Dr. Pangloss

Jerry Coyne FUD, part III

2009-09-28T10:04:00.000-07:00

In this final post I will discuss those aspects of Coyne's two-part critique with which I partially agree. I will also add a couple of my own criticisms of the ARH.

Unlike Coyne, however, I do not believe any of these criticisms come close to undermining the adaptive rumination hypothesis. At most they suggest avenues for the future development and testing of an hypothesis that I strongly suspect will turn out to be true.

(Here are links to part 1 and part 2 of Coyne's critique, and here are links to my first and second posts on the critique.)

Does depression help solve complex problems?

Coyne dismisses the evidence that depressive rumination actually helps solve tough life problems, concluding

the evidence is very, very weak. The authors cite only one “pertinent mood induction experiment”, which may not be relevant at all.

And:

as a strong piece of evidence for depression helping solve thorny social dilemmas, it’s weak. It’s certainly not enough evidence to tell people to go off their meds!

Coyne's first error, as I noted in my previous post, is failing to mention the overwhelming evidence that depressed folks ruminate a lot, they ruminate about their problems, and they themselves say they are trying to understand and solve their problems (Nolen-Hoeksema et al. 2008 and references therein). The question is whether this rumination actually helps solve the problem that triggered the depression, or whether it impedes solving the problem.

The current view is that, when depressed, thinking intensely about one's problems impedes solving them. But A&T point out, as I also noted earlier, that all studies supporting the current view involved depressed people attempting to solve tasks unrelated to their life problems. It's not too surprising that performance on cognitive puzzles, such as random number generation, will be impaired if one is ruminating about the death of a close relative or abandonment by a spouse.

Because no one has yet explored whether depressive rumination helps solve the problem(s) that actually triggered the depression, A&T have been forced to build their case on common sense; the weak empirical case for the current view; evidence that depression is conducive to rumination and analysis; and what they themselves readily admit (e.g., p. 633) is the limited direct evidence supporting the ARH.

Coyne's second, and more egregious error, is to ignore the lengthy discussion in A&T (pp. 628-633) of the evidence that depression promotes an analytical style of reasoning. As A&T summarize:

The analytical rumination hypothesis predicts that depression coordinates changes in body systems to promote an analytical problem-solving approach that is concordant with the analytical, difficult problems that trigger it. Consistent with this, studies of preexisting and experimentally induced mood have consistently shown that depressed affect promotes an analytical processing style in which information is processed more carefully, thoroughly, and methodically and is processed in smaller chunks (Ambady & Gray, 2002; Edwards & Weary, 1993; Gasper, 2004; Gasper & Clore, 2002; Schwarz, 1990; Schwarz & Bless, 1991; Yost & Weary, 1996).

Although A&T, Coyne, and I all agree that currently there is little direct evidence that depression actually helps solve the triggering problem (because the appropriate studies simply have not yet been done), A&T have assembled considerable empirical evidence that depression promotes intense, focused analysis. The most obvious explanation for these results is that depressed people have very important yet complex problems to solve.

Cost-benefit analyses

In his first post, Coyne implies that A&T do not consider the costs of depression:

Against [the proposed benefits of depression], however, must be set the maladaptive consequences of depression....[and] we do know that there is one hugely maladaptive consequence of depression: suicide...It’s telling that in the entire 34-page article by Andrews and Thomson, the word “suicide” is not mentioned once.

In his second, Coyne makes this explicit:

The authors give no cost-benefit analysis for depression, despite the fact that the costs are certainly severe. At present they include an appreciable frequency of suicide. And, as one alert reader pointed out, a loss of appetite or desire for sex would have been seriously maladaptive in our savanna-dwelling ancestors. Imagine an ancestral H. erectus, curled up on the floor of his cave, ruminating obsessively because he suspects his mate of infidelity. He doesn’t sleep; he doesn’t eat; he doesn’t have sex or go hunting with his mates. Does this really give him an adaptive advantage? This scenario is a bit facetious, but the point is serious.

