Meeting Abstract
In 1992, Folstad and Karter published the immunocompetence handicap hypothesis, suggesting that testosterone not only influences male sexually-selected traits, but also results in immunosupression, hence indicating a handicap; only those individuals with superior immune systems can afford the cost of producing and maintaining elaborate sexually-selected traits, while simultaneously being able to fight off parasites and pathogens. We (Braude et al., 2009) challenged this idea by proposing the immunoredistribution hypothesis. We argued that, under stressful conditions, the immune cells in the blood migrate to more vulnerable areas of the body where they are most needed, such as to the skin when there is a danger of superficial injuries. The loss of immune cells in the blood can then lead to the mistaken conclusion that immunosuppression has occurred. The general view, however, continues to be that testosterone inevitably suppresses the vertebrate immune system. Here we examine and review empirical data showing that, at least in some species, there is scant unequivocal evidence that testosterone is immunosuppressive. Studies on parasites, testosterone, and immunity do not always support the hypothesis. Some meta-analyses likewise have failed to find strong support. Other studies find that results obtained under natural, field conditions may differ (less likely to show immunosupression) compared to those obtained in the lab. Moreover, testosterone may have indirect effects on body condition, or other steroid hormones, that can confound the interpretation of results. These disparate threads of evidence suggest that the widely-held belief that testosterone is unquestionably immunosuppressive needs to be re-evaluated.
