Husemoen Lise Lotte Nystrup, Fenger Mogens, Friedrich Nele, Tolstrup Janne Schurmann, Beenfeldt Fredriksen Stine, Linneberg Allan
Research Centre for Prevention and Health, Glostrup Hospital, Glostrup, Denmark.
Alcohol Clin Exp Res. 2008 Nov;32(11):1984-91. doi: 10.1111/j.1530-0277.2008.00780.x. Epub 2008 Sep 6.
Genetic variation in ethanol metabolism may have an influence on both alcohol drinking habits and the susceptibility to health effects of alcohol drinking. Such influences are likely to bias exposure-disease associations in epidemiologic studies of health effects of alcohol drinking. In a Caucasian population, we examined the association of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) genetic variants with alcohol drinking habits, biomarkers of alcohol exposure, and risk factors for cardiovascular disease.
The study population consisted of 1,216 Danish men and women aged 15-77 years participating in a health examination in 1998. The health examination included a self-administered questionnaire (alcohol drinking habits), a physical examination (blood pressure), and various blood tests [alanine aminotransferase (ALAT), erythrocyte mean corpuscular volume (E-MCV), and lipids]. ADH and ALDH gene variants were determined by standard techniques. Data were analyzed by regression analyses adjusted for relevant confounders.
Self-reported alcohol drinking was significantly associated with increasing levels of ALAT, E-MCV, high-density lipoprotein cholesterol, and blood pressure. The ALDH1b ala69val variant was associated with nondrinking and total alcohol intake. The ALDH2 promoter variant was associated with binge-drinking, and the ALDH1b1 ala69val polymorphism was associated with diastolic blood pressure. We did not find any statistically significant interactions between any of the gene variants and alcohol consumption in relation to the various outcomes.
In this Caucasian population sample, we found evidence to support that genetic variation in ethanol metabolism may influence drinking habits, but no statistically significant gene-environment interactions. More large-scale epidemiologic studies are needed to confirm theses results and to further investigate genetic susceptibility to the effects of alcohol drinking.
乙醇代谢中的基因变异可能会对饮酒习惯以及饮酒对健康影响的易感性产生影响。这种影响可能会使饮酒对健康影响的流行病学研究中的暴露-疾病关联产生偏差。在一个白种人群体中,我们研究了乙醇脱氢酶(ADH)和乙醛脱氢酶(ALDH)基因变异与饮酒习惯、酒精暴露生物标志物以及心血管疾病风险因素之间的关联。
研究人群包括1998年参加健康检查的1216名年龄在15 - 77岁之间的丹麦男性和女性。健康检查包括一份自我填写的问卷(饮酒习惯)、一次体格检查(血压)以及各种血液检测[丙氨酸转氨酶(ALAT)、红细胞平均体积(E - MCV)和血脂]。ADH和ALDH基因变异通过标准技术进行测定。数据通过针对相关混杂因素进行调整的回归分析进行分析。
自我报告的饮酒情况与ALAT、E - MCV、高密度脂蛋白胆固醇水平升高以及血压显著相关。ALDH1b ala69val变异与不饮酒和总酒精摄入量有关。ALDH2启动子变异与暴饮有关,而ALDH1b1 ala69val多态性与舒张压有关。我们未发现任何基因变异与酒精消费之间在各种结局方面存在统计学上显著的相互作用。
在这个白种人群体样本中,我们发现有证据支持乙醇代谢中的基因变异可能会影响饮酒习惯,但未发现统计学上显著的基因-环境相互作用。需要更多大规模的流行病学研究来证实这些结果,并进一步研究饮酒影响的遗传易感性。