Why Evolution is True is a blog written by Jerry Coyne, centered on evolution and biology but also dealing with diverse topics like politics, culture, and cats.
The Sedalia High School evolution tee-shirt poll is apparently still open, though it was reportedly closed earlier today. As of a few minutes ago (2:50 pm Monday), a big YAY:
Fig. 1. The militant Darwinian horde has spoken
Vote here (bottom of right-hand column), and undo the damage that Richard Dawkins has wrought in Missouri.
. . . at Richard Dawkins, who caused the big tee-shirt kerfuffle in Sedalia, Missouri.
by Greg Mayer
Last Monday I spent a few hours at the Smithsonian‘s National Museum of Natural History (originally known as the United States National Museum, and still known as the USNM to scientists, even after the Smithsonian began collecting art, airplanes, tchotchkes, etc., and thus gave its museums more specific names), and came across WEIT in their gift shop.
I moved this copy about two feet to the right to photograph it, because I thought Jerry would appreciate the surroundings: it’s almost a diorama.
The great natural history museums, such as the USNM, are among the world’s premier scientific institutions. The mission of the Smithsonian Institution, 
bequeathed to it by its founding benefactor, James Smithson, is the “increase and diffusion of knowledge”, and it is a fitting mission, encompassing both research and education, for not only museums, but also universities. Having been a postdoctoral fellow at the USNM twenty years ago, but not having had a chance for many years to go through the exhibits (which are a chief way in which the USNM diffuses knowledge), I wanted to see how the exhibits had changed.
The old evolution exhibit had been taken down some years ago, and a new Ocean Hall stood in its place; I was anxious to see how the newer exhibits covered evolution and the history of life, which had always been a theme throughout exhibits such as Dinosaurs and Life in the Ancient Seas, and of course are the major themes of the work of the USNM’s researchers. I didn’t think that the Smithsonian would have succumbed to any external pressures: they successfully fought off a creationist legal attack in 1980, eliciting from the DC Circuit Court of Appeals the memorable ruling that the balance between freedom of religion and learning
…was long ago struck in favor of diffusion of knowledge based on responsible scientific foundations, and against special constitutional protection of religious believers from the competition generated by such knowledge diffusion.
I’m happy to report that the presentation of evolution is even more forthright than I’d anticipated. This sign greets visitors in the Rotunda, at the feet of the USNM’s iconic elephant:
Note particularly the line “Evolution is at the heart of this museum.”
In the Ocean Hall, one of the main galleries is devoted to the origin and history of life on earth, including everything from stromatolites, to a very nice exhibit on the origin of whales (see here, too), a story highlighted in chapter 2 of WEIT. Hung from the ceiling are skeletons of the sea lion-like Maiacetus, and the fully marine, yet hind-legged, Dorudon and Basilosaurus.
There are also two temporary evolution exhibits opening next month. Darwin’s Legacy will be about Darwin and how his “theory soon found supporters at the Smithsonian, including Joseph Henry, the first Secretary of the Smithsonian Institution, and it continues to guide research at the National Museum of Natural History.” The exhibit Since Darwin: the Evolution of Evolution
focuses on the significant role that Darwin’s theories have played in explaining and unifying all the biological sciences. Specimens from the Museum’s diverse collections, along with documentation from our ongoing research, illustrate the importance of evolution as a scientific foundation, and how our knowledge of evolution has evolved over the last 150 years.
I was also interested to see how the USNM had fared with regard to two other issues facing modern museums: commercialization and exhibit design. Museums are under increasing financial pressure, and even publicly supported institutions have had to seek at least supplementary private funding. There are potential pitfalls with such funding though: private funding might distort the mission or the message of the museum. The USNM had experienced a controversy over this while I was there, when the insect extermination company Orkin sponsored, and had its name put on, the Insect Zoo. There have been other controversies concerning donors since. I found that the named-by-sponsor exhibits were still there, but had not increased substantially. The new Ocean Hall was named for Roger Sant, a member of the Smithsonian’s Board of Regents, and a major donor. And there was a temporary exhibit on forensic anthropology co-sponsored by the History Channel, but the exhibit contents largely allayed my fears that the exhibit might be made to cable TV standards of quality. Most annoying, but not at the USNM, but rather across the mall in The Castle, was a heavily hawked tie-in to the movie Night at the Museum: Battle of the Smithsonian.
In its exhibit halls, the USNM seems to have avoided the worst of corporate sponsorship, such as the garish corporate-advertising-masquerading-as-sponsorship I’ve seen in some zoos and even national parks.
