Jump to content



Photo

Is There Permanent Nerve Or Brain Damage?


  • Please log in to reply
10 replies to this topic

#1 fishinghat

fishinghat

    Site Partners

  • Active Members
  • PipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPip
  • 13,869 posts
  • LocationMissouri

Posted 18 September 2019 - 09:10 AM

Nerve Cell Atrophy

Summary

Dendrites are branched extensions of a nerve cell (also known as a neuron) that transfers the signal from another neural cell to the axon which transfers the signal on to the dendrites of the next neve cell.

Drawing of a nerve cell.
 https://simple.wikip...org/wiki/Neuron
 
 
Chronic stress increases production of glucocorticoids (primarily cortosol) which produces these reversible structural alterations in nerve cells These changes are characterized by decreased dendrite lengths and reduced number of branches.
 
Drawing of changes in a nerve cell due to stress (see figure 5)
https://www.hindawi....12/914947/fig5/

Stress decreases brain-derived neurotrophic factor*.

 

Decreases in BDNF causes changes in genes in the synapses including the BDNF gene.

 

*Brain-derived neurotrophic factor, (BDNF), is a protein that is responsible for nerve growth and repair. BDNF acts on nerve cells helping to support the survival of existing neurons, and encourage the growth and development of new neurons and synapses.

Serotonin transport is influenced by BDNF levels.

Lower BDNF will lower dopamine production and is closely linked to depression as well as some links to anxiety. Low BDNF is common in major depressive disorder and especially treatment resistant depression.

Neuron atrophy reduces the size of the amygdala, hippocampus and prefrontal cortex in the brain.

Increased BDNF production reverses neuron atrophy and reduces anxiety and depression symptoms.

Why is this important?

 

Stress in life limits our production of BDNF and makes us more susceptible to DNA, nerve and synapse changes. This makes us more vulnerable to anxiety/depression. Once we are on an antidepressant the BDNF levels raise and provide some relief along with the drugs effects on serotonin and other neurotransmitters. If/when we decide to taper of the drugs we enter a deep state of stress. We not only lose much of our BDNF production dues to this stress but we also lose the BDNF production we were getting from the antidepressant. This all makes the withdrawal worse. Nearly all of the research on the compounds that raise BDNF say that the supplements are better at preventing loss of BDNF if taken before the stress begins. For those who are going to wean off of ANY medicine that has a withdrawal it would be wise to raise the BDNF levels prior to starting the withdrawal. The one exception is the withdrawal from addictive compounds which involve dopamine and BDNF imbalances .

Best ways to increase BDNF, repair DNA damage, avoid cellular damage from oxidation and reduce the effects of aging.

 

Increase BDNF and prevent loss of BDNF during stress

500 mg of ALA/DHA Omega 3 daily, 1000 mg of curcumin twice a day, L-Theanine at 400 mg per day, Astaxanthin at 12 to 18 mg/day.
Routine Exercise
Get plenty of sunlight
Cut refined sugar
Cut saturated fat
Cut high fructose corn syrup
7 hours or more sleep

 

Volumes of research showing that by increasing BDNF one can reduce the risk of developing Parkinson's, Alzheimer's Disease and dementia as well as bringing some relief from symptoms of these diseases. It can also help treat nerve damage and stroke symptoms if therapy is begun soon after the damage occurs. Omega 3 has also been shown to reduce plague buildup in the brain in persons with Alzheimer's Disease.

Reverse/minimize DNA damage from sun and radioactive imaging as well as extending life span

 

DNA damage is important. We have often discussed the gene mutations that are associated with anxiety/depression but you may not have been born with those mutations. They may have developed due to the aging process, sun exposure, radiation, etc. Being able to reverse some of that damage is a great asset.

 

600-1200 mg N-Acetyl Cysteine per day or 500 mg of Vitamin C per day. Shown to reverse significant damage done by aging and radioactive imaging/sun and slow the aging process.

 

Nicotinamide mononucleotide is an effective anti-aging intervention that could be translated to humans, recommended dose 100 to 200 mg/day.

 

Astaxanthin at 12 to 18 mg/day significantly reduces DNA damage from radiation/sun and is anti-aging.

 

Coenzyme q10, while not helping with DNA damage it does have anti-aging effects.

 

Quercetin has anti-aging effects and also improves BDNF levels but it does not show signs of repairing DNA.

 

L-Theanine slows the aging process and increases BDNF.

 

Recommendations;

 

I have NOT included dozens of supplements and herbal compounds that show signs of these properties due to unknown or potential bad side effects, no human data and even limited animal data. I have stuck with those compounds that are well established as supplements and are considered relatively safe .

 

1) 600-1200 mg N-Acetyl Cysteine per day or 500 mg of Vitamin C per day. to reverse DNA damage, limit further damage to DNA, raise BDNF and anti-aging.

 

2) Astaxanthin, Quercetin and L-Theanine are good alternatives.


