Critique 024: Moderate alcohol consumption lowers risk of metabolic diseases in a population with high mean alcohol intake. – 28 November 2010
Clerc O, Nanchen D, Cornuz J, Marques-Vidal P, Gmel G, Daeppen J-B, Paccaud F, Mooser V, Waeber G, Vollenweider P, Rodondi N. Alcohol drinking, the metabolic syndrome and diabetes in a population with high mean alcohol consumption. Diabet Med 2010;27:1241–1249.
Authors’ Abstract
Aims To investigate the relationship of alcohol consumption with the metabolic syndrome and diabetes in a population-based study with high mean alcohol consumption. Few data exist on these conditions in high-risk drinkers.
Methods In 6,172 adults aged 35–75 years, alcohol consumption was categorized as 0, 1–6, 7–13, 14–20, 21–27, 28–34 and ≥ 35 drinks ⁄ week or as non-drinkers (0), low-risk (1–13), medium-to-high-risk (14–34) and very-high-risk (≥ 35) drinkers. Alcohol consumption was objectively confirmed by biochemical tests. In multivariate analysis, we assessed the relationship of alcohol consumption with adjusted prevalence of the metabolic syndrome, diabetes and insulin resistance, determined with the homeostasis model assessment of insulin resistance (HOMA-IR).
Results Seventy-three per cent of participants consumed alcohol, 16%were medium-to-high-risk drinkers and 2%very-high risk drinkers. In multivariate analysis, the prevalence of the metabolic syndrome, diabetes and mean HOMA-IR decreased with low-risk drinking and increased with high-risk drinking. Adjusted prevalence of the metabolic syndrome was 24% in nondrinkers, 19% in low-risk (P < 0.001 vs. non-drinkers), 20% in medium-to-high-risk and 29% in very-high-risk drinkers (P = 0.005 vs. low-risk). Adjusted prevalence of diabetes was 6.0% in non-drinkers, 3.6% in low-risk (P < 0.001 vs. nondrinkers), 3.8% in medium-to-high-risk and 6.7% in very-high-risk drinkers (P = 0.046 vs. low-risk). Adjusted HOMA-IR was 2.47 in non-drinkers, 2.14 in low-risk (P < 0.001 vs. non-drinkers), 2.27 in medium-to-high-risk and 2.53 in very-high-risk drinkers (P = 0.04 vs. low-risk). These relationships did not differ according to beverage types.
Authors’ Conclusions Alcohol has a U-shaped relationship with the metabolic syndrome, diabetes and HOMA-IR, without differences between beverage types.
Forum Comments
With the emergence of an epidemic of obesity and type 2 diabetes (DM) throughout the world, the association of lifestyle habits that may affect the risk of metabolic diseases is especially important. Most prospective studies have shown that moderate drinkers tend to have about 30% lower risk of developing DM than do non-drinkers,1-3 and moderate drinkers also tend to be at considerably lower risk of developing metabolic syndrome (MS).4-7 This cross-sectional analysis of subjects in Switzerland related varying levels of alcohol intake to the presence of DM, MS, and an index of insulin resistance (HOMA-IR).
Several Forum members commented on potential problems when considering a number of physiologic conditions as the “metabolic syndrome” and focusing therapy on the syndrome. Whether referred to as the insulin resistance syndrome, the deadly quartet, or the metabolic syndrome, it does not help clarify etiology nor does it provide help for medical care. Risk factors such as hypertension, hypercholesterolemia, unfavorable TC/HDL-C ratio, diabetes mellitus, and last but not least obesity and lack of physical activity should be considered singly. The so-called metabolic syndrome can be looked at simply as an agglomeration of risk factors with a major cause, namely obesity or metabolic overload. The MONICA project and the EUROASPIRE project have refrained from using the definition “metabolic syndrome,” as all participants thought that defining these findings as a syndrome does not produce any additional benefit.
Comments on this paper: The strengths of this paper include being population-based and having a reasonable number (> 1,000) subjects who reported that they consumed 14 or more drinks/week. (Many previous studies have had few subjects reporting this level of alcohol intake). Also, there was a good percentage (27%) of subjects reporting no alcohol intake during the one week of assessment used for classifying subjects. A strength worth mentioning is the careful confirmation of drinking status with state-of-the-art laboratory tests. It is a cross-sectional analysis, so a causative relation between alcohol intake and the metabolic outcomes cannot be assessed. Still, the data support much that has been shown in prospective studies.
