The Evolutionary Calculus of Depression: Page 2 of 3
The Evolutionary Calculus of Depression: Page 2 of 3
Andrews and Thomson don’t do this, or even try. And if they did try, they probably wouldn’t succeed, for everything we know about depression suggests that rather than enhancing fitness, it reduces it. The most obvious issue is suicide, a word that, curiously, does not appear in Andrews and Thomson’s text. Statistics show that those with major depression are 20 times more likely to kill themselves than are individuals in the general population.4 Evolutionarily speaking, this is a strong selective penalty. Depression also appears to reduce libido and may make one unattractive as a sexual partner. Andrews and Thomson point out depression’s “adverse effect on women’s fertility and the outcome of pregnancy.”1(p638) Other health problems are comorbid with depression, although it’s not clear whether depression is the cause or consequence of these problems. Finally, studies show that depressed mothers provide poorer care of their children.
If there is counterevidence that depressive rumination outweighs all these problems and enhances reproduction, Andrews and Thomson don’t provide it. The evolutionary calculus for depression—as for any psychological “adaptation”—demands an answer to the question: how does that condition affect your expected number of offspring? It is odd that evolutionary psychiatrists neither answer this question nor, with rare exceptions, consider it, especially because data on reproductive output are not hard to gather.
If the evolutionary calculus is not favorable, one can still appeal to history: while depression may not be adaptive now, maybe it was reproductively advantageous in our ancestors. Perhaps the symptoms of depression were less debilitating in the past, or there was a lower possibility of suicide. Such appeals often smack of ad hoc special pleading, especially because we’re largely ignorant of the conditions under which our ancestors lived. But Andrews and Thomson try this plea:
A design analysis does not require depressive rumination to be currently adaptive because modern and evolutionary environments may differ in important ways. . . . All that is required is that on average, depressive rumination helped people analyze and solve the problems they were ruminating about in ancestral environments.1(p644)
This is wrong. Appeals to problem solving in the past, as in the present, must ultimately involve reproduction. Note, too, that if depressive rumination no longer helps us solve problems, we can ignore Andrews and Thomson’s suggested therapies.
But we need to consider other data as well—data about the genetic basis of depression. And here the ARH also fails.
The ARH does not explain the existence of genetic variation for depression. No evolutionary hypothesis about depression is credible without specifying the nature of genetic variation. It is most crucial to propose whether the genes producing depression are fixed or segregating. And both hypotheses come with problems.
“Fixed genes” are those for which all individuals have the same genes, presumably those genes producing a form of depressive rumination that was favored in all human populations. Under this scenario, individuals do not vary genetically in their liability to depression, so variation in the disorder reflects only the different environments faced by different individuals (these environments include nongenetic accidents of development).
Under the fixed-gene model it is impossible to show by pedigree analysis that there is a “genetic basis” of depression, for those methods require the existence of genetic variation among individuals. For the same reason one could not demonstrate an evolutionary advantage of genes causing depression, since everyone currently carries the same “depression genes.”
Thomson and Andrews apparently reject this model because they recognize that individuals do differ genetically in their susceptibility to depression. They thus accept the second scenario: segregating “depression genes,” in which variation among individuals results from variation in both genes and the environmental circumstances that precipitate the disorder.
But adopting the “segregating-gene” hypothesis creates other problems, for now one has to explain not only the selective advantage of depression but also why genes producing it are segregating at non-trivial frequencies. Genes with a uniform advantage should not show this kind of variation. And population genetics theory tells us that the biological conditions under which natural selection maintains genetic variation for a trait are quite restrictive. One requires either that heterozygotes (individuals carrying one copy of a depression gene and one copy of a “nondepression gene”) have a higher fitness than individuals having two identical copies of either gene, or that environments vary over time or space in a way that depression genes are favored at some times or places, and disfavored at others. And even in this latter scenario, different environments have to appear in precisely the correct frequency or spatial distribution lest a single, generally adaptive form of the gene becomes fixed.
Neither Andrews and Thomson nor, as far as I know, any proponent of adaptive explanations for mental disorders, describes what form of selection they see as maintaining genetic variation. Without such a hypothesis, any adaptive theory cannot be taken seriously, much less experimentally tested.
There is no reason to think that depression is an adaptation rather than a pathology. Lacking evidence for a reproductive advantage of depression, Andrews and Thomson see the malady as an evolutionary adaptation for three other reasons: it is an “orderly” syndrome (“there is a neurological orderliness [anhedonia and biochemical effects on serotonin concentration that affect rumination] that appears to specifically and proficiently promote analysis in depressive rumination and is not likely to have evolved by chance”1[p622]); it is relatively common both within and among cultures; and it has a partial genetic basis.