![]() This response is modified in accordance with the competing demands of the potential costs of parasite infection versus that of increased reproductive success afforded by exaggerated signals. ![]() We propose a negative-feedback loop between signal intensity and parasite burden by suggesting that testosterone-dependent signal intensity is a plastic response. This "double-edged sword" creates a physiological trade-off that influences and is influenced by parasite burden. The primary androgenic hormone, testosterone, has a dualistic effect it stimulates development of characteristics used in sexual selection while reducing immunocompetence. Here, we have presented a phenomenological model, operating on an intraspecific level, which views the cost of secondary sexual development from an endocrinological perspective. To a large extent, handicap hypotheses have relied on energetic explanations for these costs. It has been argued that females should be able to choose parasite-resistant mates on the basis of the quality of male secondary sexual characters and that such signals must be costly handicaps in order to evolve.
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