Search J Rheum

Advanced Search


Current Issue


Guidelines for Authors & Reviewers

Classified Ads


Search PubMed


Subscriber Registration

Guidelines for Website Users

JRheum Update Service

Contact Info


Hyperuricemia, Gout, and Lifestyle Factors

Clinical Lecturer and Consultant Rheumatologist,
Arthritis Research Campaign National Primary Care Centre,
Primary Care Sciences,

Download PDF

View Table of Contents

Keele University,
Staffordshire ST5 5BG, United Kingdom

Address reprint requests to Dr. Roddy. E-mail:

Gout, one of the most prevalent inflammatory arthritides, arises from the formation and deposition of monosodium urate (MSU) crystals in and around joints. Hyperuricemia and the saturation of body tissues with urate are essential prerequisites for the development of gout, MSU crystals forming as serum urate (SUA) concentrations rise and exceed the physiological saturation threshold of urate. Recent epidemiological surveys have suggested that the prevalence and incidence of hyperuricemia and gout are rising1-4. Frequent suboptimal treatment5 may also contribute to the prevalence of clinically important, symptomatic gout. Numerous risk factors for the development of hyperuricemia and gout have been described, with the role of dietary and alcohol excess being recognized since ancient times. Historically, epidemics of gout are described in Roman times and in 19th century England that were attributed to a diet excessively rich in purines and alcohol, although the widely recognized association with port is now thought to have been due to lead poisoning that arose from lead contamination of fortified wines6,7. More recently, robust prospective epidemiological evidence of the roles played by dietary purines and alcohol in the development of hyperuricemia and gout has emerged. In the Health Professionals Follow-up Study, 47,150 men were followed for 12 years, observing 730 incident cases of gout. The development of gout was associated with alcohol consumption [multivariate relative risk (RR) 1.17 per 10 g increase in daily intake, 95% confidence interval (CI) 1.11–1.22] and intake of meat (RR 1.41, highest vs lowest quintile, 95% CI 1.07–1.86) and seafood (RR 1.51, 95% CI 1.17–1.95)8,9. Interestingly, beer conferred greater risk than spirits, whereas consumption of wine and vegetable-purines did not predispose to the development of gout. In a study of 14,809 participants from the Third National Health and Nutrition Examination Survey (NHANES-III), SUA level was found to increase with increasing consumption of meat, seafood, beer, and spirits10,11. Similarly, SUA levels were greater with beer than spirits, whereas wine consumption was not associated with hyperuricemia. Further analyses from these studies have suggested that consumption of sugar-sweetened soft drinks and fructose also predispose to hyperuricemia and gout12,13 and that a number of other dietary factors might protect against their development, for example, vitamin C (see Gao, et al in this issue14), coffee15,16, and dairy products8,11.

In this issue of The Journal, Miao and colleagues report the results of an epidemiological survey from China that provides further insights into the effects of dietary factors on the prevalence of hyperuricemia and gout17. In this cross-sectional study, 5003 subjects aged between 20 and 80 years across 5 districts underwent a home interview that collected data concerning personal medical history including hyperuricemia and gout, dietary intake within the preceding 7 days, and important comorbidities, and blood samples for measurement of SUA. The prevalences of hyperuricemia and gout in this population were found to be 13.19% and 1.14%, respectively, which are similar to estimates from recent epidemiological studies18-20. A previous study undertaken in the same region of China found a higher prevalence of hyperuricemia of 25.3%, yet a lower prevalence of gout of 0.36%21, providing further evidence that the prevalence of gout may be rising. Higher levels of consumption of meat, fish, seafood, beer, and wine were seen in those with hyperuricemia and gout compared with control subjects. An interesting observation was that the prevalence of hyperuricemia was greater in urban than rural areas. Similarly, both hyperuricemia and gout were more prevalent in the most economically developed city in the region compared with the least developed city. Consumption of meat and seafood but not alcohol was also greater in the city residents compared with countryside residents and in the most economically developed city compared with the least developed. The authors concluded that the prevalence of hyperuricemia and gout is strongly associated with economic development and lifestyle factors.

