Primary Hypothesis: The behavioral and morphological traits associated with social monogamy emerge during development due to the combined actions of steroids and peptides |
• A shift from a reliance on androgens to a stronger dependence on peptides may facilitate the prosocial traits of social monogamy |
Testosterone: Features of social monogamy emerge in part via a reduction in the functional effects of androgens |
• Mutations in the androgen receptor gene reduce the effects of androgens, reducing morphological and behavior sex differences and masculinization |
• Variations in the 5-α reductase gene reduce sexual dimorphism by reducing the conversion of testosterone to the more potent dihydrotestosterone |
• High levels of glucocorticoids outcompete testosterone for the androgen receptor, reducing sexual dimorphism |
Estrogens: Created as a metabolic by-product of testosterone, estrogens play a role in the regulation of the traits of social monogamy and sexual differentiation |
• Testosterone is aromatized to estradiol, which in turn facilitates actions of peptides, allowing for displays of the behavioral traits of social monogamy |
Peptides: Oxytocin has the capacity to prevent masculinization by acting as an anti-inflammatory agent that inhibits the actions of androgens |
• Variation in the oxytocin and vasopressin systems is shaped by factors such as genetics, epigenetics, and developmental experiences; differences in these systems help to explain the variation in sociality among species and between individuals within a species |