Skip to main content

Volume 8 Supplement 1

Gout and Hyperuricemia

  • Review
  • Published:

Epidemiology, risk factors, and lifestyle modifications for gout


Gout affects more than 1% of adults in the USA, and it is the most common form of inflammatory arthritis among men. Accumulating data support an increase in the prevalence of gout that is potentially attributable to recent shifts in diet and lifestyle, improved medical care, and increased longevity. There are both nonmodifiable and modifiable risk factors for hyperuricemia and gout. Nonmodifiable risk factors include age and sex. Gout prevalence increases in direct association with age; the increased longevity of populations in industrialized nations may contribute to a higher prevalence of gout through the disorder's association with aging-related diseases such as metabolic syndrome and hypertension, and treatments for these diseases such as thiazide diuretics for hypertension. Although gout is considered to be primarily a male disease, there is a more equal sex distribution among elderly patients. Modifiable risk factors for gout include obesity, the use of certain medications, high purine intake, and consumption of purine-rich alcoholic beverages. The increasing prevalence of gout worldwide indicates that there is an urgent need for improved efforts to identify patients with hyperuricemia early in the disease process, before the clinical manifestations of gout become apparent.


Assessing the incidence and prevalence of gout is challenging because of its episodic nature. In the USA gout estimates vary, depending on the population being described. For example, male veterans are at heightened risk for developing gout because of their numerous risk factors, as seen in the Normative Aging Study conducted by the US Department of Veterans Affairs (Fig. 1) [1]. In contrast, white male physicians exhibited a cumulative incidence of gout over a 30-year period of approximately 8.6%, with 5.9% having primary gout (gout without a history of diuretic use) [2]. African-American physicians may have an even higher rate of gout [3]. Although data on physicians cannot accurately be generalized to the public, doctors do more accurately self-report suspected gout than the lay population, from whom many of the other gout estimates were derived.

Figure 1
figure 1

Cumulative incidence of gouty arthritis by prior urate levels. Reproduced from [1]. Copyright 1987 with permission from Excerpta Medica Inc.

The Rochester epidemiology study [4] has reported on the change in gout incidence over time. Comparing men and women from two cohorts – one from 1977 to 1978 and another from 1995 to 1996 – Arromdee and coworkers found that the age- and sex-adjusted annual incidence rate for primary gout in the USA rose from 20.2/100,000 persons to 45.9/100,000 persons; no change in the incidence of secondary gout related to thiazide diuretic therapy was observed. Gout has also been shown to increase somewhat linearly over a person's lifespan. This perceived rise in gout prevalence is primarily associated with an aging population, but it is also potentially associated with a number of changing societal trends. Based on self-reported gout from the National Health Interview Survey [5], in 1992 about 2 million people were characterized as having gout. In 1996 there were increases in gout incidence of up to 4.6% in men and 2% in women among those in the higher risk age range of 65 years or older, leading to an estimated overall prevalence of between 0.5% and 1%.

The prevalence of gout also appears to be rising in certain populations. A multicenter study conducted in the UK in 1991 found that the prevalence of gout had increased threefold compared with estimates from the 1970s [6]. In a 1999 examination of gout epidemiology from the UK General Practice Research Database [7], gout prevalence was found to be approximately 2% among men and about 1% among men and women combined. Prevalence was highest among those aged 75–84 years; among the men gout incidence approached 8%. Gout prevalence varies substantially by geographic region. In New Zealand among the Maoris gout is relatively endemic with prevalence estimated as high as 5% [8, 9]. The prevalence of gout in particular geographic regions suggests that both genetic factors and environmental factors predispose individuals to developing gout [10].

The varied methods of reporting epidemiological data on gout and the sometimes imperfect data sources available make it difficult to document the public health impact accurately. In the Sudbury study [11], for example, in as many as half of the patients who claimed to have gout, this could not be confirmed by history and physical examination. Although it is best to rely on a crystal diagnosis to confirm cases of gout, this is not practical at the population level.

Why is the prevalence of gout potentially rising? One reason may be changes in gout risk factors, not the least of which is increased longevity. As Americans get older and heavier, there has been a concordant rise in the prevalence of hypertension [12, 13]. Both the metabolic syndrome and hypertension have a strong association with gout [14, 15] (see below), and treatments for hypertension (e.g. thiazide diuretics) can result in the development of secondary gout [16]. Results from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack (ALLHAT) trial [17] have led to the recommendation that diuretics be given as first-line therapy in most patients with hypertension; some therefore speculate that the incidence of secondary gout related to diuretic use is likely to grow in the near future. The ubiquitous use of low-dose aspirin for the prevention of cardiovascular disease may be another reason for the rise in gout prevalence [18, 19].