The expected associations were seen between the reported amount of alcohol intake and potentially confounding variables. For example, moderate drinkers had the lowest weight, tryglycerides, and blood pressure. All drinkers had higher HDL-cholesterol values than did non-drinkers. For the specific components of the MS, lower occurrences of high waist circumference, high tryglycerides, and high blood pressure were seen for moderate drinkers than for non-drinkers or for heavy drinkers; there was a continuous, inverse association between alcohol intake and low HDL. There was little association with high fasting glucose.
The key finding is that there is a U-shaped association between alcohol intake and DM, MS, and insulin resistance. The prevalences of all of these outcomes were lowest among moderate drinkers. There were no significant differences noted in this study by type of beverage; the majority of subjects consumed mainly wine, although beer was more frequent among heavier drinkers.
References from Forum Comments
1. Rimm EB, Chan J, Stampfer MJ, Colditz GA, Willett WC. Prospective study of cigarette smoking, alcohol use, and the risk of diabetes in men. BMJ 1995;310:555-559.
2. Perry IJ, Wannamethee SG, Walker MK, Thomson G, Whincup PH, Shaper AG. Prospective study of risk factors for development of non–insulin dependent diabetes in middle aged British men. BMJ 1995;310:560-564.
3. Koppes LL, Dekker JM, Hendriks HF, Bouter LM, Heine RJ. Moderate alcohol consumption lowers the risk of type 2 diabetes: a meta-analysis of prospective observational studies. Diabetes Care 2005;28;719-725.
4. Djousse L, Arnett DK, Eckfeldt JH, Province MA, Singer MR, Ellison RC. Alcohol consumption and metabolic syndrome: does the type of beverage matter? Obes Res 2004;12:1375-1385.
5 Freiberg MS, Cabral HJ, Heeren TC, Vasan RS, Ellison RC. Alcohol consumption and the prevalence of the metabolic syndrome in the US: a cross-sectional analysis of data from the Third National Health and Nutrition Examination Survey. Diabetes Care 2004;27:2954-2959.
6. Fan AZ, Russell M, Naimi T, Li Y, Liao Y, Jiles R, Mokdad AH. Patterns of alcohol consumption and the metabolic syndrome. J Clin Endocrinol Metab 2008;93:3833-3838.
7. Alkerwi A, Boutsen M, Vaillant M, Barre J, Lair ML, Albert A, Guillaume M, Dramaix M. Alcohol consumption and the prevalence of metabolic syndrome: a meta-analysis of observational studies. Atherosclerosis 2009;204:624-635.
Forum Summary
This cross-sectional analysis of subjects in Switzerland related varying levels of alcohol intake to the presence of DM, MS, and an index of insulin resistance (HOMA-IR). The strengths of this paper include being population-based and having a large number of subjects who reported that they consumed 14 or more drinks/week. Also, there was a good percentage (27%) of subjects reporting no alcohol intake during the one week of assessment used for classifying subjects. Another strength is the careful confirmation of drinking status with state-of-the-art laboratory tests. In multivariate analysis, the prevalence of the metabolic syndrome, diabetes and mean HOMA-IR decreased with low-risk drinking and increased with high-risk drinking. No differences were noted according to the type of beverage consumed.
This is a cross-sectional analysis, so a causative relation between alcohol intake and the metabolic outcomes cannot be assessed. Still, the data support much that has been shown in prospective studies. Several Forum members commented on potential problems when considering a number of physiologic conditions as the “metabolic syndrome” and focusing therapy on the syndrome. They believed that each metabolic factor should be evaluated and treated singly.
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Contributions to this critique by the International Scientific Forum on Alcohol Research came from the following:
Arne Svilaas, MD, general practice and lipidology, Oslo University Hospital, Oslo, Norway
Creina Stockley, clinical pharmacology, Health and Regulatory Information Manager, Australian Wine Research Institute, Glen Osmond, South Australia, Australia.
Erik Skovenborg, MD, Scandinavian Medical Alcohol Board, Practitioner, Aarhus, Denmark
Ulrich Keil, MD, PhD, Institute of Epidemiology and Social Medicine, University of Münster, Münster, Germany
Harvey Finkel, MD, Hematology/Oncology, Boston University Medical Center, Boston, MA, USA
R. Curtis Ellison, MD, Section of Preventive Medicine & Epidemiology, Boston University School of Medicine, Boston, MA, USA