From an evolutionary perspective, it shouldn’t even exist. Most psychiatric disorders are at least somewhat genetic, and most psychiatric disorders decrease reproductive fitness. Biologists have equations that can calculate how likely it is that maladaptive genes can stay in the population for certain amounts of time, and these equations say, all else being equal, that psychiatric disorders should not be possible. Apparently all else isn’t equal, but people have had a lot of trouble figuring out exactly what that means. A good example of this kind of thing is Greg Cochran’s theory that homosexuality must be caused by some kind of infection; he does not see another way it could remain a human behavior without being selected into oblivion.
Del Giudice does the best he can within this framework. He tries to sort psychiatric conditions into a few categories based on possible evolutionary mechanisms.
First, there are conditions that are plausibly good evolutionary strategies, and people just don’t like them. For example, nymphomania is unfortunate from a personal and societal perspective, but one can imagine the evolutionary logic checks out.
Second, there are conditions which might be adaptive in some situations, but don’t work now. For example, antisocial traits might be well-suited to environments with minimal law enforcement and poor reputational mechanisms for keeping people in check; now they will just land you in jail.
Third, there are conditions which are extreme levels of traits which it’s good to have a little of. For example, a little anxiety is certainly useful to prevent people from poking lions with sticks just to see what will happen. Imagine (as a really silly toy model) that two genes A and B determine anxiety, and the optimal anxiety level is 10. Alice has gene A = 8 and gene B = 2. Bob has gene A = 2 and gene B = 8. Both of them are happy well-adjusted individuals who engage in the locally optimal level of lion-poking. But if they reproduce, their child may inherit gene A = 8 and gene B = 8 for a total of 16, much more anxious than is optimal. This child might get diagnosed with an anxiety disorder, but it’s just a natural consequence of having genes for various levels of anxiety floating around in the population.
Fourth, there are conditions which are the failure modes of traits which it’s good to have a little of. For example, psychiatrists have long categorized certain common traits into “schizotypy”, a cluster of characteristics more common in the relatives of schizophrenics and in people at risk of developing schizophrenia themselves. These traits are not psychotic in and of themselves and do not decrease fitness, nor is schizophrenia necessarily just the far end of this distribution. But schizotypal traits are one necessary ingredient of getting schizophrenia; schizophrenia is some kind of failure mode only possible with enough schizotypy. If schizotypal traits do some other good thing, they can stick around in the population, and this will look a lot like “schizophrenia is genetic”.
How can we determine which of these categories any given psychiatric disorder falls into?
One way is through what is called taxometrics — the study of to what degree mental disorders are just the far end of a normal distribution of traits. Some disorders are clearly this way; for example, if you quantify and graph everybody’s anxiety levels, they will form a bell curve, and the people diagnosed with anxiety disorders will just be the ones on the far right tail. Are any disorders not this way? This is a hard question, though schizophrenia is a promising candidate.
Another way is through measuring the correlation of disorders with mutational load. Some people end up with more mutations (and so a generically less functional genome) than others. The most common cause of this is being the child of an older father, since that gives mutations more time to accumulate in sperm cells. Other people seem to have higher mutational load for other, unclear reasons, which can be measured through facial asymmetry and the presence of minor physical abnormalities (like weirdly-shaped ears). If a particular psychiatric disorder is more common in people with increased mutational load, that suggests it isn’t just a functional adaptation but some kind of failure mode of something or other. Schizophrenia and low-functioning autism are both linked to higher mutational load.
Another way is by trying to figure out what aspect of evolutionary strategy matches the occurrence of the disorder. Developmental psychologists talk about various life stages, each of which brings new challenges. For example, adrenache (age 6-8) marks “the transition from early to middle childhood”, when “behavioral plasticity and heightened social learning go hand in hand with the expression of new genetic influences on psychological traits such as agression, prosocial behavior, and cognitive skills” and children receive social feedback “about their attractiveness and competitive ability”. More obviously, puberty marks the expression of still other genetic influences and the time at which young people start seriously thinking about sex. So if various evolutionary adaptations to deal with mating suddenly become active around puberty, and some mental disorder always starts at puberty, that provides some evidence that the mental disorder might be related to an evolutionary adaptation for dealing with mating. Or, since a staple of evo psych is that men and women pursue different reproductive strategies, if some psychiatric disease is twice as common in women (eg depression) or five times as common in men (eg autism), then that suggests it’s correlated with some strategy or trait that one sex uses more than the other.
This is where Del Giudice ties in the life history framework. If some psychiatric disease is more common in people who otherwise seem to be pursuing some life strategy, then maybe it’s related to that strategy. Either it’s another name for that strategy, or it’s another name for an extreme version of that strategy, or it’s a failure mode of that strategy, or it’s associated with some trait or adaptation which that strategy uses more than others do. By determining the association of disorders with certain life strategies, we can figure out what adaptive trait they’re piggybacking on, and from there we can reverse engineer them and try to figure out what went wrong.
This is a much more well-thought-out and orderly way of thinking about psychiatric disease than anything I’ve ever seen anyone else try. How does it work?
Unclear. Psychiatric disorders really resist being put into this framework. For example, some psychiatric disorders have a u-shaped curve regarding childhood quality — they are more common both in people with unusually deprived childhoods and people with unusually good childhoods. Many anorexics are remarkably high-functioning, so much so that even the average clinical psychiatrist takes note, but others are kind of a mess. Autism is classically associated with very low IQ and with bodily asymmetries that indicate high mutational load, but a lot of autistics have higher-than-normal IQ and minimal bodily asymmetry. Schizophrenia often starts in a very specific window between ages 18 and 25, which sounds promising for a developmental link, but a few cases will start at age 5, or age 50, or pretty much whenever. Everything is like this. What is a rational, order-loving evolutionary psychologist supposed to do?
Del Giudice bites the bullet and says that most of our diagnostic categories conflate different conditions. The unusually high-functioning anorexics have a different disease than the unusually low-functioning ones. Low IQ autism with bodily asymmetries has a different evolutionary explanation than high IQ autism without. In some cases, he is able to marshal a lot of evidence for distinct clinical entities. For example, most cases of OCD start in adulthood, but one-third begin in early childhood instead. These early OCD cases are much more likely to be male, more likely to have high conscientiousness, more likely to co-occur with autistic traits, and have a different set of obsessions focusing on symmetry, order, and religion (my own OCD started in very early childhood and I feel called out by this description). Del Giudice says these are two different conditions, one of which is associated with pathogen defense and one of which is associated with a slow life strategy.
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There is a part of me that thinks this book is a beautiful example of what solving a complicated field would look like. You take all the complications, and you explain by layering of a bunch of different simple and reasonable things on top of one another. The psychiatry parts of Evolutionary Psychopathology: A Unified Approach do this. I don’t know if it’s all just epicycles, but it’s a heck of a good try.