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Starting The Process


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#1 sc00ter18

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Posted 23 March 2015 - 10:55 PM

Hello All,

So after reading this forum and having gone through a pristiq discontinuation I am very stressed about this process again.

A bit about myself , I am 32 years old been on medication for the past 6 years . Pristiq for 2 years and Cymbalta for 2 years and some trial and error in between. I have been taking these meds for GAD.

This time I am switching from Cymbalta 60mg to Fetzima 40mg.

The suggested method from my psychiatrist is to reduce Cymbalta to 40mg at night and taking Fetzima 20mg in the AM for 10 days . Then another reduction of 20mg of cymbalta and increasing Fetzima to 40mg for 10 days then stopping Cymbalta completely .

Today is my second day on Cymbalta 40mg and Fetzima 20mg. Today was fine , nothing worth mentioning which is a blessing but yesterday I had severe headache, nausea, skin burning , cold sweat .... Basically I felt extremely hung over and panic attacks that lasted for about an hour or so at the end of the day before taking my regular 40mg Cymbalta dose. Went to sleep and woke up ok.

While today was fine I am worried about the bumpy ride a head of me so any helpful tips are welcome!

Thank you all for being here to help each other , I really appreciate all of you.

#2 lady2882Nancy

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Posted 24 March 2015 - 04:07 AM

Hi sc00ter

 

I looked up the information on Fetzima and I would say that what you experience yesterday was start up side effects of the Fetzima rather than any withdrawal from Cymbalta.

Since these two medications are both SNRI antidepressants the transition should be relatively smooth.

 

I hope this works for you as I see that this new SNRI antidepressant also has the insane short 12 hour half life.

 

Take care of you and be well


#3 fishinghat

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Posted 24 March 2015 - 08:30 AM

Lady Nancy is right. It should be a smooth transition. Just for your information Fetzima has a 12 hour half life so you can expect a similar withdrawal for it when the time comes.


#4 sc00ter18

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Posted 26 March 2015 - 03:37 PM

Hi All, so I questiond my MD about her decision to go from one Med to the other and here is the reply she gave me. I am sure a lot of members will find it useful

"
Hello Adam.

Fortunately, I'm already aware of this, but the science is more complicated than the half-life. I hope you can appreciate the tone I intend when I say this, which is not meant to be negative: if anyone with internet access could do the same thing as a physician, we wouldn't need to send people to school for an extra decade for more education. The same goes for other scientific fields, too, like people who get PhD's in physics, advanced mathematics, chemistry, biology, engineering, etc.

Let me explain: If we were converting you from one med to another purely for withdrawal reasons, and the half-life was the only determinant of potential for withdrawal, then having the same half-life would be important, although even in that situation not the only thing to take into account. But neither of those things are true. Keep in mind that duloxetine/Cymbalta and levomilnacipran ER/Fetzima are not actually the same chemical, despite both working on serotonin and norepinephrine. That would be like saying Prozac, Zoloft, and Lexapro are all the same chemical because they are all SSRIs. So even though there are significant similarities in their function, this does not take into account many, many other factors. Here are just a few reasons: there are more than a dozen serotonin receptor subtypes. SSRIs/SNRIs may or may not work on the actual serotonin transporter. They differ in things such as anticholinergic effects, effects on dopamine (often indirectly impacted by variations in serotonin), effects on alpha and beta receptors, and many, many more. Even this detail does not take into account that changes in one subtype of serotonin receptor action in one part of the brain has a markedly different impact than in other parts of the brain, because just a few of the major brain areas most pertinent to psychiatry are the prefrontal cortex (particularly the dorsolateral and orbital sub-sections), the mesolimbic area, the mesocorticol region, the basal ganglia, the hippocampus, etc. SSRIs and SNRIs mostly impact mood and anxiety, but also has significant effects on cognition, memory, energy level, motivation, apathy vs concern, perceived pain levels, not to mention possible effects on the gastrointestinal system, cardiovascular system, and virtually any organ system in your entire body.

