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Autoimmune and Inflammatory Disorders · Journal article
Korean Journal of Family Medicine · August 18, 2026
Well-designed and adequately powered for the question it asks.
This two-sample Mendelian randomization study provides genetic evidence that diabetes liability and higher alcohol intake are causally associated with increased Dupuytren's disease risk, while obesity and smoking show no clear causal effects. Although effect sizes are modest, consistent with disease multifactoriality, the findings support glycemic control and reduced alcohol consumption as potential preventive strategies.
Two-sample Mendelian randomization with meta-analysis. European ancestry individuals with genetic data and defined Dupuytren's disease outcomes in UK Biobank and FinnGen. Intervention: Genetic liability for diabetes, genetically predicted alcohol intake (overall and drinks per week), obesity-related traits, and smoking intensity. Compared with: Lower genetic liability or exposure (reference). UK Biobank and FinnGen (Finland); European ancestry populations.
Diabetes genetic liability: OR 1.0157 (95% CI 1.0070–1.0245, P<0.001) Alcohol intake genetically predicted: OR 1.0150 (95% CI 1.0087–1.0212, P<0.001) Drinks per week: OR 1.0062 (95% CI 1.0015–1.0110, P=0.0103)
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Clinicians should counsel patients with diabetes on the importance of glycemic control and those with high alcohol intake on moderation to reduce DD risk. However, modest effect sizes indicate these are contributors within a multifactorial disease model, not sole determinants.
Rigorous two-sample Mendelian randomization with meta-analyzed summary statistics from large cohorts (UK Biobank and FinnGen), clear causal estimates for primary exposures, adequate instrument strength, and sensitivity analyses supporting robustness, though effect sizes are modest.
As stated by the source record.
Quoted from the source exactly as published.
Clinicians should counsel patients with diabetes on the importance of glycemic control and those with high alcohol intake on moderation to reduce DD risk. However, modest effect sizes indicate these are contributors within a multifactorial disease model, not sole determinants.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Background: Dupuytren's disease (DD) is associated with metabolic and lifestyle traits. However, these associations remain uncertain because exposures frequently cluster, and conventional studies are vulnerable to residual confounding and reverse causation. Methods: A two-sample Mendelian randomization (MR) analysis using genetic instruments for diabetes, obesity-related, smoking, and alcohol-related traits from genome-wide association studies of large European ancestry was conducted. Summary statistics of DD were obtained from UK Biobank and FinnGen and combined using meta-analysis. Multiplicative random-effects inverse variance weighted MR was used as the primary method, with complementary sensitivity analyses to test robustness. Results: Genetic liability for diabetes was associated with a higher risk of DD (meta-analyzed odds ratio [OR], 1.0157; 95% confidence interval [CI], 1.0070-1.0245; P<0.001). Genetically predicted alcohol intake was also positively associated with DD (alcohol intake OR, 1.0150; 95% CI, 1.0087-1.0212; P<0.001; drinks per week OR, 1.0062; 95% CI, 1.0015-1.0110; P=0.0103). However, we found no convincing evidence that obesity traits or smoking intensity had causal effects on DD. Sensitivity analyses were directionally consistent, the instruments were adequately strong, and there was no substantial evidence of horizontal pleiotropy for the main associations. Although the observed effect sizes were modest, consistent with the multifactorial nature of DD, supporting directional risk associations rather than large individual-level effects. Conclusion: This MR study supported diabetes liability and higher alcohol intake as causal risk factors for DD, whereas genetically proxied obesity and smoking traits showed no clear causal effects. These findings suggest that better glycemic management and lower alcohol exposure may help reduce the risk of DD.
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