In fact, A&T do mention "suicidal behaviors," on p. 644, and they do discuss the trade-off between costs and benefits multiple times (I count 14 uses of the term "trade-off"), e.g.,:

Stress response mechanisms often require trade-offs between fitness-related goals to produce an effective response to the triggering problem. Like fever, then, the impairments associated with depression are usually the outcome of adaptive trade-offs rather than disorder. (p. 623)

The evolutionary benefits of depressive rumination must have been great enough to compensate for the substantial costs, many of which we have discussed. (p. 643)

Nevertheless, A&T leave the distinct impression that most depression symptoms, even quite costly ones, play a functional role in rumination. I agree that depression has substantial costs that are not well-explained by the ARH, of which suicidality is only one. Another is the loss of interest in virtually all activities that, along with depressed affect, is the core defining feature of major depression.

A&T persuade me that many depressive symptoms, including anhedonia, function, at least in part, to promote an analytical mode of reasoning and to reduce distraction from the analysis required to solve major life problems. Yet they haven't convinced me that reducing distraction is enough of a benefit to explain loss of interest in virtually all activities. Individuals with major depression often don't groom, bathe, and sometimes don't even use the toilet. Depressed parents reduce care of their own offspring, including highly vulnerable newborns. Over the weeks and months that major depression can last, a failure to groom or bathe would probably have exposed a depressed person to a significantly increased risk of infection, and reduced investment in childcare, as occurs in postpartum depression, would have detrimental effects on child survival, growth, and development. Each of these would plausibly have had a serious negative effect on fitness that would not easily be offset by more uninterrupted time to think.

Loss of appetite would have been another serious cost of depression, a fact mentioned by a reader of Coyne's blog. On loss of appetite A&T again speculate that eating distracts from thinking, and that's why depression is associated with a loss of appetite:

Depression may also decrease disruption of analysis through psychomotor changes, including a preference for solitude, fatigue, changes in appetite, and changes in sleep or activity patterns....[N]eurobiological evidence indicates that oral or buccal activity interferes with the processing of stimuli (Jacobs & Fornal, 1999). The reduced appetite often seen in depression may sustain processing by reducing oral and buccal activity. (p. 632)

I find this pretty unconvincing, at least for depressions that last more than a day or two. Cognitive processing, the very heart of the ARH, takes a lot of energy. The brain is one of the biggest energy consumers in body, consuming about 20% of calorie intake though comprising only about 2% of body mass. Among hunter-gatherers, hunting success rates are often pretty low (see, e.g., Kelly 1995, p. 103), which means that human ancestors should have eaten whenever food was available, especially if they were in the midst of analyzing a complex life problem that required sustained, intensive cognitive functioning.

If depression is an adaptation then plausible explanations must be found for its costliest symptoms: loss of appetite, loss of interest in virtually all activities, including grooming, bathing and care of one's own children, and suicidality.

In a series of papers my colleagues Paul Watson, Peter Hammerstein, and I have proposed that these extremely costly features of depression function to deliberately hurt oneself as a means to (a) credibly signal need (a la costly signaling theory) and (b) threaten and hurt interdependent others to force concessions from them (see here, here, here, and here).

This work dovetails nicely with the ARH because it also sees depression as a functional response to a complex life problem. The difference is that we argue such problems can often be solved only if other people change their behavior. In many cases, other people would only change their own behavior if they were convinced that the complex problem was genuine, which would require a credible signal of need. Moreover, others would often only change their behavior if they were compelled to do so. We posit that the costly symptoms of depression serve both functions.

Andrews and Thomson cite this body of work, and, if Coyne had bothered to dig a bit deeper, he would have found that Andrews is a co-author on one of these papers (this one). So, elsewhere, Andrews (and Thomson) endorse other evolved functions for some of depression's most costly symptoms, and I think the current paper would have been strengthened if A&T had conceded that the ARH probably does not explain them.

Final thoughts

Critiques of the illness model of depression are especially urgent because antidepressants, some of the most widely used medications (and also some of the most profitable), have profound, and largely unknown, effects on the brain. These compounds have certainly not been shown to correct a brain "chemical imbalance."

