Is the Science of Antidepressants Backwards?

At least one researcher thinks so. Assistant Professor of Evolutionary Psychology Paul Andrews, PhD, JD conducted an evolutionary analysis of the effects of antidepressant medications as an offshoot of his main research interest: the evolution of depression as an emotional response to complex problems.

If he’s right about that, depression itself has a function, or it once did in evolutionary terms: his idea is that depression evolved to promote the kinds of changes in body systems that promote analysis of the complex problems that trigger depression.

Serotonin and depression

His analysis of antidepressant medications revealed that almost all commonly prescribed antidepressants disturb serotonin levels somehow, and that they therefore have adverse health effects on every major bodily process regulated by serotonin. The scientific research has traditionally stated that depression and low levels of serotonin in the brain are linked. The antidepressant medications most frequently prescribed — like Prozac, Paxil and Zoloft — are selective serotonin re-uptake inhibitors (SSRIs) which prevent cells that release serotonin from re-absorbing it. In this way, SSRIs are intended to maintain higher levels of serotonin.

However, Andrews found that people with depression have higher levels of serotonin, not lower levels, and antidepressants may be making them worse. Since there is no way to directly measure serotonin in the brain and doctors instead must rely on how patients feel, the medical establishment has no definitive way to put this specific issue to bed.

Conflict in the community

This is a controversial conclusion that was refuted in some detail by, for example, Jerry Coyne, who argues cogently that clinical depression, which must be distinguished from basic sadness, cannot be seen as an adaptation or advantage enhancing fitness from an evolutionary standpoint. Furthermore, various studies of people with serious clinical depression have shown improved outcomes for people who take antidepressants.

Perhaps the issue that Andrews is really pointing to is a possible trend in overprescription. While there is no doubt that millions suffer from clinical depression, it’s less clear how many people might be suffering from situational depression—from living in miserable conditions, for example.

Although terrible circumstances or an overly stressful lifestyle don’t cause everyone to feel depressed, they might push some people over the edge. Maybe for that smaller subset, SSRIs are not helpful compared to larger lifestyle changes.

So, are brains with depression recovering in spite of antidepressants? Are antidepressants helping some, but not others? Is this a continuum or a range of problems that are as yet poorly understood, which is causing this conflict? Whatever the answer, tread carefully before changing your brain’s neurochemistry.