Here’s an interesting, longish item in New Atlantis (2014):
Together with the popular success of psychoactive medications like Prozac and Xanax, the change in the commitments of psychiatry has created ways of talking about mental illness that would have seemed outrageous or even nonsensical less than a century ago. Many of us now blithely accept that depression results from an imbalance of neurotransmitters. While the neurobiological understanding of mental disorders is still at a rudimentary stage, drugs that alter brain chemistry have definite palliative effects, and we increasingly look for and accept explanations of mental illness in neuroscientific terms. We might still take older explanations drawn from psychoanalysis or social psychiatry to hold some value, but we tend to assume that they can be reduced to neurobiology.
And how’s that working out?
Many patients find that antidepressants do not alleviate their depression, and some find that the drugs have no impact on their moods at all. A 2002 meta-analysis published in the journal Prevention and Treatment found that for six of the most prescribed antidepressants, placebo control groups matched 82 percent of the medication response. This situation led a 2014 article in Nature to claim that “five decades of work on antidepressant drugs have not made them more likely to lift people out of depression.” It has also led pharmaceutical companies to develop secondary drugs intended to enhance the effectiveness of antidepressants, with multi-drug treatment becoming more common.
Of course, the real story here is not that antidepressants never work but that the placebo effect is much more powerful than many suppose.
Despite the limited effectiveness of antidepressants and the theoretical gaps in understanding how they work, they have immensely shaped the theory and practice of psychiatry. The drugs provided clues to chemical processes involved in depression, which fueled attempts to formulate hypotheses for neurobiological causes of depression. These hypotheses were first formulated by looking at the biochemical effects of antidepressant drugs and attempting to infer the neurobiological abnormalities they were thought to fix.
But antidepressants were much more than an example of new technology changing the course of scientific research; they also helped widen the range of symptoms thought to be caused by depression. The Food and Drug Administration loosened restrictions on direct-to-consumer advertisements in the late 1990s, allowing pharmaceutical companies to run ads for antidepressants in national magazines, television shows, and elsewhere. Many of these advertisements limned the most general and benign symptoms included in the DSM’s criteria for depression (like irritability and fatigue) and their role in interpersonal problems and workplace difficulties, implicitly pushing the idea that drugs could relieve everyday human troubles. More.
One outcome that should concern us is the loss of a distinction between clinical depression (can’t go to work or maintain relationships for no clear reason) and specific or general unhappiness (friend dies, one realizes one will not attain life goals, etc.)
There is no cure for the human condition, after all. 😉
See also: Is there a good reason to believe that the human mind is and must bea fully natural object?