#2 fishinghat

fishinghat

    Site Partners

  • Active Members
  • PipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPip
  • 13,869 posts
  • LocationMissouri

Posted 18 September 2019 - 09:18 AM

Effects of antidepressants

Fluoxetine (Prozac) (more effective when taken with melatonin), mirtazapine (Remeron), milnacipran (Savella), citalopram (Celexa) and Agomelatine have been shown to renormalize dendrite atrophy and elevates BDNF.

 

Administration of serotonin uptake inhibitor tianeptine (Stablon/Coaxil) prevents atrophy during stress.

 

Research results vary on whether Paroxetine (Paxil), sertraline (Zoloft), venlafaxine (Effexor), escitalopram (Lexapro) or desvenlafaxine (Pristiq), raises serum BDNF levels.

 

Nortriptyline and fluvoxamine (Luvox) do not raise BDNF values.
 


#3 invalidusername

invalidusername

    Site Admin

  • Site Supporter
  • 6,195 posts
  • LocationKent, UK

Posted 19 September 2019 - 09:47 AM

Interesting read - so in sum for the context of the forum - this explains why we have a reduced threshold for stress during taper and withdrawal.

 

Well timed considering the last 7 days I have endured with my stress levels. So NAC shows a good benefit in increasing BDNF which can restore any potential damage cause by the severe stress. Surely the 500mg Vitamin C can be obtained through a good diet - unless this is to be considered supplementary to that which is provided by the diet?

 

It worries me that when stress gets to that pivotal point where your brain simply says "enough is enough" and this is when you begin bordering on fear rather than just anxiety. I need a preventative as well as a remedy to reverse the damage as inevitably, the damage will leave me vulnerable to further attacks of the same?


#4 fishinghat

fishinghat

    Site Partners

  • Active Members
  • PipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPip
  • 13,869 posts
  • LocationMissouri

Posted 19 September 2019 - 12:25 PM

"So NAC shows a good benefit in increasing BDNF which can restore any potential damage cause by the severe stress."

It can not restore 'any' damage but will restore considerable damage.

"Surely the 500mg Vitamin C can be obtained through a good diet - unless this is to be considered supplementary to that which is provided by the diet?"

Good point. This is supplementary to your diet. Very high doses vitamin C (25,000 mg by IV were used at the Fukushima Power Plant in Japan, see below) and N-acetylcysteine have been used to reverse DNA damage as well as to increase BDNF.

Fukushima Power Plant story.
http://www.orthomole...ns/v08n06.shtml
Four workers who took intravenous vitamin C (25,000 mg) therapy before they went in, and continuously took anti-oxidative supplements during the working period, had no significant change in both free DNA and overall cancer risk.

"I need a preventative as well as a remedy to reverse the damage as inevitably, the damage will leave me vulnerable to further attacks of the same?"

Absolutely. That is exactly why I added the section "Recommendations;"

"1) 600-1200 mg N-Acetyl Cysteine per day or 500 mg of Vitamin C per day. to reverse DNA damage, limit further damage to DNA, raise BDNF and anti-aging.

2) Astaxanthin, Quercetin and L-Theanine are good alternatives."

These would be used for preventative as well as damage control. My wife has been on the Vitamin C and Astaxanthin now for 2 years and is a believer. Just feels better and more resilient. There have been hundreds of lab tests done in the last 4 years documenting the correction of nerve damage and reversing the aging process. Now researchers are trying combinations of compounds in the effort to further reverse the effects of the aging process. Most of the successful tests so far provide an estimated increase of 2 to 5 years for the average individual. Unluckily many have also provided severe side effects. Those I chose to recommend have been around a long time and have established safety levels.

#5 invalidusername

invalidusername

    Site Admin

  • Site Supporter
  • 6,195 posts
  • LocationKent, UK

Posted 20 September 2019 - 05:43 PM

It is a topic that is becoming more and more prominent in this day and age. It is all about "age" being the enemy and that all diseases and issues are related to the aging process. I follow the work of a very bright, but very extravagant academic, Aubrey de Grey, who set up the SENS foundation. His primary area of research is reversing the aging process - you may have heard of his work? If not, you really do need to look him up. 

 

I will admit, he has had some strange ideas that haven't exactly panned out comparable to the likes of Ray Kurzweil and Ben Goertzel, but much like these two, he is a very clever chap with a lot to give to the cause. 

 

I meant to ask you, not wanting to change the thread of what you have written, but along the same lines of stress reduction and reversal of damage, have you heard much in the way of agmatine for such therapy?


#6 fishinghat

fishinghat

    Site Partners

  • Active Members
  • PipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPip
  • 13,869 posts
  • LocationMissouri

Posted 21 September 2019 - 07:44 AM

Agmatine is a new one on me but I will certainly do some reading on it. Thanks for bringing it to my attention.

