Salivary cortisol and affective responses to acute psychosocial stress among adolescents.

BACKGROUND

Acute psychosocial stress activates the hypothalamic-pituitary-adrenal (HPA) axis and triggers the release of cortisol, a commonly used biomarker of stress reactivity. Yet only 25 % of studies have reported a correlation between cortisol and affective responses to stress. This study aimed to examine whether cortisol reactivity following an acute psychosocial stressor in the laboratory correlated with concurrent positive and negative affect in adolescents, and whether early life adversity (ELA) moderated this relationship.

METHODS

The current study examined the salivary cortisol response of 89 adolescents (46.1 % female) following administration of the Trier Social Stress Test for Children (TSST-C). Using 7 simultaneous measurements, changes in cortisol were compared to changes in concurrent affect using the Positive and Negative Affect Schedule (PANAS). Parents reported their child's exposure to ELA.

RESULTS

Within-person variability in cortisol was associated with higher negative affect at baseline, b = 1.43 (SE =.41), p < .001, as well as more rapid negative affective recovery following stress, b = -0.003 (SE =.002), p = .04. ELA-exposed participants were not more sensitive to this effect. Within-person variability in cortisol was not associated with positive affect at baseline or following the TSST-C on average, all ps > .27. However, within-person increases in cortisol were associated with decrements in positive affect among ELA-exposed individuals, all ps < .01, suggesting differential sensitivity to anhedonic effects of glucocorticoids.

CONCLUSIONS

Stress impacts affective states, in part through acute increases in HPA axis activity. The present data show that negative affect is more vulnerable to this than positive affect among adolescents. Further, adolescents with high ELA may be more vulnerable to decrements in positive affect in the acute aftermath of HPA axis activation. Whether this is a modifiable source of vulnerability to stress-related disease in this high-risk population remains to be understood.