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Cortisol reactivity and weight gain among adolescents who vary in prenatal drug exposure
Author(s) -
Armstrong B.,
BuckinghamHowes S.,
Black M. M.
Publication year - 2018
Publication title -
pediatric obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.226
H-Index - 69
eISSN - 2047-6310
pISSN - 2047-6302
DOI - 10.1111/ijpo.12430
Subject(s) - weight gain , medicine , reactivity (psychology) , endocrinology , stressor , mediation , hydrocortisone , obesity , physiology , body weight , clinical psychology , alternative medicine , pathology , political science , law
Summary Objective Low inhibitory control is linked with weight gain among youth. Inhibitory problems are associated with disruption to the hypothalamic–pituitary–adrenal axis cortisol response. Increased cortisol predicts appetite and weight gain (though may be gender specific). This study hypothesized that cortisol reactivity explains the association between inhibition and weight gain while considering the moderating factors of early stressors to the hypothalamic–pituitary–adrenal axis (e.g. prenatal‐drug exposure) and gender. Methods Adolescents with prenatal‐drug exposure ( n  = 76) and non‐exposed comparison adolescents (NE; n  = 61) completed the Conner's Continuous Performance Test and provided salivary cortisol samples. BMI z ‐score were measured at the initial and 12‐month follow‐up evaluations. A bootstrapped moderated mediation analysis was conducted to test for conditional indirect effects of cortisol reactivity. Results Lower inhibition was associated with increased cortisol reactivity among youth who were NE, and increased cortisol reactivity was associated with weight gain among girls. Cortisol reactivity mediated the relation between inhibition and BMI z ‐score change for the girls in the group who was NE. Conclusion Increased cortisol reactivity may play a mechanistic role in predicting weight gain among non‐prenatally drug‐exposed girls. Cortisol reactivity may be a biomarker for targeted interventions to improve biological regulation and ultimately health risk among girls.

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