Is depression an evolutionary adaptation? Part 1.
I’ve been a critic of evolutionary psychology over the years — perhaps too much of a critic, since there is some good stuff being done in that field. But I won’t pull my punches with one of its subdisciplines: evolutionary psychiatry. Exponents of evo-psychiatry spend their time ruminating about how “mental disorders” in humans might really be adaptations that have evolved either recently or, more often, in our savanna-dwelling ancestors. (Here I mean “adaptation” in the evolutionary sense: a mental disorder is a module of neurons selected as a unit because the behavior it produces causes its carriers to leave more genes than do individuals lacking the “disorder”.)
The reason why I’ve often come down on evolutionary psychology — and evolutionary psychiatry — is that often its practitioners don’t just idly speculate about the evolutionary origin of our behavior. Many of their “speculations” have real world consequences and lead to prescriptions about how we should change society.
Nowhere is this more evident than in the latest offering of evo-psychiatry, a pair of papers by Paul W. Andrews and J. Anderson Thomson, Jr. — a long one in Psychological Review and a précis in Scientific American. In these articles, Andrews and Thomson float the idea that both clinical and subclinical depression are not pathologies, but adaptive traits built into our ancestors by natural selection. Why? Because, they say, depression enables people who have encountered difficult life circumstances a way to kick back, engage in deep and long-lasting rumination, and analytically solve those thorny problems. They call this the “analytical rumination hypothesis” (henceforth ARH) for depression.
Well, ideas like this have been floated before. What is new is the authors’ prescription that because depressive rumination is good, and because drugs that alleviate depression also alleviate the adaptive rumination, the best way to treat depression is not through drugs but through psychotherapy that helps the patient solve problems. Drugs only make things worse — they may alleviate the symptoms of depression, but they don’t alleviate the cause (life problems).
I’m not taking either a pro- or anti-drug stand here. What I am saying is that it seems unwise, especially in light of the insubstantial evidence that Andrews and Thomson offer for their evolutionary theory, to tell doctors to back off from a therapy that seems to help people. And if you read the Psychological Review paper with a critical eye, you’ll find that it’s a tissue of tissue — paper thin evidence that in some cases is almost laughable. But such are the data of evolutionary psychiatry. Let’s look at those data. Today I’ll set out the reasons why Andrews and Thomson see depression as an adaptation, and discuss what, exactly, is so adaptive about it. In tomorrow’s installment I’ll discuss the experimental support — or lack thereof — for their assertions.
WHY MIGHT DEPRESSION BE CONSIDERED AN ADAPTATION? The authors give several reasons:
It is common. The Scientific American paper says “between 30 to 50 percent of people have met current psychiatric diagnostic criteria for major depressive disorder sometime in their lives. But the brain plays crucial roles in promoting survival and reproduction, so the pressures of evolution should have left our brains resistant to such high rates of malfunction. Mental disorders should generally be rare — why isn’t depression?”
There appears to be some discrepancy about statistics here, for in the Psychological Review paper the authors note that only 16.6% of Americans meet the criteria for MDD (46.4% are said to have met criteria for “at least one mental disorder”), while a New Zealand study gives 37% and another American study gives 7% for “major depression.” It’s not clear how they get 30-50% for depression alone. Leaving that aside, though, I note that the commonness of a malady says nothing about whether that “malady” is really an adaptation. The frequency of appendicitis is roughly 7%. Does that make it an adaptation? A huge proportion of males experience enlarged prostate glands beginning at about age 40 (an age at which men are still fertile). Are enlarged prostate glands an adaptation? Probably not — they’re almost certainly a pathology. So why can’t depression be a pathology?
The authors also note, and I’ve read this elsewhere, that depression is found in all societies, including those supposedly resembling the hunter-gatherer societies of our ancestors (the authors, however, give no statistics about depression in tribes like the !Kung!). This shows that depression cannot be completely an artifact of living in modern societies, but it doesn’t say whether it could be exacerbated by modern societies.
The authors assert that the “high prevalence estimates” of depressive disorders, and their worldwide presence “suggest[s] that much of what is currently classified as depressive disorder represents normal psychological functioning.” This suggests nothing of the sort, any more than the frequency and ubiquity of toothaches suggests that these are part of normal dental functioning. The only way around this grotesque conclusion is the semantic tactic that anything that occurs in more than 15% of people is “normal” by definition.
There is a structure whose absence reduces depression. As the Scientific American article notes, “One reason to suspect that depression is an adaptation, not a malfunction, comes from research into a molecular in the brain known as the 5HT1A receptor. The 5HT1A receptor binds to serotonin [5HT, or 5-hydroxytryptamine], another brain molecule that is highly implicated in depression and is the target of most current antidepressant medications. Rodents lacking this receptor show fewer depressive symptoms in response to stress, which suggests that it is somehow involved in promoting depression.”