Nonmodifiable risk factors for gout


The prevalence of gout increases in direct association with age; therefore, the increased longevity of populations in industrialized nations may contribute to a higher prevalence of gout through the disorder's association with age-related diseases (e.g. metabolic syndrome and hypertension) and treatments for aging-related diseases (e.g. thiazide diuretics) [1416]. Moreover, the prevalence of the clinical manifestations of gout increases with the duration of hyperuricemia. Thus, elderly patients with longstanding hyperuricemia are more likely to present with the signs and symptoms of gout. In one study conducted by Wallace and coworkers [20], individuals older than 75 years exhibited an increase in the rate of gout from 21/1000 persons in 1990 to 41/1000 persons in 1999, and in the 65–74 year age group the increase was from 21/1000 to 24/1000 persons from 1990 to 1992 to more than 31/1000 from 1997 to 1999. In contrast, prevalence rates in persons younger than 65 years remained consistently low throughout the study. In those older than 75 years, the prevalence per 1000 is quite sizable compared with that in younger age ranges; these findings are similar to some of the data from the General Practice Research Database (discussed below).


Clinically, gout is often considered a male disease. Although gout prevalence has increased in both sexes, among patients younger than 65 years men have a fourfold greater prevalence than women [20]. However, gout in the elderly has a more equal sex distribution, most likely reflecting the loss of the uricosuric effect of estrogen following the menopause. In patients older than 65 years, the sex gap narrows to one woman to every three men with gout and/or hyperuricemia (3:1 ratio). With the declining use of estrogen therapy, the percentage of elderly female patients with gout may increase.

Modifiable gout risk factors

Serum urate

Serum urate level is the most important risk factor for gout. In the Normative Aging Study [1], 2046 initially healthy participants were followed for 14.9 years. Those with baseline serum urate levels of ≥ 9 mg/dl had a 22% cumulative incidence of gout over a 6-year period. Among patients with urate levels of ≤ 7.0 mg/dl and 7.0–8.9 mg/dl, the annual incidences of gouty arthritis were 0.5% and 0.1%, respectively (Fig. 1). Large percentages of people in the USA [21] and Japan [22], men in particular, have urate levels above the solubility threshold of approximately 6.7 mg/dl. In patients with gout who are older than 60 years, however, about half are women and the prevalence in women increases as they age.


Gout is associated with a number of different medications, including diuretics (noted above), low-dose aspirin, and drugs that are commonly used in organ transplantation.

Currently, approximately 46% of women and 59% of men who are at high risk for cardiovascular events take aspirin. Many persons at low risk for cardiovascular events also take low-dose aspirin in response to the positive publicity surrounding the prevention trials and guidelines [18]. Aspirin has been shown to have a bimodal effect on renal handling of uric acid. At high dosages (>3 g/day) aspirin is uricosuric, whereas at low dosages (1–2 g/day) it causes uric acid retention [23]. At 75 mg/day aspirin resulted in a 15% decrease in the rate of uric acid excretion (P = 0.045) and a small but significant increase in serum levels of uric acid (P = 0.009) [19]. These effects declined with increasing dosages of aspirin. Concomitant use of diuretics exacerbated the effects of aspirin on uric acid levels.

Renal and other major organ transplants

Hyperuricemia and gout are common complications of renal and other major solid-organ transplants. Gouty joint damage is accelerated in transplant patients with hyperuricemia compared with patients with primary hyperuricemia, and gout is frequently polyarticular [24]. Of transplant patients 13% will experience new-onset gout, and as many as 50% will become hyperuricemic [25]. Among patients receiving heart transplants rates of hyperuricemia are as high as 81%, with 8–12% experiencing new-onset gout [24].

Kidney transplant recipients may develop increased levels of uric acid because its secretion diminishes with the decreasing glomerular filtration rate [26]. Pharmaceutical agents that are commonly prescribed to transplant recipients – including diuretics, antimicrobials such as ketoconazole, ethambutol and pentamidine, and certain immunosuppressive agents such as cyclosporine – are strongly associated with hyperuricemia and gout [27].

Cyclosporine, a calcineurin inhibitor, is thought to increase uric acid levels by reducing tubular uric acid secretion and inhibiting glomerular filtration rates because of its ability to increase renal arterial vasoconstriction [28, 29]. A study conducted by Lin and coworkers [30] examined the frequency of hyperuricemia and gout in renal transplant patients who were treated with either cyclosporine and prednisone or azathioprine and prednisone. Hyperuricemia was significantly more common among patients who received cyclosporine than among those who received azathioprine (84% versus 30%; P = 0.0001), as was gout (7% versus 0%). Progression from acute gout to chronic, tophaceous gout can occur in as fewer as 6 months in some transplant patients.

The immunosuppressive agent tacrolimus has the potential to increase uric acid through its effect on glomerular filtration rate [31]. However, studies suggest that hyperuricemia occurs in under 3% of patients who receive tacrolimus, and so transplant recipients who receive this agent may be at lower risk for gout than those who receive cyclosporine.

