Jump to content



Photo

And The Answer To Your Question Is.....


  • Please log in to reply
21 replies to this topic

#1 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 05 August 2017 - 05:03 PM

I have just finished reading about 60,000 old posts on this site. My object is use this topic to post the reviews of all of our members concerning every drug, method, technique they have tried to handle their Cymbalta withdrawal. This will include their mistakes, successes, warnings, etc. My hope is that this can be a one stop shopping for information, especially new people.

 

If any of you have ANY suggestions. something you want to add, corrections, etc. just let me know and I will add it on to the posts. Lets make this as good as we can for everyone to use.

 

Sincerely

Fishinghat.


#2 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 05 August 2017 - 05:13 PM

Nausea Vertigo Treatments

 

Recommendations - Use of ginger root or other ginger product. No withdrawal or drug interactions and all natural. Member reviews are very positive. Second choice would be Original Dramamine.
 
Dimenhydrinate/Meclizine/Garlic and others - 8/7/17
Dimenhydrinate - an antihistamine - Tell your doctor or pharmacist if you are taking other products that cause drowsiness such as opioid pain or cough relievers (such as codeine, hydrocodone), alcohol, drugs for sleep or anxiety (such as alprazolam, lorazepam, zolpidem), muscle relaxants (such as carisoprodol, cyclobenzaprine), or other antihistamines (such as cetirizine, diphenhydramine, hydroxyzine).
 
Dramamine
71 member mentions.... 62 positive, 7 no help, 2 intermittent help, 13 says causes sleepiness,
Helps with lightheadedness, jolts, dizzy spells, sleep, nausea, brain swooshes, calming, motion sickness, brain zaps, Sloshy head, and anxiety.
 
Caution - some members state that "dramamine did..." but as listed below there is a difference in ingredients and dosing for different kinds of dramamine.  Dimenhydrinate is available in 98 products approved in the USA other than dramimine so please check label ingedients before using with other products .Nearly all nausea, cold, flu, sleep aides and dizziness medicines contain antihistamines and are incompatable with each other. Check ingredient list closely.
 
Seven members admit to taking two or more of these products at the same time OR taking double doses. This has lead to comments like...
"...and chucked my guts all day"
"and afterward had stomach cramps for hours"
 
Sarah noted "Dramamine II (not the original Dramamine) contains the same active ingredient as Bonine. Some places also sell generic Meclizine and I have found it at CVS. Some very closely related drugs are buclizine, and cyclizine.
Some brand names that contain meclizine, buclizine, or orcyclizine are:
Bonine
Bonamine
Dramamine II
Marezine
Marzine
Meclicot
Medivert"
 
Will NOT contribute to Serotonin Syndrome.
 
Tips from members -
1) Careful with the Benadryl and the Dramamine together. (causes you to be sick)
Also one member warned of 'DO NOT take both NyQuil and Dramamine.... '
2) Be careful taking dramamine during the day - it knocks me out!
3) Dramamine can also be doubled up at the initial dose. It all depends on your size and what you may or may not be sensitive to.
4) Take a low dose and I don't fall asleep
5) ORIGINAL FORMULA DRAMAMINE. (NOT THE NONDROWSY, just hypes you up and makes the dizziness worse.)
6) One said it can cause nightmares.
7) One said it does not cause nightmares
8) So, I was taking this ginger gravol and it did nothing for my nausea. I started taking half of a regular gravol and its finally working
9) 2 said - the ginger gravol version does not cause sleepiness
10) if taken on a regular basis, it stops working
 
Contents:
Original Dramamine - Active Ingredient (in each tablet) Dimenhydrinate 50 mg. Inactive ingredients anhydrous lactose, colloidal silicon dioxide, croscarmellose sodium, magnesium stearate, microcrystalline cellulose.

Dramamine Motion Sickness Relief Less Drowsey Formula - Active Ingredient (in each tablet) Meclizine HCI 25 mg. Inactive Ingredients: Anhydrous Lactose, Corn Starch, Colloidal Silicon Dioxide, D&C Yellow 10 Aluminum Lake, Magnesium Stearate, Microcrystalline Cellulose.
 
Dramamine Non-Drowsy Naturals with Natural Ginger - Active ingredients - Ginger  Inactive Ingredients: Gelatin, Vegetable Magnesium Stearate, Silica
 
Dramamine All Day Less Drowsy Tab  - Meclizine 25 mg. Inactive Ingredients: Anhydrous Lactose, Corn Starch, Colloidal Silicon Dioxide, D&C Yellow 10 Aluminum Lake, Magnesium Stearate, Microcrystalline Cellulose.
 
Safety Warning
Do not give to children under 2 years of age unless directed by a doctor.
Ask a doctor before use if you have:
A breathing problem such as emphysema or chronic bronchitis.
Glaucoma.
Trouble urinating due to an enlarged prostate gland.
Ask a doctor or pharmacist before use if you are taking sedatives or tranquilizers.
When using this product:
Marked drowsiness may occur.
Avoid alcoholic drinks.
Alcohol, sedatives, and tranquilizers may increase drowsiness.
Be careful when driving a motor vehicle or operating machinery.
If pregnant or breast-feeding, ask a doctor before use.
----------------------------------------------------------------------------------------------------------
Meclizine
Taken for headaches, nausea, dizziness, brain zaps.
 
Meclizine (an antihistamine) is available in 104 products approved in the USA other than Bonine so please check label ingredients before using with other products.
 
Will NOT contribute to Serotonin Syndrome.
 
Tell your doctor about all medicines you use, and those you start or stop using during your treatment with meclizine, especially the antidepressants bupropion, duloxetine, fluoxetine, paroxetine, or sertraline.
 
Using meclizine together with DULoxetine may increase side effects such as dizziness, drowsiness, confusion, and difficulty concentrating. Some people, especially the elderly, may also experience impairment in thinking, judgment, and motor coordination. (Drugs.com)
 
15 members have used this product, 6 positive, 4 negative, 4 helps intermittantly.
2 said it makes them sleepy/groggy.
 
Common side effects include blurred vision, dry mouth, constipation, dizziness, drowsiness, headache, vomiting, or tiredness
Before using this medication, tell your doctor or pharmacist your medical history, especially of: breathing problems (such as asthma, emphysema), high pressure in the eye (glaucoma), heart problems, high blood pressure, seizures, stomach/intestine problems (such as ulcers, blockage), overactive thyroid (hyperthyroidism), difficulty urinating (for example, due to enlarged prostate), liver problems, kidney problems.
 
Bonine - Active ingredients (in each tablet) Meclizine HCI 25 mg. Inactive ingredients:
Croscarmellose sodium, crospovidone, FD&C red #40 lake, lactose, magnesium stearate, raspberry flavor, silica, sodium saccharin, stearic acid, vanilla flavor.
 
Rugby Travel Med - Meclizine HCI 25 mg and they contain the artificial sweetener Aspartame, also contains Phenylalanine 0.28 mg per tablet (can cause anxiety and nervousness in some people). Inactive ingredients aspartame, croscarmellose sodium, dextrose, FD&C Red #40 Lake, magnesium stearate, maltodextrin, microcrystalline cellulose, natural and artificial flavors, silicon dioxide, sodium sulfate, sugar, tricalcium phosphate.
 
Truck Princess commented that "I have found that taking the Rugby travel sickness med 25mg took away ALL my withdrawal symptoms for the majority. I don't get any brain zaps, dizziness, head swooshing, none of that. Also with the Rugby it's 24hrs so you only take one or two. The Rugby I took because of the nausea was so bad and just discovered it really got rid of most of the withdrawals and I didn't get the crying spells like you and others have."
 
This may partly be due to the fact it also contains Phenylalanine which other members report as helping their symptoms. See cold and flu medicine section.
 
Caution - Many of the above products contain Lactose, a concern if you are lactose intolerant. They may also contain artificial colors that may irritate the nervous system and artificial sweeteners that can irritate the stomach in some people.
------------------------------------------------------------------------------------------------------------
Ginger
Helps with nausea and stomach issues.
 
24 positive remarks and 4 negative.
 
Tips from members...
FN - ginger tea (really strong), ginger ale (old home remedy for sure), and ... candied ginger, raw ginger.
Even it sounds disgusting, eating Ginger raw is the most effective way cured my nausea in 5-10 minutes
 
AH - Ginger root works very well for nausea. I have 550mg ginger root capsules, and this has helped with a lot of the nausea and stomach upset.I'd totally recommend buying the ginger root in capsule form at the health food store. Mine was $8.99 for 100 capsules, and I will take 2-3 whenever my stomach is upset. And of course we can't forget ginger tea. It is soothing, relaxing, and will also help your stomach feel better.
ta2ed - You can try ginger root... Wont make you tired.
 
Betty - I'd recommend trying ginger ale -- not Canada Dry but the real strong stuff, sometimes labeled Jamaican ginger ale or ginger beer. It's sold in four-packs here, in the health food or imported section of the store. I've had "irritable bowel" problems for years and have found this is real medicine, with no downside I can see! It also works for nausea.
 
FN - made a "tea concoction" of turmeric and ginger
Carleeta - yippee..The ginger works. ginger ale helps me a lot too at room temperature.
Considering - Ginger is good for nausea. If you don't have any tea, make some with either grated fresh ginger or dry ginger with a little honey added. This may help.
 
Anna - I thought I would give just smelling ginger a try. I put 2-3 drops of ginger essential oil on a cotton ball and my nausea pretty much disappeared almost instantly.
 
Tria - About the nausea, some weird things help mine - ice pops, room temperature root beer soda, and oatmeal. Ginger is a good herb for nausea. I cant stand ginger tea but some people swear by it. You can also buy ginger in capsules.
 
FCB - Dr. Sanjay Gupta's turmeric tea:
Ingredients
⦁ 1 cup almond milk (I'll try coconut milk too)
⦁ 1/2 tsp turmeric
⦁ 1 tsp cinnamon
⦁ 1 tsp honey (or maple syrup)
⦁ 1/4 tsp ginger
Directions: Heat the almond milk, stir in the spices and drizzle the honey on top.
 
Latte - ginger candy for nausea - I swear by it, particularly the Gin-Gin brand
Amberd - I tried ginger tea, but it only gave me indigestion on top of it all.
 
Travelcalm Natural -
Travacalm natural contains 100mg of dried root extract that offers faster relief in conjunction with 400mg of root powder that helps sustain the soothing effect. Each tablet contains: Zingiber officinale (ginger) 500mg as root powder 400mg and dried root extract equivalent to 100mg of root powder.
 
EOTR - I am taking 'Travelcalm' Natural - costs $4.50 for 10 tablets and ......it works!
------------------------------------------------------------------------------------------------
Misc. Nausea treatments
 
Vertigoheel (Caution - read carefully)
 
Composition: Tablets: 1 tablet cont.:
Anamirta cocculus D4 210 mg; is a Southeast Asian and Indian climbing plant. Its fruit, Cocculus indicus, is the source of picrotoxin, a poisonous alkaloid with stimulant properties.)
Conium maculatum D3, (hemlock or poison hemlock) is a highly poisonous biennial herbaceous flowering plant in the carrot family Apiaceae, native to Europe and North Africa. Since no specific antidote is available, prevention is the only way to deal with the production losses caused by the plant.
Ambra grisea D6, Ambergris, Latin: ambra grisea, Old French: ambre gris), ambergrease or grey amber, is a solid, waxy, flammable substance of a dull grey or blackish colour, produced in the digestive system of sperm whales.[1] It is illegal to possess or sell in many countries)
Petroleum rectificatum D8 (purified crude oil or petroleum is distilled, diluted with sulfuric acid, and succussed. The result is a very powerful homeopathic remedy that has a wide range of uses) 30 mg each.
 
http://www.biopathic...heet.pdf       Data sheet
History of the Heel Corporation
founding father, Dr. Hans-Heinrich Reckeweg. Established in Berlin in 1936,
 
FDA violations
In 1984 BHI received letters and warnings from the Food and Drug Administration that it was in violation of FDA regulations in regards to marketing of homeopathic remedies.[1] BHI was given multiple FDA citations and fines during the 1980s and early 1990s for violation of the Compliance Policy Guidelines labelling guidelines established by the FDA in 1988. These were corrected and have not recurred,[2][3] though in August 2013 the company again agreed to dial down its health claims tied to its over-the-counter remedies and pay a $1 million class settlement to resolve accusations that it exaggerated the products’ effectiveness to consumers.[4] (Wiki)

http://edzardernst.c...n-subsidiaries/
"Homeopathic manufacturer to close North American subsidiaries"
In the USA and Canada (Heel) has been confronted with accusations through class action lawsuits.  the Heel Group decided to focus on strengthening its excellent position in South America, Central Europe and Eastern Europe and to withdraw from business activities in the USA and Canada for the time being.
Heel’s operations in both the USA and Canada will accordingly be discontinued as of August 31, 2014.

<a href="http://vincentverhey...om/node/4#Heel"data-ipb="nomediaparse" data-cke-saved-href="http://vincentverheyen.com/node/4#Heel" s"="">http://vincentverheyen.com/node/4#Heel'sfortune comes from Nazi Germany: The Quandts were rich enough to escape the Nuremberg trials
Heel's fortune comes from Nazi Germany: The Quandts were rich enough to escape the Nuremberg trials
Unfortunately, the Quandt family has had a long history of concealing the truth and lying in favor of financial profits. Not particular important regarding pseudo-science, but ever so sadly: their family and its wealth is linked to Nazi Germany, providing weapons (e.g. via their German Weapons and Munitions public limited company & their Accumulatoren Fabrik AG Berlin-Hagen (AFA) (now VARTA)) & owning ±50,000 forced and/or concentration camp slave workers, as professor of history Joachim Scholtyseck
 
http://de.wikipedia....him_Scholtyseckhttp://de.wikipedia....im_Scholtyseck| University of Bonn has, during 3 years, researched in his (> 1000 pages) study "The rise of the Quandts"13. They even signed a contract with the SS to create the concentration camp KZ-Außenlager Hannover-Stöcken (Akkumulatorenwerke) at their factory to provide slaves from the Neuengamme concentration camp, to work under conditions which the company (explicitly written) expected to murder ± 80⁄month .131415 Direct Nazi relative Sven Quandt (Stefan Quandt's brother), the only member of the family who didn't decline interviews for the German documentary "The silence of the Quandts", even advised to forget the holocoust history of the Quandts, stating it is bad for Germany to remember the holocoust:
Heel announced to cease all its activities in North America. To me, its activities seem rather continued, covered up by a mere name-change
On 23/5/2014, Heel announced to close down its business activities in the United States and Canada, supposedly due to the accusations through class action lawsuits. It also said it was negotiating with a company called MediNatura® & that the transaction wouldn't include a number of Heel's products. Actually, Heel's products have just changed their names (cf. this picture159); and thus sadly enough, the products (including some of the products which supposedly were not to be transacted) are being still sold: on 30/5/2014, MediNatura® announced to be buying Heel and selling their discontinued products under different names. First of all, I have not been able to found any account of any existence of any company named MediNatura®, as anyhow related to medical products, before 2014. Secondly, Cliff Clive
https://www.linkedin.com/in/cliffclivehttps://www.linkedin.../in/cliffclive| https://twitter.com/cliffclive https://twitter.com/cliffclivehas been the CEO & general manager of Heel in the U.S.A for many years, right up until Heel changed its name to MediNatura® in 5/2014160, which is when Cliff Clive became the founder & CEO of MediNatura®161. Thirdly, the official address of MediNatura®, is the exact same address as Heel's: in an official notice of a meeting on 10/12/2014 of the Arizona State Board of Pharmacy162, it is noted that the address of MediNatura® is 10421 Research Road SE, Albuquerque, NM 87123. Guess what's Heel's official U.S.A address? So, the company MediNatura® is actually just registered at the building where Heel has been since 2003163164, in Albuquerque, where Heel has been since 1978165. Going to Heel's American website, actually just leads you to MediNatura®'s website.166 Further more, MediNatura even sells a whole line of products which are labeled "BHI", which is actually the name of yet another company of Heel. In fact, products in this line were sold identically by Heel in the U.S. (cf. the product on the far right159). Lastly, Heel has filled 2 trademark applications for the name MediNatura®, for which (by the way) the procedures started as early as 14/2/2014, far before the so-called "negotiations" with MediNatura®:
 
Uriel - Try a homeopathic called VERTIGOHEEL it really helped me out alot i took 3 a day you just let them melt under your tongue....
 
Medical Research on Vertigoheel.
https://www.ncbi.nlm...pubmed/20852360
https://www.ncbi.nlm.../pubmed/8414621
https://www.ncbi.nlm...pubmed/15750375
------------------------------------------------------------------------------------------------------


#3 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 09 August 2017 - 10:28 AM

Increasing your GABA production and efficiency
by proper diet and supplements. -
8/10/17

Summary - Eating foods high in GABA or taking GABA supplements have little success in treating anxiety or depression because while they enter the blood system they do NOT cross the Blood/Brain Barrier. However many flavinoids have been shown to facilitate GABA activity in the brain and help with anxiety and depression.
 
Recommendations - Gaba supplements provide little if any help. A better approach would be to use flavonoids. Try focusing of eating vegetables from the lists below and/or using flavonoid supplements Flavonoid supplements are varied and there is no standard dosage so  I would recommend a good bioflavonoid (citrus based) and start ut around 10% of the dosage recommended on the package and build up from there as tolerated.
GABA is a neurotransmitter that blocks impulses between nerve cells in the. Low levels of GABA may be linked to anxiety or mood disorders like depression, epilepsy and chronic pain. Researchers suspect that GABA may boost mood or have a calming, relaxing effect on the nervous system.
http://www.livestron...e-highest-gaba/
GABA is not an essential nutrient but has been used therapeutically for anxiety, insomnia, stress and hypertension. Some prescription depressant drugs and sleeping medications act on GABA by facilitating its ability to bind to receptor sites in the brain. This produces a calming effect and can induce sleep. Taking a commercial GABA supplement is ineffective for this purpose because it is unable to penetrate the barrier surrounding the brain. This is why more powerful prescription medications are used to stimulate existing GABA in the body.

Importance -
https://www.ncbi.nlm...les/PMC3412149/
Increasing evidence points to an association between major depressive disorders (MDDs) and diverse types of GABAergic deficits. Many references
Low levels of GABA have been associated with insomnia, depression and anxiety; however, to date there are very few human studies demonstrating the anti-anxiety benefits of GABA supplementation.
Flavonoid-Rich Foods and GABA Receptors
Flavonoids are phytonutrients found in plant-based foods, tea and wine and are known to enhance GABA function.
Foods high in GABA - Cheese, kefir, miso, sauerkraut, tempeh, yogurt, soy sauce and Thai Fermented Shrimp (Kung-Som) have NOT been shown to fight anxiety or depression.
Many probiotics react to ferment foods and produce GABA but there is little evidence that these foods cross the blood brain barrier or has an effect on depression or anxiety.

A study published in 2011 in the British Journal of Pharmacology illustrates the impact flavonoids have on specific GABA receptors in the brain.

https://www.ars.usda...77Flavonoid.pdf
Detailed list of flavinoid containing foods.
General list of the Best Sources of Flavonoids
flavonols flavan-3-ols* flavones flavonones anthocyanidins
onions apples parsley oranges blueberries
apples bananas bell peppers grapefruit bananas
romaine lettuce blueberries celery lemons strawberries
tomatoes peaches apples tomatoes cherries
garbanzo beans pears oranges pears
almonds strawberries watermelon cabbage
turnip greens chili peppers cranberries
sweet potatoes cantaloupe plums
quinoa lettuce raspberries
garbanzo beans

Medical Research
https://www.ncbi.nlm...pubmed/25109791
citrus flavonoids ....including antidepressant (activity)

https://www.ncbi.nlm...pubmed/25656001
...the flavonoid fraction (F1C) with anxiolytic activity which is dose dependent, and has the ability to interact with the serotonergic system.

https://www.ncbi.nlm...pubmed/23596160
Grape powder supplementation prevents oxidative stress-induced anxiety-like behavior, memory impairment, and high blood pressure in rats.

https://www.ncbi.nlm...pubmed/24121702
Generalized anxiety disorder (GAD): efficacy of standardized Matricaria recutita (German chamomile) extract in the treatment of generalized anxiety disorder.

https://www.ncbi.nlm...pubmed/24679021
Purple grape juice as a protector against acute x-irradiation induced alterations on mobility, anxiety, and feeding behaviour in mice. This beneficial effect on short-term anxiety and mobility related activities could probably be included in the list of flavonoid bio-effects.

https://www.ncbi.nlm...pubmed/23603526
The experiments with different receptor blockers suggest an involvement of GABAergic system in the anxiolytic action of this bioflavonoid. However, this action is not seems to be mediated through serotonergic system.
https://www.ncbi.nlm...pubmed/26190180
https://www.ncbi.nlm...pubmed/25600371
https://www.ncbi.nlm...pubmed/21244373
https://www.ncbi.nlm...pubmed/25449359
These results suggest that spinosin exerts anxiolytic-like effects, and its mechanism of action appears to be modulated by GABAA and 5-HT1A (Serotonin) receptors.
https://www.ncbi.nlm...pubmed/21924247
Taken together, these data suggest that 3-OH-2'MeO6MF (a flavonoid) is an anxiolytic without sedative and myorelaxant effects acting through positive allosteric modulation of the α2β2/3γ2L and direct activation of α4β2/3δ GABA(A) receptor subtypes.

And many many more research articles show the anxiety fighting characteristics of various flavonoids.
https://www.ncbi.nlm...les/PMC4997290/
Higher flavonoid intakes may be associated with lower depression risk, particularly among older women.
https://www.ncbi.nlm...pubmed/23460966
https://www.ncbi.nlm...pubmed/24717328
https://www.ncbi.nlm...pubmed/24947870
And dozens more.

Members and foods they have consumed on the high flavinoid list.
garbanzo beans -1
NLFSS - Chickpeas (garbanzo beans), tofu, walnuts, sesame seeds, pumpkin seeds and almonds are just a few more items high on the food list that fight depression.

raspberries - 3

lettuce - 1

quinoa - 3
Anothermind - I already eat a lot of Red Quinoa (marvellous!)
Xiaojie - Red Peruvian quinoa. I thank God every day for his creating it. It is a protein-packed, vitamin and mineral-packed seed that you throw in your rice cooker and cook the same way you would cook rice (but I add a couple of tablespoons of coconut oil to it). Keeps you feeling energetic, and keeps your digestive system doing what it's meant to do, only more efficiently - so helps purge the body of crap - literally, lol. I HIGHLY recommend it eating a bowl of it every day. Sometimes I eat a bowl of it twice a day. I can tell by how good I feel after eating it that my body loves it. And it has weight loss benefits, as well. Eating lots of fresh vegetables, fish, nuts, coconut oil, and quinoa (very high in protein) daily.

sweet potatoes - 3
Lady Nancy - The sweating is a side effect of stopping the Crapalta, It messes with our hormone levels and the sudden drop in estrogen can be a cause. I found that eating sweet potatoes a couple of times a week really helped. They are a nature source of estrogen.

cantaloupe - 1

plums, cranberries, chili peppers, cabbage. peaches. romaine lettuce
None

turnip greens (Grrens in general) - 13
JDH - I put in just 20 minutes on my mini trampoline in the morning and down my fruits and greens and my days go a WAY better than when I didn't.
FCB - And I have also found eating salad greens and gourmet coleslaw mixes help
SSRI - Lots if leafy greens. ...help the zaps, but that's about it
Raphi - With no limits on the greens, I'm not hungry and was beginning to feel better.
Mendozen - Also, eat fruits and vegetables (I drank greens I got from a vitamin store). A well balanced diet truly helps with fogginess and fatigue
Tuke - friends told me about The Healing Diet. they recommend fresh pineapple, fresh greens(even cilantro and parsley), salmon, and lemon juice in tea or water whenever you can. (note - all contain flavinoids except the salmon.)

watermelon - 2
Sandlion - My husband got out the blender and made a mixture of mostly crushed ice with a tiny bit of watermelon blended in.... the ice felt so good, I was able to "drink" it down and the little bit of sugar from the watermelon gave me some energy. Second post - I woke up feeling nauseous again this morning so the first thing my husband did was make the watermelon drink... so far, so good....

strawberries - 4
JK61 - I use 2 Tablespoons of the Tart Cherry juice in my smoothie. I add a vegetable protein powder and strawberries and half of a banana. I just use water, some people use apple juice or other juices. When my depression was really bad and I couldn't eat I would have two of these a day.

almonds - 11
TM - First, foods rich in tyrosine are thought to stimulate the production of dopamine. These foods include bananas, almonds, avocados, low-fat dairy and meats, sesame seeds, and pumpkin seeds.
FN - then I started craving eggs....and prunes and almonds....
LadyNancy - but I am allergic to tree nuts with almonds and walnuts being deadly (I carry an Epi-pen because of it).
NoLonger - Foods highest in the tryptophan ratio are tofu, almonds and sesame seeds, sesame seeds being the highest. Chickpeas (garbanzo beans), tofu, walnuts, sesame seeds, pumpkin seeds and almonds are just a few more items high on the food list that fight depression.
KK - hopefully along with some dietary changes like adding lots of bananas and almonds to give you a quick boost in levels. This can apparently be accomplished by increasing the foods that raise dopamine levels, such as almonds, avocados, bananas, dairy products, lima beans, pumpkin seeds, and sesame seeds, and removing those things from my diet that cause dopamine levels to drop... such as alcohol, caffine, sugar, saturated fats, and refined foods.
Jeannie - I've been eating foods that support acetylcholine production such as peanuts, almonds, spinach, wheat germ, and whole eggs. Beef liver is also a good source of choline but who wants to eat that!
IAA - Food sources of dopamine increasing tyrosine include almonds, avocados, bananas, dairy products, lima beans, pumpkin seeds, and sesame seeds.
Michellah - I am also eating almonds and soup. The potato at night helps the body make its own serotonin and I highly encourage anyone going off to try the potato at night.
SarahJ - Also, raw almonds (without salt) are good filling food.

oranges - (Icluding the mention of citrus) - 9
WTKF - I drink a lot of water, take fish oil and eat protein and fruits/veggies without much carbs (apples, oranges, soups). The diet stuff seems to help.
LadyNancy - As far as the fruit goes you are better off with citrus like oranges or tropical like pineapple as long as your stomach can handle it. ...citrus fruit (oranges, lemons, limes) help the brain make GABA (the feel good neurotransmitter).
I am Who I Am - Poppy seeds, dates and citrus fruits are recommended as good remedies for vertigo.
tomatoes - 4
Rebecca - Two to three simple bananas and kiwi's, an egg-sandwich, 2-3 glasses of milk, a few tomatoes and an avocado a day provides many of the essential vitamins, (trace)minerals & amino acids you need on a daily base.
Jane -Eggs with tomatoes seems to be the best bet for me, followed off with a banana or applesauce.

apples - 8
WTKF - I drink a lot of water, take fish oil and eat protein and fruits/veggies without much carbs (apples, oranges, soups). The diet stuff seems to help.
CCOD - For instance, apples cause me to feel nauseated now.
MC - here are a couple of remedies that has helped my nausea in the past . Mint tea, peppermint tea, green apples and life saver 'wint-o-green' flavor.

cherries - 4
GK61 - I put the Tart Cherry in my morning smoothie for help with pain. It's been very beneficial for me.
Ctina - This week I had a strong craving for black cherries, due to my pregnancy. I discovered that they have an ingredient that helps with sleep patterns, Muscluler, and here is the kicker, skeletal pain!! I felt fantastic last night after drinking two glasses of cherrie soda. Which only after I drank it, I decided to look it up and discovered its benefits. It has meletonin to calm and help you sleep along with a natural pain reliever, called Anthocyanins. Many of us are suffering with pain and restlessness.
VV - In addition to the rhodiola, I increased intake of foods containing tryptophan. Tryptophan converts to 5-HTP which converts into serotonin. Thereby increasing my intake of tryptophan, increased my serotonin levels.

VV - Foods that help:
oatmeal
peanut butter
eggs
chicken
dark cherries
dark chocolate
yogurt
turkey
and many others if you search the web you can find them.

lemons - 2

celery - 3
Kitty - I also got three chinese herbal meds from the doc. Boswellia complex, Ligaplex 2, and Evergreen neck and shoulder chronic. Btw, all these meds are natural esp, Boswellia complex (main ingredients; turmeric powder, ginger, and celery seeds/ roots)

blueberries - 6
PPT - I also bought fresh blueberries: This lessened all my symptoms and gave me a little energy (who knows why)

bananas
BRZ -as for the nausea, since that is a direct symptom of anxiety - getting that under control would help, in the meantime, bananas work well for me.
TM - First, foods rich in tyrosine are thought to stimulate the production of dopamine. These foods include bananas, almonds, avocados, low-fat dairy and meats, sesame seeds, and pumpkin seeds.
aMarie - try b vitamins, multivitamins eggs, bananas, fish oils and red bull - this all helped greatly with my withdrawals.
LadyNancy -The bananas are good for when you have been throwing up sick or have bad diarhea or just can't eat much.
Anxiety Beating Treat
Banana chocolate dessert or spread -
2 very ripe bananas
1/8 to 1/4 cup unsweetened cocoa powder
Mash bananas then beat in cocoa until completely mixed and serve.
Irritableme - This is what I've taken to help feel a bit more human (thanks to this site): Res-Q fish oil capsules, vitamin B-12, multi-vitamin, lots of water, lots of healthy food (flaxseed ground up, Odwalla vitamin B juice, apples, bananas, salmon, fresh veges), lessened my caffeine intake, Claritin-D. I was already taking Vitamin D and magnesium before I stopped Cymbalta.
JWBH - Try to eat a bite of banana if you can. Bananas are a great source of potassium and serotonin which your brain is severely lacking after you quit Cymbalta.
Chimera - bananas are great little powerhouses when you feel weak!
Jenni - Rice cakes, bananas, nuts are working better for me than when I was eating cakes all the time - no surprise there! Also, try a regular anti-nausea medicine from the drugstore.
MixiePixie - Also, eating bananas and eggs, has helped me- which others on this site recommended.
MS -I swear to you that between a little exercise, a standard multi-vitamin that I was taking the whole time anyway, the protein whey, and a few extra bananas in my diet, I am kicking the Cymbalta withdrawals butt!
Lori - Since weaning off the Cymbalta, I have not had as much a craving for bananas, but I seem to have pain in my joints, sore muscles, and my back ITCHES!! I seem to be weaker physically, than what I used to be.

bell peppers - 1

grapefruit - (also see 'citrus' above) - 3
FH - Buspirone (Buspar) is a seratonin 5-HT1A receptor partial agonist and a dopamine antagonist at the D2 receptor, D3 receptor and D4 receptors. It functions as a weak anti-anxiety medication similar to diazepam in strength (a weak benzo). DO NOT take with grapefruit or grapefruit juice.
Member warnings
I think we would have to know more, like how much grapefruit juice has the potential to increase the levels in your system, depending on dose, other medications, etc. (False)
You aren't supposed to drink grapefruit juice while taking Cymbalta, because it changes how your body metabolizes it and increases the risk of Serotonin Syndrome, (False)
Just read that one should not drink grapefruit juice while taking Zoloft...bad interaction (True) See ...https://www.ncbi.nlm...pubmed/10890261for details.
Autimom - Did you know that GRAPEFRUIT products can cause an interaction with the following medications: Buspirone (BuSpar), Antiarrhythmia - Amiodarone (Cordarone), Antidepressant - Sertraline (Zoloft),
Antihistamine - Fexofenadine (Allegra),. Anti-seizure - Carbamazepine (Carbatrol, Tegretol), Calcium channel blocker (BP medication) - Nifedipine (Procardia), nimodipine (Nimotop), nisoldipine (Sular), Statin - Simvastatin (Zocor), lovastatin (Mevacor), atorvastatin (true)
rebecca - Avoid Grapefruit Juice. Grapefruit juice is an inhibitor of the cytochrome P-450 enzymes. These enzymes are known to metabolise (break down) (SSRI) antidepressants in the liver. Drinking grapefruit juice whilst you are taking an (SSRI) antidepressant can create a serious toxic reaction, because the (SSRI) antidepressant will build to toxic levels in the bloodstream! (only certain antidepressants) (true)
Note - Because both CYP1A2 and CYP2D6 are responsible for duloxetine metabolism, potential exists for clinically important drug interactions when duloxetine is concurrently administered with CYP1A2 inhibitors, CYP2D6 inhibitors, and CYP2D6 substrates.1 (See Interactions.)( Drugs.com) while cytochrome P – 450 3A4 substrates, has also been implicated to be inhibited by grapefruit juice. There is NO medical research to show that grapefruit juice interacts with Cymbalta. This is confirmed by the FDA ...
See https://www.fda.gov/...g/ucm093664.htm
https://www.ncbi.nlm...pubmed/10851844
Several actual examples on interactions with selective serotonin re-uptake inhibitors, HMG-CoA reductase inhibitors, mibefradil, sildenafil, protease inhibitors and with grapefruit juice are discussed.

parsley - 2
Chrism - So its been a lot of parsley, carrots, and especially broccoli. No luck.
onions (red) - 3

tea - A great many and will be addressed by types of tea tried.
chamomile flowers (tea) - 17
FN - chamomile tea helps some folks with the gastro issues (I wasn't one of them) but...helped me (with sleep) chamomile and valerian tea
FH - "There is a new sleep aide out called Somnapure. It is flying off the shelfs and being hailed as a wonder cure for insomnia. BUT.....As you can see the ingredients are listed below;

Supplement Facts
Serving Size: 2 Tablets
Servings Per Container: 30
Valerian (Valeriana Officinalis) Root Extract 500 mg*
Lemon Balm Extract Leaf 300 mg*
L Theonine 200 mg*
Hops Extract Strobile 120 mg*
Chamomile Flower Extract 50 mg*
Passion Flower Extract Aerial 50 mg*
Melatonin 3 mg*
* Daily Value not established.

All of these ingredients have strong drug interactions and/or side effects except for melatonin. There has been a rash of people landing in the hospital for reactions to this med, especially if they are on antidepressants. Use with caution."
Xanazul - *Lots of infusions (valerian, chamomile, limeflower...) all the day long, specially before going to bed.
TXC - Chamomile tea helps a little
Bahara - So yogurt, chamomile tea, orange juice helped me a lot.
CE - Chamomile tea seems to help the nausea and calms down any jitters I have. I practically live on it now.
Abbyg - The other thing that really helped was Chamomile tea.
Kate - Organic chamomile tea (especially helpful if you are prone to naseua or greater anxiety during the withdrawals)
GracesG - Also, the Chamomile Tea is helping me get to sleep.
Schmb - Chamomile Tea, or Sleepytime tea with Valerian (this helps me to sleep. I finally acquired a taste for chamomile tea, and that is soothing.
feverfew - 1
Tria - The herb Feverfew was given to me by a doctor but I was allergic to it.
Wiki - Long-term use of feverfew followed by abrupt discontinuation may induce a withdrawal syndrome featuring reb ound headaches and muscle and joint pains. Feverfew can cause allergic reactions, including contact dermatitis. Other side effects have included gastrointestinal upset such as nausea, vomiting, abdominal pain, diarrhea, and flatulence. When the herb is chewed or taken orally it can cause mouth ulcer and swelling and numbness of the mouth. Feverfew should not be taken by pregnant women. It may interact with blood thinners and increase the risk of bleeding, and may also interact with a variety of medications metabolized by the liver.
linden flowers - 2
mirmca - I did not try the apple vinegar, but I drank Linden Tea to calm my nerves at night so I could fall asleep.
cookie - Linden tea, as any other natural alternative brings very mild relief to anxiety.
passionflower - 6
LadyNancy - If you don't take any OTC sleeping aids you can also try some lemon balm or passionflower tea made quite strong at night. It helps relax the muscles which eases the pressure in the head. So far I have found that Lemon Balm, Passionflower and omega3 are very good. For nervousness, try Passionflower 2ml up to 3 times a day.
Mit90 - I had a couple of bad days when i got to 30 because i did the last drop a lttle fast but my naturopath gave me some passionflower which helped.
Freeme2 - The kava kava, passionflower, and Gaba really help keep me super calm.
cocoa (unsweetened dark cocoa only) -
BRZ - my new anti anxiety drug is Lindt's 90% cocoa chocolate
LadyNancy -
Anxiety Beating Treat
Banana chocolate dessert or spread -
2 very ripe bananas
1/8 to 1/4 cup unsweetened cocoa powder
Mash bananas then beat in cocoa until completely mixed and serve.
 

Definitely worth a try for most. Lemon balm is another good suggestion but it does contain a low concentration of beta-blockers. Beta blockers like atenolol are often used to help with anxiety and heart palpitations. One of their side effects is to lower blood pressure (this is part of their calming effect). The effect is so small that it isn't an issue for most unless they are already on BP medicine.

LNancy -What I did find helpful was Lemon Balm Tea which I can drink at any time of the day and it helps. When I have it at night with the meds that relax me I am sure to sleep though so if you are going to try it then do so in the evening in case it makes you sleepy.


wine - 22 - Alcohol is dangerous when taking Cymbalta but small amounts may help GABA production after coming off Cymbalta.
FH - when they (cramps) get real bad she can take about 6 or 7 tablespoons of wine and in 15 minutes they are gone.
TFL - I am having wine at the moment cuz it helps!
Carletta - but should have stayed on one glass of wine, the other half had me feeling fidgety and crying.
Wagtail - I can feel the effects today & my balance is very bad so I have learned a lesson , NO wine whilst suffering w/d . I find that when I drink wine the side effects are worse
DonnaP - Be careful with the amount of wine tho. I think it's ok to have some wine to take the edge off,
Zappalta - I am 80% better -I do find if I get overtired or have a glass of wine I have some symptoms return-so no wine when i dine out for now.
Zazzed - slight buzzing had a glass of wine it went away.... go figure
LazyDaisey - Last night the anxiety lifted at about 8pm. I had 2 glasses of wine...not usually recommended, but I also watched a few funny panel shows I love so I was actually in great form. It was lovely to feel happy.
CV - There is nothing you can do (I found that a couple of glasses of red wine in the evening made a big and positive impact - which is ironic because one of the main reasons I came off Cymbalta was the weird increase in my cravings for alcohol, which turned me from a mild social imbiber into a hopeless drunk
Shaun - -a glass of wine every couple nights has helped me a lot
HZN - I only drink a small glass of wine occasionally. On March 19 I became so sick with nausea that I thougt 4 ounces might help. WRONG! It made me feel so much WORSE!
Drugfree - Alcohol is a definite no-no. I had a glass of wine a few days ago and had a horrible sleep followed by a full day of feeling hung over. One glass of wine should not make me hung over.
Jen - Someone on this board recommended red wine in the evening ... and absolute Godsend. The red wine took away the symptoms completely and helped me get to sleep.
Flavinoid supplements
...a typical person should consume 20 to 100 grams of flavonoids each day. Other sources say 250 to 750 milligrams per day (0.25 to 0.75 grams per day). It is recommended to start dosage low and build slowly until you are comfortable. As of this date NO medical research has been done to determine the daily requirement for flavonoid intake. There are over 4000 flavonoids that have been identified and each act at slightly different doses. Bioflavonooids (from citrus sources) help to facilitate Vitamin C usage but some are sensitive to them (1 member) and heartpounding, skip beats and other cardiac arrhythmias may occur. No studies have been done yet that determine which flavonoids work best for anxiety or depression.
Gaba Supplements
The only way to deliver GABA effectively is to circumvent the blood-brain barrier. Indeed, there are a small, limited number of over-the-counter supplements that are derivatives of GABA, such as phenibut and picamilon combines niacin and GABA and crosses the blood–brain barrier as a prodrug that later hydrolyzes into GABA and niacin.
Phenibut
There are numerous reports of withdrawal symptoms on Internet forums and blogs including "nervousness and shakiness, psychomotor agitation, feeling easily annoyed and irritated, fatigue, poor appetite, heart pounding and racing, nausea, insomnia, and feeling tense and keyed up", consistent with its GABAB agonist properties. There has been no systematic study of this problem. Very limited data to show it can be both anti-anxiety and antidepressant in nature.
http://www.ncbi.nlm....pubmed/23391959
http://www.ncbi.nlm....pubmed/21476277
http://www.ncbi.nlm....pubmed/20841974
http://www.ncbi.nlm....pubmed/19899708
http://www.ncbi.nlm....pubmed/19334514
http://www.ncbi.nlm....pubmed/18607733

Picamilon
Picamilon is able to cross the blood–brain barrier and then is hydrolyzed into GABA and niacin. The released GABA in theory would activate GABA receptors potentially producing an anxiolytic response. The second released component, niacin acts as a strong vasodilator, which might be useful for the treatment of migraine headaches. Very limited data to show it can be both anti-anxiety and antidepressant in nature.
Reported side effects include, but are not limited to, lightheadedness and decrease in blood pressure.
Phemibut has been researched more completely than picamilon. Neither are to be taken with benzos,
http://www.ncbi.nlm....pubmed/14558352
http://www.ncbi.nlm..../pubmed/2736292
Member comments on taking Gaba supplements...
pag - The doc increased my GABA intake
Turbolag - I take GABA, made by now. but it's been 1 a day. The instructions say 2-3 capsules daily. So I guess I could try going to 2?
1 capsule has 500mg of GABA and 2mg of vitamin B-6.
AKA -By the way, I'm taking 400mg of SAM-e in the morning and 500 of GABA once in the morning and once at night. I've been feeling pretty good mood wise for the last two weeks on this combination. My persistent issue is sleep disturbances.
FH - both SAM-e and GABA can cause sleep disturbances including constant dreaming, erratic sleep and disturbing dreams.
FN - Caution -Aspartame causes "The ATP stores [adenosine triphosphate] in the cells are depleted, indicating that low concentrations of glucose are present in the cells, and this in turn will indirectly decrease the synthesis of acetylcholine, glutamate and GABA (gamma-aminobutyric acid)."
Note - Indicates one should decrease the use of aspartame during withdrawal.
Flossy - Apparently xanax depletes your natural gaba. The gaba is actually helping a lot! I am so angry and agitated at the moment due to Cymbalta withdrawal and gaba is calming me a lot.
Note as mentioned above, benzos compete with gaba for the same receptors it does not deplete the gaba in your brain.
tt2k - They specialize in 5 htp, GABA, and other amino acids that totally help your body regulate and produce the chemicals your body needs to fight anxiety and depression. TOTALLY WAS A BLESSING!!!
Cez - The GABA acts as a balancer of other chemical processes in the brain and helps to reduce anxiety and induces relaxation and sleep. It was suggested taking 250 mg mid afternoon and late evening and working up if needed. TAKE THE FIRST DOSE AT HOME IN CASE IT MAKES YOU TOO SLEEPY TO DRIVE!! I only found 750 mg in the local GNC. I am splitting the capsules to lower the dosage until my mail order lower doses come.
phtech - How it works: Gaba is an inhibitory neurotransmitter that slows activity in th ebrain and makes it easier to fall asleep. How to use:Take 500mg to 1000 mg one hour before bedtime if you have trouble getting to sleep. IF your problem is that you wake in the middle of the night and cant go back to sleep, then take it then. Do not exceed recommended doses on the package. Do this for two weeks. If it doesn't help, talk to your doctor. Caution: combining GABA with prescription or over-the counter sleep aids can cause excessive sedation."
Cam - GABA - 250 mg when I'm feeling restless (helps your neurotransmitters kick in to relax,
GABA calm - 1 member
Contains magnesium, GABA, glycine, n-acetyl l-tyrosine and taurine also sorbitol, mannitol, stearic acid, modified cellulose gum, natural orange flavor, and magnesium stearate.

Gaba Plus - 1 member
maccacat - He started taking a supplement called Gaba Plus and told me he feels a difference.
Ingredients: GABA, glutamine, passionflower aerial parts, taurine and spirulina.

https://www.cymbalta...-advice-please/
Includes a detailed discussion on Gaba

Medicines that react with the Gaba receptors....
See ... https://en.wikipedia...eceptor_agonistAgonists which stimulate the gaba receptors.
and https://en.wikipedia...ptor_antagonistAntagonists which inhibit the gaba receptors.
FN - Trazadone works on the GABA receptors....
Note - to some extent bit it also reacts with over 20 other receptors.

See - https://www.ncbi.nlm...pubmed/15610924
Both klonopin and baclofen work on the GABA receptors Wiki

Drug Interactions
https://link.springe...?no-access=true

Not involved with Serotonin Syndrome
 
Vitamin C
https://www.ncbi.nlm...les/PMC2649700/
Ascorbate is proposed as a neuromodulator (effects the performance of other neurons) of glutamatergic, dopaminergic, cholinergic and GABAergic transmission and related behaviors.

Antihistamines
The H2 antihistamine receptor is found throughout the hypothalamus, thalamus and central nervous system including neurons (nerve cells). It stimulates formation of cAMP (a compound used to transport energy), protein formation, muscle contraction, blood pressure and much more. The receptor is found in neurons and when stimulated it acts to inhibit other neurotransmitter formation including dopamine, GABA, acetylcholine, noradrenaline, histamine and serotonin.

Antidepressants -
http://www.ncbi.nlm....pubmed/15451391
In comparison with saline, citalopram (Celexa) produced a mean increase of 35% in relative brain GABA concentration in the occipital cortex.

https://www.ncbi.nlm...pubmed/25082715
Zolpidem (Ambien) increases GABA in depressed volunteers maintained on SSRIs.

https://www.ncbi.nlm...pubmed/11925309
A significant increase in occipital cortex GABA concentrations was seen after SSRI treatment.

Articles On How Anti-Depressants Effect Gaba
http://www.cymbaltaw...nts-effect-gaba

Other Supplements that efffect Gaba
Details on these supplements will be given in another section.
Thiamine (Vitamin B1) is used in the biosynthesis of the neurotransmitters acetylcholine and gamma aminobutyric acid (GABA). Humans must obtain it from their diet. Thiamine deficiency has a potentially fatal outcome if it remains untreated. There are no reports available of adverse effects from consumption of excess thiamine by ingestion of food and supplements. Thiamine increases the flow of glutamate into the cells for use in neurotransmitter formation. Wiki
Note - Use of thiamine supplements may increase gaba concentrations in the brain but it may also increase acetylcholine. This may account for the variety of responses by members.

No research found to indicate Thiamine is anxiolytic.
B6 (pyridoxine) is involved in many aspects of macronutrient metabolism, neurotransmitter synthesis, histamine synthesis, hemoglobin synthesis and function, and gene expression. It is a factor in the biosynthesis of five important neurotransmitters: serotonin, dopamine, epinephrine, norepinephrine, and gamma-aminobutyric acid (GABA).
https://www.ncbi.nlm...pubmed/10746516
50 mg B6 with Mg
https://www.ncbi.nlm...pubmed/15554143
Magne-B6 (a magnesium lactate/pyridoxine combination), effective. 14 days to start.
Antihistamines
The H2 antihistamine receptor is found throughout the hypothalamus, thalamus and central nervous system including neurons (nerve cells). It stimulates formation of cAMP (a compound used to transport energy), protein formation, muscle contraction, blood pressure and much more. The receptor is found in neurons and when stimulated it acts to inhibit other neurotransmitter formation including dopamine, GABA, acetylcholine, noradrenaline, histamine and serotonin.

Benzodiazipines
https://www.ncbi.nlm...les/PMC2943829/
Based on collective findings in this benzodiazepine withdrawal-anxiety model, we propose a functional model illustrating the changes in glutamate receptor populations at excitatory synapses during benzodiazepine withdrawal.
(Physically alters GABA receptor shape and function during withdrawal.)
http://www.ncbi.nlm....les/PMC3494928/
Chronic BZ treatment results in allosteric uncoupling of the GABA and BZ binding sites, suggesting changes in receptor subunit composition and/or receptor function (reviewed in ref. 7). Chronic dosing of animals with BZ leads to a reduction in GABAAR synaptic inhibition (8\l "–10) and produces diverse changes in GABAAR transcripts across the brain (7). Direct comparison and interpretation of these and other studies assessing mRNA levels has been challenging due to differences in treatment paradigm (time and dose), brain regions assessed, and the BZ ligand used. Radioligand binding studies have reported mixed results, ranging from decreases to no change in CNS BZ binding sites, likely due to methodological limitations in assessing subtype-specific GABAAR changes.
(Multiple references to changes in the receptors)
Benzodiazepines enhance the effect of the GABA at the GABAAa receptor. Wiki
During withdrawal, fluoroquinolone-based antibiotics are best avoided if possible; they displace benzodiazepines from their binding site and reduce GABA function and, thus, may aggravate withdrawal symptoms.

L-theanine
L-theanine is an amino acid precursor to glutamate (involved in the synthesis of GABA) and glutamine. It can cross the blood brain barrier. It is only produced by plants and fungi and a component in some teas. It inhibits glutamine transporters and glutamate transporters, and thus blocks the reuptake of glutamine and glutamate. Theanine increases serotonin, dopamine, GABA, and glycine levels in various areas of the brain. Caution – Most plants that contain L-theanine also contain caffeine and it can be a significant contaminant in L-theanine supplements. It is synthesized from glutamate using the enzyme glutamate decarboxylase and pyridoxal phosphate (which is the active form of vitamin B6) as a cofactor. This process converts glutamate, the principal excitatory neurotransmitter, into the principal inhibitory neurotransmitter (GABA).
http://en.wikipedia.org/wiki/Theanine

https://www.ncbi.nlm...pubmed/21208586
Effective, 400 mg/day
https://www.ncbi.nlm...pubmed/15378679
Not effective on anxiety, 200 mg/day
https://www.ncbi.nlm...les/PMC4137547/
Used to treat PTSD. It was successful in treating 8 gene problems associated with PSTD in the hippocampus and amygdala.

#4 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 14 August 2017 - 10:12 AM

                                                         Increasing production of Endorphins

When you are low in endorphins, you are more likely to feel anxious, depressed, stressed out, and unable to enjoy life or experience joy.

https://en.wikipedia...wiki/Endorphins
Endorphins are endogenous opioid neuropeptides and peptide hormones in humans and other animals. They are produced by the central nervous system and the pituitary gland. The principal function of endorphins is to inhibit the transmission of pain signals; they may also produce a feeling of euphoria (pleasure,happiness) very similar to that produced by other opioids.

How to increase endorphon levels

1. Sniff some vanilla or lavender - Vanilla causes an increase in production of endorphins. This is wht it can help so many with anxiety. The endorphins released when inhaling lavender creates a calming effect that may even enhance sleep and relieve depression.

https://www.ncbi.nlm...les/PMC4325408/
http://www.sciencedi...221169115001033
Ward, A., & Ward, K. (2006). U.S. Patent Application 11/609,330.

Vanilla Oil - Comments from Members

Plzhelp - i just recently learned that 'vanilla' is now something i am currently allergic to (i get headaches).
Lavender Oil - Members 12 positive and 1 negative comment.

SCL - I also have a sleep blend of Serenity, lavender, sandalwood, and bergamot. The calming blend even helped me with a headache without meds!

Gail - What helps me is bubble bath with lavender essential oil.

CurlyKate - The tips on bathing aren't working, my skin feels so tingly and creepy crawly that even my hair and clothing are painful...lavender and any other smells are triggering migraines...lost all appetite...can't sleep...this really sucks!

Gene - I agree 100% with the lavender scent, amazing how calming it is

Warning - Many essential oils are toxic to the liver and may collect there. Especially if taken orally or applied on the skin in large quantities or frequently.

The oils listed underneath are banned (FDA) and can cause toxicity if taken internally as well as dermally (eg. in a massage blend).
⦁ Almond butter
⦁ Boldo leaf
⦁ Calamus
⦁ Camphor
⦁ Horseradish
⦁ Jaborandi leaf
⦁ Mugwort
⦁ Mustard
⦁ Nightshade
⦁ Pennyoyal (both European and North American)
⦁ Rue
⦁ Sassafras
⦁ Savin
⦁ Southernwood
⦁ Stinging nettles
⦁ Tansy
⦁ Thuja
⦁ Wintergreen
⦁ Wormseed
⦁ Wormwood

http://essentialoils.../toxic-oils.htmgives details on each of these oils.
Medical research on DERMAL toxicity of essential oils.
https://www.ncbi.nlm...les/PMC3546250/
https://www.ncbi.nlm...pubmed/23663182
https://www.ncbi.nlm...pubmed/15771186
https://www.ncbi.nlm...pubmed/16324777
https://www.ncbi.nlm...pubmed/25272759
About lemon, ginger and clove toxicity.

https://www.ncbi.nlm...pubmed/15895251
Recent growth in aromatherapy sales has been accompanied by an unfortunate increase in accidental poisoning from these products. Clove oil warrants special attention.

2. take ginseng (red ginseng preferably)

https://www.ncbi.nlm...pubmed/16450289
http://muskrat.middl...ch/ginseng.html

Members - 6
Butterflygt - Combining that with breathing techniques, drinking lots of water and even green tea with ginseng and lemon it made everything bearable.

3. Exercise

https://www.ncbi.nlm...pubmed/18604371
Overtraining (OT) is a complex and multifactorial sport phenomenon, and there is no independent marker that can diagnose OT. The main stimulus for beta-end(1-31) secretion is to exercise because its secretion is volume/intensity dependent for both aerobic and anaerobic exercise. Excess training, however, may reduce beta-end(1-31) concentrations, thus altering its beneficial effects. Therefore, beta-end(1-31) could be used as an additional OT marker, mainly because its effects are strongly related to OT symptoms.

https://www.ncbi.nlm.../pubmed/1553453
https://www.ncbi.nlm.../pubmed/6091217
https://www.ncbi.nlm.../pubmed/9257407
and many more

As indicated by the first research article, the degree of exercise determines the quantities of endorphins. As many of our members related that light to moderate activities often made them feel better but heavy exercise often brought on an increase in withdrawal symptoms. Stretching also releases endorphins.

4. laughter

5. sex

6. chocolate (unsweetened cocoa) - One of the more unique neurotransmitters released by chocolate is phenylethylamine. This so called "chocolate amphetamine" causes endorphin levels to rise significantly.

https://www.ncbi.nlm.../pubmed/1805284
http://www.sciencedi...16503270600084X
https://www.elsevier...about-chocolate
and more.

Members on Cocoa - 4. all positive.

BRZ - my new anti anxiety drug is Lindt's 90% cocoa chocolate

Members on Chocolate - 18 comments, 6 mention dark unsweetened chocolate, and 4 negative comments about a sugar rush followed by a crash.

FN - for example, Lindt makes choco bars in different % ... the darkest is 90% chocolate ... bitter, but I've gotten to love it ... big boost.

Boot2 - i found if i combined chocolate (i am using unsweetened health food store kind now) and valerian- it feels like i am almost normal again...thought i;d pass that along.

7. music

8. Eat something spicy

Capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide) is a naturally occurring alkaloid derived from plants of the genus Capsicum, better known as chili pepper fruit. It is a member of the vanilloid family of compounds (e.g., vanillin from vanilla, eugenol from bay leaves, cloves, and zingerone from ginger) (Hayman and Kam, 2008).

https://www.research...ions_in_the_rat
http://www.phytochem...s/capsaicin.php
https://www.ncbi.nlm.../pubmed/2944026
http://www.rspublica.../april13/54.pdf
and many more articles.

9. Eat your very favorite food.

10. Meditation - 49 members tried it, 48 positive reviews and 1 negative review.

Meditation has been shown to in crease the production of endorphins.

https://www.ncbi.nlm.../pubmed/7669835
https://www.ncbi.nlm.../pubmed/9748098
Harte JL, Eifert GH, Smith R. The effects of running and meditation on beta-endorphin, corticotropin-releasing hormone and cortisol in plasma, and on mood. Biol Psychol. 1995;40:251–65. [PubMed]
Yadav RK, Magan D, Mehta N, Sharma R, Mahapatra SC. Efficacy of a short-term yoga-based lifestyle intervention in reducing stress and inflammation: preliminary results. J Altern Complement Med. 2012;18:662–7. [PubMed]
And more.

Member tips and comments

VanEttan - I've found drug-free methods like meditation that help a GREAT deal most of the time but like today, when I'm in panic mode to that extent,

CCod - Meditate daily for 20 minutes/day minimum. I use the Insight Timer app on my iPad or the Calm app. Use the Calm app if you have never tried meditation. Calm is really great if you have never meditated because she starts out with beginner instructions and short meditations that last 10minutes. It WORKS every single time. For headaches, anxiety, extreme anxiety, and yesterday, nausea got better. It is not religious or dogmatic; it's. Breathing.

Farkle - I gotta share with all here that the trauma based meditation approach is incredibly helpful as a coping mechanism for times like this,

FH - Meditation does help but only to a point. Once the anxiety gets too bad it becomes overwhelming.

Uriel - Just wondering if you all went cold turkey or did the weaning off slowly thing. It may sound bizarre but I have been doing meditation for 15 min a day to a meditation cd and its pretty amazing how the breathing calms your whole system.

Butterfly - The name of the app is "Relieve Depression Hypnosis-Guided meditation and Mental Health". There is a few different ones on the app store you can try and they are free, I really liked this one.

TM - I spent a few months listening to guided Mindfulness Meditation sessions at bedtime, and found it useful for winding down and falling asleep. You can find them on YouTube, on CD's, and elsewhere on the net.

considering - I think meditation has helped me deal with bouts of low grade depression that I've experienced in the last seven years since I've been on Cymbalta. So I would highly recommend it to anyone. But I recommend that you have a teacher, even if it's meditation CDs of teachings from Sharon Saltzberg or Pema Chodron.

Tinajuli - Somehow I have an anti-reaction when I think of relaxing methods like meditation and yoga. I tried them so much when I had that real depression and they didn't help, and I was despaired because they didn't help.

Karen - The guided meditation takes my anxiety down a lot. It might not be for you, but it really helped me
Check out this site: http://www.30minutem...meditation.html

Shanna - Go to http://www.self-compassion.org(my psychologist recommended this resource). Download the 'Loving Kindness / Self-Compassion' meditation and the 'Soften, Soothe, Allow' meditation - they are free and they are a great way to start cutting yourself a bit of slack and help you feel a bit more on top of yourself.

TXc - I also think meditation is helpful. There are some guided meditations you can download that are encouraging and reinforce the strength you have and can tap into to get through this. It's also nice when my senses are overly sensitive to shut down the noise, stay still, and focus on healing.

TBS - I'd also recommend a cd set by Buddhist teacher Jack Kornfield (Not to be confused with Jack Canfield!!!) called The Inner Art of Meditation. It's a workshop he ran with talks and short meditations and probably my favorite of all time.

Imdone - Meditation and visualization are powerful tools. I would recommend that everyone here practice visualization daily.

Zombie - I replaced the Cymbalta with Autogenics and Guided Meditations (not exotic meditation). My Pain Clinic has a psychologist who started me on Autogenics. I now do them daily. For guided meditations, I like this one: Susie Mantrell's Your Present: A Half-Hour of Peace. If you have access to a large library system, you will find many audio CDs on all of this so you can preview "programs" before buying CDs. Also, there are samples or mini-examples on youtube.

Chrism - And for me, meditation focused on breathing helps immensely, but that is not a skill you can pick up right away.

11. Increased exposure to sunlight.

https://www.ncbi.nlm...pubmed/24949966
https://www.ncbi.nlm...pubmed/26774381
https://www.ncbi.nlm...pubmed/16635689
https://www.ncbi.nlm...les/PMC2290997/
and more

There are numerous comments from members concerning getting enough sunlight each day. About half of the posts are in reference to the Vit D3 deficiency that member is suffering from and the rest are just general comments that sunlight is good for you especially if you have depression.

12. Certain touchs (hugs, massages...etc)

6 members mentioned messages in relation to their withdrawal. 5 positive. Many others got routine massages for their fibro and frequently mentioned how relaxed they were afterward.

TFL - Today was massage and am feeling better.

Paul - I ended up going to a spa and massage resort yesterday with the wife - didnt really find it relaxing at all!

13. Acupuncture

https://www.ncbi.nlm...pubmed/22073885
https://www.ncbi.nlm...pubmed/22073888
https://www.ncbi.nlm...pubmed/24215920
https://www.ncbi.nlm...pubmed/26896946
https://www.ncbi.nlm...pubmed/25595195
https://www.ncbi.nlm.../pubmed/7455665
and more

Member comments and tips - 15 reviews 14 positive.

FH - Many of my friends and family members have had acupuncture over the years. I think it is a great tool BUT there are a lot more idiots doing acupuncture than experts. In fact my family has only found one so far in the states that new what he was doing (I am sure there are others though).

Traceyish - I've been trying acupuncture, and a host of natural remedies but nothing is working.

GMI - I found a lot of relief from acupuncture in the early stages of withdrawal. I’ve mentioned in prior posts that I was never one to believe in acupuncture even though so many people have told me what wonders it's done for them. These types of acupuncture facilities are all over the country and one near you can be found on this link if you’re is interested in giving it a try: https://www.pocacoop...earch-by-state/

Zeus - However, my general practitioner thought different. She uses a combination of eastern and western medicine and suggested acupuncture. Wow what an improvement. I had one treatment this morning and no nausea since. Even the fatigue is better and I feel like eating again.

considering - Check out the U.S. network of Community Acupuncture Clinics. They are a great way to get low cost acupuncture treatment.

BCH - I used acupuncture, which helped amazingly well. Over a period of about 4 months I suffered very few side effect.

ECU - the auriculotherapy (like acupuncture, only done on the ear alone) was based on a 5 point protocol designed to treat heroin addicts in withdrawal, and got rid of all the physical symptoms (temporarily) and enabled me to function while my body adjusted.

cmonk - I had been going for acupuncture treatments and yes they are wonderful

Sarahj - Oh yeah, I realized how much acupuncture was helping me after the third treatment, I went once a week. So, I hope that it provides some benefit to you. One thing that I tried during the worst of the withdrawal is acupuncture. It really made a difference in my overall outlook on everything, not in a magic bullet kind of way, but my sense of being aware and wanting to take better care of myself seem to be heightened by the experience.

Rogerwilco -Acupuncture is definitely the best way I've found to treat withdrawal discomfort from pharma drugs. The thing about acupuncture is that it has side effects too... but they're all GOOD! I mean, like, WOW :!:

Ramona - acupuncture regularly now. It doesn't take away all the withdrawal symptoms, but it balances the systems in your body to help you feel better while you're going through this. Really calms down the anxiety, quiets your mind.

14. Deep breathing, sighs, yawns....

These activities cause an increase in the release of dopamine, endorphins and serotonin. This fact has been used by psychologists for decades to help control anxiety, depression and sleep. By causing yourself to yawn several time over a 10 or 15 minute period it will release enough of these neurotransmitters to help relax and induce sleep. Sighs work much in the same fashion but to a lesser degree, Breathing exercises are the most effective. A good psychologist should be used to teach the most effective techniques.

 

https://www.ncbi.nlm.../pubmed/9551709

Member comments and tips - deep breathes, breath(ing) - 22 comments all positive

Raven - Breathe it deep calming breaths and hold them for about 5 seconds before slowly letting them out.

Gail - you need to breathe, yes breathe in and out slowly.

Wagtail - Breathe deeply & slowly & DONT BE SCARED ..

FH - Deep breathing. Close your eyes—and try taking deep, slow breaths— making each breath even deeper than the last. If you have a psychologist who could teach you relaxation techniques, controlled breathing and heart rate, etc. These techniques really do work.

Raven - Just do you best to stay calm and use breathing techniques. My husband and FH have given me great tips on breathing when anxiety strikes. FH because he is a veteran and my husband because he has asthma.

Keys to breathing:
** Take slow deep breaths (breath in deeply and slowly)
** Hold for at least 15 secs if you can
** Exhale slowly
***repeat as needed*

FN - What helped me the most with this was yoga ...the breathing exercises ... once learned, they can be done anywhere, anytime .... the release of the built up anxiety in my body was tremendous ...

WAH - Some things that have helped me:

Practice breathing techniques. I'm one of those people who holds her breath a lot, and I don't even know that I'm doing it.

Janson - . i've learned a few breathing exercises via yoga and that helps immensely to calm down those nerves that are about to snap. even without knowledge of specific breathing exercises, just take deep full breaths with hands on your stomach and see your tummy rise on the breath in and then fully breath out. so simple, so effective.

Note - There must have been well over 100 members that had posts similar to the one below. Shortness of breath, heart pounding, skip beats, tightness in the chest or chest pain. These are classic anxiety symptoms and are the result of elevated adrenalin e levels. Adrenaline is a vasoconstrictor and bronchiole constrictor. These shallow rapid breaths allow CO2 to build in the lungs and worsens the symptoms. Alpha-agonists (eg. clonidine) and beta blockers (atenolol) work well t o block the effects of this excess adrenaline. Breathing exercises also help considerably in breaking this Cycle. As you can see below ZA got it really right.

Snap87 - Just scared with the shortness of breath and heart palpitations more than anything.

ZA - the 'out of breath' symptom is actually ;shallow breathing and I had that for about 2days it is very exhaustingas it cuauses your ozygen saturation to drop. what worked for me 'was awareness -slow deep breathing -then a little aerobics. it helped to up my b/p and neuteralize by blood gases

15. Conditioned Response -
One of the methods that can have a dramatic effect on anxiety is the development of a phrase in association with breathing exercises and relaxation techniques. This usually takes time to develop but is very effective. The process is begun by selecting a phrase...say the word "easy" for example. When you notice that you begin to get too anxious then lay down, close your eyes and begin your deep breathing exercises while also doing relaxation like 'progressive relaxation' all the time repeating the word 'easy' in your mind. With practice this becomes very effective and the need to lay down to achieve success is not necessary. You simply stop in place, close your eyes and say the word 'easy" to yourself while relaxing and breathing deeply. You then proceed on with your activities. This can be further used by your spouse to help you control your anxiety. If your spouse notices you becoming anxious they can simply develop a certain place she/he touches you gently as a signal that you need to stop, breath and relax. With practice this becomes automatic and can easily be done in public without drawing attention to your state of mind. The is a conditioned response so it MUST be practiced until it is a reflex action to be most helpful.

Three members report using this technique with excellent results.

Other Medical Research
https://www.ncbi.nlm...pubmed/15639542
it is suggested that melatonin exerts its analgesic actions not by binding to opioid receptor subtypes but by binding to its own receptors and increasing the release of beta-endorphin.

As well as ...
https://www.ncbi.nlm...pubmed/12579851
https://www.ncbi.nlm.../pubmed/3361078
https://www.ncbi.nlm.../pubmed/1668619
https://www.ncbi.nlm...les/PMC5038497/
and more.

Also....
https://www.ncbi.nlm...pubmed/12043836
Inhibition of dopamine release by melatonin has been demonstrated in specific areas of the mammalian central nervous system (hypothalamus, hippocampus, medulla-pons, and retina). Antidopaminergic activities of melatonin have been demonstrated in the striatum.

https://www.ncbi.nlm.../pubmed/6291701
The data of this study provide evidence for a further mechanism by which beta-endorphin may alter dopaminergic neurotransmission, namely by increasing dopamine reuptake into dopaminergic nerve endings.

https://www.ncbi.nlm.../pubmed/6263592
The data are consistent with the hypothesis that endorphins act at a presently unknown brain site(s) to increase the central sympathetic outflow to adrenal medulla and peripheral sympathetic nerve endings, thus stimulating peripheral catecholamine release and increasing plasma concentrations of epinephrine, norepinephrine, and dopamine.

https://www.ncbi.nlm.../pubmed/9588760
CSF (cerebrospinal fluid) levels of both neuropeptides (beta-endorphins and P factor) were observed to peak during the first year of life, and showed a negative correlation with increasing age. A significant positive correlation was observed between the CSF level of beta-endorphin and that of substance P.

https://www.ncbi.nlm...cles/PMC432218/
In cerebral cortex, brainstem, caudate nucleus, and thalamus, most responsive cells were inhibited by the peptides (endorphins) and by normorphine, while in hippocampus all responsive cells were excited. These results are consistent with the hypothesis that the endorphins and enkephalins may represent a new class of central neurotransmitters; among other functions, these peptides may play a role in the regulation of behavior and the expression of psychopharmacological agents such as the opiate alkaloids.
 


#5 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 28 August 2017 - 10:03 AM

                                                                            Increasing Dopamine levels
Summary;

 

⦁ The dopamine cycle is: tyrosine converts to L-Dopa to dopamine to norepinephrine and then epinephrine. Therefore caution should be used when trying to raise dopamine to treat depression. Begin with small doses until relief is obtained. Do not take larger doses as any extra unused dopamine will be changed to noradrenaline and adrenaline and the result could be anxiety.

⦁ An overabundance of bad bacteria leaves toxic byproducts called lipopolysaccharides which destroy the brain cells that make dopamine. (⦁ 14) Therefore a good probiotic should be used.
And don’t reach for artificial sweeteners. Aspartame decreases brain levels of both dopamine and serotonin, another important mood-boosting neurotransmitter. (⦁ 17)
L-tyrosine is the first dopamine supplement to consider. L-tyrosine and phenylalanine compete with tryptophan for absorption. Tryptophan is converted to serotonin by the body so if too much L-tyrisine is present n the blood stream then serotonin levels may decrease.
⦁ One of the functions of Vitamin C include the synthesis norepinephrine from dopamine and the synthesis and catabolism (breakdown) of tyrosine. So vitamin C may increase tyrosine or decrease tyrosine in the body depending on conditions.

Melatonin decreases dopamine and may make depression worse.

Bananas raise dopamine levels. Many members have relied on bananas to help with their depression and withdrawal symptoms.

 

Dopamine plays several important roles in the brain and body. It is synthesized from a molecule of L-Dopa, which is synthesized in the brain and kidneys. Some animals and humans make it via biosynthesis from the amino acid L-tyrosine. L-DOPA is the precursor to the neurotransmitters dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline) collectively known as catecholamines. The cycle is: tyrosine converts to L-Dopa to dopamine to norepinephrine and then epinephrine.

Dopamine is also synthesized in plants and most animals. In the brain, dopamine functions as a neurotransmitter - a chemical released by nerve cells to send signals to other nerve cells. The brain includes several distinct dopamine pathways, one of which plays a major role in reward-motivated behavior. Most types of rewards increase the level of dopamine in the brain, and many addictive drugs increase dopamine neuronal activity. Other brain dopamine pathways are involved in motor control and in controlling the release of various hormones. It does not cross the blood brain barrier.

Dopamine deficiency can also manifest as certain psychiatric disorders including depression, addiction, attention deficit disorder (ADD), bipolar disorder, and Parkinson’s disease.

Major depressive disorder (MDD), The cause is believed to be a combination of genetic, environmental, and psychological factors. Risk factors include a family history of the condition, major life changes, certain medications, chronic health problems, and substance abuse. About 40% of the risk appears to be related to genetics. There is no laboratory test for major depression.

 

Testing, however, may be done to rule out physical conditions that can cause similar symptoms. Much scientific evidence links lack of dopamine to depression and sometimes anxiety.

Nicotine increases dopamine by 200%, cocaine 400%, and amphetamines a jaw-dropping 1,000%.

Few people realize that they are “self-medicating” to get a dopamine boost when they engage in potentially addictive and self-destructive behaviors. The use and abuse of caffeine, alcohol, sugar, drugs, shopping, sex, video games, online porn, power, and gambling are all effective, but temporary, dopamine boosters.

Here’s a list of foods, drinks, and spices known to increase tyrosine or dopamine directly: (6, 7, 8, 9, 10, 11, 12)
⦁ all animal products
⦁ almonds
⦁ apples
⦁ avocados
⦁ bananas
⦁ beets
⦁ chocolate
⦁ coffee
⦁ fava beans
⦁ green leafy vegetables
⦁ green tea
⦁ lima beans
⦁ oatmeal
⦁ olive oil
⦁ oregano
⦁ peanuts
⦁ rosemary
⦁ sea vegetables
⦁ sesame and pumpkin seeds
⦁ soy products
⦁ turmeric
⦁ watermelon
⦁ wheat germ

I’m going specifically mention bananas because they are a particularly good source of dietary dopamine. (13)

 

Surprisingly, the health of your intestinal flora impacts your production of neurotransmitters. An overabundance of bad bacteria leaves toxic byproducts called lipopolysaccharides which destroy the brain cells that make dopamine. (14) Therefore a good probiotic should be used.

Dopamine-Depleting Foods to Avoid
Eating a lot of saturated fat also decreases dopamine receptor sensitivity. (15)

Sugar has been found to boost dopamine, but this is a temporary, unhealthy boost that is more drug-like than food-like and ultimately contributes to deficiency. (16)

And don’t reach for artificial sweeteners instead. Aspartame decreases brain levels of both dopamine and serotonin, another important mood-boosting neurotransmitter. (17)

Here’s a look at some of the best supplements that raise dopamine levels naturally. Caution should be used when trying to raise dopamine to treat depressison. Begin with small doses until releif is obtained. Do not take larger doses as any extra unused dopamine will be changed to noradrenaline and adrenaline and the result could be anxiety.

L-tyrosine is the first dopamine supplement to consider.

This amino acid is the precursor to dopamine.
If you don’t get enough l-tyrosine in your diet, or your body doesn’t properly convert it, you won’t be able to synthesize adequate dopamine. When looking for a supplement, consider n-acetyl-l-tyrosine. This is a highly absorbable form of l-tyrosine that readily enters the brain. L-tyrosine and phenylalanine compete with tryptophan for absorption. Tryptophan is converted to serotonin by the body so if too much L-tyrisine is present n the blood stream then serotonin levels may decrease. One of the functions of Vitamin C include the synthesis norepinephrine from dopamine and the synthesis and catabolism (breakdown) of tyrosine. So vitamin C may increase tyrosine or decrease tyrosine in the body depending on conditions.

L-tyrosine can make headaches/migraines and existing thyroid issues worse. The body uses tyrosine to make thyroxine, a thyroid hormone. Tyrosine seems to be safe when used in doses up to 150 mg/kg per day for up to 3 months. Some people experience side effects such as nausea, headache, fatigue, heartburn, and joint pain. (Webmd)

Mucuna pruriens is a tropical legume that contains l-dopa, a dopamine precursor. Mucuna pruriens supplements are sold to enhance mood, memory, overall brain health, anti-aging, and libido. (19) This herb was found to work even better than levodopa medications for Parkinson’s, a disease characterized by low dopamine. (20) The plant contains relatively high (3–7% dry weight) levels of L-Dopa; some people are sensitive to L-DOPA and may experience nausea, vomiting, cramping, arrhythmias, and hypotension. The seeds of the plant contain about 3.1–6.1% L-Dopa,[14] with trace amounts of serotonin, nicotine, and bufotenine (a tryptamine related to aerotonin.)

Side effects include, if too high of a dosage is taken, users may experience vomiting, headaches, and sleeplessness. Other serious side effects, like high blood pressure, hair loss, and hallucinations are also possible. No more than 500 mg a day is generally necessary to experience all of Mucuna’s effects. If you take Mucuna too frequently, you may start to develop tolerances over time which cause you to increase dosage too quickly. https://nootriment.c...s-side-effects/

https://www.ncbi.nlm...pubmed/26058043
An average of 52.11% degradation of L-dopa was found in seeds of M. pruriens varieties. Since M. pruriens seeds and/or L-dopa are used for treatment of Parkinson's disease and as an aphrodisiac both in modern and/or traditional systems of medicine, the finding of high level of L-dopa degradation (in pure form and in M. pruriens extracts) into damaging quinones and ROS is very significant.

https://www.ncbi.nlm...les/PMC3942911/
Great review of this plant and its properties.

https://www.ncbi.nlm...les/PMC4213977/
Overview of its use in treating depression.

 

This product has a large number of drug interactions, especially with psychiatric meds so please check drug compatibilities carefully.

