Traversy G, Chaput JP. Alcohol Consumption and Obesity: An Update. Curr Obes Rep 2015;4:122–130. DOI 10.1007/s13679-014-0129-4
Recreational alcohol intake is a widespread activity globally and alcohol energy (7 kcal/g) can be a contributing factor to weight gain if not compensated for. Given that both excessive alcohol intake and obesity are of public health interest, the present paper provides an update on the association between alcohol consumption and body weight.
In general, recent prospective studies show that light-to-moderate alcohol intake is not associated with adiposity gain while heavy drinking is more consistently related to weight gain. Experimental evidence is also mixed and suggests that moderate intake of alcohol does not lead to weight gain over short follow-up periods. However, many factors can explain the conflicting findings and a better characterization of individuals more likely to gain weight as a result of alcohol consumption is needed. In particular, individuals who frequently drink moderate amounts of alcohol may enjoy a healthier lifestyle in general that may protect them from weight gain.
In conclusion, despite the important limitations of current studies, it is reasonable to say that alcohol intake may be a risk factor for obesity in some individuals, likely based on a multitude of factors, some of which are discussed herein.
While it would be assumed that, among drinkers, the excess calories provided by alcohol would add to their risk of obesity, current data suggest that the association may be more complex. For example, alcohol is metabolized differently from other foods, which suggests that its calories may not be as readily available as those from fat, carbohydrate, and protein. Also, it is unclear to what extent people who consume alcohol may modify other aspects of their diets, either decreasing or increasing other sources of calories. Further, while the focus of this critique is on “alcohol,” it is realized that in mixed drinks, many of the calories are not just from alcohol but from sugar, juices, or other added substances.
The present paper provides an update on scientific data on the association between alcohol consumption and obesity. It summarizes results from cross-sectional observational studies, longitudinal observational studies, and the limited number of clinical trials that have been done; most of the latter were relatively short-term studies. In a previous study on this topic, Suter stated: “Regarding the effects of alcohol on obesity, there seems to be a large individual variability according to the absolute amount of alcohol consumed, the drinking frequency as well as genetic factors. Presently it can be said that alcohol calories count more in moderate nondaily consumers than in daily (heavy) consumers. Further, they count more in combination with a high-fat diet and in overweight and obese subjects.”
The overall conclusions of this present update on the topic are that light-to-moderate drinking does not increase the risk of obesity, while heavier drinking (or even moderate drinking among obese subjects) may lead to weight gain. Given the key role of obesity in terms of impairing health, and the tendency of some people (especially women) to avoid alcohol because of fears that it will increase their weight, it seems important that a balanced message on this topic be made widely available to the public and to officials setting health policy.
Specific Comments on the Paper by Forum Members: Most Forum members appreciated the well-done summary of data that was presented in this review article. Many, however, agreed that the mechanisms for the effects of moderate drinking remain unclear. Review Finkel wrote: “For a number of years studies published on this subject have reported similar results, and mysterious relationships that still elude neat explanation. The law of conservation of energy and matter seems to be sometimes broken, and gender equality sometimes violated. Nevertheless, this paper seems to me well done and helpful.” Forum member Stockley agreed: “From my investigations over the years, I completely agree with Finkel here. There are so many factors that make precise analysis difficult, or impossible.” Reviewer Lanzmann-Petithory considered this to be a “high-quality review article.”
Wrote Forum member Puddey: “The authors correctly highlight ‘the mixed and conflicting available evidence on the topic of alcohol consumption and obesity’ and have offered a balanced and interesting critique. Many of the referenced studies are of varying size and quality and have often led to contrasting conclusions. If evidence-based recommendations are to be made, however, this subject really deserves a systematic review and meta-analytic approach with carefully pre-defined inclusion and exclusion factors for all studies ultimately reviewed.
“Given the very large and equally confusing literature on alcohol consumption in relation to prevalence and incidence of the metabolic syndrome [of which obesity is a key element], it is imperative a better understanding is developed of not just the potential positive or negative effects of alcohol on body weight but also on body fat distribution. A meta-analysis by Sun et al suggests a J-shaped relationship between alcohol and the metabolic syndrome with RR reduction of 0.86 (CI 0.75, 0.99) in light drinkers (up to 5 g/day of alcohol) and increased RR of 1.84 (95% CI 1.34-2.52) in those drinking >35g/day. This relationship could to a considerable extent underpin the J-shaped relationship between alcohol and cardiovascular disease.”