Diet and alcohol intake

The association of purine-rich foods (e.g. meat, seafood, purine-rich vegetables such as peas, beans, and lentils), high protein intake, and dairy intake was examined in a study conducted by Choi and coworkers [32] in 47,120 men who had no history of gout at baseline. During 12 years of follow up, 730 confirmed new cases of gout were documented. Diet was assessed using the Willett Food Frequency Questionnaire, an instrument that is the 'gold standard' in nutritional epidemiology. Increased meat and seafood intake were associated with 1.41-fold and 1.51-fold increases in risk for gout, respectively, for the highest versus the lowest quintiles of intake. No increase in risk for gout was associated with the intake of purine-rich vegetables or total protein intake. The risk for gout was reduced by nearly 50% in persons in the highest quintile of dairy intake compared with those in the lowest quintile. The majority of these associations were independent of body mass index (BMI), older age, hypertension, alcohol use, diuretic use, and chronic renal failure. Although it was not surprising that meat and seafood had significant associations with the incidence of gout, the lack of effect of purine-rich vegetables in predisposing to gout was a more novel finding. It was also notable that there was a 50% reduction in gout incidence among those consuming the most dairy products (particularly low-fat dairy products).

Alcohol consumption, particularly consumption of purine-rich alcoholic beverages such as beer, is also correlated with an increase in the risk for hyperuricemia. In a second report by Choi and coworkers [33], and including the same cohort as in the previously cited report, a dose–response relationship of alcohol consumption to gout risk was found, after adjusting for other potential confounders. Beer consumption and, to a lesser extent, liquor consumption was shown to increase a person's risk for gout. It should be noted that beer is rich in guanosine, and this was thought to provide a biologic basis for this association. Of note, wine was not a significant risk factor for gout. Although the investigators did an excellent job of accounting for potential confounders, there are clear differences between people who consume wine and those who consume beer and mixed drinks, and the possibility for unmeasured confounding persists. However, adding to the strength of these findings, a subsequent investigation by Choi and Curhan [34] evaluated the relationship between intakes of beer, liquor, and wine and serum uric acid levels using data from 14,809 participants in the Third National Health and Nutrition Examination Survey (NHANES). Both before and after adjustment for other risk factors for hyperuricemia, beer and liquor intake was positively associated with increased serum urate levels (P for trend < 0.001). In contrast, wine intake was significantly associated with reduced serum urate before, but not after, adjustment for other risk factors.


Obesity is a growing epidemic in the USA. Presently, approximately 60% of Americans are overweight, and childhood obesity is increasing at an alarming rate [35]. BMI is significantly associated with risk for gout: compared with persons with a BMI of 21–22.9 kg/m2, the age-adjusted relative risk for gout is 1.40 for a BMI of 23–24.9 kg/m2, 2.35 for a BMI of 25–29.9 kg/m2, 3.26 for a BMI of 30–34.9 kg/m2, and 4.41 for a BMI of 35 kg/m2 or higher [15]. Weight gain over time is also associated with risk for gout, even after adjusting for initial weight and other risk factors.

Data suggest that obesity increases serum urate by eliciting both increased production and decreased renal excretion of urate [36]. In the Normative Aging Study [37], weight gain between the first and third visits was positively associated with increases in serum urate. In contrast, weight reduction has been shown in prospective studies to be associated with declines in uric acid levels [38].

Gout and chronic disease associations

A number of diseases have a strong association with gout. This raises the question of cause and effect – do these conditions result from gout, or do these diseases predispose individuals to gout?

The metabolic syndrome

The recent increase in the prevalence and clinical complexity of gout may partly be attributable to hyperuricemia associated with the metabolic syndrome, a clinical entity that is mediated primarily by insulin resistance. The majority of obese patients meet the criteria for metabolic syndrome, which is characterized by a clustering of central obesity; dyslipidemia (hypertriglyceridemia and low high-density lipoprotein [HDL] cholesterol); hypertension (≥130/85 mmHg); insulin resistance, glucose intolerance, or type 2 diabetes mellitus; hyperuricemia; and a prothrombotic and proinflammatory state [39]. In an analysis of data from 8814 men and women aged 20 years or older, the age-adjusted prevalence of the metabolic syndrome was 23.7% from 1988 to 1994 [40]. The prevalence of the metabolic syndrome also varied by ethnicity; for example, among Mexican Americans the age-adjusted prevalence of the metabolic syndrome is 31.9% [41]. Given that the incidence of obesity is rapidly increasing, it is likely that the prevalence of the metabolic syndrome has grown substantially in the intervening decade since these data were recorded.