As regards design, there has for many years been a tension between exhibits that are rich in the number and diversity of labeled specimens they contain, and those that are “interactive”. The modern trend in design, as Steve Gould (Natural History, January 1994; see also his “Dinomania” in the NYRB) put it, has been
…fewer specimens, more emphasis on overt pedagogy, and increasing focus on “interactive” display (meaning good and thoughtful rapport of visitor and object when done well, and glitzy, noisy, push-button-activated nonsense when done poorly)…
The former notion of what makes for a good exhibit, which Gould admired and called “cabinet museums”, still informs, if not dominates, most of the USNM’s exhibits, including the newer ones such as Ocean Hall. While not consisting of row after row of specimens in the Victorian model, the newer exhibits continue to be rich in the diversity and number of specimens exhibited, and in the excellence of their labeling. A small exhibit in The Castle harks back to the Victorian model, but the best example of this approach I know of today is the marvelous Sense of Wonder at the Milwaukee Public Museum, a deliberate recreation of the older style. The juxtaposition of specimens is a major intellectual benefit of a such a style: it practically mandates that viewers begin composing “compare and conrast” essays in their heads. Such comparisons are a source of wonder, and an inspiration for systematics, comparative anatomy, and , indeed, much of the whole of biology. As a graduate student, I spent many hours “animalizing” (as we called it) studying the skeletons in the Museum of Comparative Zoology‘s Hall of Mammals (which is also close to the Victorian model). The USNM’s Osteology Hall, with its many vertebrate skeletons, has something of the same flavor.
My major criticism of the newer exhibits, especially the Hall of Mammals, is that they have largely left out dioramas, which, to me, have always been among the most compelling components of a natural history museum. A late Victorian development of the cabinet style pioneered by Carl Akeley at the Milwaukee Public Museum, and reaching perhaps its apogee at the American Museum of Natural History, a diorama associates animals and plants that live together in a natural setting. Most suited for exhibits with a biogeographic arrangement, their richness and frequency serve as a means to distinguish the great, from the merely good, public exhibit museums.
In the mammal hall, the mammals have been removed from the environmental context provided by the diorama, and presented against stark backgrounds painted in neutral colors, with a minimal or stylized attempt to portray the environment. Glass-panel walls and overhanging girders dominate the main exhibit hall. In part, this separation of organism from environment harks back to the early Victorian cabinet museum, with its unadorned skeletons and taxidermy mounts. These early exhibits are redeemed by the richness and density of the specimens, but this only partly mitigates the present exhibit. I think there are advantages to both the diorama and the starker style evident here, but to give up the one almost entirely is a mistake. This is seen most clearly in a segment of the mammal hall entitled “Savanna Waterhole“, where a giraffe and zebra stretch to drink, but there is no waterhole, and another zebra looks back at a glass wall.
Despite this criticism, there is much to admire in the mammal hall, and much to learn in it. This hall, and the museum as a whole, is a wonder, and one of the nations, and the world’s, scientific and educational treasures. To walk through the USNM’s exhibit halls is a marvelously enjoyable, richly rewarding, and deeply edifying intellectual and aesthetic experience.
Addendum. In response to some of the comments, here are a couple more items.
I just miss hundreds of different birds in a long, long hallway.
It’s a curved hallway, and somewhat obscurely placed outside the Baird Auditorium, but the Birds of DC exhibit is hundreds of birds in a longish hallway. Here’s the cabinet that contains mostly owls, but also a passenger pigeon and a Carolina parakeet.
Is the life-size fiberglass blue whale still there??
No, but a life-size northern right whale is, right in the middle of the new Ocean Hall. It’s modeled after an actual individual whale, named Phoenix, studied by scientists from the New England Aquarium. The story of its creation is here.
I’m not sure where the blue whale is now. It was part of the Life in the Sea exhibit, which was in what is now the Hall of Mammals (I think– I’m trying to recall the hall layout from years ago, and don’t have an old floorplan). It’s story, up to 1996, is told here in Smithsonian magazine.
A band at Smith-Cotton High School in Sedalia, Missouri had the cute idea of wearing tee shirts showing a sequence of human evolution that culminated in a trumpet player. We’re all familiar with these ape-to-human diagrams; Steve Gould even wrote an article about them. They’re somewhat misleading, implying as they do that evolution is progressive and (sometimes) that we evolved from modern apes. But they don’t really do any harm, and they do promote the fact that humans evolved.
But that’s the rub. As reported in the Sedalia Democrat, some irate parents forced the band to abandon its shirts,
[Assistant Superintendant] Pollitt said the district is required by law to remain neutral where religion is concerned.
“If the shirts had said ‘Brass Resurrections’ and had a picture of Jesus on the cross, we would have done the same thing,” he said.
Band parent Sherry Melby, who is a teacher in the district, stands behind Pollitt’s decision. Melby said she associated the image on the T-shirt with Charles Darwin’s theory of evolution.
“I was disappointed with the image on the shirt.” Melby said. “I don’t think evolution should be associated with our school.”