Curcumin is the main active ingredient in the spice turmeric. It readily crosses the blood-brain barrier where it boosts levels of dopamine. (21, 22, 23) Curcumin has been found to be as effective for treating depression as the popular antidepressant Prozac. (24) When buying a curcumin supplement look for one that contains piperine, a compound found in black pepper that increases curcumin absorption by a remarkable 2,000%. (25)

https://www.ncbi.nlm...pubmed/28074653
According to a 2017 review of over 120 studies, curcumin has not been successful in any clinical trial, leading the authors to conclude that "curcumin is an unstable, reactive, non-bioavailable compound and, therefore, a highly improbable lead".

https://www.ncbi.nlm...pubmed/26024538
In Phase I clinical trials, curcumin had poor bioavailability, was rapidly metabolized, retained low levels in plasma and tissues, and was extensively and rapidly excreted, factors that make its in vivo bioactivity unlikely and difficult to accurately assess.

https://www.ncbi.nlm...pubmed/26972530
Also, curcumin normalizes the levels of dopamine, noradrenaline, and 5-hydroxyindoleacetic acid in the frontal cortex of rats. Taking all these results together, it may suggest that curcumin is potent compound acting against the depression in the male albino rats.

https://www.ncbi.nlm...pubmed/21928724
Curcumin increased both the swimming and climbing behavior in FST, thus its antidepressant like activity could be due to an increase in serotonin, norepinephrine and dopamine levels in the brain. Curcumin can be a useful antidepressant especially in cases which respond to drugs having mixed effects on serotonin and catecholamines levels in the brain.

https://www.ncbi.nlm...pubmed/20230279
Curcumin prevents dopaminergic neuronal death through inhibition of the c-Jun N-terminal kinase pathway.
Our study suggests that the neuroprotective effect of curcumin is not related simply to its antiinflammatory and antioxidant properties, but involves other mechanisms, particularly by targeting the JNK pathway

https://www.ncbi.nlm...pubmed/18766332
Antidepressant activity of curcumin: involvement of serotonin and dopamine system.
The study provides evidences for mechanism-based antidepressant actions of curcumin. The coadministration of curcumin along with piperine may prove to be a useful and potent natural antidepressant approach in the management of depression.
And many other articles.

Side effects - Turmeric isn't approved by the U.S. Food and Drug Administration to treat any diseases, and taking turmeric supplements can cause unpleasant or dangerous side effects. The most common gastrointestinal side effects are stomachache, gas, nausea and indigestion and taking turmeric for long periods can cause ulcers in some people due to increasing stomach acid.
The curcumin in turmeric encourages the gallbladder to produce more bile, which may improve digestion. Because of the extra bile production, people who have gallstones or other conditions that block bile passages shouldn't take turmeric before consulting with their doctors. Turmeric may also contribute to the formation of kidney stones, particularly in people who have conditions that increase the risk of kidney stones.

Pregnant women shouldn't take turmeric as a supplement. According to MedlinePlus, the curcumin can stimulate the uterus or encourage the uterine lining to shed, which could increase the risk of miscarriage.

Because turmeric can increase stomach acid, it can interfere with the efficacy of drugs that reduce acid, such as acid reflux medications. The spice can also increase the effectiveness of some drugs, including blood thinners and diabetes medications. Taking turmeric with blood thinners can increase the risk of bleeding. This includes taking it with other herbs that act as blood thinners, including ginger, garlic, clove, ginseng and willow. Diabetics who take medication to help lower their blood sugar levels shouldn't take turmeric because it can drop blood sugar to potentially dangerous levels.

Ginkgo biloba is traditionally used for a variety of brain-related problems such as poor concentration, memory problems, headaches, fatigue, mental confusion, depression, and anxiety. (26) One of the ways ginkgo works is by raising dopamine. (27, 28)
Ginkgo LEAF EXTRACT is LIKELY SAFE for most people when taken by mouth in appropriate doses. It can cause some minor side effects such as stomach upset, headache, dizziness, constipation, forceful heartbeat, and allergic skin reactions.

There is some concern that ginkgo leaf extract might increase the risk of liver and thyroid cancers. However, this has only occurred in animals given extremely high doses of ginkgo. There is not enough information to know if it could happen in humans.

Ginkgo fruit and pulp can cause severe allergic skin reactions and irritation of mucous membranes. Ginkgo might cause an allergic reaction in people who are allergic to poison ivy, poison oak, poison sumac, mango rind, or cashew shell oil.

There is some concern that ginkgo leaf extract might increase the risk of bruising and bleeding. Ginkgo thins the blood and decreases its ability to form clots. A few people taking ginkgo have had bleeding into the eye and into the brain, and excessive bleeding following surgery. Ginkgo leaf extract can cause allergic skin reactions in some people.

The ROASTED SEED or CRUDE GINKGO PLANT is POSSIBLY UNSAFE when taken by mouth. Eating more than 10 roasted seeds per day can cause difficulty breathing, weak pulse, seizures, loss of consciousness, and shock. The FRESH SEED is even more dangerous. Fresh seeds are poisonous and are LIKELY UNSAFE. Eating fresh ginkgo seeds could cause seizures and death.

There isn't enough reliable information available to know if ginkgo is safe when applied to the skin.

Special Precautions & Warnings:
⦁ Pregnancy and breast-feeding: Ginkgo is POSSIBLY UNSAFE when taken by mouth during pregnancy. It might cause early labor or extra bleeding during delivery if used near that time. Not enough is known about the safety of using ginkgo during breast-feeding. Do not use ginkgo if you are pregnant or breast-feeding.

Infants and children: Ginkgo leaf extract is POSSIBLY SAFE when taken by mouth for a short time. Some research suggests that a specific combination of ginkgo leaf extract plus American ginseng might be safe in children when used short-term. Do not let children eat the ginkgo seed. It is LIKELY UNSAFE.

Bleeding disorders: Ginkgo might make bleeding disorders worse. If you have a bleeding disorder, don't use ginkgo.

Diabetes: Ginkgo might interfere with the management of diabetes. If you have diabetes, monitor your blood sugar closely.

Seizures: There is a concern that ginkgo might cause seizures. If you have ever had a seizure, don't use ginkgo.

Deficiency of the enzyme glucose-6-phosphate dehydrogenase (G6PD): Ginkgo might cause severe anemia in people have G6PD enzyme deficiency. Until more is known, use cautiously or avoid using ginkgo if you have G6PD deficiency.

Infertility: Ginkgo use might interfere with getting pregnant. Discuss your use of ginkgo with your healthcare provider if you are trying to get pregnant.

Surgery: Ginkgo might slow blood clotting. It might cause extra bleeding during and after surgery. Stop using ginkgo at least 2 weeks before a scheduled surgery.

Drug Interactions

https://www.drugs.co...2&generic_only=
Ginkgo Biloba can react with over 500 different medications to primarily increase the risk of bleeding and seizures. Please review the list of meds at the above site to be sure you are not at risk of these interactions.

Talk to your doctor before using ginkgo together with DULoxetine. Some preparations of ginkgo biloba have caused seizures, and combining them with other medications that can also cause seizures such as DULoxetine may increase that risk.

Medical Research

https://www.ncbi.nlm...pubmed/25346240
Our results suggest that EGb 761 may be useful for reducing anhedonic depressive-like behavior.

https://www.ncbi.nlm...pubmed/21672588
It is suggested that EGb761 produces an antidepressant-like effect, and that an antioxidant effect against oxidative stress may be partly responsible for its observed neuroprotective effects.

https://www.ncbi.nlm...pubmed/20105177
The Ginkgo biloba extract EGb 761® and its main constituent flavonoids and ginkgolides increase extracellular dopamine levels in the rat prefrontal cortex.
The present results demonstrate that chronic but not acute treatment with EGb 761 increased dopaminergic transmission in the PFC. This finding may be one of the mechanisms underlying the reported effects of G. biloba in improving cognitive function.

https://www.ncbi.nlm...pubmed/22784425
https://www.ncbi.nlm...pubmed/20411379

L-theanine is a unique compound found in green, black, and white teas.
It increases levels of dopamine as well as serotonin and the relaxing neurotransmitter GABA (gamma-aminobutyric acid). (29)

 

L-Theanine improves recall, learning, and positive mood. (30) You can get a dopamine boost by either taking an l-theanine supplement or by drinking tea.

See the section on "raising serotonin levels) for details on this supplement.

Phosphatidylserine acts as your brain’s “gatekeeper,” regulating nutrients and waste in and out of your brain. It can increase dopamine levels and improve memory, concentration, learning, and symptoms of ADHD. (32, 33, 34)

Boost Dopamine with Exercise

But you don’t need to exercise strenuously to enhance your brain. Taking walks, or doing gentle, no-impact exercises like yoga, tai chi, or qi gong all provide powerful mind-body benefits. (38, 39, 40, 41)

And if you can get your exercise outdoors, that’s even better. Sunlight can increase the number of dopamine receptors and create vitamin D which activates the genes that release dopamine. (42, 43)

Increase Dopamine with Meditation

The benefits of meditation have been proven in over 1,000 studies. (44) Regular meditators experience an enhanced ability to learn, increased creativity, and deep relaxation. It’s been shown that meditation increases dopamine, improving focus and concentration. (45) Creative hobbies of all kinds, including knitting, quilting, sewing, drawing, photography, woodworking, and home repair, bring the brain into a meditative state. These activities increase dopamine, ward off depression, and protect against brain aging. (46)

Music Gets Dopamine Flowing

Listening to music can cause release of dopamine. Brain scans show that the brain’s pleasure center lights up when listening to music similarly to when we eat, make love, or take drugs. (47)

Boost Dopamine with Touch

All kinds of pleasurable touch increase dopamine. A therapeutic massage increases dopamine and serotonin and reduces the stress hormone cortisol. (49, 50) Stroking your dog can give both you and your pet a boost of dopamine and a slew of other feel-good brain chemicals. (51) There’s evidence that having sex increases dopamine in lab rats. (52) This has yet to be proven in humans.

The Role of Dopamine and Sleep

Research has found that dopamine plays a bigger role in sleep regulation than previously believed. It controls the production of the sleep hormone melatonin. (53) Research suggests that lack of sleep may reduce the number of dopamine receptors. (54)

https://www.ncbi.nlm...pubmed/18057326
https://www.ncbi.nlm...pubmed/12043836
https://www.ncbi.nlm.../pubmed/7534345
and others
Inhibition of dopamine release by melatonin has been demonstrated in specific areas of the mammalian central nervous system (hypothalamus, hippocampus, medulla-pons, and retina).

Note - This would indicate that patients with depression may want to limit their use of melatonin due to possible lowering of dopamine and increased depression.

The Dopamine-Weight Loss Connection

There’s a strong link between obesity and dopamine dysfunction. (55) Interestingly, people who are obese have fewer dopamine receptors than average. (56) In fact, their brains behave much like that of a drug addict. (57) Thus, since dopamine is in charge of the brain’s pleasure center, obese people will receive less pleasure and satisfaction from eating, making them want to eat more. If you struggle with your weight, you may be caught in a vicious cycle.

Blast Dopamine with a Cold Shower

If you’re game, take a cold shower or at least end your shower with a cold blast.
Taking a shower with 14C°/57F° water can increase dopamine substantially — up to 250%! (58) Proponents of cold showers swear it boosts their mood and productivity all day, even more than drinking coffee

Acheiving Results

Dopamine is released when you achieve a goal, large or small.
If your big goal is to get organized, break it down into many small goals. Each goal can be as simple as organizing your emails, cleaning a closet, or emptying your junk drawer. Every time you cross one item off your to-do list, it gives you a nice spurt of dopamine.

Ideally, your goal should be hard — like quitting a bad habit or sticking with a budget to pay down your debt. The harder your goal, the more accomplishment you’ll feel, and that translates into more dopamine. Get a calendar, virtual or paper, and cross off each day that you’ve actively worked toward your goal. This “don’t break the chain” concept is a proven way to rewire your brain. Acknowledge and savor your victories every day for a daily dopamine boost.

A link to all references can be found at https://bebrainfit.c...rease-dopamine/
The remaining information came from either Wiki or NCBI medical abstracts.





 


#6 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 10 November 2017 - 11:36 AM

Effects of Various Over the Counter (OTC) Meds
Excedrin
Caution - Most Excedrin contains caffeine and may make anxiety worse.
 
TBH - Headaches - Advil and Excedrin made no difference
 
sanctuarie - Headaches - Nothing I've tried helps the headaches, motrin, tylenol, aspirin, excedrin, even norco gives me no relief.
 
CB - I took Excedrin Migraine today....no relief.
 
GW - mild occasional headache, which excedrin took care of.
 
Mjoy - and got a headache this afternoon that fortunately went away with some excedrin.
 
BF - By the end of the day yesterday I was getting really, really dizzy. I took an Excedrin and laid down. After a restful night's sleep I am feeling pretty good. The biggest problem overall with this withdrawal seems to be the dizziness. Taking Excedrin Migraine seems to help, but I don't wanna get caught in a trap of taking a bunch of Excedrin because I tend to get jittery from the caffeine if I take it too often.
 
ITWYS - but today (first time to try it) I took two extra strength excedrin for the headache and the brain zaps have subsided also. You might try this. It has worked so far!
 
BZ - the headache that will NOT go away (which right now is the worst part of it) Claritan D nor Excedrin are putting a dent in it.
 
GD - I was taking ibuprofen for pain, but it was adding to the nausea. I found that Excedrin helps best with dulling the pain and keeps me less nauseous
 
Extra Strength Excedrin - Acetaminophen 250 mg, Aspirin 250 mg, and Caffeine 65 mg.
Excedrin Migraine - Acetaminophen 250 mg, Aspirin 250 mg Caffeine 65 mg
Excedrin Tension Headaches - Acetaminophen 500 mg Caffeine 65 mg
--------------------------------------------------------------------------------------------------------
Activated charcoal capsules
 
https://www.ncbi.nlm...tacidsCymbalta
"Pharmacokinetic results from drug interaction studies show that activated charcoal decreases duloxetine exposure" (absorption)
 
Jillybean - Activated charcoal capsules- (Solaray brand name 280 mg I take 3 capsules twice a day. Lots of water or fluids, it is highly absorbable so it needs to be taken 2 hrs b4 or after other meds, vits etc. It helps to pull the poison from yours system. It may cause diarrhea or constipation hence another reason to boost fluids. Even though diarrhea is uncomfortable, do not take something to stop it as it is necessary to flush this poison out of your system. You can adjust amount based on how you feel.
 
Jillybean - I think the activated charcoal is working too as I am feeling better.
 
DonMH - One of the most harmless remedies for the stomach problems is capsules of Activated Charcoal. You can buy them over the counter. They are often used in overdose patients to prevent the absorption of ingested drugs. Completely natural and harmless - only side effect -your poop will turn black as the charcoal passes through your body. It works - I know!
 
FH - After reviewing the medical journal abstracts I found many research articles that looked at testing if activated charcoal would remove toxins from our body. None of the research showed beneficial effects. They are however very effective at absorbing (thus reducing) medicines and nutrients in the stomach.
----------------------------------------------------------------------------------------------------------
Bragg's Apple Cider Vinegar
 
Tfaff - I'm trying to " detox" by eating well, finding foods that help detox the liver. I drink that apple cider vinegar/ honey/cinnamon mix that came up in another post here.
 
Fivenotions - I took myself off completely a few months ago and went back to home remedies (ginger tea and ginger slices, as well as Bragg's vinegar) ... the home remedies work pretty well (not perfectly) for the acid reflux ... but the "stomach worms"/anxiety every so slowly started to ratchet up ...
Another "home remedy" that really helped me (still does, I'm still taking it) is Bragg's Apple Cider Vinegar ... it's also available in most health food stores, as well as from the internet (Amazon, and Bragg's directly) ... can be put in water, with honey, etc.... during early withdrawal, I drank it straight ... my food cravings were totally weird, and at the time it actually tasted great just like that ... blech ... there've been studies (which I now can't find, typical) that indicate it's a food that naturally increases serotonin levels ... it also cured my arthritis ... (Grandma knew more than I gave her credit for!)
The Bragg's ACV, which is unpasteurized and has what they call the "mother" in it...weird term, but that's the stuff that would otherwise be pasteurized out ....what starts to form when apple cider begins to go "hard" ....

Here's the link ...
http://bragg.com/

I started taking it early in withdrawal ... totally by self-discovery ... I was having an amazing craving for vinegar tasting stuff...like dill pickles...actually, the juice they come in...so I did some googling...

It was very helpful to me with the withdrawal ... seemed to help with the zaps, my constant tiredness and the body "shakes" I got .... now, I've found that it's pretty much cured my arthritis...
 
Equuswoman - Organic apple cider vinegar, raw honey and cinnamon mixed with water.been just a few days on this.
 
Fishinghat - By the way some have had very good success with Bragg's Apple Cider Vinegar for their fibro. There is some medical research that supports this. If you do a search on this site you will find several discussions about it. Be aware it is acidic so it can upset the stomach. The reason the Bragg's is the only Apple Cider Vinegar that works is that it is unpasteurized and therefore has all the original components. If you have any questions about the Braggs let me know and I will try to answer them.
 
Lady Nancy - I could not resist the urge to search and found several references to Bragg's Apple Cider Vinegar which is an unfiltered and unpasteurized apple cider vinegar. Many are unable to take it due to stomach issues in which case a good alternative is Malic Acid/Magnesium in pill form as it works the same.
The dose for the Bragg's is two teaspoons in a cup of water. It is much stronger than regular Apple Cider Vinegar which is probably why it causes stomach aches for some even with some sugar or honey added. I know that I would not be using sugar at all if possible as it actually adds to joint pain and feeds the inflammation. .
 
Fishinghat - A little caution on the vinegar, which has been shown effective, added vinegar ingestion by women has been linked to increases in vaginal infections due to changes in blood and vaginal pH.
katrand - I also add Bragg's apple cider vinegar to my orange juice every morning to aid in absorption of my thyroid meds and supplements.
 
TFL - Are you taking anything for the joint pain? I found that Apple Cider Vinegar (Braggs is the best - natural!) is a great help - you can mix a couple of spoonfuls in a cup of warm water with 1 spoon of honey and some cinnamon - almost tasty! I have arthritis and fibro and this really helps - give it a couple of weeks...
 
BJinFl - I have tried ACV, fishinghat, thank you. Unfortunately, I have one of those stomachs that can't stomach anything.
 
Fishinghat - For fibromyalgia I would try Braggs brand Apple Cider Vinegar. The dosage is 2 tablespoons in about a cup of cold water once a day. There has been some medical research that this juice has benefit for fibro and arthritis pain. This brand is the only one that works because it is the only one that is unfiltered and not pasteurized. Many find this solution to be too acidic for their stomach to handle, if you have that problem then buy some malic acid/magnesium tablets at your local health store. Malic acid and magnesium are the active ingredients in the Apple Cider vinegar.
 
Gail - ....each capsules contains 500mg apple cider vinegar powder, 300mcg potassium and 4mcg bore.
 
Cinders - I'm drinking apple cider vinegar (with must) with agave and cinnamon.
 
Fishinghat - He said to use a 50/50 blend of Braggs (sp) apple cider vinegar and water on the area on her back where the nerves are pinched. It may take a couple months to make a difference but will reduce the arthritis and the pain greatly. He recommends it to many of his patients as a way to reduce there use of pain meds for arthritis. I asked him if he has ever heard of using it on fibro and he said that the ACV worked better on the fibro than it did the arthritis.
 
http://www.ehow.com/...bromyalgia.html
This article explains the basics of using ACV to treat Fibro. I found maybe 50 articles or so that say basically the same thing and many forums that say it works.

http://www.ncbi.nlm..../pubmed/8587088
This research article demonstrates that malic acid is very beneficial in treating fibro. AND malic acid is one of the main ingredients in ACV. It is suggested that there must be magnesium present for it to work and there is nagnesium in ACV.
 
Natural diuretics include:
⦁ Apple cedar vinegar- it regulates the level of potassium in the body

Bragg Organic Apple Cider Vinegar is the type most often mentioned on the forums.

Gonnamakeit - Well, I decided to give this a try and started this morning with this recommended by Whycee a while back: "A cup of hot water, 1/2 teaspoon of cinnamon, two tablespoons of apple cider vinegar and a teaspoon of honey every morning" minus the cinnamon as I'm allergic and I have to say that it seems to be working! I had two servings this morning and this is the first good day since last Friday and I even woke up with my period in full force AGAIN--it just ended Sunday (apologies to the men!) and even those cramps are so much better.
 
FiveNotions -
Drinking to Cure: Apple Cider Vinegar and Cherry Juice for Arthritis?
http://www.healthlin...juice-arthritis

This isn't an article, but a collection of links to info about the ACV arthritis connection...also, we had an interesting discussion here a while back about tart cherry juice as a remedy for withdrawal... https://www.cymbalta...l=+tart+cherry

The healing powers of vinegar
http://www.dailymail...rs-vinegar.html

http://www.anyvitami...inegar-info.htm

Serotonin/tryptophan connection mentioned . . .
http://health.usnews...e-cider-vinegar

This is an interesting discussion about ACV from the Social Anxiety Forum....
http://www.socialanx...a-relief-47323/
 
Wagtail - I think it was Fivenotions that recommended the apple cider vinegar , so I decided to try it . I can't say if it's a coincidence or not , but I do feel better since I've been taking it ... Less s/e's & more energy .. I'm happy with that !..:-)
 
Carleeta - Holy Moly...Apple cider vinegar...wow...I use it daily with Iceberg lettuce...I use it on my fish and on my potatoes..Also, I mix apple cider with fresh caused garlic and fresh ground black pepper, place it in a small bowl and dip pieces of meat (steak, pork chops) on it and eat them...I also soak crispy friend pork rinds in the bowl mixture and eat them...I guess I use apple cider vinegar a lot. It's possible this is what keeps me going forward...I like that it does burn fat also... So great to know it's helping you out with your cymbalta withdrawl....
 
JBhibbard - Drink lots and lots of water. Have you tried the apple cider vinegar detox? I believe it helps.
Andreamarie - For supplements I'm taking B Complex, Omega 3s, and apple cider vinegar.
 
Whychee - A cup of hot water, 1/2 teaspoon of cinnimon, two tablespoons of apple cider vinegar (Braggs) and a teaspoon of honey every morning.
 
plezhelp - i cannot say what will work for you but i continue to try different things = being open to change as the fkn side-effects change too! the best thing i am still doing is tepid Epsom-salt baths with baking soda, and apple cider vinegar - which has helped a lot with the itching; i have no idea which one of those things are the best/better 'healing' but know that they are all currently helping me.
 
happyzappynot - I found that adding a teaspoon of cider vinegar to a glass of water helped my gut.
andie - I have bought some omega 3 6 9 and taking apple cider vinegar. everything has been very bearable so far so good xx
 
Nmood2talk - I started taking apple cider vinegar over a week ago to help with metabolism and weight issues - it does - more energy than ever - less appetite but amazing result is how I didn't know it helped get off
Cymbalta - I tried before because when I didn't have money for meds at times I had terrible brain zaps(like electric shocks in my head) and terrible nightmares- and the pain in my legs got so much worse -
the apple cider vinegar has worked 3rd day off minimal leg discomfort - no brain zaps - no nightmares - have felt better than I can remember ever - look up apple cider vinegar on Web MD and other places - don't drink straight as it will irritate throat - harsh to teeth - look to see if any side effects - says it could interact with meds ... just research it - but I'm telling you - it's an answer for me so far when I thought there were no answers - apple cider vinegar - look it up - nothing fancy although they say organic is better - got mine at the dollar store and like I said took it initially for weight loss - which it is curbing my appetite and making me feel so much better and I'm losing weight but the off cymbalta without terrible withdrawals was the unexpected unbelievable finding - look it up - research it - and let me know
 
IamwhoIam - Prepare a mixture of apple cider vinegar and honey. Consume this mixture; this home remedy is highly effective in relieving vertigo.
----------------------------------------------------------------------------------------------------------
Imodium AD
 
Fishinghat - If the dry heaves are bothering her you might try a half dose of Imodium. It helps relax the GI muscles but don't use it if constipation is an issue. In the case of constipation you can have her suck on a peppermint lozenge. This relaxes the esophagus/stomach but does not affect the lower intestines and does not aggravate constipation or diarrhea. Be sure it has real peppermint not peppermint flavoring. I have occasional esophageal spasms (a weaker form of dry heaves) and they work well for me. I buy mine at a health food store for about $3 for 10 lozenges.
When I went through mine I lived off of Imodium and Pepto for the digestive issues.
 
LauraM - I can't sleep all I can do is run to the bathroom. Imodium isn't helping.
 
TFL - I used Pepto-Bismol for the nausea and Imodium for the diarrhea. It did the trick.
Fivenotions - ...new arrivals of urinary incontinence and diarrhea ( for which I've got no immediate remedies, except Imodium) ...
 
Equuswoman - The GI symptoms are rough. I took OTC Imodium and sipped G2.
 
kirksd55 - I also had big problems with diarrhea. Imodium helped pretty good but took until about a week ago.
 
Baclaker - I also took imodium for the first time last night and it has greatly helped my nausea.
Houdi - Imodium - for diarrhea
-----------------------------------------------------------------------------------------------------------
pepto
 
Fishinghat - I know I lived off of pepto, Imodium and antacids. I had some good success with Pepto. I used it for occasional relief as too much can cause constipation and ringing in the ears.
 
FiveNotions - I tried the pepto, Gas-X, and a few other OTC remedies, but they didn't help (each of us is so different, frustrating that we seem to have to try different stuff until we hit what works)
 
Sandinanth - I did have a LOT of stomach/bowel issues as a symptom of getting off the Cymbalta. I won't go into detail but it was a full month's worth of not so pleasant bathroom visits and LOTS of Pepto Bismol.
 
silverseed - I've eating Tums and drinking Pepto like it's going out of style.
 
amberd - Ladies, I am sorry if this is TMI. I will call my doctor on Monday if this persist through tomorrow. Some of you have said you have had diarrhea. Mine started Thursday. Tonight it is black. Like, BLACK. I have always heard black means blood is in it. I have been drinking pepto since yesterday. Wondering if it has anything to do with it, but now I am worried. On the bright side, less dizziness and nausea today.I actually ate soup and it stayed down. (Note - FH - yes, pepto can turn your stools black.)
cse - I think I drank half a bottle of Pepto to put the fire out.
 
TFL - I used Pepto-Bismol for the nausea
 
Writeratheart - When my stomach is really, really bothering me, I take some Pepto Bismol, but it tends to make me sleepy, so I make sure it's at a time when I'll be able to take a good hour-long nap.
 
lexini - I am throwing up and nausouis all day long. I am taking pepto bismol and ginger ale, but it isn't alleviating anything.
 
jgbounds - I am so nausiated and the vertigo seem like its getting worse. Pepto Bismo helps, pepperment candy helps
 
ebudae - is there anything that will help get rid of this nausea? I have tried Pepto...nope...
 
Carla - There is one thing that has helped my stomach and bowel problems. The doctor told me to take Pepto Bismol pills...you swallow them...three x three a day and ordered me some prescription Lomotil as the Immodium wasn't helping. Those have helped somewhat.
 
gippos - Hopefully the nausea and dizziness will go away soon - pepto bismol doesn't seem to help with that.
 
vickster - I live on Pepto Bismo and Antacids.
--------------------------------------------------------------------------------------------------------
epsom salts
 
Merete - My go-to solutions are Epsom salt baths and mint tea to sooth aches and calm the body and mind. The salts can also help with the itchy, crawly skin sensations. The only caution is if you have acute nerve pain (pins and needles or sharp stinging) in hands and feet then the warm salty water can make the feeling worse
.
Gran - Drink a lot of water, take epsom salts baths, and I massage my stomach when it feels like it's squeezing.
 
Fivenotions - Have you tried Epsom Salts hot soaks? That did wonders for me, along with the chelated magnesium ...
 
Sis - I also strongly recommend Epsom salt baths, especially in the evening. I had a hard time believing that we absorb and properly process magnesium through out skin, we do but the concentration has to be fairly high. I routinely add 2 cups of epsom and a couple drops of Lavender
 
Lundilez - I've tried Epsom salt bath which helps a little.
 
ShadyLady - .I bought a 20lb bag of epsom salts and 5lbs of baking soda, yep, more is better thinking, and it does help with the fibro pain. The problem is, even with the baking soda added, I have to take a shower and rinse off or I am itching up a storm! I have looked up the amount of salts to use and the baking powder is supposed to be a natural skin softener, but still come out itchy and shriveled up like a raisin. So far, it is more work with all that soaking and showering, I end up exhausted from the energy spent to ease the pain:( Good Lord, we will try anything for relief)
 
Buzzbuzz - I just remembered that my mother used to say that soaking in a hot bath with Epsom Salt before bed is helpful.
 
bobbie - 4) Warm baths with epsom salts help.
 
plezhelp - the best thing i am still doing is tepid Epsom-salt baths with baking soda, and apple cider vinegar - which has helped a lot with the itching; i have no idea which one of those things are the best/better 'healing' but know that they are all currently helping me.
 
freeme2 - My legs hurt the other day, maybe from all the new walking I have done. I took a nice bath with Epsom salts and I felt much better.
 
Cab - 2. Epsom salts baths helped. Since I am having extreme hot flashes since withdrawing it was hard to get in a tub of hot water so I made it lukewarm and it helped relax me.
 
chauceriangirl - I do soak with epsom salts, and it helps some.
 
imwmn - soaking in "detox baths". 1 cup epsom salts 1 cup baking soda and ESSENTIAL Lavender. I took a long detox bath every day
 
sickandtiredofit - A great therapy for the muscle aches and pains that is cheap. Run a warm bath and place 2-4 cups of epsom salt in the bath water. Add a cap of olive oil to the water. Epsom salt and oilve oil are suppose to be great fro sore achy muscles and it really helps. I also place a little drop of lavendar oil to help me relax.
 
mkhackler - I soaked last night with 2 cups of epsom salt and perfume oil.........ahhhhhhhhh.
 
schmb - I have filled the tub with hot water, 1 cup of Epsom Salts, and a few drops of patchouli oil, and just soaked until the water got cool. I read a book, and just let go. It quieted my head, eased the aches and pains, and smelled really good! (You can use whatever fragrance you like, and use oils sparingly.)
------------------------------------------------------------------------------------------------------
diaper rash cream (most contain zinc oxide)
 
Pitbullmama- The diaper rash cream actually helped soothe the itch some.
 
Runni - Anyway, back to itching I found that Calamine Lotion was helpful, Pure Aloe Vera gel was very cooling and also cream that can be bought for diaper rash in babies is especially good.
 
Vickif - hey even diaper rash cream works(by generic it cheaper)
--------------------------------------------------------------------------------------------------------
Dr Redwig R22
 
Lynn - One thing she gave me too take 3x daily was Dr Redwig R22 drops for mood.
Fishinghat - WOW, WOW and WOW again. You guys have got to read the details at the end of this information about 2 of the ingredients.

http://dkonatural.co...41&categoryId=7
R22 Reckeweg Nervous Disorders
Active ingredients:
Grindelia X4, Lachesis mutus X12, Naja tripudians X12, Ethanol, Aqua purificata.

Inactive ingredients:
36-37 vol.-% alcohol, distilled water.

Suggested Use:
Generally 10-15 drops in some water 3 times daily before meals. Reduce dosage gradually after improvement, but continue treatment for several months.

** Please read all label information on delivery.

https://www.my-ayurv...heart-medicines
DR. RECKEWEG R22 - Najasthen Drops for Nervous Disorder Anginous Condition 22 ml
Indications:
Nervous disturbance, oppression and suffocation, also following flatulence.
Anginous condition of the heart.
Ingredients:

MODE OF ACTION OF MAIN INGREDIENTS:

Naja trip: Soreness at forehead and temples due to the anginous condition of the heart. Palpitations of the heart, oppression, general nervousness. Cardiac weakness and irritations caused by nervous coughing, acute condition.

Grindelia rob.: Feels as if heart were too large for thoracic cavity, cardiac and pulmonary weakness, sensation of suffocation in bed.

Lachesis: Nervousness, spiritual animosity, headaches especially above the left eye, palpitations with sensation of suffocation, symptoms worse at bed time and by warmth.

http://homeopathictr...vous-disorders/
Same as above reference.

http://www.reckeweg-...com/company.php
Dr.Roshanlal Aggarwal & Sons Pvt.Ltd. Representing Dr.Reckeweg in India, Nepal & Bangladesh
Pioneers in Homoeopathy for over 60 years

https://homeomart.ne...isorders-drops/
Dr. Reckeweg R22 Drops for nervous disorders (anginous condition of the heart) indicated for Chest pain that is typically described as heaviness, squeezing, pressure, tightness or pain (Anginous condition of the heart). R 21 treats nervous disturbances, headaches, rapid heartbeat due to exertion (oppression) and suffocation, also following flatulence. Sense of suffocation in bed due to pulmonary weakness

A search of the medical journals has shown no scientific research has been done on this specific product.
Ingredient review:
Naja tripudians X12 - An extract from the venom of The monocled cobra.
The major toxic components in cobra venoms are postsynaptic neurotoxins, which block the nerve transmission by binding specifically to the nicotinic acetylcholine receptor, leading to flaccid paralysis and even death by respiratory failure. The major α-neurotoxin in Naja kaouthia venom is a long neurotoxin, α-cobratoxin; the minor α-neurotoxin is different from cobrotoxin in one residue. The neurotoxins of this particular species are weak. The venom of this species also contains mtotoxins and cardiotoxins.
Purchase of cobra venom and its extracts require federal permits before the products can be marketed. Current permit limitations are very restrictive and do not include medicinal applications except for antivenom use.
No medical journal information on this material other than its toxic effects.

Grindelia Robusta -
Both Grindelia Robusta and Grindelia Robusta squarrosa have been used for the symptoms here recorded. There is practically no difference in their action, although the G. Squarrosa is credited with more SPLENIC symptoms, dull pains and fullness in left hypochondrium; chronic malaria; gastric pains associated with splenic congestion. Induces paralysis, beginning in extremities. Its action is shown on the heart first quickening, then retarding it.
Acts on the cardiopulmonary distribution of the pneumo gastric in dry catarrh (tart Emetic in muco-purulent). Produces a paresis of the pneumo-gastric, interfering with respiration. Smothering after falling asleep. Asthmatic conditions, chronic bronchitis. Bronchorrhea with tough mucus, difficult to detach. Raises the blood pressure. Nausea and retching of gastric ulcer. Sugar in urine An effective antidote to Rhus-poisoning, locally and internally; also for burns, blisters, vaginal catarrh and herpes zoster. Hyperchlorhydria when attended with asthmatic and other neurotic symptoms. Hyperaemia of gastric mucous membrane with difficult respiration.

https://www.ncbi.nlm...pubmed/24603350
"Since the health-promoting effects of natural phenolic compounds against brain disorders is of increasing interest, HT and HME were also tested against oxygen and nitrogen reactive species and against enzymes related with Alzheimer's disease and depression. Extracts displayed strong in vitro scavenging activity and monoamine oxidase-A (MAO-A) inhibitory activity. The anti-MAO-A capacity was observed at non-toxic concentrations for SH-SY5Y human neuroblastoma cell line, reinforcing the benefits of G. robusta HT."
 
https://www.ncbi.nlm...pubmed/21031629
The results suggest that G. robusta extract possesses an antiinflammatory therapeutic potential through its capacity to reduce the accumulation of inflammatory mediators and MMPs.
 
https://www.ncbi.nlm...pubmed/19278665
The flavonoid pattern of an acetonic extract of Grindelia robusta Nutt. was investigated in detail. The flavonoids were enriched by CC. In addition to twelve known methylated exudate flavonols four compounds were identified for the first time in G. robusta. Several substances of the flavonoid complex, among them the main compounds quercetin-3-methylether and 6-OH-kaempferol-3,6-dimethylether, were tested for their activity to inhibit neutrophil elastase. Quercetin-3-methylether was shown to be most active with an IC(50) of 19 microM, thus obviously contributing to the anti-inflammatory activity of the drug.
 
https://www.ncbi.nlm.../pubmed/2236296
Certain components in the leaves break down red blood cells.

Lachesis mutus (The Bushmaster) - An extract of a venomous pit viper from South America.
http://natural-heali...hesis-mutus.htm
The poison of the bushmaster, a greatly feared snake native to Central and South America, is deadly if it enters the human bloodstream. It can paralyze the heart and central nervous system and disrupt the blood-clotting process. If the poison is injected into a muscle, it can induce server swelling. These reactions are why many people find it surprising that this snake venom is used in homeopathic medicine to treat various circulatory and nervous-system disorders. But the remedy, Lachesis mutus, is so dilute that only almost undetectable amounts of the poison remain. Like other homeopathic remedies, it is considered most effective in people who have particular modes of behavior. Before prescribing Lachesis mutus, the homeopath will look for such personality traits as strong self-confidence and a tendency toward envy and vengefulness. In addition, the remedy is often prescribed when symptoms of any ailments start on the left side and worsen after waking.
Lachesis mutus type
Two types of people are most likely to benefit from Lachesis mutus: One is slim and pale but energetic; the other is somewhat obese with a blotchy, reddish, complexion. Both types share a strong dislike of tight cloths, particularly around the neck.
To determine if you're a Lachesis mutus type, Check those characteristics that apply to you.
⦁ You are afraid of water.
⦁ You are very jealous.
⦁ Your symptoms are aggravated by grief.
⦁ You act erratically, can't concentrate or lose your train of thought.
⦁ You sometimes feel as if you're suffocating or not getting enough air.
⦁ Your symptoms are worse on hot days or in stuffy rooms.
If you checked more than 3 times, turn to the back of the card for additional information about the benefits of Lachesis mutus.
Therapeutic effect
The most important effect of Lachesis mutus is its blood-thinning, or anticoagulant, function. This action enbances blood flow and facilitates the bealing process by bastening the removal of toxins from the blood. The remedy is effective against many bleeding disorders.
------------------------------------------------------------------------------------------------------------
AproDerm Emollient cream
 
Katherine - (Red Face Rash) If anyone else is suffering from this I just wanted to give hope that this side effect only lasted a few days and that I eased it with AproDerm Emoillent cream,
Ingredients:
White soft paraffin, liquid paraffin, cetostearyl alcohol, macrogol cetostearyl ether, ceteareth-20, purified water, sodium hydrogen phosphate, euxyl PE 9010, phosphoric acid / sodium hydroxide.
------------------------------------------------------------------------------------------------------------
Zofran (is a medication used to prevent nausea and vomiting) It is a serotonin 5-HT3 receptor antagonist (reduces the activity of serotonin receptors). Decreases serotonin production in the intestinal tract.
 
ConnieStar - I have a medication called Zofran (ondansetron) which is working very well for nausea. I recommend it.
 
Nancydear - My doctor said zofran and bonnie for the dizziness and to call if need too.
 
Cymsufferer - I got a message from my pharmacy that Zofran was finally filled. I've been taking it for 2 weeks now. It's helped with the nausea, but the diarrhea and overall gag feeling is still around.
sanctuarie - And finally zofran 8mg odt, which is doing *nothing* for my nausea.
 
Lundetz - Also bad nausea. The doctor had given me Zofran so I tried one today. It helped a lot.
 
Equuswoman - Nausea has a biggie for me mostly. But I am able to control that w/generic Zofran.
 
TheComposer - 1. Nausea: Daily and inconsistent. Benedryl/Dramamine help sometimes, but not always.
Zofran (anti nausea medication used for chemo) completely ineffective.
 
Justmyreality - They gave me Zofran, same drug they give to chemo patients to deal with nausea and vomitting. It worked but I worried it may be masking bigger issues so i only took it a couple days.
 
Crazycatgirl - I've noticed that generic zofran helps a lot with the nausea. I used to use this when I was pregnant and it seems to help a lot now.
 
autimomforever - ask your doc for a prescription for zofran (it helps nausea/vomitting)..
 
MissAmber - I also had a prescription for Zofran and used it when i couldn't take the Dramamine because I needed to not be drowsy for work. It seemed to help too, but often gave me headaches.
 
watchdog - The Zofran is keeping the nausea in check,
 
JustJulz - However, Zofran is a nice one, dissolves in your mouth, and does not mess with your center of well-being (serotonin, etc.). I had no problems at all when I needed to stop using it. Only drawback is that it is constipating.
 
cymthia - My doctor gave me zofran for the nausea which has helped.
 
kelpme2 - My md prescribed Zofran and it has helped a little but I have no desire to eat (which has been going on) and the nausea still there a bit but better I guess.
 
patches - They gave me Zofran in IV and it stopped the non-stop nausea and intermittant cramping. I was able to eat a solid food that night after a good two months of broth and crackers and soft foods. What a nightmare.
 
Caution - 5.3 Serotonin Syndrome
The development of serotonin syndrome has been reported with 5-HT3 receptor antagonists alone. Most reports have been associated with concomitant use of serotonergic drugs (e.g., selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), monoamine oxidase inhibitors, mirtazapine, fentanyl, lithium, tramadol, and intravenous methylene blue). Some of the reported cases were fatal. Serotonin syndrome occurring with overdose of ZOFRAN alone has also been reported. The majority of reports of serotonin syndrome related to 5-HT3 receptor antagonist use occurred in a post-anesthesia care unit or an infusion center.
 
Symptoms associated with serotonin syndrome may include the following combination of signs and symptoms: mental status changes (e.g., agitation, hallucinations, delirium, and coma), autonomic instability (e.g., tachycardia, labile blood pressure, dizziness, diaphoresis, flushing, hyperthermia), neuromuscular symptoms (e.g., tremor, rigidity, myoclonus, hyperreflexia, incoordination), seizures, with or without gastrointestinal symptoms (e.g., nausea, vomiting, diarrhea). Patients should be monitored for the emergence of serotonin syndrome, especially with concomitant use of ZOFRAN and other serotonergic drugs. If symptoms of serotonin syndrome occur, discontinue ZOFRAN and initiate supportive treatment. Patients should be informed of the increased risk of serotonin syndrome, especially if ZOFRAN is used concomitantly with other serotonergic drugs [see Drug Interactions (7.1), Overdosage (10)].
 
Medical research articles which show that Zofran can help with anxiety.
https://www.ncbi.nlm...pubmed/26188166
https://www.ncbi.nlm...pubmed/22374255
https://www.ncbi.nlm...pubmed/25284215
https://www.ncbi.nlm.../pubmed/9151286
https://www.ncbi.nlm...pubmed/10650519
and more....
----------------------------------------------------------------------------------------------------------
Pseudoephedrine/Phenylephrine containing meds
Caution - Pseudoephedrine can raise blood pressure and cause nervousness in some people.
 
Tylenol Cold and Flu
Active ingredients
Dextromethorphan HBr 10 mg in each caplet
Guaifenesin 200 mg in each caplet
Phenylephrine HCl 5 mg in each caplet
Not to be taken with Cymbalta
 
gail - Tylenol flu is good for the brain zaps.
 
hailsmarie - Tylenol Cold and Flu completely took away my brain zaps,
 
dstanek - My husband said try some Nyquil I didn't have any but tried tylenol cold nighttime. In 20 min symptoms disappeared. I slept great no soaking night sweats. No nightmares. Zaps gone, I even had to shake my head to be sure. Woke up this morning feeling normal. I am going to get non drowsy version today and see if this truly is the miracle helper.
 
Caution - tylenol cold nighttime contains
Acetaminophen 325 mg in each 15 mL
Dextromethorphan HBr 10 mg in each 15 mL
Doxylamine succinate 6.25 mg in 15 mL
Phenylephrine HCl 5 mg in each 15 mL
As such it should not be taken with Cymbalta (because of the Dextromethorphan) or diphenhydramine (because of Doxylamine).

Mucinex D
Active Ingredients: Guaifenesin (600 mg), Pseudoephedrine HCl (60 mg).
 
Coastgirl - Just wanna say I ran out of Mucinex D and got Advil Cold And Flu (behind the counter with pseudophedrine) and it also works to combat the brain zaps for me. My vertigo and zaps are 98% gone.
 
Sudafed PE
Dextromethorphan HBr 10 mg
Guaifenesin 100 mg
Phenylephrine HCl 5 mg
 
Caution -As such it should not be taken with Cymbalta (because of the Dextromethorphan)
 
Coastgirl - Tried to not take sudafed this morning and I feel so messed up! Just dizzy and can't think straight. I feel so out out of it.
(I mentioned in another post the Sudafed helps with the brain zaps....unfortunately it doesn't help too much with the mild nausea feeling).
 
Houdi - some days I had to take sudafed, the REAL sudafed and only 1/2 the dose cuz it reves me up.
 
Johnnyz - earlier today I read a topic in here about pseudoephedrine and its supposed effectiveness to alleviate SSRI withdrawal symptoms. I take 12-hour sudafed (the real, behind the counter sudafed) 1-2x daily as I have persistent nasal congestion. Yesterday evening, soon after the morning sudafed tab had worn off, I had a very stressful situation which caused an emotional low that had me sitting for 10 minutes feeling very depressed. I was able to talk myself out of that stupor and continue on in a neutrally emotional state until bedtime. I took a 12-hr sudafed around 11pm and woke up at 6am this morning feeling very good physically and emotionally, like I had a decent sleep. My point here is that, looking back at the previous 5 days of my Cymbalta/ Trintillex withdrawal plan and its relative low and tolerable symptoms, I wonder how much my daily use of sudafed has been a factor in my light symptoms.

Claritin-D 24 hour extended release tablets
10 mg loratadine for immediate release
240 mg pseudoephedrine sulfate is released slowly allowing for once-daily administration.

ittybittysmitty - WHAM, today I got blasted with three times as much dizziness and zapping...I feel zombie-like. Thinking it was part allergy symptoms I took a Claritin...that helped somewhat...less dizziness while seated.
 
irritableme - I started taking a Claritin-D and that seems to help. When I don't take the Claritin-D the brain swooshes and zaps return.

Advil Cold & Sinus
Ibuprofen 200 mg
Pseudoephedrine Hydrochloride 30 mg
Chlorpheniramine Maleate 2 mg
 
Chlorpheniramine (over the counter) is an antihistamine {H(1)R antagonist} used to treat allergy symptoms. It does cause sleepiness like other antihistamines and has significant anxiolytic effects. Caution - It has also been shown to function as an ssri and snri. As such it should never be taken in combination with those medications as it can cause seratonin syndrome. Due to its anticholenergic effects it frequently causes constipation. As with diphenhydramine do not take with other medicines that can cause sleepiness. Recommended dose is 4 mg every 4 to 6 hrs not to exceed 32 mg/day. Widely sold as an allergy treatment.
Begins working in 30 minutes to an hour
Peak levels - 2 to 4 hrs
Half Life – 12 to 43 hrs
 
https://www.ncbi.nlm...les/PMC3854398/
(8mg dose)
https://www.ncbi.nlm...pubmed/16876927
https://www.ncbi.nlm...pubmed/16156843
https://www.ncbi.nlm...pubmed/12951198
https://www.ncbi.nlm...pubmed/10541737

Coastgirl - Just wanna say I ran out of Mucinex D and got Advil Cold And Flu (behind the counter with pseudophedrine) and it also works to combat the brain zaps for me. My vertigo and zaps are 98% gone.
 
Carleeta - Have been taking advil cold and sinus daily..Seems to work.
 
Heartfeatherss - Try taking 4 ( yes 4) Advil LIQUID BLUE GELCAPs with a Coke. It has to be the blue gel caps and it cannot be a diet Coke. My neurologist told me to do this and I was so miffed, thinking he was just not understanding how bad it hurt... but dang! It works!! Hope this gives you relief.
 
Contains ibuprofen and dihydramine. Should not be taken with other amines like benadryl.

Medical information on ingredients of above meds
 
Dextromethorophan
 
FiveNotions - I didn't check, but my bet is that Tylenol Cold contains DMX -- "dextromethorphan" .... it's a serotonin agonist (enhancer - reuptake inhibitor) ...
Nyquil contains a lot of it, which is why someone taking Cymbalta (duloxetine) or any other SSRI shouldn't use Nyquil ... there are case studies about the combo causing severe serotonin syndrome ...

Loratadine

https://www.ncbi.nlm...pubmed/10444229
Loratadine, No effect on 'mood'.

While this is the only research I found it is interesting to note that around 4% of people taking loratadine report anxiety as a side effect. This is about the same number of diphenhydramine (Benadryl) users that report depression as a side effect. (FDA)

From Drugs.com
Cardiovascular side effects have included hypertension, hypotension, palpitation, supraventricular tachyarrhythmias, syncope and tachycardia.

Wiki
As a "nonsedating" antihistamine, loratadine causes less (but still significant, in some cases) sedation and psychomotor retardation than the older antihistamines because it penetrates the blood/brain barrier to a smaller extent.
 
Note - inability to significantly penetrate the blood brain barrier would make it an unlikely anxiolytic medicine.
 
Do not take with Tagamet or other antihistamines.
 
Half life - 8 hours.
 
Metabolism
Loratadine is an H1 receptor antagonist (blocks the action of histamine on the H1 histamine receptor). Does NOT cross the blood brain barrier.
Diphenhydramine is an potent H1 receptor inverse agonist (blocks the action of histamine on the H1 receptors but crosses the blood brain barrier readily. Has been shown to reduce anxiety.
Hydroxyzine is a potent H1 receptor inverse agonist as well and has been shown to have substantial effect on anxiety and readily crosses the blood brain barrier.
 
Pseudoephedrine
Wiki
Patients who are prone to anxiety or panic attacks should use pseudoephedrine with caution, as anxiety and restlessness are common side effects, mostly due to the drug's stimulant properties.
http://www.sciencedi...080552323624882
Can cause anxiety as a side effect.

http://research.omic...Pseudoephedrine
Adverse effects
Common adverse drug reactions (ADRs) associated with pseudoephedrine therapy include: CNS stimulation, insomnia, nervousness, excitability, dizziness and anxiety. Infrequent ADRs include: tachycardia or palpitations.

https://www.ncbi.nlm...pubmed/10999495
"...the drug tended to increase anxiety scores (p=0.092). Depth resulted in a significant increase in anxiety scores (p=0.021) and a significant decrease in verbal fluency test scores (p=0.041)"

https://www.ncbi.nlm...les/PMC4518702/
Over-the-counter cold preparations contain phenylpropylamine and pseudoephedrine, obvious stimulants. Yet patients with unexplained dyspnea may believe they have allergies and take these medications frequently in order to treat their anxiety symptom, further exacerbating their dyspnea and anxiety symptoms. The use of energy drinks with combinations of both caffeine and stimulants is another important example.
And many more research articles....

http://www.ehealthme...loride/anxiety/
(FDA website)
140 people reported to have side effects when taking Pseudoephedrine Hydrochloride.
Among them, 12 people (8.57%) had Anxiety as a side effect.

Pseudoephedrine: Pseudoephedrine is an agonist at both alpha- and, to a lesser degree, beta-adrenergic receptors. Like ephedrine, pseudoephedrine also has an indirect effect by releasing norepinephrine from its storage sites. By stimulating alpha-adrenergic receptors in the mucosa of the respiratory tract, pseudoephedrine shrinks swollen nasal mucous membranes; reduces tissue hyperemia, edema, and nasal congestion; and increases nasal airway patency. Also, drainage of sinus secretions is increased, and obstructed eustachian ostia may be opened. Oral administration of pseudoephedrine usually produces negligible effects on blood pressure. In some patients, especially those with preexisting cardiac disease receiving higher doses, pseudoephedrine may increase blood pressure or irritability of the heart muscle and may affect ventricular conduction. Wiki
Phenylephrine is a selective alpha1-adrenergic receptor agonist (stimulates adrenaline receptors) used primarily as a decongestant, as an agent to dilate pupils, and to increase blood pressure. Wiki
 
Medical research emphasizing that phenylephrine can cause anxiety.
https://www.ncbi.nlm...pubmed/20937329
https://pubchem.ncbi...d/phenylephrine
https://everipedia.o.../Phenylephrine/
People with a history of anxiety or panic disorders, or on anticonvulsant medication for epilepsy should not take this substance.
--------------------------------------------------------------------------------------------------------
Phenylephrine is a selective α1-adrenergic receptor agonist of the phenethylamine class used primarily as a decongestant, as an agent to dilate the pupil, and to increase blood pressure. Phenylephrine is a sympathomimetic drug, which means that it mimics the actions of epinephrine (commonly known as adrenaline) or norepinephrine. Phenylephrine selectively binds to alpha receptors which cause blood vessels to constrict. Phenylephrine may cause side effects such as headache, reflex bradycardia, excitability, restlessness and cardiac arrhythmias. Phenylephrine is not suggested for use in patients with hypertension.
Available as Oral and nasal spray.

While considerable medical research indicates that Phenylephrine can cause anxiety the following research indicates differently.

https://www.ncbi.nlm...pubmed/20937329
Helps with anxiety

https://mdanderson.i...amatergic-synap
https://mdanderson.i...tially-regulate
https://www.ncbi.nlm...les/PMC4252518/
Increases the release of gaba.

---------------------------------------------------------------------------------------------------------------------------------------


naproxin, advil, tylenol, ibuprofen, allevee, aspirin, motrin, acetaminophen, excedrin and other over the counter analgesics do not fair well for body aches and headaches. Just as many say they don't work as say they help. No clear cut option here.
---------------------------------------------------------------------------------------------------------
Himalaya Herbal Healthcare StressCare

http://www.cymbaltaw...elps#entry65192
----------------------------------------------------------------------------------------------------------
Ylang-ylang
Note - Cananga odorata, known as the cananga tree is a tropical tree. It is valued for the perfume extracted from its flowers, called ylang-ylang which is an essential oil used in aromatherapy.
 
Carleeta - Ylang-ylang is still one of my favorites....it's wonderful for lifting your mood...and helps with positivity....
 
mimmie - Dill oil on my wrists and Joy oils (mixture of Bergamot, Ylang Ylang, Geranium and others) on my chest right over my heart.
 
sarahj - Ylang Ylang for in the day, for the beauty of the smell also. You can just smell them straight from the bottle, or put some in your bathwater.
-------------------------------------------------------------------------------------------------------------
Zantac (Ranitidine) is an H2 histamine receptor antagonist that works by blocking histamine and thus decreasing the amount of acid released by cells of the stomach.

http://www.cymbaltaw...tion#entry66071
Zantac (Ranitidine) For Anxiety And Depression

FiveNotions - I've stumbled onto the discovery that Zantac, which I'd been taking for severe acid reflux, seems to help my post-crapalta anxiety ... did some research, and found a number of old (really old) articles that seem to confirm this ... here's one of the freely available ones ...
jimmcg - Now, with a week on the Zantac, I feel much more in control of these feelings. I may wake up worrying about something in the middle of the night, but, unlike before, I can talk myself through it and go back to sleep.
 
Caution : but be aware that new research is showing that extended use of Zantac, and / or use of the highest dose, may cause kidney/liver damage.
 
http://pmj.bmj.com/c...03/353.full.pdf
Effect of the H2-receptor antagonist ranitidine on depression and anxiety in duodenal ulcer patients
Depression and anxiety were measured during the course of a double-blind, placebo-controlled trial
of the histamine H2-receptor antagonist, ranitidine (150 mg twice daily), in patients suffering from
duodenal ulcer but free of systemic disease. There were 25 patients in the ranitidine group (mean age: 33-2 years) and 28 in the placebo group (mean age: 37-2 years). In both groups there was a highly significant and progressive decrease in depression and anxiety scores over the 4 weeks of treatment. There were no instances of mental confusion. In our group of otherwise physically healthy patients, ranitidine appeared to be free of neuropsychiatric complications.

https://www.ncbi.nlm.../pubmed/9833631

The H1- and H2-histamine blockers chlorpheniramine and ranitidine applied to the nucleus basalis magnocellularis region modulate anxiety and reinforcement related processes.
In summary, these findings show that H1- and H2-receptor antagonists differentially modulate reinforcement and fear-related processes in the NBM and thus, provide the first evidence for a behavioral relevance for the histaminergic innervation of this brain site.

https://www.ncbi.nlm...les/PMC3854398/

H1 but not H2 histamine antagonist receptors mediate anxiety-related behaviors and emotional memory deficit in mice subjected to elevated plus-maze testing
As well as...
https://www.ncbi.nlm...pubmed/18275952
https://www.ncbi.nlm...pubmed/17109942
https://www.ncbi.nlm...pubmed/16600315
https://www.ncbi.nlm...pubmed/23535246
https://www.ncbi.nlm...pubmed/22952484
Plus many more....

Drug interactions -
Caution - Zantac (Ranitidine) may significantly increase the blood levels of loperamide (Imodium). This can lead to serious and potentially fatal complications such as irregular heart rhythm and cardiac arrest, especially if you use more than the recommended doses of loperamide.
 
Zantac CAN be taken with Benadryl. They are different types of antihistamines. Drugs.com
-------------------------------------------------------------------------------------------------------------
http://www.cymbaltaw...tion#entry37106
Kratom information and discussion.
-------------------------------------------------------------------------------------------------------------
Benadryl -Antihistamine and sleep aide containing 50 mg diphenhydramine
 
Diphenhydramine, (over the counter) also known as Benadryl, is an antihistamine and as such is not only used for allergies/colds but also as a sleep aide. It does have a mild anxiolytic effect. May lower blood pressure and cause irregular heartbeats. Long-term use of Benadryl often affects mental cognition, especially in the elderly. Your body does build up tolerance to it after a few weeks. There is evidence of dependence in cases of long-term heavy uses, It is a histamine H(1)R antagonist in the brain. Do not take this medicine with any other medicine that can cause sleepiness including benzos, most blood pressure medicines, ssri/snri, buspar and others. Please check for compatibility before using. This medicine has many drug interactions.
Begins working in 15 to 30 minutes
Peak levels - 2 to 2.5 hrs
Half Life – 4 to 6 hrs
 
https://www.ncbi.nlm...pubmed/24530460
Moderately effective
https://www.ncbi.nlm...pubmed/19415242
(50mg dose)
https://www.ncbi.nlm...pubmed/16156843
Effective
https://www.ncbi.nlm...pubmed/16111835
Effective
Can cause dependence with constant heavy use. Some moderate withdrawal symptoms possible.

Diphenhydramine should NOT be taken with hydroxyzine. Drugs.com
 
Use by members for anxiety releif and to help sleep is too numerous to mention.
Products containing diphenhydramine...
Brand names
⦁ Aler-Dryl®
⦁ Allergia-C®⦁ ¶
⦁ Allermax®⦁ ¶
⦁ Altaryl®⦁ ¶
⦁ Banophen®⦁ ¶
⦁ Ben Tann®⦁ §
⦁ Benadryl®
⦁ Bromanate AF®⦁ ¶
⦁ Compoz Nighttime Sleep Aid®⦁ ¶
⦁ Dicopanol®⦁ §
⦁ Diphedryl®⦁ ¶
⦁ Diphen®⦁ ¶
⦁ Diphenadryl®⦁ ¶
⦁ Diphenhist®
⦁ Diphenylin®⦁ ¶
⦁ Dytan®⦁ ¶
⦁ Hydramine®⦁ ¶
⦁ Nytol®
⦁ Pardryl®⦁ ¶
⦁ PediaCare Children's Allergy®
⦁ Siladryl®
⦁ Silphen®
⦁ Sominex®
⦁ Unisom®
Brand names of combination products
⦁ Advil PM® (containing Diphenhydramine, Ibuprofen)
⦁ Alahist LQ® (containing Diphenhydramine, Phenylephrine)
⦁ Aldex CT® (containing Diphenhydramine, Phenylephrine)
⦁ Aleve PM® (containing Diphenhydramine, Naproxen)
⦁ Anacin P.M. Aspirin Free® (containing Acetaminophen, Diphenhydramine)⦁ ¶
⦁ Bayer Aspirin PM® (containing Aspirin, Diphenhydramine)
⦁ Benadryl-D Allergy Plus Sinus® (containing Diphenhydramine, Phenylephrine)
⦁ Children's Dimetapp Nighttime Cold and Congestion® (containing Diphenhydramine, Phenylephrine)
⦁ Doans PM® (containing Diphenhydramine, Magnesium Salicylate)⦁ ¶
⦁ Endal HD® (containing Diphenhydramine, Phenylephrine)⦁ §
⦁ Excedrin PM® (containing Acetaminophen, Diphenhydramine)
⦁ Goody's PM® (containing Acetaminophen, Diphenhydramine)
⦁ Legatrin PM® (containing Acetaminophen, Diphenhydramine)
⦁ Masophen PM® (containing Acetaminophen, Diphenhydramine)⦁ ¶
⦁ Midol PM® (containing Acetaminophen, Diphenhydramine)
⦁ Motrin PM® (containing Diphenhydramine, Ibuprofen)
⦁ PediaCare Children's Allergy and Cold® (containing Diphenhydramine, Phenylephrine)
⦁ Robitussin Night Time Cough and Cold® (containing Diphenhydramine, Phenylephrine)
⦁ Sudafed PE Day/Night Cold® (containing Acetaminophen, Dextromethorphan, Diphenhydramine, Guaifenesin, Phenylephrine)
⦁ Sudafed PE Day/Night Congestion® (containing Diphenhydramine, Phenylephrine)
⦁ Sudafed PE Severe Cold® (containing Acetaminophen, Diphenhydramine, Phenylephrine)
⦁ Tekral® (containing Diphenhydramine, Pseudoephedrine)⦁ §
⦁ Theraflu Nighttime Severe Cold and Cough® (containing Acetaminophen, Diphenhydramine, Phenylephrine)
⦁ Triaminic Night Time Cold and Cough® (containing Diphenhydramine, Phenylephrine)
⦁ Tylenol Allergy Multi-Symptom Nighttime® (containing Acetaminophen, Diphenhydramine, Phenylephrine)
⦁ Tylenol Severe Allergy® (containing Acetaminophen, Diphenhydramine)
⦁ Unisom with Pain Relief® (containing Acetaminophen, Diphenhydramine)

------------------------------------------------------------------------------------------------------
Omeprazole
 
Significant drug interactions.
omeprazole ↔ citalopram
Applies to:omeprazole and Celexa (citalopram)
Talk to your doctor before using citalopram together with omeprazole. Combining these medications may increase the blood levels of citalopram and increase the risk of certain side effects, including an irregular heart rhythm that may be serious or life-threatening.
 
Omeprazole causes the increased absorption of nearly 500 medications. It should NOT be taken with.....
Benzos, Atenolol, Celexa, Lexapro and many other ssri and snri, st. john's wort,
------------------------------------------------------------------------------------------------------
Baking soda
 
Shady Lady - I hate baths, but needed fast relief and the epsom salt baths, I also pour in a half to one cup of baking soda for softness as the bath salts made me itchy, another pesky issue.
 
FiveNotioins - I'd also add in baking soda/water ... I made a paste of it, and put it on the worst welted/itchy/scratchy parts of my skin ... then rinse of with cool water ..
 
plezhelp - i am still doing is tepid Epsom-salt baths with baking soda, and apple cider vinegar - which has helped a lot with the itching;
 
freeme2 - I took a nice hot bath with baking soda and Epson salts The baking soda really calms down the skin.
 
sage - I had digestion issues with Cymbalta as well, especially as I've started weaning off of it. The two things that seem to totally work (for me) are dill pickles with garlic (and sipping the juice!)... and 1/2 tsp of baking soda mixed with a little water (instant appeasement of symptoms, which means Cymbalta has probably made my stomach more acidic?).
 
irnwmn - They suggested soaking in "detox baths". 1 cup epsom salts 1 cup baking soda and ESSENTIAL Lavender.
Many members use baking soda as an antacid as well.
------------------------------------------------------------------------------------------------------------
probiotics
http://www.cymbaltaw...rove#entry45197
It begins on post #68 and continues to post #73.
Info and discussion on probiotics.

http://www.cymbaltaw...ics/?hl=improve
Great Details on benefits of probiotics.

probiotic and serotonin,
https://www.ncbi.nlm...pubmed/28607543
After probiotic supplementation, we observed a significant increase in concentration of serum serotonin (P = .008) and a decreased level of tryptophan in plasma.
https://www.ncbi.nlm...les/PMC5102282/
Summary of the effects of pro and prebiotics on psychiatric functions.
https://www.huffingt...4b064e1b4b3a842
A layman's summary of the effects of pro and prebiotics on psychiatric functions.
https://www.ncbi.nlm...pubmed/25470391
https://www.ncbi.nlm...pubmed/24554471
https://www.ncbi.nlm...pubmed/20974015
https://www.ncbi.nlm...pubmed/21983070
https://www.ncbi.nlm...pubmed/25879690
https://www.ncbi.nlm...pubmed/23384445
and many more
----------------------------------------------------------------------------------------------------------
Phosphatidylserine (Theoretically reduces corticol.)
 
Phosphatidylserine is an important phospholipid cellular membrane component which plays a key role in cell cycle signaling, specifically in relationship to apoptosis (programmed cell death). When the Phosphatidylserine in the cell membrane turns around (The head of the molecule pointing out and the tail pointing in) it acts as a signal for macrophages to engulf the cell.
In May, 2003 the FDA gave "qualified health claim" status to phosphatidylserine thus allowing labels to state "consumption of phosphatidylserine may reduce the risk of dementia and cognitive dysfunction in the elderly" along with the disclaimer "very limited and preliminary scientific research suggests that phosphatidylserine may reduce the risk of cognitive dysfunction in the elderly. FDA concludes that there is little scientific evidence supporting this claim.
Originally acquired from the bovine brain, mad cow disease put an end to that. Most is now extracted from soybeans. Phosphatidylserine can cause side effects including insomnia and stomach upset, particularly at doses over 300 mg.

http://www.ncbi.nlm....pubmed/24759145
Involved in the formation of clots.

http://www.ncbi.nlm....pubmed/23312676
Well tolerated.

http://www.ncbi.nlm....pubmed/24172938
Those with elevated levels of phosphatidylserine are more likely to form thrombosis (blood clots).

http://www.ncbi.nlm....pubmed/23926688
Phosphatidylserine is critical in the production of good quality sperm.

http://www.ncbi.nlm....pubmed/23723695
safe for human consumption.

http://www.ncbi.nlm....pubmed/21807480
Well tolerated

http://www.ncbi.nlm....pubmed/12385596
Soy derived Phosphatidylserine is safe for human consumption.

http://www.ncbi.nlm....les/PMC4237891/
A Phosphatidylserine/phosphatidic acid complex normalized the hypothalmus-pituatary-adrenal axis in acutely stressed males. It normalized cortisol levels. They used PAS 200 (200 mg of both compounds) and PAS 400 (400 mg of both compounds). Only the PAS 400 showed the beneficial response.


http://www.ncbi.nlm....les/PMC2503954/
Reduces cortisol levels after exercise.


Several of these studies showed that the compound Phosphatidylserine had no effect on blood pressure or pulse. With the combination (PAS) returning the hypothalmus-pituatary-adrenal axis to normal function in the chronically fatigued. Adrenaline increases and cortisol decreases with an increase in energy levels. This increase in energy is what causes the insomnia side effect. Should be taken in the morning.
Not compatable with adrenergic agonists (eg. Clonidine). Most reviews of this product are positive but do reflect that it is an adaptogen (your body adapts to it in time and begins reducing its natural production). Many reviews state it only helps for a couple months at a time. There are many who say it makes them sleep like a baby and many who say it causes insomnia. This is probably due to whether or not the person is suffering from a chronic adrenergic state (stress over a long period of time elevating adrenaline levels) OR from adrenal fatigue which is due to a relatively short term intense stress which causes a burst of adrenaline followed by a drop in adrenaline. This is what causes the knees to shake and a person to feel exhausted after say a car accident.

http://www.cymbaltaw...rove#entry59862

Ramona - I've read that there is a supplement called Phosphatidylserine that reduces the amount of cortisol your adrenals are over-producing. Anyone familiar with this? I checked with a pharmacist over the weekend and he said I shouldn't take Seriphos while on Cymbalta.

Bethhalffull - I saw a new shrink. She recommended ... phosphatidylserine. When I investigated the second ingredient it is supposed to limit cortisol.
Seriphos - Phosphorylated Serine - An amino acid not to be confused with Phosphatidylserine although similar in structure and action and is mostly used to improve clotting and cognition. Taking it with Cymbalta reduces the essential amino acid serine in the body and should be avoided. NCBI

I could find no medical journal article associating Phosphorylated Serine with lower cortisol levels. I did find several articles on its effects on the adrenal gland but no reference to its efficacy for either anxiety or depression.
----------------------------------------------------------------------------------------------------------
Rescue Remedy
 
Ingredients
Active Ingredients: 5 x dilution of:- Prunus cerasifera HPUS (Crab Apple), Clematis vitalba HPUS (Clematis), Impatiens glandulifera HPUS (Impatiens), Helianthemum nummularium HPUS (Rock Rose), Ornithogalum umbellatum HPUS (Star of Bethlehem). Inactive Ingredients: 27% Alcohol
 
Uriel - You can get Rescue Remedey from the health food store its a tincture you put under your tongue for anxiety. It helps the body cope well.
-------------------------------------------------------------------------------------------------------
Genius Joy
INGREDIENTS

Serving Size: 4 Delayed Release Veggie Capsules
Servings Per Container: 25

Amount Per Serving

Vitamin B Energy Complex

Vitamin B1 (as Thiamine HCL) – 1.5mg
Vitamin B2 (as Riboflavin 5 Phosphate) – 1.7mg
Vitamin B3 (as Niacinamide) – 20mg
Vitamin B5 (as D-Calcium Pantothenate) – 10mg
Vitamin B6 (as pyridoxal-5-phosphate) – 2mg
Vitamin B12 (as methylcobalamin) – 6mcg
Vitamin D3 (as cholecalciferol) – 1000IU

S-adenosylmethionine (SamE) – 1000mg
N-Acetyl L Tyrosine – 350mg
Rhodiola5Plus Rhodiola rosea [root](std. 3% Rosavins and 2% Salidrosides) – 300mg
Red Panax Ginseng Powder – 250mg
HTPurity 5-hydroxytryptophan Griffonia simplicifolia [seed] (Std. 98% 5-HTP) – 100mg
Neuro Factor Coffea Arabica [Fruit] Extract – 100mg
TheaKalm Natural L-Theanine – 100mg
 
mimi - I'm still only taking 2 Genius Joy supplements when I first get up and by 10am I can do all that I wish to accomplish for the day, I can be outside without itching, I can drive safely, I can do my household finances and communicate effectively.
 
While this product contains many components that may be benificial they may also be incopatable with a variety of drugs and other natural remedies. You should closely check for drug interactions before use.
-----------------------------------------------------------------------------------------------------------


#7 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 15 December 2017 - 01:28 PM

                                                                Other OTC Products

Standard Process

TFL - I found the Min Tran on Amazon -- 90 tabs for 11.97 -- Brand is Standard Process. Suggested dosage 4 tabs w/each meal.
Jessielee - Here are some vitamins & other things that are helping me.
*Standard Process Vitamins: Min-Chex (9/day) & Cataplex G (6/day)

Dawson - I take all natural, whole food supplements that I got from my Doctor. The brand name is Standard Process, and I take several to help restore the balance as well as replenish the minerals that cymbalta has robbed my liver of. I have been on them several months now, and feel really good, however, like I said in my posting, I was off the cymbalta for a week, and was a mess! So who knows what, if anything, is making me feel better?

Jeff - Standard Process Brands is a whole food supplement of really high quality. I get it from my Chiropractor. You cannot get it at a store, check online for resources.
---------------------------------------------------------------------------------------------------------------------------
Gatorade

Amysgarden - I've increased my protein and salt intake and also b vitamins and electrolyte drinks such as Gatorade and Vitalyte. It's helping, but I think with our entire systems being under so much stress from withdrawal and healing, we just have to slow down for awhile and pay close attention to how our bodies respond to nutrient intake.

Fivenotions - I also drank an awful lot of Gatorade during the first weeks.

Carleeta -.For me, I always carry a bottle of gatorade with me where ever I go..

ZappAlta - Eat light but eat often -get some gatorade -keep fluids in most important.

Kindorf - Also I have been avoiding caffeine so I cut out my coffee and sweet tea.
I replaced then with fruit juice, ( mainly apple juice ) water and Gatorade. Today no stomach cramps I think they are done. No diarrhea, Lord I hope that is gone. No dizzy spells today and that felt good.

shvarner - I've been drinking a lot of water & gatorade,

Uriel - I am eating good healthy meals and also drinking gatorade.

Judy - I knew that Gatorade helped with the light-headed, "floating brain" feelings.

watchdog - Drinks LOTS of GREEN gatorade..... don't know what the deal is, but it helps.

wiraz - Drink at least one G2 Gatorade a day – stay away from the full sugar version, leads to a higher chance of diarrhea. I drink one 32 oz bottle every day plus tons of water!!

caroline - Vit E also for head and joints and then Gatorade's G2. I didn't want the sugars so I went with the G2

Rafael - I have mild brain zaps but I believe the omega 3 Fish Oil and Gatorade are helping.

Sandlion - I took fish oil/other Omega 3 and also found that Gatorade helped -- maybe it's the salt replacement after all the nightsweats.

guppie - I'm a month off the drug so only minor zaps now and then. Whoever gave the gatorade advice is a genius. That treats them instantly (make sure you get the low calorie gatorade since regular is high calorie). Brain zaps are minor. I grab a gatorade and that gets rid of those for a bit (electrolytes).

Alisha - gatorade-had one of the big bottles yesterday and it did seem to help,

mkhackler - I have started drinking a ton of G2, the lighter version of Gatorade because I think I'm getting dehydrated as well.

Summary - Many members medtioned drinking Gatorade for the electrolytes after diarrhea, night sweats and when having brain zaps. G2 was often mentioned because it has no sugar (not true, see below). Also, it was suggested that one should not just rely on Gatorade alone for hydrated but should also drink plenti of water. Green Gatorade is highly recommended by some members. Vitylite and Powerade wer also mentioned a couple times for electrolytes. I would also recommend Isopure as it comes with and without sugars and proteins with a similar amount and type of electrolytes as Gatorade.


Original Gatorade - One 12.5 fl oz bottle contains 21 grams sugar. It also contains 160 mg sodium (sodium is a stimulant to some people, raising bp and and metabolism). It contains no phosphorus, calcium or magnesium.
Lemon/lime has same ingredients as other Gatorade except it has Yellow #5.

G2 Gatorade - It has the same amount of sugar as regular Gatorade and nearly all the same ingredients and electrolytes.

Gatorade Fierce Green Apple Sports Drink - This may be the "green gatorade" that members spoke of. It contains malic acid, the active ingredient in apple cider vinager which has proved so helpful to other members. Other ingredients are the same.

Isopure Zero Carbs - No sugar, with some calcium. Contains Malic acid
Isopure Mass - With sugar and proteins, with calcium, Contains Malic acid
Isopure zero carb with proteins - no sugar, contains proteins. With calcium Contains Malic acid

-----------------------------------------------------------------------------------------------------------------------
valerian root

Fishinghat - A caution for those who use or are considering using valerian root. It greatly slows down the bodies ability to process and eliminate benzos. This allows the benzos to build to very high values in the body. Caution should be used when taking the two at the same time.

Fivenotions - Ditto to the valerian caution.....I tried it as tea....wasn't using benzos, but it whacked me out somehow....a tip I got from Fishinghat is to start whatever it is you're trying....amino, herb, etc....in very small amounts/doses....and work up gradually....

Boot2 - i found if i combined chocolate (i am using unsweetened health food store kind now) and valerian- it feels like i am almost normal again...thought i;d pass that along.

LadyNancy - I had a reaction to valerian but then that is nothing new for me.

RussellSprout - The valerian/mag combo (when I remember to do both) doesn't act like a sleeping pill or anything of that sort, but it does physically relax me so I can drift to sleep more easily. Unfortunately, the valerian smells like death.

Hornet - I too am enjoying the dreams. Additionally, I have been taking Valerian root to help sleep and it exacerbates the dreams.

brzghoff - valerian works for some, gives me a headache.

jillybean - I also use valerian root (from puritan's pride) 450 mg capsules 1 capsule late afternoon and 1 before bed. This is considered nature's valium and though it does not make me drowsy I do feel it is helping with anxiety. I missed the late afternoon dose yesterday and had one hell of a panic attack. I won't do that again.

