Evolutionary Psychology: Deadweight or Paydirt?

According to Jerry Coyne [1], in science's pecking order, evolutionary psychology is a deadweight, dragging evolutionary biology closer to phrenology than physics. Certainly, that is not all-wrong. Outlandish popularized and scholarly accounts of the causes of emotional and moral trait evolution (including pathologies) are sometimes nearly baseless and generally lacking any pretense of rigor. Loose banter about 'theories' associated with evolution--even in name alone--is not exactly what we need. But it is inevitable because, "evolutionary psychology satisfies our hunger for a comprehensive explanation of human existence [...] Freud is no longer the preferred behavioral paradigm. Now Darwin is ascendant. Blame your genes, not your mother" [1]. As it turns out. some of the blame may fall on your genes, mother, and father.

I was in for a small surprise when, in preparation for my evolution class, which will be taught to a mostly pre-med audience, I read some fabulously interesting papers by Bernie Crespi and Chris Badcock [2,3; and popular accounts in NYT, Science]. Briefly, taking a cue from the early work on sexual conflict by W. D. Hamilton, and expanded by D. Haig, they contend that asymmetric expression of maternally and paternally imprinted genes may be responsible for a wide spectrum of seemingly unrelated mental illnesses.

Given that intragenomic conflict can drive the evolution of paternal and maternal imprinting, and imprinting can affect the development of the parts of the brain involved in social interactions in an opposite manner, Crespi and Badcock argue that balanced expression of those two components results in 'normal' cognitive and social development. Alternatively, a wide imbalance can have a strong negative outcome. If the mother's genetic self-interest wins, this can lead to hypermentalism (e.g. paranoid schizophrenia; pathologically conspiracy-prone with delusions of grandeur, ambivalence). Conversely, male imprinting can lead to hypomentalism (autism spectrum; poor inference of intention, inability to decieve, deficit in personal agency, single-mindedness). The key prediction of the theory is that autism and schizophrenia occupy ends of a 'social brain' [4] spectrum. This is significant because of the puzzling and hopelessly contradictory medical evidence. Autism and schizophrenia do not obey simple Mendelian inheritance, and this paralyzed the search for clinical treatments.

Although definitive evidence is still lacking, and some individuals can show signs of both spectrum disorders, the imprinted social brain theory is now supported by the frequent genomic co-localization of the two end-spectrum disorders, the distribution of copy number variants, predicted correlations with other mental conditions, as well as anatomical and epidemiological data (but see critiques in [3] and elsewhere). At the very least this contention is testable and, if it holds up, it may show outstanding clinical payoffs. It seems that the deadweight could have paydirt potential, afterall.

Notes
[1] Coyne, J.A. 2000. “The fairy tales of evolutionary psychology.” Review of A Natural History of Rape: Biological Bases of Sexual Coercion, by Randy Thornhill & Craig T. Palmer, MIT Press, 2000. The New Republic, March 4, 2000.
[2] Badcock C. and B. Crespi. 2008. Battle of the sexes may set the brain. Nature 454:1054-1055. (Photo credit: J. Robinson)
[3] Crespi, B. and C. Badcock. 2008. Psychosis and autism as diametrical disorders of the social brain. [with commentary] Behavioral and Brain Sciences 31:241-320.
[4] Dunbar, R.I.M. 1998. The Social Brain Hypothesis. Evolutionary Anthropology 6:178-190. (Dechro peeps: we should totally get and re-analyze this data).