Hormones, and hormone responses to social contexts, are the proximate mechanisms of evolutionary pathways to pair bonds and other social bonds. Testosterone (T) is implicated in tradeoffs relevant to pair bonding, and oxytocin (OT) and arginine vasopressin (AVP) are positively tied to social bonding in a variety of species. Here, we present the Steroid/Peptide Theory of Social Bonds (S/P Theory), which integrates T and peptides to provide a model, set of predictions, and classification system for social behavioral contexts related to social bonds. The S/P Theory also resolves several paradoxes apparent in the literature on social bonds and hormones: the Offspring Defense Paradox, Aggression Paradox, and Intimacy Paradox. In the S/P Theory, we partition aggression into antagonistic and protective aggression, which both increase T but exert distinct effects on AVP and thus social bonds. Similarly, we partition intimacy into sexual and nurturant intimacy, both of which increase OT and facilitate social bonds, but exert distinct effects on T. We describe the utility of the S/P Theory for classifying 'tricky' behavioral contexts on the basis of their hormonal responses using partner cuddling, a behavior which is assumed to be nurturant but increases T, as a test case of the S/P Theory. The S/P Theory provides a comparative basis for conceptualizing and testing evolved hormonal pathways to pair bonds with attention to species, context, and gender/sex specificities and convergences.

Testosterone (T) and other androgens are incorporated into an increasingly wide array of human sexuality research, but there are a number of issues that can affect or confound research outcomes. This review addresses various methodological issues relevant to research design in human studies with T; unaddressed, these issues may introduce unwanted noise, error, or conceptual barriers to interpreting results. Topics covered are (1) social and demographic factors (gender and sex; sexual orientations and sexual diversity; social/familial connections and processes; social location variables), (2) biological rhythms (diurnal variation; seasonality; menstrual cycles; aging and menopause), (3) sample collection, handling, and storage (saliva vs. blood; sialogogues, saliva, and tubes; sampling frequency, timing, and context; shipping samples), (4) health, medical issues, and the body (hormonal contraceptives; medications and nicotine; health conditions and stress; body composition, weight, and exercise), and (5) incorporating multiple hormones. Detailing a comprehensive set of important issues and relevant empirical evidence, this review provides a starting point for best practices in human sexuality research with T and other androgens that may be especially useful for those new to hormone research.

Previous research suggests that sexual stimuli increase testosterone (T) in women and shows inconsistent effects of sexual arousal on cortisol (C), but effects of cognitive aspects of arousal, rather than behaviors or sensory stimuli, are unclear. The present study examined whether sexual thoughts affect T or C and whether hormonal contraceptive (HC) use moderated this effect, given mixed findings of HC use confounding hormone responses. Participants (79 women) provided a baseline saliva sample for radioimmunoassay. We created the Imagined Social Situation Exercise (ISSE) to test effects of imagining social interactions on hormones, and participants were assigned to the experimental (sexual) or one of three control (positive, neutral, stressful) conditions. Participants provided a second saliva sample 15 min post-activity. Results indicated that for women not using HCs, the sexual condition increased T compared to the stressful or positive conditions. In contrast, HC using women in the sexual condition had decreased T relative to the stressful condition and similar T to the positive condition. The effect was specific to T, as sexual thoughts did not change C. For participants in the sexual condition, higher baseline T predicted larger increases in sexual arousal but smaller increases in T, likely due to ceiling effects on T. Our results suggest that sexual thoughts change T but not C, baseline T levels and HC use may contribute to variation in the T response to sexual thoughts, and cognitive aspects of sexual arousal affect physiology.

Testosterone is typically understood to contribute to maleness and masculinity, although it also responds to behaviors such as competition. Competition is crucial to evolution and may increase testosterone but also is selectively discouraged for women and encouraged for men via gender norms. We conducted an experiment to test how gender norms might modulate testosterone as mediated by two possible gender→testosterone pathways. Using a novel experimental design, participants (trained actors) performed a specific type of competition (wielding power) in stereotypically masculine vs. feminine ways. We hypothesized in H1 (stereotyped behavior) that wielding power increases testosterone regardless of how it is performed, vs. H2 (stereotyped performance), that wielding power performed in masculine but not feminine ways increases testosterone. We found that wielding power increased testosterone in women compared with a control, regardless of whether it was performed in gender-stereotyped masculine or feminine ways. Results supported H1 over H2: stereotyped behavior but not performance modulated testosterone. These results also supported theory that competition modulates testosterone over masculinity. Our findings thus support a gender→testosterone pathway mediated by competitive behavior. Accordingly, cultural pushes for men to wield power and women to avoid doing so may partially explain, in addition to heritable factors, why testosterone levels tend to be higher in men than in women: A lifetime of gender socialization could contribute to "sex differences" in testosterone. Our experiment opens up new questions of gender→testosterone pathways, highlighting the potential of examining nature/nurture interactions and effects of socialization on human biology.T estosterone is a major influence on bodily and behavioral features seen as male and/or masculine. Not surprisingly, then, research on testosterone in humans mainly focuses on men, with some notable exceptions (e.g., refs. 1-3). Women, however, also have naturally occurring testosterone, and testosterone sometimes functions via conversion to estradiol (4). Although testosterone exists and functions similarly in women and men, men have markedly higher average testosterone than women. This difference in testosterone is widely presumed to be a sex difference, that is, one that reflects maleness and femaleness caused by innate and evolved influences (3). Together, this leads to characterizations of testosterone as the essence of maleness, fixed and unchanging, and determined by only innate factors (3,5). This occurs despite growing understandings of biology that emphasize plasticity and social modulation (for example in the brain, immune system, and genetics).The view of testosterone as fixed and innate is empirically dubious, given a surprisingly large and underexplored nongenetic influence (6). This nongenetic influence includes meaningful and predictable variation from factors such as seasonal or diurnal rhythms (6). In addition, there are profound social influences on...

Cross-cultural evidence links pair bonding and testosterone (T). We investigated what factors account for this link, how casual relationships are implicated, and whether gender/sex moderates these patterns in a North American sample. We gathered saliva samples for radioimmunoassay of T and self-report data on background, health, and social/relational variables from 115 women and 120 men to test our predictions, most of which were supported. Our results show that singles have higher T than long-term (LT) partnered individuals, and that casual relationships without serious romantic commitment are more like singlehood for men and LT relationships for women-in terms of T. We were also able to demonstrate what factors mediate the association between partnering and T: in women, frequency of partnered sexual activity mediated the effect in men, interest in more/new partners mediated the effect. This supported our prediction of relationship status interpretations in women, but relationship orientation in men. Results replicated past findings that neither sexual desire nor extrapair sexuality underlie the T-partnering link. We were able to rule out a large number of viable alternative explanations ranging from the lifestyle (e.g., sleep) to the social (e.g., social support). Our data thus demonstrate pattern and mediators for the development of T-pair bonding associations, and emphasize the importance of neither under- nor overstating the importance of gender/sex in research about the evolution of intimacy.