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Alcohol Use Disorder Masks the Effects of Childhood Adversity, Lifetime Trauma, and Chronic Stress on Hypothalamic–Pituitary–Adrenal Axis Reactivity
Author(s) -
Zhang Alice,
Price Julianne L.,
Leonard David,
North Carol S.,
Suris Alina,
Javors Martin A.,
Adinoff Bryon
Publication year - 2020
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.14334
Subject(s) - stressor , hypothalamic–pituitary–adrenal axis , reactivity (psychology) , adrenocorticotropic hormone , corticotropin releasing hormone , confounding , psychology , medicine , trier social stress test , hydrocortisone , population , psychosocial , hormone , alcohol use disorder , endocrinology , clinical psychology , psychiatry , fight or flight response , alcohol , biochemistry , chemistry , alternative medicine , environmental health , pathology , gene
Background Individuals with alcohol use disorder (AUD) and those who have experienced traumas or chronic stress exhibit dysregulated hypothalamic–pituitary–adrenal (HPA) axis reactivity. Whether and how trauma and stress histories interact with AUD to affect HPA axis reactivity has not been assessed. Methods In the present study, 26 healthy male controls and 70 abstinent men with AUD were administered a pharmacologic probe [ovine corticotropin–releasing hormone (oCRH)] and psychosocial stressor to assess HPA axis reactivity. Plasma adrenocorticotropin hormone (ACTH) and cortisol were assessed every 10–20 minutes. Hierarchical clustering of multiple measures of trauma and stress identified 3 distinct clusters: childhood adversity, lifetime trauma, and chronic stress. General linear model procedures were used to examine main effects of group (AUD/control) and interaction effects of the 3 clusters upon net‐integrated ACTH and cortisol response. Results We found that higher levels of childhood adversity, lifetime trauma, and chronic stress were each associated with blunted oCRH‐induced ACTH reactivity in controls, but not in the AUD group. Recent chronic stress within the prior 6 months had the strongest influence upon ACTH reactivity in the control group, and lifetime trauma, the least. Conclusions Childhood adversity, lifetime trauma, and chronic stress likely exert persistent, measurable effects upon HPA axis functioning in healthy controls. This association appears to be masked in individuals with AUD, potentially confounding studies examining the effects of stress, adversity, and/or trauma upon the HPA axis in this population during the protracted withdrawal phase of recovery. Future work targeting stress exposure and reactivity should consider the heightened effect of previous alcohol use relative to past adversity and trauma.