背景:由于生物应激反应系统的长期激活,合金静态负荷(AL)与疾病易感性升高有关。已知酒精使用障碍(AUD)激活这些系统。本研究的主要目的是检查AL和AUD之间的关系。
方法:参与者为男性(100%),患有DSM-IV酒精依赖(n=48),健康参与者无物质使用障碍史(n=17)。AUD参与者禁欲4-6周。AL指数使用皮质醇,interluken-6(IL-6),纤维蛋白原,肿瘤坏死因子-α(TNFa),C反应蛋白(CRP),葡萄糖,胰岛素,瘦素,脉搏,收缩压读数,舒张压读数,体重指数(BMI)。基于第25或第75百分位数内的值确定每个生物学量度的生理失调;AL被计算为生理失调生物学量度的总数。
结果:病例和对照组之间的平均AL评分没有差异(t(63)=0.48,p=0.63)。在案件中,AL与每个饮酒日的终生饮酒量无关(F(2,42)=.42,p=.66),终生总饮料(F(2,42)=0.48,p=0.62),参加研究前6个月的总饮料(F(2,43)=.58,p=.56),或在3个月随访时每天饮用饮料(F(2,35)=1.93,p=.16)。参与研究前6个月,AL与每饮酒日的饮酒量呈负相关(F(2,42)=3.71,p=0.033)。
结论:假设未得到支持。鉴于酒精可能导致生理失调,AL显示的累积应激生物标志物与饮酒状态之间明显缺乏关系,这既是意料之外的,也是显著的.根据结果,在饮酒状况或AUD男性饮酒的情况下,AL可能不适用。
BACKGROUND: Allostatic load (AL) is associated with a heightened predisposition to disease due to prolonged activation of biological stress-response systems. Alcohol use disorder (AUD) is known to activate these systems. The primary aim of the current
study was to examine the relationship between AL and AUD.
METHODS: Participants were males (100%) with DSM-IV Alcohol Dependence (n = 48) and healthy participants with no history of substance use disorder (n = 17). Participants with AUD were 4-6 weeks abstinent. The AL index used cortisol, interleukin-6 (IL-6), fibrinogen, tumor necrosis factor-alpha (TNFα), C-reactive protein (CRP), glucose, insulin, leptin, pulse, systolic blood pressure readings, diastolic blood pressure readings, and body mass index (BMI). Physiological dysregulation for each biological measure was determined based on values within the 25th or 75th percentiles; AL was calculated as the total number of physiologically dysregulated biological measures.
RESULTS: No differences in mean AL scores between the cases and controls [t(63) = .48, p = .633] were observed. Among cases, AL was not associated with lifetime drinks per drinking day (F(2,42) = .42, p = .662), lifetime total drinks (F(2,42) = 0.48, p = .620), total drinks 6 months prior to participating in the
study (F(2,43) = 0.58, p = .563), or drinks per drinking day at 3-month follow-up (F(2,35) = 1.93, p = .161). AL was negatively associated with drinks per drinking day 6 months prior to
study participation (F(2,42) = 3.71, p = .033).
CONCLUSIONS: The hypotheses were not supported. Given that alcohol is likely to lead to physiological dysregulation, the apparent absence of a relationship between biomarkers of cumulative stress as indicated by AL and drinking status was both unanticipated and remarkable. Based on the results, AL in the context of drinking status or drinking among males with AUD may not be applicable.