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Effect of alcohol consumption on biological markers associated with risk of coronary heart disease: systematic review and meta-analysis of interventional studies

BMJ 2011; 342 doi: https://doi.org/10.1136/bmj.d636 (Published 22 February 2011) Cite this as: BMJ 2011;342:d636
  1. Susan E Brien, postdoctoral fellow1,
  2. Paul E Ronksley, doctoral student1,
  3. Barbara J Turner, professor of medicine and director2,
  4. Kenneth J Mukamal, associate professor of medicine3,
  5. William A Ghali, scientific director and professor14
  1. 1Calgary Institute for Population and Public Health, Department of Community Health Sciences, Faculty of Medicine, University of Calgary, Alberta, Canada T2N 4Z6
  2. 2REACH Center, University of Texas Health Science Center, San Antonio, TX, USA
  3. 3Harvard Medical School, Division of General Medicine and Primary Care, Beth Israel Deaconess Medical Center, Boston, MA, USA
  4. 4Department of Medicine, University of Calgary, Alberta, Canada
  1. Correspondence to: W A Ghali wghali{at}ucalgary.ca
  • Accepted 12 December 2010

Abstract

Objective To systematically review interventional studies of the effects of alcohol consumption on 21 biological markers associated with risk of coronary heart disease in adults without known cardiovascular disease.

Design Systematic review and meta-analysis.

Data sources Medline (1950 to October 2009) and Embase (1980 to October 2009) without limits.

Study selection Two reviewers independently selected studies that examined adults without known cardiovascular disease and that compared fasting levels of specific biological markers associated with coronary heart disease after alcohol use with those after a period of no alcohol use (controls). 4690 articles were screened for eligibility, the full texts of 124 studies reviewed, and 63 relevant articles selected.

Results Of 63 eligible studies, 44 on 13 biomarkers were meta-analysed in fixed or random effects models. Quality was assessed by sensitivity analysis of studies grouped by design. Analyses were stratified by type of beverage (wine, beer, spirits). Alcohol significantly increased levels of high density lipoprotein cholesterol (pooled mean difference 0.094 mmol/L, 95% confidence interval 0.064 to 0.123), apolipoprotein A1 (0.101 g/L, 0.073 to 0.129), and adiponectin (0.56 mg/L, 0.39 to 0.72). Alcohol showed a dose-response relation with high density lipoprotein cholesterol (test for trend P=0.013). Alcohol decreased fibrinogen levels (−0.20 g/L, −0.29 to −0.11) but did not affect triglyceride levels. Results were similar for crossover and before and after studies, and across beverage types.

Conclusions Favourable changes in several cardiovascular biomarkers (higher levels of high density lipoprotein cholesterol and adiponectin and lower levels of fibrinogen) provide indirect pathophysiological support for a protective effect of moderate alcohol use on coronary heart disease.

Footnotes

  • Contributors: All authors conceived the study and developed the protocol. SB and PR carried out the search, abstracted the data for the analysis, and did the statistical analysis. SB, PR, and WG wrote the first draft of the manuscript. All authors critically reviewed the manuscript for important intellectual content and approved the final version of the manuscript. WG will act as guarantor for the paper.

  • Funding: This work was supported by a contracted operating grant from Program of Research Integrating Substance Use Information into Mainstream Healthcare (PRISM) funded by the Robert Wood Johnson Foundation project No 58529, with cofunding by the Substance Abuse and Mental Health Services and the Administration Center for Substance Abuse Treatment. SB is supported by a postdoctoral fellowship award from the Alberta Heritage Foundation for Medical Research. PR is supported by a Frederick Banting and Charles Best Canada graduate scholarship from the Canadian Institutes of Health Research. WG is supported by a Canada research chair in health services research and by a senior health scholar award from the Alberta Heritage Foundation for Medical Research. Other than funding, research in this manuscript was done independent of funding agencies. None of the funding agencies played an active role in the preparation, review, or editing of this manuscript.

  • Competing interests: All authors have completed the Unified Competing Interest form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declare: All authors had support from a contracted operating grant from Program of Research Integrating Substance Use Information into Mainstream Healthcare (PRISM) funded by the Robert Wood Johnson Foundation project No 58529, with cofunding by the Substance Abuse and Mental Health Services and the Administration Center for Substance Abuse Treatment for the submitted work; no financial relationships with any organisations that might have an interest in the submitted work in the previous 3 years; no other relationships or activities that could appear to have influenced the submitted work.

  • Ethical approval: Not required.

  • Data sharing: Statistical code and datasets available from the corresponding author at wghali{at}ucalgary.ca.

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