Consumption of alcohol and cardiovascular disease mortality: a 16 year follow-up of 115,592 Norwegian men and women aged 40–44 years

  • Aage Tverdal
  • Per Magnus
  • Randi Selmer
  • Dag Thelle
MORTALITY

Abstract

We tested whether teetotalism explains the upturn in cardiovascular risk for non-drinkers and whether wine is a more favorable alcohol type. We studied 115,592 men and women aged 40–44 years who participated in the age 40 program in Norway in 1994–1999 and were followed for an average of 16 years with 550 cardiovascular deaths. Self-reported number of glasses of beer, wine and spirits during 14 days was transformed to alcohol units/day. One unit is approximately 8 grams of pure alcohol. The mean and median number of alcohol units/day were 0.70 and 0.46. Teetotallers had higher risk of dying from cardiovascular disease than alcohol consumers, multivariate adjusted hazard ratio (95% CI) 1.97 (1.52–2.56). The use of alcohol-related deaths as endpoint substantiated a selection of previous alcohol users to the teetotal group. Without teetotallers there was no association between alcohol consumption and cardiovascular disease mortality. However, the multivariate adjusted hazard ratio per one unit/day of wine was 0.76 (0.58–0.99). The corresponding figures for beer and spirits were 1.04 (0.94–1.15) and 0.98 (0.75–1.29). The upturn in risk for non-drinkers could be explained by a higher risk for teetotallers who likely included previous alcohol users or teetotalers who started to drink during follow-up. Wine gave the most favorable risk estimates.

