Adinoff Bryon, Ruether Keith, Krebaum Steven, Iranmanesh Ali, Williams Mark J
Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, USA.
Alcohol Clin Exp Res. 2003 Sep;27(9):1420-7. doi: 10.1097/01.ALC.0000087581.13912.64.
Cortisol, the primary glucocorticoid in humans, is intimately involved in the regulation of such varied and critical biological processes as emotion, cognition, reward, immune functioning, and energy utilization. A persistent increase in cortisol concentration as a result of chronic intoxication could therefore result in alcohol-related disorders such as sleep disruption, cognitive deficits, diabetes, and mood disturbances. Although moderate levels of acute alcohol ingestion are reported to produce an increase in cortisol levels, it is uncertain whether cortisol remains persistently increased during long-term chronic intoxication.
Salivary cortisol and breath alcohol concentrations (BAC) were obtained on 73 subjects with primary alcohol dependence on initial presentation for treatment and 22 alcohol-dependent subjects participating in a residential treatment program.
Both intoxicated alcohol-dependent subjects (n = 38) and nonintoxicated subjects in acute alcohol withdrawal (n = 30) demonstrated significantly increased salivary cortisol concentrations compared with abstinent subjects (n = 27; p < 0.001). Nonintoxicated subjects in acute withdrawal demonstrated significantly increased salivary cortisol concentrations compared with highly intoxicated subjects (BAC >100 mg/dl) but were similar to subjects with lower levels of intoxication (BAC, 10-100 mg/dl).
Chronic alcohol-dependent subjects experience continuously increased concentrations of cortisol during both intoxication and withdrawal. Increased levels of cortisol during chronic intoxication seem to progressively increase with the onset of withdrawal. This suggests a daily cycle of hypercortisolemia during the active drinking phase, with further increases on the cessation of drinking and the emergence of withdrawal symptoms. Persistently increased levels of cortisol may extract a costly allostatic load, resulting in significant central nervous system and peripheral organ morbidity.
皮质醇是人类主要的糖皮质激素,密切参与多种关键生物过程的调节,如情绪、认知、奖赏、免疫功能和能量利用。因此,慢性中毒导致的皮质醇浓度持续升高可能会引发与酒精相关的疾病,如睡眠障碍、认知缺陷、糖尿病和情绪紊乱。尽管据报道适度的急性酒精摄入会使皮质醇水平升高,但长期慢性中毒期间皮质醇是否持续升高尚不确定。
对73名初次就诊接受治疗的原发性酒精依赖患者和22名参加住院治疗项目的酒精依赖患者采集唾液皮质醇和呼气酒精浓度(BAC)。
与戒酒者(n = 27;p < 0.001)相比,醉酒的酒精依赖患者(n = 38)和急性酒精戒断期未醉酒的患者(n = 30)唾液皮质醇浓度均显著升高。与高醉酒程度患者(BAC >100 mg/dl)相比,急性戒断期未醉酒的患者唾液皮质醇浓度显著升高,但与低醉酒程度患者(BAC,10 - 100 mg/dl)相似。
慢性酒精依赖患者在中毒和戒断期间皮质醇浓度持续升高。慢性中毒期间皮质醇水平的升高似乎随着戒断的开始而逐渐增加。这表明在饮酒活跃期存在每日高皮质醇血症循环,在停止饮酒和出现戒断症状时进一步升高。持续升高的皮质醇水平可能会带来高昂的代偿性负荷,导致显著的中枢神经系统和外周器官病变。