Albergo - Made things worse: Valerian root (really bad reaction - BIG WARNING), benzodiazepines (clonozepam .5mg, took 1-2 weeks to recover from),

Around 20 members mention taking valerian, especially in their SleepyTime Tea. I would estimate around 60% said it helped with around 40% saying no. Several had bad reactions/interactions with it.

Drug.com list 581 drug interactions for Valerian, including sleep aides, benzos, cold medicines, and more.
---------------------------------------------------------------------------------------------------------------------------
damiana tea

FiveNotions - Instead of valerian, I use damiana tea...from the fresh herb.....but a caution there....it can lower blood pressure, esp. Systolic....that's a benefit for me, but not if you already run low or take meds for bp.....

Fishinghat - Interesting. I couldn't find anything about damiana (Turnera diffusa) treating anxiety in the medical journals. But I found several articles on Turnera aphrodisiac being as effective as diazepam. The active ingredient on Turnera aphrodesiacis, Apigenin, which works on benzo receptors. (see reference below )

Kumar, S; Madaan, R; Sharma, A (2008), "Pharmacological evaluation of Bioactive Principle of Turnera aphrodisiaca", Indian Journal of Pharmaceutical Sciences, 70: 740–4, doi:10.4103/0250-474X.49095, PMC 3040867  , PMID 21369434
Apigenin is a potent inhibitor of CYP2C9 an enzyme responsible for the metabolism of many pharmaceutical drugs in the body. Ingestion of this substance would significantly reduce the absorption of medicines and supplements absorbed via the CYP2C9 enzyme. It also effects opiod and adenosine receptors as well. It can increase testosterone levels, decrreases cortisol levels, (See reference below for source references).
https://examine.com/...ments/apigenin/

Many references state that Turnera diffusa and T. aphrodisiaca are generally regarded as the same plant in herbal commerce. This may explain why some supplements have a better reputation than others. Many mention that damiana is also an aphrodesiac but again this is not damianas but Turnera aphrodisiac.

Research;

http://www.ncbi.nlm....pubmed/16635964
http://www.ncbi.nlm....pubmed/15864356
http://www.ncbi.nlm....les/PMC1062162/


http://www.herbaldb....iolytic-action/
The article here talks about the anti-anxiety properties of damianas in research BUT the research they quote was done on Turnera aphrodesiac not Turnera diffusa (damianas).
-------------------------------------------------------------------------------------------------------------------
essential oils

Tea tree oil
kmrek - Some things I tried when I weaned the first time: tea tree oil under my nose (for some reason, the smell was calming),

Ylang-ylang
Note - Cananga odorata, known as the cananga tree is a tropical tree. It is valued for the perfume extracted from its flowers, called ylang-ylang which is an essential oil used in aromatherapy.

Carleeta - Ylang-ylang is still one of my favorites....it's wonderful for lifting your mood...and helps with positivity....

mimmie - Dill oil on my wrists and Joy oils (mixture of Bergamot, Ylang Ylang, Geranium and others) on my chest right over my heart.

sarahj - Ylang Ylang for in the day, for the beauty of the smell also. You can just smell them straight from the bottle, or put some in your bathwater.

Sniff some vanilla or lavender - Vanilla causes an increase in production of endorphins. This is why it can help so many with anxiety. The endorphins released when inhaling lavender creates a calming effect that may even enhance sleep and relieve depression.
https://www.ncbi.nlm...les/PMC4325408/
http://www.sciencedi...221169115001033
Ward, A., & Ward, K. (2006). U.S. Patent Application 11/609,330.

Vanilla Oil -
Plzhelp - i just recently learned that 'vanilla' is now something i am currently allergic to (i get headaches).

Lavender Oil - Members 12 positive and 1 negative comment.
SCL - I also have a sleep blend of Serenity, lavender, sandalwood, and bergamot. The calming blend even helped me with a headache without meds!

Gail - What helps me is bubble bath with lavender essential oil.

CurlyKate - The tips on bathing aren't working, my skin feels so tingly and creepy crawly that even my hair and clothing are painful...lavender and any other smells are triggering migraines...lost all appetite...can't sleep...this really sucks!

Gene - I agree 100% with the lavender scent, amazing how calming it is

Warning - Many essential oils are toxic to the liver and may collect there. Especially if taken orally or applied on the skin in large quantities or frequently.
The oils listed underneath are banned (FDA) and can cause toxicity if taken internally as well as dermally (eg. in a massage blend).
⦁ Almond butter
⦁ Boldo leaf
⦁ Calamus
⦁ Camphor
⦁ Horseradish
⦁ Jaborandi leaf
⦁ Mugwort
⦁ Mustard
⦁ Nightshade
⦁ Pennyoyal (both European and North American)
⦁ Rue
⦁ Sassafras
⦁ Savin
⦁ Southernwood
⦁ Stinging nettles
⦁ Tansy
⦁ Thuja
⦁ Wintergreen
⦁ Wormseed
⦁ Wormwood

http://essentialoils...c-oils.htmgivesdetails on each of these oils.
Medical research on DERMAL toxicity of essential oils.
https://www.ncbi.nlm...les/PMC3546250/
https://www.ncbi.nlm...pubmed/23663182
https://www.ncbi.nlm...pubmed/15771186
https://www.ncbi.nlm...pubmed/16324777
https://www.ncbi.nlm...pubmed/25272759
About lemon, ginger and clove toxicity.

https://www.ncbi.nlm...pubmed/15895251
Recent growth in aromatherapy sales has been accompanied by an unfortunate increase in accidental poisoning from these products. Clove oil warrants special attention.

RevTom - Yes, we had some empty veggie caps lying around, for essential oils.

Carleeta - Rosemary oil rubbed on your temples makes you think clearer

FiveNotions - I found the scent of lavender to be very soothing, helpful to me for getting calmed down and drifting off to sleep .

Fishinghat - A caution on the essential oils. Being oils they are absorbed readily through the skin into the blood stream where (along with other oils and fats) and can contribute to non-alcoholic fatty liver disease. I know they are real popular right now but the FDA is considering a warning on topical use. Lemon oil is the only one tested to not contribute to this condition. These oils combine with cholesterol and triglycerides in fat/oil saturation of the liver.
You might consider just putting them on your collar or label for the aroma.

smacoy - I am using Young Living Essentil Oils. There are so many oils to use for so many things. I diffuse them, take them orally, apply them topically. My favorite right now is the supplement called Ningxia Red. It's a mixture of fruit juices and essential oils. It gives me energy and even curbs my appetite some. It's also great for your immune system. I also have lavender, frankincense and lemon which are supposed to be great for depression. I have a pendant that I'm going to put them in and wear them so that I'm inhaling them all day

CatLeeJones - What I've come across for the pain is absolutely amazing. It is called 'oil pulling'. Oil pulling is putting about a tablespoon of oil in your mouth, gently swishing it through for about 20 minutes. Then you spit it out. I did this for the first time yesterday with 3 sessions and it is nothing short of a miracle in how it released my pain. I've just started this process, with others I've read up on stating their pain is completely gone. There are so many more benefits from this process. This is something Im sure big pharma doesn't want too popular. The oils recommended are sesame seed oil, olive oil and coconut oil. I used organic sesame seed oil. I've read that sesame seed oil has properties that is most beneficial for fibromyalgia sufferers. It will take a bit to get used to but I'd rather do this than take pills that poison my body.

https://www.ncbi.nlm...pubmed/25584309
Oil pulling with sesame oil is equally efficacious as chlorhexidine in reducing oral malodor (bad breath) and microbes causing it. It should be promoted as a preventive home care therapy.

https://www.ncbi.nlm...pubmed/27084861
The Effect of Coconut Oil pulling on Streptococcus mutans Count in Saliva in Comparison with Chlorhexidine Mouthwash.

https://www.ncbi.nlm...pubmed/27966509
Oil pulling for bad breath.

And many more articles all dealing with oil pulling for bad breath and oral bacterial control.

https://www.ncbi.nlm...pubmed/29070291
https://www.ncbi.nlm...pubmed/24429325
https://www.ncbi.nlm...pubmed/26518258
lipoid pneumonia caused by repeated sesame oil pulling
Note - he membranes in the mouth are very adept at absorbing materials. This would be a way to directly absorb oils (especially if exposed for 20 minutes, directly into the blood stream without digestion.

grtree - the next step was to meet with an aromatherapist,she performed a thorough intake survey,we tried several different essential oils to see how I responded,then she mixed them and put into an inhaler(absolutely fantastic!)Then I kept pushing back the time I took the meds daily,just kept waiting until the zaps and dizzy feelings were getting to me,over the course of three weeks,I gained a full two days in time so to speak,then one day my body said...enough.The first 72 hours were a breeze,then things got ugly with the withdrawal symptoms.

I am who I am - To relieve dizziness or vertigo symptoms you can even opt for aromatic essential oils like lavender, peppermint, etc. Gentle forehead massage with the essential oils will be helpful in restoring normalcy and improves blood circulation.

SCL - have a calming blend of doTerra Serenity, frankinsence, and something else (someone made it for me). I also have a sleep blend of Serenity, lavender, sandalwood, and bergamot. The calming blend even helped me with a headache without meds! It could all be in my head, but I don't care.

---------------------------------------------------------------------------------------------------------------------------
Jujube (also called San Zao Ren) (Genera Ziziphus)


FH - San Zao Ren is the same thing as Jujube. It does have anxiolytic effects but can also reduce bp so please monitor carefully.
Geebers - She gave me an herbal powder called San Zao Ren (Chao). This is to help with the anxiety and sleep.
https://www.ncbi.nlm...pubmed/19260286
The alcohol extracts of Semen Ziziphi Spinosae have the anti-anxiety effects instinctively. Its mechanism may be related to increasing the GABA and expression of GABAAR1 and reducing the Glu and expression of NMDAR1.

https://www.ncbi.nlm...pubmed/19101585
It is concluded that sanjoinine A may have anxiolytic-like effects in the elevated plus-maze, hole-board test and open field test, and these effects may be mediated by GABAergic transmission.
https://www.ncbi.nlm...pubmed/19505549
ZE (jujube) with the 5-HT(1B) (serotonin) receptor.

https://www.ncbi.nlm...pubmed/10996283
https://www.ncbi.nlm...pubmed/14531016
All the above mention anxiolytic effects.

https://examine.com/...iziphus-jujuba/
Traditional usage of Jujube is taking 50g of the fruits (20 individual 2-2.5cm diameter fruits) and doing a hot water extract, either a soup of a beverage.
There currently is not enough evidence in humans to establish an effective oral dose of Zizyphus Jujube supplements but estimating from animal studies finding benefits with 500mg/kg for anxiety reduction, an estimated human dose would be:
⦁ 5,500 mg for a 150lb person
⦁ 7,300 mg for a 200lb person
⦁ 9,000 mg for a 250lb person
The seeds of Ziziphus jujube have been implicated in reducing anxiety, in accordance with their traditional usage. Oral administration of 0.5, 1, and 2g/kg of the ethanolic seed extract in mice was able to exert anxiolytic effects, and although it was equally effective as Buspirone and Diazepam (2mg/kg and 1mg/kg, respectively) at a black and white test (anxiety model) at 500mg/kg, it appeared to become less potent at anxiolysis at 1 and 2g/kg while becoming more sedative in nature.
Highly regarded as a sedative in traditional chinese medicine with minimal Western trials on its efficacy, it appears to induce sedation in a relatively dose dependent manner and is synergistic with 5-HTP in this regard.
Good for constipation. May be acutely anti-fertility, but there is limited evidence to support this notion.
Above reference contains support references.
As no human toxicity tests have been performed care should be used when taking this supplement.
---------------------------------------------------------------------------------------------------------------------------
Multivitamins

Caution -Vitamin Toxicity. More than 60,000 instances of vitamin toxicity are reported annually to US poison control centers.
USP – A sign of synthesized vitamins. Most vitamins can be purchased as natural food vitamins.

Vitamins should always be consumed with at least a small amount of foods which contain the same vitamin. This way any natural covitamins, enzymes or poteins needed to process the vitamin will be available.

A (β-carotene) is a group of unsaturated nutritional organic compounds, that includes retinol, retinal, retinic acid and several provitamin A carotenoids, among which beta-catotene is the most important. Vitamin A has multiple functions: it is important for growth and development, for the maintenance of the immune system and good vision. Vitamin A is needed by the retina of the eye in the form of retinal. Vitamin A also functions as retinoic acid which is an important hormone-like growth factor for epithelial and other cells. Recommended Daily Allowance is from 600 to 900 micrograms/day (Maximum is 1700 to 3000 micrograms/day). Vitamin A toxicity is very serious and as it is fat soluble it may be stored in the human body. Consult with physician before taking Vitamin A supplements. Anxiety is a side effect of Vitamin A deficiency and as such Vitamin A will bring the anxiety under control but it is recommended that this be done by dietary changes rather than by supplements due to the risk of toxicity. Vitamin A allergy is rare.

https://www.ncbi.nlm...pubmed/21521362
Not anxiolytic.
https://www.ncbi.nlm...pubmed/24777547
RA not anxiolytic.
https://www.ncbi.nlm...pubmed/17727954
Causes anxiety

Hypervitaminosis A (elevated Vitamin A levels)
Toxicity results from ingesting too much preformed vitamin A from foods (such as fish or animal liver), supplements, or prescription medications and can be prevented by ingesting no more than the recommended daily amount.
Diagnosis can be difficult but there are effective tests available. Hypervitaminosis A is usually treated by stopping intake of the offending food(s), supplement(s), or medication. Most people make a full recovery.

Wiki

"Per tablespoon (13.6 g), cod liver oil contains 136% of the established daily Tolerable Upper Intake Level (UL) for Preformed Vitamin A (Retinol). Vitamin A accumulates in the liver, and can reach harmful levels sufficient to cause hypervitaminosis A. Pregnant women may want to consider consulting a doctor when taking cod liver oil because of the high amount of natural forms of vitamin A such as retinol.

The risks of fatty acid oxidation, hypervitaminosis, and exposure to environmental toxins are reduced when purification processes are applied to produce refined fish oil products."

The environmental toxins are important, especially mercury, other heavy metals and pesticides.
http://ajcn.nutritio...t/83/2/191.full
In developed nations, the increasing availability of and interest in fortified foods and supplements resulted in a large percentage of the population with preformed vitamin A intakes higher than recommended. Indeed, observational studies suggest that more than 75% of people may be routinely ingesting more than the recommended dietary allowance (RDA) for vitamin A, much of it as preformed vitamin A

https://www.ncbi.nlm...t00572-0157.pdf
Chronic hypervitaminosis A may exist for many years among members of the general
public without recognition, resulting eventually in hepatocellular (liver) damage and hepatic fibrosis. Pre-existing liver disease may also affect the capacity of the organ to transport the vitamin into the circulation, thus potentiating its hepatotoxicity..

Symptoms may include:
Abnormal softening of the skull bone (in infants and children)
Blurred vision
Bone Pain or swelling Bulging of the soft spot in an infant's skull
Changes in alertness or consciousness
Devreased Appitite
Dizziness
Double vision (in young children)
Drowsiness
Hair changes, such as hair loss and oily hair
Headache
Irritability
Liver damage
Nausea
Poor weight gain (in infants and children)
Skin changes, such as cracking at corners of the mouth, higher sensitivity to sunlight, oily skin, peeling, itching, and yellow color to the skin
Vision changes
Vomiting

Dosages -
Liver is high in vitamin A. The liver of certain animals are particularly toxic. Supplements - usually when taken above recommended dosages - can be toxic. Cod Liver Oilis particularly high in vitamin A.

http://nutritiondata...-and-oils/628/2
One tablespoon of Cod Liver oil contains 13,500 IU (4,500 μg/day) which exceeds the tolerable upper limit for an adult human by 50% for daily intake.

Most Vitamin A supplements deliver 5,000 to 25,000 IU (which is 1,667 to 8,333 μg/day)
Amazon

https://www.ncbi.nlm...ooks/NBK222318/
The half-life o0f Vitamin A is 128 days and allows for rapid build up of toxic levels.

Daily Tolerable Upper Level
Life stage group category Upper Level (μg/day)
Infants
0–6 months
7–12 months
600
600
Children
1–3 years
4–8 years
600
900
Males
9–13 years
14–18 years
19 – >70 years
1700
2800
3000
Females
9–13 years
14–18 years
19 – >70 years
1700
2800
3000
Pregnancy
<19 years
19 – >50 years
2800
3000
Lactation
<19 years
19 – >50 years
2800
3000
Source for above information is wiki

B complex is a class of water-soluble vitamins that play important roles in cell metabolism. Though these vitamins share similar names, research shows that they are chemically distinct vitamins that often coexist in the same foods. In general, supplements containing all eight are referred to as a vitamin B complex. General side effects, (usually transient) may include restlessness, nausea and insomnia. Vitamin B allergies are rare and are usually associated with Vitamin B 3, 6 and 12. Some allergic reactions can be severe. See individual B vitamin. The raw form of B vitamins are difficult to absorb. The methylated or phosphated forms (sometimes referred to as coenzyme form)is more readily absorbed. Since the B vitamins are so essential in our handling of stress many psychiatrists begin new patients off with a vitamin B blood assessment. There is little evidence that B vitamins are effective against anxiety but only helps protect against the effect of further stress.

FH - One caution to add. If this is your first time taking B vitamins start with a low dose and work up from there. I was put on B complex when I was first diagnosed with anxiety and had a severe allergic reaction to it.. Allergy to B vitamins is uncommon but does happen. I can't even take the little kiddy pills without nausea and vomiting.

FN - Also, take them in the morning.....I learned that if I take a b complex any later than noon, it seems to interfere with my sleep....they seem to give me an energy boost, which isn't what I need at nighttime.....I've read that this is the case for quite a few people....

http://www.ncbi.nlm....pubmed/23738221
Used Max Stress B, effective, 30 days to start

Caution – Max Stress B contains many more active ingredients than just B Vitamins.

https://www.ncbi.nlm...pubmed/21905094
B complex not effective

B1 (thiamine) is the most active form is thiamine pyrophosphate (TPP), a coenzyme in the breakdown of sugars and amino acids. Synthetically thiamin is usually marketed as thiamin hydrochloride or thiamin mononitrate and is a made from Grewe diamine (a coal tar derivative) processed with ammonia and other chemicals.
Thiamine is used in the biosynthesis of the neurotransmitters acetocholine and gamma=aminobutyric Acid (GABA). Humans must obtain it from their diet. Thiamine deficiency has a potentially fatal outcome if it remains untreated. The RDA is set at about 1.0 mg. There are no reports available of adverse effects from consumption of excess thiamine by ingestion of food and supplements. Vitamin B1 toxicity is very rare but high doses can lower other vitamins.
No research found to indicate Thiamine is anxiolytic.

B2 (riboflavin) has reactions including activation of other vitamins. There is no evidence for riboflavin toxicity produced by excessive intakes, as its low solubility keeps it from being absorbed in dangerous amounts within the digestive tract. Allergic reactions are rare.
No research found to indicate riboflavin is anxiolytic.

B3 (niacin) is changed to NAD and NADP which are used in catabolism of fat, carbohydrate, protein, and alcohol, as well as cell signaling and DNA repair, and NADP mostly in anabolism reactions such as fatty acid and cholesterol synthesis. Niacin is involved in both DNA repair and the production of steroid hormones in the adrenal gland. Due to high energy use in the brain it is the most susceptible organ for niacin deficiency. RDA is 14 to 16 mg/day. Intake should not exceed 35 mg/day. Extended release tablets increase the risk of liver toxicity. The FDA does not recommend the taking of niacin supplements. Niacinamide does not seem to cause gastrointestinal upset or hepatotoxicity that the synthetic time-released niacin can cause.

It comes in 3 forms (nicotinic acid, niacinamide and nicotinamide). Taking niacin also might worsen allergies, gallbladder disease and symptoms of certain thyroid disorders. If you have diabetes, niacin can interfere with blood glucose control. Use niacin with caution if you have the complex form of arthritis gout. Niacin can cause an excess of uric acid in the blood (hyperuricemia), putting you at risk of gout. (Mayo Clinic)

No research found to indicate niacin is anxiolytic.

FH - Niacin is a B Vitamin (B2) and like so many B vitamins it can help with anxiety. CAUTION....Niacin can build up in the system and cause flushing, liver toxicity and really agitate your stomach. I would start with low doses around 0.25 to 0.5 mg per day and see how you handle it.

B5 (pantothenic acid) is a water soluble vitamin that is essential to synthesize and metabolize proteins, carbohydrates, and fats. The RDA is 5mg/day. There is no upper limit for consumption. Extremely high doses have been found to produce panic attacks. Synthetic pantothenic acid is processed with formaldehyde (a strong cancer causing agent. It exists in 2 other forms; pantotheno and calcium pantothenate.
No research found to indicate pantothenic acid is anxiolytic.

B6 (pyridoxine) is involved in many aspects of macronutrient metabolism, neurotransmitter synthesis, histamine synthesis, hemoglobin synthesis and function, and gebe expression. It is a factor in the biosynthesis of five important neurotransmitters: serotoniin, dopamine, epinephrine, norepinephrine, and gamma-aminobutyric acid (GABA). The RDA is 1 – 3 mg/day. Doses of pyridoxine in excess of the RDA over long periods of time result in painful and ultimately irreversible neurological problems. There are 7 forms; Pyridoxine (most common), Pyridoxine 5'-phosphate, Pyridoxal, Pyridoxa 5'-phosphate, the metabolically active form (sold as 'P-5-P' vitamin supplement) Pyridoxamine (PM), Pyridoxamine 5'-phosphate (PMP) and 4-Pyridoxic acid (PA). Due to its half life of up to 25 days it is easy to buildup mtoxic amounts in the blood stream. Vitamin B6 toxicity is on the rise in the USA.

Vitamin B6 Toxicity

https://www.ncbi.nlm...pubmed/26417231
Fenugreek seed extract treats peripheral neuropathy in pyridoxine induced neuropathic mice. Our data showed that fenugreek has anti neuropathic effect and restores the function of nerve fibers
The German Commission E monograph recommends 6 grams per day, which can be taken all at once or divided between three meals. Since most fenugreek capsules are available in either 580 or 610 milligrams, a common dosing scheme would be 2-3 capsules three times a day.

https://www.ncbi.nlm.../pubmed/6308447
We describe seven adults who had ataxia and severe sensory-nervous-system dysfunction after daily high-level pyridoxine (vitamin B6) consumption. Four were severely disabled; all improved after withdrawal. Weakness was not a feature of this condition, and the central nervous system was clinically spared. Although consumption of large doses of pyridoxine has gained wide public acceptance, this report indicates that it can cause sensory neuropathy or neuronopathy syndromes and that safe guidelines should be established for the use of this widely abused vitamin.

https://www.ncbi.nlm...ooks/NBK114313/
Half-Life is 15 to 24 days.

https://www.ncbi.nlm.../pubmed/3041185
Pyridoxine neuropathy.
A case of sensory neuropathy in a young woman due to long-term ingestion of pyridoxine, with subsequent recovery, is described. Pyridoxine neuropathy may occur after the long-term ingestion of doses as low as 200 mg a day. Because of its widespread use in the community, both the general public and the medical community need to be aware of this recently described complication of megavitamin therapy.

https://www.ncbi.nlm.../pubmed/3630649
A newly recognized neurotoxic syndrome due to pyridoxine (B6) overdose is described. It is the largest series of B6 intoxication hitherto reported. A raised serum B6 level was present in 172 women of whom 60% had neurological symptoms, which disappeared when B6 was withdrawn and reappeared in 4 cases when B6 was restarted. The mean dose of B6 in the 103 women with neurological symptoms was 117 +/- 92 mgs, compared with 116.2 +/- 66 mgs in the control group. There was a significant difference (P less than 0.01) in the average duration of ingestion of B6 in the neurotoxic group of 2.9 +/- 1.9 years compared with 1.6 +/- 2.1 years in controls. The symptoms were paraesthesia, hyperaesthesia, bone pains, muscle weakness, numbness and fasciculation, most marked on the extremities and predominantly bilateral unless there was a history of previous trauma to the limb. These women were taking a lower dose of B6 than previously described (1,2), which may account for the complete recovery within 6 months of stopping B6.

https://www.ncbi.nlm...pubmed/10746516
50 mg B6 with Mg
https://www.ncbi.nlm...pubmed/15554143
Magne-B6 (a magnesium lactate/pyridoxine combination), effective. 14 days to start.
A total of four articles were found linking vitamin B6 to the treatment of anxiety and/or depression.
https://www.livestro...icity-symptoms/
Vitamin B-6 toxicity cannot occur from eating natural foods, but it can occur from supplementing with its synthetic form, pyridoxine. The recommended dietary allowance of vitamin B-6 for adults is no more than 2 mg daily, but toxicity is not thought to occur until ingesting at least 100 mg daily, if not 500 mg daily, for many weeks consecutively. Some people do mega-dose pyridoxine for long enough to cause toxicity, which leads to symptoms ranging from temporarily irritating to permanent and disabling.

https://www.ncbi.nlm...pubmed/16320662
Vitamin B6 (pyridoxine) causes neuropathy at intakes of 1000 mg per day or more, which is about 800 times the daily intake from foods. There have also been occasional reports of toxicity at intakes of 100-300 mg per day. The US authorities set the no-observed-adverse-effect-level at 200 mg per day and the safe upper limit at 100 mg per day.

https://www.ncbi.nlm...pubmed/25137514
Supplementation with pyridoxine at doses greater than 50 mg/d for extended duration may be harmful and should be discouraged.
https://www.ncbi.nlm...pubmed/25056196

B7 (Biotin) no reported side effects or toxicity.
No research found to indicate biotin is anxiolytic.

B9 (Folic acid, folate) is essential for numerous bodily functions. Humans cannot synthesize folic acid, therefore, folic acid has to be supplied through the diet to meet their daily requirements. Folic acid is not found naturally but folate is. Some recent research has indicated that synthetic folic acid may interfer with the bodies ability to process folate. The human body needs folate to synthesize DNA, repair DNA, and methylate DNA as well as to act as a cofactor in certain biological reactions. It is especially important in aiding rapid cell division and growth, such as in infancy and pregnancy. Children and adults both require folate to produce healthy red blood cells and prevent anemia. Low risk of toxicity. RDA is 400micrograms/day and not to exceed 1000.
http://www.ncbi.nlm....pubmed/22528830

B12 (methylcobalamin) (do not use cyanocobalamin, contains cyanide molecule.) oral use may lead to several allergic reactions such as hives; difficult breathing; swelling of the face, lips, tongue, or throat. Less-serious side effects may include headache, nausea, stomach upset, diarrhea, joint pain, itching, or rash. Cyanocobalamin is synthetically manufactured but the body can convert it to all forms of vitamin B12. Vitamin B12 is essential to growth, cell reproduction, hematopoiesis, and nucleoprotein and myelin synthesis.

http://www.ncbi.nlm....pubmed/12796225
Not anxiolytic.

Vitamin C (ascorbic acid ) is a cofactor in at least eight enzyme reactions, including several collagen synthesis reactions that, when dysfunctional, cause the most severe symptoms of scurvy. In animals, these reactions are especially important in wound-healing and in preventing bleeding from capillaries. Vitamin C may also act as an antioxidant against oxidative stress. The functions of Vitamin C include the synthesis of collagen, carnitine, and neurotransmitters (norepinephrine from dopamine); the synthesis and catabolism of tyrosine; and the metabolism of microsome. RDA is 75 to 90 mg/day with no more than 2000 mg/day maximum. The signs and symptoms of overdose is nausea, vomiting, diarrhea, flushing of the face, headache, fatigue and disturbed sleep. Vitamin C's anxiolytic properties is beleived to primarily be from its ability to repair oxidative effects from stress.

http://www.ncbi.nlm....pubmed/24511708
Effective at 1000 mg/day
http://www.ncbi.nlm....les/PMC2885294/
Effective
https://www.ncbi.nlm...pubmed/24979594
Effective
https://www.ncbi.nlm...pubmed/21036190
Effective and lowers cortisol levels.
https://www.ncbi.nlm...les/PMC2649700/
Ascorbate is proposed as a neuromodulator of glutamatergic, dopaminergic, cholinergic and GABAergic transmission and related behaviors.
https://www.ncbi.nlm...les/PMC3964749/
A paper explaining the relationship between oxidative stress and anxiety.

Vitamin D - Cholecalciferol and ergocalciferol
No Research shows Vitamin D, in any form, anxiolytic.

FH - You are definitely correct about taking the D3 with the calcium but would caution about watching out for immediate changes in behavior, clarity of thought, (not that I am sure I could tell right now lol), constipation, nausea and vomiting as these are symptoms of an allergic reaction that require immediate medical attention. If taking vit d3 you should have your calcium and D3 levels checked each 6 months. Long term use can cause hypercalcemia (too high calcium levels).

Vitamin E refers to a group of compounds that include both tocopherols and tocotrienols. Regular consumption of more than 1,000 mg (1,500 IU) of tocopherols per day may be expected to cause hypervitaminosis E with an associated risk of vitamin K deficiency and consequently of bleeding problems. Vitamin E has many biological functions, the antioxidant function being the most important and best known. Other functions include enzymatic activities, gene expression, and neurological function(s). RDA is 15 mg/day.

Hypervitaminosis E is a state of vitamin E toxicity. Since vitamin E can act as an anticoagulant[citation needed] and may increase the risk of bleeding problems, many agencies have set a tolerable upper intake levels (UL) for vitamin E at 1,000 mg (1,500 IU) per day.[1] This UL was established due to an increased incidence of hemorrhaging with higher doses of supplemental vitamin E. Doses of vitamin E above the UL can also magnify the antiplatelet effects of certain drugs such as anti-coagulant medications and aspirin, which can cause life-threatening symptoms in ill patients. Hypervitaminosis E may also counteract vitamin K, leading to a vitamin K deficiency.

http://jn.nutrition....138925.full.pdf
Half life is 2 - 3 days.

http://www.ncbi.nlm....pubmed/24511708
Not effective

https://www.ncbi.nlm...pubmed/21036190
Effective

Members comments

Many used vitamins without any real comment on their perceived effectiveness.
One member did recommend Vitamin B complex.
And two stated that Vit B complex may have caused increased anxiety.
Another stated....."B Vitamins - "
"Some of the recommendations I've heard are: stay away from Vitamin B as it ramps up the nervous system and can actually increase anxiety."

Resources
Major sources of information includes NCBI, webmd, emedicine and drugs.com.
--------------------------------------------------------------------------------------------------------------------
Centrum Forte

Lady nancy - A really good vitamin & mineral supplement (I used Centrum Forte) has helped me.

Nutrient Info
Select a vitamin or mineral to learn more.
Vitamins
Vitamin A
1,000 IU
Beta- Carotene
3,000 IU
Vitamin E
50 IU
Vitamin C
90 mg
Folate
0.4 mg
Vitamin B1
2.25 mg
Vitamin B2
3.2 mg
Niacinamide
15 mg
Vitamin B6
5 mg
Vitamin B12
20 mcg
Vitamin D
600 IU
Biotin
45 mcg
Pantothenic Acid
10 mg
Vitamin K1
25 mcg
Minerals
Calcium
200 mg
Iodine
0.15 mg
Iron
10 mg
Magnesium
50 mg
Copper
1 mg
Manganese
5 mg
Potassium
80 mg
Chromium
35 mcg
Molybdenum
45 mcg
Selenium
55 mcg
Zinc
7.5 mg
Other Ingredients
Lutein
500 mcg
Lycopene
600 mcg

-------------------------------------------------------------------------------------------------------------------------
Calms Forte

Arcelus - Right now I'm also taking 300mg of chelated magnesium and I might take calms forte for sleep as well.
Uriel - Different things work for different people I have found a homepathic called Calms Forte for me they work great for the anxiety and down moods while i went thru withdrawl.

Active Ingredients | Purposes:
Avena Sativa 4X HPUS: stress, nervousness
Calcarea Phosphorica 3X HPUS: restlessness
Chamomilla 4X HPUS: nervous irritability
Ferrum Phosphoricum 3X HPUS: nervousness
Humulus Lupulus 4X HPUS: occasional sleeplessness
Kali Phosphoricum 3X HPUS: irritability
Magnesia Phosphorica 3X HPUS: mental anxiousness
Natrum Phosphoricum 3X HPUS: anxiousness
Passiflora 4X HPUS: restless sleep from exhaustion

Caution - Carefully investigate the possibility of interactions with your medications.

 


#8 gail

gail

    God-like

  • Site Supporter
  • 4,600 posts
  • LocationSherbrooke, PQ
  • why_joining:
    5 months on cymbalta, scary side effects, never felt good.
    Needed understanding and support, and a place where I was not alone. To read others stories and realizing that I was not the only one going through all that crap.
    In hope that one day, I can return the favors in some kind of way.

Posted 16 December 2017 - 09:44 AM

Oh wow! I just saw this.

I think that we should ask Ken to add another, short of English words here, subject line called Different Medical information or something like that. We get lost searching for different info.

You could put all those info in there with links. This subject would be without possible posts from us. And add below Different Medical Information another subject called Questions About Medical Information. That would be great.

What do you think Fishinghat? I'm excited about this possibility. Thank you sir!

#9 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 16 December 2017 - 10:33 AM

Gail, could you give me a small sample of an outline for these two threads? I am having a hard time putting this together in my mind. When the last of my info us loaded on the current thread I was going to reformat the information anyway. For right now any member can go to this thread and do a search for a symptoms (eg. zaps), supplement (eg magnesium) or other term and find the information fairly easily but to just set down and read it is difficult for sure.


#10 gail

gail

    God-like

  • Site Supporter
  • 4,600 posts
  • LocationSherbrooke, PQ
  • why_joining:
    5 months on cymbalta, scary side effects, never felt good.
    Needed understanding and support, and a place where I was not alone. To read others stories and realizing that I was not the only one going through all that crap.
    In hope that one day, I can return the favors in some kind of way.

Posted 17 December 2017 - 10:29 AM

Fishingbrain, I do find that Different medical information would be a good title. Most important, it would be for us impossible to post back on this because we'll be lost again and again and if Ken can arrange this, that must be possible.

Example, when you gave me the difference between Dyskenisia and the two others, I don't remember in what category it was. But I wrote it all down, thank God! This post should be in Different Medical information.

Just below this different medical info, the title should be questions about DMI. I'm not sure that I answered your question here. Of course you can answer people about DMI on any posts, but this information should be reposted on DMI.

Lots of work? In a way, it would prevent you of repeating and repeating. And refer them to DMI. On that, a good Sunday to you and your so loving wife.

#11 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 17 December 2017 - 11:12 AM

Very interesting. O understand your approach. Here is what I am going to do.

 

1) Finish entering my info on the existing thread.

 

2) Reorganize my information on that thread.

 

3) Deveolp an outline for that thread.

 

4) Rename the thread

 

5) Return to the subject of how to better present the info with you and other members and possible get Ken to help if we decide to go that route.

 

6) Reread the posts for 'other medical information' like the one on muscle movement syndromes and incorporate them as well.

 

This will take some time but with everyone's input we can make a good document out of this.

 

Thanbk you for your input Gail and let me know of this sounds reasonable.


#12 gail

gail

    God-like

  • Site Supporter
  • 4,600 posts
  • LocationSherbrooke, PQ
  • why_joining:
    5 months on cymbalta, scary side effects, never felt good.
    Needed understanding and support, and a place where I was not alone. To read others stories and realizing that I was not the only one going through all that crap.
    In hope that one day, I can return the favors in some kind of way.

Posted 20 December 2017 - 11:43 AM

Sounds great Fishinghat, sorry for the late reply. Exhaustion took over my body. Normal, as the oncologist said yesterday.

Yes, a lot of work, I really think that this would be beneficial for all members. And as I said, prevent you of repeating. Prevent me from losing my mind while searching. And there is so many valuable informations, we need this! Like a plant that needs watering!

Perhaps we can get the members here also, to get their output. Thismoment, we could use your thoughts about this, where ever you are! Smoking a cigar in Italy??

#13 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 23 December 2017 - 01:03 PM

                                          Reading Material and Treatment Programs
                  Informational Reading
     A Mind Of Your Own
blanam - A great book is Kelly Brogan's "A Mind Of Your Own".
FH - Kelly Brogan, MD is absolutely correct. I remember my crying spell. It lasted about 3 or 4 weeks. I remember going for long walks in the park and crying every step, for no apparent reason. Everyone was asking me if I was OK. I waited for those spells to end before I went walking again.
blanam - Kelly Brogan, MD suggests that it can take from 6 month to 2 years for the brain/body to recalibrate.
kr15sy - I have been focusing on going Paleo to get healthy and lose weight, and after reading Dr. Kelly Brogan's A Mind of Your Own, and Dr. Perlmutter's Grain Brain, found out about the connection between your gut and your brain.

     The Gifts of Imperfection
FN - If you're a reader, I highly recommend Brene Brown's The Gifts of Imperfection.

AngryinHouston - If you're a reader, I highly recommend Brene Brown's The Gifts of Imperfection.

     The Antidepressant Solution
Jekaufman - BUY THE BOOK- "THE ANTIDEPRESSANT SOLUTION" By. Joseph Glenmullen. He writes a step-by-step guide to overcoming Antidepressant Withdrawl, Dependence and Addiction!
Unitedwecan - This book, The Antidepressant Solution, was written in 2005. It is by Joseph Glenmullen, M.D.. He also wrote Prozac Backlash. He teaches at Harvard Medical School. This book tells of the way money and power have corrupted the pharmecutical companies, the FDA and everyone involved. It also has a 5 step program that basically says to GO SLOW when weaning off these drugs.
pheonixjazzmine - I would like to suggest a book called "The Antidepressant Solution" by Joseph Glenmullen, M.D. Dr. According to Glenmullen, many doctors these days do not taper patients off of SSRI's slowly enough. His book guides people off of these drugs through verrrry gradual tapering schedules.
agrace - I have a book called "The Antidepressant Solution" by a Dr. Glenmullen which devotes a whole chapter on determining whether a symptom is that of an actual illness or just withdrawal. It's very good, although I don't think he goes nearly far enough in discussing the long term implications of these symptoms, although he briefly mentions that they have been documented to continue past a year,and he has a chart of over fifty side effects that cover everything from physical to mental/emotional to neurological.
Norther - In Joseph Glenmullen's book, 'The Antidepressant Solution' (devoted to withdrawal), he states the situation very clearly, on p.97:
"Q. Can antidepressants be taken every other day as part of tapering off them?
A. None of the short acting antidepressants should be taken every other day as a method of tapering them. Because of their short half-lives, the every other day schedule can result in roller coaster levels of the drugs and roller coaster levels of withdrawal symptoms."
However, patients seem to be told, time after time, to withdraw by alternating doses or missing out days - a surefire recipe for destabilising drug levels, and putting the patient through needless physiological chaos and withdrawal nightmares
rogerwilco - I found Dr Glenmullen's book very revealing of the situation I find myself in, and you can find it at addall.com.

     Full Catastrophe Living
Gail - Full Catastrophe Living: Using the Wisdom of Your Body and Mind to Face Stress, Pain and Illness (Delta, 1991);
This book treats all ailments the same way. Depression, anxiety, cancer, fibromalgia, anything, you name it.
Same (remedy) applies to all, mindfulness.
A really interesting book. Step by step. Easy to understand,

xanaxul - I forgot, I agree with you "Full catastrophe living..." Other of the John Kabat-Zinn books offers many cues for trauma survivors to cope and begin to rebuilt from the emotional wreckage that trauma lefts behind.
Limbo - A book that has always helped me is Dr. Jon Kabatt-Zinn's books. He has a mindfullness-based stress reduction program that is extremely helpful for chronic pain and depression. He runs these programs in hospitals but you can buy the books and audio CDs.
http://www.amazon.co...nn/e/B000AQ12GA
http://www.umassmed....t.aspx?id=41252

     Walking with God through Pain and Suffering
IBS - I'm not sure what you like to read but I am reading a great book on suffering by Timothy Keller..called 'Walking with God through Pain and Suffering' It's completely biblical, based on the foundation you mentioned and I highly recommend it.

     The Ragamuffin Gospel
SL - Praying like never before & have deriving the most comfort from (other than the Psalms) a book called 'The Ragamuffin Gospel' by Brennan Manning (awesome, you might wanna check it out) 'written for the bedraggled, beat up & burnt out.'

     Anatomy of an Epidemic
TM - I introduced the topic because the no-proof-for-serotonin-deficiency is high on the list of SSRI critics; Robert Whitaker's book, Anatomy of an Epidemic is representative of this, and I recommend it.
BHF - One of the things I would like to share is the books that I have learned from. One of my favorites is Anatomy of an Epidemic by Robert Whittaker. I felt that the references to research let me use my own judgement to reach conclusions. He studied a wide range of psychotropic drugs. I bought copies of his book to lend and/or give away. I am particularly worried about some of my son's teenaged friends who are ripe for the industry to chew up. I also appreciated Unhinged and The Emperors New Drugs.
Papin - For anyone interested in learning more about recent research on long-term anti-depressant use, check out the book Anatomy of an Epidemic, by Robert Whitaker. He goes into a lot of detail about the history of psychotropic drugs and the efforts the APA goes to in order to cover up evidence that these drugs are, in fact, doing more harm than good.
Imdone - I encourage everyone to read Whitaker's "Anatomy of an Epidemic" and Breggin's "Your Drug May Be Your Problem."
Jesselee - Also, educate yourself and uplift yourself. I found the book, "Anatomy of an Epidemic" by Robert Whitaker to be helpful,
     The Mood Cure
K65 - You may find the book "The Mood Cure" helpful. It addresses the underlying diet and medical causes (for me, hypothyroidism) of pain (both mental and physical). I have found it to be very useful in understanding and learning about natural and dietary means of treating that pain. The book also references 5HTP, as well as other supplements, as being helpful for people weaning off of antidepressants.
 
     At Last A Life
Jennifer - I have read Claire Weekes and got a lot of helpful info there but the book that is truly helping me is At Last A Life by Paul David. It's up to date and hit the nail on the head on everything I am going through. He suffered for 10 years with severe anxiety and has gotten his life back.

     The Healing Power of Vitamins, Minerals, and Herbs
Tria - It has info on most of the more common vitamins and supplements - The Healing Power of Vitamins, Minerals, and Herbs by Reader's Digest. I don't think it's in print anymore, but you may be able to find used copies online.

     Essential Help for the nerves
Gail - If you have a chance to get her book, it will soothe you, at least for a while. Title ESSENTIAL HELP FOR YOUR NERVES.

     Various Suggested reading by members
http://www.cymbaltaw...book#entry41552
     Suggested readings

TM
Anatomy of an Epidemic, Robert Whitaker (2010)
Let Them Eat Prozac, David Healey (2006)
Pharmageddon, David Healey (2013)

Boundaries
IBS -I'm reading the book "Boundaries" by Cloud and Townshend...it's a great read...should have read a decade ago, but that's okay...

Surviving Panic Disorder: What You Need to Know
TM - Here's a link to a book you might wish to look into.
http://www.amazon.co...disordershipko

The Power of Anxious Thinking
BRZ - i highly recommend his latest podcast, The Power of Anxious Thinking: http://www.anxietygu...xious-thinking/its about an hour, the first 6 min or so is just chit chat, but then he gets into the meat of his topic. there is an article and then at the bottom a link for the podcast on that topic. the actual podcast section is the archives - also good stuff in there.
-------------------------------------------------------------------------------------------------------------
                                       Programs
http://www.theroadba...withdrawal.aspx
The Road Back is put out by the Church of Scientology

http://www.cymbaltaw...tion#entry45468
http://www.cymbaltaw..."the road back"
Discussions and information on the Road Back program.

http://www.cymbaltaw...book#entry44953
A discussion and information on TheRoadBackProgram.

Tinajuli - something that might be a joke, I don't know: Have you heard about The Road Back Programme? It might be just using the desperation of people who feel very silly afterwards but I thought screw it and ordered the stuff. They advise to take a supplement that kind of calms the reactions that take place in your body as soon as you take an anti-depressant, and when you go into withdrawal. It has to do with the JNK gene. (If you know whether that company is a joke, let me know!) What are ALA supplements? I really need something to help me with that fatigue, because work gets really hard when you're constantly extremely tired.

LadyNancy - I know someone who used The Road Back program to try to get off of Cymbalta and the last time I had any contact with her she was doing everything the book said to do and taking all the supplements and still not off it so unless you just like to pray a lot then in my opinion you should just go out and buy some Omega 3, a good Vitamin B complex and drink lots of water.
I haven't found anyone who had severe symptoms that found the program very helpful in actually getting through withdrawal symptoms.
-------------------------------------------------------------------------------------------------------------
                                   Psychological treatments
     General
FH - Psychiatrists only regulate meds but a good psychologist can help you control the anxiety without meds. They can teach you relaxation techniques, control your heart rate and breathing and much more. I would highly recommend one. These techniques can help you greatly reduce your need for meds. Pick a psychologist who has experience with Cognitive Behavioral Therapy or Mindfulness. These seem to be the best techniques for anxiety.
Way to many members recommended a good psychologist to list all quotes here.
     REBT
brzghoff - my therapist who specializes in REBT, rational emotive behavioral therapy,
FN - You're young, and there are lots of other good alternatives for managing depression, anxiety and any other issues that landed you on the meds in the first place ... CBT and REBT are two ...
http://rebtnetwork.o...rary/ideas.html
REBT Website

FN - What is Rational Emotional Behavior Therapy (REBT)?
Understanding the Approach by Considering the Four Elements of its Name
Wyndy Dryden, Goldsmith's University of London
http://windydryden.c...nts_article.pdf

Excellent overview and introduction to REBT.

Brz -
1) go to http://rebtnetwork.org/library.html
2) look on the right hand side
3) scroll down in the box "news"
4) look for "New ebook released" How to Conquer Your Frustrations by Dr. William J. Knaus. the link is right there and says in blue hypertext "download the free ebook.

EQ - i would like to share a downloadable booklet i found last night that is free. great stuff. check it out if you like. its called "How To Conquer Your Frustrations" http://www.rebtnetwo...strations.pdf
it can be found on a web site i haven't been to in a long time: www.rebtnetowork.org .
https://www.ncbi.nlm.../pubmed/9479090
The results suggest that the treatment approach was successful in modifying irrational beliefs and anxiety.

https://www.ncbi.nlm...les/PMC5036761/
The findings revealed significant effects of a REHCT intervention program on problematic assumptions, death anxiety, and psychological distress reduction among the cancer patients and their family caregivers at the end of the intervention.
https://www.ncbi.nlm...les/PMC5428629/
REBC is a time-efficient and solution-focused therapeutic modality for assisting occupationally stressed employees

Scientific research into the efficacy of this method is limited.

      Cognative Behavioral Therapy
FH - Therapy is a must. I was blessed with a dr who was adept at cognitive behavioral therapy (mindfulness therapy is also good). She taught me how to do breathing exercises, reduce heart rate, refocus my thinking from obsessive thoughts, and many more coping mechanism. It has proved very beneficial.
Brz - i also highly recommend seeing a therapist who specializes in cognitive behavioral therapy - and visit on as regular basis as much as you can possibly afford - like once a week. that combined with a conservative tapering schedule can be the difference between self destruction and preserving the relationships with those you love. i won't say there will be no struggle - because there will - but the idea is to minimize suffering and avoid permanent or long term damage.
Brz - i got good sleep and deployed some good cognitive strateges and things started to improve a little.

https://www.ncbi.nlm...pubmed/24314926
Treatment-resistant depression: definitions, review of the evidence, and algorithmic approach
Manual based psychotherapies remain a treatment option, with the most compelling evidence for cognitive behavioral therapy.

https://www.ncbi.nlm...pubmed/25433401
Systematic review of management for treatment-resistant depression in adolescents.
The combination of antidepressant medication and psychotherapy should be recommended for adolescents who present with treatment-resistant depression.

https://www.ncbi.nlm...pubmed/24458008
The integrative management of treatment-resistant depression: a comprehensive review and perspectives.
Evidence suggests that cognitive therapy (CT) is an effective strategy for TRD.

https://www.ncbi.nlm...pubmed/26635099
Treatment-resistant panic disorder: a systematic review.
Augmentation of the pharmacological treatment with cognitive-behavioral therapy demonstrated some short-term efficacy in treatment-resistant PD.

https://www.ncbi.nlm...pubmed/16847460
Treatment-resistant anxiety disorders.
Anxiety disorders are treatable conditions and respond to the front-line interventions such as serotonin reuptake inhibitors and cognitive behavioral therapy.
Acceptance and Commitment Therapy for Generalized Anxiety Disorder in Older Adults: A Preliminary Report (full text)
Behavioral Therapy, March 2011

http://www.ncbi.nlm....les/PMC3496779/

Abstract excerpt: Some evidence suggests that acceptance-based approaches such as Acceptance and Commitment Therapy (ACT) may be well-suited to geriatric generalized anxiety disorder (GAD). The primary goal of this project was to determine whether ACT was feasible for this population. Seven older primary-care patients with GAD received 12 individual sessions of ACT; another 9 were treated with cognitive-behavioral therapy. No patients dropped out of ACT, and worry and depression improved. Findings suggest that ACT may warrant a large-scale investigation with anxious older adults.
Cathill - I just finished up with 4 months of cognitive behavioral therapy to help with my life long battle of depression. I have been on and off antidepressants for most of my adult life (usually very low levels). I have been on Cymbalta for over two years now, 40mg once a day, and now that I am armed with my new tools that I learned in therapy, fianlly ready to say good bye to this drug. I have tried getting off in the past, so I am well aware of the hell you go through getting off.
gsmommy - I did have anxiety and panic attacks nearly 10 years ago and took a med for it, paxil. I went through very aggressive cognitive behavioral therapy and weaned from the med and have not had panic attack since.
There are dozens and dozens of medical research articles showing the benefit of CBT on anxiety treatment primarily but also more limitedly on depression as well.
     Mindfulness
Xana - JON KABAT-ZINN, PH.D., is founding Executive Director of the Center for Mindfulness in Medicine, Health Care, and Society at the University of Massachusetts Medical School. He is also the founding director of its renowned Stress Reduction Clinic and Professor of Medicine emeritus at the University of Massachusetts Medical School. He teaches mindfulness and Mindfulness-Based Stress Reduction (MBSR) in various venues around the world. He received his Ph.D. in molecular biology from MIT in 1971 in the laboratory of Nobel Laureate, Salvador Luria.

He is the author of numerous scientific papers on the clinical applications of mindfulness in medicine and health care, and of a number of books for the lay public: Full Catastrophe Living: Using the Wisdom of Your Body and Mind to Face Stress, Pain and Illness (Delta, 1991); Wherever You Go, There You Are: Mindfulness Meditation in Everyday Life (Hyperion, 1994); Coming to Our Senses: Healing Ourselves and the World Through Mindfulness (Hyperion, 2005); and Arriving at Your Own Door: 108 Lessons in Mindfulness (Hyperion, 2007). He is also co-author, with his wife Myla, of Everyday Blessings: The Inner Work of Mindful Parenting (Hyperion, 1997); and with Williams, Teasdale, and Segal, of The Mindful Way Through Depression: Freeing Yourself from Chronic Unhappiness (Guilford, 2007). Overall, his books have been translated into over 30 languages.

I did the training (half of it as I told you) with a former Z Segal PhD student. The book I've is the one by Williams, Teasdale, Segal and Kabat-Zinn, that comes with a CD with all the exercises guided by Kabat-Zinn. The book is about mindfulness applied to prevent depression relapse, but since it was written Minfulness that was developed as a technique to cope with stress by J Kabat-Zinn, has proven to be equally efective in treating the whole spectrum of anxiety disorders.
Pepe - The following technique (which I picked up from a book) has worked for me to slow down this constant train of thoughts and anxiety several times, and it still does.
1) Make yourself as comfortable as you can (sit or or lie down and close your eyes)
2) Try to get your respiration under control (inhale deep through your nose for 4 seconds, keep the air in for 3 seconds exhale for 7 seconds)
3) When your respiration has stabilized,try to observe yourself as a silent 'spectator'
4) You are NOT your thoughts or feelings, your thoughts and feelings should not kidnap you as a person. Try to observe your thoughts/feelings without any judgement. Just try to observe them. Don't ask yourself any questions regarding these thoughts/feelings.
5) Realize you are *observing* your thoughts/feelings. You, as a full person, are observing 'some thoughts/feelings' which are....just there.
6) Realize that these thoughts/feelings are just a (small) part of you, they are NOT you.
7) If you are able to objectively observe your thoughts/feelings they will gradually decrease in strength and speed.

TM - I spent a few months listening to guided Mindfulness Meditation sessions at bedtime, and found it useful for winding down and falling asleep. You can find them on YouTube, on CD's, and elsewhere on the net.
considering - I think meditation has helped me deal with bouts of low grade depression that I've experienced in the last seven years since I've been on Cymbalta. So I would highly recommend it to anyone. But I recommend that you have a teacher, even if it's meditation CDs of teachings from Sharon Saltzberg or Pema Chodron.
newbeginning - Im hoping just to try to relax do some relaxation techniques from my mindfulness tape, and not to think this is what my life will always be like. ive never realised how bad anxiety can be as ive manly suffered depression and ocd thinking.
turbolag - I work with a therapist, that works with me on mindfulness and meditation, I also use Gert's anxiety CD course.
jimmcg -The good news is that all the work I've been doing — therapy, mindfulness study, meditation and reading — has paid dividends in other areas of my life, especially my personal relationships.
IBS - One therapy I've benefited from is DBT...it incorporates mindfulness and was designed by Dr. Marsha Linehan for people with Borderline personality disorder...so i better get going on it.
TM - 1. The Mindfulness & Acceptance Workbook for Depression by Kirk D. Strosahl and Patricia J. Robinson.
2. The Mindfulness & Acceptance Workbook for Anxiety by George H. Elfert and John P. Forsyth.
These books come with CD, guided imagery, and Mindfulness exercises. As a strategy for broadening your Mindfulness understanding and practice, look into Mindfulness classes in your area. You might inquire through your therapist, medical community, community college, night classes, or university. Search on YouTube for Vipassana Mindfulness Meditation
TM - Start with something to keep the anxiety down-- that's the wild card! I could not imagine using Mindfulness to intervene in a skyrocketing episode of anxiety or rage. Impossible!
I agree that the physical symptoms occupy too much band-width to enable Mindfulness or other therapy to be up-loaded early on in discontinuation-- there's just too much activity in your head at this time.
brz - i wish i could find the web site i found with a good description, but a great technique i use is sensory mindfulness. focus on one of your five senses, like sound. just listen to all the sounds around you, , don't judge them, just let them come and go and be aware of them. do that for 5-10 minutes, then switch to a different sense, sight - notice all the imgaes before you, again, don't judge them, just notice them and be aware - you can do the same with touch , taste - chew something flavorful like chocolate, savor it, note the subtleties. the idea is to take your focus away from the intrusive thoughts. same with focusing on your breath, in out, full but normal breathing. don't hyperventilate. just feel your breath go in and out, no judgement. it takes practice. i work on it ALL the time, so when the anxiety isn't as strong, it is easier and it can become a habit.
anothermind - are you referring to Prof Mark Williams - he has researched mindfulness and happiness? ... https://www.youtube....h?v=WY08aXxor20( here's a great talk from him at Alain de Botton's School of Life in London)
Andrew Solomon is another amazing speaker on anxiety and depression: http://www.ted.com/t...secret_we_share
and dozens of others with positive things to say about mindfulness therapy.
There are large amount of research showing the benefits of mindfulness for both anxiety and depression.
----------------------------------------------------------------------------------------------------------
                                                 Home Care
     Sleep
Many members recommend sleeping as much as possible during withdrawal.
http://www.cymbaltaw...elps#entry72205
The document "How to sleep better"

FN - Sound machine/radio - I pick out which of the sounds (often I have high and low pitch, hissing, humming, and whirring all at the same time) I find most pleasing ... and somehow that helps me drift off to sleep ... It helps cover up outside noises.
Raven - I also sometimes find that putting headphones on and listening to your favorite music as loud as you can stand it helps drown out anything that might make you panic, it might even help you fall asleep.

https://www.ncbi.nlm...pubmed/26047492
This meta-analysis indicates that short and long sleep duration was significantly associated with increased risk of depression in adults.

https://www.ncbi.nlm...pubmed/26179204
Geriatric Depression Scale and Geriatric Anxiety Inventory scores are both significantly correlated with sleep disturbance. Geriatric Depression Scale scores are uniquely associated with daytime dysfunction, and Geriatric Anxiety Inventory scores are uniquely associated with perceived sleep quality, sleep latency, and global Pittsburgh Sleep Quality Index scores.
https://www.ncbi.nlm...les/PMC3900629/
Contributions to depressive symptoms increase at both short and long sleep durations.
Many articles exist that show this relationship of sleeping to much or to little contributes to anxiety and depression symptoms.
There are many studies that reflect the fact that withdrawal decreases sleep and increases withdrawal symptoms. Many studies also reflect that by increasing sleep by use of natural or prescription drugs help with withdrawal sympotoms.

     Diet
Please refer to previous sections on diet to improve serotonin, endorphin and dopamine levels.
Increase protein intake to help body to heal. Protein is very big in helping to overcome any illness. Can be added as a powder to a smoothie or other liquid.
FN - the amino acids ... just be very cautious, and research every single thing he/she tells you on your own ... they're powerful, and if not used with great care and caution, can be harmful.

     Blood pressure monitoring
FH - Just wanted to pass along a growing trend in a new way drs can get accurate feedback on your anxiety levels and how to adjust your medicine.

As we have discussed many times on this site most antidepressants and especially antianxiety drugs will lower you blood pressure to some degree. Ever wonder why a dr will start you out on a low dose of a medicine first and then slowly increase it as needed? Well part of the reason is to be sure you do not take any more meds then necessary. The other part is to make sure your body has a chance to adjust to any changes in blood pressure. Any dr who puts you on a full dose to begin with is doing you no favors unless you are just desperate for help. By ramping up slowly you can see if you will develop any significant side effects before they overwhelm you; you can see if you have a reaction to a medicine before you get carried away with a full dose and to give your body a chance to adjust to any changes in BP.

What drs are doing now (and we can do this as well) is to monitor the systolic part of our blood pressure. The systolic is the top large number of our blood pressure. So if your bp is 120/80 then the 120 is the systolic number. The general guidelines are that if the systolic is over 120 then the anxiety levels are to high and an increase in meds may be necessary. If the systolic drops to near 90 (say 90/50) then this indicates that there is more medicine in your system than you need and the dr may cut back on a dose.
Now drs are using this method along with the information on how you feel to determine if any changes are needed. Of course you don't always carry a dr around in your back pocket so it is important to realize that you can use this method as well.
As many of you know I take clonidine and hydroxyzine to control my anxiety. Both of course can affect bp but have no withdrawal. So by monitoring my bp I can tell when I need to get more medicine in my body (systolic over 120) or to drop a little in medicine dose (systolic near 90). By the way if you get dizzy when you stand up too fast this is an indication your bp is getting low and you need to check it. This is also a way to determine if you are stable enough to start weaning again. As your bp drops it indicates your stress levels are decreasing and it may be time to start weaning again. If your bp starts to go over 120 on the systolic then it may be time to slow down or pause a little bit BEFORE it gets too bad.
PLEASE READ; Important.
Blood pressure must be taken the same way each time. You must be sitting or lying still for 2 minutes or more. This is called a resting blood pressure. If you choose to set then it must always be taken in a setting position each time. DO NOT base any of your decisions on one single bp. Bp fluctuates due to many factors. Activity around you, your health, when and what you eat, etc. So when I need to check things out I take 2 or 3 blood pressures during the day. You are looking for a pattern. I have found that at least in my case it is easy to quickly determine that my bp is rising or falling after a few bp readings. Do not take a bp within 5 minutes of another blood pressure. It takes the vessels in the arm or wrist time to adjust back to normal. It is best to wait 10 minutes if you need to try and get another bp.
I know for me this has helped as a early warning system on when my withdrawal is ramping up and gives me better control. I hope it helps you all as well.

     Taking Meds
FH - At this point, like with most medicines I would recommend the teaspoon tea cup rule. For those new to the site this is the safety approach to taking a new medicine to avoid allergic reactions, severe side effects or incompatible reactions. If the medicine calls for, example, 100 mg every 8 hours start with 10 mg (part of a tablet), then 20 then 50 then 75, etc. Some sort of step mechanism to be sure your body can handle the medicine appropriately before going to a full dose. This helps avoid a lot of needless suffering.

     Mediatation
See section earlier in this thread.
     GI Disturbances
FH - Remember if your stomach is an issue you shouldn't drink anything hot or cold as this caused the muscles to tighten even more. Slightly warm water is the best and sometimes a hot pad on the stomach help calms it as well.
FH - It is like the old question, which came first the chicken or the egg. Anxiety causes an increase in adrenaline and serotonin activity. Adrenaline affects the heart and serotonin in the stomach and intestines. What most people do not realize is that the heart and stomach are controlled by the vagus nerve. So if anxiety increases then the stomach problems increase and vice versa, if stomach problems increase then anxiety increases. Anxiety increases due to feed back from the stomach and the vagus nerve. Old drs use to call this the head/gut connection. Stomach issues are also another stressor for the body and any time you can reduce a source of stress your anxiety will improve. Consider when you have had a bad case of the flu. You are tired and sick but also irritable, agitated, etc. The flu makes you stressed. As the flu subsides your psychological symptoms reduce as well. Chronic long-term stress usually causes IBS (irritable bowel syndrome) because of constant increase in serotonin activity in the GI tract.
Jim - He put me on 150 mg of Zantac twice a day in order to reduce production of stomach acid. Within 2 hours of taking the first dose I was shocked to feel my anxiety reduce by probably 75%. I was astonished at how my stomach was exacerbating my anxious feelings. Sometimes even when I didn't feel particularly anxious about anything, my stomach would well up and I would suddenly feel like I was about to go into the most important job interview on my life.
FH - Stomach issues, IBS, acid refux, etc have long been correlated to the severity of anxiety. During my own withdrawal I found that relief of heartburn by zantac and antacids would not only relieve my heartburn but also reduce my anxiety levels some. You need to realize that stomach ailments are a source of more stress on the body and would add to your anxiety symptoms. It is also believed that by returning the acid levels in the stomach to normal allows your medicine to be absorbed more efficiently and therefore it does a better job.
FN - I remembered this discussion, and I had some Zantac on hand. So, I figured I'd try an experiment to see how it works on anxiety .... I'm having no acid reflux/GERD symptoms of the sort that tell me I need to take it ... and I haven't associated my weird stomach sensation with acid reflux ...
Anyway, I took 75 mg...about 7 a.m.... and amazingly, shortly thereafter, the anxiety stuff dropped down several notches ... so, at about 9 a.m. I took another 75 mg tab (can't take more than two in a 24 hr period) ...
Well, the anxiety/weird stomach stuff that I call "anxiety" totally cleared up ... I mean totally ....
https://draxe.com/gu...ain-connection/
A fairly good overview of the brain/gurt connection.

FH - Basically with stress proper digestion and acid production changes. Bad bacteria in the stomach are able to better compete with good bacteria. With poor digestion improper nutrition increases to the body and has an inflamatory effect on many organs including the brain. Stress reduction, probiotics and a good diet are essential in bringing things back into balance. See the section on probiotics for details on what conditions can be caused by this inproper digestion. See the earlier section in this thread on Probiotics.

     Peppermint
Fishinghat -You can have her suck on a peppermint lozenge. This relaxes the esophagus/stomach but does not affect the lower intestines and does not aggravate constipation or diarrhea. Be sure it has real peppermint not peppermint flavoring. I have occasional esophageal spasms (a weaker form of dry heaves) and they work well for me. I buy mine at a health food store for about $3 for 10 lozenges. Peppermint contains menthol, which has an antispasmodic effect that relaxes the muscles of the digestive tract.
notsobad - I've had issues with motion sickness (that I didn't have when I was a kid)...and I wonder if it's all connected somehow. I went through phases with ginger and chewing peppermint gum, which made the situation survivable but still unpleasant.
MC - here are a couple of remedies that has helped my nausea in the past . Mint tea, peppermint tea, green apples and life saver 'wint-o-green' flavor.
Many members mention the GI benefits they recieve from using peppermint. Peppermint contains high amounts of menthol which is an antispasmotic and smooth muscle relaxant.

     Keeping a Journal
Many members promote the keeping of aq journal. You will find that this type of record is much more accurate trhan our memories plus it is a good reference when talking to the dr or going back to look for similar experiences. My journal has helped me immensely over the years.

     Cravings
Chart: what do food cravings mean (nutrient shortage indicated by cravings)... scroll down the page, chart is at bottom)
http://betterraw.com...-you-chart.html

Members frequently mention cravings during withdrawal. Ten mention craving sugar, 7 mention craving carbs, 3 salt, 2 coffee, and they also mention ice, ice cream, oranges and orange juice, pineapple.
It is interesting that these items has a unique dietary profile.
Coffee raises tyrosine and dopoamine
Salt and ice cream are high in sodium, calcium and magnesium (electrolytes)
Oranges, orange juice and pineapple are high in bioflavanoids and vitamin C as well as sugar.
The sugar craving may be because of low blood sugar during withdrawal which has been mentioned by many members.

16 members mention developing low blood sugar during withdrawal, usually associated with headaches or dizziness. 2 members mentioned that their blood sugar readings were like a rollercoaster during withdrawal and 4 mentioned it stayed normal. I could not find any research articles linking Cymbalta withdrawal to hypoglycemia.

     Stimulants (Make anxiety worse)
Caffeine
Over-the-counter cold preparations contain phenylpropylamine and pseudoephedrine*
Sleep deprivation
m*********
Magnesium*
MSG
Alcohol
Stress
amphetamines
ecstasy
nicotine
Ginseng
L-Tyrosine
B Vitamins*
aspartame
Coconut Oil
Taurine
DHEA
Ginkgo
Iodine
Arginine
Sugar
Kava
* - Only some people have this reaction.

Things containing caffeine..
Coffee, Espresso, Cappuccino, some Teas, Low calorie, non-cola soda containing aspartame, Low calorie colas containing aspartame or saccharine, Energy drinks, Some types of alcoholic drinks.
Chocolate ....Baking, Dark, Sweet and semisweet, Pudding, Cereals, Fudge , Milk chocolate, Syrup, Mousse, Soymilk, Fat free cookies, Cookies, Cake, Frozen Yogurt, Ice cream, Frosting, and Shakes .
Java Pops, Chai Mints, Green Tea, Warp Mints, Penguin mints, and cinnamons. Caffeinated Energy Strips, Caffeinated Fruity Lollipops, HyDrive Energy Chews, Caffeinated Nixie Tubes, Foosh Energy Mints, Atomic Energy Bites, Buzz Bites, KickBricks, Energy Chews, Reload Energy Strips, Movit Gummies, Caffeinated jellybeans, Morning Spark, Oatmeal, Sumseeds (caffeinated sunflower seeds), Lightning Rods (beef sticks), Engobi "Energy Go Bites" (crispy snacks), Jolt Gum, Blitz Energy Gum, Think Gum Stay Alert, Vibe Black, Black Go Fast!, Dozens and dozens of herbal supplements.
https://www.caffeine...ffeine-database
List of energy drinks with caffiene. (over 100)

FCB - Air, I'd think coffee is better than the diet coke! Those artificial sweeteners can really mess with your body and mind (anxiety-creating, among other effects) plus the other junk that is in pop. Coffee on the other hand, has been found to have health benefits. Dark roast coffee has less caffeine. Sweeten it with honey or maple syrup - they have a medium glycemic index and have other health benefits, and sweeter than sugar so you use less (or try stevia, I heard the body does not process stevia as a sugar).

http://www.cymbaltaw...ety/?hl=improve
What makes anxiety worse.

     Depressants (Make depression worse)
Oxalic acid is found in members of the spinach family and cabbage, broccoli, brussels sprouts, chives and lamb's quarters are high in oxalates, as are sorrel and parsley. Rhubarb leaves contain about 0.5% oxalic acid.
Can cause depression, lack of minerals, kidney stones, and more. Cooking does not affect oxalic acid. People with kidney disease, a history of kidney stones or suffer from depression should avoid these foods.
Aspartame
Gluten
High Fat Dairy
Sugar
alcohol
Trans fats
Sodium
Caffiene
Pesticide residue on foods
GHB
Organic solvents (paint, varnish, stains, cleaning solvents, paint thinner, etc).
------------------------------------------------------------------------------------------------------
                             Mammalian diving reflex
The diving reflex, also known as the diving response and mammalian diving reflex is a response to immersion that overrides the basic homeostatic reflexes, which is found in all air-breathing vertebrates. It optimizes respiration by preferentially distributing oxygen stores to the heart and brain which allows staying underwater for extended periods of time. It is exhibited strongly in humans, in particular babies up to 6 months old. The greatest bradycardia effect is induced when the subject is holding breath with face submerged.
Method description - The Dive Reflex, originally noted in cold water diving, is a first rate vagus nerve stimulation method capable of rapidly chilling down anxiety, panic, stress and body-wide inflammation as well as elevating moods. At first the dive reflex was done by dipping the face from the lips to the scalp line into very cold water for 30 seconds to 1 minute. This would quickly melt away anxiety and stress. Later it was found that a large zip-lock plastic bag filled with ice or ice cubes applied to the face from the scalp line to the lips would perform as well without leaving the user appearing like they just emerged from a river. The Dive Reflex, because of its ability to stimulate the vagus nerve, has proved helpful for:
Swift reduction of all forms of anxiety.
Rapidly dampening down a panic attack.
Performance anxiety, test anxiety, and phobia work.
Reducing body-wide inflammation.
Use in lowering intense fight/flight in PTSD work.
Reducing stress.
Lowering anger.
Thwarting worry and rumination.
Elevating moods.

https://www.ncbi.nlm...les/PMC3768097/
Harnessing the suprabulbar circuits of origin that control diving physiology may promote feedback therapies designed to remedy high HR and hypertension associated with anxiety.
------------------------------------------------------------------------------------------------------------
sk8 - also started reiki... I noticed since reiki i have been able to wean way easier (not sure if it is a coincidence or not but anything helps)...
ExCymbaltaUser - i am a reiki student, and received an attunement august 19, which sent me into a massive detox (like the worst flu ever) after which all my withdrawal symptoms completely evaporated over the next week or so, while I continued giving myself reiki healing every day.
Christene - I have some wonderful Reiki music to plug into and used visualization with this process. I know this has keep me centered and help in the cleansing and healing process.
and others
Reiki is a form of alternative medicine developed in 1922 by Japanese Buddhist Mikao Usui. Since originating in Japan, Reiki has been adapted into varying cultural traditions across the world. Reiki practitioners use a technique called palm healing or hands-on healing through which a "universal energy" is allegedly transferred through the palms of the practitioner to the patient in order to encourage emotional or physical healing.
Reiki is pseudoscience. It is based on qi ("chi"), which practitioners say is a universal life force, although there is no empirical evidence that such a life force exists. Clinical research has not shown Reiki to be effective as a medical treatment for any medical condition. The American Cancer Society, Cancer Research UK, and the National Center for Complementary and Integrative Health state that Reiki should not be a replacement for conventional treatment.
Wiki

https://www.ncbi.nlm...pubmed/24582620
Although the number of studies is limited, based on the size Cohen's d statistics calculated in this review, there is evidence to suggest that Reiki therapy may be effective for pain and anxiety.

https://www.ncbi.nlm...pubmed/25835541
As this included only 25 people with anxiety and 17 with depression and 20 more with either anxiety or depression, but which was not specified, the results could only be reported narratively. They show no evidence that Reiki is either beneficial or harmful in this population.

https://www.ncbi.nlm...pubmed/26163604
The results of this study indicate that Reiki may decrease pain, anxiety and fatigue in oncology patients.

https://www.ncbi.nlm...pubmed/20635803
Significant differences were observed between the experimental and treatment groups on measures of pain, depression, and anxiety; no changes in heart rate and blood pressure were noted. Content analysis of treatment notes and interviews revealed five broad categories of responses: Relaxation; Improved Physical Symptoms, Mood, and Well-Being; Curiosity and a Desire to Learn More; Enhanced Self-Care; and Sensory and Cognitive Responses to Reiki.

and many many more.

#14 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 26 December 2017 - 04:20 PM

                                                   Major Natural Human Supplements

SAMe - S-Adenosyl methionine is a common substrate involved in methylmethyl group transfers, transsulfuration, and aminopropylation. Although these reactions occur throughout the body, most SAM-e is produced and consumed in the liver. More than 40 methyl transfers from SAM-e are known, to various substrates such as nucleic acids, proteins, lipids etc. The half-life is about 100 minutes. Wiki

Safety and side effects

Side effects from SAMe are rare and, if they occur, usually mild.
SAMe can cause:
⦁ Upset stomach
⦁ Nausea
⦁ Mild insomnia
⦁ Dizziness
⦁ Irritability
⦁ Anxiety
⦁ Sweating
⦁ Constipation
⦁ Diarrhea Mayo

Possible interactions include:

⦁ Antidepressants and other drugs and supplements that increase levels of serotonin. Don't take SAMe with antidepressants. The combination could cause effects similar to a condition caused by high levels of the chemical serotonin to accumulate in your body (serotonin syndrome).
⦁ Antipsychotics. Be cautious when taking these drugs with SAMe. The combination could increase the risk of serotonin syndrome.
⦁ Amphetamines. Be cautious when taking these drugs with SAMe. The combination could increase the risk of serotonin syndrome.
⦁ Dextromethorphan. Taking SAMe with this cough suppressant could increase the risk of serotonin syndrome.
⦁ Narcotics. Taking SAMe with meperidine (Demerol) or tramadol (Ultam, ConZip) could increase the risk of serotonin syndrome.
⦁ St. John's wort. Be cautious when taking this supplement with SAMe. The combination could cause serotonin syndrome.
Mayo

https://nccih.nih.go...upplements/SAMe
S-Adenosyl methionine (SAM-e); In Depth
At least 40 studies in people have evaluated SAMe for depression, and many of them showed evidence of beneficial effects. However, most of these trials lasted only a few weeks, included a small number of participants, and were not of the highest scientific quality. Also, some studies used injected SAMe rather than an oral form (taken by mouth).

https://examine.com/...syl-methionine/
Detailed summary of scientific studies including safety, dose, interactions, etc.
Great info.

https://www.ncbi.nlm...pubmed/27727432
Not useful in treating depression.

-------------------------------------------------------------------------------------------------------
5HTP
http://www.umm.edu/h...tryptophan-5htp
Overview
5-hydroxytryptophan (5-HTP) is a chemical that the body makes from tryptophan (an essential amino acid that you get from food). After tryptophan is converted into 5-HTP, the chemical is changed into another chemical called serotonin (a neurotransmitter that relays signals between brain cells). 5-HTP dietary supplements help raise serotonin levels in the brain.
A 2002 review concluded that although the data evaluated suggests that 5-HTP is more effective than placebo in the treatment of depression, the evidence was insufficient to be conclusive due to a severe lack of high quality research. More and larger studies are needed to determine if 5-HTP is truly effective in treating depression. Wiki

Safety

5-HTP is POSSIBLY SAFE when taking by mouth appropriately. 5-HTP has been used safely in doses up to 400 mg daily for up to one year. However, some people who have taken it have developed a condition called eosinophilia-myalgia syndrome (EMS), a serious condition involving extreme muscle tenderness (myalgia) and blood abnormalities (eosinophilia). Some people think EMS might be caused by an accidental ingredient or contaminant in some 5-HTP products. However, there is not enough scientific evidence to know if EMS is caused by 5-HTP, a contaminant, or some other factor. Until more is known, 5-HTP should be used cautiously.

Other potential side effects of 5-HTP include heartburn, stomach pain, nausea, vomiting, diarrhea, drowsiness, sexual problems, and muscle problems.

5-HTP is POSSIBLY UNSAFE when taken by mouth in large doses. Doses from 6-10 grams daily have been linked to severe stomach problems and muscle spasms.

