Ick, not sick! hormonal modulation of physiological and behavioral responses to pathogen threat

Abstract

The Behavioral Immune System (BIS) helps reduce infection risk through responses such as disgust and pathogen avoidance. The Compensatory Prophylaxis Hypothesis (CPH) proposes that immunomodulation associated with heightened progesterone increases BIS reactivity to offset this vulnerability. This dissertation examined how endogenous progesterone and exogenous progestin (via oral contraceptives [OCs]) shape behavioral and physiological responses to pathogen threat across three studies. It further tested the prediction that behavioral and physiological defenses would show complementary coordination under low vulnerability and compensatory coordination under conditions of heightened vulnerability.In Study 1, pathogen-salient cues increased state disgust, and progestogenic activity shaped when individual differences in perceived infectability (PI) were associated with pathogen avoidance motivation. In Study 2, pathogen cues again increased disgust, which in turn predicted greater pathogen avoidance and reduced inflammatory reactivity (IL-6), supporting a compensatory pattern of coordination between behavioral and physiological responses. These effects were moderated by PI and hormonal context, with the compensatory pathway emerging among naturally cycling luteal-, but not follicular-, phase women, consistent with the CPH, and across OC users, although attenuated at higher levels of progestogenic activity. In Study 3, there was little evidence that pathogen threat or hormonal context reliably predicted intergroup attitudes. Across studies, state disgust emerged as the most consistent indicator of BIS activation and had a central role in linking pathogen threat to downstream defensive responses. Overall, this dissertation supports a flexible, context-dependent coordination between behavioral and physiological immune responses and refines the CPH by demonstrating that hormonal influences shape pathogen defense.