We do know, however, that fluoxotine (Prozac) and imiprimine (a tricyclic antidepressant) interfere with adaptive stress responses in at least one species. Guinea pigs pups, who possess central 5-HT_1D receptors similar to humans, cry when they are separated from their mother, except when, in studies screening novel compounds for antidepressant effects, they're given doses of fluoxetine, imipramine and other known antidepressants. These antidepressants suppress the guinea pig pup separation cries, interfering with a clearly adaptive stress response. As hard as it is to believe, compounds intended for human use as antidepressants are screened based on their ability to interfere with stress responses in other animals.* It was wise, not reckless, for A&T to raise the possibility that antidepressants might also interfere with a functional stress response in humans.

In summary, A&T use a standard method in evolutionary biology to argue that depressive rumination might be functional. They base this hypothesis on the substantial evidence (though not proof) that severe negative life events, in part, cause major depression; the overwhelming (and undisputed) evidence that depressed individuals ruminate a lot about their problems, trying to solve them; evidence that depressive symptoms, at least in part, are conducive to rumination and analysis; and the admittedly limited evidence that depressive rumination helps solve the problem that originally triggered the depression.

Combine this with the work of Watson, Hammerstein and myself, and the strategy for treating depression becomes straightforward, though rarely simple: if most depressions are caused by genuine life problems then "treating" depression will involve solving these problems -- sometimes this will require changes on the part of the depressed person as a result of analytical rumination, sometimes this will require changes on the part of others as a consequence of credible signals of need and arm-twisting, and often it will require both. There's nothing at all kooky about this hypothesis and nothing reckless or unwise about its clinical implications. As for its truth, only future empirical research can establish that.

*Unlike the guinea pig pup vocalization test paradigm, it is difficult to tell whether the stress responses exhibited in other animal models of depression, such as the forced swim test with rats or mice, are functional.

Jerry Coyne FUD, part II

2009-09-28T10:02:00.000-07:00

In my first post on Coyne's two part critique of Andrews and Thomson's paper on depression, I argued that Coyne's hand-wringing about the paper was either paternalistic, naive, or, most likely, just a means to sow FUD about evolutionary psychology and evolutionary psychiatry. In this post and the next I discuss the critique itself.

It is obviously legitimate to critique A&T but this requires reading the entire paper and knowing something about the topic. Coyne's critique is sloppy at best. It shows he didn't read large chunks of the paper and is ignorant of well-known findings in depression research. Coyne also fails to recognize basic elements of his own field. This post will focus on points of strong disagreement between myself and Coyne, and the next will focus on points of partial agreement.

My gloss of Andrews and Thomson's analytical rumination hypothesis (ARH)

Before I continue, I'll provide my gloss of the Andrews and Thomson argument, which is essentially a refinement of the psychic pain hypothesis for depression first put forward by evolutionary biologists Richard Alexander and Randy Thornhill, and then taken up by the psychiatrist Randy Nesse and others. The psychic pain hypothesis proposes that psychic pain, such as depression, is analogous to physical pain. Physical pain is undoubtedly an adaptation whose function is to detect and avoid physical injuries. If you break your ankle, the pain informs you that you have seriously injured your ankle, it inhibits you from walking, thereby preventing further damage to the ankle, and it helps teach you not to repeat whatever you might have done to break your ankle in the first place.

According to the psychic pain hypothesis, depression has a similar function. If your valued spouse leaves you, the psychic pain informs you that something very bad has happened (as measured in the currency of fitness), it inhibits you from increasing the social damage (e.g., stop being a workaholic and maybe your spouse will return), and it helps teach you not to repeat whatever you might have done to cause your spouse to leave (e.g., if your spouse returns or you get another spouse, spend more time with him or her and less time at work).

In the Andrews and Thomson update of the psychic pain hypothesis, complex life problems, such as abandonment by a spouse, trigger depression, which then causes the depressed person to ruminate intensely about this problem, thereby increasing the chances that he or she will find some solution, such as a way to convince the spouse to return or to obtain another spouse.

Although Coyne doesn't mention it, the evidence is overwhelming that depressed folks ruminate a lot, they ruminate about their problems, and they say they are trying to understand and solve their problems (Nolen-Hoeksema et al. 2008 and references therein). What is unresolved is whether such rumination actually helps the depressed solve their problems, or instead impedes problem solving, thereby prolonging depression.

Andrews and Thomson make the case that rumination is actually helpful, contrary to the prevailing view that such rumination impairs cognitive performance and is therefore dysfunctional and harmful.

