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.
____________
*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.
After reading what you said these authors hypothesize, all I can say is “What are they thinking?”
I wont go into my (negative)take on (evo- or otherwise) psychology and psychiatry, but I do not see how they can be serious about their claims.
How do articles like this get through the peer review process? From what I have seen (which is not extensive), the peer review process can be relentless in NOT letting people get away with unsubstantiated claims. How did these studies get through?
newenglandbob I think studies like this that get through the peer review process shows psychology and psychiatry still haven’t completely crossed the bar into science.
The peer review process has nothing to do with the definition of science. Could the peer review process be better? Certainly, but that doesn’t make these studies unscientific.
My impression from reading Ben Goldacre is that the Serotonin Hypothesis is more and more looking to be ever so much bullshit.
But that is not to say the SSRIs don’t work – it’s just that we have no friggin’ clue how they work. I seem to recall the eminent Derek Lowe mentioning that reuptake enhancers may have a similar positive benefit on depression sufferers.
Anecdote time: I can obviously only speak for myself, but I needed the drugs (and still do). I have had therapy, too, and it has done me a world of good, but I truly did not have the mental excess to concentrate on my thoughts and feelings and engage in introspection until I was fully medicated. And my depression was never as bad as some of the worst cases from what I can gather from the descriptions by the victims.
On the serotonin model of depression and why it’s at best incomplete, see here.
I think that the serotonin hypothesis of depression is just too simplistic. It may be just 1 of the reasons people suffer from depression.
In my research which is summarised in my latest book I’ve found that there are over 20 different physical causes for depression including hormonal imbalances, nutrient deficiencies, adverse reactions to food and toxic overload.
Apologies for this shameful self-promotion, but may I submit this post I wrote a couple of days ago on the same study? I only read the SciAm article. Reading the full 34 pages seems like a true waste of time. To me, the really funny theme in the story is that the authors suggest that ruminating over your social problems was more adaptive than actually eating and having sex. Last I heard sex and food were among the very things that are thought to increase fitness.
When people are depressed eating and relationships are negatively affected and may stay that way for a long time. Taking time out whether it is to ruminate or just recover from a stressful life event helps recover normal functioning.
Then ruminating would be the adaptation to fix the malady of depression.
Your article is excellent, and covers my frustration with psychiatry in general vis: that its dogmas are based on little, no (or even truckloads of countervailing) evidence.
(Mostly the “NO evidence” model.)
You state that you have seen no-one propose that schizophrenia is adaptive.
The late psychologist Julian Jaynes did exactly this in his controversial tome “The Origin of Consciousness in the Breakdown of the Bicameral Mind”.
I do not agree with him, but I merely point out that he proposed this theory.
Now you cannot say that no-one has forwarded the notion! 😉
Very nice write up. It is imperative that scientists openly criticize other scientists’ work, because for us laymen people every scientifically-sounding idea sounds amazing until presented with a counter-argument.
“they may alleviate the symptoms of depression, but they don’t alleviate the cause (life problems).”
I’m sorry to inform, but many times depression arises REGARDLESS of whether you have ‘life problems’ or not. One can have essentially no real problems and still be afflicted with crippling depression thank you very much…
Depression isn’t like going off on a hike to get some time alone and think without distraction. It skews the cognitive faculties, lowering one’s estimation of one’s own capabilities. You can see your problems, but you don’t think you can do anything about them. Depression makes a person less able to function.
That saves me some trouble – I was going to say – I thought depression was supposed to be very for cognitive functioning.
very bad for cognitive functioning, I said – I must have screwed up the italics. How depressing.
You accidentally the whole thing.
“Modularity” is another thing which makes me wary of evo-psych. As somebody who actually does research on network modularity, I can tell you, it ain’t simple. Even when your system is just a heap of nodes connected by lines — glossing over all the biological complexity of neurons — defining what one means by “modules” and partitioning a network into them is not a trivial problem. Add to this the complexity of the genotype-phenotype map and the relation between neural structures and behaviours. . . well.
I’m just curious about what Jerry thinks about Randolph Nesse’s work.
As for depression, my wild uneducated speculation would be the ability to feel sad gets supernormally stimulated to a point that the behaviour it leads to ultimately perpetuates the depressed feeling and makes it worse in a kind of self perpetuating feedback loop that gradually leads to more and more depressed behavior.
Making up “theories” is fun!
It’s not just about feeling sad, feeling worthless is a huge part of it. And good news doesn’t help, because you can’t see how it applies to you. Hope this helps.
I think that cycle of feedback between the depressed person’s feelings and behaviour is pretty much the behaviourist theory of depression. Recently, some studies have shown that breaking the feedback cycle by changing the depressed person’s behaviour and encouraging them to explicitly avoid rumination by focussing on their behaviour has results equal to the cognitive-behavioural model, indicating that the cognitive components of the theory were actually inert and that the efficacy was due to the behavioural components. So maybe your “made-up” theory hits the nail square on the head!
