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Alcohol Consumption, Genetic Variants in Alcohol Deydrogenases, and Risk of Cardiovascular Diseases: A Prospective Study and Meta-Analysis

Author

Listed:
  • Dagmar Drogan
  • Abigail J Sheldrick
  • Madlen Schütze
  • Sven Knüppel
  • Frank Andersohn
  • Romina di Giuseppe
  • Bianca Herrmann
  • Stefan N Willich
  • Edeltraut Garbe
  • Manuela M Bergmann
  • Heiner Boeing
  • Cornelia Weikert

Abstract

Objective: First, to investigate and compare associations between alcohol consumption and variants in alcohol dehydrogenase (ADH) genes with incidence of cardiovascular diseases (CVD) in a large German cohort. Second, to quantitatively summarize available evidence of prospective studies on polymorphisms in ADH1B and ADH1C and CVD-risk. Methods: We conducted a case-cohort study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam cohort including a randomly drawn subcohort (n = 2175) and incident cases of myocardial infarction (MI; n = 230) or stroke (n = 208). Mean follow-up time was 8.2±2.2 years. The association between alcohol consumption, ADH1B or ADH1C genotypes, and CVD-risk was assessed using Cox proportional hazards regression. Additionally, we report results on associations of variants in ADH1B and ADH1C with ischemic heart disease and stroke in the context of a meta-analysis of previously published prospective studies published up to November 2011. Results: Compared to individuals who drank >0 to 6 g alcohol/d, we observed a reduced risk of MI among females consuming >12 g alcohol/d (HR = 0.31; 95% CI: 0.10–0.97) and among males consuming >24 to 60 g/d (HR = 0.57; 95% CI: 0.33–0.98) or >60 g alcohol/d (HR = 0.30; 95% CI: 0.12–0.78). Stroke risk was not significantly related to alcohol consumption >6 g/d, but we observed an increased risk of stroke in men reporting no alcohol consumption. Individuals with the slow-coding ADH1B*1/1 genotype reported higher median alcohol consumption. Yet, polymorphisms in ADH1B or ADH1C were not significantly associated with risk of CVD in our data and after pooling results of eligible prospective studies [ADH1B*1/1: RR = 1.35 (95% CI: 0.98–1.88; p for heterogeneity: 0.364); ADH1C*2/2: RR = 1.07 (95% CI: 0.90–1.27; p for heterogeneity: 0.098)]. Conclusion: The well described association between alcohol consumption and CVD-risk is not reflected by ADH polymorphisms, which modify the rate of ethanol oxidation.

Suggested Citation

  • Dagmar Drogan & Abigail J Sheldrick & Madlen Schütze & Sven Knüppel & Frank Andersohn & Romina di Giuseppe & Bianca Herrmann & Stefan N Willich & Edeltraut Garbe & Manuela M Bergmann & Heiner Boeing &, 2012. "Alcohol Consumption, Genetic Variants in Alcohol Deydrogenases, and Risk of Cardiovascular Diseases: A Prospective Study and Meta-Analysis," PLOS ONE, Public Library of Science, vol. 7(2), pages 1-11, February.
    • Handle: RePEc:plo:pone00:0032176
    DOI: 10.1371/journal.pone.0032176
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    References listed on IDEAS

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    1. Lina Chen & George Davey Smith & Roger M Harbord & Sarah J Lewis, 2008. "Alcohol Intake and Blood Pressure: A Systematic Review Implementing a Mendelian Randomization Approach," PLOS Medicine, Public Library of Science, vol. 5(3), pages 1-11, March.
    2. Guohong Zhang & Ruiqin Mai & Bo Huang, 2010. "ADH1B Arg47His Polymorphism Is Associated with Esophageal Cancer Risk in High-Incidence Asian Population: Evidence from a Meta-Analysis," PLOS ONE, Public Library of Science, vol. 5(10), pages 1-5, October.
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    1. Golder, Su & McCambridge, Jim, 2021. "Alcohol, cardiovascular disease and industry funding: A co-authorship network analysis of systematic reviews," Social Science & Medicine, Elsevier, vol. 289(C).

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