Variations in heritability of cortisol reactivity to stress as a function of early familial adversity among 19-month-old twins

Abstract

CONTEXT: Cortisol reactivity is a marker of vulnerability for a variety of stress-related diseases that likely arise from the contributions of both genetic and environmental sources of influence. However, little is known about gene-environment interplay in early cortisol reactivity. OBJECTIVES: To examine the genetic and environmental contributions to early cortisol reactivity in a population-based sample of 19-month-old twins and to determine whether these contributions vary as a function of early familial adversity. DESIGN: A variant of the twin method, with genetic and environment contributions to cortisol reactivity estimated as a function of familial adversity. Familial adversity was defined as the presence of 7 risk factors during perinatal and postnatal development (eg, at 6 and 19 months of age): maternal smoking during pregnancy, low birth weight, low family income, low maternal educational level, single parenthood, young motherhood, and maternal hostile or reactive behaviors. Twins exposed to 4 or more risk factors at either time were considered as having been exposed to high (vs low) familial adversity (23.4% of the sample). SETTING: Centre de Recherche Fernand-Seguin at the Hôpital Louis-Hyppolite Lafontaine, Montréal, Quebec. Patients Participants were families of twins from the Québec Newborn Twin Study recruited between April 1, 1995, and December 31, 1998, in the greater Montréal area. A total of 346 twins, 130 monozygotic and 216 dizygotic, were included in the study. MAIN OUTCOME MEASURES: Salivary cortisol samples were collected before and after the participating twins had been exposed to unfamiliar situations; change in cortisol over time was used as a measure of cortisol reactivity. RESULTS: Distinct patterns of genetic and environmental contributions to cortisol reactivity were evidenced as a function of familial adversity, suggesting a possible gene-environment interplay. In low-familial adversity settings that characterized most families, both genetic and unique but not shared environmental factors accounted for individual differences in cortisol reactivity, with shared genes explaining the similarity observed within twin pairs. By contrast, in conditions of high familial adversity, both shared and unique environmental factors, but not genetic factors, accounted for the variance in cortisol reactivity. CONCLUSION: This pattern of differing genetic and environmental contributions according to familial adversity suggests that, early in life, high familial adversity may have a programming developmental effect on cortisol reactivity.