Happiness has had a tough time of it lately. The backlash against the seemingly endless stream of books about the subject (Amazon returned 426,789 titles when I used that search term, including one that calls happiness "life's most important skill") had already set in last year. At the time, I pointed out that "among people with late-stage illnesses, those with the greatest sense of well-being were more likely to die in any given period of time than the mildly content were. Being 'up' all the time can cause you to play down very real threats," and channeled the arguments of scholars who lamented the medicalization of the normal human emotion of sadness. (Click here to follow Sharon Begley)
These and other critiques of happiness and the happiness industry, however, came mostly from psychologists, philosophers, and sociologists who are concerned about the effect of a message that says modest levels of well-being aren't enough, and that we all practically have a duty to be really, really happy—and that what was once considered normal sadness is something to be smothered, even shunned. I was therefore interested to see a new scientific paper taking a more brain-based perspective. (My thanks to The Psych Student blog for drawing my attention to it.)
Writing in the journal Psychological Review, postdoctoral fellow Paul Andrews of Virginia Commonwealth University and psychiatrist J. Anderson Thomson Jr. of the University of Virginia present research suggesting that depression is present in the species, and in individuals, for a purpose, and we're playing with fire if we try to eradicate it. In evolution-speak, depression is an "adaptation," they argue. That is, it evolved because it made individuals who experienced it fitter, under natural selection, than individuals who did not experience it. Andrews and Thomson—who is best known for research on the psychology of religious belief, and who has also studied whether antidepressants threaten love and fidelity—offer as evidence the presence of a molecule in the brain called the 5HT1A receptor. This serves as a docking port for the neurochemical serotonin, which the Prozac/Zoloft/Paxil class of antidepressants targets. Human brains are not the only ones with the 5HT1A receptor. Rats also have it.
Here's the really interesting part: the rat version is 99 percent identical to the human one. This suggests that in the evolution from the shared ancestor of rats and people (hold those creationism letters!), natural selection did not mess with the receptor much. That leave-well-enough-alone history tends to happen when the function of some trait is so important that tinkering with it evolutionarily would produce more harm than good. What kind of harm? Rodents that have a mutation causing them to lose this receptor exhibit fewer symptoms of depression when they suffer some stress, a 1998 paper reported. In other words, losing the receptor that promotes depression in response to stress is something evolution thought would be a very bad move. Ergo: depression is not something to be thrown out lightly.
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