Special precautions & warnings:

Pregnancy and breast-feeding: There is not enough reliable information about the safety of taking 5-HTP if you are pregnant or breast feeding. Stay on the safe side and avoid use.

Surgery: 5-HTP can affect a brain chemical called serotonin. Some drugs administered during surgery can also affect serotonin. Taking 5-HTP before surgery might cause too much serotonin in the brain and can result in serious side effects including heart problems, shivering, and anxiety. Tell patients to stop taking 5-HTP at least 2 weeks before surgery.

Are there interactions with medications?

Major Do not take this combination.
Medications for depression (Antidepressant drugs)
5-HTP increases a brain chemical called serotonin. Some medications for depression also increase serotonin. Taking 5-HTP along with these medications for depression might increase serotonin too much and cause serious side effects including heart problems, shivering, and anxiety. Do not take 5-HTP if you are taking medications for depression.

Some of these medications for depression include fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft), amitriptyline (Elavil), clomipramine (Anafranil), imipramine (Tofranil), and others.

Medications for depression (MAOIs)
5-HTP increases a chemical in the brain. This chemical is called serotonin. Some medications used for depression also increase serotonin. Taking 5-HTP with these medications used for depression might cause there to be too much serotonin. This could cause serious side effects including heart problems, shivering, and anxiety.

Some of these medications used for depression include phenelzine (Nardil), tranylcypromine (Parnate), and others.
Moderate Be cautious with this combination.

Carbidopa (Lodosyn)
5-HTP can affect the brain. Carbidopa (Lodosyn) can also affect the brain. Taking 5-HTP along with carbidopa can increase the risk of serious side effects including rapid speech, anxiety, aggressiveness, and others.

Dextromethorphan (Robitussin DM, and others)
5-HTP can affect a brain chemical called serotonin. Dextromethorphan (Robitussin DM, others) can also affect serotonin. Taking 5-HTP along with dextromethorphan (Robitussin DM, others) might cause too much serotonin in the brain and can result in serious side effects including heart problems, shivering, and anxiety. Do not take 5-HTP if you are taking dextromethorphan (Robitussin DM, and others).

Meperidine (Demerol)
5-HTP increases a chemical in the brain called serotonin. Meperidine (Demerol) can also increase serotonin in the brain. Taking 5-HTP along with meperidine (Demerol) might cause too much serotonin in the brain and serious side effects including heart problems, shivering, and anxiety.

Pentazocine (Talwin)
5-HTP increases a brain chemical called serotonin. Pentazocine (Talwin) also increases serotonin. Taking 5-HTP along with pentazocine (Talwin) might increase serotonin too much. This might cause serious side effects including heart problems, shivering, and anxiety. Do not take 5-HTP if you are taking pentazocine (Talwin).

Sedative medications (CNS depressants)
5-HTP might cause sleepiness and drowsiness. Medications that cause sleepiness are called sedatives. Taking 5-HTP along with sedative medications might cause too much sleepiness.

Some sedative medications include clonazepam (Klonopin), lorazepam (Ativan), phenobarbital (Donnatal), zolpidem (Ambien), and others.

Tramadol (Ultram)
5-HTP increases a brain chemical called serotonin. Tramadol (Ultram) can also increase serotonin. Taking 5-HTP along with tramadol (Ultram) might cause too much serotonin in the brain and might result in side effects including confusion, shivering, stiff muscles, and others.

Are there interactions with herbs and supplements?

Herbs and supplements with sedative properties

5-HTP can cause sleepiness or drowsiness. Using it along with other herbs and supplements that have the same effect might cause too much sleepiness. Some of these herbs and supplements include calamus, California poppy, catnip, hops, Jamaican dogwood, kava, St. John's wort, skullcap, valerian, yerba mansa, and others.

Herbs and supplements with serotonergic properties
5-HTP increases a brain chemical called serotonin. Taking 5-HTP along with other herbs and supplements that increase serotonin might lead to too much serotonin and cause side effects including heart problems, shivering and anxiety. Other herbs and supplements that increase serotonin levels include Hawaiian baby woodrose, L-tryptophan, S-adenosylmethionine (SAMe), and St. John's wort.

A total of 74 drugs (242 brand and generic names) are known to interact with 5-hydroxytryptophan.
55 major drug interactions
19 moderate drug interactions
For the complete list and to see what the interaction is go to:
http://www.drugs.com...3&generic_only=

Member comments

No brain zaps in 5 days

I decided to stop taking it completely b/c I really didn't think it was doing much of anything for me/I wasn't withdrawl-ing and started taking 25 to 50 mg 5-HTP about a week ago. The 5-HTP doesn't really seem to be helping me. I am feeling more depressed...

The brain zaps are horrid, but 5-HTP really does ease them dramatically. I'm taking 100mg in the morning, and 50mg before bed. It really does help you sleep, and lifts your mood.

Tria - My head seems clearer and I just seem to feel more normal (knock on wood - don't want to jinx myself!) I can't say this is all due to the 5-HTP as she started me on a few other supplements as well but I only start one new supplement at a time, give it a couple weeks then start another, and my mood did improve after starting the 5-HTP.

AKAnole - I took 150mg of 5HTP every day for a few months. I stopped in December thinking I no longer needed it then over the holidays the depression came back suddenly.

brz - i am still not sure how best to take 5htp, it seems to work on a delayed "as needed" basis. does that make sense? it takes about a day to kick in but as soon as i get my anxiety under control it doesn't seem to be a problem to just stop. - which is not what i was expecting when i started last october. since many people take it on a regular basis, that is what i do. i take one 100mg time release pill every morning. just wanted to pass along my experience. however, while i have had good results from the 5htp for anxiety, i can't speak to its effectiveness as a sleep aid.

Analreland - Someone also suggested 5HTP, which is not for sale in Ireland

Penguin1982 - There was a post I read that even though the half life is only 12 hrs, it can stay in your liver and fat stores for months. Didn't realize that when I started supplementing with 200mg 5htp and 750mg GABA at night only to find myself peeing every ten min and shivering beyond control. After seeing that post I realized I was getting waaaay too much serotonin and creating serotonin syndrome for myself . I've since stopped both and seem to b coming back around .

AKAnole - 5 HTP to supplement the lack of serotonin that I was experiencing. It helped but didn't curb the anxiety I would experience at times. L-Tryptophan which I think works better for me mood wise but I can't take it at night or else it disrupts my sleep

brzghoff - most recently i've experimented with 5htp which has been effective.

FN - 5HTP worked/works great for me as well ... I did stop using it daily, and have been using it just once in a while, and was doing just fine ... however, I'm now actually considering going back on it daily, as I've been working a really stressful temp job, and I'm starting to feel a bit "unsteady" ...

There is a rebound effect from 5-htp if it is stopped cold turkey. Next time try phasing it out over a 2 week period and you will do a lot better

http://www.cymbaltaw...5-htp/?hl=helps
5thp information and discussion.

https://examine.com/supplements/5-htp/
Detailed summary of scientific studies on 5HTP including anxiety and depression.

https://www.ncbi.nlm...les/PMC3415362/
Lack of effectiveness and dangers of its use.

5-HTP is not found in the foods we eat, although tryptophan is. Eating foods with tryptophan does not increase 5-HTP levels very much, however. As a supplement, 5-HTP is made from the seeds of an African plant called Griffonia simplicifolia.
Source: http://www.umm.edu/a...m#ixzz2Q0VyOr4w

1. 5-HTP is changed into serotonin
2. Our body uses tryptophan to make 5-HTP
3. Vitamin B6, vitamin C, folic acid and magnesium are necessary for the metabolization of tryptophan. In addition, tyrosine and phenylalanine compete with tryptophan for absorption.
4. Several dietary, lifestyle, and health factors reduce the conversion of tryptophan to serotonin, including cigarette smoking, high sugar intake, alcohol abuse, excessive consumption of protein, hypoglycemia and diabetes.
5. Depression, anxiety, irritability, impatience, impulsiveness, inability to concentrate, weight gain or unexplained weight loss, slow growth in children, overeating and/or carbohydrate cravings, poor dream recall, and insomnia can all be signs that a person may need more tryptophan.
6. The following foods contain tryptophan: red meat, dairy products, nuts, seeds, legumes, soybeans and soy products, tuna, shellfish, chicken and turkey.

5-HTP can be a wonder drug for anxiety and depression but MUST be used correctly.
1st – Start out slow. Build slow
50 mg once per day for 3 days
50 mg twice a day for 3 days
50 mg three times per day for 3 days then
50-50-75 for 3 days
50-75-75 for 3 days
75-75-75 dor 3 dats and then
100-75-75
100-100-75
100- 3 times a day (maximum dose).
As you ramp up watch for stomach upset (stop at that point)
If at anytime your symptoms are minimal do not go up any more.

2nd – Absolutely do not take with a ssri/snri as it may cause seratonin syndrome (easily recognized by a fever over 102F.
3rd – Check list of incompatable drugs. Drugs.com
4th – After you have been emotionally stable for a couple weeks you need to slowly, slowly decrease the 5-HTP as your system may not need as much now that it has had a chance to catch up. Many people start out using 150 mg/day and feel fine and then taper down to 75 mg for the long haul. This is important as with long term usage 5-HTP can deplete some necessary nutrients in the body.
5th – 5-HTP can be gotten for our body by consuning foods rich in tryptophan along with a small supplement of Vitamin B6, vitamin C, folic acid and magnesium. Foods high in tryptophan include red meat, dairy products, nuts, seeds, legumes, soybeans and soy products, tuna, shellfish, chicken and turkey.
6th - Depression, anxiety, irritability, impatience, impulsiveness, inability to concentrate, weight gain or unexplained weight loss, slow growth in children, overeating and/or carbohydrate cravings, poor dream recall, and insomnia can all be signs that a person may need more tryptophan.
7th - Several dietary, lifestyle, and health factors reduce the conversion of tryptophan to serotonin, including cigarette smoking, high sugar intake, alcohol abuse, excessive consumption of protein, hypoglycemia and diabetes.
-----------------------------------------------------------------------------------------------------------
L-theanine:

Member's comments

(puritan's pride) 200 mg capsules 2- 3/ day. I have been taking this prior to cymbalta detox. It helped me reduce my dosage of clonazepam. Within 20-30 mins I feel more calm. I do believe it is helping keep the anxiety in check.

Tinabee - For now I have started taking fish oil and a supplement called Theanine Serene that is supposed to help with anxiety. I know it sounds silly since I've only taken the anxiety supplement for a couple days but I really feel like it has helped.

200mg L-Theanine in the morning with a full glass of water on an empty stomach, you can take again in late afternoon 100 to 200 mg if needed (make sure it is suntheanine - it helps with headaches and pain as any painkiller I had just did not cut it)

Member's comments were generally favorable.

http://www.cymbaltaw...page-2?hl=helps
Page 1 and 2, detailed information on L theanine and its usage.

Research

The research shows that all green tea leaves contain both L-theanine and D- theanine BUT only the special processing used by the manufacturer produces pure L-Theanine and is the choice of many of the research biologists.

https://www.ncbi.nlm...pubmed/22214254
https://www.ncbi.nlm...pubmed/16759779
https://www.ncbi.nlm...pubmed/14755608

Rapid Commun Mass Spectrom. 2004;18(3):251-6.
Analysis of derivatized and underivatized theanine enantiomers by high-performance liquid chromatography/atmospheric pressure ionization-mass spectrometry.
⦁ Abstract
Theanine, a naturally occurring non-proteinic amino acid found in tea leaves, has demonstrated wide-ranging physiological activity, from lowering blood pressure to enhancing the anti-tumor activity of chemotherapeutic drugs. The chiral nature of theanine suggests that enantiospecificity plays a significant role in its various pharmacological functions. Using the Chirobiotic T (teicoplanin) chiral stationary phase, native and derivatized theanine enantiomers were separated and detected via high-performance liquid chromatography (HPLC) coupled to atmospheric pressure ionization mass spectrometry (API-MS). With the use of flow rates compatible with each ionization source, native theanine standards achieved excellent sensitivity and detection limits (10 ng/mL) for both atmospheric pressure chemical ionization (APCI) and electrospray ionization (ESI). Optimum sensitivity and detection limits for derivatized theanine standards were achieved using ESI-MS. The enantiomeric composition of six commercially available L-theanine samples was evaluated using the high-flow APCI-MS method and confirmed with photodiode array detection. Five of the six products contained significant amounts of D-theanine. Only one product, SunTheanine, appeared to contain only the L-theanine enantiomer.

https://www.ncbi.nlm...les/PMC3049752/
Note - Suntheanine is the pure ingredient and that is what you want. That is the pure L-theanine. D-theanine is not absorbed by our bodies.
L-theanine is an amino acid precursor to glutamate and glutamine.

Key Points

It can cross the blood brain barrier. It is only produced by plants and fungi. It inhibits glutamine transporters and glutamate transporters, and thus blocks the reuptake of glutamine and glutamate. Theanine increases serotonin, dopamine, GABA, and glycine levels in various areas of the brain. Caution – Most plants that contain L-theanine also contain caffeine and it can be a significant contaminant in L-theanine supplements.Theanine has been studied for its potential ability to reduce mental and physical stress, improve cognition, and boost mood and cognitive performance in combination with caffeine. In combination with caffeine it may increase anxiety.

Scientific Information

A National Standard monograph that reviews current research on theanine reports that it is likely safe in doses of 200–250 mg up to a maximum daily dose of 1,200 mg. Theanine is used to help with anxiety, blood pressure control, mood, and cognition. Natural Standard rates the evidence to support the usage for anxiety, blood pressure control, and mood as “unclear or conflicting scientific evidence” and the evidence for cognition as “fair negative scientific evidence.” Many of the studies of theanine were done in combination with caffeine as found in tea. While the studies found that the combination had some effect on mood, the studies found that theanine alone had little effect. More sufficiently designed studies in humans are warranted to further our understanding of the effects of theanine.

https://www.ncbi.nlm...pubmed/21208586
Effective, 400 mg/day
https://www.ncbi.nlm...pubmed/15378679
Not effective on anxiety, 200 mg/day
https://www.ncbi.nlm...les/PMC4137547/
Used to treat PTSD. It was successful in treating 8 gene problems associated with PSTD in the hippocampus and amygdala.


Recommendations

"The basic metabolic process is ...
Tryptophan to 5HTP to seratonin to melatonin."

First of all assess if you may need additional dietary input.

"Depression, anxiety, irritability, impatience, impulsiveness, inability to concentrate, weight gain or unexplained weight loss, slow growth in children, overeating and/or carbohydrate cravings, poor dream recall, and insomnia can all be signs that a person may need more tryptophan." The most common of these seam to be the anxiety traits (eg. irritability) and the craving of carbohydrates.

Second determine what is needed for this process.

This includes Vitamin B6, vitamin C, folic acid and magnesium which are necessary for the metabolization of tryptophan. In addition, tyrosine and phenylalanine compete with tryptophan for absorption. A review of your diet can shed some light on how much of each is currently available to your body. Adding unneeded amounts of some of these can actually be detrimental. Blood test can be done for the B vitamins (a standard test for new psychiatric pstients with may pdocs). A blood test is also available for blood magnesium levels.

One complication is the interference of tyrosine and phenylalanine to the uptake of L-tryptophan. A recommended daily intake for phenylalanine and tyrosine is 25 mg per kilogram of body weight, or 11 mg per pound. For a 70 kg person this is 1750 mg (phenylalanine + tyrosine).

Unluckily these compounds are found in nearly the same food as L-Tryptophan. Tyrosine, which can also be synthesized in the body from phenylalanine, is found in many high-protein food products such as chicken, turkey, fish, milk, yogurt, cottage cheese, cheese, peanuts, almonds, pumpkin seeds, sesame seeds, soy products, lima beans, avocados, and bananas. For example, the white of an egg has about 250 mg per egg, while lean beef/lamb/pork/salmon/chicken/turkey contains about 1000 mg per 3 ounces (85 g) portion. So increasing you ingestion of these foods may not provide more L-tryptophan to your body and therefore a supplement might be considered.

Third, what else interfers with the conversion of tryptophan to serotonin.

Several dietary, lifestyle, and health factors reduce the conversion of tryptophan to serotonin, including cigarette smoking, high sugar intake, alcohol abuse, excessive consumption of protein, hypoglycemia and diabetes. So..no smoking, keep blood sugar levels in normal range, no drinking (alcoholic) and moderate protein ingestion. Again the excessive protein ingestion may cause interference by tyrosine and phenylalanine to the uptake of L-tryptophan.

How else to control seratonin levels.

The conversion of seratonin to melatonin at night helps our body deplete excessive seratonin and gives the brain a chance to rest/relax and repair. Once light dims below 25 watts the pineal gland in the brain begins to convert seratonin to melatonin which is used to cause sleepiness in the evenings. Many block ut the windows in there bedroom and regulate light levels carefully after 5 PM.

How to try to get L-tryptophan levels increased in the body.

Can not be synthsized by our bodies and must be part of our diets. DO NOT EXCEED FDA LIMIT ON DOSES. The normal recommendation is for dietary intake is chicken or turkey. White poultry meat contains about 40% more L tryptophan then dark meat.

http://nutritiondata.self.com/The RDA for tryptophan is 0.2 gm (200 mg) per day, while the average daily intake is 1-1.5gm per day. The therapeutic range is up to 4gm per day, and medical supervision of treatment can be helpful. The 0.2 mg equates out to around 0.2 lbs of white poultry meat per day with an upper limit of 4 lbs per day (not practical). I would suggest around 0.5 lbs of white poultry meat per day. Increasing the L-Tryptophan levels will give your body a chance to absorb additional amounnts if the interferences are minimal.

FH - Do I follow this diet? Yes I do. I can't say it has cured my anxiety but I do find it slightly improved and definitely more stable.

What if it is not effective.

If this regime is not effective then the substitution of L-Tryptophan supplements might be in order as described above. This would eliminate the risk of tyrosine and phenylalanine interference. Work with your dr and the schedule above to build up slowly and cut back once stabilized.

-------------------------------------------------------------------------------------------------------------
L- tyrosine

An amino acid. Tyrosine is a hydrophilic amino acid and is significantly less soluble in water than its precursor, phenylalinine.
L-phenylalinine is converted by the body to L-tyrosine which is changed to L-DOPA then to dopamine followed by norepiniphrine and finally epinephrine (adrenaline).

Tyrosine is a precursor to neurotransmitters and increases plasma neurotransmitter levels (particularly dopamine and norepinephrine),but has little if any effect on mood in normal subjects. The effect on mood is noted in humans subjected to stressful conditions.

A number of studies have found tyrosine to be useful during conditions of stress, cold, fatigue, prolonged work and sleep deprivation, with reductions in stress hormone levels, reductions in stress-induced weight loss seen in animal trials, and improvements in cognitive and physical performance seen in human trials. Wiki

Member Comments

a neurostransmitter to help mental alertness and helps support glands especially the thyroid. I take 750 mg capsule 2x's/day
doriono - I was having anxiaty attacks all the time. I trid all sorts of supplements and finnally tried L-Tyrosine. It work like a miracle! I used NOW L-Tyrosine for 3 month and never got an attack again. It's been 6 months now.

Tomitsu - L-Tyrosine also helped me

https://examine.com/...nts/l-tyrosine/
Details the results of over 50 research articles on L-tyrosine.

No significant link found for L-tyrosine in fighting anxiety or depression.
-------------------------------------------------------------------------------------------------------------
L Tryptophan is an amino acid essential for human life and cannot be synthesized by our body, and therefore must be part of our diet. In addition, tryptophan functions as a biochemical precursor for Serotonin synthesized via tryptophan. Serotonin, in turn, can be converted to melatonin. Niacin is synthesized from tryptophan. L-tyrosine and phenylalanine compete with tryptophan for absorption.

If you don’t get enough l-tyrosine in your diet, or your body doesn’t properly convert it, you won’t be able to synthesize adequate dopamine. When looking for a supplement, consider n-acetyl-l-tyrosine. This is a highly absorbable form of l-tyrosine that readily enters the brain. L-tyrosine and phenylalanine compete with tryptophan for absorption. Tryptophan is converted to serotonin by the body so if too much L-tyrisine is present n the blood stream then serotonin levels may decrease. One of the functions of Vitamin C include the synthesis norepinephrine from dopamine and the synthesis and catabolism (breakdown) of tyrosine. So vitamin C may increase tyrosine or decrease tyrosine in the body depending on conditions. Webmd.com

Key Points

Can not be synthesized by our bodies and must be part of our diets. DO NOT EXCEED FDA LIMIT ON DOSES. The normal recommendation is for dietary intake is chicken or turkey. White poultry meat contains about 40% more L tryptophan then dark meat.

http://nutritiondata.self.com/The RDA for tryptophan is 0.2 gm per day, while the average daily intake is 1-1.5gm per day. The therapeutic range is up to 4gm per day, and medical supervision of treatment can be helpful. The 0.2 mg equates out to around 0.2 lbs od white poultry meat per day.

This supplement must be taken together with vitamin C, magnesium and B-complex vitamins to support the transformation of tryptophan into serotonin.

L tryptophan reacts with most antidepressants (seratonin syndrome), MAOIs, benzos and sedatives. There is an extensive number of drug interactions. Please research before use.

Scientific Information

Dietary sources

Tryptophan is a routine constituent of most protein-based foods or dietary proteins. It is particularly plentiful in chocolate, oats, dried dates, milk, yogurt, cottage cheese, red meat, eggs, fish, poultry, sesame, chickpeas, almonds, sunflower seeds, pumpkin seeds, buckwheat, spirulina, bananas, and peanuts. Contrary to the popular belief that turkey contains an abundance of tryptophan, the tryptophan content in turkey is typical of poultry.

Tryptophan (Trp) Content of Various Foods
Food Tryptophan
[g/100 g of food] Protein
[g/100 g of food] Tryptophan/Protein [%]
egg white, dried 1.00 81.10 1.23
spirulina, dried 0.93 57.47 1.62
cod, atlantic, dried 0.70 62.82 1.11
soybeans, raw 0.59 36.49 1.62
cheese, Parmesan 0.56 37.90 1.47
sesame seed 0.37 17.00 2.17
cheese, cheddar 0.32 24.90 1.29
sunflower seed 0.30 17.20 1.74
pork, chop 0.25 19.27 1.27
turkey 0.24 21.89 1.11
chicken 0.24 20.85 1.14
beef 0.23 20.13 1.12
oats 0.23 16.89 1.39
salmon 0.22 19.84 1.12
lamb, chop 0.21 18.33 1.17
perch, Atlantic 0.21 18.62 1.12
chickpeas, raw 0.19 19.30 0.96
egg 0.17 12.58 1.33
wheat flour, white 0.13 10.33 1.23
baking chocolate, unsweetened 0.13 12.9 1.23
milk 0.08 3.22 2.34
rice, white, medium-grain, cooked 0.028 2.38 1.18
quinoa, uncooked 0.167 14.12 1.2
quinoa, cooked 0.052 4.40 1.1
potatoes, russet 0.02 2.14 0.84
tamarind 0.018 2.80 0.64
banana 0.01 1.03 0.87


L-tryptophan is possibly unsafe when taken by mouth. It has been linked to over 1500 reports of eosinophilia-myalgia syndrome (EMS) and 37 deaths. EMS is a neurological condition with symptoms that include fatigue; intense muscle pain; nerve pain; skin changes; baldness; rash; and pain and swelling affecting the joints, connective tissue, lungs, heart, and liver. Symptoms tend to improve over time, but some people may still experience symptoms up to 2 years after they develop EMS. Some people report that their symptoms have never gone away completely. Since the FDA has limited the doses available the occurrence of EMS has markedly dropped.

L-tryptophan can cause some side effects such as heartburn, stomach pain, belching and gas, nausea, vomiting, diarrhea, and loss of appetite. It can also cause headache, lightheadedness, drowsiness, dry mouth, visual blurring, muscle weakness, and sexual problems. This supplement must be taken together with vitamin C and B-complex vitamins to support the transformation of tryptophan into serotonin. Dosages range from 5 to 1000 mg/day.

http://www.ncbi.nlm....les/PMC3195213/
http://www.ncbi.nlm....les/PMC2908021/

brz - how well does the st john's wort work for anxiety? it makes it worse for me, same with L tryptophan. i checked into l tryptophan. after doing a lot of research i picked some up and took one 500 mg capsule tuesday night. within 20-30 min it kicked in. real mellow, i wasn't able to go to sleep right away, but was very comfortable for an hour before dozing off. slept all night the next day i felt great! wednesday night i took one 500 mg capsule. within 20-30 min i felt hyper, my heart rate went up and boom! anxiety! it was terrible. i was up for several hours

TM - The experiment with L-Tryptophan didn't work. That's okay-- forget about it. I'm old school: I'm suspicious of supplements and won't take any. I think they are another crap-shoot.

General Comments

http://www.cymbaltaw...rove#entry72249
In formation on SAM-e, L-tryptophan and 5htp.

Special Note

Metabolic limitations - All of these items mentioned above are 'natural' in our diets and/or body. However, each has to have certain enzymes, vitamins (such as B6, B12, Vit C, etc.), minerals or other components to be processes into dopamine, serotonin, adrenaline or other neurotransmitters. They may also have items which compete with them in the body such as tyrosine or phenylalanine. The reactions may or may not produce more or less of a neurotransmitter but will that even get to the brain? Many of these products just don't cross the blood brain barrier (a membrane around the brain) so even though they are produced they do no good for mood. Some require special enzymes, insulin, certain proteins, etc to cross the barrier and all these items have their own requirements and limitations. This becomes clearly evident in looking at all the individual comments on these supplements. The effects are all over the place. Each persons body is different and has its own nutritional shortages or overages and therefore it may be im possible to tell in advance what reaction may occur to one of these supplements.




 


#15 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 09 February 2018 - 12:58 PM

Nutritional Causes of Anxiety and Depression

Unless otherwise noted all information is either from http://www.rightdiagnosis.com/or
https://www.ncbi.nlm.nih.gov/pmc/
-----------------------------------------------------------------------------------------------------------

Omega-3 fatty acids
High levels of Omega 3 fatty acids can cause anxiety
https://www.ncbi.nlm...pubmed/17991818

Omega 3 deficiency linked to depression.
https://www.ncbi.nlm...pubmed/23890734
https://www.ncbi.nlm...pubmed/21838665
https://www.hindawi....cl/2014/313570/
and other articles as well.

This is an increasingly common occurrence in advanced societies that no longer consume significant levels of fish or seafood.

EPA
https://academic.oup...5/3/244/1448354
High levels of EPA are linked to anxiety. Rare

DHA
https://www.nih.gov/...itary-personnel
Study links low DHA levels to suicide risk among U.S. military personnel. Increasing in occurrence.

Omega-6 fatty acids
https://www.scienced...50525161319.htm
High levels of Omega 6 linked to depression. Rare

Testing
http://www.questdiag...dc=TS_Omega_3_6
Blood sampling for individual Omega 3 and 6 components.
--------------------------------------------------------------------------------------------------------
Amino Acids
Testing
https://www.mayomedi...terpretive/9265
The Mayo clinic does a complete detailed analysis of all amino acids in the body.

Amino Acid Imbalance
http://journals.lww....chronic.12.aspx
As early as in the 1960s of the last century especially Harper has investigated the potential effects exerted by amino acid imbalances. Adverse effects have been observed in experimental animals consuming diets containing disproportionate amounts of amino acids. Such effects may also appear in humans when homeostatic mechanisms regulating amino acid concentrations in body fluids are deficient or defective because of liver or kidney damage, malnutrition or a genetic defect of amino acid metabolism. Moreover, also an overload associated with parenteral or enteral supplied amino acids/proteins can lead to amino acid imbalances.
Note - Many amino acids compete directly with each other in the body, when that is combined with taking supplements, imbalanced diet, genetic limitations and digestive issues it can easily lead to an amino acid imbalance.
----------------------------------------------------------------------------------------------------------
Tryptophan
https://www.ncbi.nlm...pubmed/22683764
Tryptophan deficiency linked to depression.
https://www.ncbi.nlm...pubmed/23904410
https://www.ncbi.nlm...pubmed/21377656
https://www.ncbi.nlm...les/PMC2908021/

The modern Western diet often is very high in fats and carbohydrates, and sometimes complete proteins (containing all the essential amino acids) are lacking. Additionally, some seemingly healthy vegetarian and vegan diets may be lacking in sources of Tryptophan. https://nootriment.c...han-deficiency/
-----------------------------------------------------------------------------------------------------------
Threonine
http://aminoacidstud...nine_deficiency
Deficiency (extremely rare) linked to emotional agitation. Mostly occurs in vegetarians,
-----------------------------------------------------------------------------------------------------------
Isoleucine
http://aminoacidstud...cine_deficiency
Deficiency rare but can include irritability.
------------------------------------------------------------------------------------------------------------
Methionine
http://aminoacidstud...g/l-methionine/
"deficiency of L-methionine can cause or exacerbate depression and allergies and lead to an excess of toxins"

https://www.ncbi.nlm...les/PMC5501805/
Our findings suggest that imbalances in specific metabolite levels (which included methionine) may be involved in the pathogenesis of MDD (Major Depressive Disorder).

http://ajcn.nutritio...76/5/1151S.full
Decades of research on the biochemical and molecular roles of SAMe in cellular metabolism have provided an extensive foundation for its use in clinical studies, including those on depression, dementia, vacuolar myelopathy, liver disease, and osteoarthritis.
S-Adenosyl-l-methionine (SAMe), first discovered in 1952 (1), is formed from the essential amino acid methionine and adenosine triphosphate.

http://www.tandurust...deficiency.html
There are several uses of methionine in our body, it is necessary in synthesis of RNA and DNA, it helps to absorb selenium. In order to make a proper utilization of methionine, it requires cofactors such as vitamin B6, B12, choline, folic acid and magnesium.
Methionine deficiency is contributory factor in causing diseases such as childhood rheumatic fever, muscle paralysis, hair loss, depression, folic acid deficiency.

Methionine deficiency is usually associated with an overall protein deficiency. http://www.ndhealthf...wiki/Methionine
------------------------------------------------------------------------------------------------------------
Phenylalanine
http://aminoacidstud...-phenylalanine/
People deficient in phenylalanine may experience symptoms such as lethargy, confusion, cognitive impairment, poor appetite, and depression.

http://www.umm.edu/h...t/phenylalanine
Same

http://www.nature.co...lication_detail
The genetic disorder phenylketonuria (PKU) is the inability to metabolize phenylalanine because of a lack of the enzyme phenylalanine hydroxylase. Phenylketonuria affects about one in 12,000 babies. Individuals treated late or never treated may develop severe behavioral or psychiatric problems (depression, anxiety, and phobias) in the third or fourth decade. In a few case reports, untreated individuals with PKU (Excess phenylalanine) with normal intelligence were diagnosed in adulthood only as a result of a sudden and severe psychiatric deterioration.

Uncommon - From eating a low protein diet or from genetic mutations.
http://www.tandurust...ncy-causes.html
-----------------------------------------------------------------------------------------------------------
Tyrosine
http://aminoacidstud...d_mental_health
Due to the important role tyrosine has in producing neurotransmitters there has been several studies looking at the relationship between this amino acid and depression. It has been established that women taking oral contraceptives tend to have lower tyrosine concentrations and this may trigger depression

It’s possible that the metabolism of tyrosine is abnormal in people suffering from depression. There is some research to suggest that tyrosine supplementation may help elevate people out of a depressed state.

The best results have been achieved when taken together with 5-HTP supplements. 5-HTP is a phytochemical similar to that amino acid tryptophan. It helps to elevate serotonin levels in the brain to improve mood.

Rose D and Cramp D. 1970. Reduction of plasma tyrosine by oral contraceptives and oestrogens: a possible consequence of tyrosine aminotransferase induction. Clinica Chimica Acta Volume 29, Issue 1, (pp. 49-53).”

Moller S. (1981). Effect of oral contraceptives on tryptophan and tyrosine availability: evidence for a possible contribution to mental depression. Neuropsychobiology. Volume 7, Issue 4, (pp. 192-200).”

Kishimoto H, and Hama Y. (1976). The level and diurnal rhythm of plasma tryptophan and tyrosine in manic-depressive patients. Yokohama Medical Bulletin, Volume 27, (pp. 89-97).”

Gelenberg A and Gibson C (1984). Tyrosine for the treatment of depression. Nutrition and Health. Volume 3, Issue 3, (pp. 163-73).”

Low energy levels and an erratic mood may be linked to a deficiency in l-tyrosine. Often the symptoms of low tyrosine are similar to that of hypothyroidism. People may experience flu-like symptoms, unexplained weight gain, poor temperature regulation, low blood pressure, sluggish metabolism, depression, dry skin, constipation and brittle hair or fingernails.

Uncommon - Due to low protein diet or genetic mutations.
----------------------------------------------------------------------------------------------------------
Vitamins

Vitamin C

Vitamin C deficiency
https://www.ncbi.nlm...pubmed/25835231
https://www.ncbi.nlm...pubmed/17372835
https://www.ncbi.nlm.../pubmed/8451160
https://www.ncbi.nlm...les/PMC3540126/
All the above link it to depression.
Rare
------------------------------------------------------------------------------------------------------------
Vitamin D - The two major forms are vitamin D2 or ergocalciferol, and vitamin D3 or cholecalciferol.

Vitamin D deficiency (depression)
https://www.ncbi.nlm...pubmed/23377209
http://ajcn.nutritio...87/4/1080S.full
Vitamin D deficiency is now recognized as a pandemic. The major cause of vitamin D deficiency is the lack of appreciation that sun exposure in moderation is the major source of vitamin D for most humans.
https://www.scienced...41202111148.htm
And many more.

Vitamin D Deficiency (anxiety)
https://link.springe...0067-006-0348-5
https://www.ncbi.nlm...iciency anxiety
https://www.ncbi.nlm...pubmed/26203431
and many more.

Fairly Common due to improper diet, not enough sun, dark pigmented skin, kidney disease, digestive absorbtion disorder, genetics, and obesity.
https://www.webmd.co...-d-deficiency#2

Vitamin D toxicity is on the increase due to over use/overdose of Vitamin D. Currently Vitamin D supplementation is very popular and routine blood levels of your vitamin D should be performed if you are taking the supplements.
----------------------------------------------------------------------------------------------------------
Vitamin E
Includes....
Alpha Tocopherol
Beta Tocopherol
Gamma Tocopherol and
Delta Tocopherol

Deficiency
https://www.ncbi.nlm...pubmed/21979061
https://www.ncbi.nlm...pubmed/19472364
Linked to anxiety.
https://www.ncbi.nlm...pubmed/15508016
Linked to depression

Rare - Caused by genetics or Fat malabsorption - Some dietary fat is needed for the absorption of vitamin E from the gastrointestinal tract. Anyone diagnosed with cystic fibrosis, individuals who have had part or all of their stomach removed or who have had a gastric bypass, and individuals with malabsorptive problems such as Crohn's disease, liver disease or exocrine pancreatic insufficiency may not absorb fat (people who cannot absorb fat often pass greasy stools or have chronic diarrhea and bloating). Abetalipoproteinemia is a rare inherited disorder of fat metabolism that results in poor absorption of dietary fat and vitamin E. - Wiki

------------------------------------------------------------------------------------------------------------
B Vitamins

General
http://ajcn.nutritio...t/92/2/269.full
http://file.scirp.or...02_49431046.pdf
Details on the relationships of various B vitamins to depression.

https://www.ncbi.nlm...pubmed/25173634
Genetic mutations commonly effect B vitamin production and use resulting in various psychological disorders.

FH - Where I am a blood work up including levels of b vitamins is sort of standard. If your levels of B vitamins is normal then they do not recommend taking a B vitamin supplement because two high a dose can cause side effects.
------------------------------------------------------------------------------------------------------------
Thiamine (B1)

Deficiency
http://www.bmj.com/r...sychosis-which-
https://www.research..._clinical_trial
Linked to depression.
http://journals.sage...533210110392941

Fairly common - Thiamine deficiency fairly common in alcoholics. Beriberi (Thiamine deficiency) may also be caused by shortcomings other than inadequate intake: diseases or operations on the digestive tract, alcoholism, dialysis, genetic deficiencies, etc. All these causes mainly affect the central nervous system, and provoke the development of what is known as Wernicke's disease or Wernicke's encephalopathy.

Wernicke's disease is one of the most prevalent neurological or neuropsychiatric diseases. In autopsy series, features of Wernicke lesions are observed in approximately 2% of general cases. https://en.wikipedia...eficiency#Cause

------------------------------------------------------------------------------------------------------------
Niacin (B3)

Deficiency
https://www.ncbi.nlm...les/PMC4198903/
https://www.research...w_of_literature
http://www.bmj.com/r...sychosis-which-
And others link low Niacin to causing depression.

Moderately common - Niacin deficiency is more likely to be caused by problems that affect absorption of niacin or tryptophan. The most common cause is alcoholism. Other possible causes include disorders of the digestive system and prolonged treatment with the tuberculosis drug isoniazid (Laniazid, Nydrazid).
https://www.webmd.co...-treatments#1-3
------------------------------------------------------------------------------------------------------------
Vitamin B6 (pyridoxine)

Deficiency
https://www.ncbi.nlm...pubmed/15479988
https://www.ncbi.nlm...pubmed/25401165
https://www.ncbi.nlm...pubmed/18838531
and other articles link low vitamin B6 to depression.

https://www.ncbi.nlm.../pubmed/4547177https://www.ncbi.nlm.../pubmed/6889807
and other articles link oral contraceptives to low B6 and depression.

A deficiency of vitamin B6 alone is relatively uncommon and often occurs in association with other vitamins of the B complex. The elderly and alcoholics have an increased risk of vitamin B6 deficiency, as well as other micronutrient deficiencies. Evidence exists for decreased levels of vitamin B6 in women with type 1 diabetes and in patients with systemic inflammation, liver disease, rheumatoid arthritis, and those infected with HIV. Use of oral contraceptives and treatment with certain anticonvulsants, isoniazid, cycloserine, penicillamine, and hydrocortisone negatively impact vitamin B6 status. Hemodialysis reduces vitamin B6 plasma levels.
https://en.wikipedia...n_B6#Deficiency

Caution
https://www.ncbi.nlm.../pubmed/3630649
Because of supplements and certain medical therapies including some chemotherapies, vitamin B6 toxicity is becoming much more common.

Note - A search of vitamin B6 supplements on Amazon shows that many supplements currently on the market are well above the recommended dietary allowances. The long half life (see below) allows for toxic levels to build rapidly.

Cin - a good mult-vitamin, but don't overdo it on the B vitamins (even though they are water soluble, I actually got vit. B6 toxicity and that caused some nerve issues that I'm not sure will ever completely reverese),

https://www.ncbi.nlm...ooks/NBK114313/
Half-Life is 15 to 24 days.
------------------------------------------------------------------------------------------------------------
Folate (Folic Acid, vitamin B9)

Deficiency
https://examine.com/...nts/folic-acid/
Bjelland I, et al. Folate, vitamin B12, homocysteine, and the MTHFR 677C->T polymorphism in anxiety and depression: the Hordaland Homocysteine Study. Arch Gen Psychiatry. (2003)
Kelly CB et al.. The MTHFR C677T polymorphism is associated with depressive episodes in patients from Northern Ireland. J Psychopharmacol. (2004)
Almeida OP, et al. Contribution of the MTHFR gene to the causal pathway for depression, anxiety and cognitive impairment in later life. Neurobiol Aging. (2005)
And others link deficiency to depression.

Moderately common -
Folate is a water-soluble vitamin. It dissolves in water and isn’t stored in your fat cells. This means that you need to keep taking folate as your body cannot develop a reserve.
A diet low in fresh fruits, vegetables, and fortified cereals is the main cause of folate deficiency. In addition, overcooking your food can sometimes destroy the vitamins. Folate levels in your body can become low in just a few weeks if you don’t eat enough folate-rich foods.

Diseases that affect absorption in the gastrointestinal tract can cause folate deficiencies. Such diseases include:
Crohn’s disease
celiac disease
⦁ certain types of cancers
⦁ severe kidney problems that require dialysis.

Some people have a genetic mutation that hinders their body from properly and efficiently converting dietary or supplemental folate to its usable form, methylfolate.

Certain medications can cause folate deficiency. These include:
phenytoin (Dilantin)
trimethoprim-sulfamethoxazole
methotrexate
sulfasalazine

Alcohol interferes with folate absorption. It also increases folate excretion through the urine.
https://www.healthli...ficiency#causes

Toxicity
https://www.livestro...d-in-your-body/
Depression

http://www.healthy-v...n-toxicity.html
Taking Pancreatic enzymes, methotrexate, genetics can cause vitamin B9 toxicity.
------------------------------------------------------------------------------------------------------------
Vitamin B12 (cobalamin)
Deficiency
https://examine.com/...ts/vitamin-b12/
Carney MW, Sheffield BF. Serum folic acid and B12 in 272 psychiatric in-patients. Psychol Med. (1978)
Penninx BW, et al. Vitamin B(12) deficiency and depression in physically disabled older women: epidemiologic evidence from the Women's Health and Aging Study. Am J Psychiatry. (2000)
Lerner V, et al. Vitamin B12 and folate serum levels in newly admitted psychiatric patients. Clin Nutr. (2006) Morris MS, et al. Depression and folate status in the US Population. Psychother Psychosom. (2003)
and many other articles link low levels of vitamin B12 to depression.

https://www.health.h...ul-201301105780

Moderately common - More common in the elderly, vegetarians, those taking proton pump inhibitors (24 hour heart burn medicine) or have Celiac Disease or serious digestive issues.

Toxicity
https://www.mayoclin...12/art-20363663
"your body is capable of storing several years' worth of vitamin B-12," May cause anxiety. The majority of B12 toxicity is from taking too much supplements or megadoses of Vitamin C.

Half-life is 6 days.
https://www.nature.c...ticles/198200a0
-----------------------------------------------------------------------------------------------------------
Pantothenic Acid (Vitamin B5)
Deficiency
http://www.sciencedi...antothenic-acid
http://www.umm.edu/h...antothenic-acid
Links to depression.

Uncommon - Groups at risk of deficiency are alcoholics, women on oral contraceptives, the elderly, and people with impaired absorption due to certain digestive disorders.
https://www.justvita...5/#.WnyZJORy65c
------------------------------------------------------------------------------------------------------------
Choline
Deficiency
http://ajcn.nutritio.../90/4/1056.full
https://www.psycholo...he-case-choline
http://folk.uib.no/m...1_jimd_34_3.pdf
Low levels linked to anxiety

Deficiency caused by fatty liver disease, alcoholics, the obese, elderly and diabetics.

Toxicity
https://www.scienced...925492717301464
https://www.hindawi....rt/2011/650450/
http://www.psy-journ...(80)90065-7/pdf
High levels linked to depression

http://lpi.oregonsta...holine#toxicity
Toxicity normally caused by diet, Methotrexate and/or taking supplements.
-----------------------------------------------------------------------------------------------------------
Minerals/Metals

Calcium
hypocalcemia
http://www.sciencedi...y/hypocalcaemia
http://psycnet.apa.o.../1989-19007-001
https://www.drugs.co...pocalcemia.html
and others link low calcium to anxiety

Causes of hypocalcemia include....
Eating disorders Prolonged vomiting (e.g. with a viral illness)
⦁ Exposure to mercury, including infantile ⦁ acrodynia
⦁ Excessive dietary magnesium, as with supplementation.
⦁ Excessive dietary zinc, as with supplementation (causes rapid hypocalcemia).
⦁ Prolonged use of medications/laxatives containing magnesium
Chelation therapy for metal exposure, particularly ⦁ EDTA
Osteoporosis treatment or preventive agents, such as bisphosphonates and denosumab.
⦁ Agents for the treatment of hypercalcemia, such as Calcitonin.

  • Chronic kidney failure
  • Absent active vitamin D

⦁ Decreased dietary intake
⦁ Decreased sun exposure
⦁ Defective Vitamin D metabolism
Anticonvulsant therapy
⦁ Vitamin-D dependent ⦁ rickets, type I
⦁ Ineffective active vitamin D
⦁ Intestinal malabsorption
⦁ Vitamin-D dependent rickets, type II
Pseudohypoparathyroidism
⦁ Severe acute  hyperphosphataemia
Tumour lysis syndrome ⦁ Acute kidney failure
Rhabdomyolysis (initial stage)
⦁ Exposure to hydrofluoric acid which can be fatal if 2.5% of skin is exposed.
⦁ As a complication of pancreatitis Alkalosis, often caused by hyperventilation
https://en.wikipedia...alcaemia#Causes

hypercalcemia
http://www.cleveland.../hypercalcemia/
http://www.amjmedsci...2436-8/fulltext
http://www.jpsmjourn...(08)00145-0/pdf
and others link high calcium to anxiety and depression.

Caused by...
Parathyroid function
Primary hyperparathyroidism
Solitary parathyroid adenoma
Primary parathyroid hyperplasia
Parathyroid carcinoma
Multiple endocrine neoplasia
Familial isolated hyperparathyroidism
Lithium use
Familial hypocalciuric hypercalcemia/familial benign hypercalcemia
Vitamin-D disorders
Hypervitaminosis D (vitamin D intoxication)
⦁ Elevated 1,25(OH)2D (see calcitriol under Vitamin D) levels (e.g. sarcoidosis and other granulomatous diseases such as  tuberculosis)
Idiopathic hypercalcaemia of infancy⦁ [15]
⦁ rebound hypercalcaemia after rhabdomyolysis
High bone-turnover rates
Hyperthyroidism
Multiple myeloma
⦁ Prolonged immobilization
Paget's disease
Thiazide use
Vitamin A intoxication
Kidney failure
⦁ Severe secondary hyperparathyroidism
Tertiary hyperparathyroidism
Aluminium intoxication
Milk-alkali syndrome
Other
Adrenal insufficiency
Zollinger Ellison syndrome

Fairly common
https://en.wikipedia...alcaemia#Causes

FH - When I think of a natural product I think of something like calcium carbonate (the active ingredient in Tums). I do not use Tums because of the other ingredients. I purchase 100% calcium carbonate (food grade) and put the right amount in an empty vegetable gelatin capsule and use that for my antacid. Cheap, safe (as long as I routinely my blood calcium levels) and effective.

http://www.cymbaltaw...nic/?hl=caution
All about calcium and zinc supplements for anxiety.
------------------------------------------------------------------------------------------------------------
Iron
Deficiency
http://www.jogc.com/...bstract?rss=yes
http://jn.nutrition..../135/2/267.full
http://journals.tbzm...JARCM-3-219.pdf
and others link deficiency to depression.
https://www.livestro...5-iron-anxiety/
Limited evidence of iron deficiency causing anxiety.

Rare - chronic bleeding (hemoglobin contains iron)
⦁ excessive ⦁ menstrual bleeding
⦁ non-menstrual ⦁ bleeding
⦁ bleeding from the ⦁ gastrointestinal tract (⦁ ulcers, ⦁ hemorrhoids, ⦁ ulcerative colitis, ⦁ stomach or ⦁ colon cancer, etc.)
⦁ rarely, ⦁ laryngological bleeding or from the ⦁ respiratory tract
⦁ inadequate intake (see below) substances (in diet or drugs) interfering with iron absorption
⦁ Fluoroquinolone antibiotics
malabsorption syndromes
inflammation where it is ⦁ adaptive to limit bacterial growth in infection, but is also present in many other chronic diseases such as ⦁ Inflammatory bowel disease and ⦁ rheumatoid arthritis
⦁ blood loss (via donation, menstruation, injury, etc.)
⦁ parasitic infection
https://en.wikipedia...ficiency#Causes

Toxicity
https://www.ncbi.nlm...pubmed/23333676
https://www.ncbi.nlm...les/PMC5581806/
Limited evidence of iron toxicity causing depression.

https://rd.springer....?no-access=true
Limited evidence that excessive iron can cause anxiety

Causes of excess iron
Haemochromatosis
Haemolytic anaemias
Haemosiderosis
Iron poisoning (Supplements/multivitamins)
Zellweger Syndrome
Moderately common -
http://www.rightdiag...on/view-all.htm
----------------------------------------------------------------------------------------------------
Magnesium
Deficiency Toxicity
https://www.ncbi.nlm...pubmed/25690713
https://www.ncbi.nlm...pubmed/23289218
https://www.ncbi.nlm...pubmed/23950577
Blood levels of magnesium do not necessarily relate to depression or anxiety. Many patients respond to magnesium therapy even though their blood levels may already be high or normal. No concrete determination has been made as to when to take magnesium for depression or anxiety.

Both deficiency and excessive levels are fairly common.

FH - Be sure and have your serum magnesium levels checked at least once per year as the supplement can elevate mag levels with time which can cause calcium to drop and create additional muscle/joint issues.

FH - I did have my routine blood magnesium drawn a couple weeks ago and it was high. This would explain my low calcium. I have been dropping my magnesium intake a little at a time and repeating the blood test. As I drop it my calcium increases. I am now off the magnesium and hopefully at my next test on the 30th my calcium and magnesium will both be back to normal. This is why I always recommend people who are taking magnesium to have a blood magnesium test run every 6 months.
----------------------------------------------------------------------------------------------------------
Potassium           Sodium
Deficiency of sodium and or potassium are linked to depression and anxiety during dehydration and low Vitamin D levels.
Toxicity
https://www.ncbi.nlm...oxicity anxiety
https://www.ncbi.nlm...pubmed/23523745
https://www.ncbi.nlm...pubmed/23653461
https://www.ncbi.nlm...pubmed/24704193
https://www.ncbi.nlm...les/PMC5536667/
High sodium levels highly correspond to anxiety and some indiation it can cause depression.
https://www.ncbi.nlm.../pubmed/2919849
Limited evidence that high potassium causes anxiety

List of causes are extensive.

FH - Sodium can be a real issue for those suffering from anxiety. Anyone under stress (physical or mental) produces lactic acid. That is why many of us get body aches during times of high stress. Salt consumption, as everyone knows, puts high amount of sodium into the blood stream. It reacts with the lactic acid in our bodies to produce sodium lactate, a very strong neurostimulant. I am particularly sensitive to it. A simple salty hotdog will double my anxiety for 2 or 3 hours. Obviously I can reduce that by forcing fluids, say 2 or 3 glasses in an hour or two. This has lead me to eating at home where I can have a salt free diet.

Salt might be nature's antidepressant
http://www.scienceda...90310152329.htm
(Because it is a neural stimulant and in high enough quantities may cause anxiety)
------------------------------------------------------------------------------------------------------------
Zinc
Deficiency
https://www.ncbi.nlm...pubmed/23806573
https://www.ncbi.nlm...pubmed/21946308
https://www.ncbi.nlm...pubmed/24367556
https://www.ncbi.nlm...pubmed/21093288
and many more articles link low blood zinc levels to depression.

https://www.ncbi.nlm...pubmed/17166602
https://www.ncbi.nlm...ubmed/23493534/
https://www.ncbi.nlm...ubmed/18975044/
and many more articles link low blood zinc levels to anxiety.

Excess zinc..
⦁ Zinc may accumulate in acute kidney injury.
⦁ Those with haemochromatosis may absorb larger amounts of zinc.
⦁ Various pesticides contain zinc salts.
⦁ Compounds used to make paints, rubber and dyes may also contain zinc.
⦁ Zinc absorption from dandruff shampoos and denture creams.
⦁ Increasing in occurrence.
⦁ Supplements

Increasing in occurrence.

Zinc Deficiency

Uncommon -
⦁ Inadequate diet.
⦁ Gastrointestinal diseases including ulcerative colitis, Crohn's disease, short bowel syndrome and chronic diarrhoea.
⦁ Chronic liver disease.
⦁ Chronic kidney disease.
⦁ Alcoholism (decreases zinc absorption and increases urinary zinc excretion).
⦁ Sickle cell disease.
⦁ Diabetes.
⦁ Pregnancy and breast-feeding.
⦁ Vegetarian diet.
⦁ People taking large amounts of iron supplementation (iron can interfere with zinc absorption).
https://patient.info...ation-pro#nav-4

http://www.cymbaltaw...nic/?hl=caution
All about calcium and zinc supplements for anxiety.
------------------------------------------------------------------------------------------------------------
Manganese
Toxicity
https://www.ncbi.nlm...pubmed/25064383
Elevated manganese linked to anxiety
https://www.ncbi.nlm...pubmed/16343629
https://www.ncbi.nlm...pubmed/16962176
https://www.ncbi.nlm...pubmed/17018581
Elevated manganese linked to anxiety and depression.

Uncommon

Cause include...
⦁ Arc welding fume
⦁ Iron anemia
⦁ naturally contaminated drinking water (typically from certain limestone
⦁ exposure to fuel exhaust which contains ⦁ methylcyclopentadienyl manganese tricarbonyl (MMT),
⦁ Consumption of ⦁ dithiocarbamate pesticides.
https://en.wikipedia...anganism#Causes
-----------------------------------------------------------------------------------------------------------
Selenium
Deficiency
https://www.ncbi.nlm...pubmed/18449137
https://www.ncbi.nlm.../pubmed/1873372
https://www.ncbi.nlm...les/PMC3566946/
and others link low selenium levels to both anxiety and depression.

Very uncommon

It can occur in patients with severely compromised intestinal function, those undergoing total parenteral nutrition, those who have had gastrointestinal bypass surgery, and also in persons of advanced age (i.e., over 90). People dependent on food grown from selenium-deficient soil may be at risk for deficiency.
https://en.wikipedia...ficiency#Causes

Toxicity
https://pubchem.ncbi...ection=Symptoms
Limited indication that high selenium can cause depression.

Getting to be fairly common.

Selenium in Chinese grains like Chinese rice have been a source of selenium poisoning. Many areas of China have soils rich in selenium and natives who eat vegetables and meats in those areas are subject to bouts of selenium poisoning. Some of the vegetables exported from China come from those regions. Periodic outbreaks of selenosis have occurred in regions of China where high concentrations of selenium are found in the soil.

The richest food sources of selenium are seafood, followed by muscle meats. Drinking water is not considered to be a significant source of selenium in North America except in areas, where high levels of selenium in soil contribute to the selenium content of the water, higher levels of selenium may be found in wells used for drinking water. This frequently occurs in areas of the upper midwest and far west in the USA. Some plants, including garlic, Brazil nuts, and multiple mustard species, garlic, onion, and broccoli, wheat, and soy are rich in selenomethionine, a form of selenium. (‘selenium accumulators’). Brazil nuts grown in areas of Brazil with selenium-rich soil may provide more than 100 μg of selenium in one nut, while those grown in selenium-poor soil provide 10 times less.

Astragalus is a medicinal herb frequently grown in China and is a significant source of selenium poisoning. The researchers investigated an outbreak of acute selenium poisoning after reports of cases of toxicity started to surface in March 2008. They defined a case as the onset of symptoms of selenium toxicity within 2 weeks of ingesting a dietary supplement. There were 227 affected persons from 9 states, including Florida, Georgia, Kentucky, Michigan, North Carolina, Pennsylvania, Tennessee, Texas, and Virginia.

Selenium toxicity is actually more common in livestock than people. All animal species are susceptible to selenium toxicosis. However, poisoning is more common in forage-eating animals such as cattle, sheep, horses, and other herbivores that may graze selenium-containing plants. This is particularly true in the western part of the United States where the soil is rich in selenium. One thing that the states of Montana, South Dakota and Wyoming have in common is high selenium in the soil, water and plants. High selenium content in soil is absorbed by plants and passed on to livestock which has been linked to human cases of selenium poisoning. In 142 adults living on farms in seleniferous regions of South Dakota, the range of serum selenium was 123–363 μg/L (mean 197, SD ± 55, median 184)

Selenium toxicity is most frequently the cause of allergic reactions to multivitamins. Most multivitamins provide 40 to 60 mcg/day (which does not include selenium from the diet) while the dietary intake is recommended at 55 mcg.
https://www.ncbi.nlm...les/PMC3153292/
------------------------------------------------------------------------------------------------------------
Fluoride

Toxicity
https://www.ncbi.nlm...pubmed/24184405
https://www.ncbi.nlm...pubmed/23222693
https://www.ncbi.nlm...les/PMC5594553/
and others link fluoride exposure to anxiety and depression.

Causes of Fluorine toxicity...
⦁ Twenty percent of modern pharmaceuticals contain fluorine.
⦁ Children may experience gastrointestinal distress upon ingesting excessive amounts of flavored toothpaste. Between 1990 and 1994, over 628 people, mostly children, were treated after ingesting too much fluoride-containing toothpaste.
⦁ Around one-third of the world’s population drinks water from groundwater resources. Of this, about 10 percent, approximately 300 million people, obtains water from groundwater resources that are heavily contaminated with arsenic or fluoride
⦁ accidental or intentional consumption of insecticides and rodenticides.
------------------------------------------------------------------------------------------------------------
Cholesterol /Triglyceride

Deficiency
www.ncbi.nlm.nih.gov/pubmed/10367605
https://www.ncbi.nlm...pubmed/16250690
https://www.ncbi.nlm...pubmed/23197842
Decreased HDL and/or LDL linked to anxiety and/or depression.

Toxicity
https://www.ncbi.nlm...pubmed/16250690
https://www.ncbi.nlm...pubmed/12211884
https://www.ncbi.nlm...pubmed/11778348
https://www.ncbi.nlm.../pubmed/8884036
https://www.ncbi.nlm.../pubmed/1536278
https://www.ncbi.nlm...pubmed/10900559
Elevated LDL and Triglyceride linked to anxiety.
------------------------------------------------------------------------------------------------------------
Nutritional Blood Tests for causes for anxiety and/or depression.

Items proceeded by an asterisk are analysis that are routinely performed by many Psychiatrists.
Omega 3 and 6
Amino Acids
to include...
      Tryptophan
      Threonine
      Isoleucine
      Methionine
      Phenylalanine
      Tyrosine
Vitamins
to include...
      C
      *D
      E
      *B vitamins
Minerals....
Calcium
Iron
Magnesium
Potassium
Sodium
Zinc
Manganese
Selenium

Lipid Profile
Cholesterol
Triglycerides

Misc.
Choline
Flouride

Psychiatrists also often perform the following tests
Testosterone
Estrogen
Thyroid Function
Liver Function - (FH - The AD manufacturers usually recommend an annual Liver Function Test (LFT) to keep an eye on that issue.
Parathyroid Function
Pituitary Function

An increasing number of psychiatrists are also opting to do a genetic screening for genetic mutations.


#16 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 09 February 2018 - 01:03 PM

So you think you are in control of your supplements?

Competition of minerals and vitamins in the body.

If you take a large dose of a mineral, it will compete with other minerals to reduce their absorption.

Doses of magnesium can also be relatively large and should, ideally, be taken apart from other minerals. Magnesium competes with calcium for absorption.

If you take high doses of zinc long-term (50 mg or more per day for 10 weeks or longer ), be aware that it can cause copper deficiency, so you may need to supplement with copper as well.

Iron, copper and zinc are competitive for absorption.

The use of prescription drugs also helps in the deficiency of minerals. Antibiotics, Tylenol, Advil, Motrin, and aspirin all inhibit the absorption of minerals especially zinc, chromium and calcium.

Research has shown the best bioavailable minerals are amino acid chelated minerals.

Fiber which contains phytates, tea which contains tannins and rhubarb and spinach which contains oxalates are known as bad chelates. This is because phytates, tannins and oxalates bind the minerals in the body to themselves in the same way that amino acids do, this results in the minerals not being absorbed by the body but excreted instead.

Methionine effects the concentration of vitamin B6, B12, choline, folic acid and magnesium.

Vitamin C can enhance iron absorption from supplements and plant foods.

The fat-soluble vitamins (A, D, E, and K) are likely to be better absorbed if taken with a meal that contains fats. In fact, one study found that taking vitamin D with dinner rather than breakfast increased blood levels of vitamin D by about 50%.

Moderate to large doses of fat-soluble vitamins reduce absorption of other fat-soluble vitamins - by about 10 to 50% - due to competition.

Absorption of vitamin K appears to be particularly reduced by taking other fat-soluble vitamins.

Vitamin A absorption is least affected and may actually be better absorbed when taken with vitamin E.

Taking vitamins D, E, or K several hours before or after other fat-soluble vitamins would seem to maximize their absorption.

Vitamin C can inhibit copper absorption, and too much copper can lead to vitamin C deficiency.

Zinc inhibits both copper and iron; magnesium, copper, iron and calcium all compete for absorption, so too much of one can lead to low blood levels of the others.

Taking antibiotics for a long time can also deplete the body's levels of several B vitamins. On the other hand, taking vitamin B-12 with the antibiotic tetracycline may interfere with the medication's absorption and effectiveness.

Weight loss medication that prevents your body from absorbing fat also prevents your body from absorbing fat-soluble vitamins.

Taking magnesium with food can reduce the occurrence of diarrhea.

Taking iron with food can reduce the chance of stomach upset.

Be aware that vitamins and minerals can also affect the absorption and effectiveness of medications.

l-leucine was inhibited by l-valine, l-isoleucine and l-methionine

l-lysine was inhibited by l-arginine, l-phenylalanine and l-histidine.

Little or no competition was observed for the glycine uptake site

Many other amino acids compete with each other for absorption.

https://www.consumer...-take-vitamins/
https://www.livestro...other-vitamins/
http://www.foodminer...human-body.html
https://www.scienced...300962977903528
-------------------------------------------------------------------------------------------------------


#17 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 09 February 2018 - 01:12 PM

List of medical/medicinal causes of Anxiety not including stress

This list does NOT include items that fall under the category of stress, That would be items like loss of job, divorce, death in a family, marrage problems, having a life threatening disease, military combat, .....

Genetic Conditions
Chromosome 17p, partial deletion -
Chromosome 22q deletion - anxiety
⦁ Genetics - There are various gene mutations that exist for nearly all vitamins, amino acids, etc that can cause deficiencies or toxicity of these items and lead to anxiety and/or depression.
Mc Leod neuroacanthocytosis syndrome -
Multiple endocrine neoplasia - Genetically caused tumors of endocrine glands
Soto's Syndrome - cerebral gigantism
Vitiligo - s a long-term genetic skin condition characterized by patches of the skin losing their pigment.
WAGR Syndrome is a rare genetic syndrome
Westphal disease - is a rare, autosomal dominant channelopathy characterized by muscle weakness or paralysis when there is a fall in potassium levels in the blood.
Wilson's disease - is a genetic disorder in which copper builds up in the body.
Wolfram's disease - is a rare autosomal-recessive genetic disorder that causes childhood-onset diabetes mellitus, optic atrophy, and deafness as well as various other possible disorders.
Porphyria - is a group of diseases in which substances called porphyrins build up, - anxiety

 

Perceptions
⦁ Phobias - feeling of panic

Poisonings
Amphetamine intoxication
Alcoholic intoxication -
Apricot seed poisoning -
⦁ Aspirin intolerance
Bearsfoot hellebore poisoning - nervousness
Bird cherry seed poisoning - nervousness
Bitter almond seed poisoning - nervousness
Carbamate insecticide poisoning - anxiety
Chemical poisoning -- Azinphos-methyl - nervousness
Chemical poisoning -- Carbaryl - anxiety
Chemical poisoning -- Carbon Disulfide - anxiety
Chemical poisoning -- Chlordecone - anxiety
Chemical poisoning -- Chloropicrin - anxiety
Chemical poisoning -- Cologne - anxiety
Chemical poisoning -- DDD - anxiety
Chemical poisoning -- DDT - anxiety
Chemical poisoning -- Ethylamine - anxiety
Chemical poisoning -- Jet Fuel-5 - nervousness
Chemical poisoning -- Lysergic Acid Diethylamide - fear
Chemical poisoning -- Manganese - nervousness
Chemical poisoning -- Monocrotophos - anxiety
Chemical poisoning -- Oil-based paint - nervousness
Chemical poisoning -- Phencyclidine - fear
Chemical poisoning -- Selenium Dioxide - nervousness
Chemical poisoning -- Sodium Monofluoroacetate - anxiety
Chemical poisoning -- Strychnine - anxiety
Chemical poisoning -- Thallium - nervousness
Chemical poisoning -- Toluene - anxiety
Chronic Chemical poisoning -- Varnish makers' and painters' Naptha - nervousness
Cherry laurel seed poisoning - nervousness
Cherry seed poisoning - nervousness
Chokecherry seed poisoning - nervousness
Chronic Pesticide poisoning -- xylene - nervousness
Cyclosporine toxicity - anxiety
Jessamine poisoning - nervousness
Lead poisoning - anxiety
Lidocaine toxicity - nervousness
Lupine poisoning - nervousness
Mercury
Moccasin snake poisoning - anxiety
Morning Glory poisoning - anxiety
Organophosphate insecticide poisoning - anxiety
Peach seed poisoning - nervousness
Poison hemlock poisoning - nervousness
Puss caterpillar poisoning - anxiety
Puss caterpillar poisoning - anxiety
Sea snake poisoning - anxiety
Venerupin shellfish poisoning - nervousness
Wild cherry seed poisoning - nervousness
Toxic Shock Syndrome is a condition caused by bacterial toxins. Symptoms may include fever, rash, skin peeling, and low blood pressure.anxiety
⦁ Bisphenol A exposure linked to anxiety and depression
https://www.ncbi.nlm.nih.gov/pmc

Adverse Reactions
Food Additive Adverse reaction -- amines - nervousness
Food Additive Adverse reaction -- MSG - nervousness
Food Additive Adverse reaction -- salicylate - nervousness
Food Additive Adverse reaction -- sulfite - nervousness
Hallucinogen
Herbal Agent adverse reaction -- Ginseng - nervousness
Herbal Agent adverse reaction -- Sassafras Oil - anxiety
Herbal Agent overdose -- Ginseng - nervousness
Herbal Agent overdose -- Golden Seal - nervousness
Herbal Agent overdose -- Sabah vegetable - anxiety
Inch ant sting - anxiety
Insect allergy - anxiety
Insect bite allergy - anxiety
Insect sting allergy - anxiety
Jack jumper ant sting - anxiety
Greenhead ant sting - anxiety
Non-Food Allergy -- Africanized honeybee - anxiety
Non-Food Allergy -- Black fire ant - anxiety
Non-Food Allergy -- Bumblebee - anxiety
Non-Food Allergy -- honey bee - anxiety
Non-Food Allergy -- Hornet - anxiety
Non-Food Allergy -- scorpion - anxiety
Non-Food Allergy -- Tropical fire ant - anxiety
Non-Food Allergy -- wasp - anxiety
Non-Food Allergy -- Yellow jacket Wasp - anxiety
Red Imported Fire ant sting - anxiety
Carukia barnesi sting - anxiety
Delphinium poisoning - nervousness
Caffeine

Withdrawals (Most withdrawals can cause some anxiety, some of the most common are listed here)
Alcohol withdrawal - fear
Ambien withdrawal - anxiety
Amphetamine withdrawal - anxiety
Antidepressants withdrawal
Cocaine withdrawal - anxiety
Crack withdrawal - anxiety
Darvocet withdrawal - anxiety
Demerol withdrawal - severe anxiety
Dilaudid withdrawal - anxiety
Ecstasy withdrawal - anxiety
m******** withdrawal - anxiety
Methamphetamine withdrawal - anxiety
Opium withdrawal - anxiety
Ritalin withdrawal - anxiety
Tranquilizer withdrawal - anxiety
Vicodin withdrawal - panic
⦁ Benzodiazepine ⦁ withdrawal - anxiety
Discontinuation syndrome - anxiety
Heroin withdrawal - panic
Percocet withdrawal - anxiety

Systemic Conditions/Diseases
Hypertension - anxiety
Adrenal hypertension - anxiety
Alcohol-induced hypertension - anxiety
Conn Syndrome-induced hypertension - anxiety
Corticosteroid-induced hypertension - anxiety
Cyclosporine-induced hypertension - anxiety
Drug-induced hypertension - anxiety
Erythropoietin-induced hypertension - anxiety
Hyperaldosteronism-induced hypertension - anxiety
Licorice-induced hypertension - anxiety
Malignant hypertension - anxiety
Nasal decongestant-induced hypertension - anxiety
Renal hypertension - anxiety
Anaemia
Chronic orthostatic hypotension - anxiety
Decreased oxygen saturation - anxiety
⦁ Diabetes
⦁ Electrolyte disturbance
Hyperglycemia
Hypoglycemia
Inborn amino acid metabolism disorder - anxiety
Orthostatic intolerance - anxiety
Renovascular Hypertension - anxiety
Anoxemia - abnormally low level of oxygen in the blood - - anxiety
⦁ Barraquer–Simons syndrome
⦁ Chronic fatigue syndrome- anxiety
Glycogen storage disease - a metabolic disorder caused by enzyme deficiencies affecting either glycogen synthesis, glycogen breakdown or glycolysis (glucose breakdown) - nervousness
Hyperoxia - occurs when cells, tissues and organs are exposed to an excess supply of oxygen (O2) - anxiety
Lupus - is an autoimmune disease in which the body's immune system mistakenly attacks healthy tissue in many parts of the body. -anxiety
⦁ Pseudopolycythaemia: An acquired condition where the blood has the normal number of red blood cells but has a reduced plasma volume. It usually occurs in males with weight and blood pressure problems who smoke
Temporal arteritis is an inflammatory disease of blood vessels.

Transfusion Reaction
Uremia It can be defined as an excess of amino acid and protein metabolism end products, such as urea and creatinine, in the blood that would be normally excreted in the urine
Volume depletion - s a state of decreased blood volume; more specifically, decrease in volume of blood plasma.
Anaphylaxis

Adrenal Ddiseases/Conditions
Adrenal Cortex Diseases - anxiety
Adrenal dysfunction
Adrenal hypofunction - anxiety
Congenital adrenal hyperplasia - anxiety
Hypoadrenalism - anxiety
Pheochromocytoma - is a neuroendocrine tumor of the medulla of the adrenal glands nervousness
Addison's Disease -primary adrenal insufficiency - anxiety

Drug addiction/abuse/overuse
Alcoholism - fear
Amphetamine abuse - chronic anxiety
Barbiturate abuse - nervousness
Benzodiazepine abuse - nervousness
Caffeine addiction - anxiety
Cocaine
c*******
Cocaine abuse - nervousness
Cocaine addiction - anxiety
Crack addiction - anxiety
Crystal meth addiction - anxiety
Dexedrine overdose - panic
Ecstasy abuse - anxiety
Ecstasy addiction - anxiety
Heroin dependence - Anxiety
m******** abuse - fear of dying
m******** addiction - anxiety
Methamphetamine overdose - panic
Narcotic addiction - anxiety
Nicotine
Opioid addiction - anxiety
Opium addiction - anxiety
Oxycontin addiction - anxiety
Pain killer addiction - anxiety
Sleeping pill addiction - anxiety
Tranquilizer addiction - anxiety
Guarana overuse - nervousness
⦁ Body-packer syndrome is the Anglo-american term for intracorporeal transport of drugs packed in rubber or plastic containers.

Respiratory Diseases/Conditions
Airway Obstruction - panic
Asthma
Chronic obstructive pulmonary disease
Chronic respiratory failure
Diaphragmatic paralysis - anxiety
Emphysema
Hyperventilation
Pneumothorax
Pulmonary edema - anxiety
Pulmonary embolism - anxiety
Respiratory depression - anxiety
Respiratory failure
Stridor - a high-pitched breath sound resulting from turbulent air flow in the larynx

Infections
Bacterial pericarditis - anxiety
Brucellosis
Encephalitis
Epstein Barr virus - anxiety
Infectious CFS - anxiety
Infectious mononucleosis
Limbic encephalitis - anxiety
Middle ear infection - labyrinthitis
Neurosyphilis
Pneumonia, Bacterial - anxiety
Pneumonia, Viral - anxiety
Post-Streptococcal Neurologic Disorders - anxiety
Post-viral CFS - anxiety
Rabies - feeling of panic
Tuberculous pericarditis - anxiety
Viral pericarditis - anxiety
Tetanus - anxiety
Cystitis - Urinary tract infection - anxiety
⦁ Candidiasis is a fungal infection due to any type of Candida (a type of yeast).
Stachybotrys chartarum - Black Mold
Variant Creutzfeldt-Jakob disease - is a type or brain disease within the transmissible spongiform encephalopathy family.It is caused by prions, which are mis-folded proteins.[6] Spread is believed to be primarily due to eating bovine spongiform encephalopathy (BSE)-infected beef.

Neurological Disorders
Alzheimer disease - Anxiety
Brain tumor
Concussion
Cerebrovascular disease
Delirium - anxiety
Delirium tremens - terror
Dementia
General somatic pain - Anxiety
Head injury
Migraine
Parkinson disease - anxiety
Post-concussion syndrome
Vascular malformations of the brain - anxiety
Whiplash - nervousness
Bilateral abductor vocal cord paralysis syndrome - anxiety
Myofascial pain syndromes - Anxiety
Neurosis
Neurotoxicity syndromes - anxiety

Sympathomimetics - Drugs that mimic the effect of adrenaline
Temporal lobe epilepsy - fear
Asperger Syndrome, - is a developmental disorder characterized by significant difficulties in social interaction and nonverbal communication, along with restricted and repetitive patterns of behavior and interests - anxiety
Autonomic Dysreflexia - anxiety (Spinal cord injury)
Barre-Lieou syndrome - symptoms which are rooted in the sympathetic nervous system, specifically the cluster of nerves located in the posterior cervical area at the back of the neck.anxiety
Benign Fasciculation Syndrome - twitching of musles.nervousness
Burning mouth syndrome a burning sensation in the mouth with no underlying dental or medical cause
Multiple sclerosis
Stiff-Person Syndrome - a rare neurologic disorder of unclear cause characterized by progressive rigidity and stiffness.
⦁ Brain ⦁ hemorrhage
Sydenham chorea - is a disorder characterized by rapid, uncoordinated jerking movements primarily affecting the face, hands and feet

Thyroid Conditions/Diseases
Autoimmune thyroid diseases - nervousness
High T4 syndrome - nervousness
Hyperthyroidism - nervousness
Subacute Thyroiditis - anxiety
Graves Disease - nervousness

Parathyroid Diseases/Conditions
Hypoparathyroidism - nervousness
Parathyroid dysfunction
Cardiac Diseases and Conditions
Cardiac arhythmia
Cardiac tamponade - pericardial effusion in which fluid, pus, blood, clots, or gas accumulates in the pericardium (the sac in which the heart is enclosed), - anxiety
Cardiogenic shock
Chest pain
Congenital heart disease
Congestive cardiac failure
Constrictive pericarditis - anxiety
Decreased cardiac output - anxiety
Heart failure
Mitral valve prolapse
Pyogenic pericarditis - anxiety
Rheumatic pericarditis - anxiety
Sinus arrhythmia - anxiety
Sinus node disease - anxiety
Sinus tachycardia - anxiety
Uremic pericarditis - anxiety

Hormonal/Reproductive/Pregnancy
Hormonal effects
Menopause - anxiety
Nymphomania - anxiety
Postpartum depression
Postpartum hyperthyroidism - Anxiety
Postpartum thyroiditis - anxiety
Premenstrual dysphoric disorder - anxiety
Premenstrual syndrome - anxiety
Puberty - anxiety
⦁ Elevated Estrogen levels
⦁ Low Estrogen levels
⦁ Elevated Testosterone

Gastrointestional Diseases/Condition
Gastrointestinal disorders
Celiac disease - anxiety
Crohn's disease
Hiatus hernia
Peptic ulcer
Ulcerative colitis
⦁ postcholecystectomy syndrome after removal of gall bladder includes depression.
Cholecystectomy - Removal of gall bladder.

