The discipline of evolutionary psychology views modern human behaviors as products of natural selection that acted on the psychological traits of our ancestors. A subdiscipline, evolutionary psychiatry, tries to find evolutionary explanations for mental disorders.
One of the most common subjects of evolutionary psychiatry is depression. Although debilitating, depression is also reasonably widespread. Estimates of its prevalence in Western nations range between 5% and 20%, and the disorder appears to depend at least partly on an individual’s genes. The relatively high frequency of an apparently maladaptive and partially genetic syndrome has led to speculation that it may really be “adaptive” in an evolutionary sense—that is, a liability to depression may have been installed in our genome by natural selection.
A recent version of this idea is the adaptive rumination hypothesis (ARH) of Andrews and Thomson,1 which posits that depression evolved as a way to solve difficult and complex problems, most of them involving social interactions. Instead of being a pathology, depression is seen as a useful complex of thoughts and behaviors that enable troubled people to withdraw from the world, deliberate intensively about their social problems, and devise solutions. Andrews and Thomson suggest this behavior evolved because it was adaptive in our ancestors, and may still be so.
The ARH has attracted a good deal of attention, much of it favorable. It was, for example, the subject of a recent article in The New York Times magazine.2 Debate about the ARH is not purely academic, for Andrews and Thomson see the idea as pointing to specific therapies, including problem-solving talk therapies and the deliberate withholding of medication. Since these suggestions stem from a specific evolutionary hypothesis, we should carefully examine that hypothesis.
I have previously discussed a number of troubling problems with the ARH.3 Andrews and Thomson deliberately conflate clinical depression and simple sadness, assuming that these are simply positions on a continuous psychological gradient. They give no evidence that depression is caused by, rather than the cause of, difficult social problems, and they fail to show that depression actually helps people solve those problems. And many of the “experiments” supporting the ARH are unrealistic, bordering on silly. One such study mimicked the effect of depression on problem solving by having people engage in mock currency trading while listening to sad music.
Rather than repeat my critique, I want to discuss how evolutionary biologists identify features as “adaptations” and relate this to evolutionary explanations of mental disorders such as the ARH. I will show that depression does not meet the minimal requirements for qualifying as a biological adaptation, and that even if it did, the evolutionary explanation of the ARH—and of other “adaptive” theories for depression—is scientifically unsound.
The ARH is unsatisfactory for three reasons:
Depression is not an adaptation in the evolutionary sense. Andrews and Thomson consider depression an “adaptation” because it supposedly helps the sufferer solve problems. But an evolutionary adaptation is more than something that is merely useful. Biologists consider a trait adaptive only if that behavior, and the genes producing it, enhance an individual’s fitness—the average lifetime output of offspring. It is this genetic advantage, and the evolutionary changes in behavior it promotes, that is the essence of adaptation by natural selection. To demonstrate that depression is an evolved adaptation, then, we must show that it enhances reproduction.
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.
None of this suggests that depression is an adaptation rather than a pathology. The “coordination” of symptoms is post facto rationalization: with sufficient imagination, one can view nearly any mental illness as an orderly and useful syndrome. Schizophrenia, for example, could be considered a cluster of “coordinated” symptoms that enable individuals to discard a reality that is simply too painful to bear. Without information that depression enhances reproduction, the idea of adaptive “coordination” is mere storytelling.
More important, there are alternative explanations for disorders that are fairly common and have some genet-ic underpinning. Take alcoholism, which has an incidence similar to that of depression (about 7%) and appears to have some genetic basis. But nobody maintains that alcoholism is adaptive. Rather, it’s almost certainly a pathological effect of an environmental change (the discovery of fermentation and distillation) on an adaptive trait (the evolved wiring and pleasure centers of our brain). Like the painful and sometimes fatal childbirth that is the by-product of selection for larger human brains, depression could simply be a maladaptive by-product of a feature that is generally adaptive—perhaps the wiring of those brains. Viewed in this way, depression could be a “spandrel,” a genetic hitchhiker that is a by-product of something else.5
Alternatively, genes that cause depression might have some advantage when they are present but do not produce the disorder. This can happen if the condition has what geneticists call “variable penetrance”: 10% of individuals carrying the dominant gene for retinoblastoma, for instance, don’t develop the disease. Or, genes that cause depression only when present in two copies could, when present in heterozygous (one-copy) conditions, have another, unknown advantage. Note that these two scenarios offer an adaptive explanation for depression genes that do not view the condition itself as adaptive. And both can be tested, for they predict that the non-depressed relatives of depressives (who carry but don’t express “depression genes”) should have higher reproductive output than do non-depressed people whose relatives are also not depressed.
This critique of the ARH applies, of course, to other adaptive explanations of depression, including the plea for help theory,6 the social rank theory,7 and the depressive realism theory.8 Some have also suggested that depression is adaptive because it and other affective disorders are associated with high creativity.9 This suggestion is also dubious because there is no evidence that depressed people who are creative have a higher reproductive output than other members of the population.
Andrews and Thomson conclude that in view of the ARH, problem-solving therapies like cognitive-behavioral therapy are the go-to treatments for depression. Further, they say, doctors should not be too hasty in prescribing antidepressant medication because the afflicted should be willing to “endure the pain”1(p645) in hopes of a more permanent, evolution-based cure. Indeed, one could read the ARH as suggesting that depression should not be cured, but cultivated!
But Andrews and Thomson’s prescriptions lose force to the extent that they rest on a flawed biological premise. Of course researchers should continue to compare talk therapies and to determine which, if any, drugs are useful in alleviating depression. But in the meantime, let’s not expropriate and distort evolutionary theory in a misguided attempt to claim mental disorders as “adaptations.”
References1. Andrews PW, Thomson JA Jr. The bright side of being blue: depression as an adaptation for analyzing complex problems. Psychol Rev. 2009;116:620-654.