Alcohol consumption as a preventive factor for developing rheumatoid arthritis: A dose-response meta-analysis of prospective studies

Title
Alcohol consumption as a preventive factor for developing rheumatoid arthritis: A dose-response meta-analysis of prospective studies
Publication type
Journal Article
Year of Publication
2013
Journal
Annals of the Rheumatic Diseases
Date published
2013
ISBN
00034967 (ISSN)
Keywords
Abstract

Objective To summarise the evidence regarding the dose-response association between alcohol consumption and risk of rheumatoid arthritis (RA). Method Studies were identified from search of MEDLINE, Embase and Web of Science databases between 1 January 1946 and 10 April 2013, and from review of the conference abstracts and the reference lists of retrieved articles. Prospective studies that reported relative risks (RRs) with 95% CIs for the association between alcohol consumption and the risk of RA were included. Results from individual studies were pooled using a dose-response meta-analysis. Results Up to 10 April 2013, 8 prospective studies contained 195 029 participants and 1878 RA cases were included. The results indicated that low to moderate alcohol consumption yielded a preventive effect on RA development (RR: 0.86; 95% CI 0.78 to 0.94), and provided some evidence of a non-linear relationship between alcohol consumption and risk of RA. Dose-response meta-analysis of the study data revealed that compared with that for no alcohol consumption, the adjusted RR was 0.93 (95% CI 0.88 to 0.98) for 3 g/day of alcohol consumption, 0.86 (95% CI 0.76 to 0.97) for 9 g/day, 0.88 (95% CI 0.78 to 0.99) for 12 g/day, 0.91 (95% CI 0.81 to 1.03) for 15 g/day, and 1.28 (95% CI 0.94 to 1.73) for 30 g/day. Subgroup analysis indicated that women who had low to moderate alcohol consumption had a 19% reduction in RA risk. Regardless of sex, a consistent low to moderate alcohol consumption for a period of at least 10 years was found to have a 17% reduction in RA risk. Conclusions Low to moderate alcohol consumption inversely associated with the development of RA in a manner that appears to be dose-dependent, timedependent and sex-dependent. Large prospective studies that investigate gene-environment interactions are required to further clarify the aetiology of RA.