Variations in Heritability of Cortisol Reactivity to Stress as a Function of Early Familial Adversity among 19-Month-Old Twins

Variations in Heritability of Cortisol Reactivity to Stress as a Function of Early Familial Adversity among 19-Month-Old Twins

Variations in Heritability of Cortisol Reactivity to Stress as a Function of Early Familial Adversity among 19-Month-Old Twins

Variations in Heritability of Cortisol Reactivity to Stress as a Function of Early Familial Adversity among 19-Month-Old Twinss

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Référence bibliographique [1775]

Ouellet-Morin, Isabelle, Boivin, Michel, Dionne, Ginette, Lupien, Sonia J., Arsenault, Louise, Barr, Ronald G., Pérusse, Daniel et Tremblay, Richard E. 2008. «Variations in Heritability of Cortisol Reactivity to Stress as a Function of Early Familial Adversity among 19-Month-Old Twins ». Archives of General Psychiatry, vol. 65, no 2, p. 211-218.

Fiche synthèse

1. Objectifs


Intentions :
« 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. » (p. 211)

2. Méthode


Échantillon/Matériau :
« 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. » (p.211)

Instruments :
« 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. » (p. 211)

Type de traitement des données :
Analyse statistique

3. Résumé


« 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. 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. » (p. 211)