Fig. 1. TIGER SHAME! The offensive and now defunct tee shirt (photo courtesy of the Sedalia Democrat).
I can see a trend coming here: evolution is said to be a “faith,” same as religion, and thus can’t be presented in the public schools. Thanks, Michael Ruse!
Thanks to ERV for bringing this to my attention via her post.
NOTE: erv (see comment below) notes that there is now an online poll about the appropriateness of the tee-shirt. Go here to vote (right-hand column below the ads).
In yesterday’s post I laid out an adaptive hypothesis for the evolution of depression — a hypothesis presented in two new papers by Andrews and Thompson. In short, their “analytical rumination hypothesis” (ARH) proposes that the “malady” we call depression is actually an adaptive behavior built into our ancestors by natural selection. When facing difficult social problems, selection is said to have promoted behaviors that make individuals withdraw from life, ceasing to engage in formerly pleasurable activities like socializing, eating, and sex. This is all in the service of rumination: freed from other activities and commitments, the depressed individual is said to analyze the problems that led to depression in the first place, eventually solving them and re-entering society. This is “adaptive” because individuals who lacked the depressive syndrome would not be able to solve their life problems so easily, and would leave fewer offspring than individuals who shut down and ruminated. In such a way the genes promoting depression increased in our ancestors.
The ARH involves more than just the above, including a hypothesis about the biochemical basis of depression, which involves an excess of the neurotransmitter serotonin. Do consult the original paper if you want more details. I also described why the authors saw depression as an adaptation. Their rationale is quite weak — in essence consisting only of a story of how analytical rumination might have been adaptive in our ancestors. 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.
Today I want to briefly examine the evidence proffered by Andrews and Thomson in support of the ARH. I’ll break it down into a series of questions.
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.
Does depression enhance analytical rumination? Again, the evidence is very, very weak. The authors cite only one “pertinent mood induction experiment”, which may not be relevant at all. In this experiment participants (finance and economics students) were offered the chance to buy and sell German marks and Swiss francs (this was before the Euro in Germany), and were given historical information about markets that could help them with their decision. Success was judged by how much profit was made.
The authors of this study (Au et al. 2003) supposedly created depression-istic conditions in the participants in this way:
Mood was manipulated by providing participants with false feedback on the first round. In the positive mood induction, participants received a high profit for their decision, regardless of what they actually did. In the sad mood induction, participants took a substantial loss. In the neutral mood induction, participants broke even. For all subsequent rounds, participants’ payoffs were determined by their actual decisions and mood was maintained with positive music, sad music, or no music.
Here’s Andrews’ and Thomson’s analysis:
People in positive moods made worse decisions by both standards: They were less accurate, and they lost more because they invested more. Sad participants made the most accurate decisions, but they tended to invest conservatively. Neutral participants were not as accurate as sad participants, but they received a higher profit because they invested more.
This experiment is very much in line with a model of depression’s causes and cognitive effects suggested by Gifford Weary and her colleagues (Weary et al., 1993). Participants experienced an increase in sad affect when they received feedback that their causal understanding of their situation (the trading situation) was
erroneous or in need of modification. Sad affect appeared to have focused their attention on the problem and helped them analyze it so that they could gain control over the situation.
Only in evolutionary psychiatry could a study like this count as “evidence” for the ARH. All it says to me is that if you lose your shirt when engaging in a financial speculation, you tend to be more cautious. If you gain a lot, you tend to be euphoric and not as cautious. Surprise! What this has to do with clinical depression is a mystery.
Does depression help people solve their social dilemmas? The authors cite some studies that, they say, support this contention (see p. 634 of the Psychological Review paper). The one they describe in detail, however, doesn’t inspire much confidence.
In this study pairs of participants played “Prisoner’s Dilemma”. There were three kinds of pairs: depressed people paired with nondepressed people, nondepressed people paired with other nondepressed people, nondepressed people paired with people with “other problems” (e.g. high “fear” tendencies). “High power” participants were those who made the first choice in the dilemma, “low power” participants went second. Overall, depressed people scored marginally better than “normals”, but the difference isn’t impressive: 97.4 versus 88.5 points, a difference that isn’t reported as statistically significant. Andrews and Thomson impute the results to the fact that “the behavior of the depressed participants was more sensitive to position. In the high power position, depressed participants tended to defect more; when in the low power position, they tended to cooperate more.
Well, this may be relevant to the problem, but 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! Ideally we’d like to examine two groups of people that face similar social dilemmas, such as infidelity. One group would consist of those who experience post-dilemma depression, the other would not. Psychologists could then assay whether the depressives had more positive outcomes.