Skelatal/Muscle Disorders/Diseases
Akathisia - a feeling of inner restlessness and inability to stay still. - anxiety
Fibromyalgia - anxiety
Rheumatoid arthritis

Urogenital Diseases/Conditions
hematuria syndrome - blood in the urine - nervousness

Pituitary Diseases/Conditions
Cushing's disease - Anxiety
⦁ Pituitary dysfunction - (tumors,

Sleep Disorders
Dysomnia (sleep disorders)
⦁ Sleep Deprivation
Hypersomnia - excessive time spent sleeping -Anxiety
Sleep apnea - anxiety

Miscellaneous Conditions
Cholesteatoma - a destructive and expanding growth consisting of keratinizing squamous epithelium in the middle ear and/or mastoid process.
Lazarus complex - A phenomenon of unclear nature that may occur in patients who have been clinically dead and then either resuscitated, or in whom there has been a spontaneous return of circulation after attempts to resuscitate fail. Patients report a continuity of subjective experience and may recall visitors and other hospital events despite virtually complete suppression of cortical activity. There have been only 38 cases documented in the medical literature worldwide.anxiety
Misanthropy - Hating the human race
Misogynism - hatred of, contempt for, or prejudice against women or girls
Mountain sickness - a pathological condition that is caused by acute exposure to low air pressure
⦁ Troell-Junet syndrome: A disorder involving enlarged extremities, diabetes, skull abnormalities and excessive thyroid hormone production

Liver Diseases/Conditions
Hepatic encephalopathy - anxiety

Medications or substances that may cause Anxiety
The following drugs, medications, substances or toxins are some of the possible causes of anxiety.
This list is incomplete and various other drugs or substances may cause your anxiety. Always advise your doctor of any medications or treatments you are using, including prescription, over-the-counter, supplements, herbal or alternative treatments.
⦁ Abilify
⦁ AccuNeb
Acebutolol
Acebutolol Hydrochloride
⦁ Adapin
⦁ Adrenalin injection
⦁ Airet
⦁ AK Beta
Albuterol
⦁ Aldopren
⦁ Alferon N
⦁ Alphagan
⦁ Alphagan P
⦁ Alphapress
Amantadine
Amantadine Hydrochloride
⦁ Ambien
⦁ Aminogluthethmide
Amiodarone
Amitriptyline Hydrochloride
⦁ Amlodipine and Benazepril
Amoxapine
Amphetamine
Amphetamine intoxication
⦁ Amvaz
Anafranil
⦁ Anapsique
⦁ Anatuss LA
⦁ Ancolan
Anticholinergic
Antihypertensive drug
⦁ Antidepressants
⦁ Apo-Amitriptyline
⦁ Apo-Atenol
⦁ Apo-Clomipramine
⦁ Apo-Doxepin
⦁ Apo-Salvent
⦁ Apresoline
⦁ Aquatab
⦁ Aratac
Arima
Aripiprazole
⦁ Aromasin
⦁ Asendin
⦁ Asmol
⦁ Atapryl
Atenolol
Atovaquone
⦁ Aurorix
⦁ Avalide
⦁ Avapro
⦁ Aventyl
⦁ Aventyl Pulvules
⦁ Benacine
⦁ Benadryl Cough Medicine
Benazepril Hydrochloride
⦁ Benzene and derivatives
⦁ Betagan
⦁ Betapace
⦁ Betapace AF
Betaxolol
⦁ Betaxolol Hydrochloride
⦁ Betaxon
⦁ Betimol
⦁ Betoptic
⦁ Betoptic S
⦁ Betoquin
⦁ Bicor
⦁ Bismatrol
Bisoprolol
Bitolterol
⦁ Blocadren
Brimonidine
Brompheniramine
⦁ Broncholate
⦁ Bronkaid Dual Action
⦁ Bupivacaine with Epinephrine
Bupropion
⦁ Buvacaina
⦁ Cafergot
Caffeine
c*******
⦁ Carbex
⦁ Carbocaine 2% with Neo-Cobefrin
⦁ Carbon disulphide
⦁ Cardinol
⦁ Cardinorm
Cardura
Carteolol
⦁ Carteolol Hydrochloride
⦁ Cartrol
⦁ Catapres tablets
⦁ Catapres-TTS-1 tablets
⦁ Catapres-TTS-2 tablets
⦁ Catapres-TTS-3 tablets
⦁ Catovit
Celexa
⦁ CellCept
Cevimeline
⦁ Chloroprocaine Hydrochloride
Chlorpheniramine
⦁ Chlorpromazine Hydrochloride
⦁ Citanest Forte
⦁ Citanest Forte with Epinephrine
⦁ Citanest Octapresin
⦁ Clindamycin
⦁ Clobemix
⦁ Clomipramine Hydrochloride
Clonazepam
⦁ Clonidine tablets
⦁ Clopra
⦁ Coldmist
⦁ Comtan
⦁ Congess
⦁ Congestac
⦁ Consupren
⦁ Contuss
Copaxone
⦁ Cordarone X
⦁ Corgard
Cyclosporine
⦁ Cytadren
⦁ Deconsal II
⦁ Deconsal Sprinkle
⦁ Defen LA
⦁ Delixir
⦁ Demazin Hot Lemon
⦁ Demolox
⦁ Desipramine Hydrochloride
⦁ Devrom
⦁ Devron
Dexchlorpheniramine
Didanosine
Diethylstilbestrol
⦁ Dimetane
⦁ Dimetriose
Distigmine
Dofetilide
Doxazosin
Doxepin Hydrochloride
Dronabinol
⦁ Druatuss
⦁ Duranest with Epinephrine
⦁ Durasal II
⦁ Dynafed Asthma Relief
⦁ Dynamo
⦁ Dynex
Ecstasy
Effexor
⦁ Effexor XR
⦁ Elavil
⦁ Eldepryl
⦁ Endal
⦁ Endal-SR
⦁ Endantadine
⦁ Endep
Enfuvirtide
⦁ Enidin
⦁ Enovil
Enoxacin
⦁ Enoxin
Entacapone
⦁ Entex LA
⦁ Entex PSE
⦁ Epipen
⦁ Epoetin
Epoetin Alfa
Epogen
⦁ Eprex
⦁ Ergamisol
⦁ Ergodryl
⦁ Etidocaine Hydrochloride with Epinephrine
⦁ Etrafon
⦁ Etrafon-A
⦁ Etrafon-Forte
⦁ Eulexin
⦁ Evoxac
Exemestane
⦁ Fedahist Expectorant
Felbamate
⦁ Felbatol
Flecainide
⦁ Flecatab
⦁ Flomax
Fluoxymesterone
Flutamide
⦁ Foradil Aerolizer
⦁ Foromoterol
⦁ Fuzeon
⦁ Gengraf
Gestrinone
⦁ GFN/PSE
⦁ Glatiramer
⦁ GP-500
⦁ Guai-Vent PSE
⦁ Guaifed
⦁ Guaifed-PD
⦁ Guaifenex GP
⦁ Guaifenex PSE
⦁ Guaimax-D
⦁ Guaimax-S
⦁ Guaipax PSE
⦁ Guaitab
⦁ Guaitex PSE
⦁ Guaituss PE
Guanabenz
⦁ H 9600 SR
Hallucinogen
⦁ Halotestin
⦁ Histalet X
⦁ Honvol
Hydralazine
Imipramine
Inderal
⦁ Inderide
⦁ Inderide LA
⦁ Ineral LA
⦁ Inerferon Alfa
⦁ Infergen
⦁ Inhaler drug
⦁ Innopran XL
⦁ Intraglobulin
⦁ Intragram
Intron A
⦁ Iosal II
⦁ Isocaine HCl 2%
⦁ Keppra
⦁ Kerlone
Klonopin
⦁ L-Deprenyl
Lamictal
⦁ Lamictal CD
Lamotrigine
Levamisole
⦁ Levate
⦁ Levatol
Levetiracetam
Levobunolol
⦁ Lexapro
⦁ Lidocaine and Epinephrine
⦁ Limbitrol
⦁ Limbitrol DS
⦁ Liquibid
⦁ Lodosyn
⦁ Loniten tablets
⦁ Lopressor
⦁ Lotensin
⦁ Lotrel
⦁ Ludiomil
⦁ Luvox
⦁ Magnesium
⦁ Maosig
⦁ Marcain
⦁ Marcaine
⦁ Marcaine with Epinephrine
m******** - a form of ⦁ c*******
⦁ Marinol
⦁ Maxair
⦁ Maxifec
⦁ Maxifed G
⦁ Maxolon
Mazindol
Meclozine
⦁ Med-RX
⦁ Melipramine
⦁ Mepivacaine with Levonordefrin
Mepron
⦁ Meridia
⦁ Methdilazinea
Metipranolol
Metoclopramide
Metoprolol
⦁ Micardis
⦁ Micardis HCT
Midodrine
⦁ Migral
⦁ MiniThin Asthma Relief
⦁ Minoxidil tablets
⦁ Miraphen PSE
Mirtazapine
⦁ Moclebemide
Moclobemide
Modafinil
⦁ Mohexal
⦁ Monitan
⦁ Mycophenolate
Naltrexone
⦁ Nardil
⦁ Nasabid
⦁ Nasabid-SR
⦁ Nasatab LA
Neoral
⦁ Nesacaine
⦁ Nesacaine-MPF
⦁ Nesstab LA
⦁ NoDoz
⦁ NoDoz Plus
Normal Immunoglobulin
⦁ Norpramin
Norvasc
⦁ Novo-Atenol
⦁ Novo-Doxepin
⦁ Novo-Salmol
⦁ Novo-Tryptin
⦁ Nu-Atenol
⦁ Octamide
⦁ Octocaine 100
⦁ Octocaine 50
⦁ Ocupress
Olanzapine
⦁ Optipranolol
Organophosphates
Orlistat
⦁ Ormazine
⦁ Oxypentifylline
⦁ Pamelor
⦁ PanMist LA
⦁ PanMist Syrup
⦁ PanMist-Jr
⦁ Parnate
Paxil
⦁ Paxil CR
⦁ PegIntron
Penicillin
⦁ Pepto-Bismol
Pergolide
⦁ Permax
⦁ PhenaVent
Phenelzine
Pindolol
⦁ Pink Bismuth
⦁ Piriton
⦁ Pisacaina
⦁ PMS-Amantadine
⦁ PMS-Clonazepam
⦁ PMS-Desipramine
⦁ Polaramine Infant Compound
⦁ Polocaine 2%
⦁ Prilocaine with Epinephrine
⦁ Primatine
⦁ ProAmatine
Procrit
⦁ Profen II
⦁ Prolintane
⦁ Propoxycaine and Procaine
Propranolol
⦁ Prostigmin
Proventil
⦁ Proventil HFA
⦁ Proventil Repetabs
⦁ Provigil
Prozac
⦁ Prozac Weekly
⦁ Pseudovent
⦁ Pseudovent-PED
Ranitidine
⦁ Ravocaine and Novocain with Levophed
⦁ Ravocaine and Novocain with Neo-Cobefrin
⦁ Reclomide
⦁ Refenesen Plus
Reglan
⦁ Remeron
⦁ Remeron SoITab
⦁ Respa-1st
⦁ Respaire
⦁ Respaire-120 SR
⦁ Respax
⦁ Respolin
⦁ Revia
⦁ Rhotral
⦁ Risperdal
⦁ Risperdal M-TAB
Risperidone
⦁ Robitussin PE
Roferon-A
⦁ Ru-Tuss DE
⦁ Rymed
⦁ Sabulin
⦁ Salbulin
⦁ Salbutalan
⦁ Sandimmun Neoral
Sandimmune
⦁ Sandoglobulin
⦁ Sanorex
⦁ Sarafem
⦁ Sectral
Selegiline
⦁ Sensorcaine
⦁ Sensorcaine with Epinephrine
⦁ Sensorcaine-MPF
⦁ Serenace
Sertraline
Sibutramine
Sildenafil
Sinemet
⦁ Sinemet CR
⦁ Sinequan
⦁ Sinufed Timecelles
⦁ Sinupan
⦁ Sinuvent PE Tablets
⦁ Sonata
⦁ Stamoist E
Stavudine
⦁ Stilphostrol
⦁ Stimulant drugs
⦁ Sudal
⦁ Sulphonamide drug
⦁ Surmontil
⦁ Sus-Phrine
⦁ Symadine
⦁ Symmetrel
⦁ Syn-RX
⦁ Tambocor
Tamsulosin
⦁ Taro-Atenol
⦁ Temodar
Temozolomide
⦁ Tenormin
⦁ Thorazine
⦁ Tikosyn
Timolol
⦁ Timoptic
⦁ Timoptic-XE
Tizanidine
Tocainide
⦁ Tofranil
⦁ Tofranil-PM
⦁ Tonocard
⦁ Toprol-XL
⦁ Tornalate
⦁ Touro LA
Tramadol
⦁ Travacalm
⦁ Trental
⦁ Triavil
⦁ Tridapin
Trimipramine
⦁ Tryptanol
⦁ Tuss-LA
⦁ Ubretid
⦁ Ultracet
⦁ Ultram
⦁ Uvega
⦁ V-Dec-M
Venlafaxine
Ventolin
⦁ Ventolin HFA
⦁ Ventolin Nebules
⦁ Ventolin Rotacaps
⦁ Versacaps
Viagra
Videx
⦁ Videx EC
⦁ Visken
Vitamin B12 deficiency
⦁ Vivactil
⦁ Volmax
Wellbutrin
⦁ Wellbutrin SR
⦁ Wellbutrin XL
⦁ Wytensin
⦁ Xenical
⦁ Xopenex
⦁ Xylocaina
⦁ Xylocaine with Epinephrine
Zaleplon
⦁ Zanaflex
⦁ Zantac
⦁ Zantac 75
⦁ Zantac EFFERdose
⦁ Zebeta
⦁ Zephrex
⦁ Zephrex LA
Zerit
⦁ Zerit XR
⦁ Ziac
Zofran
⦁ Zofran ODT
Zoloft
Zolpidem
⦁ Zonegran
Zonisamide
⦁ Zyban
⦁ Zyprexa
⦁ Zyprexa Zydis


#18 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 09 February 2018 - 01:16 PM

List of causes of non-stress Depressive symptoms

This section shows a full list of all the diseases and conditions listed as a possible cause of Depressive symptoms in our database from various sources.

This list does NOT include items that fall under the category of stress, That would be items like loss of job, divorce, death in a family, marrage problems, having a life threatening disease, military combat, .....

22q11.2 deletion syndrome - Depression
⦁ Oxalic acid is found in members of the spinach family and cabbage, broccoli, brussels sprouts, chives and lamb's quarters are high in oxalates, as are sorrel and parsley. Rhubarb leaves contain about 0.5% oxalic acid.
Aceruloplasminemia - depression
ACTH Deficiency - depression
Acute Bokhoror - depression
Acute Chemical poisoning -- Varnish makers' and painters' Naptha - depression
Acute intermittent porphyria - depression
Acute Pesticide poisoning -- Triforine - depression
Acute Viliuisk Encephalitis - depression
Acute Viliuisk Encephalomyelitis - depression
Addiction - depression
Addington disease - mental depression
Addison's Disease - Depression
Adhesive abuse - depression
Adhesive addiction - depression
Adrenal Cortex Diseases - depression
Adrenal Cortex Neoplasms - depression
Adrenal gland hyperfunction - depression
Adrenal gland hypofunction - depression
Adrenal hyperplasia - depression
Adrenal incidentaloma - depression
Aerosol abuse - depression
Aerosol addiction - depression
Aging brain syndrome - depression
Alcohol abuse
Alcohol Withdrawal - depression
Alzheimer's Disease - depression
Ambien withdrawal - suicidal thoughts
Amphetamine abuse - suicidal thoughts
Amphetamine withdrawal - suicidal thoughts
Anaemia, sideroblastic, X-linked -- ataxia - depression
Andropause - (Low testosterone) depression
Asperger syndrome - depression
Attenuated congenital adrenal hyperplasia - depression
Autoimmune limbic encephalitis - depression
Autoimmune thyroid disease associated Celiac Disease - Depression
Autoimmune thyroid diseases - depression
Balance disorders - depression
Baltic myoclonic epilepsy - depression
Barre-Lieou syndrome - depression
Basal ganglia calcification, idiopathic 1 - depression
Basilar artery insufficiency - depression
Bearsfoot hellebore poisoning - depression
Benzodiazepine abuse - depression
Bilateral abductor vocal cord paralysis syndrome - depression
Binswanger's Disease - depression
Black locust poisoning - depression
Borna disease - depression
Bottlebrush buckeye poisoning - depression
Brain tumor
Breathing-related sleep disorder - depression
Briquet syndrome - depression
Brucellosis
Burnett's syndrome - depression
California buckeye poisoning - depression
Celiac Disease - depression
Cerebral tumor
Cerebrovascular disease
Chat room addiction - depression
Chemical poisoning -- Amitrole - depression
Chemical poisoning -- Chloralose - depression
Chemical poisoning -- Chloromethane - depression
Chemical poisoning -- Nitrotoluene - depression
Chemical poisoning -- Phencyclidine - depression
Chemical poisoning -- Propoxur - depression
Childbirth
Cholestasis disease of pregnancy - depression
Choreoacanthocytosis amyotrophic - depression
Chronic fatigue syndrome - depression
Chronic Hepatitis B - depression
Chronic pain
Circadian rhythm sleep disorder - depressed mood
Coastal leucothoe poisoning - depression
Cocaine abuse - depression
Cocaine addiction - depression
Cocaine withdrawal - depression
Collagenous celiac disease - Depression
Congenital adrenal hyperplasia (CAH) - depression
Congenital hepatic porphyria - depression
Cope's syndrome - depression
Corsican Hellebore poisoning - depression
Cotard syndrome - suicidal thoughts
Crack addiction - depression
Crack withdrawal - depression
Creutzfeldt-Jakob Disease - depression
Crystal meth addiction - depression
Cushing's disease - Depression
Cycad nut poisoning - depression
Cyclical edema syndrome - depression
Cyclothymic disorder - depressive symptoms
Cystitis - depression
Decreased oxygen saturation - depression
Dementia
⦁ F⦁ ibromyalgia - depression
Dercum syndrome - mental depression
Dexedrine overdose - depression
Dexedrine withdrawal - depression
DiGeorge syndrome - depression
Disseminated lupus erythematosus
Dysomnia - Depression
Dysthymia - depression
Dysthymia/seasonal depression disorder, PND - empty feeling
Dystonia-Parkinsonism, Adult-Onset - depression
Ecstasy abuse - depressive symptoms
Ecstasy addiction - depression
Ecstasy withdrawal - depression
Ectopic ACTH Syndrome - depression
Elective mutism - depression
Encephalitis
Epstein Barr - depression
Familial dysautonomia - depression
Familial hypopituitarism - depression
Familial hypothyroidism - depression
Fatigue
Fecal incontinence - depression
Fetterbush poisoning - depression
Florida leucothoe poisoning - depression
Food Additive Adverse reaction -- chocolate - depression
Food Additive Adverse reaction -- sulphite - depression
Food Allergy -- beef - depression
Food Allergy -- buckwheat - depression
Food Allergy -- chicken meat - depression
Food Allergy -- duck meat - depression
Food Allergy -- goose meat - depression
Food Allergy -- lamb - depression
Food Allergy -- meat - depression
Food Allergy -- pork - depression
Food Allergy -- red meat - depression
Functioning pancreatic endocrine tumor - depression
Gaming addiction - depression
General somatic pain - Depression
Genetic Parkinson disease - depression
Genetics - There are various gene mutations that exist for nearly all vitamins, amino acids, etc that can cause deficiencies or toxicity of these items and lead to anxiety and/or depression.
Glucagonoma syndrome - depression
Graeck-Imerslund disease - Depression
Grand mal epilepsy - Depressed mood
Grand mal seizures - depressed mood
Grasbeck-Imerslund Disease - depression
Hashimoto's Thyroiditis - depression
Head injury
Hepatic encephalopathy syndrome - depression
Hepatitis
Herbal Agent overdose -- Golden Seal - depression
Hereditary hypothyroidism - Depression
Heroin dependence - depression
Honey intoxication - Depression
Human T-lymphotropic virus type 3 - depression
Huntington's chorea
Huntington's Disease - depression
Hydrocodone withdrawal - depression
Hyper IgE - depression
Hyperadrenalism - depression
Hyperadrenocorticalism
Hypercalcemia
Hyperostosis frontalis interna - depression
Hyperparathyroidism - depression
Hyperparathyroidism, primary - depression
Hypoadrenalism - depression
Hypoadrenocorticalism
Hypokalemia - mental depression
Hypoparathyroidism
Hypopituitarism
Hypothyroidism - depression
Idiopathic edema - depression
Idiopathic Parkinson's disease - depression
Infectious CFS - depression
Infectious mononucleosis
Influenza
Inhalant abuse - depression
Inhalant addiction - depression
Japanese andromeda poisoning - depression
Job syndrome - depression
Kartagener syndrome - depression
Kawasaki disease - depression
Lazarus complex - depression
Lead poisoning - depressive symptoms
Lenten rose poisoning - depression
Lidocaine toxicity - depression
Limbic encephalitis - depression
LSD addiction - depression
Lupus - depression
Lymphomatous thyroiditis - depression
Macrocytosis - depression
m******** addiction - depression
Marsh marigold poisoning - depression
Mc Leod neuroacanthocytosis syndrome - depression
Mediterranean myoclonic epilepsy - depression
Megaloblastic Anemia 1 - depression
Menopause - Depression
Metabolic Syndrome - depression
Metachromatic Leukodystrophy - depression
Methamphetamine withdrawal - depression
Mild Traumatic Brain Injury - Depression
Milk poisoning - Milk poisoning is a condition where the body is too alkaline and the blood contains too much calcium. It can be caused by drinking large quantities of milk or using too many alkaline antacid remedies. High vitamin D intake can make the condition worse. - depression
Milk-Alkali syndrome - depression
Mitochondrial Parkinson's disease - depression
Mountain andromeda poisoning - depression
Multi-infarct dementia
Multiple sclerosis
Myoclonus progressive epilepsy of Unverricht and Lundborg - suicide
Myofascial pain syndromes - Depression
Narcotic addiction - depression
Neurosyphilis - depression
Neurotoxicity syndromes - depression
Niemann-Pick disease, type D - depression
Non Classic Congenital Adrenal Hyperplasia - depression
Nymphomania - depression
Obesity hypoventilation syndrome - depression
Obstructive sleep apnea - depression
Opioid addiction - depression
Opium withdrawal - depression
Osteoarthritis - depression
Oxycontin addiction - depression
OxyContin withdrawal - depression
PANDAS - depression
Paraneoplastic limbic encephalitis - depression
Parkinson's disease - depression
Pediatric AIDS - depression
Pellagra - depression
Pernettya poisoning - depression
Phosphate diabetes - depression
Pick's disease
Pickwickian syndrome - depression
Pituitary tumors, adult - depression
Plant poisoning -- Acetylandromedol - depression
Plant poisoning -- Andromedotoxin - depression
Plant poisoning -- Grayanotoxin - depression
Plant poisoning -- Rhodotoxin - depression
Polycystic ovary syndrome - Depression
Polymyalgia rheumatica - depression
Porphyria - depression
Post-natal depression
Post-viral CFS - depression
Postpartum hypothyroidism - depression
Postpartum thyroiditis - depression
Pregnancy - baby blues
Premenstrual dysphoric disorder - Suicidal thoughts
Premenstrual syndrome - depression
Primary Fibromyalgia - depression
Primary hypothyroidism - Depression
Primary Parkinsonism - depression
Prion diseases - depression
Progressive External Opthhalmoplegia- depression
Progressive Supranuclear Palsy - depression
Psoriatic arthritis, juvenile form - depression
Rabies - mental depression
Red buckeye poisoning - depression
Refractory Celiac Disease - Depression
Riedel syndrome - depression
Sensory ataxic neuropathy, dysarthria, and ophthalmoparesis - depression
Sheep laurel poisoning - depression
Short Bowel Syndrome - depression
Sleep apnea - depression
Sleep Apnea Syndromes - depression
Sleep disorders - Depression
Sleepiness
Sleeping pill addiction - depression
Solvent abuse - depression
Solvent addiction - depression
Sopite syndrome - mental depression
Spastic paraplegia 4, autosomal dominant - depression
Spinocerebellar ataxia 27 - depression
Stachybotrys chartarum - depression
Staggerbush poisoning - depression
Steroid abuse - depression
Steroid withdrawal syndrome - depression
Stroke
Subarachnoid hemorrhage
Substance Withdrawal Syndrome - suicide
Systemic Lupus Erythematosus - depression
Teeth grinding - Depression
Temporal lobe contusion
Temporal lobe epilepsy
Thyroid disorders - depression
Thyroid hormone plasma membrane transport defect - depression
Toxoplasmosis
Tranquilizer addiction - depression
Tranquilizer withdrawal - suicidal thoughts
Traumatic Brain Injury - depression
Turner Syndrome - depression
Turner syndrome associated Celiac Disease - Depression
Ultram withdrawal - depression
Underactive Thymus - depression
Unverricht-Lundborg disease - depression
Uremic encephalopathy - depression
Vacinko syndrome - suicidal tendency
Van Bogaert's disease - depression
Van Bogaert-Scherer-Epstein Disease - depression
Variant Creutzfeldt-Jakob disease - Depression
Variegate porphyria - depression
Vascular malformations of the brain - depression
Velocardiofacial syndrome - depression
Vitiligo - depression
WAGR Syndrome - depression
Weinstein Kliman Scully syndrome - Depression
Westphal disease - Depression
Whiplash - depression
Wilson's Disease - depression
Wolfram's disease - Depression
Xanthomatosis cerebrotendinous - depression
Young Simpson syndrome - Depression
Zadik Barak Levin syndrome - Depression

Medications or substances causing Depressive symptoms
The following drugs, medications, substances or toxins are some of the possible causes of depression.
This list is incomplete and various other drugs or substances may cause your symptoms Always advise your doctor of any medications or treatments you are using, including prescription, over-the-counter, supplements, herbal or alternative treatments.

⦁ Accure
⦁ Aches-N-Pain
Acitretin
⦁ Activella
⦁ Adalat Oros
Advil
Agenerase
⦁ Agon SR
⦁ Agrylin
⦁ AK Beta
⦁ AL-R
Aldomet
⦁ Aldopren
⦁ Alesse
⦁ Aleve
⦁ Alferon N
⦁ Aller-Chlor
⦁ Alora Transdermal System
⦁ Alpha-Baclofen
⦁ Alphamethyl dopa
⦁ Alphapress
⦁ Alpidine
⦁ Alpraclonidine Hydrochloride
⦁ Alprax
Alprazolam
⦁ Ambien
⦁ Ameblin
⦁ Amen
⦁ Aminogluthethmide
Amlodipine
⦁ Amodopa
Amprenavir
Amylobarbitone
Anabolic Steroids
Anagrelide
⦁ Anapolon 50 tablets
⦁ Anaprox
⦁ Anaprox DS
Anastrozole
⦁ Androcur
⦁ Androderm Transdermal System
⦁ Androgel
Android
⦁ Anitrim
⦁ Anpec
⦁ Ansaid
⦁ Apo-Atenol
⦁ Apo-Carbamazepine
⦁ Apo-Chlordiazepoxide
⦁ Apo-Clorazepate
⦁ Apo-Diflunisal
⦁ Apo-Ibuprofen
⦁ Apo-Metronidazole
⦁ Apo-Naproxen
⦁ Apo-Sulfatrim
⦁ ApraClonidine tablets
⦁ Apresoline
⦁ Apri
⦁ Apro-Flurbiprofen
Aricept
Arimidex
⦁ Aromasin
⦁ Arthrotec
ASA
⦁ Aspirin and Codeine
⦁ Asprodeine
⦁ Atapryl
Atazanavir Sulfate
Atenolol
⦁ Atiquim
⦁ Ativan
⦁ Atretol
⦁ Atrofen
⦁ Aviane
⦁ Aygestin
⦁ Baclo
Baclofen
⦁ Baclohexal
⦁ Bactelan
⦁ Bactrim
⦁ Bactrim DS
⦁ Bactrim Pediatric
⦁ Batrizol
⦁ Bayer Select Pain Relief Formula
Beta blocker
⦁ Betaferon
⦁ Betagan
⦁ Betapace
⦁ Betapace AF
Betaxolol
⦁ Betaxolol Hydrochloride
⦁ Betaxon
⦁ Betimol
⦁ Betoptic
⦁ Betoptic S
⦁ Betoquin
Bicalutamide
⦁ Bicor
⦁ Biphasil
Bisoprolol
⦁ Blocadren
⦁ Brenda
⦁ Brevicon
⦁ Bromaline Elixir
⦁ Bromanate Elixir
⦁ Bromarest
⦁ Bromatapp
⦁ Brombay
⦁ Bromphen
Brompheniramine Maleate
⦁ BuSpar
⦁ BuSpar Dividose
Buspirone
Buspirone Hydrochloride
⦁ Butacortelone
Butobarbitone
⦁ Cabaser
Cabergoline
⦁ Camilla
⦁ Candyl
Carbamazepine
⦁ Carbatrol
⦁ Carbazep
⦁ Carbazina
⦁ Carbex
⦁ Carbrital
⦁ Cardinol
Cardura
Carteolol
⦁ Carteolol Hydrochloride
⦁ Cartrol
Carvedilol
⦁ Cataflam
⦁ Catapres tablets
⦁ Catapres-TTS-1 tablets
⦁ Catapres-TTS-2 tablets
⦁ Catapres-TTS-3 tablets
⦁ Catovit
⦁ CellCept
⦁ Cenestin
⦁ Centrax
⦁ Cerebyx
⦁ Children’s Advil
⦁ Children’s Motrin
⦁ Chlo-Amine
⦁ Chlor-Pro
⦁ Chlor-Trimeton
⦁ Chlor-Tripolon
Chlorate
Chlordiazepoxide
Chlorotrianisene
Chlorpheniramine Maleate
Chlorpromazine
Clemastine
⦁ Clemastine Fumarate
⦁ Climara
⦁ Climara Pro Transdermal System
⦁ Climen
⦁ Clinoril
Clobazam
⦁ Clofen
Clonazepam
⦁ Clonidine tablets
Clopidogrel
Clorazepate
Clorazepate Dipotassium
⦁ Cognex
⦁ CombiPatch
⦁ Combivir
⦁ Consupren
⦁ Corax
⦁ Corbeton
⦁ Cordilox
⦁ Coreg
⦁ Corgard
Corticosteroid
⦁ Coryphen Codeine
⦁ Cosopt
⦁ Cosudex
⦁ Cotrim
⦁ Cotrim DS
⦁ Cotrim Pediatric
⦁ Crestor
⦁ Crinone
⦁ Cryselle
⦁ Curretab
⦁ Cyclessa
Cycloserine
Cyclosporine
⦁ Cycrin
⦁ Cylert
⦁ Cyprone
⦁ Cyprostat
Cyproterone Acetate
⦁ Cystagon
Cysteamine
⦁ Cytadren
⦁ Dalmane
⦁ Dantrium
Dantrolene
⦁ Dantrolene Sodium
⦁ Daypro
⦁ Daypro ALTA
⦁ Demulen 1/35
⦁ Demulen 1/50
⦁ Depacon
⦁ Depakene
⦁ Depakote
⦁ Depakote ER
⦁ Depakote Sprinkle
⦁ Depo-Provera
⦁ Desogen
Desogestrel
⦁ Diamine T.D
⦁ Diane
⦁ Diastat
⦁ Diazemuls
Diazepam
⦁ Diazepam Intensol
⦁ Dibufen
Didanosine
Dienestrol
Diethylpropion
⦁ Diethylpropion Hydrochloride
Diethylstilbestrol
Dilantin
⦁ Dilantin Kapseals
⦁ Dimaphen Tablets
⦁ Dimetapp 4-hour Liqui-Gel Capsule
⦁ Dimetapp Extentabs
⦁ Dimetapp Tablet
⦁ Dolac Injectable
⦁ Dolac Oral
Dolobid
Donepezil
⦁ Dopar
⦁ Dostinex
Doxazosin
Dronabinol
⦁ Durabolin Injection
⦁ DV Cream
⦁ EC-Naprosyn
Ecstasy
⦁ Ectaprim
⦁ Ectaprim-F
Efavirenz
⦁ Eldec
⦁ Eldepryl
⦁ Eldisine
⦁ Elmiron
⦁ Empirin with Codeine
Emtricitabine
⦁ Emtriva
Enfuvirtide
Enoxacin
⦁ Enoxin
⦁ Enpresse
⦁ Enterobacticel
⦁ Epitol
Epivir
⦁ Epivir-HBV
⦁ Ergamisol
⦁ Errin
⦁ Esclim
Estazolam
⦁ Esteprim
⦁ Estinyl
⦁ Estrace
⦁ Estraderm
⦁ Estrasorb
⦁ Estratab
⦁ Estratest
⦁ Estratest HS
⦁ Estring
⦁ Estrostep 21
⦁ Estrostep Fe
⦁ Ethyloestrenol
Etodolac
Etonogestrel
⦁ Eulexin
Evista
⦁ Excedrin
⦁ Excedrin Extra Strength
⦁ Exelon
Exemestane
⦁ Fareston
Felbamate
⦁ Felbatol
⦁ Feldene
⦁ Feldene Gel
Felodipine
⦁ Felodur ER
⦁ Femhrt
⦁ Femoden
⦁ FemPatch
⦁ Femring
⦁ Fensaid
⦁ Flagenase
⦁ Flagyl
⦁ Flagyl ER
Flecainide
⦁ Flecatab
⦁ Flexen
⦁ Flogen
⦁ Flomax
⦁ Flumadine
Fluoxymesterone
⦁ Fluphenazine Hydrochloride
Flurazepam
⦁ Flurbiprofen Sodium
Flutamide
⦁ Forteo
⦁ Fosfesterol
Fosfestrol
Frisium
⦁ Froben
⦁ Froben-SR
⦁ Fuxen
⦁ Fuzeon
⦁ Gabitril
Galantamine
⦁ Gelpirin
⦁ Gen-Xene
⦁ Genatap Elixir
⦁ Gengraf
⦁ Genpril
⦁ Goody’s Headache Powders
Goserelin
Guanabenz
⦁ Gynodiol
Hallucinogen
⦁ Halotestin
⦁ Haltran
Herceptin
⦁ Hicin
⦁ Honvan
⦁ Honvol
Hydralazine
⦁ Hytrin
⦁ IBU
⦁ Ibuprin
Ibuprofen
⦁ Ibuprohm
⦁ Implanon
⦁ Imukin
Inderal
⦁ Inderide
⦁ Inderide LA
⦁ Indo-Spray
⦁ Indochron E-R
Indocin
⦁ Indocin SR
⦁ Indomed
Indomethacin
⦁ Indomethicin
⦁ Ineral LA
⦁ Inerferon Alfa
⦁ Infants’ Motrin
⦁ Infergen
⦁ Innofem
⦁ Innopran XL
⦁ Insensye
Interferon
Intron A
⦁ Iopidine
⦁ Isobac
⦁ Isocover
⦁ Isohexal
Isoniazid
⦁ Isoptin
Isotretinoin
⦁ Isotrex
⦁ IsotrexGel
⦁ Isox
Itraconazole
⦁ Itranax
⦁ Jolivette
⦁ Juliet
⦁ Kalma
⦁ Kariva
⦁ Kedvil
⦁ Kelfiprim
⦁ Keppra
⦁ Kerlone
Ketorolac - injection and tablets
Ketorolac Tromethamine
⦁ Kinson
Klonopin
⦁ Kloromin
⦁ L-Deprenyl
L-dopa
Labetalol
Lamictal
⦁ Lamictal CD
Lamivudine
Lamotrigine
⦁ Lessina
⦁ Leucoprorelin
Levamisole
⦁ Levatol
Levetiracetam
⦁ Levlen
⦁ Levlite
Levobunolol
Levodopa
Levonorgestrel
⦁ Levora
⦁ Libritabs
Librium
Lioresal
⦁ Lipex
⦁ Lo/Ovral
Lodine
⦁ Lodine Retard
⦁ Lodine XL
⦁ Lodosyn
⦁ Loestrin 1/20
⦁ Loestrin 21 1.5/30
⦁ Loestrin 21 1/20
⦁ Loestrin Fe 1.5/30
⦁ Loestrin Fe 1/20
⦁ Loette
⦁ Logynon
⦁ Lonavar tablets
⦁ Loniten tablets
⦁ Lopressor
⦁ Lorazepam Intensol
⦁ Lotronex
⦁ Low-Ogestrel
⦁ Lucrin Depot Injection
⦁ Lucrin Injection
⦁ Madopar
⦁ Marinol
⦁ Marvelon
⦁ Mazepine
Mazindol
⦁ Meclomen
⦁ Medilium
⦁ Medipren
Medroxyprogesterone Acetate
⦁ Mellaril
⦁ Mellaril-S
Meloxicam
⦁ Menadol
⦁ Menest
⦁ Meridia
⦁ Mesantoin
⦁ Mesoridazine Besylate
Metaxalone
Methyldopa
Methyltestosterone
Metipranolol
Metoprolol
⦁ Metoxiprim
⦁ Metric 21
⦁ Metro I.V
⦁ MetroCream
⦁ MetroGel
⦁ MetroLotion
Metronidazole
⦁ Micorgynon
⦁ Microgestin Fe 1.5/30
⦁ Microgestin Fe 1/20
⦁ Microlevlen
⦁ Microlut
⦁ Microval
⦁ Midol
⦁ Midol-IB
⦁ Midoride
⦁ Milezzol
Minipress
⦁ Minipress XL
⦁ Minizide
⦁ Minoxidil tablets
⦁ Minulet
⦁ Mircette
⦁ Mirena
⦁ Mitran
⦁ Mixogen tablets
Mobic
Modafinil
⦁ Modavigil
⦁ Modicon
⦁ Monofeme
⦁ Motrin
Motrin IB
⦁ Mycophenolate
⦁ Myphetapp
Nabumetone
Nafarelin
⦁ Nalfon
⦁ Naprelan
⦁ Naprodil
Naprosyn
Naproxen
Naproxen Sodium
⦁ Nasahist B
⦁ Navelbine
⦁ Naxen
⦁ Naxil
⦁ ND-Stat
⦁ Necon 1/35
⦁ Necon 1/50
⦁ Necon 10/11
⦁ Necon 7/7/7
⦁ Neocon 0.5/35
Neoral
⦁ Neotigason
⦁ Neugeron
⦁ Neurontin
⦁ Neurosine
⦁ Neurotonin
⦁ Nicorette
⦁ Nicorette DS
⦁ Nicorette Plus
Nicotine
⦁ Nicotine chewing gum
⦁ Nicotinell-TTS
⦁ Nicotrol
⦁ Nifecard
Nifedipine
⦁ Nifehexal
Nimodipine
⦁ Nimotop
⦁ Nobesine
Nolvadex
⦁ Nor-Q.D
⦁ Nora-BE
⦁ Nordette
⦁ Norflohexal
Norfloxacin
⦁ Norinyl 1+35
⦁ Norinyl 1+50
⦁ Noritate
⦁ Normodyne
⦁ Noroxin
⦁ Norplant II
⦁ Nortrel 0.5/35
⦁ Nortrel 1/35
⦁ Norvas
Norvasc
⦁ Novo-Atenol
⦁ Novo-Carbamaz
Novo-Clopate
⦁ Novo-Diflunidal
⦁ Novo-Flurprofen
⦁ Novo-Naproxen
⦁ Novo-Nidazol
⦁ Novo-Poxide
⦁ Novo-Profen
⦁ Novo-Trimel
⦁ Noxitem
⦁ Nu-Atenol
⦁ Nu-Carbamazepine
⦁ Nu-Cotrimox
⦁ Nu-Diflunisal
⦁ Nu-Flurprofen
⦁ Nu-Ibuprofen
⦁ Nu-Naproxen
⦁ Nuprin
⦁ NuvaRing
⦁ Nyefax
⦁ Ocupress
⦁ Ogen
⦁ Ogestrel
⦁ Oncovin
⦁ Opioid intoxication
⦁ Optipranolol
⦁ Orabolin Tablets
Oral Contraceptive
⦁ Oraminic II
⦁ Oratane
⦁ Oreton Methyl
Orlistat
⦁ Ortho Dienestrol
⦁ Ortho Tri-Cyclen
⦁ Ortho Tri-Cyclen Lo
⦁ Ortho-Cept
⦁ Ortho-Cyclen
⦁ Ortho-Est
⦁ Ortho-Micornor
⦁ Ortho-Norvum 1/50
⦁ Ortho-Novum 1/35
⦁ Ortho-Novum 10/11
⦁ Ortho-Novum 7/7/7
⦁ Ortho-Prefest
⦁ OrthoEvra
⦁ Orudis KT
⦁ Ospolot
⦁ Otrozol
⦁ Ovcon-35
⦁ Ovcon-50
⦁ Ovral
⦁ Ovrette
Oxprenolol
Oxymetholone
⦁ Pactens
⦁ Pamprin IB
⦁ Parstelin
⦁ Paxam
⦁ Paxipam
⦁ Pediacare Fever
⦁ PediaProfen
Peganone
⦁ PegIntron
⦁ PemADD
Pemoline
⦁ Pentobarbitone
Pentosan Polysulfate Sodium
Pericyazine
Perindopril
⦁ Permitil
⦁ Pheneizine
⦁ Phenetron
⦁ Phenytek
Phenytoin
Pindolol
⦁ Pirox
Piroxicam
⦁ Plan B
⦁ Plavix
⦁ Plendil ER
⦁ PMS-Baclofen
⦁ PMS-Carbamazepine
⦁ PMS-Clonazepam
⦁ Ponstel
⦁ Portia
Prazosin
Premarin
⦁ Premphase
⦁ Prempro
⦁ Preven
⦁ Pro-Trin
⦁ Proartinal
Procainamide
⦁ Procan-SR
⦁ Procanbid
⦁ Procur
⦁ Progestasert
⦁ Prograf
⦁ Prolintane
⦁ Prolixin
⦁ Prometrium
⦁ Promine
⦁ Pronaxil
⦁ Pronestyl
⦁ Pronestyl-SR
Propranolol
⦁ ProSom
⦁ ProStep
⦁ Protostat
Provera
⦁ Provigil
⦁ Pyralin
⦁ Quadrax
Raloxifene
⦁ Ralozam
Ramipril
Ranitidine
⦁ Rebetron
⦁ Relafen
⦁ Reminyl
⦁ Reposans-10
Reserpine
⦁ Reyataz
⦁ Rimantidine
Rivastigmine
Rivotril
⦁ Roaccutane
Roferon A
⦁ Roubac
⦁ Roxin
⦁ Rufen
⦁ Salazopyrin
⦁ Salazopyrin EN
⦁ Saleto-200
⦁ Saleto-400
⦁ Sandimmun Neoral
Sandimmune
⦁ Sanorex
Selegiline
⦁ Septra
⦁ Septra DS
⦁ Sequilar
⦁ Serax
⦁ Serenace
⦁ Serentil
Sibutramine
Simvastatin
Sinemet
⦁ Sinemet CR
⦁ Sinusol-B
⦁ Skelaxin
⦁ Solareze-Gel
⦁ Solium
⦁ Solvin
⦁ Sonazine
⦁ Soneryl
⦁ Soriatane
Sporanox
⦁ Sprintec
⦁ Stalazine
Stavudine
⦁ Stilphostrol
⦁ Striant
⦁ Sulfamethoprim
⦁ Sulfamethoprim DS
Sulfasalazine
⦁ Sulfatrim
⦁ Sulfatrim DS
⦁ Sulfoxaprim
⦁ Sulfoxaprim DS
Sulphasalazine
⦁ Sulthiame
⦁ Supradol
Sustiva
⦁ Synarel Nasal Spray
⦁ Syntest DS
⦁ Syntest HS
⦁ Syraprim
⦁ Tabalon
⦁ TACE
Tacrine
Tacrolimus
⦁ Tambocor
⦁ Tamine
Tamoxifen Citrate
Tamsulosin
⦁ Taro-Atenol
⦁ Tavegyl
⦁ Tavist
⦁ Tegretol
⦁ Tegretol-XR
⦁ Telachlor
⦁ Teldrin
⦁ Temodar
Temozolomide
⦁ Tenormin
⦁ Tenuate
⦁ Tenuate Dospan
⦁ Tepanil
⦁ Terazosin hydrochloride
⦁ Teril
Teriparatide
⦁ Testin
⦁ Testoderm Transdermal System
⦁ Testomet
⦁ Testopel
Testosterone
⦁ Testred
Tetrabenazine
Thiethylperazine
⦁ Thioridazine Hydrochloride
⦁ Thorazine
⦁ Thorazine Spansules
Tiagabine
Timolol
⦁ Timoptic
⦁ Timoptic-XE
Tizanidine
⦁ TMP-SMZ
⦁ Tolectin
⦁ Topamax
⦁ Topamax Sprinkle
Topiramate
⦁ Toprol-XL
⦁ Torecan
Toremifene
⦁ Trandate
Tranxene
⦁ Tranxene T-Tab
⦁ Tranxene-SD
Tranylcypromine
⦁ Trasicor
Trastuzumab
⦁ Travist
⦁ Trendar
⦁ Tri-Levlen
⦁ Tri-Minulet
⦁ Tri-Norinyl
Triamterene
⦁ Trifeme
⦁ Trifluoperazine Hydrochloride
⦁ Trimesuxol
⦁ Trimetoger
⦁ Trimetox
⦁ Trimzol
⦁ Trioden
⦁ Triphasil
⦁ Triquilar
⦁ Trisulfa
⦁ Trisulfa-S
⦁ Trisulfam
⦁ Trivora
⦁ Trizivir
⦁ Uni-Pro
⦁ Uroplus DS
⦁ Uroplus SS
⦁ Vagifem
Valium
Valproic Acid
⦁ Valrelease
⦁ Vatrix-S
⦁ Velbe
⦁ Velsay
⦁ Veltane
⦁ Veracaps
⦁ Verahexal
Verapamil
⦁ Vertisal
⦁ Vesanoid
⦁ Vicks DayQuil Allergy Relief 4 Hour Tablet
Videx
⦁ Videx EC
Vinblastine
Vinca alkaloids
Vincristine
⦁ Virilon
⦁ Visken
⦁ Vivelle
⦁ Vivelle-Dot
Voltaren
⦁ Voltaren Emugel
⦁ Voltaren Rapid
⦁ Voltaren-XR
⦁ Withdrawal from amphetamine
⦁ Withdrawal from cocaine
⦁ Withdrawal from phencyclidine
⦁ Wytensin
Xanax
⦁ Xenical
⦁ Yasmin
⦁ Zanaflex
⦁ Zantac
⦁ Zantac 75
⦁ Zantac EFFERdose
⦁ Zebeta
Zerit
⦁ Zerit XR
⦁ Ziac
⦁ Zoladex Depot Injection
Zolpidem
⦁ Zonegran
Zonisamide
⦁ Zovia 1/35E
⦁ Zovia 1/50E


#19 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 12 February 2018 - 05:18 PM

Precription Meds

Cautions and Warnings – Stress starts a series of actions that include the release of adrenaline and other neural stimulants. This causes an increase in respiration, pulse, and blood pressure as well as general metabolism. Any medicine which will help alleviate anxiety will have the effect of lowering the pulse, blood pressure and respiration. This decrease helps explain the frequent weight gains when taking anxiety medicine. The taking of more than one anxiety medicine at a time or too much of an anxiety medicine can pose a risk of low blood pressure and pulse. Not only is it essential that these medications be discussed with your physician but they should still be approached with care. When prescribed an anxiety medicine you should consider starting with a partial dose and gradually working your dose upward as you feel comfortable with any side effects. Nearly all medicines can have side effects. The risk of a serious side effect may be very low BUT you never know, you could be the one. By starting with a low dose it will give you a chance to determine what side effects or allergic reaction will occur before a larger dose is attempted.

Cimetidine – (Tagamet) Increases the absorption of a great many medicines. Please check your meds to see if they can be taken with Tagamet.

Liver and kidney damage is frequent with use of most of these medicines and patients should insist upon a liver function blood test (LFT) and to have their kidney functions checked at least annually. The liver is a detoxification organ for our body and processes most of the medicines we take.

http://www.cymbaltaw...xiety/?hl=helps
Contains list of prescription and OTC antidepressants and there effects and cautions.
Also contains lists of anxiety medications and research on treatment resistant anxiety and depression.

http://www.cymbaltaw...mend#entry68953
Alternate Treatments for Anxiety
-----------------------------------------------------------------------------------------------------------
Clonidine

Clonidine (Catapres, Kapvay, Nexiclon, Clophelin) is a classic blood pressure medicine BUT it is very effective on anxiety. It is an alpha adrenergic antagonist which means it stimulates the alpha adrenaline synapses located in the frontal lobes of the brain. When these synapses are stimulated by the clonidine the brain thinks that it is due to adrenaline and it tells the adrenal gland to produce less adrenaline. It is a little slow to kick in, about an hour and a half. It has a 12 hour half life. Most drs prescribe 0.1 mg twice a day. One to be taken about an hour before bedtime and the other in the morning. Because it decreases adrenaline it has a strong calming effect which helps a person get to sleep and stay a sleep. It is not unusual for people to have a little drowsiness from clonidine until they get use to it (1 or 2 weeks). It does NOT work faster sublingual (under the tongue) like benzos. These have no withdrawal but your blood pressure may spike for a couple weeks if you cold turkey. Due to the lowering of blood pressure and sleepiness it is common for the patient to start with ½ tablet at bedtime. Once the patient adjusts to the medicine they begin a ½ tablet in the morning. As sleepiness and blood pressure stabilize they are slowly worked up to the 2 tablets (0.1 mg each) a day. They also make a slow release patch for clonidine which avoids the peaks up and down in blood pressure and sleepiness associated with taking clonidine every 12 hours.

Begins working 60 to 90 minutes
Peak levels – 3 to 5 hrs
Half Life – 12 - 16 hrs

There are too many research articles on clonidine's anxiolytic properties to list here.

FH -The clonidine I have upped a half tablet and has helped take the edge off

FH - I started clonidine but it was a relief to me NOT to be able to feel my heart pound through my chest. As long as your bp is OK you shouldn't have a problem.
That is why the slow start up. This gives your heart a chance to adapt to the new med. I did the same slow start up and my bp stayed within normal range. Just keep monitoring your bp and you should be OK.

FN - clonidine worked wonders for me

http://www.cymbaltaw...elps#entry71818
Cymbalta, clonidine and hydroxyzine and alcoholism information
---------------------------------------------------------------------------------------------------------
Hydroxyzine, (Vistaril, Atarax) - is an H(1)R antagonist, is very effective against anxiety in most people but some get no help from it at all. It is not addictive nor does it have withdrawal but it also can lower blood pressure some but that usually goes away with time. This medicine should be started slowly to give your body a chance to adjust to the blood pressure effect. Normal dose is 25 mg four times a day but can go as high as 400mg/day.

Begins working in 30 minutes or less
Peak levels - 2 hrs
Half Life – 15 to 20 hrs

https://www.ncbi.nlm...pubmed/21154375
https://www.ncbi.nlm...pubmed/12444816
https://www.ncbi.nlm.../pubmed/7875114
Anxiolytic, Sleepiness begins to subside after 1st week and no withdrawal.
https://www.ncbi.nlm.../pubmed/9809861
https://www.ncbi.nlm.../pubmed/2430410
Do not take with cimetidine as it increases hydroxyzine levels in the blood.
https://www.ncbi.nlm...les/PMC1512309/
Effective, sleepiness slowly decreases.

http://www.cymbaltaw...elps#entry71818
Cymbalta, clonidine and hydroxyzine and alcoholism information
-----------------------------------------------------------------------------------------------------------
Atenolol is a beta 1 adrenergic receptor antagonist, also known as a beta blocker. It does not pass through the blood brain barrier which limits its side effects compared to other beta blockers. It has been linked to a higher risk of type 2 diabetes. It may cause drowsiness and lower blood pressure. Typical dosage around 25 mg four times/day. Dosage should be slowly increased.

Begins working in 30 minutes to an hour
Peak levels – 2 – 4 hrs
Half Life – 6 - 8 hrs

https://www.ncbi.nlm.../pubmed/3549876
Effective but blood pressure drops.
https://www.ncbi.nlm.../pubmed/4054193
Side Effects
https://www.ncbi.nlm.../pubmed/1777372
https://www.ncbi.nlm.../pubmed/4047384
Not effective
https://www.ncbi.nlm.../pubmed/2196620
30% found it effective.
--------------------------------------------------------------------------------------------------------
Buspirone (Buspar) is a seratonin 5-HT1A receptor partial agonist and a dopamine antagonist at the receptors. It functions as a weak anti-anxiety medication similar to diazepam in strength (a weak benzo). No withdrawal or tolerance issues. Dosage should be kept low if taking a ssri and/or snri or St. John's Wort as it may cause seratonin syndrome. DO NOT take with grapefruit or grapefruit juice. May lower blood pressure. Typical dosage is 10 to 20 mg three times per day.

Begins working 3 to 7 days after begin dosing
Peak levels - 1 hrs
Half Life – 2 - 4 hrs

https://www.ncbi.nlm...les/PMC3608295/
With Sesamol
https://www.ncbi.nlm...pubmed/22998742
Buspar (15mg) and Melatonin (3 mg) yielded the best anti-depressant effect of any combination concentration tested. 
https://www.ncbi.nlm...pubmed/25156283
Buspar and melatonin in combination is anxiolytic.
------------------------------------------------------------------------------------------------------------
Benzodiazipines and Z-Drugs


Usage data

https://www.ncbi.nlm...pubmed/25517224
In 2008, approximately 5.2% of US adults aged 18 to 80 years used benzodiazepines. The percentage who used benzodiazepines increased with age from 2.6% (18-35 years) to 5.4% (36-50 years) to 7.4% (51-64 years) to 8.7% (65-80 years). Benzodiazepine use was nearly twice as prevalent in women as men. The proportion of benzodiazepine use that was long term (> 120 days) increased with age from 14.7% (18-35 years) to 31.4% (65-80 years), while the proportion that received a benzodiazepine prescription from a psychiatrist decreased with age from 15.0% (18-35 years) to 5.7% (65-80 years). In all age groups, roughly one-quarter of individuals receiving benzodiazepine involved long-acting benzodiazepine use.

https://www.ncbi.nlm...pubmed/25613443
Estimates of the number of benzodiazepine-dependent persons in Germany range from 128 000 to 1.6 million.

Use benzodiazepines for only 4 weeks or less to minimize risk of addiction.

https://www.ncbi.nlm...les/PMC4318457/
Dependency problems with benzodiazepines have been a familiar phenomenon for
about 40 years for this reason, pharmaceutical companies and the German Federal Institute for Drugs and Medical Devices (BfArM) have restricted the standard period of use to 2–4 weeks since the 1980s. According to the current law on prescriptions of medical drugs, hypnotics and tranquillizers can be prescribed for period can be extended if sound reasons exist.

http://www.smw.ch/co...smw-2011-13277/
Within weeks of chronic use, tolerance to the pharmacological effects can develop and withdrawal becomes apparent once the drug is no longer available, which are both conditions indicative of benzodiazepine dependence.
Withdrawal symptoms are observed following discontinuation or abrupt reduction of BDZs dosage, even after a relatively short treatment period (three to four weeks). Such physiological symptoms are the main signs of physical dependence. The most frequent are insomnia, gastric problems, tremors, agitation, fearfulness and muscle spasms. Less frequently observed are irritability, sweating, depersonalisation, hypersensitivity to stimuli, depression, suicidal behaviour, psychosis, seizures and delirium tremens. Over-rapid withdrawal from BDZs also increases the severity of the symptoms. Slow and gradual reduction of dosage customised to the individual accompanied by psychological support are the most effective way of managing withdrawal. Complete withdrawal can require four weeks to several years.

National Health Committee. Guidelines for assessing and treating anxiety disorders. Wellington (New Zealand): National Health Committee; 1998.
Recommend restricting their use to no more than 3–4 weeks

https://www.ncbi.nlm...pubmed/17535048
Recommend restricting their use to no more than 3–4 weeks

https://www.ncbi.nlm...t1-ndt-11-1885/
Review of research listing proper use of benzos.
In general, compounds with higher potency and a shorter half-life are associated with a greater likelihood of developing withdrawal syndromes and dependence.
A significant risk of dependence is recognized in some patients receiving treatment for longer than one month, and health professionals should be aware of this when considering the relative treatment benefits and risks.

https://www.ncbi.nlm...pubmed/16639148
Benzodiazepine dependence could be prevented by adherence to recommendations for short-term prescribing (2-4 weeks only when possible).

Clinical Guideline 22 (amended). Anxiety: management of anxiety (panic disorder, with or without agoraphobia, and generalised anxiety disorder) in adults in primary, secondary and community care" (PDF). National Institute for Health and Clinical Excellence. 2007. pp. 23–25. Retrieved 2009-08-08.
According to National Institute for Health and Clinical Excellence (NICE), benzodiazepines can be used in the immediate management of GAD, if necessary. However, they should not usually be given for longer than 2–4 weeks. The only medications NICE recommends for the longer term management of GAD are antidepressants.

McIntosh A, Cohen A, Turnbull N, et al. (2004). "Clinical guidelines and evidence review for panic disorder and generalised anxiety disorder" (PDF). National Collaborating Centre for Primary Care. Retrieved 2009-06-16.
Barbui C, Cipriani A (2009). "Proposal for the inclusion in the WHO Model List of Essential Medicines of a selective serotonin-reuptake inhibitor for Generalised Anxiety Disorder" (PDF). WHO Collaborating Centre for Research and Training in Mental Health. Retrieved 2009-06-23.
Based on the findings of placebo-controlled studies, they do not recommend use of benzodiazepines beyond two to four weeks, as tolerance and physical dependence develop rapidly, with withdrawal symptoms including rebound anxiety occurring after six weeks or more of use.

https://www.ncbi.nlm...pubmed/25613443
Benzodiazepines are generally highly effective when first given, but they should generally be given only for strict indications and for a limited time. If these drugs still need to be given beyond the short term, timely referral to a specialist is indicated, and possibly also contact with the addiction aid system.

http://www.rcpsych.a...diazepines.aspx
Royal College of Psychiatrists
How long should I take a benzodiazepine for?
Up to 4 weeks - no longer. This should really be just to give other (often psychological) treatments a chance to work.

Limited effectiveness/Long-term use and Addiction
http://www.ncbi.nlm....pubmed/16933543
The Canadian Psychiatric Association (CPA) recommends benzodiazepines alprazolam, bromazepam, lorazepam, and diazepam only as a second-line choice, if the treatment with two different antidepressants was unsuccessful. Although they are second-line agents, benzodiazepines can be used for a limited time to relieve severe anxiety and agitation. CPA guidelines note that after 4–6 weeks the effect of benzodiazepines may decrease to the level of placebo, and that benzodiazepines are less effective than antidepressants in alleviating ruminative worry, the core symptom of GAD. However, in some cases, a prolonged treatment with benzodiazepines as the add-on to an antidepressant may be justified.

https://www.ncbi.nlm...pubmed/16639148
Tolerance to anti-anxiety effects develops more slowly with little evidence of continued effectiveness beyond four to six months of continued use.

Curran, H. V.; Collins, R.; Fletcher, S.; Kee, S. C. Y.; Woods, B.; Iliffe, S. (2003-10-01). "Older adults and withdrawal from benzodiazepine hypnotics in general practice: effects on cognitive function, sleep, mood and quality of life". Psychological Medicine 33 (7): 1223–1237. doi:10.1017/s0033291703008213. ISSN 0033-2917. PMID 14580077.
"Holbrook AM. %282004%29. Treating insomnia. - PubMed - NCBI". www.ncbi.nlm.nih.gov. PMID 25282004. Retrieved 2015-12-10.
Poyares, Dalva; Guilleminault, Christian; Ohayon, Maurice M.; Tufik, Sergio (2004-06-01). "Chronic benzodiazepine usage and withdrawal in insomnia patients". Journal of Psychiatric Research 38 (3): 327–334. doi:10.1016/j.jpsychires.2003.10.003. ISSN 0022-3956. PMID 15003439.
Friedman MJ (1998). "Pharmacotherapy for posttraumatic stress disorder: a status report". Clinical Neurosciences Supplement 52: S115–S121.
Heather N, Bowie A, Ashton H, McAvoy B, Spencer I, Brodie J, Giddings D (2004). "Randomised controlled trial of two brief interventions against long-term benzodiazepine use: outcome of intervention". Addiction Research and Theory 12 (2): 141–154. doi:10.1080/1606635310001634528.
Bandelow, Borwin; Zohar, Joseph; Hollander, Eric; Kasper, Siegfried; Möller, Hans-Jürgen; Zohar, Joseph; Hollander, Eric; Kasper, Siegfried (2008-01-01). "World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for the pharmacological treatment of anxiety, obsessive-compulsive and post-traumatic stress disorders HYPERLINK

"http://www.ncbi.nlm....49648"HYPERLINKhttp://www.ncbi.nlm....ubmed/18949648" The World Journal of Biological Psychiatry 9 (4): 248–312. doi:10.1080/15622970802465807. ISSN 1562-2975. PMID 18949648.
Ashton, Heather (2005-05-01). "The diagnosis and management of benzodiazepine dependence". Current Opinion in Psychiatry 18 (3): 249–255. doi:10.1097/01.yco.0000165594.60434.84. ISSN 0951-7367. PMID 16639148.
Morin, Charles M.; Bélanger, Lynda; Bastien, Célyne; Vallières, Annie (2005-01-01). "Long-term outcome after discontinuation of benzodiazepines for insomnia: a survival analysis of relapse". Behaviour Research and Therapy 43 (1): 1–14. doi:10.1016/j.brat.2003.12.002. ISSN 0005-7967. PMID 15531349.
Michelini S, Cassano GB, Frare F, et al. (2016). "Long-term use of benzodiazepines: tolerance, dependence and clinical problems in anxiety and mood disorders.". Pharmacopsychiatry 29: 127–134
http://www.ncbi.nlm....pubmed/24434093
Several studies (listed above) have confirmed that long-term benzodiazepines are not significantly different from placebo for sleep or anxiety. This may explain why patients commonly increase doses over time and many eventually take more than one type of benzodiazepine after the first loses effectiveness.

https://www.ncbi.nlm...pubmed/15078112
Discontinuation of benzodiazepines or abrupt reduction of the dose, even after a relatively short course of treatment (three to four weeks), may result in two groups of symptoms—rebound and withdrawal. Rebound symptoms are the return of the symptoms for which the patient was treated but worse than before. Withdrawal symptoms are the new symptoms that occur when the benzodiazepine is stopped. They are the main sign of physical dependence.

https://www.ncbi.nlm...pubmed/26164054
While benzodizapines may have short-term benefits for anxiety, sleep and agitation in some patients, long-term (i.e., greater than 2–4 weeks) use can result in a worsening of the very symptoms the medications are meant to treat.

https://www.ncbi.nlm...pubmed/26545257
The relative proportion of long-term BZD users in adult BZD users ranged from 6% to 76% (mean 24%) The estimates were higher in studies only on the elderly (47%). Long-term use involved typically steady treatment with low BZD doses. However, in elderly patients long-term BZD use and exceeding recommended doses was relatively common. Several characteristics associated with long-term use were found.

https://www.ncbi.nlm.../pubmed/2222129
Patients who were able to remain free of benzodiazepines for at least 5 weeks obtained lower levels of anxiety than before benzodiazepine discontinuation.

Part 2
Effects of long-term use.
Alzheimer's Disease
https://www.ncbi.nlm...pubmed/26011780
During the 4-year follow-up, we found that 45% of individuals with Alzheimer's Disease (AD) and 38% of individuals without AD used BZDRs. The prevalence of long-term (≥ 180 days) BZDR use was more common among individuals with AD (30%) than individuals without AD (26%). The high prevalence of long-term BZDR use among individuals with AD is especially a cause for concern because long-term use may further impair cognition and may be associated with serious adverse events.

https://www.ncbi.nlm...pubmed/25208536
No association for Alzheimer's disease was found for a cumulative dose <91 prescribed daily doses. The strength of association increased with exposure density 1.32 for 91-180 prescribed daily doses and 1.84 for >180 prescribed daily doses). Benzodiazepine use is associated with an increased risk of Alzheimer's disease. The stronger association observed for long term exposures reinforces the suspicion of a possible direct association, even if benzodiazepine use might also be an early marker of a condition associated with an increased risk of dementia. Unwarranted long term use of these drugs should be considered as a public health concern.

https://www.ncbi.nlm...pubmed/25491057
Taking benzodiazepine is associated with an increased risk of Alzheimer disease

Cancer Risk
https://www.ncbi.nlm...pubmed/25674736
Clonazepam was associated with a higher risk for cancers. Moreover, specific cancer risk among BZDs use was observed significantly increased 98% for brain, 25% for colorectal, and 10% for lung, as compared with non-BZDs use. Diazepam, chlordiazepoxide, medazepam, nitrazepam, and oxazepam are safe among BZDs use for cancer risk.

https://www.ncbi.nlm...pubmed/24314718
In this population-based study, we found a significant increase in the risk of benign brain tumor development in a cohort of long-term (>2 months) BZD users.

https://www.ncbi.nlm...pubmed/23043261
BZRD use was not associated with an overall increase in cancer risk.

Dementia
https://www.ncbi.nlm...pubmed/25691075
Out of the ten studies retrieved, nine reported an increased risk of dementia in benzodiazepine users. The risk increased with cumulative dose and treatment duration and when long-acting molecules were used. Even if the causal nature of this association remains unproved, the reviewed material provides arguments for evoking a causal link. Further research would be necessary to elucidate the mechanism of this effect, if any, to evaluate the risk of exposure in younger population and the influence of risk factors such as depression. In any case, the body of evidence seems sufficient for avoiding prescriptions or renewals that are not fully justified and indiscriminate long-term use.

https://www.ncbi.nlm...pubmed/26016483
The risk of dementia increased by 22% for every additional 20 defined daily dose per year. Long-term benzodiazepine users have an increased risk of dementia compared with never users.

https://www.ncbi.nlm...les/PMC4737849/
The risk of dementia is slightly higher in people with minimal exposure to benzodiazepines but not with the highest level of exposure. These results do not support a causal association between benzodiazepine use and dementia.

https://www.ncbi.nlm...les/PMC3460255/
In this prospective population based study, new use of benzodiazepines was associated with increased risk of dementia. The result was robust in pooled analyses across cohorts of new users of benzodiazepines throughout the study and in a complementary case-control study.

Memory/Cognative Function
https://www.ncbi.nlm...pubmed/21494764
In the course of the 10 year-follow-up, 3.9% of subjects were defined as occasional users of benzodiazepine and 7.5% as long-term users. The analysis revealed a significant alteration of long-term memory in women whereas there was no significant association in men.

https://www.ncbi.nlm...pubmed/22705064
Chronic use of benzodiazepine was significantly associated with a lower latent cognitive level, but no association was found between chronic use and an acceleration of cognitive decline, neither on the latent cognitive process, nor on specific neuropsychological tests. Our results suggest that chronic benzodiazepine use is associated with poorer cognitive performance but not with accelerated cognitive decline with age.

https://www.ncbi.nlm.../pubmed/7639085
This study confirmed earlier observations of neuropsychological deficits in long-term benzodiazepine-using patients and demonstrated that these changes (decrease in general intelligence and of nonverbal memory) are at least partly reversible (within a year) by discontinuing drug intake.

Sleep
https://www.ncbi.nlm...pubmed/23692988
Our findings do not support long-term effectiveness of BZDs; long-term users slept more poorly than nonusers and were even more outspoken in users of long-acting BZDs.

Tasman A; Kay J; Lieberman JA, eds. (2008). Psychiatry (3rd ed.). Chichester, England: John Wiley & Sons. pp. 1186–1200, 2603–2615. ISBN 978-0470065716.
Disrupting REM sleep by inhibiting deep stage sleep

https://www.ncbi.nlm...pubmed/20963787
Long-term benzodiazepine users were more likely to report poor sleep quality.

https://www.ncbi.nlm...pubmed/26547856
Melatonin ineffective in helping sleep during benzo withdrawal.

https://www.ncbi.nlm...pubmed/22704915
Benzodiazepines may be efficient in reducing symptoms in the short term, but evidence from this long temporal follow-up study indicates limited positive influences in the long term.

https://www.ncbi.nlm...pubmed/25145751
Sleep quality in chronic BZD/Z users significantly decreased over 1 year and was significantly worse than in nonusers at the end of this period. This study suggests that using BZD/Zs chronically does not maintain or improve sleep quality.

https://www.ncbi.nlm...pubmed/15003439
Benzos decrease REM sleep.

Elderly
https://www.ncbi.nlm...pubmed/15001721
Jackson SG, Jansen P, Mangoni A (22 May 2009). Prescribing for Elderly Patients
The long-term effects of benzodiazepines and benzodiazepine dependence in the elderly can resemble dementia, depression, or anxiety syndromes, and progressively worsens over time. Adverse effects on cognition can be mistaken for the effects of old age. The benefits of withdrawal include improved cognition, alertness, mobility, reduced risk incontinence, and a reduced risk of falls and fractures. The success of gradual-tapering benzodiazepines is as great in the elderly as in younger people. Benzodiazepines should be prescribed to the elderly only with caution and only for a short period at low doses.

https://www.ncbi.nlm...pubmed/16639148
McIntosh A, Semple D, Smyth R, Burns J, Darjee R (2005). "Depressants". Oxford Handbook of Psychiatry (1st ed.). Oxford University Press. p. 540. ISBN 0-19-852783-7.
American Geriatrics Society 2012 Beers Criteria Update Expert Panel (2012). "American Geriatrics Society updated Beers Criteria for potentially inappropriate medication use in older adults" (PDF)
The elderly are at an increased risk of suffering from both short- and long-term adverse effects, and as a result, all benzodiazepines are listed in the Beers List of inappropriate medications for older adults.

https://www.ncbi.nlm...pubmed/26545257
The relative proportion of long-term BZD users in adult BZD users ranged from 6% to 76% (mean 24%) The estimates were higher in studies only on the elderly (47%). Long-term use involved typically steady treatment with low BZD doses. However, in elderly patients long-term BZD use and exceeding recommended doses was relatively common. Several characteristics associated with long-term use were found.

https://www.ncbi.nlm...les/PMC1934057/
Patients achieved withdrawal or reduced their dose by at least 50% after 6 and 12 months.

Seizures
https://www.ncbi.nlm...pubmed/21815323
Since the first report of benzodiazepine withdrawal seizure in 1961, many case reports have followed. Withdrawal seizures have occurred with short, medium, and long halflife benzodiazepine, if discontinued abruptly. Withdrawal seizures usually occur in patients who have been taking these medications for long periods of time and at high doses. Seizures have also been reported with less than 15 days of use and at therapeutic dosage. Almost all the withdrawal seizures reported were grand mal seizures. The severity of seizures range from a single episode to coma and death. Benzodiazepine dose tapering can be done faster in a hospital setting in high-dose abusers, but must be done more slowly in the outpatient setting in therapeutic dosage users.
Many many other articles also address this issue.

Part 3

From the manufacturer drug inserts

https://dailymed.nlm...8f-880eced0239f
Xanax (generic name is alprazolam) (Pfizer)
Warnings (Pfizer)
"Even after relatively shortterm use at the doses recommended for the treatment of transient anxiety and anxiety disorder (ie, 0.75 to 4.0 mg per day), there is some risk of dependence. Spontaneous reporting system data suggest that the risk of dependence and its severity appear to be greater in patients treated with doses greater than 4 mg/day and for long periods (more than 12 weeks). "
"Seizures attributable to XANAX were seen after drug discontinuance or dose reduction in 8 of 1980 patients with panic disorder or in patients participating in clinical trials where doses of XANAX greater than 4 mg/day for over 3 months were permitted. The duration of use in the above 8 cases ranged from 4 to 22 weeks. There have been occasional voluntary reports of patients developing seizures while apparently tapering gradually from XANAX. The risk of seizure seems to be greatest 24–72 hours after discontinuation."
Adverse Reactions
"It is suggested that the daily dosage of XANAX be decreased by no more than 0.5 mg every three days. Some patients may benefit from an even slower dosage reduction. In a controlled postmarketing discontinuation study of panic disorder patients which compared this recommended taper schedule with a slower taper schedule, no difference was observed between the groups in the proportion of patients who tapered to zero dose; however, the slower schedule was associated with a reduction in symptoms associated with a withdrawal syndrome."
Drug Abuse and Dependence
"When necessary, immediate management of withdrawal symptoms requires re-institution of treatment at doses of XANAX sufficient to suppress symptoms."

Also from Pfizer;
"Demonstrations of the effectiveness of XANAX by systematic clinical study are limited to 4 months duration for anxiety disorder and 4 to 10 weeks duration for panic disorder; however, patients with panic disorder have been treated on an open basis for up to 8 months without apparent loss of benefit. The physician should periodically reassess the usefulness of the drug for the individual patient."
"Withdrawal reactions may occur when dosage reduction occurs for any reason. This includes purposeful tapering, but also inadvertent reduction of dose (eg, the patient forgets, the patient is admitted to a hospital). Therefore, the dosage of XANAX should be reduced or discontinued gradually."
"There have been reports of failure of other benzodiazepines to fully suppress these withdrawal symptoms. These failures have been attributed to incomplete cross-tolerance but may also reflect the use of an inadequate dosing regimen of the substituted benzodiazepine or the effects of concomitant medications."

https://dailymed.nlm...0a-41a0946f956c
Valium (generic name is diazepam) (Genentech)
Drug Abuse and Dependence
"Diazepam is subject to Schedule IV control under the Controlled Substances Act of 1970. Abuse and dependence of benzodiazepines have been reported. Addiction-prone individuals (such as drug addicts or alcoholics) should be under careful surveillance when receiving diazepam or other psychotropic agents because of the predisposition of such patients to habituation and dependence. Once physical dependence to benzodiazepines has developed, termination of treatment will be accompanied by withdrawal symptoms. The risk is more pronounced in patients on long-term therapy."
"Since the risk of withdrawal phenomena and rebound phenomena is greater after abrupt discontinuation of treatment, it is recommended that the dosage be decreased gradually."
No additional information on the Genentech website.

https://dailymed.nlm...b6-30936715d73b
Klonopin (generic name is clonazepam) (Genentech)
Drug Abuse and Dependence
"After extended therapy, abrupt discontinuation should generally be avoided and a gradual dosage tapering schedule followed."
"Following the short-term treatment of patients with panic disorder, patients were gradually withdrawn during a 7-week downward-titration (discontinuance) period."
Dosage and Administration
"There is no body of evidence available to answer the question of how long the patient treated with clonazepam should remain on it. Therefore, the physician who elects to use Klonopin for extended periods should periodically reevaluate the long-term usefulness of the drug for the individual patient."
"Treatment should be discontinued gradually, with a decrease of 0.125 mg bid every 3 days, until the drug is completely withdrawn."
No additional information on the Genentech website.

Ativan (generic name is lorazepam) (Valeant Pharmaceuticals)
Indication and usage
"Ativan (lorazepam) is indicated for the management of anxiety disorders or for the short-term relief of the symptoms of anxiety or anxiety associated with depressive symptoms.The effectiveness of Ativan (lorazepam) in long-term use, that is, more than 4 months, has not been assessed by systematic clinical studies."
Warnings
"The dependence potential is reduced when lorazepam is used at the appropriate dose for short-term treatment."
"In general, benzodiazepines should be prescribed for short periods only (e.g., 2 to 4 weeks). Extension of the treatment period should not take place without reevaluation of the need for continued therapy. Continuous long-term use of product is not recommended. Withdrawal symptoms (e.g., rebound insomnia) can appear following cessation of recommended doses after as little as one week of therapy. Abrupt discontinuation of product should be avoided and a gradual dosage-tapering schedule followed after extended therapy."
No additional information on the Valeant Pharmaceuticals website.

