Department of Public Health Solutions, Finnish Institute for Health and Welfare, 00271 Helsinki, Finland.
Doctoral Programme in Population Health, University of Helsinki, Helsinki, Finland.
Int J Epidemiol. 2021 Jan 23;49(6):1836-1846. doi: 10.1093/ije/dyaa113.
Despite reporting lower levels of alcohol consumption, people with lower socio-economic status (SES) experience greater alcohol-related harm. Whether differential biases in the measurement of alcohol use could explain this apparent paradox is unknown. Using alcohol biomarkers to account for measurement error, we examined whether differential exposure to alcohol could explain the socio-economic differences in alcohol mortality.
Participants from eight representative health surveys (n = 52 164, mean age 47.7 years) were linked to mortality data and followed up until December 2016. The primary outcome was alcohol-attributable mortality. We used income and education as proxies for SES. Exposures include self-reported alcohol use and four alcohol biomarkers [serum gamma-glutamyl transferase (available in all surveys), carbohydrate-deficient transferrin, alanine aminotransferase and aspartate aminotransferase (available in subsamples)]. We used shared frailty Cox proportional hazards to account for survey heterogeneity.
During a mean follow-up of 20.3 years, totalling 1 056 844 person-years, there were 828 alcohol-attributable deaths. Lower SES was associated with higher alcohol mortality despite reporting lower alcohol use. Alcohol biomarkers were associated with alcohol mortality and improved the predictive ability when used in conjunction with self-reported alcohol use. Alcohol biomarkers explained a very small fraction of the socio-economic differences in alcohol mortality, since hazard ratios either slightly attenuated (percent attenuation range 1.0-12.1%) or increased.
Using alcohol biomarkers in addition to self-reported alcohol use did not explain the socio-economic differences in alcohol mortality. Differential bias in the measurement of alcohol use is not a likely explanation for the alcohol-harm paradox.
尽管报告的饮酒量较低,但社会经济地位较低的人(SES)所经历的与酒精相关的伤害更大。目前尚不清楚测量饮酒时的差异偏差是否可以解释这种明显的悖论。本研究使用酒精生物标志物来解释测量误差,我们检验了酒精暴露的差异是否可以解释酒精死亡率的社会经济差异。
我们将来自八个代表性健康调查(n=52164,平均年龄 47.7 岁)的参与者与死亡率数据相关联,并随访至 2016 年 12 月。主要结局是酒精相关性死亡率。我们使用收入和教育作为 SES 的代表。暴露因素包括自我报告的饮酒量和四种酒精生物标志物[血清γ-谷氨酰转移酶(所有调查均可用)、糖缺乏转铁蛋白、丙氨酸氨基转移酶和天冬氨酸氨基转移酶(在亚样本中可用)]。我们使用共享脆弱性 Cox 比例风险来解释调查异质性。
在平均 20.3 年的随访期间,总计有 1056844 人年发生了 828 例与酒精相关的死亡。尽管报告的饮酒量较低,但 SES 较低与更高的酒精死亡率相关。酒精生物标志物与酒精死亡率相关,并且当与自我报告的饮酒量一起使用时,提高了预测能力。酒精生物标志物仅解释了酒精死亡率的社会经济差异的一小部分,因为危险比要么略有减弱(减弱幅度为 1.0-12.1%),要么增加。
除了自我报告的饮酒量外,使用酒精生物标志物并不能解释酒精死亡率的社会经济差异。酒精使用测量的差异偏差不太可能是酒精危害悖论的解释。