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Re: Which way on Serotonin Cam? Cam W.

Posted by terra miller on May 30, 2001, at 11:51:26

In reply to Re: Which way on Serotonin Cam? moonman, posted by Cam W. on May 29, 2001, at 17:21:18

I'm on wellbutrin. After riding through that initial phase (which seems lightyears ago) of increased agitation(diff than anxiety)and rage, things leveled off. I have recently increased my dose to total 300mg/day and here's the deal: I have more cognitive ability to make choices over what my chemicals are causing me to feel. That is the major aid. I also appreciate the benefit of additional concentration and energy, but it's the added ability to calm internally that is very helpful.

I don't know that wellbutrin has increased my anxiety or decreased it. I have too much other stuff going on right now (PTSD) to run an appropriate scientific method on myself.

I couldn't go anywhere on the SSRI's either. And I, too, wonder if too much serotonin might be a culprit. (In fact, I got so suicidal on Zoloft it was extreme. Dropped it and it was gone. I went the total other direction.)

So I wanted to add that I've got this internal calming thing going on as well. I still have to use Ativan on the shortterm, but the wellbutrin acts like a consistent undercurrent that's extremely helpful.

More for you to chew on. :-)


> Moonman - An deficiency of serotonin is thought to cause anxiety (and depression and panic and OCD and PTSD, etc.). Each of these disorders is thought to be a deficiency in a particular serotonin pathway originating from the raphe nuclei (the body's main wake/sleep mechanism within the reticular activating system). This being said, the above is a very reductionist view of what is actually going on in the brain. You alter one neurotransmitter, you are altering them all, even ones we do not know of, yet. I am not saying that Wellbutrin will not help anxiety; it's "proposed" mechanism of action does not fit with the current "anxiety theory". Like I said, I have read of Wellbutrin alleviating anxiety, but this does go against the reductionist view. Obviously, the reductionist view is wrong (or the true mechanism of action of Wellbutrin is wrong - this is a definite possibily). Hey, if you've found something that works, stick with it. I'll keep an eye open to see if this can be explained by someone with a better grasp of depression than me.
> Theorectially, your anxiety should be worse. It's not, and that is a hazard of proposing a theory, but remember, it is only a theory and is subject to revision. It is the "what ifs" and "not in this cases" that keep me in a job.
> As an example, I will use the theory of the mechanism of action of atypical antipsychotics. For the past couple of years we have been told that it is the 5-HT2A receptor blockade that prevents EPS (except for Risperdal) and that D2 blockade is less important than previously thought. Then Phil Seemans (father of the receptor site theory) comes up with the "tweaking" of D2 receptors, rather than irreversible binding of an antipsychotic to D2 receptors that stops psychosis and prevents EPS and 5-HT2A really have little or no function. I was at the lecture where he proposed this (actually, he changed his whole lecture to integrate this theory - and showed why). At the time, I sat there with a respected psychiatrist and we said, "Bullshit!". Now that I have had time to integrate what Seemans said, I do see that he is probably right. I do realize that it is the "excepts" that kill you and your theories. This may be what is happening with Wellbutrin; it is an "except". God, I love this field; never a dull moment. Once we figure it out we will say, "How could it be any other way." As they say, it is not the end of the journey that is exciting, it is the getting there.
> Sorry for rambling - Cam




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