Part 4

Effects of Discontinuation/Withdrawal

Guina, Jeffrey; Rossetter, Sarah R.; DeRHODES, Bethany J.; Nahhas, Ramzi W.; Welton, Randon S. (2015-07-01). "Benzodiazepines for PTSD: A Systematic Review and Meta-Analysis". Journal of Psychiatric Practice 21 (4): 281–303. doi:10.1097/PRA.0000000000000091. ISSN 1538-1145. PMID 26164054.
Michelini S, Cassano GB, Frare F, et al. (2016). "Long-term use of benzodiazepines: tolerance, dependence and clinical problems in anxiety and mood disorders.". Pharmacopsychiatry 29: 127–134
Gelpin, E.; Bonne, O.; Peri, T.; Brandes, D.; Shalev, A. Y. (1996-09-01). "Treatment of recent trauma survivors with benzodiazepines: a prospective study". The Journal of Clinical Psychiatry 57 (9): 390–394. ISSN 0160-6689. PMID 9746445.
Rosen, Craig S.; Greenbaum, Mark A.; Schnurr, Paula P.; Holmes, Tyson H.; Brennan, Penny L.; Friedman, Matthew J. (2013-12-01). "Do benzodiazepines reduce the effectiveness of exposure therapy for posttraumatic stress disorder?". The Journal of Clinical Psychiatry 74 (12): 1241–1248. doi:10.4088/JCP.13m08592. ISSN 1555-2101. PMID 24434093.
Wilhelm, F. H.; Roth, W. T. (1997-09-01). "Acute and delayed effects of alprazolam on flight phobics during exposure". Behaviour Research and Therapy 35 (9): 831–841. doi:10.1016/s0005-7967(97)00033-8. ISSN 0005-7967. PMID 9299803.
Matar, Michael A.; Zohar, Joseph; Kaplan, Zeev; Cohen, Hagit (2009-04-01). "Alprazolam treatment immediately after stress exposure interferes with the normal HPA-stress response and increases vulnerability to subsequent stress in an animal model of PTSD". European Neuropsychopharmacology 19 (4): 283–295. doi:10.1016/j.euroneuro.2008.12.004. ISSN 1873-7862. PMID 19167197.
Curran, H. V.; Collins, R.; Fletcher, S.; Kee, S. C. Y.; Woods, B.; Iliffe, S. (2003-10-01). "Older adults and withdrawal from benzodiazepine hypnotics in general practice: effects on cognitive function, sleep, mood and quality of life". Psychological Medicine 33 (7): 1223–1237. doi:10.1017/s0033291703008213. ISSN 0033-2917. PMID 14580077.
Pary R, Lewis S (2008). "Prescribing benzodiazepines in clinical practice". Resident and Staff Physician 54 (1): 8–17.

Withdrawal symptoms or rebound symptoms in between doses mimicking or exacerbating underlying anxiety or sleep disorders, inhibiting the benefits of psychotherapy by inhibiting memory consolidation and reducing fear extinction, and reducing coping with trauma/stress and increasing vulnerability to future stress. Anxiety, insomnia and irritability may be temporarily exacerbated during withdrawal, but psychiatric symptoms after discontinuation are usually less than even while taking benzodiazepines. Fortunately, for those with benzodiazepine-induced problems, functioning significantly improves within 1 year of discontinuation.

https://www.ncbi.nlm...pubmed/16639148
https://www.ncbi.nlm...pubmed/19062773
Royal Pharmaceutical Society of Great Britain (2009). British National Formulary (BNF 57). BMJ Group and RPS Publishing. ISBN 978-0-85369-845-6.
Opinion as to the time needed to complete withdrawal ranges from four weeks to several years. A goal of less than six months has been suggested, but due to factors such as dosage and type of benzodiazepine, reasons for prescription, lifestyle, personality, environmental stresses, and amount of available support, a year or more may be needed to withdraw.

https://www.ncbi.nlm...les/PMC2943829/
Based on collective findings in this benzodiazepine withdrawal-anxiety model, we propose a functional model illustrating the changes in glutamate receptor populations at excitatory synapses during benzodiazepine withdrawal.
(Physically alters GABA receptor shape and function during withdrawal.)

https://www.ncbi.nlm.../pubmed/1675688
Protracted withdrawal syndromes from benzodiazepines.
Benzodiazepines can give rise not only to slowly reversible functional changes in the central nervous system, but may also occasionally cause structural neuronal damage.

http://www.ncbi.nlm....pubmed/25466558
This occurred independently of neuronal activity and intracellular calcium and involved GABA(A)R–gephyrin interactions, suggesting that the changes in GABA(A)R diffusion depend on conformational changes of the receptor.

https://www.ncbi.nlm...pubmed/20935233
Similar to above.

http://www.ncbi.nlm....les/PMC3494928/
Chronic BZ treatment results in allosteric uncoupling of the GABA and BZ binding sites, suggesting changes in receptor subunit composition and/or receptor function (reviewed in ref. 7). Chronic dosing of animals with BZ leads to a reduction in GABAAR synaptic inhibition (8\l "–10) and produces diverse changes in GABAAR transcripts across the brain (7). Direct comparison and interpretation of these and other studies assessing mRNA levels has been challenging due to differences in treatment paradigm (time and dose), brain regions assessed, and the BZ ligand used. Radioligand binding studies have reported mixed results, ranging from decreases to no change in CNS BZ binding sites, likely due to methodological limitations in assessing subtype-specific GABAAR changes.
(Multiple references to changes in the receptors)

https://www.ncbi.nlm...pubmed/15219633
Impaired hypothalamic-pituitary-adrenocortical (HPA) system is related to severity of benzodiazepine withdrawal in patients.

https://www.ncbi.nlm...pubmed/20140603
BDNF plasma levels decrease during benzodiazepine withdrawal in patients suffering from comorbidity of depressive disorder and benzodiazepine dependence.

https://www.ncbi.nlm...pubmed/17132385
Patients achieved withdrawal or reduced their dose by at least 50% after 6 and 12 months. Abstinence and withdrawal symptoms were also measured.

https://www.ncbi.nlm.../pubmed/7439058
Among the benzodiazepines, lorazepam seems to have a particularly high addiction potential.

https://www.ncbi.nlm.../pubmed/2880872

https://www.ncbi.nlm.../pubmed/3676860
Specificity and intensity of BDZ withdrawal symptoms were the same for those dependent upon high doses of BDZs and those dependent upon low doses, but a protracted withdrawal was only observed in low-dose BDZ-dependent patients.

http://www.ncbi.nlm..../pubmed/9063050
Protracted benzodiazepine withdrawal syndrome mimicking psychotic depression.


Withdrawal Notes

http://www.benzosupp...ey_contents.htm
See..
http://www.benzosupp...instatement.htm
29% had to go over the ORIGINAL DOSE to stabilize or could not reach a dose high enough to stabilize.

Updosing during withdrawal
http://www.benzosupp...g/up_dosing.htm
24% said it was unsuccessful.

Ashton, H. (1984). Benzodiazepine withdrawal: An unfinished story. British Medical Journal, 288, 1135-1140.
Ashton, H. (1987). Benzodiazepine withdrawal: Outcome in 50 patients. British Journal of Addiction, 82, 665-671.
These symptoms have often been temporarily alleviated by a moderate increase in dosage or the addition of another benzodiazepine, but eventually re-emerge during further chronic use and only disappear after the benzodiazepine is stopped.

http://www.smchealth...per08-12-13.pdf
If symptoms to bad stabilize dose or go up in dose for 1-2 weeks.

https://www.ncbi.nlm...d00117-0138.pdf
Small "extra dose" on any day they feel a special need for
extra help. This helps them to feel in control.

http://www.btpinfo.o...benzodiazepines
Never abruptly stop any benzodiazepine or Z drug. The shock caused by such an abrupt withdrawal is so severe that even after resumption of your drug at the previous dose, it may take weeks or months to "stabilise", and in some cases, you may never stabilise from a cold turkey withdrawal until after you have completed your reduction.


Withdrawal

Suicide
http://www.ncbi.nlm....les/PMC2047018/
Two recent studies have examined the role of benzodiazepines on actual or attempted suicide. A study examining elderly suicides in Sweden found that between 1992 and 1996, benzodiazepine hypnotics dominated drug-poisoning suicides (216 of 548, 39%) in those aged over 65 years.4 During the same time frame, a population-based cohort study in Canada found a significant association between suicide attempts and benzodiazepine usage (odds ratio = 6.2). While disinhibition and paradoxical reactions inducing suicidal impulses were considered, the authors believed that confounding by the original indication was a more likely explanation.5 Neither study reported withdrawal symptoms as a factor, although both advised examining for depression and restrictive prescribing for groups at risk of suicide.

Part 5

Withdrawal Treatment

https://riordanclini...ical-rationale/
Benzodiazepine withdrawal treatment. GABA, Vitamin C and niacin.

Flumazenil
https://www.ncbi.nlm...pubmed/14578014
FLU (iv injection) immediately reversed BZD effects on balance task and significantly reduced withdrawal symptoms in comparison with oxazepam and placebo on both self-reported and observer-rated withdrawal scales. The partial agonist also reduced craving scores during the detoxification procedure. In addition, during oxazepam tapering, group B patients experienced paradoxical symptoms that were not apparent in FLU patients. Patients treated with FLU showed a significantly lower relapse rates on days 15, 23 and 30 after the detoxification week. Our data provide further evidence of FLUs ability to counteract BZD effects, control BZD withdrawal and normalize BZD receptor function.

https://www.ncbi.nlm...les/PMC4014019/
Preliminary data suggest that continuous intravenous or subcutaneous flumazenil infusion for 4 days significantly reduces acute benzodiazepine withdrawal sequelae.

https://www.ncbi.nlm...pubmed/26096314
The most common AEs (adverse events) in the flumazenil group were agitation and gastrointestinal symptoms, whereas the most common SAEs (significant adverse events)were supraventricular arrhythmia and convulsions.

https://www.ncbi.nlm...pubmed/27166362
This paper reports the data related to 214 subjects addicted to high doses of benzodiazepine and treated with the FLU-SSI method between 2012 and 2014. This technique is less invasive and requires less nursing intervention than intravenous infusion. Our data support FLU-SSI as a possible efficient strategy for the treatment of patients with long-term, high-dose benzodiazepine addiction

https://www.ncbi.nlm...pubmed/22596209
This small proof-of-concept study indicates that subcutaneous flumazenil infusion has excellent tolerability, efficacy and improvement on measures of psychological distress.

Cyamemazine (antihistamine)
https://www.ncbi.nlm...pubmed/22421069
Therefore, the anxiolytic efficacy of cyamemazine in benzodiazepine withdrawal can be due to a 5-HT(2AR) antagonistic activity at the cortical level.

cyamemazine vs. bromazepam
https://www.ncbi.nlm...pubmed/16243418
28 patients (total 618) in the cyamemazine group and 18 in the bromazepam group had an adverse event, including anxiety, insomnia, dry mouth and somnolence. No extra-pyramidal symptoms were reported. In conclusion, cyamemazine was comparable to bromazepam in ensuring successful benzodiazepine withdrawal and in controlling the acute benzodiazepine withdrawal syndrome. Cyamemazine may be useful to facilitate benzodiazepine withdrawal in those patients where bromazepam substitution is not appropriate.

Pregabalin (Lyrica)
"Common side effects include: sleepiness, confusion, trouble with memory, poor coordination, dry mouth, problem with vision, and weight gain.[6] Potentially serious side effects include angioedema, drug misuse, and an increased suicide risk.[6] It is moderately addictive both physically and psychologically.[1]"
Wiki
https://www.ncbi.nlm...pubmed/24532157
Our findings suggest that successful treatment of long-term BDZ use with PGB is associated with a substantial, though only partial, recovery of BDZ-compromised neuropsychological functioning, at least at a 2-month follow-up.

https://www.ncbi.nlm...pubmed/21334859
The success rates did not differ according to either the benzodiazepine of abuse or the presence of other substance use disorders. Significant and clinically relevant improvements were observed in withdrawal and anxiety symptoms, as well as in patients' functioning. At week 12, tolerability was rated as good or excellent by 90% and 83% of the clinicians and patients, respectively. Our results suggest that pregabalin is an efficacious and well-tolerated adjunctive treatment for benzodiazepine withdrawal.

https://www.ncbi.nlm...pubmed/22568872
Available evidence suggests that monotherapy with pregabalin, within the dosage range of 150 - 600 mg/d, is a promising "novel" option for the safe and efficacious relapse prevention of both AD and BD. However, its efficacy as monotherapy in the acute treatment of AD withdrawal syndrome is still controversial.

https://www.ncbi.nlm...pubmed/22545971
Between 15% and 29% of the patients were able to stop using benzodiazepines after starting pregabalin or gabapentin treatment. Psychiatric patients who started pregabalin were able to reduce the amount of benzodiazepines used by 48%, compared to only 14% among starters of gabapentin. This study shows that some patients reduced their use of benzodiazepines substantially after starting pregabalin.

Gabapentin
"Serious side effects may include an increased risk of suicide, aggressive behaviour, and drug reaction with eosinophilia and systemic symptoms.[4] It is unclear if it is safe during pregnancy or breastfeeding.[8] Lower doses should be used in people with kidney problems. Gabapentin does not affect the activity of the inhibitory neurotransmitter γ-aminobutyric acid (GABA); how it works is unclear.[4}"
Wiki

Possible links to pancreatic and other cancers (below)
http://clinicaltrial...how/NCT01138124
http://www.bioportfo...ancer-gprd.html
http://clinicaltrial...how/NCT01236053
http://www.ncbi.nlm....les/PMC3314779/

https://www.ncbi.nlm...pubmed/22545971
Between 15% and 29% of the patients were able to stop using benzodiazepines after starting pregabalin or gabapentin treatment. Psychiatric patients who started pregabalin were able to reduce the amount of benzodiazepines used by 48%, compared to only 14% among starters of gabapentin. This study shows that some patients reduced their use of benzodiazepines substantially after starting pregabalin.

Afobazole (fabomotizole)
Clinical trials have shown fabomotizole to be well tolerated and reasonably effective for the treatment of anxiety. Fabomotizole has found little clinical use outside Russia and has not been evaluated by the FDA.
https://www.ncbi.nlm...pubmed/25076752
Afobazole (5.0 mg/kg, i.p.) effectively (i) ameliorated withdrawal-induced anxiety, returning behavioral pattern in the elevated plus maze test up to levels comparable to that in vehicle-treated animals, and (ii) increased withdrawal-reduced dopamine level (+23.8%, p < 0.05) in striatum. It is suggested that afobazole, due to its multitarget receptor action, can be useful in the diazepam withdrawal-induced anxiety blockade through modulation of dopaminergic system activity.
nitric oxide synthase inhibitors

https://www.ncbi.nlm...pubmed/21857078
Administration of the non-selective NO synthase inhibitors N(G)-nitro-L-arginine (L-NOARG) and N(G)-nitro-L-arginine methyl ester hydrochloride (L-NAME) significantly attenuated the withdrawal syndrome (i.e., pentetrazole-induced seizures) in diazepam-dependent mice. L-NOARG significantly suppressed hypermotility in clonazepam-dependent rats and inhibited the decrease in body weight observed after 12 h of withdrawal in chlordiazepoxide- and clonazepam-dependent rats. Moreover, a clear propensity of L-NOARG to protect benzodiazepine-dependent rats against audiogenic seizures was observed

Phenobarbital
Side effects include a decreased level of consciousness along with a decreased effort to breathe. There is concern about both abuse and withdrawal following long term use. It may also increase the risk of suicide. It is pregnancy category B or D in the United States and category D in Australia.
Wiki
Many research articles have been written on its withdrawal.

https://www.ncbi.nlm.../pubmed/1575069
https://www.ncbi.nlm.../pubmed/2147093
https://www.ncbi.nlm...pubmed/22285834
We reviewed the medical records of 310 patients treated with a 3-day fixed-dose phenobarbital taper for benzodiazepine dependence over a 5-year period between 2004 and 2009. We recorded the incidence of seizures, falls, delirium, and emergency department (ED) visits or readmission to our institution within 30 days as markers for safety; we also recorded how many patients had doses held because of sedation. The taper was well tolerated, although one quarter of the patients had at least one dose held because of sedation. There were no seizures, falls, or injuries reported. Six percent had a readmission, and 7% had an ED visit at our institution within 30 days of discharge, but only 3 patients required readmission for withdrawal symptoms. Overall, this protocol appears to be safe and effective.

βCCT
βCCT, an antagonist selective for α1GABAA receptors.
https://www.ncbi.nlm...pubmed/23149168
Acute challenge with either flumazenil (10mg/kg) or βCCt (1.25, 5 and 20 mg/kg) alleviated the diazepam withdrawal-induced anxiety. Moreover, both antagonists induced an anxiolytic-like response close, though not identical, to that seen with acute administration of diazepam. These findings imply that the mechanism by which antagonism at GABA(A) receptors may reverse the withdrawal-induced anxiety involves the α(1) subunit and prompt further studies aimed at linking the changes in behavior with possible adaptive changes in subunit expression and function of GABA(A) receptors.

https://www.ncbi.nlm...pubmed/24695241
In conclusion, the current study suggests that the role of α1-containing GABAA receptors in mediating the development of physical dependence may vary based on the effect being studied and duration of protracted treatment. Moreover, the present data supports previous findings that the lack of activity at α1-containing GABAA receptors is not sufficient to eliminate physical dependence liability of ligands of the benzodiazepine type.

https://www.ncbi.nlm...les/PMC4066304/
Variable effectiveness.

GB-115 dipeptide
https://www.ncbi.nlm...pubmed/22238979
It is established that, in 24-48 h following BZ withdrawal, GB-115 dipeptide administered in doses of 0.1 and 0.5 mg/kg, i.p., produced an anxiolytic effect in all animals, which was manifested by increasing the stay time and number of entries in EPM. In the striatum of outbred rats, GB-115 increased DOPAC (+25%) and DA (+31.6%) levels that were decreased during diazepam withdrawal syndrome. The obtained results showed the GB-115 efficiency in attenuating the anxiety caused by BZ withdrawal.

Captodiamine
Captodiame, also known as captodiamine, is an antihistamine sold under the trade names Covatine, Covatix, and Suvren which is used as a sedative and anxiolytic. It is a derivative of diphenhydramine.
Wiki
https://www.ncbi.nlm...pinewithdrawal
Analysis of the primary study criterion revealed a statistically significant difference (p < 0.0001) in the emergence of withdrawal symptoms between the two groups in favour of captodiamine at two, six and eight weeks following initiation of therapy. These results were supported by significant beneficial effects of captodiamine on the majority of secondary outcome measures. The switch to captodiamine was associated with an improvement in vigilance, which may be an advantage for the overall safety of the anxiolytic treatment, for example with regard to road safety. Discontinuation of captodiamine was not associated with the emergence of rebound anxiety.

Dothiepin (a tricyclic antidepressant not available in the USA)
https://www.ncbi.nlm.../pubmed/8730942
Not significant efficacy.

Varied treatments evaluated
https://www.ncbi.nlm...pubmed/16856084
Results support the policy of gradual rather than abrupt withdrawal of benzodiazepine. Progressive withdrawal (over 10 weeks) appeared preferable if compared to abrupt since the number of drop-outs was less important and the procedure judged more favourable by the participants. Short half-life benzodiazepine, associated with higher drop-out rates, did not have higher withdrawal symptoms scores. Switching from short half-life benzodiazepine to long half-life benzodiazepine before gradual taper withdrawal did not receive much support from this review. The role of propanolol in benzodiazepine withdrawal was unclear; adding tricyclic antidepressant (dothiepin) decreased the intensity of withdrawal symptoms but did not increase the rate of benzodiazepine abstinence at the end of the trial. Buspirone and Progesterone failed to suppress any benzodiazepine symptoms. Carbamazepine might have promise as an adjunctive medication for benzodiazepine withdrawal, particularly in patients receiving benzodiazepines in daily dosages of 20 mg/d or more of diazepam (or equivalents).

Buspirone
https://www.ncbi.nlm.../pubmed/2880872
It was concluded that buspirone does not help benzodiazepine withdrawal and does not suppress benzodiazepine withdrawal symptoms.
https://www.ncbi.nlm...pubmed/11097963
The success rate of the taper in this study was significantly higher for patients who received imipramine (82.6%), and nonsignificantly higher for patients who received buspirone (67.9%), than for patients who received placebo (37.5%). The imipramine effect remained highly significant even after the analysis adjusted for three other independent predictors of taper success: benzodiazepine dose, level of anxious symptoms at baseline, and duration of benzodiazepine therapy.
https://www.ncbi.nlm.../pubmed/2878622
This finding supports preclinical studies indicating that buspirone has no clinically significant benzodiazepine receptor activity.
https://www.ncbi.nlm.../pubmed/2211568
Buspirone and alprazolam may be used together safely, and buspirone may be started early in the alprazolam tapering process. Thirty-six patients received placebo t.i.d. and 36 received buspirone 5 mg. t.i.d. Findings included significantly greater anxiety (as measured by the Hamilton Rating Scale for Anxiety) in the placebo group and significantly reduced manifestations of abstinence (as measured by the Abstinence Rating Scale) in the buspirone group
https://www.ncbi.nlm...pubmed/22298398
Buspirone-treated patients tended to have lower anxiety levels than placebo-treated patients.
https://www.ncbi.nlm.../pubmed/2885432
Failure of buspirone to protect against lorazepam withdrawal symptoms.

Tianeptine and Carbamazepine
https://www.ncbi.nlm...pubmed/12647454
It appears from this study that both drugs (carbamazepine and tianeptine) are comparable, safe and efficient in treating benzodiazepine withdrawal symptoms.

Carbamazepine
Common side effects include nausea and drowsiness. Serious side effects may include skin rashes, decreased bone marrow function, suicidal thoughts, or confusion. It should not be used in those with a history of bone marrow problems. Use during pregnancy may cause harm to the baby; however stopping it in pregnant women with seizures is not recommended. Its use during breastfeeding is not recommended. Care should be taken in those with either kidney or liver problems.
Wiki

https://www.ncbi.nlm.../pubmed/9005346
Compared with a gradual tapering off of benzodiazepines, abrupt withdrawal plus CBZ medication seems to be better tolerated

https://www.ncbi.nlm.../pubmed/1297907
Thirty-six outpatients aged > or = 60 yrs suffering from general anxiety disorders and benzodiazepine abuse underwent gradual discontinuation of benzodiazepine therapy in two groups, one treated with carbamazepine and one with placebo. The carbamazepine-treated group demonstrated a lower incidence of withdrawal symptoms rated according to the Physician Withdrawal Check List

https://www.ncbi.nlm.../pubmed/2929759
All patients tolerated rapid discontinuation well and none developed significant withdrawal symptoms.

https://www.ncbi.nlm.../pubmed/2021297
The results of this pilot investigation suggest that carbamazepine might have promise as an adjunctive drug therapy for the benzodiazepine withdrawal syndrome, particularly in patients receiving benzodiazepines in daily dosages of 20 mg/d or greater of diazepam equivalents.
https://www.ncbi.nlm.../pubmed/1854420
These geriatric patients experienced no major withdrawal symptoms, but mild symptoms were common. There was no correlation between dose or duration of alprazolam use and extent of withdrawal symptoms. We recommend use of this treatment regimen in a hospital setting only, where close monitoring can occur.
https://www.ncbi.nlm.../pubmed/1686406
Fundamental withdrawal symptoms (like hypersensitivity to sensory stimuli, abnormal perception of movement, depersonalisation or derealisation) were also less severe in the group treated with CBZ compared with the group not receiving that treatment. These findings support the results of previous reports indicating a therapeutical effect of CBZ in BZD withdrawal.
Widely used by detox centers.
Topiramate (Topomate)
People taking topiramate should be aware of the following risks:
⦁ Avoid activities requiring mental alertness and coordination until drug effects are realized.
⦁ Topiramate may impair heat regulation, especially in children. Use caution with activities leading to an increased core temperature, such as strenuous exercise, exposure to extreme heat, or dehydration.
⦁ Topiramate may cause visual field defects.
⦁ Topiramate may decrease effectiveness of estrogen-containing oral contraceptives.
⦁ Taking topiramate in the 1st trimester of pregnancy may increase risk of cleft lip/cleft palate in infant.
⦁ As is the case for all antiepileptic drugs, it is advisable not to suddenly discontinue topiramate as there is a theoretical risk of rebound seizures.
Wiki

There is an extensive list of side effects on Wiki and the FDA websites. Too numerous to list here.

https://www.ncbi.nlm...pubmed/12858324
A case is presented of a rapid benzodiazepine-withdrawal treated successfully with topiramate.
https://www.ncbi.nlm...pubmed/17071548
In our case of a patient with recurrent major depressive disorder, subthreshold anxiety disorder and addiction to alprazolam, topiramate appears to be efficient and safe in alprazolam withdrawal.

Alpidem
Clinical trial to obtain US FDA approval were halted in 1992 and the drug never received FDA approval. It was withdrawn from the French market by 1994 and is not approved for marketing anywhere in the world.. In 1995, Alpidem was withdrawn from the market in most of the world following reports of severe liver damage.

https://www.ncbi.nlm.../pubmed/8097214
It was concluded that alpidem is not helpful in helping patients withdrawing from a benzodiazepine withdrawal perhaps because of partial agonist properties

https://www.ncbi.nlm...pubmed/19698430
A severe WS was diagnosed in 11.1% of the patients in the alpidem group and in 31.6% of the placebo group. If not having been withdrawn from the market, alpidem could have been useful for the prevention of BZ withdrawal syndrome.

Valproate
https://www.ncbi.nlm...pubmed/22915484
Non-fatal and fatal liver failure associated with valproic acid.
Many research articles om serious side effects, some fatal for this drug.

Placebo
https://www.ncbi.nlm...pubmed/11205424
Thus, females had the highest base-line ratings and were the only group that showed a significant reduction in symptom ratings after placebo injections on the first occasion. Gender differences were also found for systolic and diastolic blood pressure.

Progesterone
is an endogenous steroid and progestogen sex hormone involved in the menstrual cycle, pregnancy, and embryogenesis of humans and other species.
This drug has its own severe withdrawal.
https://www.ncbi.nlm.../pubmed/7604143
There was no progesterone versus placebo difference in the severity of taper withdrawal.
https://www.ncbi.nlm.../pubmed/9000261
The principal finding of the present work is that the intensity of diazepam withdrawal syndrome was significantly reduced by acute administration of progesterone

Clonidine
https://www.ncbi.nlm.../pubmed/2872826
The intensity, severity, and duration of the abstinence syndrome were not altered by clonidine at a dose sufficient to markedly reduce blood pressure and plasma free 3-methoxy-4-hydroxyphenylglycol.

https://www.ncbi.nlm.../pubmed/8577798
Finally, low doses of clonidine (0.03 mg/kg, i.p.) were shown to have anxiolytic properties and to reverse the anxiogenic effects of lorazepam on withdrawal.

Ipsapirone
https://www.ncbi.nlm.../pubmed/1676531
Ipsapirone causing true potentiation of BZ withdrawal

Not approved by the FDA yet.

Propranolol (Beta-Blocker)
https://www.ncbi.nlm.../pubmed/1971767
Those in the propranolol group suffered more severe symptoms.

https://www.ncbi.nlm.../pubmed/7910743
This paper describes pharmacological treatments that can reverse the anxiogenic response detected in animal tests when rats are withdrawn from chronic treatment with diazepam. Concurrent treatment with the calcium channel antagonist verapamil prevented this withdrawal response and the benzodiazepine-receptor antagonist flumazenil reversed the anxiogenic response and restored the system to a drug-naive state. Other treatments that reversed the anxiogenic response were the GABAB agonist baclofen, the 5-HT1A receptor agonist buspirone, and the 5-HT3 receptor antagonist (R,S)-zacopride (GABA = gamma-aminobutyric acid; 5-HT = 5-hydroxytryptamine). Both the enantiomers of zacopride contributed to this reversal. These behavioural reversals are interpreted in the light of biochemical studies showing increased 45Ca2+ flux and [3H]5-HT release from the hippocampus, during benzodiazepine withdrawal .

Hydroxyzine (Atarax) (antihistamine)
https://www.ncbi.nlm...les/PMC3598901/
Benzo use was reduced by 25% every 2 to 4 weeks.
25 mg Hydroxyzine/day.

https://www.ncbi.nlm.../pubmed/9417395
The patients had to be long term consumers (at least 3 months) of 2 mg daily of lorazepam and were withdrawn using transiently an antihistaminic anxiolytic (hydroxyzine or placebo TAD) according to 6 different procedures defining 6 parallel groups: hydroxyzine 50 mg, abrupt or progressive withdrawal; hydroxyzine 25 mg, abrupt or progressive withdrawal; placebo, abrupt or progressive withdrawal. Following this 4 week-period of withdrawal, the patients were without any treatment for a post-study follow up 2 month-period.
After a one-month period of withdrawal (under placebo or hydroxyzine) followed by a 2 month-period without any treatment, 75% patients were totally free of any drug and their level of anxiety was significantly decreased
Levels of anxiety were significantly improved in hydroxyzine 50 mg group and in hydroxyzine 25 mg group but not in placebo group. Withdrawal symptoms between D0 and D28 were improved only in hydroxyzine 50 mg group and the number of side effects was significantly improved in both the hydroxyzine (25 et 50 mg) groups but not in placebo group.
When a patient is engaged to be withdrawn from of a lorazepam long term treatment, it can therefore be proposed as a support a transient prescription of hydroxyzine 25 mg TAD to markedly anxious patients and of hydroxyzine 50 mg TAD to patients presenting a withdrawal symptomatology.

https://www.ncbi.nlm...pubmed/18379511
The study aimed at investigating of efficacy of hydroxyzine (atarax) as a substitutive drug used in case of benzodiazepine tranquilizers (BDT) withdrawal in patients who received BDT for more than 3 months. Fifty-nine patients with protracted chronic anxiety-phobic disorders were divided into 2 groups: in the first (main) one, BDT were withdrawn at once with the following assignment of substitutive therapy with atarax and in the second (control) group the withdrawal was continuous during 14 days with the simultaneous assignment of a substitutive placebo therapy. In the first group (resumed the BDT therapy because of worsening of their state 23,3% patients finished their participation in the study ahead of time as compared to 65,6% of those in the control group. The Hamilton Anxiety Scale scores were more reduced in the main group than in the control one. The results obtained suggest that atarax is worth to be used as a substitutive drug for BDT.

Z Drugs

Definition - Z-drugs are a group of nonbenzodiazepine drugs with effects similar to benzodiazepines, which are used in the treatment of insomnia, and most of whose names start with the letter "Z". Some Z-drugs may have advantages over benzodiazepines. (Wiki)

Eszopiclone (Lunesta) (Zopiclone )
Zaleplon (Sonata).
Zolpidem (Ambien)

Benzodiazepines and Z Drugs

https://www1.ghc.org...benzo-zdrug.pdf
Benzodiazepine and Z-Drug Safety Guideline
This guidance document is an excellent over view of these two drug groups. It explains how the Z-Drugs act just like benzos, a little less effective on anxiety and a little more effective on sleep. They are just as addictive, severe withdrawal and because their action is the same as benzos they should not be taken with benzos as it increases the rate of addictiveness and severity of withdrawal.

https://www.ncbi.nlm...pubmed/25474727
The risk to develop BZD/z-drugs dependence is significantly associated with psychiatric history and with the quantity of BZD/z-drugs that is taken.

https://www.ncbi.nlm...pubmed/24774720
Dependence on benzodiazepines (BZDs) or Z-drugs (zolpidem, zopicline and zaleplon) is a common clinical phenomenon.
https://www.ncbi.nlm...pubmed/18505619
There were no significant differences in patients' perceptions of efficacy or side-effects reported by those on Z drugs compared to patients taking benzodiazepines. Side-effects were commonly reported, which may have contributed to a high proportion of responders, particularly patients on Z drugs who were wishing to stop, or who had previously tried to stop taking this medication. Reported prescribing practices were often at variance with the licence for short-term use.
About half of those with sleep problems seek medical help, which often involves a prescription of hypnotic drugs including benzodiazepines like temazepam, or Z drugs such as zopiclone, zolpidem, or zaleplon. Most hypnotic prescribing takes place in primary care, and drug treatments may be inappropriately prescribed for 4 weeks or longer in up to 50% of new prescriptions.
No significant differences between Z drugs and benzodiazepines were found in respect of perceived benefits or adverse effects, including withdrawal or dependence.

https://www.nice.org...522015122913515
Guidance document from NICE (National Institute for Health and Care Excellence, UK)on the use of Benzos and Z-drugs.
"There is no firm evidence of differences in the effects of zaleplon, zolpidem, zopiclone and the shorter-acting benzodiazepines."
"If treatment with one of these hypnotic medicines does not work, the doctor should not prescribe one of the others."
A drug used to induce sleep is described as a 'hypnotic'.
The Summary of Product Characteristics (SPC) specifies that treatment (with Zaleplon) should be as short as possible with a maximum duration of 2 weeks. The SPC states that the duration of treatment (with Zolpidem) should usually vary from a few days to 2 weeks with a maximum of 4 weeks, including tapering off where appropriate. The SPC also states that the duration of treatment (with Zopiclone) should be 2–5 days for transient insomnia and 2–3 weeks for short-term insomnia.
http://www.nhsgrampi...zo_649_1014.pdf
In practice short-term prescribing should be limited to a maximum of two weeks as signs of psychological and physical dependence can develop if prescribed for longer periods.

*Z- drugs which include zaleplon, zolpidem and zopiclone are non benzodiazepine hypnotics, they carry the same risks and dependence problems as benzodiazepines.

Z drugs are indicated only for the short term management of severe insomnia that interferes with normal daily life, and should be prescribed for short periods of time only (up to two to four weeks for Zopiclone, Zolpidem and up to two weeks for Zaleplon).[2], [3]

There is no justification for prescribing more than one benzodiazepine or Z-drug concurrently, except during the period of conversion.

If the patient is struggling with symptoms of withdrawal, halt the reduction and maintain the current dose until symptoms improve. Increases in dose are to be discouraged.

http://www.setrust.h...and_Z_Drugs.pdf
There is no significant difference in adverse effects between benzodiazepines and zopiclone and not enough data to choose one over the other. There is no significant difference in sleep latency between benzodiazepines and zopiclone. The risk of hip fracture is as likely with z drugs as with other benzodiazepines.

They offer no clinically significant advantages over benzodiazepines

Only use for the short-term treatment of severe anxiety or insomnia (anxiety maximum of 4 weeks, insomnia maximum of 10 nights)

Ambien (Zolpidem)
https://dailymed.nlm...96-8702a28e6e76
Note - The following is from the drug insert supplied with Ambien (Manu; Sanofi-aventis) and is an example of a typical drug insert for Z-Drugs. See above website for inserts from other Z-drugs and manufacturers.

"Sleep-driving" and other complex behaviors while not fully awake. Risk increases with dose and use with other CNS depressants and alcohol. Immediately evaluate any new onset behavioral changes.
Depression: Worsening of depression or, suicidal thinking may occur. Prescribe the least amount of tablets feasible to avoid intentional overdose.
Withdrawal effects: Symptoms may occur with rapid dose reduction or discontinuation
Observed reactions include anaphylaxis and angioedema.
Additive effects occur with concomitant use of other CNS depressants (e.g. benzodiazepines, opioids, tricyclic antidepressants, alcohol), including daytime use. Downward dose adjustment of AMBIEN CR and concomitant CNS depressants should be considered.
Abnormal thinking and behavior changes have been reported in patients treated with sedative/hypnotics, including AMBIEN CR. Some of these changes included decreased inhibition (e.g. aggressiveness and extroversion that seemed out of character), bizarre behavior, agitation and depersonalization. Visual and auditory hallucinations have been reported.
Other complex behaviors (e.g., preparing and eating food, making phone calls, or having sex) have been reported in patients who are not fully awake after taking a sedative-hypnotic. As with "sleep-driving", patients usually do not remember these events. Amnesia, anxiety and other neuro-psychiatric symptoms may also occur.
In primarily depressed patients treated with sedative-hypnotics, worsening of depression, and suicidal thoughts and actions (including completed suicides), have been reported. Suicidal tendencies may be present in such patients and protective measures may be required.

Zolpidem can cause drowsiness and a decreased level of consciousness, which may lead to falls and consequently to severe injuries. Severe injuries such as hip fractures and intracranial hemorrhage have been reported.
Data from a clinical study in which selective serotonin reuptake inhibitor- (SSRI-) treated patients were given zolpidem revealed that four of the seven discontinuations during double-blind treatment with zolpidem (n=95) were associated with impaired concentration, continuing or aggravated depression, and manic reaction.
Zolpidem tartrate is classified as a Schedule IV controlled substance by federal regulation.

https://www.ncbi.nlm...pubmed/14519173
Zolpidem and zopiclone can cause dependence.

https://www.ncbi.nlm...pubmed/24531568
We found that subchronic zolpidem and diazepam administration produced ...increased anxiety-like behaviors 1 day after drug termination.
https://www.ncbi.nlm...pubmed/26776243
This study demonstrated a significant association between using zolpidem and suicide or suicide attempt in people with or without comorbid psychiatric illnesses.
https://www.ncbi.nlm...pubmed/22444504
In 83.5% of cases, psychoactive substances other than zolpidem were detected, most commonly antidepressants (46.2%), benzodiazepines (35.2%), opioids (26.4%), and alcohol (39.6%). In summary, zolpidem was a factor contributing to death in a large proportion of cases, predominately involving drug toxicity and suicide.
https://www.ncbi.nlm...pubmed/24931450
Results revealed medium effect sizes for zopiclone and zolpidem on measures of verbal memory. An additional medium effect size was observed for zolpidem on attention. Finally, smaller effect sizes were observed for zolpidem speed of processing and for zopiclone on working memory. It is clear from these data that the use of a single dose of the z-drugs in healthy adults as measured in the morning following the exposure does produce a specific rather than a generalized negative effect on cognitive function. However, there were only enough studies to evaluate the individual cognitive effects of the zolpidem and zopiclone medications; the specific effects of zaleplon and eszopiclone cannot be ascertained because only one study met the inclusion and exclusion criteria for the review.
https://www.ncbi.nlm...les/PMC3906775/
This case showed that zolpidem can exert abuse capability, euphoric mood, tolerance, and withdrawal syndrome.
http://www.benzo.org.uk/ashtonad.htm
Do not change type or dose of antidepressants while withdrawing from a benzo. Wait for 4 weeks or more after withdrawal complete to change.
------------------------------------------------------------------------------------------------------------
Atenolol is a beta 1 adrenergic receptor antagonist, also known as a beta blocker. It does not pass through the blood brain barrier which limits its side effects compared to other beta blockers. It has been linked to a higher risk of type 2 diabetes. It may cause drowsiness and lower blood pressure. Typical dosage around 25 mg four times/day. Dosage should be slowly increased.
Begins working in 30 minutes to an hour
Peak levels – 2 – 4 hrs
Half Life – 6 - 8 hrs
https://www.ncbi.nlm.../pubmed/3549876
Effective but blood pressure drops.
https://www.ncbi.nlm.../pubmed/4054193
Side Effects
https://www.ncbi.nlm.../pubmed/1777372
https://www.ncbi.nlm.../pubmed/4047384
Not effective
https://www.ncbi.nlm.../pubmed/2196620
30% found it effective.
SF - So now I am on one. It is called Atilonol (Atenolol?) and calms down your heart rate too.
-----------------------------------------------------------------------------------------------------------
Diphenhydramine, (over the counter) also known as Benadryl, is an antihistamine and as such is not only used for allergies/colds but also as a sleep aide. It does have a mild anxiolytic effect. May lower blood pressure and cause irregular heartbeats. Long-term use of Benadryl often affects mental cognition, especially in the elderly. Your body does build up tolerance to it after a few weeks. There is evidence of dependence in cases of long-term heavy uses, It is a histamine H(1)R antagonist in the brain. Do not take this medicine with any other medicine that can cause sleepiness including benzos, most blood pressure medicines, ssri/snri, buspar and others. Please check for compatibility before using. This medicine has many drug interactions.

http://www.cymbaltaw...elps#entry68017
Technical information on Diphenhydramine(Benadryl)

serendipity - I found Benadryl to produce hangover effects, and cause palpitations when taken long term. Even if you wake up in the middle of the night, and can't get back to sleep, even a teeny amount (say, 15mg) can induce sleep again.

Schmb - Benadryl worked on a limited basis for me, because sometimes it makes me jittery, and that only made the zaps much worse, so just use some caution in case you are sensitive to it.

FH - One caution on benadryl. It is famous for bad reactions with other medicine so check your compatability closely. The maximum dosage of benadryl is 25 to 50 mg every 4 to 6 hours and do not surpass 300 mg in a day.


Begins working in 15 to 30 minutes
Peak levels - 2 to 2.5 hrs
Half Life – 4 to 6 hrs

https://www.ncbi.nlm...pubmed/24530460
Moderately effective
https://www.ncbi.nlm...pubmed/19415242
(50mg dose)
https://www.ncbi.nlm...pubmed/16156843
Effective
https://www.ncbi.nlm...pubmed/16111835
Effective

-----------------------------------------------------------------------------------------------------------


#20 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 28 February 2018 - 06:44 PM

Effects of Cymbalta on the Body
------------------------------------------------------------------------------------------------------------
Hypothyroidism. It is a common side effect of the use of ssri/snri antidepressants. The medicine inserts that come with antidepressants nearly always warn of the risk of developing hypothyroidism and/or liver damage. These chemicals (medicines) are often suppressive to the function of these tissues. It is standard procedure that a psychiatrist will stop the use of ssri/snri for 3 months to allow the thyroid to recover (which it almost always does unless actual damage is done to the tissue). At that point a different ssri/snri will be used to see if it can be used without effect on the thyroid. Zoloft is the one with the best record. It is important to note that it is essential to consider any radiological testing that may have been done around the same time. It has been shown that around 30% of the abdominal cat scans use enough contrast iodine to produce hypothyroidism. It is usually asymptomatic and does return to normal within a 6 to 9 month period. A simple 24 hour urine sample can show if iodine toxicity (from cat scans/radiation imaging) is the source of the hypothyroidism.
 
FH - NO good endocrinologist would put you on thyroid medicine immediately after blood tests suggesting hypothyroidism unless you are very symptomatic and in despite need for help. I was diagnosed with HypoT after being on Cymbalta. My primary care dr said I would have to be on thyroid medicine for life. I went to my endocrinologist and he threw a fit. I was informed, but was already aware, that many conditions can causes hypoT blood test results including the radiation, aspirin usage and some of the other nsaids, many other medicines, as well as infections. All clear when the causative agent is removed. Even a seafood diet and/or heavy iodine salt usage can cause this.
http://www.cymbaltaw...tion/?hl=helped
List of AD that can cause thyroid issues.
http://www.cymbaltaw...rove#entry46513
Hypothyroidism and depression information.

Antidepressants
reboxetine - TSH reduced and T4 increased.
sertraline - TSH increased and T4 reduced.
https://www.ncbi.nlm.../?term=18262705

sertraline and fluoxetine showed reductions in TSH,T3 and T4 levels.
https://www.ncbi.nlm.../?term=15486607

Fluoxetine decreased T3 and T4, increased TSH
https://www.ncbi.nlm...d/?term=6413229

Do not treat with thyroid hormones if hypothyroidism is asymptomatic.
These are often accompanied by findings such as low blood pressure, low blood glucose (N), low sodium (N), high potassium (N), and high calcium(N).

https://www.ncbi.nlm...pubmed/22450350
Escitalopram-induced subclinical hypothyroidism. A case report.

https://www.ncbi.nlm...pubmed/20851281
Reversible escitalopram-induced hypothyroidism.

https://www.ncbi.nlm...pubmed/17874352
Reversible paroxetine-induced symptomatic hypothyroidism.

https://www.ncbi.nlm...pubmed/11054982
Depressed patients should be screened for hypothyroidism. In hypothyroid patients, depression may be more responsive to a replacement regimen that includes T3 rather than T4 alone. Therefore, inclusion of T3 in the treatment regimen may be warranted after adequate trial with T4 alone.

https://www.ncbi.nlm.../pubmed/7779834
Effects of long term treatment with sertraline (Zoloft) simulating hypothyroidism in an adolescent.

And many more articles.

ssri/snri replacement is a viable option.

https://www.drugs.com/pro/effexor.html
Side effects
"Endocrine system—Rare: goiter, hyperthyroidism, hypothyroidism, thyroid nodule, thyroiditis."

https://dailymed.nlm...54-00144ff88e88
The same is mentioned in the section on 'adverse reactions' in the drug insert for Effexor.


http://www.ehealthme...hypothyroidism/
65,121 people reported to have side effects when taking Effexor.
Among them, 420 people (0.64%) have Hypothyroidism

http://www.ehealthme...hypothyroidism/
An FDA supported website.
84,701 people reported to have side effects when taking Cymbalta.
Among them, 292 people (0.34%) have Hypothyroidism

https://dailymed.nlm...f2-c185fbad64ba
Drug insert. (Cymbalta)
Endocrine Disorders — Infrequent: hypothyroidism.

-------------------------------------------------------------------------------------------------------
Tinnitus
Partial list of entries on this site referring to tinnitus.
You will see a pattern, the faster the withdrawal the worse the tinnitus and the longer lasting the occurrence. It also seems to be more common in those on the generic form.

Medical journal info to follow.

Bee 11/29/11
I have been on Cymbalta for 6+ years, also taking 60mg 2x day. I have constant tinnitus.

Marcia 1/24/12
On my journey I am a few days off cymbalta and have the brain zaps, inc tinnitus, aches and pains, chills.

Marcia 1/26/12
Not 10 minutes go by without brain zaps of varying degrees as well as severe tinnitus. At times its just the usual ocean sound, but at times it is a whooshing, pulsating pressure feeling/sound that is very disconcerting.

Jenni 1/26/12 (during withdrawal)
My osteopath found that my neck was very seized up which doesn't help with neck/head/sinus/ear pain and tinnitus. All my symptoms felt better after my appt including the whooshing noise. Maybe a back massage or even just lying in a hot, shallow bath.

BuzzBuzz 3/23/13 (during withdrawal)
The brain zaps and tinnitus are pretty bad,...

SusanMoore 3/28/13 (during withdrawal)
I have also developed what I now know as Tinnitus and this I am told, does not go away.

Answer from lady Nancy
Don't worry Susan the Tinnitus does go away, it takes awhile but it will go away

THP 3/30/13 (during withdrawal)
I started at 60 mg per day and tried to go to every other day which was a nightmare. Severe tinnitus, nausea, emotions, etc.

Lady Nancy 4/16/13 and many many other times. An excert from section 5.7 of the drug insert for Cymbalta.
"During marketing of other SSRIs and SNRIs (serotonin and norepinephrine reuptake inhibitors), there have been
spontaneous reports of adverse events occurring upon discontinuation of these drugs, particularly when abrupt, including
the following: dysphoric mood, irritability, agitation, dizziness, sensory disturbances (e.g., paresthesias such as electric
shock sensations), anxiety, confusion, headache, lethargy, emotional lability, insomnia, hypomania, tinnitus, and seizures.
Although these events are generally self-limiting, some have been reported to be severe."

Fishinghat 4/17/13 Posted full excert.
5.7 Discontinuation of Treatment with Cymbalta
Discontinuation symptoms have been systematically evaluated in patients taking duloxetine. Following abrupt or tapered discontinuation in placebo-controlled clinical trials, the following symptoms occurred at 1% or greater and at a significantly higher rate in duloxetine-treated patients compared to those discontinuing from placebo: dizziness, headache, nausea, diarrhea, paresthesia, irritability, vomiting, insomnia, anxiety, hyperhidrosis, and fatigue. During marketing of other SSRIs and SNRIs (serotonin and norepinephrine reuptake inhibitors), there have been spontaneous reports of adverse events occurring upon discontinuation of these drugs, particularly when abrupt, including the following: dysphoric mood, irritability, agitation, dizziness, sensory disturbances (e.g., paresthesias such as electric shock sensations), anxiety, confusion, headache, lethargy, emotional lability, insomnia, hypomania, tinnitus, and seizures.
Although these events are generally self-limiting, some have been reported to be severe.
Patients should be monitored for these symptoms when discontinuing treatment with Cymbalta. A gradual reduction in the dose rather than abrupt cessation is recommended whenever possible. If intolerable symptoms occur following a decrease in the dose or upon discontinuation of treatment, then resuming the previously prescribed dose maybe considered. Subsequently, the physician may continue decreasing the dose but at a more gradual rate [see Dosage and Administration (2.4)].

Zappinist 5/19/13 during withdrawal
No tinnitus right now, which has been bad recently, but zaps are still there.

Tomitsu 6/11/13 dw
I do have tinnitus and I get the odd brain zap here and there.

Dogs Rule 7/2/13 7 weeks off
This withdrawal will not stop. The really hideous days of zaps and sweating and nausea are over, but lingering symptoms remain: dizziness, tinnitus, and milder zaps.

Irish Eyes 3/21/13
I quit taking Cymbalta in June 2012. I had brain zaps, impaired mental processing, the swishing sound when you move your eyes side to side and tinnitus.
By the end of August I felt almost normal. Then my left foot started tingling. Then in October I got tinnitus.
Last week I start having the swishing sound when I move my eyes back and forth but just when I first wake up.
It's been 9 months and I'm having some of the same symptoms I had in July. Anybody else out there experiencing this?

Afg1202 10/4/13
And this tuning-fork-in-my-head feeling is horrible. And there is so little literature on what helps tinnitus

Thismoment 1/5/14
I might describe my own withdrawal experience like this- bead counting from 30 mg over 6 weeks @ 2.3%.
Difficult// weeks 1-2 smooth/ weeks 3-6 coarse/ weeks 7-12 medium/ weeks 13-24 fine + some medium/ weeks 25-48 fine/ weeks 49-52 smooth/ weeks 53-68 smooth and still improving subtly. I still have two symptoms that are probably permanent- a continuous tension-type headache and tinnitus in my right ear.

Thismoment 1/7/14
My last Cymbalta bead was the end of July 2012, which is getting close to a year and a half now. I still have two symptoms I didn't have before I started the drug. I have a constant headache, and tinnitus in my right ear. Both are tolerable, and I consider myself lucky because after 2 years on the drug I was fried...

FiveNotions 2/18/14
I've had severe tinnitus thanks to cymbalta....it had been so bad that I cldnt hear people talking directly to me...now it's faded a bit, and I have periods of time where it's almost gone...last week I was able to hear my kitchen clock tick! Today, it's bad, like a jet engine in my head...I've had it so long, years, that I've trained myself not to notice it....

Clara 2/26/14
I wish I had a cure for this constant tinnitus. It drives me nuts at times. Just another Cymbalta gift that refuses to go away!

BelaLugosisDad 3/5/14
Tinnitus. - non stop in both ears.

ThisMoment 3/14/14

I've been off Cymbalta for nearly 20 months, and I think I'm probably 95% back; I'm still a little achy in my muscles, I have tinnitus in my right ear, and I have a constant (24/7) tension-type headache that no NSAID will touch. These items are probably chronic, but I'll report back when I hit the 2 year mark this summer.

ThisMoment 3/23/14

Currently at 95%+ function with a few residual withdrawal artifacts: tinnitus, chronic headache, low dopamine. I am back to "normal", but I have a palpable 'different' feeling of myself compared to before I started this adventure, but that was 4 years ago and certainly the passage of time alone has an effect

ThisMoment 4/3/14

I have a constant headache, tinnitus, and fatigue. My level of depression is about the same as when I started Cymbalta.

Phillyguy1 4/24/14
....being off in that 8-10 week window. I pretty much went off cold turkey. I've experienced similar with good and bad days. My biggest issue has been acute vertigo and tinnitus in my right ear. Some days it's been better than others for sure.

Sodone61 4/24/14 Off 5 weeks
No more paresthesia and headaches and the tinnitus (both ears, bad) is gone.

FiveNotions 4/24/14
Tinnitus...I hadn't thought about it in weeks....which meant I haven't had much of it (cymbalta gave it to me big time)....then, just this afternoon, kaboom....it's back, and with a vengeance....sounds like I've got a toilet flushing, sink running, and crickets chirping simultaneously inside my head....when I had it all the time I learned to ignore it....then, when it went away, I was astonished at being able to hear clocks tick and birds sing....now it's driving me nuts because Ive forgotten how to ignore it....it's gonna keep me awake tonight for sure....

Xman 4/25/14
Mine is much better, although I still have it in my right ear intermittently. I am intrigued that there is a pattern forming regarding the right ear tinnitus...
My tinnitus started during crapalta. Never had it before and have no inner ear problems whatsoever. My right ears--
Hickupp 5/8/14
Sorry Clara but at least for me it has never gone away and I've been off for several years. It doesn't happen every day but it still happens.
Clara 6/18/14 6 to 8 months off.
FINALLY coming alive again! And the tinnitus seems to have mostly GONE AWAY!!!!! So grateful about that!!!!
Xman 5/25/14
Thankfully. Also the buzzing in my ears and tinnitus like noise is less in severity. I am a little over 3 months post crapalta.

ThisMoment 5/5/14
After 42 days of tapering off by bead-counting, I swallowed my last bead on July 31, 2012. That was 22 months ago (approximately 660 days)!
I have two lingering side-effects that are probably permanent-- tinnitus in my right ear, and a constant (24/7) tension-type headache that I've had since i began the withdrawal more than two years ago

Must read...
http://www.cymbaltaw...om/?hl=tinnitus

Downtongirl 6/29/14 dw
Lots of ear pressure, pain, and the already existing tinnitus that I have developed from benzo tolerance/withdrawal was worse.
Downtongirl 7/3/14 dw
I developed tinnitus/hyperacusis last summer from what I believe to be tolerance withdrawals from klonopin but this Cymbalta makes it much worse. Anyone else experience this?
FiveNotions
As for the tinnitus, oh yeah, that was one of my long lasting effects....it got much much worse during the first weeks of withdrawal...then it almost disappeared, and I got all excited because I could hear my kitchen clock ticking....never knew it did that!....but then it came back.....it's faded a bit, and comes and goes....
MichB 7/7/14 dw
Oh yes! I have tinnitus too. If there is other noise around me it's not so bad but I can still hear it. Anytime it's quiet it sounds like an attack of locusts!! It's irritating but sadly I'm used to it. If its one of the few lasting permanent effects from getting off this poison I'll be fine.
Gail 7/21/14 5 months off
Tinnitus, which I can tolerate and on and off headaches that I can handle.

brzghoff 7/30/14 11 weeks off
For me getting off C has been rough, for the first month and a half or so it was a lot of physical stuff, joint and muscle pain - lots - serious gastro issues, nausea, the runs, etc, confusion, tinnitus.

Guest_Notsureaboutit_* 8/2/14 1 week off
Ears Whirring, Like A I Have A Helicopter In Them.

Response by Donewithcrap 8/2/14 Off
I have ringing in both ears and have had this for years now. I gets worse at tines but never goes away. I have tried "Ring Stop" but it didn't help me.

Response by ShadyLady 8/3/14 Off
I had the 'whirring swooshies' (great description!) for about 3 weeks after stopping the C-dope!

Pheobster 8/3/14 dw
Tinnitus has set in. Not super loud but enough to be another irritant.

tomitsu 9/2/14 off
I have anxiety and depression I didn't have before taking cymbalta. I have tinnitus and suicidal ideation is a reality. I have memory loss. I believe my symptoms are permanent as they have not gone away. I'm deeply disturbed by the symptoms.

nerdluvin 10/13/14 3 days off
For the past couple of weeks, I get intense migraine-level headaches (no brain zaps) and tinnitus in my ears.

FiveNotions 10/13/14 Off 10 months
I had tinnitus ... actually, after 10 months off, I still have it ... think it's permanent, due to the cold turkey

Thread Titile - Off Crapalta 6 Mos. Or More - What Symptoms Do You Still Have? 10/15/14
FiveNotions - 8 months off - The tinnitus returned several months ago, and is even louder and more constant than ever.
Clara - Tinnitus comes and goes, much less intense.
Gail - 8 mths - Tinnitus

Thisbetterpass 10/17/14
Looking back, I did start having problems with tinnitus when they switched me over to generic probably about two years ago.

Downtongirl 11/20/14 Off
I have developed tinnitus about 1 1/2 years ago and don't want to take anything to make that worse and nsaids are listing as being ototoxic...

FiveNotions 12/6/14 1 yr off
I am (so far) left with some apparently long-lasting after effects ... severe tinnitus,....

Shouldclean 3/31/15 3 mths off
Over a years time I weaned from 60 mg to 0. I was due to finish the end of January and was weighing the microscopic beads of 20 mg pills. I was in so much muscle pain that my husband suggested I go cold turkey, which I did on Christmas Day. My pain almost immediately was cut by 75%. I also had dizziness and tinnitus.

Sfava987 6/18/15
But after stopping the 20mg, I had the full blown discontinuation syndrome and could not drive or function. So, I went back on the 20mg and stayed there for a couple months, but the Tinnitus and some brain fog remained along with burning pain in my heels and the bottom of my feet.

ThisMoment 8/1/15 3 years off
I still have short-lived events that feel like ripples of withdrawal, and I still have a few symptoms that continue to fade: tinnitus, headache, unsteady balance, and GI instability

Things that list tinitus as a common symptom during dicontinuation;
Benzos
Coffee
Alcohol
Opium
SSRI
SNRI
Bath Salts
Dilantin and more...

Seven complete articles on treating tinitus.
Each link is followed by the title of the article in bold.
Articles concerning rTMS have the word "note" in front of the title.

https://www.ncbi.nlm...les/PMC4637057/
Note - Efficacy and Safety of Repeated Courses of rTMS Treatment in Patients with Chronic Subjective Tinnitus.
"Repeated application of rTMS seems to be useful in tinnitus management and should preferentially be offered to patients who experience a worsening of their tinnitus during the intertreatment interval, irrespective of their response to the first treatment course."

https://www.ncbi.nlm...les/PMC4678896/
Note - Combined rTMS treatment targeting the Anterior Cingulate and the Temporal Cortex for the Treatment of Chronic Tinnitus.
"This pilot study demonstrated the feasibility of combined mediofrontal/temporoparietal-rTMS-stimulation with double cone coil in tinnitus patients but failed to show better outcome compared to an actively rTMS treated control group."

https://www.ncbi.nlm...les/PMC4772792/
Note- Triple-site rTMS for the treatment of chronic tinnitus: a randomized controlled trial.
"We report a tendency towards a modest, sustained long-term effect of the triple-site stimulation protocol in comparison to the single-site protocol."
Table 2
Adverse events for both treatment groups.
single-site rTMS triple-site rTMS
transient adverse events
muscular tension 1 -
headache 6 3
blurred vision 1 -
increase in tinnitus loudness 3 -
mood swings 1 -
dizziness - 1
feeling of heaviness in the legs - 1
ongoing adverse events
increase in tinnitus loudness 3* -
broadening of the frequency range of the tinnitus - 1
/pmc/articles/PMC4772792/table/t2/?report=objectonly
*One of those three patients dropped out after two days of treatment.

https://www.ncbi.nlm...les/PMC2832848/
Emerging pharmacotherapy of tinnitus
Summary og medicines used for tinitus.

https://www.ncbi.nlm...les/PMC3563643/
Note - rTMS Induced Tinnitus Relief Is Related to an Increase in Auditory Cortical Alpha Activity
"Several studies indeed show tinnitus relief after rTMS, however effects are moderate and vary strongly across patients."

https://www.ncbi.nlm...les/PMC3227628/
Treatment options for subjective tinnitus: Self reports from a sample of general practitioners and ENT physicians within Europe and the USA
"A structured online questionnaire was conducted with 712 physicians who reported seeing at least one tinnitus patients in the previous three months. They were 370 general practitioners (GPs) and 365 ear-nose-throat specialists (ENTs) from the US, Germany, UK, France, Italy and Spain."
"Despite a large variety of treatment options, the low success rates of tinnitus therapy lead to frustration of physicians and patients alike. For subjective tinnitus in particular, effective therapeutic options with guidelines about key diagnostic criteria are urgently needed."

https://www.ncbi.nlm...les/PMC4761664/
Sensorineural Tinnitus: Its Pathology and Probable Therapies
"The most common form of treatment of tinnitus is pharmacological agents and behavioral treatment combined with sound therapy. Less common treatments are hypnosis and acupuncture. Various forms of neuromodulation are becoming in use in an attempt to reverse maladaptive plastic changes in the brain."

Summaries of articles on treating tinitis.

https://www.ncbi.nlm...pubmed/26960786
Therapeutic role of Vitamin B12 in patients of chronic tinnitus: A pilot study.
"This pilot study highlights the significant prevalence of Vitamin B12 deficiency in North Indian population and improvement in tinnitus severity scores and VAS in cobalamin-deficient patients receiving intramuscular Vitamin B12 weekly for 6 weeks further provides a link between cobalamin deficiency and tinnitus thereby suggestive of a therapeutic role of B12 in cobalamin-deficient patients of tinnitus. "
http://www.ncbi.nlm..../pubmed/8484483
Vitamin B12 deficiency in patients with chronic-tinnitus and noise-induced hearing loss.
"These observations suggest a relationship between vitamin B12 deficiency and dysfunction of the auditory pathway. Some improvement in tinnitus and associated complaints were observed in 12 patients following vitamin B12 replacement therapy. The authors recommend that routine vitamin B12 serum levels be determined when evaluating patients for chronic tinnitus."
https://www.ncbi.nlm...les/PMC3645155/
The Role of Plasma Melatonin and Vitamins C and B12 in the Development of Idiopathic Tinnitus in the Elderly
"Comparing the plasma levels of the markers between elderly with and those without tinnitus, the plasma levels of melatonin (p=0.01) and vitamin B12 (p=0.03) were significantly lower among the elderly with tinnitus compared to those without, while the difference in the plasma level of vitamin C (p=0.6) was not.)
https://www.ncbi.nlm...les/PMC4765244/
Tinnitus: Is there a place for brain stimulation?
Nothing "to support or discourage the application of brain stimulation in tinnitus."

https://www.ncbi.nlm...pubmed/26938213
Electroacupuncture for Tinnitus: A Systematic Review.
"Due to the poor methodological quality of the primary studies and the small sample sizes, no convincing evidence that electroacupuncture is beneficial for treating tinnitus could be found. "

https://www.ncbi.nlm...pubmed/26910854
Randomized Controlled Trial of a Perceptual Training Game for Tinnitus Therapy
"The results suggest that the attention training game may have reduced focus on the tinnitus, potentially through improved selective attention. "Terrain" was superior to "Tetris" in the population tested and therefore shows promise as a management option for tinnitus. Further testing in a larger, more general, population would be enabled through improving the game's accessibility."

https://www.ncbi.nlm...pubmed/26901425
Cortical Reorganisation during a 30-Week Tinnitus Treatment Program.

https://www.ncbi.nlm...pubmed/26890094
Neuronavigated left temporal continuous theta burst stimulation in chronic tinnitus.
"In our study, verum cTBS was not superior to sham which highlights the persistent need for improving non-invasive brain stimulation techniques for the treatment of tinnitus."

https://www.ncbi.nlm...pubmed/26868680
Maladaptive plasticity in tinnitus - triggers, mechanisms and treatment
"Maladaptive neural plasticity seems to underlie these changes: it results in increased spontaneous firing rates and synchrony among neurons in central auditory structures, possibly generating the phantom percept. This Review highlights the links between animal and human studies, and discusses several therapeutic approaches that have been developed to target the neuroplastic changes underlying tinnitus."

https://www.ncbi.nlm...pubmed/26867083
Internet-Delivered Cognitive-Behavior Therapy for Tinnitus: A Randomized Controlled Trial
"Using a randomized controlled trial design, we replicated prior findings regarding positive effects of Internet-delivered CBT on tinnitus-related distress and associated symptoms."

https://www.ncbi.nlm...pubmed/26817797
Note -Long-Term Distributed Repetitive Transcranial Magnetic Stimulation for Tinnitus: A Feasibility Study.
"Our study demonstrated that rTMS can be delivered in a distributed schedule that is well-tolerated, feasible and may prove to be clinically beneficial. A long-term distributed rTMS schedule for tinnitus may warrant investigation as an alternative to the short-term aggregated treatment schedules more frequently used previously. For the many varied therapeutic uses of rTMS (established and investigational), treatment schedules are relatively unexplored, and deserve further attention."

https://www.ncbi.nlm...pubmed/26790209
[Deep needling and shallow needling at three acupoints around ear for subjective tinnitus: a randomized controlled trial].
"Acupuncture at the three acupoints around ear deeply could apparently improve tinnitus, and reduce tinnitus sound levels for subjective tinnitus. The effect is better than that by shallow needling at the three acupoints."

https://www.ncbi.nlm...pubmed/26773752
Auditory and visual 3D virtual reality therapy as a new treatment for chronic subjective tinnitus: Results of a randomized controlled trial.
"Virtual Reality appears to be at least as effective as CBT in unilateral subjective tinitus patients."

https://www.ncbi.nlm...pubmed/26771015
Feasibility and Safety of Transcutaneous Vagus Nerve Stimulation Paired with Notched Music Therapy for the Treatment of Chronic Tinnitus.
"After 10 treatment sessions, 15/30 patients (50%) reported symptom relief."
"This study has demonstrated the feasibility and safety of tVNS paired with notched music therapy in patients with chronic tinnitus, with the use of a pad-type electrode attached to the auricular concha."

https://www.ncbi.nlm...pubmed/26747828
Tinnitus and its current treatment-Still an enigma in medicine.
"As yet, there are no Food and Drug Administration approved drugs available and the quest for a new treatment option for tinnitus focus on important challenges in tinnitus management. A number of options have been used to treat patients with tinnitus, but outcomes have been limited."

https://www.ncbi.nlm...pubmed/26649534
Clinician-Supported Internet-Delivered Psychological Treatment of Tinnitus
"For the 6 studies comparing Internet treatment against a no-treatment control condition, a moderate effect size was found (Hedges's g = 0.58). The 3 studies comparing Internet treatment against face-to-face group treatments showed a small difference."

https://www.ncbi.nlm...pubmed/26632254
The efficacy of individual treatment of subjective tinnitus with cognitive behavioural therapy.

https://www.ncbi.nlm...pubmed/26619701
[Therapeutic perspectives in the treatment of chronic subjective tinnitus].
"There are no effective therapies for the treatment of chronic subjective tinnitus. The present study aims to compare two therapeutic approaches: Tinnitus Retraining Therapy (TRT) and a Biopsychosocial Approach (BPS). Results show no difference in evolution of tinnitus' perception between the beginning of the study and after 12 months of treatment in both treatment groups."
https://www.ncbi.nlm...pubmed/26609769
Potassium channels as promising new targets for pharmacologic treatment of tinnitus: Can Internet-based 'crowd sensing' initiated by patients speed up the transition from bench to bedside?

https://www.ncbi.nlm...pubmed/26557055
Note - Repetitive transcranial magnetic stimulation induces oscillatory power changes in chronic tinnitus.
"This is the first study to show tinnitus-related alterations of neuroplasticity that were specific to stimulation site and oscillatory frequency."
"Moreover our findings confirm the role of the left temporal and the right frontal areas as relevant hubs in tinnitus related neuronal network. Our results underscore the value of combined TMS-EEG measurements for investigating disease related changes in neuroplasticity."

https://www.ncbi.nlm...pubmed/26547700
Antioxidant therapy in the elderly with tinnitus.
Prospective, randomized, double-blinded, placebo-controlled clinical trial. The sample consisted of 58 subjects aged 60 years or older, with a complaint of tinnitus associated with sensorineural hearing loss. The treatment regimens were: Ginkgo biloba dry extract (120mg/day), α-lipoic acid (60mg/day)+vitamin C (600mg/day), papaverine hydrochloride (100mg/day)+vitamin E (400mg/day), and placebo.There was no benefit from the use of antioxidant agents for tinnitus in this sample.
https://www.ncbi.nlm...pubmed/26541232
Effectiveness of sound therapy in patients with tinnitus resistant to previous treatments: importance of adjustments.
"There was improvement in quality of life (Tinnitus Handicap Inventory), with good response to sound therapy using customized settings in patients who did not respond to previous treatments for tinnitus."

https://www.ncbi.nlm...pubmed/26498289
Repeated sessions of transcranial direct current stimulation for treatment of chronic subjective tinnitus: a pilot randomized controlled trial.
"No statistically significant difference was found between anodal and sham stimulation regarding either immediate or long-lasting effects over the 2 weeks follow-up period. Deterioration of symptoms and alteration in tinnitus characteristics were reported by a few patients. There were no significant long-term beneficial effects following tDCS of the left temporoparietal area. "

https://www.ncbi.nlm...pubmed/26467416
The Management and Outcomes of Pharmacological Treatments for Tinnitus.
Table 1.
Pharmaceutical treatment effects on tinnitus.
Drugs Authors Subjects Placebo Controlled Dosage Results Side Effects
Lidocaine Melding,
et al. (1978) 78 Open-label 1-2 mg per kg of body weight intravenously for 3-4 minutes Highly effective in patients with Organ of Corti damage None
Nortriptyline Sullivan
et al. (1989) 19 Placebo-washout Maximum 50 to 150 mg per day Tinnitus loudness and severity decreased Dry mouth, dyspepsia, constipation, orthostatic hypotension
Sullivan
et al. (1993) 92 Placebo controlled 50 to 150 mg/mL for six weeks Depression and tinnitus loudness decreased Anticholinergic side effects, sedation
Amitriptyline Podoshin
et al. (1995) 218 Placebo controlled 10 mg 3x/day for 10 weeks Improvement in more than 40% Sedation
Bayar et al. (2001) 37 Placebo controlled 50 to 100 mg daily for six weeks Decreased tinnitusintensity and subjective relief Sedation, dryness of mouth
Mendis
et al. (2008) 1 Case study 10 mg for three days Neurologic foot pain resolved Tinnitus
Imipramine Tandon
et al. (1987) 475 Chart review 150 to 250 mg per day Depression improved Tinnitus
Evans et al. (1981) 1 Case study 15 to 45 mg per day No improvement in depression Tinnitus
Sertraline Zoger et al. (2006) 76 Placebo controlled 25 to 50 mg daily for 16 weeks Improved loudness, severity Sexual side effects
Paroxetine Robinson
et al. (2005) 115 Placebo controlled Maximum of 50 mg per day for 100 days No better than placebo Sexual dysfunction, drowsiness,
dry mouth, sweating,
insomnia, gastrointestinal distress, tremor, headache
Alprazolam Johnson
et al. (1993) 36 Placebo controlled 0.25 or 0.5 mg for one week, increased to maximum of 1.0 mg for some for 56 days Reduction in loudness Excessive drowsiness; more dreams
Jalali et al. (2009) 36 Placebo controlled 0.5 mg 1-3 times per day for 8 weeks No improvement None
Clonazepam
Ginkgo biloba Han et al. 2012) 38 Open-label 0.5 mg Clonazepam; 4.0 mg GB increased from 1 to 4 doses per day for 5 weeks Clonazepam more effective than GB; tinnitus annoyance, duration, and loudness decreased Drowsiness
Gabapentin Bauer et al. (2006) 39 Placebo controlled Maximum 2,400 mg for 20 weeks Decrease in annoyance Dizziness, fatigue
Witsell et al. (2006) 76 Placebo controlled 1800 mg daily for five weeks No significant difference Mouth sores, decreased libido
Amino-oxyacetic Acid Reed et al. (1985) 10 Placebo controlled 50 to 75 mg four times a day for one week Subjective lessening of tinnitus in 3/10 Worsening of tinnitus upon withdrawal; dizziness, lightheadedness, disequilibrium, nausea, and headache at higher doses (400 mg/day)
Lamotrigine Simpson
et al. (1999) 31 Placebo controlled 25 to 100 mg daily for 8 weeks No significant difference Nausea, vomiting, headache
Carbamazepine Donalson I (1981) 62 Placebo controlled 100 mg No significant difference Tinnitus returned rapidly post-injection
Memantine Figueiredo
et al. (2008) 43 Placebo controlled 5 to 10 mg 1-2 times per day for 90 days No significant difference Dizziness, high blood pressure, insomnia, stomachache
Flupirtine Salembier
et al. (2006) 24 Open-label 100 mg twice a day for three weeks No significant difference Amnesia and concentration disorders
Neremexane Suckfull et al (2011) 320 Placebo controlled 25 to 75 mg daily for 16 weeks Decreased annoyance and impact on life at higher dosage Dizziness, headache, vertigo, fatigue, hypertension
Acamprosate Azevedo et al. (2007)
Sharma et al. (2012) 50

40 Placebo controlled
Placebo controlled 333 mg 3x daily for
three months
333 mg TDS 3x daily
for 45 days Improvement
over placebo
Significant improvement over placebo Epigastralgia, choking

Worsening intensity
(2 participants)
Cyclobenzaprine Coelho at al. (2011) 49 open-label max high dose: 30 mg; max low dose: 10 mg high dosage saw a reduction in THI dry mouth, sleepiness, constipation
Vanneste et al. (2013) 95 open-label 10 mg 2x/day for 4 weeks reduction in distress and intensity worsening intensity
Naltrexone Vanneste et al. (2013) 106 open-label up to 50 mg for four weeks tinnitus distress reduced in some none
Deanxit Meeus et al. (2011) 28 placebo-controlled 1 mg per day for three weeks 3/28 report tinnitus improvement none
Betahistine Sonmez et al. (2013) 68 placebo-controlled 48 mg per day for three months slight improvement in loudness and on THI pyrosis, nausea
Pramipexole Sziklai et al. (2011) 40 placebo-controlled maximum dosage: 0.7 mg 3x/day for 4 weeks 35% of pramipexole group improved dizziness, allergic reactions
Piribedil De Azevedo
et al. (2009) 56 Placebo-controlled 50mg daily No difference from placebo Nausea, dizziness
Simvastatin Canis et al. (2011) 94 placebo-controlled 40 mg/day for 4 months reported improvement but not significant worsening tinnitus
Vitamin B12 Berkiten et al. (2013) 83 placebo-controlled 1 g/mL injected daily for 5 days, then once a month for 12 months no significant change N/A
Zinc Coelho et al. (2013) 89 placebo-controlled 220 mg zinc sulphate daily for 4 months no significant change indigestion

https://www.ncbi.nlm...pubmed/26459345
Slow Cortical Potential Neurofeedback in Chronic Tinnitus Therapy: A Case Report.
https://www.ncbi.nlm...pubmed/26433054
Cannabinoids, cannabinoid receptors and tinnitus.
https://www.ncbi.nlm...pubmed/26430749
Note - A Pilot Study of EEG Source Analysis Based Repetitive Transcranial Magnetic Stimulation for the Treatment of Tinnitus.
"Low-frequency rTMS decreased tinnitus significantly after active, but not sham, treatment. Responders in the EEG source analysis-based rTMS group, 71.4% (5/7) patients, experienced a significant reduction in tinnitus loudness, as evidenced by VAS scores. The target site of neuronal generators most consistently associated with a positive response was the frontal lobe in the right hemisphere, sourced using high-density EEG equipment, in the tinnitus patients. After left temporoparietal rTMS stimulation, 42.8% (3/7) patients experienced a decrease in tinnitus loudness."

https://www.ncbi.nlm...pubmed/26422238
The effect of noninvasive brain stimulation on neural connectivity in Tinnitus: A randomized trial.
"Sixteen patients received active rTMS treatment; 14 patients received sham treatment. There were no differences between the active and sham groups in baseline functional connectivity. Neither treatment with rTMS nor sham therapy resulted in statistically significant functional connectivity changes in the examined brain networks."

https://www.ncbi.nlm...pubmed/26413574
The Effect of Korean Red Ginseng on Symptoms and Quality of Life in Chronic Tinnitus: A Randomized, Open-Label Pilot Study.
"Fifty-nine patients completed the planned protocol. Significant improvements were observed between initial and post-treatment THI scores in patients receiving 3000 mg/day KRG. Treatment with 3000 mg/day KRG for 4 weeks significantly improved role emotional and mental health scores in the SF-36 survey.These results suggest that KRG may improve tinnitus symptoms and mental wellbeing in chronic tinnitus patients."

https://www.ncbi.nlm...pubmed/26406286
An evaluation of the Reltus ear massager for short-term tinnitus relief.
'Supression of tinitus loadmess to auditory stimulation was found in 87% of participants and to tactile stimulation in 83%. No significant differences were found in the effectiveness between the four vibration stimulation points, or between the left and right ear of the participants. The Reltus produced a sound that resulted supression of tinitus.'
"It is the auditory artifact of the Reltus that was responsible for short-term tinnitus suppression."
This device rates a 2.5 out od 5 stars on Amazon.
https://www.ncbi.nlm...pubmed/26388055
The Development of Acceptance of Chronic Tinnitus in the Course of a Cognitive-Behavioral Group Therapy.
"CBT is considered an effective treatment for tinnitus distress in patients with chronic tinnitus. Acceptance of chronic tinnitus clearly improved within a CBT group therapy."

https://www.ncbi.nlm...pubmed/26261868
Treatment of tinnitus.

https://www.ncbi.nlm...pubmed/26248783
The effectiveness of psychological interventions among tinnitus sufferers: A review.
"Psychological interventions were more effective in reducing psychological impacts of tinnitus than non-psychological interventions such as the use of tinnitus maskers. Nevertheless, the combination of the treatments yielded more superior outcomes."

http://www.cymbaltaw...lped#entry71820
and
http://www.cymbaltaw...elps#entry65067
Research and treatments for tinnitus.
http://www.cymbaltaw...rove#entry72117
Information on tinnitus.
---------------------------------------------------------------------------------------------------------
Restless Leg Syndrome
(Synopsis from PubMed)
Causes
Research and brain autopsies have implicated both dopaminergic system and iron insufficiency in the The substantia nigra plays an important role in reward, addiction, and movement and is composed of dopaminergic neurons. This area is one of the primary areas for the production of dopamine. Iron is an essential cofactor for the formation of L-dopa, the precursor of dopamine and adrenaline.
Magnesium deficiency.
Magnesium deficiency showed important disorders of sleep organization, agitated sleep with frequent periods of nocturnal awakenings, increase of the durations and percentages of light sleep, a decrease of duration and percentage of deep sleep, a decrease of duration and percentage of REM sleep caused by magnesium deficiency with the disappearance in the REM sleep in some.

