1Institute of Biotechnology, University of Helsinki, 2School of Anthropology, University of Arizona, 3Department of Anthropology, Stony Brook University
Saturday 2:00-2:15, Grand Ballroom II
Testosterone is thought to be an underlying cause of immunosuppression in males. It results in costly secondary sexual characteristics which compete with the immune system for resources, leading to an increase in parasite intensities. This is widely known as the immunocompetence handicap hypothesis (ICHH) and has been examined extensively (with conflicting results) in numerous organisms in both captive and wild conditions. However, these studies have only examined the parasitic response to testosterone in males. We previously found that in the wild, female brown mouse lemurs (Microcebus rufus) have testosterone levels comparable to the males of the species which possess elaborate secondary sexual characteristics. Here we test to see if the ICHH applies to both sexes, by comparing tesosterone values to ecto- and endoparasite intensities. Data was collected from August 2008 through November 2009, and samples were analyzed for fecal testosterone(n=541) at the Wisconsin National Primate Research Center using enzyme linked immunoassays. Our results show that while males do experience an increase in ectoparasite loads during the breeding season, there is no correlation between fecal testosterone and ecto- or endoparasite load. Similarly, fecal testosterone in females shows no significant trend fitting the ICHH. We found that during the breeding season males experience a dramatic increase in ectoparasite loads, but our data fail to support testosterone as the primary underlying cause of this mechanism. Instead we suggest a much more complex cause of decreased immunocompetence in males.