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Part IV SOCIALITY AND MEDICINE M ost biologists probably work in biomedical fields. If nothing in biology makes sense except in the light of evolution, then medi - cine should have much to learn from evolutionary reasoning. The rapidly growing field of Darwinian medicine (Williams and Neese, 1991) is based on this premise and seeks to provide insight on topics such as the evolution of virulence and diseases of altered evolutionary envi - ronments. A subfield recently called Hamiltonian medicine (Foster, 2005) investigates the impact of social evolution, cooperation, and conflict on disease. In Chapter 11, Andrew Read and colleagues treat the vital problem of how to minimize the evolution of pathogen resistance and thereby extend the useful lives of our arsenal of antibiotic drugs. This involves a complex set of interacting causes, some of which have a social element and others do not. The authors challenge the dogma that we minimize the evolution of resistance by “radical pathogen cure”: using enough of a drug to try to eliminate the pathogen from the patient’s body. The reasonable rationale behind this practice is to lower the pathogen population size and minimize the occurrence of novel resistance mutations. But the authors argue that this ignores the selective phase, which may be more important in deter- mining the time to drug impotence, particularly when resistance muta - tions arise with relative ease. In this selective phase, the radical pathogen cure provides the strongest possible selection for resistance. According to Read and colleagues, the social structure of the pathogen can power- fully augment this selection. When a host is infected by multiple strains 235
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236 / Part IV of the pathogen (as is often true of malaria) and the total density of the pathogen is regulated, then wiping out susceptible strains with antibiotics can greatly increase the frequency of formerly rare resistant strains. This raises the possibility that the medical community is ignoring an important human social dilemma: that the best treatment for a patient may not be the best outcome for society as a whole. Some human disorders can spring not from a failure of adaptation per se, but from disagreement and conflict over what is the correct adaptation. This is particularly so in the realm of human interpersonal relations, start - ing with fundamental conflicts between parent and offspring. Haig (1993) has argued that such conflicts can lead to pathologies in pregnancy when there is an upset in the precarious resolution of embryo-maternal conflict. Taking a radical step further, he has pointed out that the optimal strategy of an embryo’s gene differs according to whether it came from the dam or the sire, with maternal loci being less selected to take resources from the mother. Remarkably, imprinted genes appear to behave in accord with this theory. In Chapter 12, David Haig extends this thinking in several directions. He notes that most of our kin belong to categories that have asymmetrical relatedness to our maternal and paternal genes, so that most of our psychological adaptations for dealing with kin, and perhaps pathologies, may reflect these kinds of conflicts. In particular, he shows how this perspective may illuminate unsolved problems surrounding the evolution of adolescence and the timing of sexual maturation in humans. In Chapter 13, Steven Frank and Bernard Crespi extend and general- ize the same theme: that conflict can lead to pathologies when oppos - ing interests that are precariously balanced become unbalanced. These authors suggest that the conflict between maternal and paternal genes in offspring, through its demonstrated effects on the regulation and patholo- gies of growth, may be responsible for some cancers. They then discuss the exciting idea that this same balance is partly responsible for a wide spectrum of psychiatric disorders, such as autism that may result from an overexpression of paternal interests in offspring selfishness. Similarly, other disorders such as schizophrenia might result from an overexpression of genes underlying the maternal goal of greater social integration. Finally, the authors present a novel theory of conflict between autosomal and X chromosomes. The latter spend two-thirds of their time in females and therefore should be selected to give greater weight to female than to male adaptation. Autosomes should give equal weight. It will be fascinating to see if empirical tests support the authors’ prediction that such conflict will underlie pathologies of expression along the male-female axis.