A key finding of A&T is that no study has ever examined whether depressive rumination improves one's ability to solve the problem that triggered the depression in the first place. Instead, the evidence for the prevailing view comes from studies in which depressed individuals solve cognitive tasks unrelated to the life problem they see as having triggered their depressions.

Imagine being depressed over a marital breakup, and then asked to generate random numbers in a lab. It's not too surprising that performance on this task will be "impaired" relative to folks who haven't recently suffered a marital breakup because, as A&T argue, the depressed folks are rightly ruminating about the marital breakup instead of focusing on random number generation.

In my opinion, the Andrews and Thomson hypothesis will eventually be viewed as simple common sense. Now, though, it's a radical revision of much current thinking on depressive rumination.

In the following discussion, I take Andrews and Thomson's Psych Review article as the authoritative source of their argument rather than their Scientific American article, because Scientific American heavily edits articles in order to shorten and simplify them for a popular audience, and this editing can distort the actual argument. I recently wrote a short piece for Scientific American, and even after I approved the final version my (heavily edited) wording was changed in a way I didn't like.

What, now, of Coyne's criticisms?

How to identify adaptations

Coyne questions the method by which Andrews and Thomson aim to demonstrate adaptation:

The authors claim that “such coordination [of features of depressive rumination] 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.

Coyne pulled the above quote from near the end of A&T's article, but this is how A&T introduce their method (p. 622):

When a trait has features that proficiently promote a specific effect, that will go a long way to demonstrating that the effect is an evolved function of the trait because it is highly unlikely that chance processes could be completely responsible for the trait’s features (Andrews et al., 2002a; Thornhill, 1990; G. C. Williams, 1966). An exploration of a trait’s features in relation to its effects for the purpose of evaluating whether it has an evolved function is often called a design analysis, which is the form of argument used in this article.

A&T are not claiming that coordination of depressive symptoms per se is evidence of adaptation. Rather, the evidence of adaptation comprises the coordination of depression-induced neurophysiological changes for the specific purpose of effectively analyzing the life problem that triggered the depression. This type of analysis is standard stuff in evolutionary biology. Here, for example, is Darwin on the coordination of woodpecker traits for the purpose of catching insects:

Naturalists continually refer to external conditions, such as climate, food, etc., as the only possible cause of variation. In one very limited sense, as we shall hereafter see, this may be true; but it is preposterous to attribute to mere external conditions, the structure, for instance, of the woodpecker, with its feet, tail, beak, and tongue, so admirably adapted to catch insects under the bark of trees. (On the origin of species, Introduction.)

A&T don't bother citing Darwin on this point, but they do cite George C. Williams, a giant of modern evolutionary biology. Here is Williams, in the cited reference, explaining the relationship between organism design and natural selection:

If...we were asked how the apple acquired it various properties, and why it has these properties instead of others, we would need the theory of natural selection, at least by implication. Only thus could we explain why the apple has a waterproof wax on the outside, and not elsewhere, or why it contains dormant embryos and not something else. We would find an impressive list of structural details and processes of the apple can be understood as elements of a design for an efficient role in the propagation of the tree from which it came. We attribute the origin and perfection of this design to a long period of selection for effectiveness in this particular role. (Adaptation and Natural Selection, p. 6.)

Note that the question I'm addressing now is not whether A&T provide a convincing case that depression shows evidence of design for analytical rumination (I think they do, but I'll examine that later), nor is the question whether design analysis is the best way to identify adaptations. Rather, the question is whether A&T employ a logic that would be familiar to an evolutionary biologist. The answer is clearly yes.

It's not obvious to me why Coyne claims he is unfamiliar with this logic. Is he really unfamiliar with a basic approach to identifying adaptations, as laid out by both Darwin and G.C. Williams? Is he being deliberately misleading? Or is he writing about an article that he didn't carefully read? On current evidence, it is impossible to tell which of these is true.

Do negative life events cause depression?