Puddey continued: “In Australia the general public is very familiar with the concept of a ‘beer belly’ in heavy drinkers but overall the evidence linking alcohol consumption independently to increased waist circumference remains quite confusing, let alone the even larger literature on alcohol in relation to cardiovascular risk factors associated with the metabolic syndrome. This paper has carefully considered many of the potential confounders in relation to alcohol and obesity. A further consideration however, might be that excessive alcohol consumption and overeating could be linked aetiologically by a common genetic predisposition, with recent evidence that genetic variants in the fat mass- and obesity-associated gene (FTO) are associated with alcohol dependence (Wang et al). Cross-sectional and intervention studies have consistently confirmed independent and additive effects of obesity, especially abdominal obesity, and heavy alcohol consumption on risks for elevated blood pressure. The take home message with respect to alcohol and obesity therefore once again needs to be a light to moderate alcohol intake together with a healthy diet and lifestyle.”
Potential mechanisms explaining why moderate drinking does not increase obesity: Reviewer Ellison commented: “Unfortunately, it is not clear to me whether adding alcohol, particularly wine, to a meal increases, decreases, or has little effect on total calorie consumption. I have found contradictions in research on this topic, perhaps partly because we have not determined the degree to which alcohol (or any nutrient) adds to or replaces other foods. However, to the extent that alcohol calories are added to total consumption, complex mechanisms related to utilization of such calories may play a role.” Forum member Skovenborg considered this to be “A meticulous review with a fair selection of references from the large body of literature. However, I missed a discussion of ‘Non-exercise Activity Thermogenesis’ (NEAT) as one of the possible explanations of the alcohol-obesity paradox (Levine et al, Orozco et al).
Reviewer Van Velden stated: “It is a well-balanced article, but the mechanism is not explained. We must remember that alcohol is classified as a carbohydrate macro nutrient. Our own research demonstrated that alcohol stimulates insulin secretion and lowers blood glucose. Insulin is an obesogenic (anabolic) hormone, that promotes storage of carbohydrates as fat. This could explain the effect of alcohol on weight gain. On the other hand, alcohol is also thermogenic, and I might note that the alcoholic patients I have treated were not obese: they were often found sleeping in the rain and in gutters, but the metabolism of the ethanol kept them warm.”
Forum member Teissedre stated that he agreed with Van Velden. “There are calories liberated by alcohol metabolism because alcohol is a nutrient with an obligation of combustion (particularly of proteins). With a restricted or normal diet it’s possible to lose weight with 3 glasses of wine daily (around 30 g of alcohol a day). With a high-caloric diet, ethanol is in addition of the other nutrients and in this case there is gain weight (possibly due to enhanced metabolism of lipids and carbohydrates).”
Reviewer de Gaetano suggested other possible confounders: “Data from the Moli-sani study indicate that a higher income and education are independently associated with a greater adherence to Mediterranean Diet-like eating patterns [that include wine] and a lower prevalence of obesity (Bonaccio et al). Obesity prevalence was higher in the lowest-income group (36%) in comparison with the highest-income category (20%, p<0.0001). Income was associated with dietary patterns in all categories of education. The possible influence of income and /or education on the relationship between Mediterranean Diet, alcohol intake, and obesity is an additional confounding factor for the complex relation between alcohol and obesity.”
Reviewer Finkel provided an anecdote related to the discussion: “A friend, a research surgeon, who had grown large in retirement, lost 30+ pounds in a relatively short time. Surprised to see this, I asked how he did it. ‘Wine,’ said he. He found that his meals, however small, if accompanied by a moderate quantity of good wine, provided the requisite satisfaction to enable him to leave the table when he should, not when some ‘satiation switch’ was tripped in his brain. Or so we thought.”
Forum member Ursini commented on the anecdote from Finkel: “A control (or at least extra information) is missing. What did your friend drink before shifting to wine? Coca-Cola, maybe? This would explain a lot.” To this, Finkel replied: “While I cannot match your biochemical dexterity, I can assure you, both from the testimony of the subject and from my time-to-time observations, my friend’s usual mealtime beverage was never high-sugar soft drinks. However, his pre-diet food consumption vastly exceeded energy expenditure requirements.”
