Association of Alcohol Drinking With Incident Type 2 Diabetes and Pre-diabetes: the Guangzhou Biobank Cohort Study

Abstract Background To examine associations of baseline alcohol drinking with incident type 2 diabetes or impaired fasting glucose, and explore whether the associations were modified by genetic polymorphisms of aldehyde dehydrogenase-2 ( ALDH2 ) and alcohol dehydrogenase-1B ( ADH1B ). Methods Information of alcohol consumption was collected at baseline from 2003 to 2008. Incident type 2 diabetes 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 type 2 diabetes and/or initiation of hypoglycemia medication or insulin during follow-up. Impaired fasting glucose was defined as fasting glucose ≥5.6 mmol/l and <7 mmol/l. Results Of 15,716 participants without diabetes and 11,232 participants without diabetes and impaired fasting glucose at baseline, 1,624 (10.33%) developed incident type 2 diabetes, and 1,004 (8.94%) developed incident impaired fasting glucose during average 4 years of follow-up. After adjusting for sex, age, education, occupation, personal annual income, smoking, physical activity, body mass index, waist/hip ratio, health status, family history of diabetes, compared with never drinking, occasional or moderate alcohol drinking was not associated with risk of incident type 2 diabetes+impaired fasting glucose (odds ratio (OR) 1.08, 95% confidence interval (CI) 0.94-1.25, and 0.89 (0.68-1.16), respectively), but heavy alcohol drinking was associated with a higher risk of incident type 2 diabetes+impaired fasting glucose (1.83, 1.25-2.69). No interactions of sex, overweight/obesity and genetic polymorphisms of ADH1B or ALDH2 genes with alcohol drinking on incident type 2 diabetes and/or impaired fasting glucose were found ( p for interaction from 0.12 to 0.81). Conclusions Our results support a detrimental effect of heavy alcohol use on impaired fasting glucose and type 2 diabetes. No protective effect was found for those carrying lower risk alleles for ADH1B and ALDH2 genes.