To elaborate – the placebo group is not just swallowing pills, but is also receiving positive attention, and therefore social support, from those who administer the treatments to them. People are showing that they care. This could make a huge difference, and i would suggest the social solidarity that is evident in the actions of the non-patients in these trials is the real placebo.

So we really have three factors at work in these trials:

1. anti-depressants
2. placebos
3. social solidarity

Both groups are receiving significant doses of either 1 and 3, or 2 and 3, and therefore the scientific ideal of altering one variable while holding all others constant is not obtained.

Do you think that competitive pressures will result in all placebos eventually being, say, big and green?

More fundamentally the failure of antidepressants represents a serious challenge to the disease model of depression. We need to start taking seriously the possibility that depression is the bad end of a distribution. Depression may be something much more like height or amount of body hair, a natural variation (affected by environmental factors) which we think requires treatment in some cases, e.g., excessive body hair or severely inconvenient shortness.

This issue poses a fundamental moral dilema to the human species. If depression can’t be easily fenced off as abnormal brain function when do we use psychoactive substances to alleviate suffering? I think the answer is whenever they prevent more suffering than they cause and the myth of antidepressants is one of the things that is holding us back from developing useful agents of this kind.

Finally saying people are individuals and vary is find and dandy but that still doesn’t provide you evidence the drugs are a net help. Heck, those individuals differences could just as well work out in the other direction. Now certainly there are some areas where despite good evidence from controlled studies we can reasonably assume that a given treatment is likely to be helpful to certain patients on the basis of a sound theoretical model but that is distinctly lacking for anti-depressants.

Ultimately though the question isn’t whether anti-depressants help some people but WHY. Is it a placebo effect or some other mechanism. Personally I suspect the remaining statistically significant effects for the very depressed result from regression to the mean (if you are way on the unhappy side then randomly fuck with your brain function and your more likely than not to end up a bit happier).

But Robin’s point still stands. It’s not an excuse for poor reasoning.

As for what else you could do. Well if the pyschiatric community really faced this problem they might start prescribing drugs with clear anti-depressant effects like Adderall. Sure there is abuse potential but that’s not a reason not to give a person a shot at happiness or to pull them out of a suicidal spiral.

Controlled studies are not and should not be the sole arbiter of truth.
Controlled studies are especially important in healthcare, because biases, illusions, wishful thinking, and placebo effects are so strong. But they also fail most dramatically in healthcare, mainly because individual reactions differ so much. The assumptions underlying standard statistical analyses don’t apply to human biology or psychology, which never have the simple distributions that the analysis requires.

When one person can repeat something many times and have an observable effect each time, then we need to take their anecdotes seriously. For instance, I get a headache from drinking two sodas with Aspartame in a row. Any respectable MD will swear up and down that this is impossible, because many controlled studies have shown that Aspartame has no ill effects. Nonetheless, my own personal experience is repeatable and reliable.

In other cases, say orthoscopic surgery, where an individual doesn’t get repeated trials, we don’t have any way to observe individual variation other than in large studies. In that case, believing the results of large studies is more appropriate than believing the impressions of doctors who have never bothered to actually count how many patients said they felt better afterwards.

Kirsch’s claims appeared to receive a big boost from a meta-analysis published in January in the Journal of the American Medical Association and widely reported. The study concludes that “there is little evidence” that antidepressants are more effective than a placebo for minor to moderate depression. But, as a Cornell psychiatrist, Richard Friedman, noted in a column in the Times, the meta-analysis was based on just six trials, with a total of seven hundred and eighteen subjects; three of those trials tested Paxil, and three tested imipramine, one of the earliest antidepressants, first used in 1956. Since there have been hundreds of antidepressant drug trials and there are around twenty-five antidepressants on the market, this is not a large sample. The authors of the meta-analysis also assert that “for patients with very severe depression, the benefit of medications over placebo is substantial”—which suggests that antidepressants do affect mood through brain chemistry. The mystery remains unsolved.

Read more: http://www.newyorker.com/arts/critics/atlarge/2010/03/01/100301crat_atlarge_menand?currentPage=all#ixzz0gxHosEfe

…anti-testimonials to drugs that definitely do nothing, such as homeopathic remedies, are rare. Anti-testimonials to antidepressants are common.

Isn’t that because homeopathic remedies do nothing, but antidepressants screw with your brain chemistry? Just because the antidepressants have bad side effect doesn’t make Horn 2 particularly more likely (unless you say “well, it screws with my brain, and my depressions is inside my brain, therefore it’s more likely to be effecting my depression than if I had no side effects”.)