What is the effect of alcohol consumption on the risk of chronic widespread pain? A Mendelian randomisation study using UK Biobank

Beasley, M., Freidin, M. B., Basu, N. , Williams, F. M.K. and Macfarlane, G. J. (2019) What is the effect of alcohol consumption on the risk of chronic widespread pain? A Mendelian randomisation study using UK Biobank. Pain, 160(2), pp. 501-507. (doi: 10.1097/j.pain.0000000000001426) (PMID:30371560)

[img]
Preview
Text
178986.pdf - Accepted Version
Available under License Creative Commons Attribution Non-commercial No Derivatives.

621kB

Abstract

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.

Item Type:Articles
Additional Information:This research has been conducted using the UK Biobank resource, application no. 1144, and was funded by the University of Aberdeen. M.B. Freidin is funded by the EU FP7 project PainOmics (contract #602736).
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Basu, Professor Neil
Authors: Beasley, M., Freidin, M. B., Basu, N., Williams, F. M.K., and Macfarlane, G. J.
College/School:College of Medical Veterinary and Life Sciences > School of Infection & Immunity
Research Centre:College of Medical Veterinary and Life Sciences > School of Infection & Immunity > Centre for Immunobiology
Journal Name:Pain
Publisher:Elsevier
ISSN:0304-3959
ISSN (Online):1872-6623
Published Online:26 October 2018
Copyright Holders:Copyright © 2018 The International Association for the Study of Pain
First Published:First published in Pain 160(2):501-507
Publisher Policy:Reproduced in accordance with the copyright policy of the publisher

University Staff: Request a correction | Enlighten Editors: Update this record