Adrenocortical sensitivity, moderated by ongoing stress, predicts drinking intensity in alcohol-dependent men.
Adrenocortical sensitivity, moderated by ongoing stress, predicts drinking intensity in alcohol-dependent men.
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由持续的压力调节的肾上腺皮质敏感性预测了酒精依赖性男性的饮酒强度。
DOI：
10.1016/j.psyneuen.2016.10.011
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发表时间：
2017-02
影响因子：
3.7
通讯作者：
Rao U
中科院分区：
文献类型：
--
作者：
Adinoff B;Leonard D;Price J;Javors MA;Walker R;Brown ES;Xiao H;Rao U
来自环境应激源和持续糖皮质激素分泌的非稳态负荷与酒精依赖的疾病严重程度相关。复发风险和/或饮酒严重程度升高，特别是，可能是对酒精和戒断引起的生理应激反应系统变化的反应，加上持续的生活压力，尽管尚未评估其对饮酒严重程度的共同贡献。研究下丘脑-垂体-肾上腺（HPA）反应性和环境应激源（例如，持续的生活压力）与治疗后酒精依赖男性的复发严重程度之间的关系，在4-6周的戒酒酒精依赖男性（n=41）中，在心理社会压力[特里尔社会压力测试（TSST）]和两种药理学刺激[绵羊促肾上腺皮质激素释放因子（oCRH）和促促皮质激素]后获得血浆促肾上腺皮质激素（ACTH）和皮质醇。治疗出院后，每周评估一次饮酒结果（主要结果：每日饮酒量（DDD）;次要结果：总饮酒量和饮酒天数），治疗出院后每两周评估一次持续生活压力，持续24周。饮酒严重程度的广义估计方程模型与基础和刺激ACTH和皮质醇浓度作为预测和持续的生活压力作为调节。更高水平的生活压力与更高的饮酒强度（DDD和总饮酒量）独立相关，但与频率（饮酒天数）无关。较高的基础皮质醇：促肾上腺皮质激素或激发皮质醇：促肾上腺皮质激素的比例与更大的治疗后DDD的个人经历了更高水平的持续压力。总之，持续的生活压力与酒精依赖男性治疗后饮酒强度相关;压力也加强了肾上腺皮质敏感性和治疗后饮酒之间的关系。非稳态负荷和环境应激的生理措施联合增加复发强度。
Allostatic load from both environmental stressors and persistent glucocorticoid secretion has been associated with disease severity in alcohol dependence. Heightened relapse risk and/or drinking severity, in particular, may be a reaction to alcohol- and withdrawal-induced changes in physiological stress response systems coupled with ongoing life stress, although their shared contributions upon drinking severity have not been assessed. To investigate the combined contribution of hypothalamic-pituitary-adrenal (HPA) reactivity and environmental stressors (e.g., ongoing life stress) to relapse severity in alcohol-dependent men following treatment, plasma adrenocorticotropin (ACTH) and cortisol were obtained in 4-6 weeks abstinent alcohol-dependent men (n=41) following a psychosocial stressor [the Trier Social Stress Test (TSST)] and two pharmacological provocations [ovine corticotropin releasing factor (oCRH) and cosyntropin]. Following treatment discharge, drinking outcomes (primary outcome: drinks per drinking day (DDD); secondary outcomes: total drinks and drinking days) were assessed weekly and ongoing life stress was assessed biweekly for 24 weeks following treatment discharge. Generalized estimating equation models of drinking severity were fit with basal and stimulated ACTH and cortisol concentrations as predictors and ongoing life stress as the moderator. Greater levels of life stress were independently associated with greater drinking intensity (DDD and total drinks) but not frequency (days drinking). Higher basal cortisol:ACTH or provoked cortisol:ACTH ratios were strongly associated with greater post-treatment DDD in individuals who experienced higher levels of ongoing stress. In conclusion, ongoing life stress is associated with post-treatment drinking intensity in alcohol dependent men; stress also strengthens the relationship between adrenocortical sensitivity and post-treatment drinking. Physiological measures of allostatic load and environmental stressors conjointly increase relapse intensity.