Psycho-Babble Medication | about biological treatments | Framed
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Re: To Those Who Switched From Celexa to Lexapro..

Posted by SLS on July 13, 2006, at 18:06:03

In reply to Re: To Those Who Switched From Celexa to Lexapro.., posted by bassman on July 13, 2006, at 16:32:50

> My theory on why that is (which is worth about 2 cents) is that clinical trials last, say, 8 weeks. During that period, there is a significant number of people that go into remission spontaneously. That makes the math messy: if 50% of the people went into remission of their own accord and the AD was effective for 30% of the people, then the statistics, without error, would be placebo 50%, AD 65%. But there is always a large error in any study involving creatures and 10% error would be great. So the results could look like 55% for placebo to 59% for AD easily. You get the idea:

I think it is quite a bit more complicated than that.

I wish I were a mathematician.

In most studies, I believe the placebo response is about 30%. That is unacceptably high. I think it needs to be brought down.

Among other things, I believe the inclusion criteria for these studies allows people in who do not have a biologically-driven mental illness. I think we need to define more rigidly what it is we are setting out to treat. I think people with 100% psychological depressions are apt to feel less depressed on a placebo if they believe they are to be helped by it. Even properly-screened people with biological depressions entering the NIMH report feeling better during the first two weeks of their admission because they are so relieved that they are to finally be cured of their illness. These people are given a placebo run-in during this period. If these people with biological depressions report feeling better, even though they really aren't, are our testing implements valid when they rely so heavily on self-reporting? I also think people with psychogenic depressions are far less apt to respond to a somatic treatments like antidepressant therapy. Sure, some of the placebo responders are biogenic spontaneous remitters, but I believe a great many of them, perhaps the majority, are psychogenic remitters. Placebo responders are too high because the number of psychogenic depressives susceptible to suggestion is too high. Active compound responders are too low because psychogenic non-responders are too high. We must more rigidly and narrowly define the illnesses we are investigating and more rigorously select our subjects for our treatment studies to obtain any meaningful results.

If we are going to treat anything that looks grossly like depression with a single class of treatments, we will fail miserably. We will have greater success once we are able to more finely differentiate between the presentations of the various syndromes.

I know this introduction represents to a great degree black-or-white thinking regarding depression as a psychobiological phenomenon. However, it does serve to underscore the reality that there is no standardization of selection criteria for clinical trials for antidepressants or even a definition of what depression is.

These drugs work. We see that this is true with our own eyes, just as we do the sun shining. There must therefore be a problem with the testing.

Oh, yeah. I almost forgot. These drugs suck. They don't work for everyone all of the time. They don't work for me. If you are reading this, they probably don't work for you. Even when they do work, they have side effects. Often, they stop working after some period of time, and you have to look for another one. A lot of times, you have to endure withdrawal syndromes when you discontinue them. They are expensive. The drug companies are taking advantage of us and are concerned only with their profit margins. Etc.

- Scott




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