Critique 131: Effects of alcohol consumption on the risk of gout — 23 December 2013
Wang M, Jiang X, Wu W, Zhang D. A meta-analysis of alcohol consumption and the risk of gout. Clin Rheumatol 2013;32:1641–1648.
Authors’ Abstract
Alcohol consumption had been linked to the risk of gout theoretically, but the results from observational studies were conflicting. Hence, a meta-analysis was conducted to assess the effect of alcohol consumption on the risk of gout. A comprehensive search was performed to identify all eligible studies on the association of alcohol consumption with gout risk. Pooled relative risks (RRs) with 95 % confidence intervals (CIs) from fixed and random effects models were calculated.
A total of 12 articles with 17 studies involving 42,924 cases met the inclusion criteria. The pooled RR for highest vs. non/occasional alcohol drinking in every study was 1.98 (95 % CI, 1.52–2.58). The RRs for light (≤1 drink/day), moderate (>1 to <3 drinks/day), and heavy drinking (≥3 drinks/day) vs. non/occasional alcohol drinking were 1.16 (95 % CI, 1.07–1.25), 1.58 (95 % CI, 1.50–1.66), and 2.64 (95 % CI, 2.26–3.09), respectively. The results suggested that alcohol consumption might be associated with increased risk of gout.
Forum Comments
Background: Traditionally, it has been assumed that gout occurs primarily from the consumption of large amounts of food, especially red meat, other purine-containing foods, and alcohol. The first large prospective analysis of alcohol and types of beverage and the risk of gout was reported in 2004 from the Health Professional’s Study. As stated by these authors, “The association between heavy alcohol consumption and increased risk of gout has long been suspected; however, the association has not been prospectively confirmed. Metabolic studies have shown that hyperuricaemia (not gout per se) can be induced by alcohol loading; furthermore, hyperuricaemia has been proposed as a marker for ethanol ingestion. These findings provided the basis that alcohol might eventually cause gout through hyperuricaemia.”
The Health Professional’s Study showed that the consumption of spirits increased risk in comparison with non-drinkers. Beer, especially, increased risk; multivariate RR for gout per 12-oz serving of beer per day was 1.49; 95% CI 1.32–1.70. However, wine consumption was not related to the risk (RR per 4-oz serving per day was 1.04; 95% CI 0.88–1.22)(Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G. Alcohol intake and risk of incident gout in men: a prospective study. Lancet 2004;363:1277–1281).
In 2011, Cea Soriano et al did a case-control analysis of gout in the UK, based on 24,768 newly diagnosed gout patients (and 50,000 controls) among a cohort of 1,775,505 individuals aged 20 to 89 years between 2000 and 2007 (Cea Soriano L, Rothenbacher D, Choi HK, García Rodríguez LA. Contemporary epidemiology of gout in the UK general population. Arthritis Res Ther 2011;13:R39. doi: 10.1186/ar3272). Data were from a UK primary care database (THIN). These authors reported that there was a slight increase (6%) for reported alcohol intake up to 10 units/week, but larger increases for greater amounts (OR of 3.0 for consumption of > 42 units of alcohol per week). Beverage-specific data were not available.
A study by Lee et al from South Korea in 2013 was based on the National Health Insurance Corporation and National Health Screening Exam (NHSE) database, which included the health-care records of 48.1 million individuals (Lee CH, Sung MY. Lee J, Bae S-C. Factors associated with gout in South Koreans: analysis using the National Health Insurance Corporation and the National Health Screening Exam databases. Clin Rheumatol 2013;32:829–837; DOI 10.1007/s10067-013-2183-9). The primary type of alcohol consumed in South Korea is soju, and the authors state that “soju is a Korean distilled beverage like whisky, a type of spirit, which is different from wine or beer. It is traditionally made from rice, and its taste is similar to vodka, but slightly sweeter because of added sweeteners. The usual alcohol content of soju and volume of one bottle is 20% and 360 mL. Therefore, the amount of alcohol in one bottle of soju is 57.6 g (360×0.2×0.8).” These authors found an increased risk for consumers of more than one-half bottle of soju, but not for smaller amounts.
An update on the subject by Harvey Simon, MD of Harvard Medical School was quoted in the December 17, 2013, issue of NY Times: “Drinking excessive amounts of alcohol can raise your risk of gout. Beer is the kind of alcohol most strongly linked with gout, followed by spirits. Moderate wine consumption does not appear to increase the risk of developing gout. Alcohol use is highly associated with gout in younger adults. Binge drinking particularly increases uric acid levels. Alcohol appears to play less of a role among elderly patients, especially among women with gout.”
The present meta-analysis by Wang et al was based on 12 studies providing almost 43,000 cases of gout. The analyses appear to be well done. Subjects reporting no alcohol or occasional drinking made up the referent category; beverage-specific data were not available. The authors conclude that even light drinking (up to 1 typical drink of 12.5 g per day) was associated with a 16-17% increased risk of gout, with greater increases for heavier drinking.
Specific comments on the present paper: Forum member Zhang wrote: “I read the paper and discussed it with my colleague, Dr. Choi, who is an expert in gout research. He has published many papers in high impact journals, including NEJM, JAMA, Ann Int Med, BMJ, Lancet, etc., on risk factors and gout using data from the Health Professional’s Follow-up Study, the Nurses’ Health Study, NHANES, MRFIT, etc. In fact, his paper was cited in this meta-analysis.