Forum member Skovenborg thought that there may be some truth in this anecdote “It is anecdotal, but true – and evidence-based. The same principle was applied with success many years ago in a study of a weight-reduction program among obese subjects by Dr. Giorgio Lolli, described below.
An interesting early paper on wine and obesity: During the discussions on this paper among Forum members, reviewer Skovenborg identified for other members a publication by Lolli in 1962, entitled: “The Role of Wine in the Treatment of Obesity.” This was a case-crossover study among 27 obese patients on a weight-reduction program who were instructed for periods of about one week each to (1) ingest no wine (a control period), and then (in varying sequences) to consume 3 ounces of a wine of their choice either (2) 30-60 minutes before dinner, (3) during dinner, or (4) 30-60 minutes after dinner.
It was found that the largest decrease in reported calories and measured weight occurred when wine was consumed in period 3 (wine with dinner). During this period, subjects reported a 12% decrease in calories and 24 of 27 subjects showed a decrease in weight, ranging up to 1.6 pounds, with a mean loss of 0.5 pounds. Wine consumed before or after the meal was associated with less effect on reported calories and weight. The author, from the International Center for Psychodietetics, also reported that wine with meals was reported by subjects showing the largest effect was related to “the relief of hunger and emotional stress associated with their weight loss program.” Forum members noted that the amount of wine reported by subjects in this study was quite small, only between 3 and 4 ounces, so not adding a large number of calories.
Reviewer Ursini commented further on potential mechanisms by which alcohol intake could affect weight. “From a biochemical and metabolic point of view, ethanol must be considered a fat. It generates AcCoA and this inhibits pyruvate dehydrogenase. Pyruvate is transformed into oxaloacetate and more citrate is produced. At the same time glyconeogenesis is activated (increasing glycemia) as well as the availability of NADPH (needed for fatty acid synthesis) from pentose phosphate shunt increases. Due to that large availability of energetic substrates (both lipids and CHO), the Krebs cycle is saturated, citrate exits to cytosol, activates acetyl CoA Carboxylase producing malonyl CoA and this inhibits acyl CaA-Carnitine transferase I. The outcome is an increased fatty acid synthesis and a decreased beta-oxidation. This can lead to more TG exported by VLDL, hyperglycaemia, and more fat in adipose tissue. A reasonable interpretation of the fat tissue decrease related to ‘moderate’ ethanol intake could be an associated decreased intake of carbohydrates. One glass of wine (150 – 190 kcal) substituting for approximately 50 g of glucose could be a reasonable mechanism for shifting the metabolism from lipogenesis to oxidation of lipids. But, no Coke for lunch!”
References from Forum Comments
Bonaccio M1, Bonanni AE, Di Castelnuovo A, De Lucia F, Donati MB, de Gaetano G, Iacoviello L; Moli-sani Project Investigators. Low income is associated with poor adherence to a Mediterranean diet and a higher prevalence of obesity: cross-sectional results from the Moli-sani study. BMJ Open 2012;2:pii:e001685. doi:10.1136/bmjopen-2012-001685.
Levine JA, Eberhardt NL, Jensen MD. Role of Nonexercise Activity Thermogenesis in resistance to fat gain in humans. Science 1999;283:212-214.
Lolli G. The role of wine in the treatment of obesity. New York State Journal of Medicine 1962;62:3438-3443.
Orozco S, de Castro JM. Effect of spontaneous alcohol intake on heart rate and dietary intake of free-living women. Pharmacol Biochem Behav 1994;49:629-638.
Sun K, Ren M, Liu D, Wang C, Yang C, Yan L. Alcohol consumption and risk of metabolic syndrome: a meta-analysis of prospective studies. Clin Nutr 2014;33:596-602.
Suter PM. Is alcohol consumption a risk factor for weight gain and obesity? Crit Rev Clin Lab Sci 2005;42:197-227.
Wang L, Liu X, Luo X, Zeng M, Zuo L, Wang KS. Genetic variants in the fat mass- and obesity-associated (FTO) gene are associated with alcohol dependence. J Mol Neurosci 2013;51:416-424.
