Alcohol consumption and incident osteoarthritis: a nationwide population-based longitudinal study.
TL;DR
Alcohol consumption was associated with incident OA in a dose-dependent manner that persisted after liver-related and weight-related restrictions, suggesting that this association is unlikely to be explained solely by hepatic dysfunction or obesity.
Abstract
Objective
To examine the association between alcohol consumption and incident osteoarthritis (OA) and whether it persists after restriction for liver-related and weight-related factors.
Design
We analyzed South Korean National Health Insurance Service data for adults aged ≥40 years who underwent health screening in 2009-2011 and had no recorded OA at baseline. Alcohol consumption was assessed by self-reported drinking frequency and estimated daily ethanol intake. Participants were followed until first claims-based OA diagnosis (ICD-10 M15-M19, excluding traumatic OA), death, or December 31, 2023. Multivariable Cox models estimated adjusted hazard ratios (HRs). Prespecified restricted analyses were conducted in participants with normal liver function and no liver disease history and in participants with normal weight and no obesity history.
Results
Among 1,233,179 participants with drinking-amount data (mean age, 50.8 years), the mean follow-up period was 9.9 years, during which 571,077 cases of OA occurred. Compared with non-drinkers, the light-drinking group had an adjusted HR of 1.037 (95% CI, 1.030-1.045), the moderate-drinking group had an adjusted HR of 1.081 (95% CI, 1.072-1.091), and the heavy-drinking group had an adjusted HR of 1.186 (95% CI, 1.174-1.197). A similar dose-response pattern was observed for drinking frequency and across sensitivity analyses. The pattern also persisted in the normal liver function and normal weight cohorts, and women showed elevated OA risk at lower levels of alcohol consumption than men.
Conclusions
Alcohol consumption was associated with incident OA in a dose-dependent manner that persisted after liver-related and weight-related restrictions, suggesting that this association is unlikely to be explained solely by hepatic dysfunction or obesity. These findings identify alcohol consumption as a factor associated with incident OA, warranting further investigation as a potentially modifiable contributor to OA risk.