Like many other commenters, I’m baffled. What definition of “depression” are these guys working with? Do they understand that it doesn’t mean “feeling sad and contemplative?” There was nothing at all adaptive or functional about my life before medication – endless sleeping (or no sleeping at all), suicidal ideation, panic attacks and obsessive-compulsive behaviors. OK, so I had a few more problems than depression alone:)
Honestly, the entire premise of their hypothesis is insane if they believe (as they appear to) that the brain is doing useful work during a bout of depression. By definition, depression is a state where the mind is not functioning well. It’s not “solving problems;” it’s creating them. This is so transparent, so uncontroversial, I cannot understand how the authors even got past the proposal stage without someone saying, “Um, I don’t think that word means what you think it means.”
JoshS’s point is the one which rang through my head as I skimmed the paper. I wish people would properly define their terms when talking about mental disorders! Depression comes in a number of flavours and forms of severity.
I can see where they’re coming from, but only in an almost-trivial sense in that feeling down can lead one to re-asses one’s life goals and priorities, or that difficult situations can be hard to bear. To conflate this with MDD, with its extreme psychomotor retardation, dissociation, and overbearing suicidal obsession and actions, is the height of muddled thinking. To go on to make treatment recommendations for the latter based on observation of the former is dangerous.
BTW, I understand ‘rumination’ from Nolen-Hoeksema’s work, where it is defined as pointless absorption and most definitely NOT useful.
Oy! And to add to other points raised, I have this:
“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*”
Now I seem to remember a recent press release where they found, or at least speculated, that the anhedonia of depression where not entirely or even in major part caused by an inability to experience rewards, but from a much depressed [sic!] ability to plan ahead.
I.e. even people who ordinarily could put off future rewards for the immediate activity necessary to achieve them lost much of that capability on the basic level that allowed them to actually do it. (As opposed to intellectually “getting” the concept.)
Even if speculation, the possibility that such hypotheses exists AFAIU mean that these authors must show that anhedonia in actuality benefits, not possibly detracts from, their hypotheses.
As a layman I’m insufficiently prepared to digest even the more basic and verified topic of evolution, but I find it easy to at least extract some papers that have made and tested predictions. (Whether I actually understand them is another question.)
Despite some browsing I have found it hard to do the same with EP. Which means that I can embrace the notion that it is pathological science on the level of Freud’s dream “analyses”, or at least a dead attempt at science. Any predictive and tested “good stuff” would of course radically change that, so I would be glad to any immediate pointers to such papers.
Lacking that I will continue to browse this log, perhaps I will get lucky on this score!
I can trace my chronic state of serotonin depression, effectively cured by taking SSRI uptake inhibitor Lexapro not to problems in life but to a 3 month extreme video game playing episode that I would participate as long as 48 hours at a time, with severe disruption in nutrition and sleeping habits.
I am convinced that my depressive state began at precisely that time.
My theory is that the brain must have gone through a mechanism to improve performance, concentration, and limit fatigue, at the cost of other non-game functions by enhancing the uptake process.
This is probably a survival mechanism that has wide aplication and may be argued to be adaptive, if it can be reduced to such behavior.
“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).”
“A design analysis does not require depressive rumination to be currently adaptive because modern and evolutionary environments may differ in important ways.”
If the former is their conclusion, then this is a bait-and-switch: you shouldn’t take anti-depressants… why? because depression was adaptive for your ancestors. I would bet Scientologists, or others with an anti-psychiatry bias, were responsible for this.
“By putting yourself into isolation and forcing your brain into rumination, depression supposedly helps you attack the precipitating problem.”
Here’s another anecdote for you, but this seems absolute nonsense to me. As someone who regularly suffers from severe depression I can tell you that when I come out the other side, I realise that the thoughts I had while depressed are often remarkably illogical and if I make any major decisions during my most depressed periods, they usually turn out to be bad ones. Lots of introspection certainly, but not necessarily productive.
spending 25 years with a narcissistic, abusive relationship, I do believe I reside in a clinical state of variable levels of depression. Yet all of my problems are dissipating through the assistance of family as I have been able to leave this relationship behind. Daily I can make personal evaluations and clear means to solve any dilemmas that arise. Yet I am a writer and artist, I do believe that my depression does allow the tools to vacate the dilemma and make thinking cleaner and more attuned to problem solving. Also I would like to point out that with the longevity of the depression, There clearly was no way to survive looking inward,I know and believe I am good and kind person to everyone I meet, therefore I was inclined to interest myself into large scale dilemmas, such as history,religion, and the sciences. And I do see and find flaws in many things, yet I do not have the educational background to justify a thing. Now I ask, how does one in this situation make their findings available for review and analysis, without criticizing the individual?
For a fuller explanation of the hypothesis under discussion here, see the more original and foundational paper, downloadable here:
http://biology.unm.edu/biology/pwatson/public_html/Watson_Andrews2002.pdf
We present an hypothesis in hopes of it being tested. That’s how scientific discoveries, including counterintuitive ones, are made. — PJW