Abstract
The offspring of depressed parents have been found to show elevated basal levels of the stress hormone cortisol. Whether heightened cortisol stress reactivity is also present in this group has yet to be clearly demonstrated. We tested whether postnatal maternal depression predicts subsequent increases in offspring biological sensitivity to social stress, as indexed by elevated cortisol reactivity. Participants (mean age 22.4-years) derived from a 22-year prospective longitudinal study of the offspring of mothers who had postnatal depression (PND group; n=38) and a control group (n=38). Salivary cortisol response to a social-evaluative threat (Trier Social Stress Test) was measured. Hierarchical linear modelling indicated that PND group offspring showed greater cortisol reactivity to the stress test than control group participants. Group differences were not explained by offspring depressive or anxiety symptoms, experiences of negative life events, elevated basal cortisol at age 13-years, subsequent exposure to maternal depression, or other key covariates. The findings indicate that the presence of early maternal depression can predict offspring biological sensitivity to social stress in adulthood, with potential implications for broader functioning.
Highlights
Research has established that the offspring of depressed parents are themselves at elevated risk of depressive disorder by early adolescence (Halligan et al, 2007b; Murray et al, 2011; Hammen et al, 2012)
Elevated basal cortisol levels have been demonstrated in association with the presence of parental depression across a number of studies (Essex et al, 2002; Halligan et al, 2004; Ellenbogen et al, 2006; Mannie et al, 2007)
These studies have each found relatively higher cortisol levels following a mild stressor in at-risk versus control group infants, but interpretation is complicated by the fact that the provocations used typically did not result in a clear cortisol stress response
Summary
Research has established that the offspring of depressed parents are themselves at elevated risk of depressive disorder by early adolescence (Halligan et al, 2007b; Murray et al, 2011; Hammen et al, 2012). Elevated cortisol reactivity is suggested by cross-sectional studies of young infants (Azar et al, 2007; Brennan et al, 2008; Waters et al, 2013) and preschool-aged children (Dougherty et al, 2011, 2013) whose parents reported having previous or current depression These studies have each found relatively higher cortisol levels following a mild stressor in at-risk versus control group infants, but interpretation is complicated by the fact that the provocations used typically did not result in a clear cortisol stress response. The limited availability of robust evidence for enhanced cortisol reactivity to stress in the offspring of depressed parents is significant, as elevations in basal cortisol levels that have been observed in this group have been proposed to reflect HPA axis dysregulation linked to increased vulnerability to stressors (Ostiguy et al, 2011). The assessment of both postnatal and subsequent maternal depression afforded a preliminary investigation of whether there is any evidence for a particular, persistent impact of the presence of maternal depression during early life, as would be predicted by animal models of HPA axis development
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