Literature DB >> 25745954

HPA-axis reactivity interacts with stage of pubertal development to predict the onset of depression.

Natalie L Colich1, Katharina Kircanski2, Lara C Foland-Ross2, Ian H Gotlib2.   

Abstract

UNLABELLED: Both elevated and blunted levels of cortisol secretion during childhood and adolescence have been linked to the subsequent onset of major depressive disorder (MDD). These mixed findings may be due to developmental changes in HPA-axis functioning, which have not been previously assessed in the context of risk. In the present study, therefore, we examined whether pubertal development moderated the influence of cortisol secretion on the subsequent development of MDD. Eighty-nine never-disordered girls ages 9-15 years, many of whom were at high risk for depression by virtue of having a maternal history of the disorder, completed a laboratory stress task. To index cortisol reactivity, salivary cortisol samples were collected at baseline and 15 min following the onset of the stressor. Girls' levels of pubertal development were measured using Tanner staging. All participants were followed through age 18 in order to assess the subsequent development of MDD. Pubertal stage moderated the effects of cortisol stress reactivity on the development of MDD. Specifically, the onset of MDD was predicted by cortisol hyporeactivity in girls who were earlier in pubertal development (Tanner stage ≤ 2), but by cortisol hyperreactivity in girls who were later in pubertal development (Tanner stage ≥ 3.5).
CONCLUSIONS: These findings demonstrate that girls' cortisol stress reactivity predicts the subsequent onset of MDD, and further, that the nature of this effect depends on the girls' level of pubertal development. Results are discussed in the context of clarifying previous findings, and directions for future research are offered.
Copyright © 2015 Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Adolescence; Cortisol; Depression; HPA-axis; Puberty

Mesh:

Substances:

Year:  2015        PMID: 25745954      PMCID: PMC4380614          DOI: 10.1016/j.psyneuen.2015.02.004

Source DB:  PubMed          Journal:  Psychoneuroendocrinology        ISSN: 0306-4530            Impact factor:   4.905


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