1Human Evolutionary Biology, Harvard University, 2California National Primate Research Center, University of California Davis, 3Psychology, University of California Davis
March 26, 2015 10:15, Grand Ballroom D
For mammals, mother’s milk is an important physiological pathway for nutrient transfer and glucocorticoid signaling. We investigated mother’s milk and infant temperament and growth in a cohort of rhesus macaque (Macaca mulatta) mother-infant dyads at the California National Primate Research Center (N=108). Glucocorticoids in mother’s milk, independent of available milk energy, predicted a more Nervous, less Confident temperament in both sons and daughters. Importantly, higher cortisol concentrations in milk were associated with lower maternal parity and greater infant weight gain across time. Taken together, these results suggest that mothers with fewer somatic resources, even in captivity, may be “programming” through milk signaling, behaviorally cautious offspring that prioritize growth above behavioral exploration. A majority of these individuals (N=84) remained in the breeding colony to assess survival, mass, and, for females (N=48/84), the age of reproductive debut. Mother’s milk and early life temperament predicted offspring outcomes. After accounting for relevant co-variates during AIC model selection, nervous temperament was associated with higher mortality in both sexes, but not growth, and delayed reproductive debut for females. Mass in juvenility was associated with milk produced by the mother years earlier, but sons were seemingly sensitive to milk glucocorticoids while daughters were seemingly sensitive to milk energy. Glucocorticoids ingested through milk may importantly contribute to the assimilation of available milk energy, development of temperament, and orchestrate, in part, the allocation of maternal milk energy among life history tradeoffs during early life biobehavioral organization with consequences persisting after the period of maternal dependence.
This research was supported by the NSF BCS-0921978; BCS-0525025 (KH); NCRR, NIH (R24RR019970 (JPC), P51RR000169 (CNPRC)); and currently Office of Research Infrastructure Programs/OD, NIH (R24OD010962 (JPC), P51OD011107 (CNPRC)).