QUOTE (teddydouglas @ Feb 26 2008, 11:37 PM)

The mechanism of action (the way it fixes the problem) of Prozac is poorly understood. Many of the physiological effects of Prozac (including the inhibition of serotonin reuptake) have been studied extensively, however we do not know why, how, or if these effects contribute to relief from the symptoms of depression.
It is known that the effect is to increase the overall level of seratonin binding itself to seratonin receptor neurons in the brain. As to how or why that effects mood is of course not fully understood since the way the brain works is not fully understood. However it is a well accepted notion that neurons with seratonin receptors (which are very long and extend into many areas of the brain from the raphe nuclei) are responsible for the mood.
QUOTE
What we do know is that it works. Not for everyone, and not immediately, and not perfectly. However, all that new study says is that it's easy to lie with statistics. Different studies use different measures for depression and different outcome measures as well. Some consider the drug a success only if it cuts a patient's depression rating score in half (regardless of the start or endpoints) others measure success as reduction to a certain fixed level.
That's not what the study says. I quote its conclusion:
QUOTE
Conclusions
Drug–placebo differences in antidepressant efficacy increase as a function of baseline severity, but are relatively small even for severely depressed patients. The relationship between initial severity and antidepressant efficacy is attributable to decreased responsiveness to placebo among very severely depressed patients, rather than to increased responsiveness to medication.
The first sentence says that the differences between prozac and a placebo are relatively small, even for severely depressed patients. This means that the placebo has basically the same effect as the drug.