Keywords

Beer Wine Spirits Risk factors 

References

  1. 1.
    St Leger AS, Cochrane AL, Moore F. Ischemic heart disease and wine. Lancet. 1979;313:1294.CrossRefGoogle Scholar
  2. 2.
    Marmot MG, Rose G, Shipley MJ, Thomas BJ. Alcohol and mortality: a U-shaped curve. Lancet. 1981;317:580–3.CrossRefGoogle Scholar
  3. 3.
    Shaper AG, Wannamethee G, Walker M. Alcohol and mortality in British men: explaining the U-shaped curve. Lancet. 1988;332:1267–73.CrossRefGoogle Scholar
  4. 4.
    Harriss LR, English DR, Hopper JL, et al. Alcohol consumption and cardiovascular mortality accounting for possible misclassification of intake: 11-year follow-up of the Melbourne Collaborative Study Cohort. Addiction. 2007;102:1574–85.CrossRefPubMedGoogle Scholar
  5. 5.
    Boffetta P, Garfinkel L. Alcohol drinking and mortality among men enrolled in an American Cancer Society Prospective Study. Epidemiology. 1999;1(5):342–8.CrossRefGoogle Scholar
  6. 6.
    Klatsky AL. Alcohol and cardiovascular diseases: where do we stand today? J Intern Med. 2015;278:238–50.CrossRefPubMedGoogle Scholar
  7. 7.
    O’Keefe JH, Bhatti SK, Bajwa A, Di Nicolantonio JJ, Lavie CJ. Alcohol and cardiovascular health: the dose makes the poison… or the remedy. Mayo Clin Proc. 2014;19(3):382–93.CrossRefGoogle Scholar
  8. 8.
    Ronksley PE, Brien SE, Turner BJ, Mukamal KJ, Ghali WA. Association of alcohol consumption with selected cardiovascular disease outcomes: a systematic review and meta-analysis. BMJ. 2011;342:d671. doi:10.1136/bmj.d671.CrossRefPubMedPubMedCentralGoogle Scholar
  9. 9.
    Roerecke M, Rehm J. Alcohol consumption, drinking pattern, and ischemic heart disease: a narrative review of meta-analyses and a systematic review and meta-analysis of the impact of heavy drinking occasions on risk for moderate drinkers. BMC Med. 2014;12:182. doi:10.1186/s12916-014-0182-6.CrossRefPubMedPubMedCentralGoogle Scholar
  10. 10.
    Tverdal A, Hjellvik V, Selmer R. Heart rate and mortality from cardiovascular causes: a 12-year follow-up study of 379,843 men and women aged 40–45 years. Eur Heart J. 2008;29(22):2772–81.CrossRefPubMedGoogle Scholar
  11. 11.
    StataCorp. Stata Statistical Software: release 13. College Station: StataCorp LP; 2013.Google Scholar
  12. 12.
    VanderWeele T. Explanation in causal inference: methods for mediation and interaction. Oxford: Oxford University Press; 2015. p. 249–85.Google Scholar
  13. 13.
    Naess O, Søgaard AJ, Arnesen E, et al. Cohort profile: cohort of Norway (CONOR). Int J Epidemiol. 2008;37(3):481–5.CrossRefPubMedGoogle Scholar
  14. 14.
    Norwegian Institute of Public Health. Alcohol and other psychoactive substances—Public Health Report 2014. https://www.fhi.no/en/online-publications/public-health-report-2014/risk–protective-factors/alcohol-and-other-psychoactive-subs/#international-comparison.
  15. 15.
    Jackson R, Scragg R, Beaglehole R. Alcohol consumption and risk of coronary heart disease. BMJ. 1991;303:211–6.CrossRefPubMedPubMedCentralGoogle Scholar
  16. 16.
    Dai J, Mukamal KJ, Krasnow RE, Swan GE, Reed T. Higher usual alcohol consumption was associated with a lower 41-y mortality risk from coronary artery disease in men independent of genetic and common environmental factors: the prospective NHLBI Twin Study. Am J Clin Nutr. 2015;102:31–9.CrossRefPubMedPubMedCentralGoogle Scholar
  17. 17.
    Tverdal A. Dødelighet av hjerteinfarkt i fylker og helseregioner i perioden 1951–1994. Norsk Epidemiologi. 1998;8(1):79–90.Google Scholar
  18. 18.
    Bjartveit K, Wøien G. Cardiovascular disease risk factors in Norway. Results from surveys in 18 counties. Oslo: National Health Screening Service; 1997.Google Scholar
  19. 19.
    Cordova AC, Jackson LSM, Berke-Schlessel DW, Sumpio BE. The cardiovascular protective effect of red wine. Am Coll Surg. 2004;. doi:10.1016/j.jamcollsurg.2004.10.030.Google Scholar
  20. 20.
    Magnus P, Bakke E, Hoff DA, et al. Controlling for high-density lipoprotein cholesterol does not affect the magnitude of the relationship between alcohol and coronary heart disease. Circulation. 2011;124:2296–302.CrossRefPubMedGoogle Scholar
  21. 21.
    De la Torre R, Corella D, Castañer O, et al. Protective effect of homovanillyl alcohol on cardiovascular disease and total mortality: virgin olive oil, wine, and cathechol-methylathion. Am J Clin Nutr. 2017;105(6):1297–304.PubMedGoogle Scholar
  22. 22.
    Holmes MV, Dale CE, Zuccolo L, et al. Association between alcohol and cardiovascular disease: mendelian randomization analysis based on individual participant data. BMJ. 2014;349:g4164. doi:10.1136/bmj.g4164.CrossRefPubMedPubMedCentralGoogle Scholar
  23. 23.
    Taylor AE, Lu F, Carslake D, et al. Exploring causal associations of alcohol with cardiovascular and metabolic risk factors in a Chinese population using Mendelian randomization analysis. Sci Rep. 2015;5:14005. doi:10.1038/srep14005.CrossRefPubMedPubMedCentralGoogle Scholar
  24. 24.
    Edenberg HJ. The genetics of alcohol metabolism. Alcohol Res Health. 2007;30(1):5–13.PubMedPubMedCentralGoogle Scholar

Copyright information

© Springer Science+Business Media B.V. 2017

Authors and Affiliations

  1. 1.Norwegian Institute of Public HealthNydalen, OsloNorway
  2. 2.Department of Genetic Research and BioinformaticsNorwegian Institute of Public HealthNydalen, OsloNorway
  3. 3.Department of PharmacoepidemiologyNorwegian Institute of Public HealthNydalen, OsloNorway
  4. 4.Department of Public Health and Community MedicineGothenburg UniversityGothenburgSweden
  5. 5.Institute of Basic Medical Sciences, Medical FacultyUniversity of OsloBlindern, OsloNorway

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