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When I developed the first, crude version of the imprinted brain theory, I realized that I needed a mental illness which it could explain, and my first idea was anorexia. Indeed, it seemed obvious. At that time—the late 1990s—I had formulated a theory which held that the mental conflicts described by Freud were caused by deeper, genetic conflicts.
David Haig had advanced an elegant theory showing how conflicts between a mother's and a father's genes were critical for growth and development. Paternal genes favor growth and development of the fetus because in mammals they get all the benefits without any cost thanks to the mother doing the gestating and lactating. The mother's genes want restraint for the same reason. The key example is IGF2: a growth factor gene which is paternally-active and maternally-silent.
In Beckwith-Wiedemann syndrome (BWS) both parents' copies of IGF2 are expressed, but in Silver-Russell syndrome (SRS) neither are. As the illustration above shows, BWS is an over-growth syndrome, and SRS an under-growth one. I believed that the Freudian id was the psychological agent of paternal, resource-demanding genes and the ego that of the maternal, resource-limiting ones.
Anorexia seemed designed to prove the idea because the vast majority of sufferers are female, and self-starvation is the ultimate in resource-limiting behavior. Anorexics, in other words, were expressing maternal genes and the ego at the expense of paternal ones and the id—and specifically the id’s demand for food. No wonder the vast majority were female: all mothers are!
But almost immediately I saw that there were problems with this. The genetic conflicts Haig described are over investment in the offspring during pregnancy and infancy, not over food-consumption in late adolescence/early adulthood—the typical age for the onset of anorexia. And Prader-Willi syndrome was incontestably the result of enhanced expression of critical maternal genes on a region of chromosome 15, yet voracious food-foraging and obesity were seen in later childhood—definitely not anorexia! Another beautiful idea bit the dust!
But now it’s back in a new guise. Given that 90% of sufferers from anorexia and 98% of those suffering from bulimia are female, a recent paper suggests that these eating disorders are good candidates for being pathologies of the so-called extreme female brain (EFB). I have published a previous post about the EFB, so won’t repeat myself here except to say that where the imprinted brain theory differs most from the EFB one is in the cognitive model it employs. For the EFB theory this is Baron-Cohen’s systemizing/empathizing one explained in the previous post on the subject. In the case of the imprinted brain theory, the diametric model of the mind proposes that whereas autism spectrum disorders are symptomatically hypo-mentalistic, psychotic spectrum disorders are symptomatically hyper-mentalistic.
Gratifyingly, this paper explicitly endorses the latter in explaining why anorexics did worse than normal controls on a test they should have done better on if anorexia is indeed an extreme female brain disorder: Reading the Mind in the Eyes (RME, example below):
An alternative interpretation is that low scores on the Reading the Mind in the Eyes task does not represent a deficit in theory of mind ability, but rather an excess that reflects hyper-mentalizing. … The test does not identify the nature of the errors that impede performance. For example, there can be errors of absence (failing to detect a mental state when it is present) and errors of excess (wrongly inferring a mental state in its absence). We suspect the second class of errors (errors of excess) account for most of the lower scores on this test among individuals with anorexia.
One reason for preferring hyper-mentalizing to "hyper-empathizing" is that it’s hard to see how you can hyper-empathize when, by definition, empathizing suggests accurately perceiving another’s feelings. You wouldn’t be empathizing if you thought someone who was crying with pain was crying from laughter, and "hyper-empathizing" by interpreting a tear shed by an eye-irritation as one shed in sorrow would be similarly erroneous. Nevertheless, this paper does highlight one context in which "hyper-empathizing" does seem to make some sense: vegetarianism. As the authors point out:
People with greater empathizing skills would be expected to be more sensitive to the pain and suffering of others. An interesting interpretation of these data involves the disproportionate rates of vegetarianism among individuals with eating disorders. For example, numerous studies have found a positive association between vegetarianism and eating disorders (…). Most investigators interpret this relationship as evidence confirming health-conscious, restrictive eating patterns among people with eating disorders. However, an alternative hypothesis consistent with the data presented here is that individual differences in empathizing may affect dietary choices as a consequence of heightened concerns about animal cruelty and animal welfare.
One development that may resolve the issue is when food technology advances to the point that you can go from stem-cell to steak without growing the rest of the animal. Indeed, the first experiments are already underway, and the final outcome is inevitable. Who would want to eat meat from a slaughtered animal infected with god-knows-what when you can get a perfect steak grown from stem cells in a sterile environment? (A recent survey of vegetarians' attitudes to lab-produced meat can be found at http://theveganoption.org/2012/05/16/lab-meat-survey-results/.)
But will anorexics be takers? They should not object if their problem is "hyper-empathizing." Yet I suspect that they will have no more taste for meat produced this way than any other because their problem is in fact hyper-mentalizing. Millions of people around the world routinely avoid certain foods thanks to the collective hyper-mentalizing we call religion—certainly not because of "hyper-empathizing": think of the ritual slaughtering practices on which some of them insist! It would be very strange if anorexics were much different, and I suspect they’re not.
On the contrary, the case that springs to mind if you are talking about "hyper-empathizing" with animals is that of Temple Grandin, the world's most famous autistic. This makes no sense if, as the empathizing/ systemizing model claims, autism is symptomatically deficient in empathy. And of course, Temple Grandin is no vegetarian!
If it is correct that hyper-mentalizing is a major factor in anorexia/bulimia, the diametric model of mental illness suggests that these may be psychotic, rather than autism spectrum disorders. And if that is so, the imprinted brain theory definitely implicates maternal (and X chromosome) genes. Perhaps I was right the first time round!
(With thanks to Diana Fleischman for bringing this to my attention.)