Iron Deficiency
The most commonly associated medical condition is iron deficiency (specifically blood ferritin below 50 µg/L), which accounts for just over 20% of all cases of RLS. Normal blood levels are 30-300 ng/mL for males and 15-200 ng/mL for females. Studies using cerebrospinal fluid, magnetic resonance imaging, ultrasound determination of iron and autopsy tissue have implicated a primary role for brain (substantia nigra) iron insufficiency in restless legs syndrome (RLS). Ferritin can deliver iron to multiple organs, including the brain. The data clearly show changes in iron status affect dopaminergic activity. The proposed etiology of RLS is the central dopaminergic dysfunction, based on the benefits of dopamine agonists and exacerbation of RLS symptoms by dopaminergic antagonists.

Iron is most available to the body when chelated to amino acids - iron in this form is ten to fifteen times more bioavailable than any other, and is also available for use as a common iron supplement. Often the amino acid chosen for this purpose is the cheapest and most common amino acid, glycine, leading to "iron glycinate" supplements. RDA for iron varies considerably based on age, gender, and source of dietary iron (heme-based iron has higher bioavailability).
Iron uptake is tightly regulated by the human body, which has no regulated physiological means of excreting iron. Only small amounts of iron are lost daily due to mucosal and skin epithelial cell sloughing, so control of iron levels is mostly by regulating uptake.[33] Regulation of iron uptake is impaired in some people as a result of a genetic defect that maps to the HLA-H gene region on chromosome 6. In these people, excessive iron intake can result in iron overload disorders, such as hemochromatosis. Many people have a genetic susceptibility to iron overload without realizing it or being aware of a family history of the problem. For this reason, it is advised that people do not take iron supplements unless they suffer from iron deficiency and have consulted a doctor. Hemochromatosis is estimated to cause disease in between 0.3 and 0.8% of Caucasians.[34]

Certain medications may worsen RLS in those who already have it, or cause it secondarily. These include: any antidepressants (SSRIs).
Genetics
More than 60% of cases of RLS are familial and are inherited in an autosomal dominant fashion with variable penetrance.
Six genetic loci found by linkage are currently known and are listed below.
12q,14q, 9p, 20p, 2p and 16p12.1.
Four genes, MEIS1, BTBD9, PTPRD and MAP2K5, were found to be associated to RLS.
Effects
Sleep - For 60%–80% of patients with RLS, sleep disturbance is their most distressing symptom. For example, impact on patients’ daytime cognitive abilities, patients report reduced concentration and attention, increased daytime sleepiness, and mood disturbance. Studies have indicated that the symptoms of RLS precede those of depression or anxiety, and others relate the severity of mood symptoms to the severity of RLS symptoms. For some patients, the effects on mental health may be so pronounced as to reach the diagnostic criteria for major depressive disorder or generalized anxiety disorder

Several studies have shown an association between the symptoms of RLS and worse mental health. The authors concluded that the presence of RLS symptoms “was probably the major determining factor for the anxiety and depression scores, with higher scores correlating with more severe RLS”.

Diagnosis

Serum ferritin levels are measured in patients as part of the iron studies workup for anemia and for restless legs syndrome. The ferritin levels measured have a direct correlation with the total amount of iron stored in the body including cases of anemia of chronic disease.
Normal blood levels are 30-300 ng/mL for males and 15-200 ng/mL for females.
Treatment
Patients with RLS and prominent anxiety symptoms may require treatment with an anxiolytic in addition to dopaminergic therapy for the RLS symptoms. The benzodiazepines have been used in the treatment of RLS. Their efficacy depends mostly on reducing insomnia, rather than managing the motor and sensory symptoms of RLS. These drugs may be useful in the management of RLS and anxiety, though there are concerns about the long-term use of these agents and patients require monitoring for dependency and declining efficacy.
Iron supplements - People with RLS should have their ferritin levels tested; ferritin levels should be at least 50 µg for those with RLS. Oral iron supplements, taken under a doctor's care, can increase ferritin levels. For some people, increasing ferritin will eliminate or reduce RLS symptoms. A ferritin level of 50 µg is not sufficient for some sufferers and increasing the level to 80 µg may greatly reduce symptoms. However, at least 40% of people will not notice any improvement. It is dangerous to take iron supplements without first having ferritin levels tested, as many people with RLS do not have low ferritin and taking iron when it is not called for can cause iron overload disorder, potentially a very dangerous condition.
RDA – 8 mg/day; UL 45 mg/day One used 200 mg ferrous sulfate 3 times per day, which equals 73.5 mg iron 3 times per day or 225 mg/day. An additional study used 7 mg of iron/day. They used iron succinylate or bisglycinate
Clonidine - Patients subjectively reported improvement in leg sensations and motor restlessness while receiving clonidine (0.05 mg/day). Sleep onset occurred faster with clonidine (12 minutes) compared with placebo (30 minutes) and baseline (47 minutes). Adverse findings with clonidine treatment included decreased REM sleep in the clonidine group (4%) compared with placebo (16%) and baseline (16%) and increased REM delay in the clonidine group (195 minutes) compared to the placebo (70 minutes) and baseline groups (89 minutes) There was a nonstatistical trend toward an increase in stage 3 and 4 sleep and a decrease in motor activity. Clonidine may be an effective treatment for RLS patients who don't have large numbers of sleep-disrupting periodic limb movements but have delayed sleep onset due to leg sensations and
An additional double-blind study was conducted in 20 patients with renal failure and symptoms of restless legs. 10 patients were treated with 0.075 mg clonidine twice daily and 10 received placebo. Three days after starting therapy. the clonidine-treated group complete relief of symptoms was noted in 9 out of 10 patients.

Gabapentin - Gabapentin, an analog of gamma-aminobutyric acid, was compared with L-dopa in a small, open-label study involving patients with RLS secondary to renal disease. After 4 weeks, both treatments improved the symptoms of RLS. Gabapentin produced significant improvements compared with baseline on three of the eight SF-36 domains. Gabapentin produced adverse events of malaise (feeling bad) and somnolence (drowsiness); but resulted in no patient withdrawal.

Magnesium/Calcium– RDA 400 mg/day Serum levels should be between .7 and 1 mmoles/L. Studies used 400 – 800 mg/day. (avg. 600 mg/day; 6 tablets) Special note - Amino Acid Magnesium most readily absorbed form of magnesium and most tolerated by the gi tract.
Studies recommend using 600 to 1,000 mg calcium with the magnesium. (800 mg/day avg.; ) RDA 1,000 mg/day, UL 2500 mg/day. The individual must allow for dietary intake. As calcium and magnesium compete in the blood system you should also have your serum calcium and magnesium nmonitored every 6 months.

Magnesium availability different Mg-sources
Mg-source Mg-content % Rel. Biological value % Rel. Available Mg g/kg
Mg-Chloride 12 89 107
Mg-Hydroxide 36 99 356
Mg-Phosphate 26 85 221
Mg-Ca-Phosphate 9 91 82
Mg-Ca-Na Phosphate 5 94 47
Mg-Oxide, granular 51 61 311
Mg-oxide, powder 51 84 428
MG-Sulphate 10 96 96
Source: EMFEMA 2002
Folic Acid – Recommended to be taken, no research to back this. Use folic acid at 4 – 10 mg/day.
http://www.cymbaltaw...rls/#entry72695
Detailed information on Restless Leg Syndrome
----------------------------------------------------------------------------------------------------------
Cymbalta and Pregnancy
http://www.ncbi.nlm....pubmed/23471302
No significant effect on fetus.

http://www.ncbi.nlm....pubmed/21359876
Low amount of cymbalta across placenta and in lactation.

http://www.ncbi.nlm....pubmed/23218163
Text not available.

http://www.ncbi.nlm....pubmed/23873363
No effects on new born health.

http://www.ncbi.nlm....pubmed/19809008
No effect on fetus, newborn at birth or during lactation.

http://www.ncbi.nlm....les/PMC3590601/
List what the negative out comes are.

http://www.ncbi.nlm....pubmed/25171134
Increase risk of club foot with ssri.

http://www.bmj.com/c.../bmj.g4835.long
SSRI increase risk of autism in new borns.

https://www.ncbi.nlm...pubmed/25551238
Little transferred to infant.

Duloxetine withdrawal syndrome in a newborn
http://cpj.sagepub.c...52/10/976.short
Clinical presentation and management of neonatal abstinence syndrome
http://www.dovepress...hp?fileID=19621

Use of selective serotonin reuptake inhibitors during pregnancy
http://contemporaryo...nancy?page=full

Neonatal paroxetine withdrawal syndrome
http://www.ncbi.nlm....les/PMC1721229/
Four term neonates presented with symptoms such as jitteriness and necrotising enterocolitis after paroxetine exposure in utero.

The use of psychotropic medication during pregnancy: how about the newborn?
http://www.ncbi.nlm....les/PMC3770341/

http://www.cymbaltaw...tion#entry40047
Info on Cymbalta and pregnancy
------------------------------------------------------------------------------------------------------------
Cymbalta and the Heart
https://www.ncbi.nlm...pubmed/27130441
Differential inhibition of cardiac and neuronal Na(+) channels by the selective serotonin-norepinephrine reuptake inhibitors duloxetine and venlafaxine.

https://www.ncbi.nlm...pubmed/23666493
"Whereas inhibitory effects of duloxetine seem negligible under therapeutically relevant concentrations, hERG block should be considered in cases of duloxetine overdose and when administering duloxetine to patients susceptible to drug-induced QT prolongation."

https://www.ncbi.nlm...pubmed/23422380
"In conclusion, in healthy adults exposed to DLX (Cymbalta) or ESC, no clinically significant effects on HRV (heart rate variability) were observed."

https://www.ncbi.nlm...pubmed/22163139
Abstract
Takotsubo cardiomyopathy is characterized by transient multisegmental left ventricular dysfunction, dynamic electrocardiographic changes that mimic acute myocardial infarction, and the absence of obstructive coronary disease. Takotsubo cardiomyopathy has been solidly associated with antecedent emotional and physical stressors that trigger catecholamine surges, which lead to coronary vasospasm or direct myocardial injury. Some medications can also cause catecholamine surges, although this phenomenon is not as well described. Duloxetine is a combined serotonin and norepinephrine reuptake inhibitor (SNRI). The basic goal of SNRIs is to increase catecholamine levels in neuronal tissue. However, the increased catecholamine levels may also affect the cardiovascular system.Herein, we report the case of a 59-year-old woman whose takotsubo cardiomyopathy was temporally associated with the titration of duloxetine. The duloxetine therapy was subsequently discontinued, and the patient's left ventricular function recovered completely 1 month after the index event. The purpose of this report is to alert clinicians to a possible association between SNRI medications and takotsubo cardiomyopathy.

https://www.ncbi.nlm...pubmed/18728105
Duloxetine-associated tachycardia
"Clinicians should be aware of the possibility of clinically significant tachycardia in patients receiving duloxetine, even in low doses."

https://www.ncbi.nlm...pubmed/18445706
Heart failure worsening and exacerbation after venlafaxine and duloxetine therapy.
"Use of drugs that increase serum norepinephrine levels, such as the SNRIs, may be potentially deleterious in individuals with unstable or advanced HF. These medications should be avoided or used with caution and monitored regularly in this patient population."

https://dailymed.nlm...f2-c185fbad64ba
"Cardiac Disorders — Frequent: palpitations; Infrequent: myocardial infarction and tachycardia. "
Post Marketing reports - supraventricular arrhythmia,

http://www.cymbaltaw...tion#entry70794
Information on Heart conditions and Cymbalta
------------------------------------------------------------------------------------------------------------
Cymbalta and High blood pressure

http://dailymed.nlm....?archiveid=1526
This is a document from Eli Lilly that in it it links high BP to Cymbalta.

http://www.nlm.nih.g...ds/a604030.html
Medline plus includes a warning about high BP as well. Medline plus is a service of the Federal government.

http://www.ehealthme...pressure - high
This article is from ehealth. It monitors reported side effects to the FDA and other sites. Over 5% of the users of cymbalta report high bp.

http://www.ncbi.nlm....pubmed/16303903
http://www.ncbi.nlm....les/PMC3661232/
http://www.ncbi.nlm....les/PMC2646646/
http://www.ncbi.nlm....les/PMC3004624/
http://www.ncbi.nlm....les/PMC3437646/
Research articles documenting elevation of bp by Cymbalta.

http://www.fda.gov/d...y/ucm088579.pdf
http://www.accessdat...0/022516lbl.pdf
FDA warns of risk of high blood pressure. Second one includes a black box warning from 2010 on elevated BP.
------------------------------------------------------------------------------------------------------------
Cymbalta's Damages/Effects
Introduction - Cymbalta is a seratonin norepinephrine reupyale inhibitor (SNRI). It is mostly prescribed for major depressive disorder, generalized anxiety disorder, fibromyalgias and neuropathic pain. Duloxetine failed to receive US approval for stress urinary incontinence amid concerns over liver toxicity and suicidal events; however, it was approved for this indication in the UK, where it is recommended as an add-on medication in stress urinary incontinence instead of surgery.
Duloxetine inhibits the reuptake (reuse) of serotonin (5-HT) and norepinephrine (NE) in the central nervous system. Duloxetine increases dopamine (DA) specifically in the prefrontal cortex, where there are few DA reuptake pumps, via the inhibition of NE reuptake pumps (NET) which is believed to mediate reuptake of DA and NE. However, duloxetine has no significant affinity for dopaminergic, cholinergic, histaminergic, opioid, and GABA reuptake transporters and can therefore be considered to be a selective reuptake inhibitor at the 5-HT and NE transporters
Serotonin (5HT) is primarily found in the gastrointestional tract (GI tract), blood platelets, and the central nervous system (CNS). It is popularly thought to be a contributor to feelings of well-being and happiness. Serotonin action is terminated primarily by uptake of 5-HT from the synapse. This is accomplished through the specific monoamine transporter for 5-HT, SERT, on the presynaptic neuron. Various agents can inhibit 5-HT reuptake, including cocaine, dextromethorphan, tricyclic antidepressants, selective seratonin reuptake inhibitors (SSRIs) and seratonin norepinephrine reuptake inhibitors (SNRIs).
Serotonin is released into the space between neurons (synapse) to activate 5-HT receptors located on the dendrites, cell bodies and presynaptic terminals of adjacent neurons.
When humans smell food, dopamine is released to increase the appetite. The serotonin released while consuming activates 5-HT2C receptors on dopamine-producing cells. This halts their dopamine release, and thereby serotonin decreases appetite. Drugs that block 5-HT2C receptors make the body unable to recognize when it is no longer hungry or otherwise in need of nutrients, and are associated with increased weight gain, especially in people with a low number of receptors. ( Cymbalta and weight gain: https://www.ncbi.nlm...pubmed/25467076, https://www.ncbi.nlm...ubmed/24898363, https://www.ncbi.nlm...ubmed/21314871)
The expression of 5-HT2C receptors in the hippocampus follows a diurnal rhythm (24 hour cycles up and down) which is characterised by a peak at morning when the motivation to eat is strongest.

In humans, levels of 5-HT1A receptor activation in the brain show negative correlation with aggression, and a mutation in the gene that codes for the 5-HT2a receptor may double the risk of suicide for those with that genotype. Serotonin in the brain is not usually degraded after use, but is collected by serotonergic neurons by seratonin transporters on their cell surfaces. Studies have revealed nearly 10% of total variance in anxiety-related personality depends on variations in the description of where, when and how many serotonin transporters the neurons should deploy.
In the digestive tract
The gut is surrounded by enterochromaffin cells, which release serotonin in response to food in the digestive system. This makes the gut contract around the food. Platelets in the veins draining the gut collect excess serotonin.
If irritants are present in the food, the enterochromaffin cells release more serotonin to make the gut move faster, i.e., to cause diarrhea, so the gut is emptied of the noxious substance. If serotonin is released in the blood faster than the platelets can absorb it, the level of free serotonin in the blood is increased. This activates 5HT3 receptors in the chemoreceptors trigger zone that stimulate vomiting.
Bone metabolism
Alterations in serotonin levels and signaling have been shown to regulate bone mass. In humans, increased blood serotonin levels have been shown to be a significant negative predictor of low bone density. Serotonin can also be synthesized, at very low levels, in the bone cells. It mediates its actions on bone cells using three different receptors. Through 5-HT1b receptors, it negatively regulates bone mass, while it does so positively through 5-HT2b receptors and 5HT2c. There is very delicate balance between physiological role of gut serotonin and its pathology. Increase in the extracellular content of serotonin results in a complex relay of signals in the osteoblasts (bone cells) culminating in FoxO1/ Creb and ATF4 dependent transcriptional events. These studies have opened a new area of research in bone metabolism that can be potentially harnessed to treat bone mass disorders. No research has been done on the effects of Cymbalta on bone mass.
Organ development
Since serotonin signals resource availability it is not surprising that it affects organ development. Rodent experiment shows that neonatal exposure to SSRI's makes persistent changes in the serotonergic transmission of the brain resulting in behavioral changes, which are reversed by treatment with antidepressants.
Human serotonin can also act as a growth factor directly. Liver damage increases cellular expression of 5-HT2a and 5-HT2b, mediating liver compensatory regrowth. Serotonin present in the blood then stimulates cellular growth to repair liver damage. 5HT2B receptors also activate osteocytes, which build up bone. However, serotonin also inhibits osteoblasts, through 5-HT1B receptors. (Cymbalta and liver damage; https://www.ncbi.nlm...les/PMC3773985/
https://www.ncbi.nlm...les/PMC3182394/
https://www.ncbi.nlm...pubmed/22772703
https://www.ncbi.nlm...bmed/21694615).

Cardiovascular growth factor
Serotonin, in addition, causes endothelial (the inside lining of blood and lymphatic vessels) nitric oxide synthase activation. In blood, serotonin is collected from plasma by platelets, which store it. It is thus active wherever platelets bind in damaged tissue, as a vasoconstrictor to stop bleeding, and also as a fibrocyte mitotic (growth factor), to aid healing. (Cymbalta slows clotting; https://www.ncbi.nlm...pubmed/22054632
https://www.ncbi.nlm...bmed/18958440.)

Norepinephrine also called noradrenaline (NA), is an chemical that functions in the human brain and body as a hormone and neurotransmitter.The general function of norepinephrine is to mobilize the brain and body for action. Norepinephrine release is lowest during sleep, rises during wakefulness, and reaches much higher levels during situations of stress or danger, in the so-called fight-or-flight response. In the brain, norepinephrine increases arousal and alertness, promotes vigilance, enhances formation and retrieval of memory, and focuses attention; it also increases restlessness and anxiety. In the rest of the body, norepinephrine increases heart rate and blood pressure, triggers the release of glucose from energy stores, increases blood flow to skeletal muscle, reduces blood flow to the gastrointestinal system, and inhibits voiding of the bladder and gastrointestinal motility. Norepinephrine can be converted by the body to epinephrine (adrenaline).
The sympathetic effects of norepinephrine include:
In the eyes, an increase in production of tears, making the eyes more moist., and pupil dilation through contraction of the iris dilator.

In the heart, an increase in the amount of blood pumped.

In brown adipose tissue, an increase in calories burned to generate body heat.

Multiple effects on the immune system. The sympathetic nervous system is the primary path of interaction between the immune system and the brain, and several components receive sympathetic inputs, including the thymus, spleen, and lymph nodes. However the effects are complex, with some immune processes activated while others are inhibited.

In the arteries, constriction of blood vessels, causing an increase in blood pressure.

In the kidneys, release of renin and retention of sodium in the bloodstream.

In the liver, an increase in production of glucose, either by glycogenolysis after a meal or by gluconeogenesis when food has not recently been consumed. Glucose is the body's main energy source in most conditions.

In the pancreas, increased release of glucagon, a hormone whose main effect is to increase the production of glucose by the liver.

In skeletal muscles, an increase in glucose uptake.

In adipose tissue (i. e., fat cells), an increase in lipolysis, that is, conversion of fat to substances that can be used directly as energy sources by muscles and other tissues.

In the stomach and intestines, a reduction in digestive activity. This results from a generally inhibitory effect of norepinephrine on the enteric nervous system, causing decreases in gastrointestinal mobility, blood flow, and secretion of digestive substances.

In the central nervous system norepinephrine is released by the locus coeruleus and affects brain function in a number of ways. It enhances processing of sensory inputs, enhances attention, enhances formation and retrieval of both long term and working memory, and enhances the ability of the brain to respond to inputs by changing the activity pattern in the prefrontal cortex and other areas. The control of arousal level is strong enough that drug-induced suppression of the LC has a powerful sedating effect.

Document #1
http://www.researchg...289a09b6b1a.pdf
Evaluation of Duloxetine as Micronuclei Inducer in an Acute and a Subchronic Assay in Mouse
Eduardo Madrigal-Bujaidar1), Isela Álvarez-González1), Eduardo Osiris Madrigal-Santillán2), José A Morales-González2)

Duloxetine is a widely used antidepressant worldwide. In the present report, we evaluated its capacity to induce micronucleated polychromatic erythrocytes (MNPEs) and micronucleated normochromatic erythrocytes (MNNEs) in mice. Two assays were performed, one with a single chemical administration and the other with daily chemical administration. In the first, we administered the antidepressant once to groups of 5 mice
by the intragastric (i.g.) route (2, 20, and 200 mg/kg) and performed the analysis at 24, 48, and 72 h postadministration. A control group administered i.g. distilled water was included in the assay, as well as another treated with the micronuclei-inducing chemical daunorubicin (2.5 mg/kg, injected intraperitoneally (i.p.)). In this assay, we found significant damage induced by duloxetine starting from the first time evaluated, showing the highest MNPE increase at the end of the assay. We observed a saturation effect as well, suggested by a decreasing relative efficiency with respect to each tested dose. In a second assay, we administered the antidepressant i.g. every day for 5 weeks (2, 6, and 12 mg/kg), and micronuclei analysis was performed at the end of each week. In this study, we also found a significant increase in both MNPEs and MNNEs which was clear by the second week of administration. Our results suggest that short-term as well as cumulative damage is produced by duloxetine. Thus, confirmation of the observed genotoxic potential in other models seems advisable, as well as caution when prescribing this antidepressant. Duloxetine, a potent serotonin and norepinephrine reuptake inhibitor which effectively desensitizes various autoreceptors and promotes neuroplasticity. The compound is used in stress urinary incontinence, and due to its analgesic efficacy it is also prescribed for chronic pain conditions such as diabetic
peripheral neuropathy, fibromyalgia, chronic low back pain,and osteoarthritis knee pain.

Translation -
Cymbalta causes the development of damaged red blod cells which may or may not benormal in color and have a very small nucleus (the nucleus contains the cells DNA).
Also, Cymbalta improves neuroplasticity. The brain's ability to reorganize itself by forming new neural connections throughout life. Neuroplasticity allows the neurons (nerve cells) in the brain to compensate for injury and disease and to adjust their activities in response to new situations or to changes in their environment. Brain reorganization takes place by mechanisms such as "axonal sprouting" in which undamaged axons grow new nerve endings to reconnect neurons whose links were injured or severed. Undamaged axons can also sprout nerve endings and connect with other undamaged nerve cells, forming new neural pathways to accomplish a needed function.
Cymbalta downregulates the activity of the bladder control nerves.

Document #2
https://www.ncbi.nlm...pubmed/18973814
Neurobehavioral and genotoxic parameters of duloxetine in mice using the inhibitory avoidance task and comet assay as experimental models.
Pereira P1, Gianesini J, da Silva Barbosa C, Cassol GF, Von Borowski RG, Kahl VF, Cappelari SE, Picada JN.
Abstract
Duloxetine is a potent inhibitor of serotonin and noradrenaline reuptake, with weak effects on dopamine reuptake, used in the treatment of major depression. It has been recognized that some antidepressants can affect memory in humans, but there is not study that report the duloxetine effect on memory using the inhibitory avoidance. The aim of this work was to investigate the effect of duloxetine on short- and long-term memory (STM and LTM) in the inhibitory avoidance task in mice. Duloxetine (10 and 20 mg/kg; i.p.) administered before or after the inhibitory avoidance training was not able to produce effects on STM e LTM (p>0.05). The group that received MK-801 (0.0625 mg/kg), an NMDA receptor antagonist, showed an impairment in STM and LTM (p<0.01). These effects were not reversed by duloxetine administration (p=0.114 and p=0.06, respectively). Duloxetine effect on memory 5 days after i.p. administration was also investigated. After this treatment both duloxetine doses used were unable to affect STM or LTM in the inhibitory avoidance task (p=0.371 and p=0.807, respectively). DNA damages were evaluated in brain tissues and blood by the comet assay, after subacute treatment (10 or 20 mg/kg by 5 days). Duloxetine did not induce genotoxic effects. However, when the cells were treated ex vivo hydrogen peroxide, a pro-oxidant effect on brain tissue from treated animals was observed with significantly higher DNA damage in comparison to untreated animals, suggesting increased susceptibility to injuries by reactive oxygen species in brain after treatment with duloxetine. Duloxetine did not produce any effect on memory after acute and subacute administration, suggesting that this antidepressant does not affect either memory acquisition or consolidation.

Translation - Cymbalta did not cause DNA damage.

Document #3
https://www.ncbi.nlm...les/PMC4713700/
Effects of duloxetine on microRNA expression profile in frontal lobe and hippocampus in a mouse model of depression
Our data showed that miRNA expression profile in frontal lobe and hippocampus was affected by duloxetine in mice model of depression. The effect was especially pronounced in the hippocampus, suggesting that hippocampus might be the action site of duloxetine, which presumably worked by regulating the expression of miRNA levels.
(This study shows the direct effect of Cymbalta on miRNA (used in translating DNA code) in the hippocampus (one of the emotional centers in the brain). Duloxetine in particular has been reported to induce embryotoxicity in aquatic organisms.
Moreover, as no explanation has been proposed for DNA/chromosomal damage induced by duloxetine and other antidepressants, the detection of specific molecular lesions or
the involved biochemical routes is a matter of research.

Translation - RNA 'reads' the genes in the DNA and then produces the appropriate product. For example if a certain part of the DNA is for a digestive protein the RNA would actually copy that part of the DNA and then use that information to produce the desired protein. A microRNA ( miRNA) is a small RNA molecule that functions in stopping the RNA process and post-'copying' transcription mechanisms that are used by cells to increase or decrease the production of specific gene products (such as proteins or RNA). In simple terms Cymbalta regulates DNA product manufacturing in the frontal lobe and hippocampus.
The frontal lobe is located at the front of the brain contains most of the dopamine-sensitive neurons (nerve cells) in the cerebral cortex. The dopamine system is associated with reward, attention, short-term memory tasks, planning, and motivation. Dopamine tends to limit and select sensory information arriving from the thalamus to the forebrain.
The hippocampus is the part of the brain that is involved in memory forming, organizing, and storing. It is particularly important in forming new memories and connecting emotions and senses to memories. Because of this it is the center for memory based psychological learned responses (such as PTSD). It is also the center of the human fear circuits. The hippocampus receives input from neurotransmitter systems, including serotonin, norepinephrine, and dopamine systems. It also receives cholinergic input (responds to the neurotransmitter acetylcholine) from the medial septum, which regulates the hippocampal physiological state. The hippocampus is highly involved in sleep patterns including REM sleep. There is evidence that humans having experienced severe, long-lasting traumatic stress show atrophy (shrinking fur to lack of use) of the hippocampus more than of other parts of the brain.

Document #4
https://www.ncbi.nlm.../pubmed/9686935
Naunyn Schmiedebergs Arch Pharmacol. 1998 Jun;357(6):600-10.
Effect of long-term administration of duloxetine on the function of serotonin and noradrenaline terminals in the rat brain.
Rueter LE1, Kasamo K, de Montigny C, Blier P.
Abstract
Duloxetine, an inhibitor of both 5-hydroxytryptamine (5-HT) and noradrenaline (NA) reuptake processes, has been developed as a potential antidepressant drug. The present study was initiated to investigate the functioning of multiple components of the 5-HT and NA systems following the long-term administration of duloxetine. In rats treated for 21 days with duloxetine (20 mg/kg/day), the recovery times of dorsal hippocampus CA3 pyramidal neurons from microiontophoretic applications of 5-HT and NA were significantly increased, indicating ongoing reuptake blockade with the minipump in place delivering the drug. The remaining experiments were performed following a 48-h washout. Electrically evoked release of [3H]5-HT from preloaded slices was enhanced in the midbrain, presumably due to a desensitization of the somatodendritic 5-HT1D and 5-HT1A autoreceptors. In addition, evoked release of [3H]5-HT was increased in the hippocampus, which could have been due to the desensitization of the alpha2-adrenergic heteroreceptors located on the 5-HT terminals. In contrast, there was no change in the evoked release of [3H]5-HT in the frontal cortex despite decreased functioning of the 5-HT transporter found in this brain region. Similar to changes in 5-HT release, electrically evoked release of [3H]NA was enhanced in the hippocampus and frontal cortex of rats treated chronically with duloxetine. These increases in [3H]NA release were most likely due to the desensitization of the alpha2-adrenergic autoreceptor in the hippocampus and to the desensitization of the NA transporter in the frontal cortex, respectively. These data suggest that long-term administration of duloxetine is able to induce changes in the 5-HT and NA systems that lead to enhanced release of both 5-HT and NA in some limbic brain areas. Duloxetine, therefore, may be a useful antidepressant compound.
Translation - This research proves that Cymbalat affects the seratonin reuptake proteins. It also shows an increase in seratonin in the hippocampus and no change in seratonin in the frontal cortex. Other studies show that past the 2 month state seratonin levels drop with Cymbalta usage.

Document #5
https://www.ncbi.nlm...les/PMC3362535/
Stress-Induced Changes of Hippocampal NMDA Receptors: Modulation by Duloxetine Treatment
Francesca Calabrese,1 Gianluigi Guidotti,1 Raffaella Molteni,1 Giorgio Racagni,1,3 Michele Mancini,2 and Marco Andrea Riva1,3,*
Abstract
It is now well established that the glutamatergic system contributes to the pathophysiology of depression. Exposure to stress, a major precipitating factor for depression, enhances glutamate release that can contribute to structural abnormalities observed in the brain of depressed subjects. On the other hand, it has been demonstrated that NMDA antagonists, like ketamine, exert an antidepressant effect at preclinical and clinical levels. On these bases, the purpose of our study was to investigate whether chronic mild stress is associated with specific alterations of the NMDA receptor complex, in adult rats, and to establish whether concomitant antidepressant treatment could normalize such deficits. We found that chronic stress increases the expression of the obligatory GluN1 subunit, as well as of the accessory subunits GluN2A and GluN2B at transcriptional and translational levels, particularly in the ventral hippocampus. Concomitant treatment with the antidepressant duloxetine was able to normalize the increase of glutamatergic receptor subunit expression, and correct the changes in receptor phosphorylation produced by stress exposure. Our data suggest that prolonged stress, a condition that has etiologic relevance for depression, may enhance glutamate activity through post-synaptic mechanisms, by regulating NMDA receptors, and that antidepressants may in part normalize such changes. Our results provide support to the notion that antidepressants may exert their activity in the long-term also via modulation of the glutamatergic synapse.
Translation - High glutamate (neurotransmitter) in the hippocampus contributes to depresssion. Cymbalta returns the glutamate gene function to normal activity in the hippocampus. Glutamate is an amino acid, one of the twenty amino acids used to construct proteins, and as a consequence is found in high concentration in every part of the body. In the nervous system it plays a special additional role as a neurotransmitter: a chemical that nerve cells use to send signals to other cells. In fact glutamate is by a wide margin the most abundant neurotransmitter in the vertebrate nervous system. It is used by every major excitatory information-transmitting pathway in the vertebrate brain, accounting in total for well over 90% of the synaptic connections in the human brain. It is no wonder that Cymbalta can cause such varied side effects and withdrawal symptoms as it can potentially effect all nerve cells in the brain and nervous system.
Comment - Is it no wonder that Cymbalta has such a tremendous and varied effect on the human body while on the srug or during recovery/withdrawal afterward.

Document #6
J Biol Chem. 2014 Sep 5; 289(36): 25177–25185.
Synergistic Regulation of Glutamatergic Transmission by Serotonin and Norepinephrine Reuptake Inhibitors in Prefrontal Cortical Neurons*
Eunice Y. Yuen,‡ Luye Qin,‡ Jing Wei,‡§ Wenhua Liu,‡ Aiyi Liu,‡ and Zhen Yan‡§,1
Abstract
The monoamine system in the prefrontal cortex has been implicated in various mental disorders and has been the major target of anxiolytics and antidepressants. Clinical studies show that serotonin and norepinephrine reuptake inhibitors (SNRIs) produce better therapeutic effects than single selective reuptake inhibitors, but the underlying mechanisms are largely unknown. Here, we found that low dose SNRIs, by acting on 5-HT1A and α2-adrenergic receptors, synergistically reduced AMPA receptor (AMPAR)-mediated excitatory postsynaptic currents and AMPAR surface expression in prefrontal cortex pyramidal neurons via a mechanism involving Rab5/dynamin-mediated endocytosis of AMPARs. The synergistic effect of SNRIs on AMPARs was blocked by inhibition of activator of G protein signaling 3, a G protein modulator that prevents reassociation of Gi protein α subunit and prolongs the βγ-mediated signaling pathway. Moreover, the depression of AMPAR-mediated excitatory postsynaptic currents by SNRIs required p38 kinase activity, which was increased by 5-HT1A and α2-adrenergic receptor co-activation in an activator of G protein signaling 3-dependent manner. These results have revealed a potential mechanism for the synergy between the serotonin and norepinephrine systems in the regulation of glutamatergic transmission in cortical neurons.
Translation - Cymbalta, by affecting both seratonin and alpha adrenaline receptors, affects glutamate receptor signaling in the prefrontal cortex of the brain.

Document #7
https://www.ncbi.nlm...pubmed/26135544
Antihyperalgesic effect of duloxetine and amitriptyline in rats after peripheral nerve injury: Influence of descending noradrenergic plasticity.
Hoshino H1, Obata H2, Saito S3.
Abstract
Antidepressants such as serotonin-noradrenaline reuptake inhibitors (SNRIs) and tricyclic antidepressants (TCAs) are frequently used for the management of neuropathic pain. Noradrenaline (NA) and serotonin (5-HT) increase in the spinal cord by reuptake inhibition is considered to be main mechanism of the therapeutic effect of antidepressants in neuropathic pain. In the present study, we examined the analgesic effects of duloxetine (SNRI) and amitriptyline (TCA) in a rat model of neuropathic pain induced by spinal nerve ligation (SNL). Intraperitoneal administration of duloxetine and amitriptyline dose-dependently (3,10 and 30 mg/kg) suppressed hyperalgesia induced by SNL. In vivo microdialysis in the lumbar spinal dorsal horn revealed that NA and 5-HT concentrations increased after intraperitoneal administration of duloxetine and amitriptyline (10 mg/kg, respectively). We further determined NA and 5-HT contents in homogenized samples from the ipsilateral dorsal spinal cord after SNL. Although the NA content in SNL rats 2 weeks after ligation was higher than that in SNL rats 4 weeks after ligation, the analgesic efficacy of duloxetine and amitriptyline was similar between two groups. The present study suggests that NA/5-HT increase in the spinal cord is crucial in the antihyperalgesic effect of duloxetine and amitriptyline. The plastic change of the descending noradrenergic system does not obviously affect the analgesic efficacy of duloxetine and amitriptyline.
Translation -Cymbalta increases seratonin and noradrenaline levels in the spinal cord and reduces associated spinal pain.

Document #8
https://www.ncbi.nlm...pubmed/25154730
Eur J Pain. 2015 May;19(5):649-60. doi: 10.1002/ejp.586. Epub 2014 Aug 25.
A selective α2 B adrenoceptor agonist (A-1262543) and duloxetine modulate nociceptive neurones in the medial prefrontal cortex, but not in the spinal cord of neuropathic rats.
Chu KL1, Xu J, Frost J, Li L, Gomez E, Dart MJ, Jarvis MF, Meyer MD, McGaraughty S.
Abstract
The noradrenergic system contributes to pain modulation, but the roles of its specific adrenoceptors are still being defined. We have identified a novel, potent (rat EC50  = 4.3 nM) and selective α2B receptor agonist, A-1262543, to further explore this adrenoceptor subtype's contribution to pathological nociception.
METHODS: Systemic administration of A-1262543 (1-10 mg/kg, intraperitoneal) dose-dependently attenuated mechanical allodynia in animals with a spinal nerve ligation injury. To further explore its mechanism of action, the activity of nociceptive neurones in the spinal cord and medial prefrontal cortex (mPFC) were examined after injection of 3 mg/kg of A-1262543 (intravenous, i.v.). These effects were compared with duloxetine (3 mg/kg, i.v.), a dual noradrenaline (NA) and serotonin (5-HT) reuptake inhibitor.
RESULTS: Systemic administration of A-1262543 or duloxetine did not alter the spontaneous or evoked firing of spinal wide dynamic range and nociceptive-specific neurones in the neuropathic rats, indicating that neither compound engaged spinal, peripheral or descending pathways. In contrast to the lack of effect on spinal neurones, both A-1262543 and duloxetine reduced the evoked and spontaneous firing of 'pain-responsive' (PR) neurones in the mPFC. Duloxetine, but not A-1262543, also inhibited the firing of pain non-responsive (nPR) neurones in the mPFC probably reflecting duloxetine's contribution to modulating non-pain endpoints.
CONCLUSIONS: These data highlight that activation of the α2B adrenoceptor as well as inhibiting NA and 5-HT reuptake can result in modulating the ascending nociceptive system, in particular, dampening the firing of PR neurones in the mPFC.
Translation - Cymbalta does not effect the pain sensing nerves in the spinal cord but does reduce the activity of the nerves bringing signals back up to the prefrontal cortex and thus reducing the perception of pain.

Document #9
https://www.ncbi.nlm...les/PMC3171868/
Br J Pharmacol. 2011 Sep; 164(1): 159–169.
A spinal mechanism of action for duloxetine in a rat model of painful diabetic neuropathy
T Mixcoatl-Zecuatl and CG Jolivalt
These results support the involvement of spinal 5-HT2A receptors in the ability of duloxetine to ameliorate painful diabetic neuropathy. Our data also suggest that the role of 5-HT2A receptors depends on the level of the neuraxis at which activation takes place, with peripheral activation contributing to tactile allodynia in diabetic rats, whereas spinal activation of this receptor alleviates tactile allodynia. The development of selective peripheral 5-HT2A receptor antagonists may offer a novel approach for the treatment of diabetic neuropathic pain.
Translation - Cymbalta seratonin receptor control helps control pain in peripheral (around the outside) nerves.
Document #10
https://www.ncbi.nlm...pubmed/24933334
Pharmacol Biochem Behav. 2014 Sep;124:238-44. doi: 10.1016/j.pbb.2014.06.005. Epub 2014 Jun 14.
Augmentation of antidepressant effects of duloxetine and bupropion by caffeine in mice.
Kale PP1, Addepalli V2.
Abstract
There is an unmet need in the treatment of depression suggesting requirement of new therapeutic approaches having better efficacy and safety profile. Patients receiving antidepressant therapy generally consume caffeine in the form of tea or coffee. The objective of the present study was to evaluate the augmentation of antidepressant effects of duloxetine and/or bupropion with caffeine. Male Swiss Albino mice received treatment of normal saline (10 ml/kg), 'caffeine alone' (10mg/kg), 'duloxetine alone' (10mg/kg), 'bupropion alone' (10mg/kg), caffeine+duloxetine (5mg/kg, each), bupropion+caffeine (5mg/kg, each), and bupropion+duloxetine (5mg/kg, each) through the intra-peritoneal route. The immobility period was analyzed 30 min after the treatment in forced swim and tail suspension tests. Norepinephrine, dopamine, and serotonin levels were analyzed in hippocampus, cerebral cortex and whole brain using HPLC with fluorescence detector. Euthanasia was performed 1h after treatment. Comparison between vehicle treated group and other groups showed significant decrease in immobility in all drug treated groups in both antidepressant models. Caffeine plus duloxetine treated group was better among the combination treated groups in terms of decrease in immobility and increase in norepinephrine, dopamine, and serotonin levels in hippocampi, cerebral cortices, and whole brain when compared to their respective monotherapy treated groups. These combination approaches may help in reducing the dose of duloxetine/bupropion, and consequently lower the associated side/adverse effects.
Translation - Caffiene in combination with Cymbalta helps decrease fatique and sluggishness (side effects of Cymbalta). It also increased concentrations of norepinephrine, dopamine and seratonin in the hippocampus, cerebral cortex and the whole brain.

Document #11
https://www.ncbi.nlm...pubmed/23522402
J Psychiatr Res. 2013 Jun;47(6):802-8. doi: 10.1016/j.jpsychires.2013.02.013. Epub 2013 Mar 19.
Chronic administration of duloxetine and mirtazapine downregulates proapoptotic proteins and upregulates neurotrophin gene expression in the hippocampus and cerebral cortex of mice.
Engel D1, Zomkowski AD, Lieberknecht V, Rodrigues AL, Gabilan NH.
Abstract
Structural alterations in the limbic system, neuronal cell loss, and low levels of neurotrophins have been implicated in the pathogenesis of depression. While it is generally accepted that increasing monoamine levels in the brain can effectively alleviate depression, the precise neurobiological mechanisms involved are unclear. In the present study, we examined the effects of two antidepressants, duloxetine and mirtazapine, on the expression of apoptotic (natural cell deatah) and neurotrophic proteins (promotes growth, survival and specialize) in the cerebral cortex and hippocampus of mice. Duloxetine (10 mg/kg) and mirtazapine (3 mg/kg) were chronically administered for 21 days, and qRT-PCR analysis was carried for the following: neurotrophins (BDNF, NGF, FGF-2, and NT-3); anti-apoptotic proteins (Bcl-2 and Bcl-xL) and pro-apoptotic proteins (Bax, Bad, and p53). Both duloxetine and mirtazapine produced antidepressant activity in the forced swimming test and induced increased cortical and hippocampal mRNA expression of BDNF. Duloxetine also increased Bcl-2, Bcl-xL, FGF-2, and NT-3 expression in the cerebral cortex, and FGF-2 expression in the hippocampus. Moreover, duloxetine reduced Bax and p53 expression in the hippocampus, and Bad expression in the cerebral cortex. Mirtazapine decreased Bcl-xL and Bax expression in the hippocampus, and Bad and p53 expression in both the hippocampus and cerebral cortex. Mirtazapine also increased the expression of neurotrophins, NGF and NT-3, in the cerebral cortex. These results suggest that duloxetine and mirtazapine could elicit their therapeutic effect by modulating the activity of apoptotic and neurotrophic pathways, thus enhancing plasticity and cell survival in depressive patients.
Translation - Cymbalta increased production of BDNF (brain-derived neurotrophic factor). BDNF acts on certain neurons of the central nervous system and the peripheral nervous system, helping to support the survival of existing neurons, and encourage the growth and differentiation of new neurons and synapses. In the brain, it is active in the hippocampus, cortex, and basal forebrain—areas vital to learning, memory, and higher thinking. It is also expressed in the retina, motor neurons, the kidneys, saliva, and the prostate. Cymbalta increases the production of one protein for apotosis (cell death), 2 for cell growth and survival and one cell membrane protein in the cerebral cortex. In addition it increases the protein for cell membranes in the hippocampus. Cymbalta decreases a protein antigen used to fight cellular tumors and 2 proteins used to promote cell death.

Document #12
https://www.ncbi.nlm...pubmed/23010381
Pharmacol Biochem Behav. 2012 Dec;103(2):408-17. doi: 10.1016/j.pbb.2012.09.011. Epub 2012 Sep 23.
The role of the NMDA receptors and l-arginine-nitric oxide-cyclic guanosine monophosphate pathway in the antidepressant-like effect of duloxetine in the forced swimming test.
Zomkowski AD1, Engel D, Cunha MP, Gabilan NH, Rodrigues AL.
Abstract
Duloxetine is a selective serotonin and noradrenaline reuptake inhibitor used as antidepressant. However, its mechanisms of action are not fully understood. This study investigated the effect of duloxetine in the mouse forced swimming test (FST) and in the tail suspension test (TST) and the involvement of the NMDA receptors and the l-arginine-NO-cGMP pathway in its effect in the FST. Duloxetine reduced the immobility time both in the FST and in the TST (dose range of 1-30mg/kg, i.p.), without changing locomotion in an open-field. Duloxetine administered orally (1-30mg/kg) also reduced the immobility time in the FST. The effect of duloxetine (10mg/kg, p.o.) in the FST was prevented by pre-treatment with NMDA (0.1pmol/site, i.c.v.), d-serine (30μg/site, i.c.v.), (l-arginine (750mg/kg, i.p.), S-nitroso-N-acetyl-penicillamine (SNAP, 25μg/site, i.c.v) or sildenafil (5mg/kg, i.p.). The administration of MK-801 (0.001mg/kg, i.p.), 7-nitroindazole (50mg/kg, i.p.), methylene blue (20mg/kg, i.p.) or 1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one (ODQ) (30pmol/site i.c.v.) in combination with a sub-effective dose of duloxetine (0.3mg/kg, p.o.) reduced the immobility time in the FST. Moreover, the administration of duloxetine (10mg/kg) produced a reduction in NOx levels in the hippocampus and cerebral cortex. Altogether the results suggest that the effect of duloxetine in the FST is dependent on either a blockade of NMDA receptors or an inhibition of NO. In addition, our results further reinforce the role of NMDA receptors and l-arginine-NO-cGMP pathway, besides the monoaminergic systems, in the mechanism of action of current prescribed antidepressant agents.
Translation - Cymbalta reduces nitrous oxide levels in the hippocampua and cerebral cortex. Since it was first identified to play an important role in relaxation of blood vessels, nitric oxide has been demonstrated to regulate many biological processes, especially in the central nervous system. Of the three types of enzymes that produce nitric oxide in humans and rodents, neuronal type is found almost exclusively in the nervous system. This gaseous molecule is a nonclassical neurotransmitter, which maintains the activities of neural cells and regulates the normal functions of brain. It appears to play a role in promoting the transfer of nerve signals from one neuron to another, maintaining the synaptic strength. Meanwhile, nitric oxide is a unique regulator on neurogenesis (new nerve cell production) and synaptogenesis, producing the positive or negative effects upon different signal pathways or cellular origins and locations. Based on its significant roles in neural plasticity, nitric oxide is involved in a number of central nervous diseases, such as ischemia, depression, anxiety, and Alzheimer's disease.
Document #13
https://www.ncbi.nlm...pubmed/21820879
Psychiatry Res. 2011 Nov 30;194(2):157-62. doi: 10.1016/j.pscychresns.2011.03.011. Epub 2011 Aug 6.
Duloxetine's modest short-term influences in subcortical structures of first episode drug-naïve patients with major depressive disorder and panic disorder.
Lai CH1, Wu YT.
Abstract
We developed this study to follow up the hanges in subcortical structures after 6 weeks' treatment with therapy of duloxetine in first episode drug-naïve patients with major depressive disorder and panic disorder. Fifteen patients received duloxetine 60mg/d therapy for 6 weeks and achieved remission. They all underwent structural magnetic resonance imaging (MRI) of the brain at baseline and week 6. Fifteen healthy controls were also scanned twice at baseline and week 6 to exclude possible biases. Structural MRI data were preprocessed with FMRIB's Integrated Registration and Segmentation Tool function (FIRST version 1.2) of FSL (FMRIB Software Library; version 4.1.1) to perform subcortical segmentations of the brain using a shape and appearance model. Nonparametric corrections of these structural volumes in an F-test between pre- and post-treatment were used to identify the changes after duloxetine therapy. A false discovery correction of the F-test by FIRST was also performed. A paired t-test using SPSS was applied to confirm the changes in these structures. The patients had consistent changes of volumes in bilateral nucleus accumbens, left putamen, left hippocampus and brainstem after 6 weeks of treatment with duloxetine. There were no consistent changes in other subcortical structures. There were modest increases of the volumes of the above areas, which were not significant after false discovery correction by FIRST F-test comparisons. The volumetric increases were correlated with responses of clinical symptoms. The results suggested that duloxetine possibly contributed to modest increases in several subcortical areas of these patients with remission.
Translation - Consistent changes of volumes in bilateral nucleus accumbens, a region of the forebrain, (As a whole, the nucleus accumbens has a significant role in the cognitive processing of aversion, motivation, pleasure, reward and reinforcement learning; hence, it has a significant role in addiction. It plays a lesser role in processing fear (a form of aversion), impulsivity, and the placebo effect. It is involved in the encoding of new motor programs as well.), left putamen (located at the base of the forebrain it's main function is to regulate movements and influence various types of learning. It employs GABA, acetylcholine, and enkephalin to perform its functions. The putamen also plays a role in degenerative neurological disorders, such as Parkinson's disease.), left hippocampus and brainstem after 6 weeks of treatment with duloxetine.

Document #14
https://www.ncbi.nlm...pubmed/20381469
Brain Res. 2010 Jun 23;1341:93-9. doi: 10.1016/j.brainres.2010.03.086. Epub 2010 Apr 8.
Comparison of neurogenic effects of fluoxetine, duloxetine and running in mice.
Marlatt MW1, Lucassen PJ, van Praag H.
Abstract
Hippocampal neurogenesis can be regulated by extrinsic factors, such as exercise and antidepressants. While there is evidence that the selective serotonin reuptake inhibitor (SSRI) fluoxetine enhances neurogenesis, the new dual serotonergic-noradrenergic reuptake inhibitor (SNRI) duloxetine has not been evaluated in this context. In addition, it is unclear whether effects of antidepressants and running on cell genesis and behavior are of similar magnitude in mice. Here, we assessed neurogenesis and open-field behavior in 2-month-old female C57Bl/6 mice after 28days of treatment with either fluoxetine (18mg/kg), duloxetine (2, 6 or 18mg/kg) or exercise. New cell survival, as measured by 5-bromo-2'-deoxyuridine (BrdU)-labeled cells, was enhanced by 200% in the running group only. Both running and fluoxetine, but not duloxetine, increased the percentage of new cells that became neurons. In the open-field test, animals treated with either drug spent less time in the center than controls and runners. In addition, fluoxetine treatment resulted in reduced locomotor activity. Together, these data show that the neurogenic response to exercise is much stronger than to antidepressants and imply a low likelihood that anxiolytic effects of these drugs are mediated by adult neurogenesis in C57Bl/6 mice.

Document #15
https://www.ncbi.nlm...pubmed/20159945
Mol Pharmacol. 2010 May;77(5):846-53. doi: 10.1124/mol.109.063081. Epub 2010 Feb 16.
Long-Term duloxetine treatment normalizes altered brain-derived neurotrophic factor expression in serotonin transporter knockout rats through the modulation of specific neurotrophin isoforms.
Calabrese F1, Molteni R, Cattaneo A, Macchi F, Racagni G, Gennarelli M, Ellenbroek BA, Riva MA.
Abstract
Dysfunction of the serotonergic system is implicated in the etiology of many psychiatric disorders, including major depression. Major vulnerability genes for mood disorders are also related to the serotonergic system: one of these genes encodes for the serotonin transporter (SERT), which represent a major target for the action of antidepressant drugs. We have demonstrated recently that SERT knockout (KO) rats, generated by N-ethyl-N-nitrosourea-induced mutagenesis, show reduced expression of the neurotrophin brain-derived neurotrophic factor (BDNF) in the hippocampus and prefrontal cortex, suggesting that depression vulnerability can be associated with impaired neuronal plasticity. In the present study, we demonstrate that chronic treatment with the antidepressant duloxetine (DLX) was able to normalize the expression of BDNF mRNA-coding exon (IX) in the hippocampus and prefrontal cortex of SERT KO rats through the modulation of selected neurotrophin transcripts, whose expression was up-regulated by DLX only in SERT KO rats. On the other hand, the modulation of BDNF protein by DLX in frontal cortex was abolished in mutant rats. These data suggest that animals with a genetic defect of the serotonin transporter maintain the ability to show neuroplastic changes in response to antidepressant drugs. Because these animals show depression-like behavior, the region and isoform-specific increase of BDNF levels may be a mechanism activated by long-term antidepressant treatment to restore normal plasticity that is defective under genetic dysfunction of the serotonin transporter.
Translation - Cymbalta returns BDNF to proper levels and a return of neural plasticity (the ability of the brain to change and develop through it's life).

Document #16
https://www.ncbi.nlm...pubmed/18751896
Neurochem Res. 2009 Mar;34(3):542-55. doi: 10.1007/s11064-008-9818-2. Epub 2008 Aug 27.
Brain region-specific effects of short-term treatment with duloxetine, venlafaxine, milnacipran and sertraline on monoamine metabolism in rats.
Muneoka K1, Shirayama Y, Takigawa M, Shioda S.
Abstract
We examined brain region-specific changes in monoamines and metabolites, and their ratios, after short-term administration of antidepressants to rats. Serotonin noradrenaline reuptake inhibitors (SNRIs; duloxetine, venlafaxine, milnacipran) and a serotonin-selective reuptake inhibitor (SSRI; sertraline) elevated serotonin (5-HT) levels in the midbrain (MB). Duloxetine and venlafaxine increased 5-HT levels in the brainstem and 5-HT terminal areas, whereas milnacipran and sertraline increased levels in the brainstem only. Significant reductions in 5-HT turnover were observed in various forebrain regions, including the hippocampus and hypothalamus, after treatment with all of the tested drugs except for milnacipran. In addition, there was reduced 5-HT turnover in the dorsolateral frontal cortex (dlFC), the medial prefrontal cortex (mPFC), and both the dlFC and the mPFC after treatment with duloxetine, sertraline, and venlafaxine, respectively. Venlafaxine significantly increased dopamine (DA) levels in the nucleus accumbens (NAc) and the substantia nigra and decreased DA turnover in the NAc. Similar changes were observed after treatment with duloxetine and sertraline in the NAc, whereas milnacipran increased DA levels in the mPFC. Limited increases in noradrenaline levels were detected after treatment with duloxetine, venlafaxine, or sertraline, but not after treatment with milnacipran. These results show that SNRIs and SSRIs induced region-specific monoaminergic changes after short-term treatment.
Translation - Cymbalta initially increased seratonin in the brain stem, reduced reuptake (reuse) in the hippocampus, hypothalmus and frontal cortex. Also, Cymbalta icreased dopamine levels and decreased reuptake of dopamine in the nucleus accumbens and the substantia nigra(plays an important role in reward and movement). It also caused small increases in noradrenaline.

Document #17
https://www.ncbi.nlm...pubmed/17327885
Neuropsychopharmacology. 2007 Nov;32(11):2351-9. Epub 2007 Feb 28.
Chronic duloxetine treatment induces specific changes in the expression of BDNF transcripts and in the subcellular localization of the neurotrophin protein.
Calabrese F1, Molteni R, Maj PF, Cattaneo A, Gennarelli M, Racagni G, Riva MA.
Abstract
There is growing evidence that brain-derived neurotrophic factor (BDNF) can be relevant to mood disorders and that modulation of its biosynthesis following prolonged antidepressant treatment may contribute to neuroplastic changes required for clinical response. In the present study, we investigated the effects of the novel antidepressant duloxetine on BDNF in the rat brain. Duloxetine is a serotonin-norepinephrine reuptake inhibitor that differs from other antidepressants by virtue of its balanced potency on both neurotransmitter systems. We found that chronic, but not acute, treatment with duloxetine produces a robust increase of exon V BDNF mRNA levels in frontal cortex when the animals were killed 1 or 24 h after the last administration. The expression of the neurotrophin was also increased in other cortical subregions, but not in the hippocampus. We also found that the increased expression of BDNF in frontal cortex was mainly sustained by enhanced mRNA levels for exons I and III, whereas the expression of exon IV was reduced. Protein analysis in different subcellular fractions showed that chronic treatment with duloxetine, but not with the prototypical SSRI fluoxetine, reduced mature BDNF in the cytosol, but markedly increased its levels in the crude synaptosomal fraction. Our data suggest that chronic treatment with the novel antidepressant duloxetine not only produces a marked upregulation of BDNF mRNA and protein, but may also affect the subcellular redistribution of the neurotrophin. These changes might improve synaptic plasticity and cognitive function that are defective in depressed subjects.
Translation - Chronic treatment with Cymbalta not only produces a marked increase in the function of the BDNF mRNA but also the manufacturing of BDNF itself, and may also affect the subcellular redistribution of BDNF).

Document #18
https://www.ncbi.nlm.../pubmed/9686935
Naunyn Schmiedebergs Arch Pharmacol. 1998 Jun;357(6):600-10.
Effect of long-term administration of duloxetine on the function of serotonin and noradrenaline terminals in the rat brain.
Rueter LE1, Kasamo K, de Montigny C, Blier P.
Abstract
Duloxetine, an inhibitor of both 5-hydroxytryptamine (5-HT) and noradrenaline (NA) reuptake processes, has been developed as a potential antidepressant drug. The present study was initiated to investigate the functioning of multiple components of the 5-HT and NA systems following the long-term administration of duloxetine. In rats treated for 21 days with duloxetine (20 mg/kg/day), the recovery times of dorsal hippocampus CA3 pyramidal neurons from microiontophoretic applications of 5-HT and NA were significantly increased, indicating ongoing reuptake blockade with the minipump in place delivering the drug. The remaining experiments were performed following a 48-h washout. Electrically evoked release of [3H]5-HT from preloaded slices was enhanced in the midbrain, presumably due to a desensitization of the somatodendritic 5-HT1D and 5-HT1A autoreceptors. In addition, evoked release of [3H]5-HT was increased in the hippocampus, which could have been due to the desensitization of the alpha2-adrenergic heteroreceptors located on the 5-HT terminals. In contrast, there was no change in the evoked release of [3H]5-HT in the frontal cortex despite decreased functioning of the 5-HT transporter found in this brain region. Similar to changes in 5-HT release, electrically evoked release of [3H]NA was enhanced in the hippocampus and frontal cortex of rats treated chronically with duloxetine. These increases in [3H]NA release were most likely due to the desensitization of the alpha2-adrenergic autoreceptor in the hippocampus and to the desensitization of the NA transporter in the frontal cortex, respectively. These data suggest that long-term administration of duloxetine is able to induce changes in the 5-HT and NA systems that lead to enhanced release of both 5-HT and NA in some limbic brain areas. Duloxetine, therefore, may be a useful antidepressant compound.
Translation - Demonstrated the blocking of seratonin reuptake by Cymbalta. It also increased seratonin levels in the hippocampus. Although seratonin reuptake was blocked in the frontal cortex seratonin levels remained constant. Chronic use (21 days is chronic?) showed increase release of noradrenaline in the hippocampus and frontal cortex.

Document #19
https://www.ncbi.nlm.../pubmed/9580577
J Pharmacol Exp Ther. 1998 May;285(2):404-12.
Electrophysiological characterization of the effect of long-term duloxetine administration on the rat serotonergic and noradrenergic systems.
Rueter LE1, De Montigny C, Blier P.
Abstract
Duloxetine is a dual serotonin (5-HT)/norepinephrine (NE) re-uptake blocker with antidepressant potential. In the present in vivo electrophysiological study, the changes in the function of the rat 5-HT and NE systems after 2- and 21-day administration of duloxetine (20 mg/kg/day) were assessed in the dorsal hippocampus and the dorsal raphe nucleus (DRN). The firing rate of DRN neurons was decreased after 2 days of duloxetine, but returned to the control level after 21-day administration. This recovery of firing rate was presumably due to the desensitization of the DRN somatodendritic 5-HT1A autoreceptors found after long-term duloxetine administration. Overall serotonergic tone was assessed by examining the ability of the 5-HT1A antagonist WAY 100635 to alter hippocampal firing. WAY 100635 increased hippocampal firing rates in 21-day treated rats to a greater extent than in 2-day treated or control rats, suggesting that long-term administration induced an increase in endogenous levels of 5-HT in postsynaptic regions. This increase in 5-HT levels was accompanied by selective changes in the 5-HT and NE systems induced by long-term duloxetine administration, i.e., the desensitization of the alpha-2 adrenergic heteroreceptor on 5-HT terminals and the continued blockade of the 5-HT transporters. In contrast, the sensitivity of the alpha-2 adrenergic and terminal 5-HT1B autoreceptors, as well as that of the postsynaptic 5-HT1A receptor after 21-day treatment was unchanged. Therefore, this study demonstrates that duloxetine increases serotonergic tone in a limbic forebrain structure and may therefore be effective in the treatment of depression.
Translation - Cymbalta initially increased the firing of nerve cells in the dorsal raphe nucleus (The dorsal raphe nucleus is located on the midline of the brainstem The dorsal raphe nucleus have long been implicated in depression. Some studies have suggested that the dorsal raphe may be decreased in size in people with depression and, paradoxically, an increased cell density in those who commit suicide.) but firing rates returned to normal after 21 days due to fatique in the seratonin receptors. It also increased seratonin in the forebrain.

Document #20
https://www.ncbi.nlm.../pubmed/9105878
Eur J Pharmacol. 1997 Mar 26;323(1):69-73.
Electrophysiological effects of fluoxetine and duloxetine in the dorsal raphe nucleus and hippocampus.
Smith JE1, Lakoski JM.
Abstract
The cellular electrophysiological effects of duloxetine (LY248686), a dual serotonin (5-hydroxytryptamine, 5-HT) and norepinephrine reuptake inhibitor, and the selective serotonin reuptake inhibitor fluoxetine were compared on spontaneously active neurons in the dorsal raphe nucleus and the hippocampus of chloral hydrate-anesthetized male rat. Systemic intravenous administration of duloxetine or fluoxetine inhibited dorsal raphe nucleus cell firing in a dose-dependent manner; duloxetine suppressed cell firing at significantly lower doses (ED100 1.4 +/- 0.3 mg/kg) than fluoxetine (ED100 10.0 +/- 2.0 mg/kg). In the hippocampus, microiontophoretic application of duloxetine or fluoxetine (0.01 M, pH 5.5; 5-40 nA) produced minimal inhibition of cell firing. When duloxetine was co-applied with 5-HT, the recovery response (RT50 values) of hippocampal pyramidal neurons to 5-HT application was not altered. In contrast, co-application of fluoxetine with 5-HT at the same iontophoretic currents significantly increased (59%) the RT50 values produced by 5-HT application alone. This physiological and pharmacological study contributes to understanding the cellular mechanisms of these agents which may be useful in the treatment of depression.
Translation - Cymbalta inhibited dorsal raphe nucleus cell firing. In the hippocampus little decrease was noted in cell firing.

Document #21
https://www.ncbi.nlm.../pubmed/8613930
J Pharmacol Exp Ther. 1996 Apr;277(1):278-86.
Blockade of the serotonin and norepinephrine uptake processes by duloxetine: in vitro and in vivo studies in the rat brain.
Kasamo K1, Blier P, De Montigny C.
Abstract
In in vitro uptake experiments, duloxetine inhibited [3H]5-hydroxytryptamine (5-HT) and [3H]norepinephrine (NE) uptake in hippocampus slices of control rats with IC50 values of 28 and 46 nM, respectively. The uptake of both[3H]5-HT and [3H]NE was equipotently inhibited in hippocampus slices prepared from rats treated for 2 days with different doses of duloxetine (5, 10, 15 and 20 mg/kg/day s.c.). In in vivo electrophysiological experiments in the hippocampus, the effects of duloxetine on the suppression of CA3 pyramidal neuronal firing activity by microiontophoretically applied 5-HT and NE were examined with two modes of administration. Five successive i.v. injections (2 mg/kg each) significantly and dose-dependently prolonged the recovery time of the firing activity of hippocampus CA3 pyramidal neurons from the 5-HT applications. A 2-day treatment (10, 15 and 20 mg/kg/day s.c.) also increased the recovery time in a dose-dependent manner. Whereas the recovery time from NE applications was unaffected by low doses of duloxetine (2 mg/kg i.v.; 10 mg/kg/day for 2 days), it was prolonged significantly by higher doses (8 and 1 0 mg/kg iv.; 20 mg/kg/day for 2 days). Acute i.v. injections of duloxetine suppressed the spontaneous firing activity of dorsal raphe 5-HT and locus ceruleus NE neurons with ED50 values of 99 and 475 microgram/kg, respectively. Taken together, the present results confirmed that duloxetine is a dual 5-HT/NE uptake inhibitor. Furthermore, the results obtained in in vivo experiments indicate that duloxetine has a preferential inhibitory effect on the 5-HT transporter.
Translation - Cymbalta inhibited the reuptake of both seratonin and noradrenaline in the hippocampus. It inhibited seratonin reuptake more than noradrenaline.

Document #22
https://www.ncbi.nlm...les/PMC3413810/
J Mol Neurosci. 2012 Sep; 48(1): 167–175.
Differential BDNF Responses of Triple Versus Dual Reuptake Inhibition in Neuronal and Astrocytoma Cells as well as in Rat Hippocampus and Prefrontal Cortex
,1,2,3 Gunter Kenis,1,2 Maria S. Quinton,3 Sharon Engel,3 Larry Melnick,3 and Rudy Schreiber3,4
Abstract
Monoamine reuptake inhibitors increase brain-derived neurotrophic factor (BDNF) activity, and this growth factor is regarded as an interesting target for developing new antidepressant drugs. The aims of this study were to evaluate whether monoaminergic reuptake inhibition increases BDNF in vivo and in vitro as predicted by the neurotrophic hypothesis of depression, and whether triple reuptake inhibition has a superior BDNF response compared to dual reuptake inhibition. Twenty-one days of oral treatment (30 mg/kg) with the dual serotonin/noradrenaline reuptake inhibitor duloxetine or the triple serotonin/noradrenaline/dopamine reuptake inhibitor DOV 216,303 restored BDNF protein levels in the rat hippocampus, which were initially decreased due to injection stress. The prefrontal cortex contained increased BDNF levels only after DOV 216,303 treatment. In vitro, neither duloxetine nor DOV 216,303 altered intracellular BDNF levels in murine HT22 neuronal cells. In contrast, BDNF release was more effectively decreased following treatment with DOV 216,303 in these cells. In rat C62B astrocytomas, both antidepressants increased intracellular BDNF levels at their highest nontoxic concentration. C62B astrocytomas did not release BDNF, even after antidepressant treatment. Increased BDNF levels support the neurotrophic hypothesis of depression, but our findings do not clearly evidence that the BDNF response after triple reuptake inhibitors is more effective than after dual reuptake inhibitors. Moreover, the data suggest that the role of BDNF in neurons and astrocytes is complex and likely depends on factors including specificity of cell types in different brain regions, cell–cell interactions, and different mechanisms of action of antidepressants used.
Translation - Cymbalta returned BDNF levels to normal in the hippocampus within 21 days.

Document #23
https://www.ncbi.nlm...les/PMC3176563/
Neuropsychopharmacology. 2011 Oct; 36(11): 2266–2275.
Short-Term Duloxetine Administration Affects Neural Correlates of Mood-Congruent Memory
Indira Tendolkar,1,2,3,* Guido van Wingen,1,4,5 Maren Urner,1,6 Robbert Jan Verkes,2 and Guillén Fernández1,4
Abstract
It is unknown how antidepressants reverse mood-congruent memory bias, a cognitive core factor causing and maintaining depression. Using a double-blind, placebo-controlled, cross-over design, we investigated the effect of a short-term treatment (14 days) with the dual reuptake inhibitor duloxetine on neural correlates of mood-congruent and mood-incongruent memory formation and retrieval in healthy volunteers who underwent a sad mood induction procedure. Duloxetine did not affect acute mood state or memory performance, but interacted with brain processes mediating mood-congruent memory. It decreased activity related to successful memory formation for mood-congruent and -incongruent items in a set of brain regions comprising the putamen and the middle frontal gyrus, as well as the middle and the anterior cingulate cortex. Duloxetine specifically increased amygdala activity related to successful memory retrieval for mood-incongruent items. Here we show that short-term administration of duloxetine affects the neural correlates of emotional memory formation and retrieval in a set of brain regions whose processing is related to affective state and its regulation. While duloxetine suppressed the neural correlates of emotional memory formation in general, it specifically enhanced amygdala processes associated with mood-incongruent memory retrieval. This pattern of results shows how an antidepressant may reduce emotional memory formation and reverse mood-congruent processing biases at retrieval.
Translation - A 14 day treatment with Cymbalta decreased activities related to memory formation in the putamen, frontal gyrus and anterior cingulate cortex. On the other hand it increased memory retrieval in the amygdala.

Document #24
https://www.ncbi.nlm...les/PMC4713700/
Int J Clin Exp Pathol. 2015; 8(11): 15454–15461.
Effects of duloxetine on microRNA expression profile in frontal lobe and hippocampus in a mouse model of depression
Bing Pan,1,* Yamei Liu2,*
Abstract
Depression is a major mood disorder affecting people worldwide. The posttranscriptional gene regulation mediated by microRNAs (miRNAs) which may have critical roles in the pathogenesis of depression. However, to date, little is known about the effects of the antidepressant drug duloxetine on miRNA expression profile in chronic unpredictable mild stress (CUMS)-induced depression model in mice. Healthy adult male Kunming mice were randomly divided into three groups: control group, model group and duloxetine group. Sucrose preference test and open field test were used to represent the behavioral change. MiRNAs levels in frontal lobe and hippocampus of mice were analyzed using miRNA microarrays assay. We observed that long-term treatment with duloxetine significantly ameliorated the CUMS procedure-induced sucrose preference decreases and mice treated with duloxetine demonstrated a reversal of the number of crossings, and rearings reduced by CUMS. A significant upregulation of miR-132 and miR-18a in hippocampus in the duloxetine treatment group compared with model group, whereas the levels of miR-134 and miR-124a were significantly downregulated. Furthermore, miR-18a showed significant upregulation in frontal lobe in the duloxetine treatment group relative to model group. Our data showed that miRNA expression profile in frontal lobe and hippocampus was affected by duloxetine in mice model of depression. The effect was especially pronounced in the hippocampus, suggesting that hippocampus might be the action site of duloxetine, which presumably worked by regulating the expression of miRNA levels.
Translation- Cymbalta increased the activity of two miRNA in the hippocampus (miRNA-132 which functions to regulate the expression levels of other genes by several mechanisms, generally reducing protein levels through the cleavage of mRNAs or the repression of their translation. Several targets for miR-132 have been described, including mediators of neurological development, synaptic transmission, inflammation and angiogenesis.; and miR-18a which triggers the function of other RNA) and decreases the function of two other miRNA (miR-134 is a brain-specific microRNA localised in hippocampal neurons and indirectly regulate synaptic development and is thought to mediate Creb protein giving it a role in higher brain functions such a memory formation; and miR-124a which has been found to be the most abundant microRNA expressed in nerve cells. It can change the structure of Glutamate receptors in the prefrontal cortex.)

Document #25
https://www.ncbi.nlm...les/PMC3055320/
Neuropsychopharmacology. 2010 Oct; 35(11): 2305–2317.
Effects of Duloxetine Treatment on Brain Response to Painful Stimulation in Major Depressive Disorder
Marina López-Solà,1,2 Jesus Pujol,1,3,* Rosa Hernández-Ribas,1,4,5 Ben J Harrison,1,6 Oren Contreras-Rodríguez,1,7 Carles Soriano-Mas,1,7 Joan Deus,1,8 Héctor Ortiz,1 José M Menchón,4,5 Julio Vallejo,2,5 and Narcís Cardoner1,4,5
Abstract
Major depressive disorder (MDD) is characterized by a constellation of affective, cognitive, and somatic symptoms associated with functional abnormalities in relevant brain systems. Painful stimuli are primarily stressful and can trigger consistent responses in brain regions highly overlapping with the regions altered in MDD patients. Duloxetine has proven to be effective in treating both core emotional symptoms and somatic complaints in depression. This study aimed to assess the effects of duloxetine treatment on brain response to painful stimulation in MDD patients. A total of 13 patients and a reference group of 20 healthy subjects were assessed on three occasions (baseline, treatment week 1, and week 8) with functional magnetic resonance imaging (fMRI) during local application of painful heat stimulation. Treatment with duloxetine was associated with a significant reduction in brain responses to painful stimulation in MDD patients in regions generally showing abnormally enhanced activation at baseline. Clinical improvement was associated with pain-related activation reductions in the pregenual anterior cingulate cortex, right prefrontal cortex, and pons. Pontine changes were specifically related to clinical remission. Increased baseline activations in the right prefrontal cortex and reduced deactivations in the subgenual anterior cingulate cortex predicted treatment responders at week 8. This is the first fMRI study addressed to assess the effect of duloxetine in MDD. As a novel approach, the application of painful stimulation as a basic neural stressor proved to be effective in mapping brain response changes associated with antidepressant treatment and brain correlates of symptom improvement in regions of special relevance to MDD pathophysiology.
Translation - Cymbalta reduced pain nerve signals in the pregenual anterior cingulate cortex (It plays a role in a wide variety of autonomic functions, such as regulating blood pressure and heart rate and is involved in certain higher-level functions, such as reward anticipation, decision-making, impulse control, and emotion.), right prefrontal cortex, and pons (The pons is part of the brainstem that conduct signals from the brain down to the cerebellum and medulla, and tracts that carry the sensory signals up into the thalamus.The pons contains nuclei that relay signals from the forebrain to the cerebellum, along with nuclei that deal primarily with sleep, respiration, swallowing, bladder control, hearing, equilibrium, taste, eye movement, facial expressions, facial sensation, and posture.).

