Perinatal Depression, Adverse Life Events, and Hypothalamic-Adrenal-Pituitary Axis Response to Cold Pressor Stress in Latinas: An Exploratory Study.

BACKGROUND

Latinas are disproportionately affected by perinatal depression (PND) as well as by adverse life events (ALEs), an independent predictor of PND. Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis has been seen both in women with PND and with a history of ALEs in non-Latinas. Although some evidence suggests that HPA axis dysregulation may mediate the link between ALEs and PND, this hypothesis has received little attention and there are no studies that have examined these pathways in Latinas. The primary aim of the present study was to explore, in a Latina sample, associations between ALEs, PND, and HPA axis stress reactivity to a physical stressor, the cold pressor test (CPT). The secondary aim was to explore whether HPA axis reactivity and PND were associated with pain sensitivity to the CPT.

METHODS

Thirty-four Latinas were enrolled in their third trimester of pregnancy and interviewed at 4 and 8 weeks postpartum. Depression status was determined using the Edinburgh Postnatal Depression Scale (≥10). At 8 weeks postpartum, 27 women underwent laboratory-induced pain testing using the CPT. Plasma adrenocorticotropic hormone and cortisol were sampled before and after the CPT to generate a stress reactivity score (post-pre). Pain sensitivity and ALEs were also assessed.

RESULTS

At enrollment, 26% of women were depressed, and 18% were depressed at 8 weeks postpartum. Fifty-two percent reported at least one childhood ALE. There was a significant and positive association between any childhood ALE and prenatal depression scores (p = .025). Infant-related ALEs were significantly associated with greater adrenocorticotropic hormone reactivity to the CPT (p = .030). Women with a history of any childhood ALE exhibited a blunted cortisol response to the CPT (p = .045). Women with a history of PND at 4 weeks had greater adrenocorticotropic hormone stress reactivity to the CPT (p = .027). No effects of PND were seen for pain sensitivity measures in response to the CPT, although there was a positive and significant correlation between pain tolerance and cortisol response to the CPT in the whole sample.

CONCLUSIONS

Given the associations between ALEs and PND and their individual effect on HPA axis stress reactivity, future studies on PND should include a larger sample of Latinas to test the mediating effects of HPA axis reactivity on associations between ALEs and PND.