#7 fishinghat

fishinghat

    Site Partners

  • Active Members
  • PipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPip
  • 13,869 posts
  • LocationMissouri

Posted 21 September 2019 - 09:30 AM

Well, once again it will not let me post anything large. I will try again later. Sorry


#8 fishinghat

fishinghat

    Site Partners

  • Active Members
  • PipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPip
  • 13,869 posts
  • LocationMissouri

Posted 21 September 2019 - 09:42 AM

Agmatine

https://www.ncbi.nlm...pubmed/23318245

Neuroscience. 2013 Mar 27;234:116-24. doi: 10.1016/j.neuroscience.2013.01.004. Epub 2013 Jan 11.

Effects of prolonged agmatine treatment in aged male Sprague-Dawley rats.

Abstract
Increasing evidence suggests that altered arginine metabolism contributes to cognitive decline during ageing. Agmatine, decarboxylated arginine, has a variety of pharmacological effects, including the modulation of behavioural function. A recent study demonstrated the beneficial effects of short-term agmatine treatment in aged rats. The present study investigated how intraperitoneal administration of agmatine (40mg/kg, once daily) over 4-6weeks affected behavioural function and neurochemistry in aged Sprague-Dawley rats. Aged rats treated with saline displayed significantly reduced exploratory activity in the open field, impaired spatial learning and memory in the water maze and object recognition memory relative to young rats. Prolonged agmatine treatment improved animals' performance in the reversal test of the water maze and object recognition memory test, and significantly suppressed age-related elevation in nitric oxide synthase activity in the dentate gyrus of the hippocampus and prefrontal cortex. However, this prolonged supplementation was unable to improve exploratory activity and spatial reference learning and memory in aged rats. These findings further demonstrate that exogenous agmatine selectively improves behavioural function in aged rats.
 


#9 fishinghat

fishinghat

    Site Partners

  • Active Members
  • PipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPip
  • 13,869 posts
  • LocationMissouri

Posted 21 September 2019 - 09:45 AM

https://www.ncbi.nlm...les/PMC4328591/
Full article

BMC Genet. 2015; 16(1): 8.

Mechanisms of amino acid-mediated lifespan extension in Caenorhabditis elegans

Abstract
Background
Little is known about the role of amino acids in cellular signaling pathways, especially as it pertains to pathways that regulate the rate of aging. However, it has been shown that methionine or tryptophan restriction extends lifespan in higher eukaryotes and increased proline or tryptophan levels increase longevity in C. elegans. In addition, leucine strongly activates the TOR signaling pathway, which when inhibited increases lifespan.

Results
Therefore each of the 20 proteogenic amino acids was individually supplemented to C. elegans and the effects on lifespan were determined. All amino acids except phenylalanine and aspartate extended lifespan at least to a small extent at one or more of the 3 concentrations tested with serine and proline showing the largest effects. 11 of the amino acids were less potent at higher doses, while 5 even decreased lifespan. Serine, proline, or histidine-mediated lifespan extension was greatly inhibited in eat-2 worms, a model of dietary restriction, in daf-16/FOXO, sir-2.1, rsks-1 (ribosomal S6 kinase), gcn-2, and aak-2 (AMPK) longevity pathway mutants, and in bec-1 autophagy-defective knockdown worms. 8 of 10 longevity-promoting amino acids tested activated a SKN-1/Nrf2 reporter strain, while serine and histidine were the only amino acids from those to activate a hypoxia-inducible factor (HIF-1) reporter strain. Thermotolerance was increased by proline or tryptophan supplementation, while tryptophan-mediated lifespan extension was independent of DAF-16/FOXO and SKN-1/Nrf2 signaling, but tryptophan and several related pyridine-containing compounds induced the mitochondrial unfolded protein response and an ER stress response. High glucose levels or mutations affecting electron transport chain (ETC) function inhibited amino acid-mediated lifespan extension suggesting that metabolism plays an important role. Providing many other cellular metabolites to C. elegans also increased longevity suggesting that anaplerosis of tricarboxylic acid (TCA) cycle substrates likely plays a role in lifespan extension.


#10 fishinghat

fishinghat

    Site Partners

  • Active Members
  • PipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPipPip
  • 13,869 posts
  • LocationMissouri

Posted 21 September 2019 - 09:48 AM

Well I had to divide it up into smaller sections but I made it. Agmatine is like so many other anti-aging compounds tested. It helps some but also has significant side effects.

#11 invalidusername

invalidusername

    Site Admin

  • Site Supporter
  • 6,195 posts
  • LocationKent, UK

Posted 21 September 2019 - 01:30 PM

Thanks Hat - I had found the first, but not the second paper.

 

Yes - this is largely what I found, and at the current level of funding, it will be a while before any further advances are likely to be seen. But this is the tagline that we have seen since the birth of modern medicine - some things will benefit, others will cause problems, but you won't know until you try. 

 

Just for anyone finding this discussion, the two reads I would recommend on the overall subject matter with a scientific base are the following;

 

https://www.amazon.com/dp/B00CXK14D2

 

https://www.amazon.c...k/dp/B01G2M4LZ4





0 user(s) are reading this topic

0 members, 0 guests, 0 anonymous users