Among people who consume alcohol, it would be assumed that the excess calories provided by the alcohol would add to their risk of obesity; however, current data suggest that the association may be more complex. It is unclear to what extent people who consume alcohol may modify other aspects of their diets, either decreasing or increasing other sources of calories. Further, alcohol is metabolized differently from other foods, which suggests that its calories may not be as readily available as those from fat, carbohydrate, and protein to increase obesity. The present paper provides an update on scientific data on the association between alcohol consumption and obesity. The overall conclusions of the authors are that light-to-moderate drinking does not increase the risk of obesity, while heavier drinking (or even moderate drinking among obese subjects) may lead to weight gain.
Forum reviewers appreciated the excellent summary of scientific reports on this topic provided by this article, and thought that the authors gave a sound and balanced update on the topic. However, mechanisms why numerous prospective epidemiologic studies show that moderate drinking does not increase the risk of obesity are unclear. Given that alcohol contains calories, and if drinking alcohol does not displace the intake of other foods, it would be assumed that such calories would increase the risk of obesity unless there are particular metabolic differences between alcohol calories and those from protein, fat, and carbohydrate.
Potential mechanisms suggested have included a decreased utilization of calories from alcohol due to what is known as ‘Non-exercise Activity Thermogenesis’ (NEAT), in which the metabolism of alcohol may create more heat than fat. Also, the Forum discussion included comments that alcohol could bring into play effects on insulin, glucose, and fat mobilization (however, in the laboratory, such mechanisms tend to increase, rather than decrease, body fat). Also, a reasonable interpretation of the fat tissue decrease related to ‘moderate’ ethanol intake seen in many studies could be an associated decrease in the intake of carbohydrates. One glass of wine substituting for approximately 50 g of glucose could be a reasonable mechanism for shifting the metabolism from lipogenesis to oxidation of lipids. Genetic factors undoubtedly play a role in the effects among individuals. Further, while the focus of this critique is on “alcohol,” it is realized that in mixed drinks, many of the calories are not just from alcohol but from sugar, juices, or other added substances, which must also be taken into account.
In summary, this update on the association of alcohol consumption and obesity concludes that most well-done prospective studies show that moderate drinkers do not have an increase in their risk of becoming obese, and in some studies there is even a slight decrease in weight among moderate drinkers, when compared with non-drinkers. One possibility is that, especially for wine with meals, satiety may occur earlier and result in less intake of food. However, precise mechanisms for a lack of increase in weight are not known, and the effect could still result from drinkers compensating for their drinks by taking in fewer calories from other sources and perhaps also by being a little more physically active. Heavier drinking may relate to an increase in body weight.
Reference: Traversy G, Chaput JP. Alcohol Consumption and Obesity: An Update. Curr Obes Rep 2015;4:122–130. DOI 10.1007/s13679-014-0129-4
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Comments on this critique were provided by the following members of the International Scientific Forum on Alcohol Research:
David Van Velden, MD, Dept. of Pathology, Stellenbosch University, Stellenbosch, South Africa
Fulvio Ursini, MD, Dept. of Biological Chemistry, University of Padova, Padova, Italy
Dag S. Thelle, MD, PhD, Senior Professor of Cardiovascular Epidemiology and Prevention, University of Gothenburg, Sweden; Senior Professor of Quantitative Medicine at the University of Oslo, Norway
Pierre-Louis Teissedre, PhD, Faculty of Oenology – ISVV, University Victor Segalen Bordeaux 2, Bordeaux, France
Arne Svilaas, MD, PhD, general practice and lipidology, Oslo University Hospital, Oslo, Norway
Creina Stockley, PhD, MBA, 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
Ian Puddey, MD, Professor, Faculty of Medicine, Dentistry & Health Sciences, The University of Western Australia, Nedlands, Australia
Dominique Lanzmann-Petithory,MD, PhD, Nutrition/Cardiology, Praticien Hospitalier Hôpital Emile Roux, Paris, France
Giovanni de Gaetano, MD, PhD, Department of Epidemiology and Prevention, IRCCS Istituto Neurologico Mediterraneo NEUROMED, Pozzilli, Italy
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