Objective

Early life interindividual variation in hypothalamic-pituitary-adrenal (HPA) reactivity to stress is predictive of later life psychological and physical well-being, including the development of many pathological syndromes that are often sex-biased. A complex and interactive set of environmental and genetic causes for such variation has been implicated by previous studies, though little attention has been paid to nonadditive effects (e.g. dominance, X-linked) or sex-specific genetic effects.

Method

We used a large pedigreed sample of captive 3-4 months old infant rhesus macaques (N = 2,661, 54% female) to fit univariate and multivariate linear mixed quantitative genetic models for four longitudinal blood cortisol samples and three reliable ratings of infant temperament (nervousness, gentleness, confidence) during a mother-infant separation protocol.

Results

Each trait had a moderate narrow-sense heritability (h², 0.26-0.46), but dominance effects caused the first two cortisol samples to have much larger broad-sense heritabilities (H², 0.57 and 0.77). We found no evidence for X-linked variance or common maternal environment variance. There was a sex difference in heritability of the first cortisol sample (h_f² < h_m²), suggesting differing genetic architecture of perception of maternal separation and relocation during infancy. Otherwise, genetic covariance matrices for the sexes were very similar. Genetic correlations between cortisol levels and temperament were weak (< |0.4|) but stronger than residual or phenotypic correlations.

Conclusions

HPA reactivity and temperament had a primarily additive genetic basis in infant macaques, but there were important complexities to the genetic architecture of including genetic dominance and sex differences in heritability at this early life stage. (PsycInfo Database Record (c) 2022 APA, all rights reserved).