Recently, Prozac and related SSRI antidepressants were dealt a blow when it was made public that Eli Lilly, Glaxo-SmithKline and the other manufacturers of the drugs had failed to disclose data from unfavorable clinical studies that showed patients using SSRIs had an increase as much as four to one in suicide risk. Now, a new study from Hull University, using the data submitted to the FDA to gain approval for the drugs, has found that for most patients, SSRIs are no more effective than a placebo.
Eli Lilly, of course, defends the drugs' effectiveness; and another researcher, the head of psychopharmacology at Bristol University, says that "if they provide some sort of placebo benefit, this shouldn't be discounted."
Now, the thing that immediately occurs to me is this: If you have the choice between a placebo that is medically inert, and has no side effects that aren't psychosomatic, or a drug that performs no better than the placebo, but has a vicious side-effect profile and may quadruple your likelihood of suicide ... aren't you better off with the placebo?
Clarification:
I should point out that I have not read the studies cited; I have only read summaries. My intention here was not to discuss the studies per se, but rather to question the idea that it's still a good idea to use a drug with known severe side-effects for it's placebo-like effect if it's (allegedly) no better than a placebo.
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The question no one has been able to answer is how they work. If it were just Seretonin, the effect would happen within minutes to an hour, yet it takes a few weeks before the effects show up. I have seen one or two theories as to why that is, (the one I like involves increasing brain cell count.) yet no one can explain how the SSRI's work. (Or what else they effect.)
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