Document #26
https://www.ncbi.nlm...pubmed/25880400
2015 Apr 14;15:82. doi: 10.1186/s12888-015-0457-2.
Multimodal functional and structural neuroimaging investigation of major depressive disorder following treatment with duloxetine.
Fu CH1,2, Costafreda SG3,4, Sankar A5, Adams TM6, Rasenick MM7,8, Liu P9, Donati R10,11, Maglanoc LA12, Horton P13, Marangell LB14.
Abstract
Participants were medication-free MDD patients (n = 32; mean age 40.2 years) in an acute depressive episode and healthy controls matched for age, gender, and IQ (n = 25; mean age 38.8 years). MDD patients received treatment with duloxetine 60 mg daily for 12 weeks with an optional dose increase to 120 mg daily after 8 weeks. All participants had serial imaging at weeks 0, 1, 8, and 12 on a 3 Tesla magnetic resonance imaging (MRI) scanner. Neuroimaging tasks included emotional facial processing, negative attentional bias (emotional Stroop), resting state functional MRI and structural MRI.
RESULTS: A significant group by time interaction was identified in the anterior default mode network in which MDD patients showed increased connectivity with treatment, while there were no significant changes in healthy participants. In the emotional Stroop task, increased posterior cingulate activation in MDD patients normalized following treatment. No significant group by time effects were observed for happy or sad facial processing, including in amygdala responsiveness, or in regional cerebral volumes. Reduced baseline resting state connectivity within the orbitofrontal component of the default mode network was predictive of clinical response. An early increase in hippocampal volume was predictive of clinical response.
CONCLUSIONS: Baseline resting state functional connectivity was predictive of subsequent clinical response. Complementary effects of treatment were observed from the functional neuroimaging correlates of affective facial expressions, negative attentional bias, and resting state. No significant effects were observed in affective facial processing, while the interaction effect in negative attentional bias and individual group effects in resting state connectivity could be related to the SNRI class of antidepressant medication. The specificity of the observed effects to SNRI pharmacological treatments requires further investigation.
Translation - Cymbalta normalized activation of the posterior cingulate. Imaging studies indicate a prominent role for the posterior cingulate cortex in pain and episodic memory retrieval. Increased size of posterior ventral cingulate cortex is related to working memory decline. The posterior cingulate cortex has been implicated as a key part of several control networks. The posterior cingulate cortex has also been firmly linked to prominent emotional experiences . Thus, it has been hypothesized that the emotional importance of personal memories may contribute to the strength and consistency of activity in the posterior cingulate cortex upon successful recollection of these memories. The posterior cingulate cortex is significantly activated by emotional stimuli.

Document #27
https://www.ncbi.nlm...pubmed/21195195
Neuroimage. 2011 Mar 15;55(2):825-31. doi: 10.1016/j.neuroimage.2010.12.051. Epub 2010 Dec 30.
Subchronic duloxetine administration alters the extended amygdala circuitry in healthy individuals.
van Marle HJ1, Tendolkar I, Urner M, Verkes RJ, Fernández G, van Wingen G.
Abstract
Neuroimaging studies have consistently linked depression to hyperactivation of a (para)limbic affective processing network centered around the amygdala. Recent studies have started to investigate how antidepressant drugs affect amygdala reactivity in healthy individuals, but the influence of their subchronic administration on the functional integrity of the affective neurocircuitry as a whole remains unknown. Therefore, we used functional magnetic resonance imaging in nineteen healthy volunteers to assess the effect of two weeks of administration of the combined serotonin and norepinephrine reuptake inhibitor duloxetine (60 mg) on reactivity and functional connectivity within the affective neurocircuitry in a double-blind, placebo-controlled, crossover design. Using an emotional face matching task we demonstrated that duloxetine reduced neural responses in affect processing regions including the amygdala, the anterior insula, the thalamus and the ventral aspect of the anterior cingulate cortex. Additionally, functional coupling between the amygdala and the anterior insula was enhanced by the drug. These results suggest that duloxetine attenuates the bottom-up processing of biologically salient information in an extended amygdala circuitry, while at the same time possibly potentiating the effective communication between its subparts. Since hyperactivation of the same affective neurocircuitry is thought to underlie emotional dysfunction in depression, these results suggest a putative neural mechanism through which duloxetine could normalize typical negativity biases in depression.
Translation - Cymbalta reduced nerve responses in the amygdala, anterior insula (The insulae are believed to be involved in consciousness and play a role in diverse functions usually linked to emotion or the regulation of the body's homeostasis. These functions include perception, motor control, self-awareness, cognitive functioning, and interpersonal experience. In relation to these, it is involved in psychopathology.), thalmus (Some of its functions are the relaying of sensory and motor signals to the cerebral cortex, and the regulation of consciousness, sleep, and alertness.) and cingulate cortex. Communication between the amygdala and the anterior insula were increased.

Document #28
https://www.ncbi.nlm...les/PMC3055320/
Neuropsychopharmacology. 2010 Oct; 35(11): 2305–2317.
Effects of Duloxetine Treatment on Brain Response to Painful Stimulation in Major Depressive Disorder
Marina López-Solà,1,2 Jesus Pujol,1,3,* Rosa Hernández-Ribas,1,4,5 Ben J Harrison,1,6 Oren Contreras-Rodríguez,1,7 Carles Soriano-Mas,1,7 Joan Deus,1,8 Héctor Ortiz,1 José M Menchón,4,5 Julio Vallejo,2,5 and Narcís Cardoner1,4,5
Abstract
Major depressive disorder (MDD) is characterized by a constellation of affective, cognitive, and somatic symptoms associated with functional abnormalities in relevant brain systems. Painful stimuli are primarily stressful and can trigger consistent responses in brain regions highly overlapping with the regions altered in MDD patients. Duloxetine has proven to be effective in treating both core emotional symptoms and somatic complaints in depression. This study aimed to assess the effects of duloxetine treatment on brain response to painful stimulation in MDD patients. A total of 13 patients and a reference group of 20 healthy subjects were assessed on three occasions (baseline, treatment week 1, and week 8) with functional magnetic resonance imaging (fMRI) during local application of painful heat stimulation. Treatment with duloxetine was associated with a significant reduction in brain responses to painful stimulation in MDD patients in regions generally showing abnormally enhanced activation at baseline. Clinical improvement was associated with pain-related activation reductions in the pregenual anterior cingulate cortex, right prefrontal cortex, and pons. Pontine changes were specifically related to clinical remission. Increased baseline activations in the right prefrontal cortex and reduced deactivations in the subgenual anterior cingulate cortex predicted treatment responders at week 8. This is the first fMRI study addressed to assess the effect of duloxetine in MDD. As a novel approach, the application of painful stimulation as a basic neural stressor proved to be effective in mapping brain response changes associated with antidepressant treatment and brain correlates of symptom improvement in regions of special relevance to MDD pathophysiology.
Translation - Cymblta reducted pain perception the pregenual anterior cingulate cortex, right prefrontal cortex, and pons.

Document #29
https://www.ncbi.nlm...pubmed/23507186
Psychoneuroendocrinology. 2013 Sep;38(9):1824-8. doi: 10.1016/j.psyneuen.2013.02.009. Epub 2013 Mar 16.
NGF serum levels variations in major depressed patients receiving duloxetine.
Martino M1, Rocchi G, Escelsior A, Contini P, Colicchio S, de Berardis D, Amore M, Fornaro P, Fornaro M.
Abstract
Nerve growth factor (NGF) is involved in the modulation of the neuro-endocrine-immune (NEI) system, whereas alterations in neuroplasticity and NEI homeostasis seem to play a role in the pathophysiology of major depressive disorder (MDD). Objective of the study was to investigate NGF levels variations in MDD patients during antidepressant treatment with duloxetine, a relatively newer SNRI.
METHODS: 30 MDD patients and 32 healthy controls were assessed using Hamilton depression scale (HAM-D) and monitored for NGF serum levels at baseline, week 6 and week 12 of duloxetine treatment (60 mg/day) and at baseline, respectively.
RESULTS: According to early clinical response to duloxetine (defined at week 6 by reduction >50% of baseline HAM-D score), MDD patients were distinguished in early responders (ER) and early non-responders (ENR), who overall reached clinical response at week 12. Laboratory analysis showed overall significant lower baseline NGF levels among depressed patients compared to healthy controls, not significantly in ER and significantly in ENR. During duloxetine treatment NGF levels further decreased in association with clinical response, reaching significantly lower values in ER at W6 compared to controls, and in ENR at W12 compared to baseline.
CONCLUSIONS: A decrease in NGF levels during duloxetine treatment in association to clinical response could be indicative of a relative restoring of NEI stress-adaptation system, since stressors, inducing neuronal instability due to neurotrophins activity changes, permits circuitry remodeling as background in the selection of alternative adaptive behaviors. However, the lower baseline NGF levels found in MDD patients that further decrease during the treatment could represent a lower neurotrophin set point, possibly reflecting a functional impairment in stress-adaptive neuroplasticity in depressive disorders.
Translation - Nerve growth factor concentrations were lower in depressed patients. Cymbalta further lowered nerve growth factor concentrations.

Document #30
https://www.ncbi.nlm...pubmed/20305306
Neuropsychopharmacol Hung. 2010 Mar;12(1):301-7.
[The effects of duloxetine on beta-actin stress response in rat brain].
Szücs S1, Pákáski M, Domokos A, Kálmán J Jr, Kálmán S, Garab D, Penke B, Szabó G, Janka Z, Kálmán J.
Abstract
Depression is a frequent prodromal symptom of Alzheimer's disease (AD). Stress factors play an important role in the etiopathology of both diseases, since increased corticosteroid levels caused by chronic stress indirectly induce neuronal damage. The aim of our experiments was to evaluate the changes induced by stress in the transcription of amyloid precursor protein (APP), mitogen activated protein kinase-1 (MAPK-1) and beta-actin, of which the latest plays a leading role in synaptic plasticity. Additionally we intended to examine how duloxetine - a serotonin-norepinephrin reuptake inhibitor type antidepressant - would modify the stress-induced changes. Wistar rats were exposed to immobilization stress for five hours daily through 21 days, while part of the animals received 45 mg/bwkg of duloxetine. At the end of the third week total RNA was purified from the cortex and hippocampus. The amount of beta-actin, APP and MAPK-1 mRNA was determined by real time PCR method. On protein level, semiquantitative measurement was performed by Western blot. The expression of beta-actin mRNA in the animals exposed to stress was four times as intense as in the control group. The increase in the beta-actin mRNA levels was repressed by the duloxetine treatment. In the case of APP and MAPK-1 no changes were detected. According to the Western blot results, the antidepressant treatment slightly, the drug along with the stress treatment strongly decreased the amount of the beta-actin protein. Our findings indicate that antidepressant treatment with duloxetine could play a protective role against the chronic stress-induced changes in the nervous system, such as disorders of synaptic plasticity, and the consequent cognitive dysfunctions in case of both affective disorders and AD.
Translation- Stress increases activity of the beta-actin mRNA (major part of muscle contractions) and Cymbalta decreased the activity of the beta-actin mRNA

Document #31
https://www.ncbi.nlm...pubmed/19020498
Neuropsychopharmacology. 2009 May;34(6):1523-32. doi: 10.1038/npp.2008.208. Epub 2008 Nov 19.
Acute stress responsiveness of the neurotrophin BDNF in the rat hippocampus is modulated by chronic treatment with the antidepressant duloxetine.
Molteni R1, Calabrese F, Cattaneo A, Mancini M, Gennarelli M, Racagni G, Riva MA.
Abstract
Compelling evidence suggests that mood disorders are characterized by reduced neuronal plasticity that might be normalized by pharmacological intervention. Our study aimed to establish whether chronic antidepressant treatment could alter the modulation of the neurotrophin brain-derived neurotrophic factor (BDNF) under a stressful condition. Therefore, adult male Sprague-Dawley rats were treated for 21 days with vehicle or with the SNRI duloxetine and, 24 h after the last injection, exposed to an acute swim stress (5 min) before being killed 15 min later. We found that chronic duloxetine treatment was able to modulate the rapid transcriptional changes of BDNF isoforms produced by an acute swim stress. Indeed whereas the mRNA levels of BDNF exon IV were upregulated by stress in vehicle as well as in duloxetine-treated rats, a significant increase of exon VI and exon IX was only found in rats that were pretreated with the antidepressant. These differential effects are in part because of selective changes in signaling pathways involved in the control of BDNF transcription. Moreover, the acute stressful episode significantly increased the levels of mature BDNF protein in the synaptosomal compartment in rats that were pretreated with the antidepressant, but not in control animals. Our results suggest that chronic antidepressant treatment might affect the responsiveness of BDNF under stressful conditions, suggesting that pharmacological intervention could 'prime' neuroprotective pathways and render them more responsive to preserve cell function and viability.
Translation - Stress increases BDNF concentration but Cymbalta treatment decreased the concentration. Pretreatment with Cymbalta had the opposite effect.

Document #32
https://www.ncbi.nlm...pubmed/18704370
Psychopharmacology (Berl). 2008 Dec;201(2):285-92. doi: 10.1007/s00213-008-1276-7. Epub 2008 Aug 14.
Basal and stress-induced modulation of activity-regulated cytoskeletal associated protein (Arc) in the rat brain following duloxetine treatment.
Molteni R1, Calabrese F, Mancini M, Racagni G, Riva MA.
Abstract
RATIONALE: Therapeutic efficacy of antidepressant drugs appears to be related to their ability in producing neuroadaptive changes that restore normal brain function. Activity-regulated cytoskeletal associated protein (Arc) is an effector immediate early gene that plays a fundamental role in activity-dependent neural plasticity in corticolimbic brain regions and has been implicated in the modulation of several functions known to be profoundly perturbed in depressive states.
OBJECTIVE: In the present study, we investigated transcriptional and translational changes of Arc in response to acute or chronic treatment with the novel antidepressant duloxetine.
RESULTS: Although a limited increase of Arc messenger RNA (mRNA) levels was found in some structures after acute antidepressant administration, a marked up-regulation of its gene expression was found after chronic treatment, primarily at the level of frontal cortex. The changes observed after prolonged duloxetine administration strongly correlates with those previously reported on brain-derived neurotrophic factor mRNA levels Calabrese et al. In addition, we found an anatomical-specific influence of chronic duloxetine on stress-dependent Arc modulation, which was limited to the frontal cortex.
CONCLUSIONS: We suggest that these neuroadaptive changes, among others, might contribute to the normalization of neuroplastic defects associated with mood disorders.
Translation - Chronic use of Cymbalta increases Arc concentrations in the frontal cortex (Arc is widely considered to be an important protein in neurobiology because of its activity regulation, localization, and utility as a marker for plastic changes in the brain. Dysfunctions in the production of Arc protein has been implicated as an important factor in understanding of various neurological conditions including: Amnesia; Alzheimer's disease; Autism spectrum disorders; and, Fragile X syndrome)

Misc.
http://www.ncbi.nlm....pubmed/23732229
With these findings, we propose a model by which acute SSRI administration, by altering neural activity in the extended amygdala and hippocampus, enhances both acquisition and expression of cued fear conditioning, but impairs the expression of contextual fear conditioning

http://www.ncbi.nlm....pubmed/23675317
We evaluated the effect of four weeks of 0.7 mg/kg fluoxetine on long-term potentiation (LTP) and long-term depression (LTD) in the CA1 hippocampal subfield. Recordings in hippocampal slices revealed profound deficits in LTP and LTD at Schaffer collateral-CA1 synapses associated to increased spine density and enhanced presence of mushroom-type spines, as revealed by Golgi staining

https://www.ncbi.nlm...pubmed/23400819
Overall, the results suggest that citalopram at the recommended human doses induces some genetic alterations, which can adversely affect the normal cellular functioning in mice. The mechanism(s) by which citalopram cause this adverse effect appear related, in part, to primary DNA strand breakage as detected by the comet assay as well as clastogenic and aneugenic events as detected by the FISH assay. Therefore, the clinical use of citalopram must be weighed against the risks of genetic damages in citalopram users.

https://www.ncbi.nlm...pubmed/23280034
The results showed that the drug fluoxetine was SCE and sperm abnormalities inducer. The response of this compound was dose-dependent, and showed that the highest tested dose increased about two times SCE and four times the sperm abnormalities control level. The cellular proliferation kinetics was not affected by the chemical, and the mitotic indexes were slightly diminished with the highest dose. The percentage of sperm count and sperm motility decreased (p < 0.01) with increased the dose of treatment.

https://www.ncbi.nlm...pubmed/23232079
Overall, this study provides that citalopram at the recommended human doses after long-term treatment is genotoxic for mouse germ cells (DNA breaks). Thus, male patients receiving citalopram may stand at higher risk for abnormal reproductive outcomes, particularly in the reproductive ages.

https://www.ncbi.nlm...pubmed/22750076
Genetic changes occurring in somatic cells of the wing's imaginal discs, cause the formation of mutant clones on the wing blade. The results of this study show that citalopram had a genotoxic effect in the Drosophila SMART. Sertraline, however, did not show any genotoxic effect in balancer heterozygous wings. This study concluded that more information is needed to be certain regarding the mutagenic effects of sertraline.

https://www.ncbi.nlm...pubmed/21937534
Olanzapine (OLZ), risperidone (RPD) and quetiapine (QTP) are atypical antipsychotic drugs and are commonly used for the treatments of schizophrenia and bipolar disorders.However, the application of the highest drug concentrations (250 mg/L and above) caused the sterility in lymphocyte cultures. It is concluded that the tested three different atypical antipsychotic drugs can be used safely, but it is necessary to consider the cytotoxic effects that are likely to appear depending on the doses exposed.

https://www.ncbi.nlm...pubmed/20542924
Our results indicated that the tested antipsychotic drug did not induce SCEs in lymphocytes of treated cultures. However, the application of the highest OLZ concentration caused oxidative stress. It is concluded that the OLZ can be used safely, but it is necessary to consider the tissue damages that are likely to appear depending on the oxidative stress.

https://www.ncbi.nlm...pubmed/18804223
Patients treated with selective serotonin reuptake inhibitors had a mean of 8.1% +/- 5.4% normal forms per ejaculate. A significant increase in the amount of denatured single strand DNA in total cellular DNA was found in patients treated with selective serotonin reuptake inhibitors compared with that in controls (43.2% +/- 11.4% vs 21.4% +/- 10.6%, p = 0.01). Each semen analysis parameter significantly correlated with treatment duration.

https://www.ncbi.nlm...pubmed/12904104
Classical antidepressants such as monoamine oxidase inhibitors (MAOIs) or tricyclic antidepressants (TCAs) seem to have the highest potential to induce liver damage compared with the newer drugs such as selective serotonin re-uptake inhibitors (SSRIs). The potential for severe hepatotoxicity associated with nefazodone is stressed. Guidelines for therapy and prevention of antidepressant-induced hepatotoxicity are also discussed.

https://www.ncbi.nlm...pubmed/11482523
The effects of acute (24 h) exposure to the antidepressants amitriptyline, imipramine (both tricyclics), fluoxetine (a selective serotonin re-uptake inhibitor) and tranylcypromine (a monoamine oxidase inhibitor) on DNA damage in cultured C6 rat glioma cells were determined using an alkaline comet assay. The data show that the antidepressants induce significant amounts DNA damage in C6 cells

https://www.ncbi.nlm...pubmed/20851831
The recombinogenic potential of this antidepressant in A. nidulans may be associated with the recombinational repair of citalopram-induced DNA strand breaks

https://www.ncbi.nlm...pubmed/15036127
Patients with both generalized anxiety disorder and major depression exposed to daily doses of sertraline do not indicate a possible clastogenic hazard.

https://www.ncbi.nlm...les/PMC3702119/
We conclude that although, Wellbutrin exerts potential genotoxic effects in cultured lymphocytes, its cytogenetic effects are very unlikely to occur in blood cultures of WB-administered subjects.

https://www.ncbi.nlm...pubmed/16751836
Neurotoxic reaction to citalopram.

Summary

Cymbalta
⦁ causes weight gain
⦁ causes liver damage
⦁ slows clotting
⦁ damages red blood cells beginning in 2 weeks and is cumulative
⦁ does not damage DNA
⦁ controls/alters RNA and miRNA performamce resulting in different effects than the DNA genes are coded for
⦁ alters BDNF mRNA but also the manufacturing of BDNF (brain-derived neurotrophic factor) itself. Thus RNA and BDNF controls nerve cell production and survival
⦁ returns the glutamate gene function to normal activity in the hippocampus. Glutamate is an amino acid, one of the twenty amino acids used to construct proteins, and as a consequence is found in high concentration in every part of the body. In the nervous system it plays a special additional role as a neurotransmitter: a chemical that nerve cells use to send signals to other cells. In fact glutamate is by a wide margin the most abundant neurotransmitter in the vertebrate nervous system. It is used by every major excitatory information-transmitting pathway in the vertebrate brain, accounting in total for well over 90% of the synaptic connections in the human brain. It is no wonder that Cymbalta can cause such varied side effects and withdrawal symptoms as it can potentially effect all nerve cells in the brain and nervous system.
⦁ increases seratonin and noradrenaline levels in the spinal cord
⦁ has great effect on nerve cell growth, survival and death.
⦁ effects nitrous oxide levels in the brain.
⦁ decreases reuptake of dopamine
⦁ increases memory retrieval in the amygdala. (fear center in the brain)
⦁ effects the pons that relay signals from the forebrain to the cerebellum, along with nuclei that deal primarily with sleep, respiration, swallowing, bladder control, hearing, equilibrium, taste, eye movement, facial expressions, facial sensation, and posture.).
⦁ lowers nerve growth factor concentrations
⦁ decreased the activity of the beta-actin mRNA Beta actin is used in muscle contractions.

http://www.cymbaltaw...elps#entry66904
Details and research on Cymbalta damage and effects.
AM - In extremely acidic conditions, or when a person's stomach contents move out of the stomach slowly, Cymbalta, unprotected by the enteric coating may undergo hydrolysis to form Naphthol. Caution is advised in using Cymbalta in patients with conditions thatmay slow gastric emptying." "Naphthol is found in pesticides and is toxic to lungs and mucous membranes. Repeated exposure to Naphthol may produce general deterioration of health by an accumulation in one or many human organs." "Naphthol may cause DNA damage to human lymphocytes."

https://dailymed.nlm...f2-c185fbad64ba
"In extremely acidic conditions, CYMBALTA, unprotected by the enteric coating, may undergo hydrolysis to form naphthol. Caution is advised in using CYMBALTA in patients with conditions that may slow gastric emptying (e.g., some diabetics). "

http://www.cymbaltaw...age/?hl=caution
Damage caused by Cymbalta and other antidepressants.
------------------------------------------------------------------------------------------------------------
Cymbalta and Alcohol
http://www.fda.gov/d...y/ucm088579.pdf
Page 5 of 6 from FDA
Use of Cymbalta concomitantly with heavy alcohol intake may be associated with severe liver injury. Avoid heavy alcohol use while taking Cymbalta.

The FDA site says that 0.46% of Cymbalta users reported increased alcohol consumption.

https://www.ncbi.nlm...pubmed/25161814
Chronic treatment with prazosin or duloxetine lessens concurrent anxiety-like behavior and alcohol intake: evidence of disrupted noradrenergic signaling in anxiety-related alcohol use.
Cymbalta lowers alcohol consumption.

https://www.ncbi.nlm...pubmed/18195589
Effects of naltrexone, duloxetine, and a corticotropin-releasing factor type 1 receptor antagonist on binge-like alcohol drinking in rats.
Decreased binge drinking in rats.

Note. The decrease in alcohol consumption would most likely not pertain to those suffering with mania and that is supported by looking at the alcohol related postings on this site where many report excessive consumption while being on Cymbalta.


Clonidine/Alcoholism
1) Clonidines effect on Alcohol consumption.
https://www.ncbi.nlm...pubmed/25085719
Alcohol. 2014 Sep;48(6):543-9. doi: 10.1016/j.alcohol.2014.07.002. Epub 2014 Jul 14.
The α2-adrenergic receptor agonist, clonidine, reduces alcohol drinking in alcohol-preferring (P) rats.
Clonidine significantly reduced alcohol intake.


https://www.ncbi.nlm...pubmed/15551068
Psychopharmacology (Berl). 2005 May;179(2):366-73. Epub 2004 Nov 17.
Role of alpha-2 adrenoceptors in stress-induced reinstatement of alcohol seeking and alcohol self-administration in rats.
To the degree that the present results are relevant to human alcoholism, alpha-2 adrencoceptor agonists should be considered in the treatment of alcohol dependence.

2) Clonidines effectiveness in treating alcohol withdrawal.
https://www.ncbi.nlm.../pubmed/3327372
Clonidine and alcohol withdrawal.
The alpha-2-adrenergic agonists in alcohol treatment seemed modestly effective for treatment of some parts of alcohol withdrawal.

https://www.ncbi.nlm.../pubmed/1969792
Drug Alcohol Depend. 1990 Feb;25(1):43-8.
The effect of clonidine and related substances on voluntary ethanol consumption in rats.
Clonidine, guanfacine and tiamenidine, in equihypotensive doses, significantly reduced alcohol intake in ethanol-preferring rats having free choice between 10% ethanol and drinking water. Water intake was only slightly reduced, especially during the first hours following the administration of clonidine. Simultaneous treatment with yohimbine attenuated the clonidine-induced reduction in ethanol intake. Putative central mechanisms underlying the observed inhibitory actions of clonidine and other alpha-2 adrenoceptor agonists on oral self-administration of alcohol are discussed.

https://www.ncbi.nlm...pubmed/21521867
https://www.ncbi.nlm.../pubmed/1103576
https://www.ncbi.nlm.../pubmed/7978098
https://www.ncbi.nlm.../pubmed/2646983
https://www.ncbi.nlm...pubmed/11091026
https://www.ncbi.nlm.../pubmed/6415735
https://www.ncbi.nlm.../pubmed/3300587
https://www.ncbi.nlm.../pubmed/3893195
https://www.ncbi.nlm.../pubmed/3441163
https://www.ncbi.nlm...pubmed/15551068
And many many more....

Hydroxyzine/alcoholism
There is no data on the use of hydroxyzine to reduce the desire/use of alcohol.
It has to be shown to not be effective in alcohol withdrawal.

Note - Neither clonidine nor hydroxyzine should be used WITH alcohol as it may cause a serious drop in blood pressure.
--------------------------------------------------------------------------------------------------------

Cymbalta and hyperglycemia

http://www.ehealthme...a/hyperglycemia
FDA and others number of reported cases of hyperglycemia

http://dailymed.nlm....F2-C185FBAD64BA
From NIH, a branch of the government.

http://www.ncbi.nlm....les/PMC3056054/
Research article on hyperglycemia.

http://www.accessdat...1427s030lbl.pdf
FDA reports of hyperglycemia.
------------------------------------------------------------------------------------------------------------

Mania/Sexual effects while taking Cymbalta.

Please note that many of these articles relate the high risk of mania as being related to bipolar disorder rather than Major Depression or Anxiety.

https://www.ncbi.nlm...pubmed/22024021
Persistent genital arousal disorder: successful treatment with duloxetine and pregabalin in two cases.
In both women, the treatment proved to be very successful over a long period of time. One of them experienced full remission (duloxetine) and the other one experienced substantial improvement (pregabalin), over a period now lasting for more than a year.

https://www.ncbi.nlm...pubmed/21091877
Sexual function during long-term duloxetine treatment in patients with recurrent major depressive disorder.
Cymbalta can cause sexual dysfunction (decreased sexual labido and performance).

https://www.ncbi.nlm...pubmed/17627739
Changes in sexual functioning associated with duloxetine, escitalopram, and placebo in the treatment of patients with major depressive disorder.
Same as above.

https://www.ncbi.nlm...pubmed/26003261
Psychiatric disorders and sexual dysfunction.
Same as above

https://dailymed.nlm...f2-c185fbad64ba

The following is from the drug insert information that come with Cymbalta.
5.8 Activation of Mania/Hypomania
In adult placebo-controlled trials in patients with major depressive disorder, activation of mania or hypomania was reported in 0.1% (4/3779) of CYMBALTA-treated patients and 0.04% (1/2536) of placebo-treated patients. No activation of mania or hypomania was reported in DPNP, GAD, fibromyalgia, or chronic musculoskeletal pain placebo-controlled trials. Activation of mania or hypomania has been reported in a small proportion of patients with mood disorders who were treated with other marketed drugs effective in the treatment of major depressive disorder. As with these other agents, CYMBALTA should be used cautiously in patients with a history of mania.
Note - Mania is a state of abnormally elevated arousal, affect, and energy level, or "a state of heightened overall activation with enhanced affective expression together with lability of affect." Symptoms include ...
⦁ Inflated self-esteem or grandiosity
⦁ Decreased need for sleep (e.g., feels rested after 3 hours of sleep.)
⦁ More talkative than usual or pressure to keep talking.
⦁ Flights of ideas or subjective experience that thoughts are racing. Increase in goal directed activity, or psychomotor acceleration.
⦁ Distractibility (too easily drawn to unimportant or irrelevant external stimuli).
⦁ Excessive involvement in activities with a high likelihood of painful consequences.(e.g., extravagant shopping, sexual adventures or improbable commercial schemes). Wiki

6.6 Effects on Male and Female Sexual Function in Adults
Changes in sexual desire, sexual performance and sexual satisfaction often occur as manifestations of psychiatric disorders or diabetes, but they may also be a consequence of pharmacologic treatment. Because adverse sexual reactions are presumed to be voluntarily underreported, the Arizona Sexual Experience Scale (ASEX), a validated measure designed to identify sexual side effects, was used prospectively in 4 MDD placebo-controlled trials. In these trials patients treated with CYMBALTA experienced significantly more sexual dysfunction, as measured by the total score on the ASEX, than did patients treated with placebo. Gender analysis showed that this difference occurred only in males. Males treated with CYMBALTA experienced more difficulty with ability to reach orgasm (ASEX Item 4) than males treated with placebo. Females did not experience more sexual dysfunction on CYMBALTA than on placebo as measured by ASEX total score. Negative numbers signify an improvement from a baseline level of dysfunction, which is commonly seen in depressed patients. Physicians should routinely inquire about possible sexual side effects.

http://www.gjpsy.uni...cle-mustafa.pdf
A Case of Possible Duloxetine-Induced Mania
"Her mood initially improved but two weeks into treatment she developed insomnia, hyperactivity and sexual arousal."

"Around the time of admission her symptoms constituted irritability, psychomotor agitation, pressure of speech, flight of ideas, insomnia, auditory and visual hallucinations, grandiose and persecutory delusions, aggressive and reckless behaviour, sexual disinhibition and lack of insight."


https://www.nami.org...tine-(Cymbalta)

The following is from the Nami data sheet on Cymbalta.
"Depression is also a part of bipolar illness. People with bipolar disorder who take antidepressants may be at risk for "switching" from depression into mania. Symptoms of mania include "high" or irritable mood, very high self esteem, decreased need for sleep, pressure to keep talking, racing thoughts, being easily distracted, frequently involved in activities with a large risk for bad consequences (for example, excessive buying sprees)."

http://www.mayoclini...ns/DRG-20067247

Some people may have trouble sleeping, get upset easily, have a big increase in energy, or start to act reckless. If you or your caregiver notice any of these unwanted effects, tell your doctor right away.

----------------------------------------------------------------------------------------------------------
Cymbalta and the Liver
https://dailymed.nlm...185fbad64ba#s23
Drug insert for Cymbalta
Section - 5.2 Hepatotoxicity (Liver toxicity)
"These cases have presented as hepatitis with abdominal pain, hepatomegaly, and elevation of transaminase levels to more than twenty times the upper limit of normal with or without jaundice, reflecting a mixed or hepatocellular pattern of liver injury."
"In most patients, the median time to detection of the transaminase elevation was about two months."
Note - More details on liver issues at this site.

https://www.ncbi.nlm...les/PMC3773985/
"All 6 patients recovered without liver transplantation even though 3 had pre-existing chronic liver disease."
"Duloxetine hepatotoxicity developed within 2 months of drug intake and led to clinically significant liver injury."

https://www.ncbi.nlm...ubmed/17257478/
'In a pooled analysis of 17,615 subjects, the incidence of serum alanine aminotransferase (ALT) levels > 3 times the upper limit of normal (ULN), > 5 ULN, and > 10 ULN were 1%, 0.5%, and 0.2%, respectively.5 Almost all subjects maintained normal values of alkaline phosphatase and total bilirubin with no case of jaundice and hepatocellular injury (“Hy’s law”) reported.'
https://www.ncbi.nlm...ubmed/18690992/
'However, post-marketing surveillance identified 406 cases with potential hepatotoxicity from duloxetine between 8/2004 and 8/2006.6 Of these, 58 cases were considered clinically significant. A careful review of these cases led to the following observations: (a) there was no dose-dependent increase in the incidence of hepatic injury, ( B) a large number of cases occurred between 2 and 8 weeks of therapy and 74% with onset within 16 weeks, © 31% had either pre-existing liver disease or clinical risk factors for liver disease, and (d) there were two fatal cases possibly related to duloxetine.'

https://www.ehealthm...balta/jaundice/
FDA statistics on side effects
"95,293 people reported to have side effects when taking Cymbalta.
Among them, 299 people (0.31%) have Jaundice"
Time on Cymbalta when people have Jaundice *:
⦁ < 1 month: 32.17 %
⦁ 1 - 6 months: 44.35 %
⦁ 6 - 12 months: 5.22 %
⦁ 1 - 2 years: 5.22 %
⦁ 2 - 5 years: 13.04 %
⦁ 5 - 10 years: 0.0 %
⦁ 10+ years: 0.0 %
-----------------------------------------------------------------------------------------------------------
Cymbalta and the skin
https://dailymed.nlm...f2-c185fbad64ba
From the drug insert for Cymbalta...
(side effects) Also includes hypoaesthesia, hypoaesthesia facial, genital hypoaesthesia and paraesthesia oral (Soreness and sensativity in the mouth)
Severe Skin Reactions — Caution patients that CYMBALTA may cause serious skin reactions. This may need to be treated in a hospital and may be life-threatening. Counsel patients to call their doctor right away or get emergency help if they have skin blisters, peeling rash, sores in their mouth, hives, or any other allergic reactions [see Warnings and Precautions (5.6)].
5.6 Severe Skin Reactions
Severe skin reactions, including erythema multiforme and Stevens-Johnson Syndrome (SJS), can occur with CYMBALTA. The reporting rate of SJS associated with CYMBALTA use exceeds the general population background incidence rate for this serious skin reaction (1 to 2 cases per million person years). The reporting rate is generally accepted to be an underestimate due to underreporting.
CYMBALTA should be discontinued at the first appearance of blisters, peeling rash, mucosal erosions, or any other sign of hypersensitivity if no other etiology can be identified.

http://www.mayoclini...es/dxc-20317107
Details on SJS can be found at the above site.
Stevens-Johnson syndrome
Stevens-Johnson syndrome signs and symptoms include:
⦁ Fever
⦁ Unexplained widespread skin pain
⦁ A red or purple skin rash that spreads
⦁ Blisters on your skin and the mucous membranes of your mouth, nose, eyes and genitals
⦁ Shedding of your skin within days after blisters form
If you have Stevens-Johnson syndrome, several days before the rash develops you may experience:
⦁ Fever
⦁ Sore mouth and throat
⦁ Fatigue
⦁ Cough
⦁ Burning eyes
When to see a doctor
Stevens-Johnson syndrome requires immediate medical attention. Seek emergency medical care if you experience signs and symptoms of this condition.
-----------------------------------------------------------------------------------------------------------------------
Cymbalta and Seizures and Sodium
https://www.ncbi.nlm...les/PMC2963463/
We believe that this is the first reported case in which a person developed duloxetine withdrawal seizure secondary to deranged electrolytes after abruptly stopping duloxetine.
Her sodium was 134, potassium was 2.5, chloride 86, glucose 110, calcium 9, and magnesium 1.5.

https://www.ncbi.nlm...les/PMC3229538/
Although the risk of seizures with antidepressants is generally very low, the association with overdose is well established. However, the molecular mechanisms by which antidepressants cause seizures have not been clarified. GIRK2 knockout mice exhibit spontaneous seizures and are more susceptible to seizures induced by pentylenetetrazol than wild-type mice. The risk of seizures in overdoses with sertraline, duloxetine, mianserin, and venlafaxine significantly increases, and amoxapine overdose is more likely to cause seizures. Brain levels of the drugs in overdose cases may be considerably higher than levels during treatment at therapeutic doses, suggesting significant inhibition of neuronal GIRK channels by the drugs. Additionally, other types of K+ channels are inhibited by antidepressants at micromolar concentrations, that is, the two-pore-domain K+ channel, TREK-1 for sertraline and voltage-gated K+ channels for amoxapine and mianserin. Therefore, the inhibition of GIRK channels by the drugs after overdose together with the different types of K+ channels may contribute to increased seizure activity and the occurrence of other neurological side effects by increasing neuronal excitability.
Note - GIRK2 is a K+ ion regulatory mechinism.

https://www.ncbi.nlm...pubmed/16534127
Duloxetine-induced syndrome of inappropriate antidiuretic hormone secretion and seizures.
Description of antidiuretic hormone
Kidney
Aantidiuretic hormone has three main effects:
Increasing the water permeability of initial and cortical collecting tubules and inner medullary collecting duct in the kidney, thus allowing water reabsorption and excretion of more concentrated urine, i.e., antidiuresis.
Increasing permeability of the inner medullary portion of the collecting duct to urea by regulating the cell surface expression of urea transporters, which facilitates its reabsorption into the medullary interstitium as it travels down the concentration gradient created by removing water from the connecting tubule, cortical collecting duct, and outer medullary collecting duct.
Acute increase of sodium absorption across the ascending loop of henle. This adds to the countercurrent multiplication which aids in proper water reabsorption later in the distal tubule and collecting duct.
Note - This could severely impact sodium and potassium levels in the blood stream.

From article - "We describe a woman who developed severe hyponatremia on exposure to duloxetine and recurrence on inadvertent rechallenge, suggesting the causative relationship of this drug to hyponatremia. "
Hyponatremia - is a low sodium level in the blood.

http://www.ncbi.nlm....pubmed/22306002
Generalized tonic-clonic seizure secondary to duloxetine poisoning: a short report with favorable out come.
Note - Tonic–clonic seizures (formerly known as grand mal seizures) are a type of generalized seizure that affects the entire brain. Tonic–clonic seizures are the seizure type most commonly associated with epilepsy and seizures in general, though it is a misconception that they are the only type.

https://www.ncbi.nlm...les/PMC2963463/
Duloxetine Withdrawal Seizure
She came to the emergency room with complaints of nausea, clear liquid vomitus, anxiety, “electical sensation” inside the body, restlessness, decreased liquid intake, abdominal pain, and decreased sleep. She stopped taking her duloxetine two days previoiusly. She had two generalized tonic clonic seizures 20 minutes apart in the hospital.

https://www.accessda...s011s013lbl.pdfFDA
Hyponatremia — Cases of hyponatremia (some with serum sodium lower than 110 mmol/L) have been reported and appeared to be reversible when Cymbalta was discontinued. Some cases were possibly due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The majority of these occurrences have been in elderly individuals, some in patients taking diuretics or who were otherwise volume depleted.

Note this article links Cymbalta to Hyponatremia caused by inappropriate antidiuretic hormone secretion.
Medical research articles linking Cymbalta to Hyponatremia
http://www.ncbi.nlm....pubmed/23075738
https://www.ncbi.nlm...les/PMC3285747/
https://www.ehealthm.../hyponatraemia/
https://www.ncbi.nlm...pubmed/25538343
https://www.ncbi.nlm...pubmed/25911354
https://www.ncbi.nlm...pubmed/18562431
https://www.ncbi.nlm...pubmed/17224730
https://www.ncbi.nlm...pubmed/17502788

---------------------------------------------------------------------------------------------------------
Cymbalta and seizures
1) Comments by Members
Grand Mal Seizure And Mouth Spasms ?
Posted by justsayno on 02 April 2017 - 07:58 PM in How to Find Support
Was trying to work it out tonight. Looking for any patterns / similarities etc
Only obvious thing being that both seizures occurred after a dosage drop from 40 to 30 mg.

Grand Mal Seizure And Mouth Spasms ?
Posted by justsayno on 01 April 2017 - 02:26 PM in How to Find Support
Hi Gail
Far as I am aware No. In 28 years I've never had any seizures until I began taking Cymbalta.

Bead Counting Advice Doesn't Jive With My Capsule Contents
Posted by PtldFrank on 04 September 2016 - 04:44 PM in Weaning Off Cymbalta
Vinpin,
Regarding seizures, that's a subject I do have personal experience with. The good news is that I'm seizure free for more than 10 years. The bad news is that I had half a dozen gran mal seizures in the 12 years prior, starting with wellbutrin. I tend to believe the seizures all came from the various meds (15-20 combinations) I went through. The only thing that seems to have stopped the seizures is the anti seizure medicine Keppra.

Involuntary Cold Turkey From 120Mg
Posted by Cassandra on 13 February 2015 - 10:32 AM in What are you feeling?
Hello world, this is Cassandra. It's been a rough month since I quit cymbalta and I think it'd be best to start from the very beginning.

I have been experiencing major depression as long as I can remember, at least from the age of 9 which is where my earliest memories are. I was put on my first antidepressant--celexa--5 or six years ago. I had been depressed before but when I started medication it just got worse. Five/six months ago I was put on cymbalta, first 60 mg then 120, and it got worse. I became violently suicidal and after a course of 12 ect treatments I attempted suicide by taking 2 bottles of cymbalta at once (my insurance had just switched me to where I could only get my meds in a 90 day supply--bad, bad idea to give someone who's suicidal a giant bag of meds.)

I woke up having seizures that went on for hours, and then on and off for a few days. When I got to the hospital, I was hallucinating, and couldn't stand or eat for days. I learned how to walk again and a month later I can ride my bike again.

Listing The Positive Events Daily Through My Cymbalta Withdrawl
Posted by FiveNotions on 24 December 2014 - 09:42 AM in ARE YOU NEW HERE? Words from the wise about Cymbalta
I was just talking with a friend about where I was last year this time ... compared to this year ... and it seemed more than worthy of a post in our "Positives" thread ...

Last year this time I was about 19 days into hard, cold turkey withdrawal ... I was overwhelmed with vertigo and nausea, confined almost totally to bed, and crawling to the bathroom to puke ... at one point, I just took my blanket and pillow in there and slept/lay curled up on the floor (less far to travel) ... I was unable to eat any solid foods, not even crackers ... and was living on broth and herb tea and water (didn't make for much to puke up, but I still did) ...
I was having constant muscle spasms, and had a couple of seizures (at least I assume that's what they were, I just blacked out and woke up on the floor) ... I was having auditory and visual hallucinations, constant cold, dripping sweats, and horrid general body aches and pains .... couldn't sleep much at all, just an hour or so at a time ... I hadn't showered, washed my hair, changed clothes, or changed my sheets, once ... and I simply did not care ...

Article: Duloxetine Withdrawal Seizure [Cold Turkey Withdrawal]
Posted by FiveNotions on 03 January 2015 - 09:32 AM in Cymbalta in the News
I think I had at least 1, possibly 2, seizures during hard, cold turkey withdrawal ... but don't know for sure, was alone and woke up on the floor ... yet another reason not to quit this poison cold turkey!
Duloxetine Withdrawal Seizure [full text]
Psychiatry (Sept 2006)
http://www.ncbi.nlm....les/PMC2963463/

From the article:

Much has been written about the use and side effects profile of duloxetine (Cymbalta®). We report a case of a patient who had generalized tonic clonic seizures after abruptly stopping duloxetine.

Case report. Ms. X was a 59-year-old Caucasian woman with a diagnosis of major depressive disorder recurrent severe without psychotic feature. She was stabilized on duloxetine 90mg p.o. daily.

She came to the emergency room with complaints of nausea, clear liquid vomitus, anxiety, “electical sensation” inside the body, restlessness, decreased liquid intake, abdominal pain, and decreased sleep.

She stopped taking her duloxetine two days previoiusly. She had two generalized tonic clonic seizures 20 minutes apart in the hospital.

Urine drug screen was negative. Urinalysis was negative. Complete blood count (CBC) was normal. Her sodium was 134, potassium was 2.5, chloride 86, glucose 110, calcium 9, and magnesium 1.5. Her blood urea nitrogen (BUN) and creatinine were normal. Her liver function tests were normal except mildly elevated alkaline phosphatase of 126. Computed tomography (CT) scan of her head was negative. There was no sign of infection at the point of admission. She was stabilized and was then started on a different antidepressant due to her history of nonadherence. She had no further seizures during her hospital stay.

Seizure?
Posted by sarahb on 04 April 2014 - 10:59 AM in What are you feeling?
My mother has been on Cymbalta I think 90mg and she recently started having seizures. I wonder if there could be any correlation. I'm the one who was on it 5 days and found your group and has decided to get off. Now my thoughts are with my mom. I know different things about her health are shorting her health but I hate to think what this drug is doing to her and God forbid she needs to get off.

And Here I Am- Am I Screwed Forever?
Posted by jenniesue on 09 December 2013 - 12:49 PM in ARE YOU NEW HERE? Words from the wise about Cymbalta
The DVT/Blood Clots were after I lost a pregnancy. Yes I was placed on Cymbalta for pain. The seizures I had started within 2 weeks of taking Cymbalta. Yes I have discussed all issues with my Dr. and they give me a diagnosis of something else, and have told me just keep taking the Cymbalta. Where do I start to get off of this evil med? I go to see my Dr. Monday Dec 15.

Seen The New Commercials?
Posted by Pixi on 10 June 2012 - 02:32 AM in Cymbalta in the News
I'd thought I was unsubscribed...but this thing emailed me for a reply so here goes. I can't believe it's almost a year to the day since I made the post on here. That means I've been totally Cymbalta free for 6 months! I took my healthcare into my own hands & I'm glad I had the fortitude to go through this & come out as well as I have.

I'm taking nothing for depression/neuropathy and still having the odd brain zap & dizziness - my "Cymbalta moments" as I call it. . Still having seizures at night, bouts of horrible dementia and just wish I'd never listened to the Doctors & allowed myself to be their labrat for this evil drug. Depression is still much better off it and bladder control is almost back to normal. The ONLY way to go is wean slowly, count the grains even tho it's tedious - over months, even if you're only just on it a few weeks, start to cut it down really slowly - your brain is way more delicate than you know. This shit does pretty weird things to you - that's how it's supposed to work - alter your neurology. Don't let them mess with you. It caused me DID/MPD, made my diabetic neuropathy 100 times worse & a host of other shit I've probably posted about elsewhere on this forum.

Seizures From Cymbalta
Posted by Namaste on 02 May 2012 - 02:04 AM in Weaning Off Cymbalta
Doctor changed celexa to cymbalta And was ok with it for a month and
I started Having hives, itching and bruises. My doctor stopped cymbalta and gave me prednisone. Then i started having seizures where i was fully aware of what was happening so I'm now on lamictal for seizures. Anyone of you having the same experience?
My Chapter Of Hell
Posted by distill on 06 December 2011 - 02:55 AM in ARE YOU NEW HERE? Words from the wise about Cymbalta
I have already wrote this once, but if I can help out another person then I've done what I set out to do.

I know some people have done great while taking it but the withdrawal is what gets them. I was not depressed, I was injured on the job crush three disc in my lower back. I was put on it for sciatic help.

I had a house, cars, and my best friend for a fiance. Within two weeks of taking it I lost my mind. Manic aggression, seizures, nightmares, etc. I did things I never wouldve done before this. Its like i either knew what i was doing and didnt care or i flat out dont remember. We were losing the house and my demeanor drove her away. Workers comp denied paying for all psychological meds and I flat out couldn't afford $400 for 90days. That was in January of this year.
Neuropathy As A Side Effect?
Posted by cookie on 28 November 2011 - 11:57 AM in Weaning Off Cymbalta
Dear Pixi

I took cymbalta for depression, other than than I was a pretty healthy person. After 6 years of taking it, I have sugar problems and now I am experiencing prickling sensations and pin & needles. I also have problems remembering names. I also experienced seizures and problems with my joints which I never had prior to the medication

Check In On Your Progress Here!
Posted by CindiEponabri on 16 October 2011 - 01:31 AM in Weaning Off Cymbalta
1) Method you're using
Counting bead method, kinda... I take out about 1/4 of the beads out of one of the two capsules for each day's dosage, for a week. The following week it will be 1/2 of the beads of one capsule.

2) Starting dose
120mg

3) Current dose
105mg (roughly)

4) Withdrawal symptoms you're having
more pain, anxiety, dizziness, tired, nausea, cold/flu symptoms, nightmares, itching,


5) Things that have improved.
Seizures.. we had thought they were being caused from the Oxycotin, but now I see it was from the Cymbalta, because for the most part they are now gone. I have a little one every now and then.

My Story
Posted by cookie on 26 July 2011 - 02:25 PM in Weaning Off Cymbalta
Dear Imdone:
.....However I learned to differentiate the initiall symptoms from withdrawals. I took the medication for severe depression. When I reduced dose I started experiencing asthma, itching, joint pain, problems finding words to talk and comprehending language, dizziness, vomiting, seizures, facial tics, sensitivity to noises and light, tremors, allergies, sore throat, etc which I definitely didn´t have when my depression appeared 6 years ago.
---------------------------------------------------------------------------------------------------------
2) Drug insert from Eli Lilley for Cymbalta
https://dailymed.nlm...f2-c185fbad64ba

5.7 Discontinuation of Treatment with CYMBALTA
Discontinuation symptoms have been systematically evaluated in patients taking CYMBALTA. Following abrupt or tapered discontinuation in adult placebo-controlled clinical trials, the following symptoms occurred at 1% or greater and at a significantly higher rate in CYMBALTA-treated patients compared to those discontinuing from placebo: dizziness, headache, nausea, diarrhea, paresthesia, irritability, vomiting, insomnia, anxiety, hyperhidrosis, and fatigue.
During marketing of other SSRIs and SNRIs (serotonin and norepinephrine reuptake inhibitors), there have been spontaneous reports of adverse events occurring upon discontinuation of these drugs, particularly when abrupt, including the following: dysphoric mood, irritability, agitation, dizziness, sensory disturbances (e.g., paresthesias such as electric shock sensations), anxiety, confusion, headache, lethargy, emotional lability, insomnia, hypomania, tinnitus, and seizures. Although these events are generally self-limiting, some have been reported to be severe.

Patients should be monitored for these symptoms when discontinuing treatment with CYMBALTA. A gradual reduction in the dose rather than abrupt cessation is recommended whenever possible. If intolerable symptoms occur following a decrease in the dose or upon discontinuation of treatment, then resuming the previously prescribed dose may be considered. Subsequently, the physician may continue decreasing the dose but at a more gradual rate [see Dosage and Administration (2.7)].

6.12 Postmarketing Spontaneous Reports
The following adverse reactions have been identified during post approval use of CYMBALTA. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure.
Adverse reactions reported since market introduction ....., seizures upon treatment discontinuation, supraventricular arrhythmia, tinnitus (upon treatment discontinuation), trismus, and urticaria.
=============================================================
3) Medical Research on Seizures and Cymbalta.
Other info on seizures,

https://www.ncbi.nlm...les/PMC3229538/
"Although the risk of seizures with antidepressants is generally very low, the association with overdose is well established [80]. However, the molecular mechanisms by which antidepressants cause seizures have not been clarified. GIRK2 knockout mice exhibit spontaneous seizures and are more susceptible to seizures induced by pentylenetetrazol than wild-type mice [37]. The risk of seizures in overdoses with sertraline, duloxetine, mianserin, and venlafaxine significantly increases [80]–[82], and amoxapine overdose is more likely to cause seizures [83]. "
80. Montgomery SA. Antidepressants and seizures: emphasis on newer agents and clinical implications. Int J Clin Pract. 2005;59:1435–1440. [PubMed]
81. Whyte IM, Dawson AH, Buckley NA. Relative toxicity of venlafaxine and selective serotonin reuptake inhibitors in overdose compared to tricyclic antidepressants. Q J Med. 2003;96:369–374. [PubMed]
82. Isbister GK, Bowe SJ, Dawson A, Whyte IM. Relative toxicity of selective serotonin reuptake inhibitors (SSRIs) in overdose. J Toxicol Clin Toxicol. 2004;42:277–285. [PubMed]
------------------------------------------------------------------------------------------------------------
https://www.ncbi.nlm...les/PMC4683813/
"Epilepsy is a serious condition which can profoundly affect an individual’s life. While there is some evidence to suggest an association between antidepressant use and epilepsy and seizures it is conflicting and not conclusive. "
"Conclusions
Risk of epilepsy/seizures is significantly increased for all classes of antidepressant. There is a need for individual risk-benefit assessments in patients being considered for antidepressant treatment, especially those with ongoing mild depression or with additional risk factors. Residual confounding and indication bias may influence our results, so confirmation may be required from additional studies."
-----------------------------------------------------------------------------------------------------------
https://www.ncbi.nlm...pubmed/16534127
Neurology. 2006 Mar 14;66(5):773-4.
Duloxetine-induced syndrome of inappropriate antidiuretic hormone secretion and seizures.
Maramattom BV1.
"The syndrome of inappropriate antidiuretic hormone secretion (SIADH) and hyponatremia is a well known side effect of older selective serotonin reuptake inhibitors (SSRIs) such as paroxetine, sertraline, fluoxetine, citalopram, escitalopram, and fluvoxamine.1,2 The frequency of hyponatremia is around 8 per 1,000 among elderly women receiving fluoxetine.2 Although the second-generation dual blockers, selective serotonin–norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine and duloxetine, are touted to have a wider therapeutic index, hyponatremia is encountered even with venlafaxine. To date, Medline searches do not reveal any reports of hyponatremia associated with duloxetine. We describe a woman who developed severe hyponatremia on exposure to duloxetine and recurrence on inadvertent rechallenge, suggesting the causative relationship of this drug to hyponatremia. "
------------------------------------------------------------------------------------------------------------
http://www.psychforu...topic69139.html
This is a thread about seizures and Cymbalta you might want to check out.
-------------------------------------------------------------------------------------------------------------
http://www.ehealthme...mbalta/seizure/
95,293 people reported to have side effects when taking Cymbalta.
Among them, 1,077 people (1.13%) have Seizures
------------------------------------------------------------------------------------------------------------
https://www.ncbi.nlm...pubmed/16534127
Duloxetine-induced syndrome of inappropriate antidiuretic hormone secretion and seizures.
-------------------------------------------------------------------------------------------------------------
http://www.ncbi.nlm....pubmed/22306002
Generalized tonic-clonic seizure secondary to duloxetine poisoning: a short report with favorable out come.
Abstract
Duloxetine is a potent and selective inhibitor of serotonin and norepinephrine reuptake (SNRI) with a weak activity over dopamine reuptake used in the treatment of major depressive disorder. Daily doses of 60 mg are effective in treatment of major depression. There are few cases of isolated duloxetine overdose in humans. We think this is the first report of a generalized tonic-clonic seizure following isolated duloxetine poisoning with a very high dosage.
------------------------------------------------------------------------------------------------------------
https://www.ncbi.nlm...les/PMC2963463/
Duloxetine Withdrawal Seizure
She came to the emergency room with complaints of nausea, clear liquid vomitus, anxiety, “electical sensation” inside the body, restlessness, decreased liquid intake, abdominal pain, and decreased sleep. She stopped taking her duloxetine two days previoiusly. She had two generalized tonic clonic seizures 20 minutes apart in the hospital.
=============================================================
4) Misc.
Benzos can trigger seizures.
------------------------------------------------------------------------------------------------------------
Hyponatremia
Note - Hyponatremia is a know cause of grand mal seizures, but low potassium is not. Cymbalta can cause Hyponatremia (low serum sodium levels). See below
https://www.accessda...s011s013lbl.pdfFDA
Hyponatremia — Cases of hyponatremia (some with serum sodium lower than 110 mmol/L) have been reported and appeared to be reversible when Cymbalta was discontinued. Some cases were possibly due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The majority of these occurrences have been in elderly individuals, some in patients taking diuretics or who were otherwise volume depleted.

http://www.ncbi.nlm....pubmed/23075738
A case of severe hyponatremia induced by duloxetine and ziprasidone.

https://www.ncbi.nlm...les/PMC3285747/
Rapid-Onset Hyponatremia Induced by Duloxetine in a Middle-Aged Male with Depression and Somatic Symptoms

https://www.ehealthm.../hyponatraemia/
95,293 people reported to have side effects when taking Cymbalta.
Among them, 649 people (0.68%) have Hyponatraemia

https://www.ncbi.nlm...pubmed/25538343
Duloxetine-induced hyponatremia in an elderly patient treated with thiazide diuretics.

https://www.ncbi.nlm...pubmed/25911354
Syndrome of inappropriate antidiuretic hormone secretion: a story of duloxetine-induced hyponatraemia.

https://www.ncbi.nlm...pubmed/18562431
Severe and symptomatic hyponatremia following duloxetine treatment.

https://www.ncbi.nlm...pubmed/17224730
Duloxetine and hyponatremia: a report of 5 cases.

https://www.ncbi.nlm...pubmed/17502788
Recurrent hyponatremia after substitution of citalopram with duloxetine.
And more....

https://www.mayoclin...ms/con-20031445
Mayo Clinic
Hyponatremia signs and symptoms may include:
⦁ Nausea and vomiting
⦁ Headache
⦁ Confusion
⦁ Loss of energy and fatigue
⦁ Restlessness and irritability
⦁ Muscle weakness, spasms or cramps
⦁ Seizures
⦁ Coma

----------------------------------------------------------------------------------------------------------
Drugs.com
Applies to: Wellbutrin (bupropion), Cymbalta (duloxetine)
Talk to your doctor before using buPROPion together with DULoxetine. Combining these medications may increase the risk of seizures, which may occur rarely with either medication. In addition, buPROPion can increase the blood levels of DULoxetine, which may increase other side effects. You may be more likely to experience seizures with these medications if you are elderly, undergoing alcohol or drug withdrawal, have a history of seizures, or have a condition affecting the central nervous system such as a brain tumor or head trauma.
------------------------------------------------------------------------------------------------------------

Cymbalta's effect on neurotranmitters in the brain.

http://www.ncbi.nlm....les/PMC2626928/

http://www.ncbi.nlm....pubmed/18751896

http://www.ncbi.nlm....pubmed/15991911

http://www.ncbi.nlm..../pubmed/8592129

http://www.ncbi.nlm..../pubmed/7576005

-----------------------------------------------------------------------------------------------------------

Cymbalta Fat soluble & tissue absorbtion.
From:
http://www.drugs.com/pro/cymbalta.html
"Duloxetine hydrochloride is a white to slightly brownish white solid, which is slightly soluble in water."
Note - From the structure we can see that the compound is primarily non-polar and therefore should be fat soluble.

From:
http://www.drugbank.ca/drugs/DB00476
Water Solubility = 0.00296 mg/mL (Vertually insoluble) ALOGPS
Note - If it is not water suluble (polar (has a negative or positive charge)) then it is non-polar (not charged) and would be lipid soluble.

From:
http://www.selleckch...l-cymbalta.html
Chemical Information

Solubility (25°C) * In vitro DMSO 67 mg/mL (200.67 mM)
Water <1 mg/mL (<1 mM)
Ethanol <1 mg/mL (<1 mM)

Note - Dissolves well in DMSO a relatively nonpolar solvent.

From:
http://toxwiki.wikis....com/Duloxetine
Soluble in dimethylformamide (nonpolar) and water.

From:
https://www.ncbi.nlm...les/PMC3299448/
Table I
Amount of Solid Lipid (fat) Required to Solubilize 20 mg of DLX and Percent Partitioning of DLX in Lipid vs Water
Solid lipid Amount (mg) % Partitioning
Glyceryl monostearates 400 92
Glyceryl behenate 700 33
Glyceryl palmitostearate 650 60
Geleol 450 60
Gelucire 44/14 800 –

From 33% to 92% lipid (fat) soluble.
Ta
https://oup.silverch...BIA4LVPAVW3QbleII.
http://www.ema.europ...776.pdfstmortemTissue

Duloxetine was highly bound to proteins in plasma, the mean percent bound to human plasma proteins at a duloxetine concentration of 150.2 ng/mL being 95.9%
Duloxetine was present in high concentrations in the stomach and intestinal contents at 3 to 12 hours
postdose. Kidney, liver, and lung contained the highest tissue concentrations.Overall, the liver was determined to be the primary organ responsible for the metabolism of duloxetine. Distribution of Duloxetine
------------------------------------------------------------------------------------------------------------
PSSD
J Clin Psychopharmacol. 2015 Jun;35(3):273-8. doi: 10.1097/JCP.0000000000000300.
Post-SSRI Sexual Dysfunction: Clinical Characterization and Preliminary Assessment of Contributory Factors and Dose-Response Relationship.
· Abstract
Emerging evidence suggests that sexual dysfunction emerging during treatment with selective serotonin reuptake inhibitors (SSRIs) and/or serotonin-norepinephrine reuptake inhibitors (SNRIs) persists in some patients beyond drug discontinuation (post-SSRI sexual dysfunction [PSSD]). We sought to identify and characterize a series of such cases and explore possible explanatory factors and exposure-response relationship. Subjects who responded to an invitation in a forum dedicated to PSSD filled out a survey via online software. Case probability was defined according to the following 3 categories of increasing presumed likelihood of PSSD. Noncases did not meet the criteria for possible cases. Possible cases were subjects with normal pretreatment sexual function who first experienced sexual disturbances while using a single SSRI/SNRI, which did not resolve upon drug discontinuation for 1 month or longer as indicated by Arizona Sexual Experience Scale scores. High-probability cases were also younger than 50-year-olds; did not have confounding medical conditions, medications, or drug use; and had normal scores on the Hospital Anxiety and Depression Scale. Five hundred thirty-two (532) subjects completed the survey, among which 183 possible cases were identified, including 23 high-probability cases. Female sex, genital anesthesia, and depression predicted current sexual dysfunction severity, but dose/defined daily dose ratio and anxiety did not. Genital anesthesia did not correlate with depression or anxiety, but pleasureless orgasm was an independent predictor of both depression and case probability. Limitations of the study include retrospective design and selection and report biases that do not allow generalization or estimation of incidence. However, our findings add to previous reports and support the existence of PSSD, which may not be fully explained by alternative nonpharmacological factors related to sexual dysfunction, including depression and anxiety.

Eur J Pharmacol. 2015 Apr 15;753:263-8. doi: 10.1016/j.ejphar.2014.11.031. Epub 2014 Dec 4.
Penile anesthesia in Post SSRI Sexual Dysfunction (PSSD) responds to low-power laser irradiation: a case study and hypothesis about the role of transient receptor potential (TRP) ion channels.
· Abstract
· Treatment of paroxetine-induced penile anesthesia in Post SSRI Sexual Dysfunction (PSSD) by Low-power Laser Irradiation (LPLI) is unknown in medical literature. The aim of the current article is to report partial efficacy of LPLI for paroxetine-induced persistent penile anesthesia. We report on a male patient who presented with a history of reversible loss of smell, taste and skin sensitivity occurring within a week after start of 20mg/day paroxetine-hemihydrate for a depressive period. Concurrently, patient suffered from penile anesthesia, scrotum hypesthesia, anejaculation and erectile difficulties with normal sexual desire. During 2.5 years of paroxetine treatment and throughout 2 years after paroxetine discontinuation, genital and sexual complaints persisted. Penile anesthesia was treated by LPLI with single and multi diode pulsed laser probes. After 20 LPLI-treatment sessions of 15min each, patient reported partial return of penile touch and temperature sensation. Clinical improvement of glans penis sensitivity was reported to 20% and 40%, compared to pre-paroxetine treatment penile sensitivity during erect and flaccid states, respectively. However, anejaculation and erectile difficulties remained unchanged. Briefly, in the current patient with early onset of PSSD, LPLI treatment reduced paroxetine-induced penile anesthesia. It is hypothesized that SSRI treatment induces disturbances of transient receptor potential (TRP) ion channels of mechano-, thermo- and chemosensitive nerve endings and receptors resulting in the penile anesthesia in PSSD. It is further hypothesized that there are two types of PSSD, one of which occurs soon after the start of SSRI treatment.

The Open Women' Health Journal, 2007, 1, 1-3
Prolonged Post-Treatment Genital Anesthesia and Sexual Dysfunction Following Discontinuation of Citalopram and the Atypical Antidepressant Nefazodone
Robert P. Kauffman* and Amanda Murdock Department of Obstetrics and Gynecology, Texas Tech University Health Sciences Center, School of Medicine, 1400 Coulter Drive, Amarillo, Texas 79106 USA

The Open Psychology Journal, 2008, 1, 42-50
1874-3501/08 2008 Bentham Open
Open Access
Persistence of Sexual Dysfunction Side Effects after Discontinuation of
Antidepressant Medications: Emerging Evidence
Audrey S. Bahrick*
http://pssd.nl/Persi... medication.pdf
Persistent Sexual Dysfunction after Discontinuation of Selective
Serotonin Reuptake Inhibitors

Antonei Csoka, PhD,* Audrey Bahrick, PhD,† and Olli-Pekka Mehtonen, MD‡
*University of Pittsburgh––Medicine, Pittsburgh, PA, USA; †University of Iowa—University Counseling Service, Iowa City,
IA, USA; ‡Kaivanto Psychiatric Hospital—Psychiatry, Helsinki, Finland
DOI: 10.1111/j.1743-6109.2007.00630.x

A B S T R A C T
Introduction. Sexual dysfunctions such as low libido, anorgasmia, genital anesthesia, and erectile dysfunction are
very common in patients taking selective serotonin reuptake inhibitors (SSRIs). It has been assumed that these side
effects always resolve after discontinuing treatment, but recently, four cases were presented in which sexual function
did not return to baseline. Here, we describe three more cases.
Case #1: A 29-year-old with apparently permanent erectile dysfunction after taking fluoxetine 20 mg once daily for
a 4-month period in 1996.
Case #2: A 44-year-old male with persistent loss of libido, genital anesthesia, ejaculatory anhedonia, and erectile
dysfunction after taking 20-mg once daily citalopram for 18 months.
Case #3: A 28-year-old male with persistent loss of libido, genital anesthesia, and ejaculatory anhedonia since
taking several different SSRIs over a 2-year period from 2003–2005.
Results. No psychological issues related to sexuality were found in any of the three cases, and all common causes of
sexual dysfunction such as decreased testosterone, increased prolactin or diabetes were ruled out. Erectile capacity
is temporarily restored for Case #1 with injectable alprostadil, and for Case #2 with oral sildenafil, but their other
symptoms remain. Case #3 has had some reversal of symptoms with extended-release methylphenidate, although it
is not yet known if these prosexual effects will persist when the drug is discontinued.
Conclusion. SSRIs can cause long-term effects on all aspects of the sexual response cycle that may persist after they
are discontinued. Mechanistic hypotheses including persistent endocrine and epigenetic gene expression alterations
were briefly discussed. Csoka A, Bahrick A, and Mehtonen O-P. Persistent sexual dysfunction after discontinuation
of selective serotonin reuptake inhibitors. J Sex Med 2008;5:227–233.

http://psychrights.o...aetal(2007).pdf
OR
http://onlinelibrary...07.00630.x/full

One hundred and twenty cases of enduring
sexual dysfunction following treatment

Carys Hogana, Joanna Le Nourya, David Healya,∗ and Derelie Manginb
aNorth Wales Department of Psychological Medicine, Bangor, Wales, UK
bDavid Braley & Nancy Gordon Chair of Family Medicine, Department of Family Medicine,
McMaster University, ON, Canada
Received 17 February 2014
Accepted 21 April 2014
Abstract.
BACKGROUND: There have been reports for over a decade linking serotonin reuptake inhibitors, finasteride and isotretinoin
with enduring sexual dysfunction after treatment stops.
OBJECTIVE: To explore the clinical pictures linked to all 3 drugs.
METHODS: We have selected 120 reports to RxISK.org reporting the problem and mined these for data on age, gender, drug
of use, and impact of the problem.
RESULTS: The data make it clear that the three drugs show extensive overlap in symptom profile, regardless of sex or country
of origin.
CONCLUSIONS: The availability of 120 reports from over 20 countries add to the case for the validity of the syndrome. This is
severe and enduring condition can result in death. An understanding of its physiology and an approach to treatment are needed.

http://wp.rxisk.org/...Is-and-PSSD.pdf
The prescriber information for Prozac from Eli Lilly's website. Halfway through the 15th page is a clause which reads, “Symptoms of sexual dysfunction occasionally persist after discontinuation of fluoxetine treatment.

Journal of Contemporary Psychotherapy June 2009, Volume 39, Issue 2, pp 135-143
Sexual Side Effects of Antidepressant Medications: An Informed Consent Accountability Gap
Abstract
Sexual side effects of antidepressant medications are far more common than initially reported, and their scope, quality, and duration remain poorly captured in the literature. Antidepressant treatment emergent sexual dysfunctions may decrease clients’ quality of life, complicate psychotherapy, and damage the treatment alliance. Potential damage to the treatment alliance is greatest when clients have not been adequately informed of risks related to sexual side effects. It had previously been assumed that sexual side effects always resolve shortly after medications are discontinued. Emerging evidence, however, suggests that in some individuals, sexual dysfunction side effects may persist indefinitely. The authors argue that all psychologists should be well-informed about sexual side effects risks of antidepressant medications, should routinely conduct a pre-medication baseline assessment of sexual functioning, and take an active role in the informed consent process.

Wikipedia article
http://www.thefullwi...ual_dysfunction

https://www.ncbi.nlm...pubmed/25483212
Eur J Pharmacol. 2015 Apr 15;753:263-8. doi: 10.1016/j.ejphar.2014.11.031. Epub 2014 Dec 4.
Penile anesthesia in Post SSRI Sexual Dysfunction (PSSD) responds to low-power laser irradiation: a case study and hypothesis about the role of transient receptor potential (TRP) ion channels.
· Abstract
· Treatment of paroxetine-induced penile anesthesia in Post SSRI Sexual Dysfunction (PSSD) by Low-power Laser Irradiation (LPLI) is unknown in medical literature. The aim of the current article is to report partial efficacy of LPLI for paroxetine-induced persistent penile anesthesia. We report on a male patient who presented with a history of reversible loss of smell, taste and skin sensitivity occurring within a week after start of 20mg/day paroxetine-hemihydrate for a depressive period. Concurrently, patient suffered from penile anesthesia, scrotum hypesthesia, anejaculation and erectile difficulties with normal sexual desire. During 2.5 years of paroxetine treatment and throughout 2 years after paroxetine discontinuation, genital and sexual complaints persisted. Penile anesthesia was treated by LPLI with single and multi diode pulsed laser probes. After 20 LPLI-treatment sessions of 15min each, patient reported partial return of penile touch and temperature sensation. Clinical improvement of glans penis sensitivity was reported to 20% and 40%, compared to pre-paroxetine treatment penile sensitivity during erect and flaccid states, respectively. However, anejaculation and erectile difficulties remained unchanged. Briefly, in the current patient with early onset of PSSD, LPLI treatment reduced paroxetine-induced penile anesthesia. It is hypothesized that SSRI treatment induces disturbances of transient receptor potential (TRP) ion channels of mechano-, thermo- and chemosensitive nerve endings and receptors resulting in the penile anesthesia in PSSD. It is further hypothesized that there are two types of PSSD, one of which occurs soon after the start of SSRI treatment.

https://www.ncbi.nlm...pubmed/25815755
Post-SSRI Sexual Dysfunction: Clinical Characterization and Preliminary Assessment of Contributory Factors and Dose-Response Relationship.
Emerging evidence suggests that sexual dysfunction emerging during treatment with selective serotonin reuptake inhibitors (SSRIs) and/or serotonin-norepinephrine reuptake inhibitors (SNRIs) persists in some patients beyond drug discontinuation (post-SSRI sexual dysfunction [PSSD]). We sought to identify and characterize a series of such cases and explore possible explanatory factors and exposure-response relationship. Subjects who responded to an invitation in a forum dedicated to PSSD filled out a survey via online software. Case probability was defined according to the following 3 categories of increasing presumed likelihood of PSSD. Noncases did not meet the criteria for possible cases. Possible cases were subjects with normal pretreatment sexual function who first experienced sexual disturbances while using a single SSRI/SNRI, which did not resolve upon drug discontinuation for 1 month or longer as indicated by Arizona Sexual Experience Scale scores. High-probability cases were also younger than 50-year-olds; did not have confounding medical conditions, medications, or drug use; and had normal scores on the Hospital Anxiety and Depression Scale. Five hundred thirty-two (532) subjects completed the survey, among which 183 possible cases were identified, including 23 high-probability cases. Female sex, genital anesthesia, and depression predicted current sexual dysfunction severity, but dose/defined daily dose ratio and anxiety did not. Genital anesthesia did not correlate with depression or anxiety, but pleasureless orgasm was an independent predictor of both depression and case probability. Limitations of the study include retrospective design and selection and report biases that do not allow generalization or estimation of incidence. However, our findings add to previous reports and support the existence of PSSD, which may not be fully explained by alternative nonpharmacological factors related to sexual dysfunction, including depression and anxiety.

https://www.ncbi.nlm...pubmed/28778697
Post-SSRI Sexual Dysfunction: A Literature Review.

https://www.ncbi.nlm...pubmed/28642048
Sex Med Rev. 2017 Oct;5(4):429-433. doi: 10.1016/j.sxmr.2017.05.002. Epub 2017 Jun 20.
Sexual Consequences of Post-SSRI Syndrome.
Abstract
INTRODUCTION:
Sexual dysfunctions are well-known side effects of selective serotonin reuptake inhibitor (SSRI) use. Altered libido, erectile dysfunction, vaginal dryness, ejaculatory disorders, and orgasmic problems are frequently reported by patients treated with SSRIs. Moreover, these antidepressant-emergent sexual dysfunctions do not always resolve after discontinuation of the medication and can persist indefinitely. These complaints are termed post-SSRI sexual dysfunctions (PSSD).
AIM:
To examine the existence of this clinical entity, possible theoretical mechanisms, possible risk factors, and possible treatment modalities.
METHODS:
Through literature research and clinical experience, the available information about PSSD is reviewed.
MAIN OUTCOME MEASURES:
Summary of the current literature with insights into possible causes and management options.
RESULTS:
There are some indications that antidepressant-emergent sexual dysfunctions do not always resolve after discontinuation of the medication and can persist indefinitely in some individuals. Although some or all sexual side effects that start with the use of SSRIs might continue after stopping the medication, other sexual complaints can develop. Decreased capacity to experience sexual pleasure is the most frequent characteristic of this syndrome.
CONCLUSION:
The research and understanding of PSSD remain limited and not well understood; however, the data support the existence of PSSD, which can have a substantial effect on the quality of life of these patients. More research is warranted to show the cause and possible mechanisms of PSSD that could lead to the correct diagnosis and treatment. Reisman Y. Sexual Consequences of Post-SSRI Syndrome. Sex Med Rev 2017;5:429-433.

http://www.wikidoc.o...ual_dysfunction
-----------------------------------------------------------------------------------------------------------


#21 gail

gail

    God-like

  • Site Supporter
  • 4,600 posts
  • LocationSherbrooke, PQ
  • why_joining:
    5 months on cymbalta, scary side effects, never felt good.
    Needed understanding and support, and a place where I was not alone. To read others stories and realizing that I was not the only one going through all that crap.
    In hope that one day, I can return the favors in some kind of way.

Posted 05 July 2018 - 05:34 AM

[quote name="fishinghat" post="72760" timestamp="1501970521"]

I have just finished reading about 60,000 old posts on this site. My object is use this topic to post the reviews of all of our members concerning every drug, method, technique they have tried to handle their Cymbalta withdrawal. This will include their mistakes, successes, warnings, etc. My hope is that this can be a one stop shopping for information, especially new people.

If any of you have ANY suggestions. something you want to add, corrections, etc. just let me know and I will add it on to the posts. Lets make this as good as we can for everyone to use.

Sincerely Fishinghat


Important, so, up we go!

#22 fishinghat

fishinghat

    God-like

  • Active Members
  • PipPipPipPipPipPipPipPip
  • 8,296 posts
  • LocationMissouri

Posted 05 July 2018 - 09:06 AM

Good timing Gail. I have just completed an update to this document and during the next few days will post it and replace this one. It is amazing how much information we collect on this site.





0 user(s) are reading this topic

0 members, 0 guests, 0 anonymous users