“Basically both of us disagree with the authors claim that findings on alcohol consumption on the risk of gout are inconsistent. They are consistent! Most researchers agree that alcohol consumption, regardless beverage type, is associated with an increased risk of gout.”
While some still state that the role that alcohol may have in the development of gout may be inconsistent, we have data indicating that, among people who have gout, alcohol can serve as a trigger of acute attacks (Zhang Y, Woods R, Chaisson CE, Neogi T, Niu J, McAlindon TE, Hunter D. Alcohol consumption as a trigger of recurrent gout attacks. Am J Med 2006;119:800.e13-800.e18). These authors carried out an internet study that monitored attacks among 197 known subjects with gout for 10 months and found that subjects consuming larger amounts of alcohol had an increased risk of a gout attack. Compared with subjects reporting no alcohol consumption, the odds ratios for recurrent gout attacks were 1.1, 0.9, 2.0, and 2.5 for 1 to 2, 3 to 4, 5 to 6, and 7 or more drinks consumed over a 2-day period, respectively. An increased risk of recurrent gout attacks with larger amounts was found for each type of beverage consumed.
Zhang stated further: “We also found that the effect of alcohol on the risk of recurrent gout attacks is reduced if subjects’s serum uric acid level is well controlled, for example, and if they took allopurinol regularly. Considering the beneficial effect of alcohol consumption on risk of CHD, and patients with gout are at high risk of developing CHD, patients and their physicians should make the decision whether they should stop drinking alcohol or maintaining the low level of drinking despite the risk of an increase in their serum uric acid. Overall, our studies indicate that alcohol consumption increases the risk of gout attack, and there is a strong dose-response relationship. I cannot imagine that ethanol in wine will act differently from that in liquor or from beer on gout attacks. Sure, there is an additional component in beer, guanosine, a purine that is highly absorbable, which may also increase gout attacks.”
Reviewer Arduino disagrees with the above comments regarding the effects of wine: “Most studies have involved alcohol intake other than wine. Interestingly, one of the very few wine studies (Choi et al) doesn’t show any significant associations. Plenty of untested confounding factors and recommendations for reducing alcohol intake are way too generic with little evidence.”
Forum member Van Velden stated: “Alcohol decreases the excretion of uric acid, and may play a role in gout if a person drinks alcohol with lots of red meat. Red wine, alone, does not cause gout.”
Several reviewers commented on other influences on serum uric acid levels and gout. Said Form member Svilaas: “As mentioned in the paper, hyperuricaemia/gout has a complex etiology and pathogenesis. Genetic factors play an important role, and there are several confounding factors. A slight increase in risk with light to moderate alcohol consumption may be caused by an unhealthy lifestyle, obesity, or the metabolic syndrome. A weakness of this meta-analysis is that there are no data on beverage type. Heavier alcohol consumption is clearly related to hyperuricemia/gout, but in the presence of a genetic predisposition.”
Reviewer Finkel commented: “I find nothing wrong with this paper, although I plan to continue to drink moderately and eat sweetbreads on occasion.”
Forum Summary
A new meta-analysis has been conducted to assess the effects of alcohol consumption on the risk of gout. A total of 12 articles with 17 studies involving 42,924 cases met the inclusion criteria. The authors report that the pooled RRs for light (≤1 drink/day), moderate (>1 to <3 drinks/day), and heavy drinking (≥3 drinks/day) vs. non/occasional alcohol drinking were 1.16 (95 % CI, 1.07–1.25), 1.58 (95 % CI, 1.50–1.66), and 2.64 (95 % CI, 2.26–3.09), respectively. The results suggested that alcohol consumption might be associated with increased risk of gout.
Forum reviewers agreed that the analytic methodology in this paper was appropriate. Considerable research has shown that alcohol intake, especially heavier drinking, increases serum uric acid levels and the risk of gout. There remain some questions about the relation of wine consumption with gout, and the present study did not have data to test beverage-specific responses.
Overall, data suggest that alcohol intake, especially heavier drinking, raises serum uric acid levels and may trigger an acute attack in persons with gout, especially those who are not controlling their disease with appropriate medication. A number of studies, including the present one, suggest that even light alcohol intake may increase the risk of developing gout. In any case, the risk appears to be rather low with light drinking, a level of alcohol intake that should reduce the risk of cardiovascular disease. Also, some studies suggest that the risk is lower for the consumption of wine than for the consumption of other beverages containing alcohol.
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Comments on this paper have been provided by the following members of the International Scientific Forum on Alcohol Research:
Arduino A. Mangoni, PhD, Strategic Professor of Clinical Pharmacology and Senior Consultant in Clinical Pharmacology and Internal Medicine, Department of Clinical Pharmacology, Flinders University, Bedford Park, SA; Australia
Harvey Finkel, MD, Hematology/Oncology, Boston University Medical Center, Boston, MA, USA
Erik Skovenborg, MD, Scandinavian Medical Alcohol Board, Practitioner,
Arne Svilaas, MD, PhD, general practice and lipidology, Oslo University Hospital, Oslo, Norway
Fulvio Ursini, MD, Dept. of Biological Chemistry, University of Padova, Padova, Italy;
David Van Velden, MD, Dept. of Pathology, Stellenbosch University, Stellenbosch, South Africa
R. Curtis Ellison, MD, Section of Preventive Medicine & Epidemiology, Boston University School of Medicine, Boston, MA, USA