All of this information does not even take into account the discussion we had about liver enzymes and their relative activity. We have many different CYP450 hepatic (liver) enzymes that usually metabolize our medications, but medications can also be metabolized and modified by glucoronidation (also involving the liver), in the kidneys, and other ways. Each person's enzyme activity level is independent of their other liver enzymes, so you can be a sluggish CYP450 3A/4 metabolizer and a ultra-rapid CYP450 2D6 metabolizer. Given the variation for each potential liver enzyme, and the number of liver enzymes that are pertinent, you can end up with endless combinations of the different enzymes' activity levels from person-to-person.

Half-lives are based on the assumption that someone is a 'normal' metabolizer for each pertinent hepatic CYP450 enzyme. Also, people often read too much into half-life anyway, as it does not determine longevity of clinical effect.

I also haven't started to mention active metabolites, which are an enormous factor in medications, too. Active metabolites have their own chemical activity, and they can significantly skew the impact on each neurotransmitter system, half-life, and every other factor relevant to a medication.

I could write a lot more just off the top of my head, but I have to start an appt. This was not a bad question, but there's a ton of information (most of which I didn't even touch on) as to just how incredibly over-simplified only looking at the half-life is when it comes to medication choices.

Let me know if you have further questions or thoughts! I hope all is going very well.

Dr C "

#5 fishinghat

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Posted 26 March 2015 - 04:26 PM

Hi Scooter

 

I have to blow off some steam here.

 

I have a Master's in physiology and understand everything the dr. said BUT so what?  It is impossible to determine which drugs work on which serotonin receptor (although a few have been determined).

 

Whether a drug slows down serotonin use by acting on a transporter or by blocking the serotonin receptor is of no importance. Both slow the use of serotonin. Both will have the same effect assuming they have the same strength in reducing serotonin use. And whether or not they have the same strength...well the drs use a comparative strength table for this as well as adrenaline, noradrenaline, histamine, dopamine, etc. Tables which can be found on the internet. This includes the affect on alpha and beta receptors (these are the adrenaline receptors). No one is saying these are the same chemicals only they are in the same family, (ssri/snri) because they have the same or similar effects.

 

She is right, no one has the same CYP 450 hepatic enzyme function and there is no test to determine an individuals status in that matter. THEREFORE, EVERY ssri/snri manufacturer in their literature states that patients MUST have a liver function test each year (LFT). This is to determine if the particular ssri/snri is having any damaging effect on the liver because this can NOT be determined ahead of time. Therefore this factor is a non-issue when choosing or changing a ssri/snri.

 

She is right half-lives are only an average value. Some absorb faster or slower than others. SO WHAT?  We can not determine that factor for an individual ahead of time so it is not a factor on selecting a ssri/snri. We only have these average values to go by.

 

Active metabolite (the part of the drug which is active when the drug is assimulated) absorbtion is a variable in the drugs effect. AGAIN, this can not be determined ahead of time so is of no importance in closing one of these drugs.

 

The only thing we have to go by is the half-life (general rule, the longer the half life the easier the withdrawal because it comes out of your body more slowly) and the comparative strength of the medicine. I always recommend Lexapro, Prozac or Zoloft as a replacement for Cymbalta because they are easier to come off of. Did I learn that in College? NO I learned it in the comparative medical research that has been done. They act like other ssri in general but do not control adrenaline or noradrenaline in any significant way. They will typically control with the same effectiveness as Cymbalta for MOST people. I have been on all 3. Lexapro and Zoloft worked fine BUT Prozac did nothing BUT there was no way to know that ahead of time. I just had to try it.

 

Whew!!  I feel better now.


#6 lady2882Nancy

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Posted 26 March 2015 - 06:08 PM

Thank you fishinghat

 

I followed enough of that doctor's information to tick me off but could not have put into words a rebuttal so I second your rebuttal.

 

A perfect example of a complicated answer that did not really answer the question

 

I feel better now that you have blown off steam for all of us.





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