Background Increased alcohol intake and fructose consumption may be associated with a lower risk of inflammatory arthritis. The mechanism of action may be related to a rise in serum uric acid (SUA), a circulating anti-oxidant.
Objectives To examine the association between intake of alcohol, red wine, beer and fructose, and SUA with risk of inflammatory polyarthritis (IP).
Methods Lifestyle data were obtained from 25,455 adults without IP and aged 40-79 using a health and lifestyle questionnaire (HLQ) in the population-based European Prospective Investigation of Cancer (EPIC-Norfolk) study from 1994-97. Over 342,916 person-years of follow-up, 184 individuals who subsequently developed IP were identified by linkage with the Norfolk Arthritis Register (NOAR), a primary-care based disease register. Controls were taken from a random sample of 4000 EPIC participants (case-cohort design), which due to overlap between cases and availability of 7-day diet diaries (7DD) resulted in a dataset of 4098 participants, of which 171 had IP.
Results Correlation between the HLQ and 7DD for alcohol intake was good (ρ =0.8). The median (IQR) SUA for cases and unaffected cohort was 280.6 (237.7, 356.4) and 287.7 (235.7, 345.6) μmol/L respectively. In linear regression SUA showed a weak but significant association with alcohol intake in men (β coeff 4.17 (2.61,5.73), p<0.001, adj r2=0.02) and a weak negative association with fructose intake (mainly from fruits) in women (β coeff -0.37 (-0.75,0.00), p=0.05, adj r2<0.01). In a Cox proportional hazards model stratified for gender and adjusted for age and smoking, there was no association between SUA and risk of IP (Table). Alcohol intake (HLQ) was associated with a lower risk of IP in women, while fructose intake was associated with a lower risk of IP in men and a similar trend in women. We found no specific effect for red wine or beer consumption.
Conclusions Fructose and alcohol intake may have gender specific influences on the development of future IP. Such effects are, however, unlikely to be mediated by the uric acid-allantoin anti-oxidant pathway.
Disclosure of Interest None Declared