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OCR for page 235
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
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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.
