Li Mei Jiao, Ren Jing, Zhang Wei Sen, Jiang Chao Qiang, Jin Ya Li, Lam Tai Hing, Cheng Kar Keung, Thomas G Neil, Xu Lin
School of Public Health, Sun Yat-sen University, Guangzhou, China.
Guangzhou Twelfth People's Hospital, Guangzhou, China.
Diabetes Metab Res Rev. 2022 Sep;38(6):e3548. doi: 10.1002/dmrr.3548. Epub 2022 May 28.
We examined associations of baseline alcohol drinking with incident type 2 diabetes (T2D) or impaired fasting glucose (IFG), and explore whether the associations were modified by genetic polymorphisms of aldehyde dehydrogenase-2 (ALDH2) and alcohol dehydrogenase-1B (ADH1B).
All participants were aged 50+ (mean = 60.45; standard deviation = 6.88) years. Information of alcohol consumption was collected at baseline from 2003 to 2008. Incident T2D was defined as fasting glucose ≥7.0 mmol/L or post-load glucose ≥11.1 mmol/L at follow-up examination (2008-2012), self-reported T2D and/or initiation of hypoglycaemia medication or insulin during follow-up. Impaired fasting glucose was defined as fasting glucose ≥5.6 mmol/L and <7 mmol/L.
Of 15,716 participants without diabetes and 11,232 participants without diabetes and IFG at baseline, 1624 (10.33%) developed incident T2D and 1004 (8.94%) developed incident IFG during an average 4 years of follow-up. After multivariable adjustments, compared with never drinking, occasional or moderate alcohol drinking was not associated with risk of incident hyperglycaemia (T2D + IFG) (odds ratio (OR) = 1.10, 95% confidence interval (CI) 0.95-1.27, and 0.90 (0.69-1.18), respectively), whereas heavy alcohol drinking was associated with a higher risk of incident hyperglycaemia (T2D + IFG) (OR = 1.82, 95% CI 1.24-2.68). No interactions of sex, overweight/obesity and genetic polymorphisms of ADH1B/ALDH2 genes with alcohol drinking on incident T2D and/or IFG were found (P for interaction from 0.12 to 0.85).
Our results support a detrimental effect of heavy alcohol use on IFG and T2D. No protective effect was found for those carrying lower risk alleles for ADH1B/ALDH2 genes.
我们研究了基线饮酒与2型糖尿病（T2D）或空腹血糖受损（IFG）发病之间的关联，并探讨这些关联是否会因乙醛脱氢酶2（ALDH2）和乙醇脱氢酶1B（ADH1B）的基因多态性而改变。
所有参与者年龄均在50岁及以上（平均年龄=60.45岁；标准差=6.88岁）。2003年至2008年在基线时收集饮酒信息。随访检查（2008 - 2012年）时，将新发T2D定义为空腹血糖≥7.0 mmol/L或负荷后血糖≥11.1 mmol/L，随访期间自我报告的T2D和/或开始使用低血糖药物或胰岛素。空腹血糖受损定义为空腹血糖≥5.6 mmol/L且<7 mmol/L。
在15716名基线时无糖尿病的参与者和11232名基线时无糖尿病且无IFG的参与者中，在平均4年的随访期间，1624人（10.33%）发生了新发T2D，1004人（8.94%）发生了新发IFG。多变量调整后，与从不饮酒相比，偶尔或适度饮酒与新发高血糖（T2D + IFG）风险无关（比值比（OR）分别为1.10，95%置信区间（CI）0.95 - 1.27和0.90（0.69 - 1.18）），而大量饮酒与新发高血糖（T2D + IFG）风险较高相关（OR = 1.82，95% CI 1.24 - 2.68）。未发现性别、超重/肥胖以及ADH1B/ALDH2基因的基因多态性与饮酒在新发T2D和/或IFG方面存在相互作用（交互作用P值为0.12至0.85）。
我们的结果支持大量饮酒对IFG和T2D有有害影响。未发现携带ADH1B/ALDH2基因低风险等位基因的人有保护作用。
