Grant: Master's Award: Canada Graduate Scholarships

The proposed study aims to examine the influences of genetic and social factors on the development of the stress response system. Maternal insensitivity has been linked to atypical cortisol (“stress hormone”) release, which in turn influences emotion regulation and immunosuppression, and places infants at risk for later physical and psychiatric disorders. Recent findings indicate that a healthy stress response is not simply about the amount of cortisol that is secreted under conditions of challenge, but rather the flexibility of the cortisol response under conditions of differentially stressful challenges. More specifically, infants reared by sensitive mothers exhibit flexible stress reactivity characterized by robust increases in cortisol in response to potent stressors and lower increases, or more dramatic decreases (which would occur following “arrival effects” or anticipatory anxiety), in response to mild challenge. In contrast, infants reared by insensitive mothers exhibit attenuated cortisol increases and decreases in response to potent and mild challenges, respectively. This lack of flexibility in the cortisol response can prevent adaptation to threat and lead to overexposure to cortisol. Despite the significant associations between maternal sensitivity and infant cortisol flexibility, significant variance remains unaccounted for, which suggests that this relation may be moderated by other factors, such as characteristics of the child. Given the heritable components in the cortisol response, one such moderator may be genetics. Specifically, DRD4, a gene involved in dopamine reception, has been linked to the cortisol response. Differential Susceptibility Theory (DST) suggests that infants with the 7 repeat variant of DRD4 are most susceptible to the negative effects of insensitive parenting as well as to the positive effects of sensitive parenting. Using a DST framework to advance previous work, this study will assess whether the DRD4-7 repeat allele moderates the relationship between maternal sensitivity and the flexibility of the infant cortisol response. This study will examine the hypothesis that infants with the DRD4-7 repeat allele will demonstrate the least flexible cortisol profile if reared by an insensitive mother, but also the most adaptive, flexible cortisol profile if reared by a sensitive mother. This hypothesis will be examined in conjunction with Dr. Leslie Atkinson’s CIHR funded study at Ryerson University, which contains a database including maternal sensitivity, genetic, and cortisol assessments of 297 mother-infant dyads. When infants were 16 months old, maternal sensitivity to the infant was assessed during a two-hour home observation of mother-infant interactions. At the same age, infants were observed in a mild challenge in which the infant was denied access to an attractive toy. At 17 months, infants were observed in a more potent challenge, which involved repeated separations and reunions with the mother. For both challenges, infant saliva was collected 5 minutes pre-challenge (baseline), and 20 and 40 minutes post-challenge. Cheek swabs were collected and will be assessed for the presence of the DRD4-7 repeat allele. The cortisol response is linked to almost all human physical and psychiatric disorders throughout the lifespan. By elucidating whether infants with the 7 repeat allele are more likely to develop both the adaptive, flexible cortisol profile in the context of sensitive parenting and the maladaptive cortisol profile in the context of insensitive parenting, this study can inform prevention programs that aim to identify and build resilience in those most susceptible to developing maladaptive stress physiology and, in turn, physical and psychiatric disorders.