It is critical for the ARH that complex life problems cause depression. Coyne questions the evidence for that:

Is depression caused by difficult social problems? On this crucial point the authors give virtually no evidence. [NOTE: It's since been called to my attention that there is work suggesting some association between depression and difficult life situations. Again, however, there is a cause-and-effect problem here: people with a tendency to be depressed may more often get themselves into difficult life situations.] People who have experience depression often say that its onset is often mysterious, not associated with an identifiable problem (see, for example, some of the commenters on yesterday’s post). But the authors wave that difficulty away: “Many people may be reluctant to disclose the reasons for their depression because the problem is embarrassing, reputationally damaging or otherwise insensitive, which is often why depressive episodes may appear to be endogenous. . .” This is almost Freudian in its hauteur. Here the authors presume that there is a social reason for depression rather than treating it as a hypothesis.
The authors do note that “interpersonal conflict is commonly associated with depression. . “. One example is that “in married couples, the risk for major depression is about 40 times greater if the couple is unhappily married.” Well, you can see the problems with this: what is the cause, and what the consequence? Perhaps the social problems result from undiagnosed depression. It’s easy to see that being married to someone with incipient or undiagnosed depression could cause unhappiness. Depressed people are often hard to get along with.

In reality, mental health researchers have known for years that severe negative life events are strongly correlated with depression and probably cause it, at least in part. The causal role of negative life events in depression is a well-supported, if not yet proven, hypothesis. As A&T say in their paper:

Depression is commonly thought to be caused by severe problems or stressors, often of a social nature (Brown & Harris, 1978; Hammen, 1992; Kendler, Karkowski, & Prescott, 1999).

And as for the haughty suggestion that some depressed people might be embarrassed to disclose the reasons for their depression, A&T cite Leff et al. (1970) on this point (but Coyne omitted this cite when he pulled the quote from A&T).

It was not A&T's job to bring Jerry Coyne up to speed on the last several decades of depression research, including all the evidence -- well known to depression researchers -- supporting a causal role for negative life events. That's why they cited three other papers in support of this assertion (and by the way, the evidence that Coyne claims was called to his attention is the Kendler et al. study cited by A&T).

This evidence includes that negative life events typically precede depression, ruling out the possibility that depression caused the negative life event (this doesn't, rule out the possibility of a confound, however). The single most powerful "predictor" of depression is the death of a close relative. Is it really plausible that depression causes close relatives to die? Or that depression and death of close relatives are only linked by a confound -- some unknown factor that causes close relatives to die and causes depression, but with no causal connection between the death and the depression?

Kessler's (1997) review on the relationship between stressful events and depression found causality in both directions:

The evidence reviewed above clearly shows that inventories of stressful events predict subsequent depression. A smaller number of controlled comparative studies of people exposed to single major life events provide strong evidence that at least part of this association is due to events causing depression. It is also clear from other studies that this relationship can be reciprocal and that depression can elicit or exacerbate certain stressful events and difficulties. (p. 209)

The empirical evidence is more than strong enough to warrant theorizing about depression as if life stressors actually do, in part, cause depression. That's certainly the assumption made by many mainstream (non-evolutionary) theories of depression, such as the hugely influential diathesis-stress model (e.g., Metalsky et al. 1987 and references therein), which posits that life stressors precipitate depression in constitutionally vulnerable individuals (the diathesis part).

The causal role of life stressors in depression is also the assumption made by the many researchers exploring the neurophysiological effects of hypothalamic-pituitary-adrenal (HPA) axis activation on the brain and subsequent depression. This latter work also explores severe stressors occurring in childhood, which are thought to predispose the adult to depression (for review, see here). These folks see depression as the dysfunctional effect of the biochemical cascades caused by stress, of course, but in their model life stressors are a cause of depression nonetheless.

If A&T are wrong about the causal role of life problems in depression, they'll have a lot of company.

A final point: many of the stressors that are most closely associated with major depression, such as death of a close relative and relationship problems, are common and almost certainly not evolutionarily novel. Hence, it seems that the brain should have evolved to respond to them without suffering serious dysfunction.

The significance of depression's high prevalence

Coyne first argues, correctly, that just because a trait is common does not mean that trait is an adaptation:

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.

In their Psych Review article, here is what Andrews and Thomson's actually say about the high prevalence of depression:

Such evidence [of the high prevalence and universality of depression] suggests that much of what is currently classified as depressive disorder represents normal psychological functioning (Horwitz & Wakefield, 2007).