There are a number of caveats to the study worthy of further discussion. The cross-sectional study design and contemporaneous dietary data collection mean that conclusions can only be drawn about the association between current dietary habits and prevalent hyperuricemia and gout. In contrast, the prospective Health Professionals Follow-up Study assessed exposure to alcohol and dietary factors prior to the onset of incident gout, and hence provides more robust evidence of the importance of lifestyle factors as causative factors in the development of gout. This methodological difference is perhaps less critical for hyperuricemia, where SUA levels are more likely to reflect current dietary habits, in contrast to gout, which usually arises after a sustained period of exposure to a risk factor and associated asymptomatic hyperuricemia. Another key difference is the relative size of the study populations, with only 57 subjects having gout compared with 730 in the Health Professionals Follow-up Study. Unexpected findings of the study were that only 2 subjects in the whole population were taking a diuretic, and that all of the subjects with hyperuricemia and/or gout had normal blood urea nitrogen and creatinine, which seems unusual in a study of hyperuricemia and gout.

Despite these caveats, the results of this study pose interesting questions concerning the contribution of lifestyle factors to the epidemiology of hyperuricemia and gout. The observation that urban areas and more economically developed cities had both the highest prevalence of hyperuricemia and gout and the highest levels of consumption of meat and seafood raises the possibility that variations in the prevalence and incidence of gout might be attributable to lifestyle factors. It then follows that the recent increase in the prevalence and incidence of gout might be explained by similar increases in adverse lifestyle habits such as purine-rich diets and excess alcohol consumption22. Clinical manifestations of gout show considerable variation, and the reasons why certain patients develop more severe disease are not well understood. It is possible that persistence of adverse lifestyle factors potentiates hyperuricemia and leads to more problematical clinically significant gout. These issues are worthy of further investigation in larger prospective studies.

The natural sequel of the findings of these epidemiological studies is the assumption that modification of adverse dietary habits will be advantageous in the treatment of hyperuricemia and gout. Indeed, recent evidence-based recommendations for the management of gout highlight the importance of a triumvirate of lifestyle modification, which includes weight reduction in addition to modification of intake of dietary purines and alcohol23,24. Unfortunately, it appears that advice to modify such risk factors is infrequently offered to patients5,25. However, this recommendation is based mainly on extrapolation from epidemiological studies, and there have been relatively few studies of lifestyle modification for the treatment of hyperuricemia and gout. Uncontrolled studies demonstrate reduction in SUA following alcohol restriction and weight reduction in patients with gout26 and following a low-purine diet in hyperuricemic subjects27. In a pilot study in 13 obese men with symptomatic gout, weight loss as a result of restricted carbohydrate intake and increased proportional intake of protein and unsaturated fat reduced both SUA levels and the frequency of acute attacks28. While the observation that target urate levels are infrequently reached with urate-lowering therapies in primary care is undoubtedly due, in part, to suboptimal dosing5, the likelihood remains that the efficacy of urate lowering measures is diminished by persistent unmodified lifestyle factors. There is a need for research studies investigating further the efficacy of lifestyle modification, the influence of adverse life factors on the success of urate-lowering therapy, and how best to implement successful lifestyle modification in patients with hyperuricemia and gout.


Search PubMed for:

1. Arromdee E, Michet CJ, Crowson CS, O'Fallon WM, Gabriel SE. Epidemiology of gout: is the incidence rising? J Rheumatol 2002;29:2403-6. [MEDLINE]

2. Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II. Arthritis Rheum 2008;58:26-35. [MEDLINE]

3. Roddy E, Zhang W, Doherty M. The changing epidemiology of gout. Nat Clin Pract Rheumatol 2007;3:443-9. [MEDLINE]

4. Wallace KL, Riedel AA, Joseph-Ridge N, Wortmann R. Increasing prevalence of gout and hyperuricemia over 10 years among older adults in a managed care population. J Rheumatol 2004;31:1582-7. [MEDLINE]

5. Roddy E, Zhang W, Doherty M. Concordance of the management of chronic gout in a UK primary-care population with the EULAR gout recommendations. Ann Rheum Dis 2007;66:1311-5. [MEDLINE]

6. Ball GV. Two epidemics of gout. Bull Hist Med 1971;45:401-8.

7. Nriagu JO. Saturnine gout among Roman aristocrats. Did lead poisoning contribute to the fall of the Empire? N Engl J Med 1983;308:660-3. [MEDLINE]

8. Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med 2004;350:1093-103. [MEDLINE]

9. Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G. Alcohol intake and risk of incident gout in men: a prospective study. Lancet 2004;363:1277-81. [MEDLINE]

10. Choi HK, Curhan G. Beer, liquor, and wine consumption and serum uric acid level: the Third National Health and Nutrition Examination Survey. Arthritis Rheum 2004;51:1023-9. [MEDLINE]

11. Choi HK, Liu S, Curhan G. Intake of purine-rich foods, protein, and dairy products and relationship to serum levels of uric acid: the Third National Health and Nutrition Examination Survey. Arthritis Rheum 2005;52:283-9. [MEDLINE]

12. Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ 2008;336:309-12. [MEDLINE]

13. Choi JW, Ford ES, Gao X, Choi HK. Sugar-sweetened soft drinks, diet soft drinks, and serum uric acid level: the Third National Health and Nutrition Examination Survey. Arthritis Rheum 2008;59:109-16. [MEDLINE]

14. Gao X, Curhan G, Forman JP, Ascherio A, Choi HK. Vitamin C intake and serum uric acid concentration in men. J Rheumatol 2008;35:1853-8.

15. Choi HK, Curhan G. Coffee, tea, and caffeine consumption and serum uric acid level: the Third National Health and Nutrition Examination Survey. Arthritis Rheum 2007;57:816-21. [MEDLINE]

16. Choi HK, Willett W, Curhan G. Coffee consumption and risk of incident gout in men: a prospective study. Arthritis Rheum 2007;56:2049-55. [MEDLINE]

17. Miao Z, Li C, Chen Y, et al. Dietary and lifestyle changes associated with high prevalence of hyperuricemia and gout in the Shandong coastal cities of Eastern China. J Rheumatol 2008;35:1859-64.

18. Lin KC, Lin HY, Chou P. Community based epidemiological study on hyperuricemia and gout in Kin-Hu, Kinmen. J Rheumatol 2000;27:1045-50. [MEDLINE]

19. Lohsoonthorn V, Dhanamun B, Williams MA. Prevalence of hyperuricemia and its relationship with metabolic syndrome in Thai adults receiving annual health exams. Arch Med Res 2006;37:883-9. [MEDLINE]

20. Mikuls TR, Farrar JT, Bilker WB, Fernandes S, Schumacher HR, Jr., Saag KG. Gout epidemiology: results from the UK General Practice Research Database, 1990-1999. Ann Rheum Dis 2005;64:267-72.[MEDLINE]

21. Nan H, Qiao Q, Dong Y, et al. The prevalence of hyperuricemia in a population of the coastal city of Qingdao, China. J Rheumatol 2006;33:1346-50. [MEDLINE]

22. Academy of Medical Sciences. Calling time: the nation's drinking as a major health issue. London: Academy of Medical Sciences; 2004.

23. Jordan KM, Cameron JS, Snaith M, et al. British Society for Rheumatology and British Health Professionals in Rheumatology guideline for the management of gout. Rheumatology Oxford 2007;46:1372-4. [MEDLINE]

24. Zhang W, Doherty M, Bardin T, et al. EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis 2006;65:1312-24. [MEDLINE]

25. Pal B, Foxall M, Dysart T, Carey F, Whittaker M. How is gout managed in primary care? A review of current practice and proposed guidelines. Clin Rheumatol 2000;19:21-5. [MEDLINE]

26. Gibson T, Kilbourn K, Horner I, Simmonds HA. Mechanism and treatment of hypertriglyceridaemia in gout. Ann Rheum Dis 1979;38:31-5.

27. Kullich W, Ulreich A, Klein G. Changes in uric acid and blood lipids in patients with asymptomatic hyperuricemia treated with diet therapy in a rehabilitation procedure [German]. Rehabilitation Stuttg 1989;28:134-7. [MEDLINE]

28. Dessein PH, Shipton EA, Stanwix AE, Joffe BI, Ramokgadi J. Beneficial effects of weight loss associated with moderate calorie/carbohydrate restriction, and increased proportional intake of protein and unsaturated fat on serum urate and lipoprotein levels in gout: a pilot study. Ann Rheum Dis 2000;59:539-43. [MEDLINE]

Return to September 2008 Table of Contents

© The Journal of Rheumatology Publishing Company Limited.
All rights reserved.