The authors cite one more bit of evidence for the use of depression to solve dilemmas:
That depression may help people solve social dilemmas is also supported by research on real-life dilemmas. When in conflict with close, cooperative social partners, people tend to show more sympathy, more support, and reduced aggression when their partner has depressive symptoms . The supportive response that depressed people get from their close social partners has led some researchers to argue that it reinforces depressive tendencies, which suggests that it may be useful in solving social dilemmas. [References omitted; see original paper.]
Well, this does bespeak the milk of human kindess,but it’s not clear whether sympathy does reinforce depressive tendencies (which the authors see as good), and even less clear that “more sympathy and support” translates into “solved social dilemmas.”
Such is the nature of the evidence in evolutionary psychiatry: tendentious, thin, and highly speculative. I’m used to that, but not to the prescription that doctors do away with antidepressants:
Our review suggests that medications treat symptoms, whereas psychotherapies are more likely to be treating cause. The analytical rumination hypothesis suggests that psychotherapies are productive when they help depressed people identify and solve important problems in their lives. It also suggests that depressive rumination is useful and that antidepressants may interfere with the ability to ruminate. For these reasons, the analytical rumination hypothesis would place greater emphasis on psychotherapy and less on medications.
The authors suggest that “problem-solving” forms of psychotherapy, like cognitive behavioral therapy (CBT) will be more useful, since they concentrate on having the depressed person solve problems. I’m not that familiar with CBT, so I don’t know whether the “problems” it helps solve are those identified as precipitating depression in the first place, but data do show that it seems to be effective. But no more effective than drugs. The most enlightened treatment of psychiatry today appears to be a combination of psychotherapy and medication. Before we do away with the latter, we’ll need a lot better analysis than that of Andrews and Thompson.
It may be worth mentioning here that if depression helps you solve life problems, one episode apparently doesn’t do the job. If you’ve had a major depression, the probability that you’ll have another within five years is nearly 80%. This suggests that the condition is a chronic pathology, although of course Andrews and Thompson might respond that this may just reflect genetic differences between people (but then why aren’t “depression genes” fixed in all humans?), or that some people just have a lot of problems and need to experience recurrent adaptive depressions.
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Worthwhile books on depression:
There are two superb accounts of depression, both written from the inside, that show the “adaptation” in all its frightening intensity. One is embryologist Lewis Wolpert’s personal/scientific account, Malignant Sadness: The Anatomy of Depression. The other is author William Styron’s account of his “adaptation,” Darkness Visible: A Memoir of Madness.
Manic depression is not the same clinical syndrome as depression, but I thought I’d include the following for general interest:
An Unquiet Mind: A Memoir of Moods and Madness and Touched With Fire: Manic-Depressive Illness and the Artistic Temperament, by Kay Redfield Jameson. Jameson is a clinical psychologist and a superb writer, who also suffers from severe manic depression. She’s written an engrossing memoir of her illness (now under control with lithium), which shows the difficulty that even a trained mental-health worker has with staying on medication. Her Touched with Fire is interesting, maintaining as it does that manic depression may be closely connected with artistic genius. She may well be right, though the book suffers a bit from making a virtue of necessity.
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Last night I was reading a new book which claimed that we’ve never seen atoms or molecules. The point the author was making is that in evolutionary biology you don’t need to actually see evolution happening, you can infer it — just as we can confidently infer the existence of atoms and molecules. The point is correct, but the example is not.
We can actually see atoms and molecules. This morning I awoke to find out that a really spiffy molecule has been visualized using a new type of microscope.
It’s pentacene, with 22 carbons and 14 hydrogens. The molecule consists of five fused benzene rings, and is used, among other things, in solar panels.
IBM researchers in Switzerland imaged the molecule using a sophisticated new technology that includes a single molecule of carbon monoxide as an imaging device.
Fig. 1. Image of pentacene from the atomic force microscope
The AFM [atomic force microscope] uses a sharp metal tip that acts like a tuning fork to measure the tiny forces between the tip and the molecule. This requires great precision as the tip moves within a nanometer of the sample.
‘Above the skeleton of the molecular backbone (of the pentacene) you get a different detuning than above the surface the molecule is lying on,’ Mr Gross said.
This detuning is then measured and converted into an image.
To stop the tip from absorbing the pentacene molecule, the researchers replaced the metal with a single molecule of carbon monoxide. This was found to be more stable and created weaker electrostatic attractions with the pentacene, creating a higher resolution image.
Here’s the conventional molecular representation of pentacene:
Fig. 2. Pentacene as you might have seen it in O-chem
And, as I say in WEIT, we’ve been able to visualize atoms ever since the scanning tunnelling microscope was created in 1981. (Its inventors got a Nobel Prize five years later.)
Here’s a bunch of atoms, looking like little balls:
Fig. 3 : A photograph of about 500 atoms of Niobium (41) and Selenium (34) neatly arranged at the surface of a crystal (darker atoms are simply lying lower in the surface).
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.