Notice that Andrews and Thomson are citing Horwitz and Wakefield (2007) on this point, so Coyne really needs to engage with the book-length argument of the latter two scholars, not with Andrews and Thomson (I'm beginning to wonder if Coyne understands the purpose of citations). I haven't yet read Horwitz and Wakefield, so I don't know how they make their case, but I'm pretty surprised that Coyne, a well-regarded evolutionary biologist, couldn't easily see why, from an evolutionary perspective, depression differs profoundly from a toothache.

Toothaches are caused by irritated nerves, and these nerves become irritated by dental infections or by physical tooth damage (I'm simplifying for the sake of argument). From an evolutionary perspective, diseases caused by infections are expected to be common because there is an evolutionary arms race between pathogens and hosts. This arms race means that the human immune system will often fail to prevent infection. Hence, many people will suffer a dental infection at some point in their life.

Diseases caused by physical damage are also expected to be common. The tooth, as an adaptation, exhibits a number of tradeoffs between strength, size, and function. Sometimes teeth will be subject to physical forces that exceed their "engineering specifications" and they will break, causing a toothache.

But, so far as we know, most depressions are not caused by pathogens and they're not caused by physical brain injuries resulting from, e.g., blunt force trauma or toxin exposure. (People with traumatic brain injuries do appear to suffer higher rates of depression, but the vast majority of depressions are not caused by traumatic brain injury.)

As Coyne should know, several evolutionary theories of senescence predict that, absent infection or physical injury, dysfunctions of critical adaptations, such as the heart or brain, should be relatively low in young adults but increase with age. That's the pattern we see, for example, with heart attacks, which are rare among young adults but common among elderly adults. That's also the pattern we see with dementia, which is very rare before the age of 60 but increases exponentially for at least the next 25 years (Finch and Zelinsky 2005).

Andrews, Thomson, Horwitz, and Wakefield are right to wonder why the brain, unlike most other organs, is thought to suffer very high rates of a major dysfunction in young adults, in the form of depression, despite no evidence that most such dysfunctions are caused by infection or physical damage. None of this proves that depression is an adaptation. There is, after all, still debate about the various evolutionary theories of aging, among other things. But it sure should make mental health researchers, and Coyne, pause and think.

Jerry Coyne FUD, part I

2009-09-28T10:00:00.000-07:00

Two posts by the evolutionary biologist Jerry Coyne, in which he paints Paul Andrews and Andy Thomson, friends and colleagues of mine, as reckless, just-so-story-telling kooks, inspired me to write my first blog posts.

Andrews and Thomson (A&T) argue, contrary to almost everyone, that major (clinical) depression is not a disorder but is instead an adaptation whose function, in part, is to direct one's thoughts towards solving a major life problem. A&T refer to this as the "analytical rumination hypothesis" (ARH).

Were A&T "unwise"? Are they kooks? Or was Coyne just spreading FUD about evolutionary approaches to human behavior? I tackle those questions in this post and the substance of Coyne's critique in my next two posts.

First, some background

Physics' Standard Model has faced, and continues to face, exhaustive empirical tests. Any physicist can name the classic empirical papers supporting the standard model. In contrast, the "illness model" of depression -- the idea that depression is a brain dysfunction -- has never been empirically tested. Ever. It has simply been assumed and asserted by countless mental health researchers. (Pop quiz: what are the classic empirical papers supporting the illness model over alternatives? Answer: there aren't any.)

Yes, depression has numerous costs, including suicidality, and yes, the brains of depressed people differ from the brains of non-depressed people in numerous ways (for a materialist, how could they not?). But those costs and those differences are assumed, a priori, to be evidence that depression is a brain dysfunction. The possibility that many of those costs and differences are functional has never been seriously considered. In principle, the truly destructive differences, which probably include reduced hippocampal volume in depressed individuals, could be unavoidable consequences of activating depression, much as damage to healthy tissue is probably an unavoidable consequence of activating the innate immune system.

Despite the intuitive appeal of the illness model of depression, by the most important measure it has clearly failed. More than 50 years of research inspired by the illness model has not improved the treatment of depression. Newer antidepressants, such as Prozac, though generally causing fewer side effects, are no more effective at treating depression than the older antidepressants introduced in the 1950's, nor are they more effective than talk therapy. And although antidepressants are effective, this generally means that they reduce the severity of depression but often do not "cure" it.

