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Comment on "Parasites as a Viability Cost of Sexual Selection in Natural Populations of Mammals"
We appreciate the study by Moore and Wilson
(1) that investigated the relation between sex-biased
parasitism (SBP)and sex-biased mortality (SBM) in mammals.
Regrettably, however,Moore and Wilson ignored the association between
SBP and a crucialfactor in parasite exposure: home range. Sex-based
differencesin home range are extremely common in mammalian species
(2).Logically, mammals that traverse a greater area are
exposed toa greater number of parasites because they interact with
moreparasite habitat and with more individuals carrying infectiousparasites. Of course, body size is correlated with home range,because
larger mammals can typically defend larger territoriesand because
maintaining a greater body size often requires foragingover a greater
area (3, 4).
We therefore argue that sexual difference in home range, rather than
body size, is a more proximate (yet unappreciated) mechanisticbasis
for SBP. For example, a doubling in body size is likelyto yield much
less additional parasitic exposure compared to adoubling in home
range. The impact of increased exposure to parasitehabitat would
presumably be most evident for free-living parasites,which may explain
why Moore and Wilson found the largest effectsize of SBP for arthropod
parasites but a nonsignificant effectsize for unicellular parasites.
Although Moore and Wilson alsoused a mating system variable
(monogamous or polygynous) to showan association between SBP and
sexual selection, they did notconsider that polygynous males
typically frequent much largerareas relative to females
(5). To secure mates, polygynousmales must thus
increase their probability of traversing parasitehabitat, while
interaction with each additional mate representsanother potential
source of infection.
Moore and Wilson (1) suggested that their findings are
consistent with male-biased mortality as a result of malesinvesting in
enhanced growth and differential resource allocationat the expense of
their immune systems. In a related Perspectivearticle, Owens
(6) used this logic to explain part ofhuman SBP
with statistics from the World Health Organization
(7).If males were truly more susceptible to
parasitic and infectiousdisease due to higher energetic or hormonal
investments in growthand function (rather than behavioral
differences), then we wouldexpect a high incidence of disease
mortality during the intensivehuman developmentbefore age 25. Although this is
obviously notthe case [see corrected figure from Owens
(8)], we questionthe validity of using the underlying data
set to investigate thisquestion in the first place: 48% of the
mortality due to parasiticand infectious disease in these data is from
AIDS, an afflictionstrongly influenced by the behavior of adult males.
Our new perspective on SBM changes little for insurance
companies--males still "out-die" females. However, it does indicatethat public-health programs can reduce mortality with behavioralinterventions, rather than assuming that males are doomed to immunesystem inferiority. We find this to be good news for males.
Brandon Brei* Durland Fish
Department of Epidemiology and Public Health Yale
University School of Medicine 60 College Street Post Office Box
208034 New Haven, CT 06520-8034, USA E-mail:
Durland.Fish{at}yale.edu