Well, it’s questionable whether depression is rodents is the same thing as depression in humans, and the authors give no proof. But setting that aside, the fact that the absence of a structure alleviates a condition certainly does not mean that the structure evolved to further or “promote” that condition. Under that logic we could say that appendicitis is an adaptation because removal of the appendix removes the possibility of appendicitis.
Depression involves a group of “coordinated” symptoms. These symptoms include “anhedonia,” the inability to experience pleasure, changes in “psychomotor” systems (e.g., desire for isolation, lethargy, loss of appetite), and increase of serotonin production* (this is a postulate; the authors have not demonstrated this, nor have they distinguished between increased serotonin as a cause of depression or merely a consequence of it), an increase that supposedly enables the parts of the brain engaged in analytical thinking to keep that up.
The authors claim that “such coordination makes it very unlikely that depressive rumination is a by-product of biological processes or is attributable to chance. Just as the highly structured and complex design of the vertebrate eye must have been constructed by selection and not by chance, it is difficult to see how chance biological processes could have generated such coordination. It suggests that depression evolved by natural selection, probably because depression helped people analyze and solve the problems about which they were ruminating.”
Do I really need to debunk this logic? It’s not a kind of logic that I’m familiar with as an evolutionist. Any disease or malady, psychological or otherwise, involves a coordinated group of symptoms. Schizophrenia also involves a coordinated group of symptoms that often includes catatonia, hearing voices, disordered thinking, and changes in neurotransmitter quantity. Does that make it an adaptation? I haven’t seen anybody claim that, despite the fact that schizophrenia is also found in nearly all cultures.
So much for the first principles suggesting depression is an adaptation. In tomorrow’s installment we’ll look at the authors’ experimental evidence that depression really does help people ruminate and solve their problems. Against that, however, must be set the maladaptive consequences of depression. I don’t know the statistics about the relative numbers of offspring produced by people who are depressive versus non-depressive (I doubt that those data exist, and the authors don’t cite any), but we do know that there is one hugely maladaptive consequence of depression: suicide. Estimates of the number of clinical depressives who kill themselves range from 2% -9% (the commonly cited figure of 15% is certainly too high). This is a huge fitness cost, especially since depression often strikes those of reproductive age. It’s telling that in the entire 34-page article by Andrews and Thomson, the word “suicide” is not mentioned once. One way around having to balance this deficit is to claim that suicide was not an option when depression evolved in our savanna-dwelling ancestors. But we don’t know that, and of course severe depression in hunter-gatherers may have some reproductive/survival costs that are even greater than those accrued in modern societies.
And, at any rate, a current cost-benefit analysis may be irrelevant: as the authors note, “A design analysis does not require depressive rumination to be currently adaptive because modern and evolutionary environments may differ in important ways.” That means that if depression reduces reproductive output in modern societies, the authors can still claim it was an evolved adaptation. That makes their hypothesis very difficult to test, as is true of any evolutionary-psychology theory that rests on fitness calculations that no longer obtain.
WHAT IS THE ADAPTIVE SIGNIFICANCE OF DEPRESSION? I briefly sketched the basics of the authors’ “analytical rumination hypothesis” (ARH), but I want to describe it in a bit more detail. The authors claim that there are two causes precipitating depression: “avoidable stressors” (the authors don’t describe what these are, but I presume they’re something like interpersonal conflicts at work), and “complex social problems” (the authors use as an example the infidelity of a mate, which puts you in the dilemma of whether to abandon that mate or stick with him/her and raise the kids). In either case, depression is an adaptive response because solving these problems require complicated and difficult analytical thinking. By putting yourself into isolation and forcing your brain into rumination, depression supposedly helps you attack the precipitating problem. The anhedonia, lethargy, and lack of sociality further make you concentrate on your problem and avoid distraction. Even the lack of appetite, say the authors, keeps your mind working instead of your mouth chewing! The supposedly high levels of serotonin keep that analytical brain grinding away. In the end, the “shutdown” of depression helps you solve your problem — or at least address it more effectively than those who don’t go through depression. In that way, your reproductive output is higher than that of nondepressives.
Note that the hypothesis does not say that everyone should be depressed. What it says is that if you’re faced with a very difficult life situation it is adaptive to become “depressed,” and that those who have that ability will, over time, leave more offspring than those who don’t. The genes that promote the “depression module” will then become more common in our species. The authors don’t address the question of whether such genes are fixed in the human species: that is, whether all of us have the ability to become depressed if we face life situations whose resolution requires depression.
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*Note that the conventional wisdom about depression is that it results from too little serotonin. That’s why the treatment of choice for depression is an SSRI (selective serotonin reuptake inhibitor, such as Prozac), a drug that prevents free serotonin from being absorbed and re-used by neurons, allowing the neurotransmitter to linger in the brain.
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