Given this poor showing -- no improvement in treatment of depression after more than half a century of research costing billions of dollars -- it's time to rethink the illness model. Maybe it will ultimately be vindicated and maybe it won't, but this model can tolerate, indeed desperately needs, a few scientific critics (it already has social critics).

The motivation for Coyne's critique

Let me now turn to the motivation for Coyne's critique of Andrews and Thomson:

Well, ideas like [the ARH] 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.

I'm not sure which is more amusing, Coyne's paternalism or his naiveté. Readers of Psychological Review, the journal in which Andrews and Thomson's paper was published, are professional psychologists and psychiatrists who are well-qualified to evaluate the ARH. They don't need Coyne warn them about the ARH or its implications. Furthermore, because almost all mental health folks researching and treating depression have based their careers on the illness model, the likelihood that they would "back off" drug therapy for depression based on a single theoretical paper is nil.

Was it nevertheless "unwise" of A&T to argue that the use of antidepressants might have negative consequences? Hardly. It is standard practice in theoretical psychiatric papers to discuss the clinical implications of the theory. I can even imagine that the reviewers insisted on it. If the ARH is correct, then Andrews and Thomson are correct that antidepressants might interfere with the evolved function of depression, just as pain killers like morphine interfere with the evolved function of physical pain. If the ARH is not correct, then, of course, the clinical implications do not follow. The two professionals who wrote this paper, and all professionals reading it, understand that the clinical implications are contingent on the hypothesis being true. And the truth of the hypothesis can only be determined by rigorous empirical tests that have yet to be done (that's why Andrews and Thomson refer to their idea as an hypothesis).

Finally, various forms of talk therapy, the alternative treatment advocated by Andrews and Thomson, are just as effective in treating depression as are antidepressants. Hence, Andrews and Thomson are recommending one effective form of treatment over another equally effective form of treatment. This is scarcely cause for hand wringing (except by insurance companies, which might have to pay more for talk therapy).

Andrews and Thomson recommend some form of talk therapy because these therapies typically include a component that emphasizes solving life problems, thereby treating what the ARH posits is the cause of the depression. Antidepressants, in contrast, would (under the ARH) merely treat depression symptoms. There is also some empirical evidence that talk therapies have more lasting effects than do antidepressants.

Because Coyne must know that psychiatrists aren't looking to him for guidance on patient treatment, and because he must also know that spelling out the clinical implications of a new psychiatric theory is standard practice, my guess is that he isn't really worried that doctors will "back off" using antidepressants. His hand-wringing and snide tone are just means to sow FUD about evolutionary psychology in general and evolutionary psychiatry in particular, something he, his adviser Richard Lewontin, and Lewontin's late colleague SJ Gould, have done for years.

For some reason, these folks worry that it is dangerous to even ask certain scientific questions, and Coyne admits he sees "evolutionary psychology as dangerous." Because these questions scare them, they often try and scare other scientists away from these questions too.

Footnote 1: sociobiology, the original target of this FUD in the 1970's, has become an extremely successful mainstream science of human and especially non-human animal behavior, with sociobiological articles regularly appearing in Science, Nature, and PNAS. To escape the FUD, however, the term sociobiology was quickly dropped, and this work now occurs in the field of behavioral ecology, which also explores non-social aspects of animal behavior.

Footnote 2: In case the above link goes away, here is the Coyne quote on ev psych:

So, why do I see evolutionary psychology as dangerous? I think it is because I am afraid to see myself and my fellow humans as mere marionettes dancing on genetic strings. I would like to think that we have immense freedom to better ourselves as individuals and to create a just and egalitarian society. Granted, genetics is not destiny, but neither are we completely free of our evolutionary baggage. Might genetics really hold a leash on our capacity to change? If so, then some claims of evolutionary psychology give us convenient but dangerous excuses for behaviors that seem unacceptable. It is all too easy, for example, for philandering males to excuse their behavior as evolutionarily justified. Evolutionary psychologists argue that it is possible to overcome our evolutionary heritage. But what if it is not so easy to take the Dawkinsian road and "rebel against the tyranny of the selfish replicators"?