Studies have shown that moderate alcohol consumption is strongly associated with reduced reporting of chronic widespread pain (CWP). The study designs used, however, are prone to confounding and are not able to establish the direction of causality. The current study overcomes these problems using the Mendelian randomisation design to determine the effect of alcohol consumption on the likelihood of reporting CWP. The UK Biobank recruited 500,000 participants aged between 40 and 69 years. Data collected included questions on chronic pain and alcohol consumption, and biological samples providing genotypic information. Alcohol consumption was categorised as “weekly consumption” or “nonfrequent or infrequent.” Participants were classified by genotype according to alleles of the rs1229984 single-nucleotide polymorphism, either “GG” or “AA/AG.” Chronic widespread pain was defined as pain all over the body for more than 3 months that interfered with activities. Associations between genotype, CWP, and alcohol consumption were tested by logistic regression. Instrumental variable analysis was used to calculate the causal effect of weekly alcohol consumption on CWP. Persons with “GG” genotype had an increased risk of CWP (odds ratio [OR] 1.17, 99% confidence interval 1.01-1.35) and were more likely to consume alcohol weekly (OR 1.76, 1.70-1.81) compared to those with “AA/AG” genotype. Weekly consumption of alcohol was associated with reduced risk of CWP (OR 0.33, 0.31-0.35), but instrumental variable analysis did not show a causal effect of alcohol consumption on reducing CWP (OR 1.29, 0.96-1.74). An interpretation of observational population studies as showing a protective effect of alcohol on CWP is not supported.
Despite the strong association of moderate alcohol consumption with lowered reporting of chronic widespread pain, Mendelian randomisation does not support a beneficial effect for alcohol.
aEpidemiology Group, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Aberdeen, United Kingdom
bAberdeen Centre for Arthritis and Musculoskeletal Health, University of Aberdeen, Aberdeen, United Kingdom
cDepartment of Twin Research and Genetic Epidemiology, School of Life Course Sciences, King's College London, London, United Kingdom
Corresponding author. Address: Epidemiology Group, Institute of Applied Health Sciences, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Health Sciences Building, Foresterhill, Aberdeen AB25 2ZD, United Kingdom. Tel.: +44(0) 1244 437087. E-mail address: email@example.com (M. Beasley).
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
Received July 26, 2018
Received in revised form September 13, 2018
Accepted October 16, 2018