Components of the metabolic syndrome have been associated with hyperuricemia. In a cross-sectional study conducted in 4053 African-American and Caucasian adults [14], BMI, fasting insulin, and triglycerides were significantly higher, and HDL-cholesterol was significantly lower in male and female individuals with hyperuricemia. BMI had the strongest correlation with urate among the metabolic syndrome components. Insulin resistance was also associated with serum urate levels. However, the influence of fasting insulin was not as strong as that of obesity. After controlling for obesity, insulin, and the other components of the metabolic syndrome, male persons with high triglycerides were more likely to have hyperuricemia. These data suggest that the relationship between hyperuricemia and the metabolic syndrome may result predominantly from the co-variation of these conditions with adiposity and secondarily with insulin level, and – at least in men – elevated triglycerides.


The relationship between hyperuricemia and hypertension is notable, because a higher serum urate level is known to be associated with hypertension. As many as 50% of untreated hypertensive persons have hyperuricemia, which often precedes hypertension, and even among children hyperuricemia has been shown to correlate with blood pressure. In the Normative Aging Study [1], gout was found to be more common among hypertensive individuals, with a strong association with thiazide diuretic use. One issue is whether thiazide diuretics confound the drug effect with hypertension. Sanchez-Lozada and coworkers [42], in their examination of the afferent arterioles in a rat model of gout, found that high urate levels may induce vascular effects that can be attenuated with the use of allopurinol, suggesting grounds for biologic plausibility for this observational association.

Cardiovascular disease

Irrespective of the outcomes of cardiovascular disease (CVD) such as coronary heart disease, ischemic heart disease, new cardiovascular events, or even cardiovascular mortality, CVD is strongly associated with gout. Two large US cohorts that have been rich resources for epidemiologic investigation are the Framingham study and NHANES, which have reached somewhat different conclusions on the associations between cardiovascular events and gout.

Using Framingham data, Culleton and coworkers [43] showed that serum urate levels were not independently associated with CVD, after adjustment for other risk factors. That study suggested that diuretic use, more than gout, was associated with CVD. According to NHANES data [44], the risk for death due to ischemic heart disease increased 1.77-fold in men and 3-fold in women when comparing the highest quartile with the lowest quartile for serum urate. For each 59.5 μmol/l increase in uric acid level, cardiovascular and ischemic heart disease mortality increased. After stratification by cardiovascular risk status, diuretic use, and menopausal status, the relationship between serum urate levels and cardiovascular mortality remained significant except among men using diuretics and men with more than one cardiovascular risk factor. It has been argued that NHANES is a more generalizable cohort than Framingham because it represents a wider spectrum of the US population. However, the Framingham study showed that serum urate may be a confounder for both hypertension and diuretic use, which has called the NHANES data into question.

Recent clinical trial data add fuel to this controversy. In the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study [45], baseline serum uric acid levels were associated with a 1.02-fold increase in the risk for cardiovascular events per 10 μmol/l increase; this association was significant in women but not in men.

Lifestyle modifications for gout

The data presented above reveal a clear relationship between diet and lifestyle and the development of hyperuricemia and gout. As metabolic disorders, hyperuricemia and gout are often amenable to changes in diet, lifestyle, and medication. As more data on the modifiable risk factors and co-morbidities of gout become available, integration of these data into gout management strategies may become essential, similar to the current management strategies for hypertension [46] and type 2 diabetes [47]. These lifestyle modifications are inexpensive and safe and, when combined with drug therapy, may result in better control of this disorder.

The lifestyle modification recommendations for the treatment or prevention of gout are similar to those for the prevention or treatment of other major chronic disorders [48, 49] (Fig. 2). Thus, the net health benefits from these general lifestyle recommendations [49] are expected to be even greater among patients with gout, particularly those with coexisting insulin resistance syndrome, diabetes, obesity, and hypertension [48]. In particular, weight control, reduced consumption of red meat, and daily exercise are important lifestyle modifications for patients with gout or hyperuricemia and parallel recommendations for the prevention of coronary heart disease, diabetes, and certain types of cancer. Available open-label, interventional data suggest that weight reduction is associated with a decline in uric acid levels [36, 38]. Furthermore, data on the relationship between purine-rich foods and urate levels indicate that restricting purine intake can reduce serum uric acid levels. For example, substitution of a purine-free formula diet over a period of days was shown to reduce the blood uric acid of healthy men from an average of 5.0 mg/dl to 3.0 mg/dl [50, 51]. In general, dietary restriction of purine-rich foods lowers urinary excretion of uric acid by about 200–400 mg/day and decreases mean serum urate levels by about 1–2 mg/dl [52]. Thus, reducing intake of purine-rich foods, particularly those of animal origin such as red meat, is recommended in the prevention and management of hyperuricemia and gout. Red meat is also the main source of saturated fats, which are positively associated with insulin resistance [53, 54], which in turn is closely associated with gout. These fats also increase low-density lipoprotein cholesterol more than HDL-cholesterol, resulting in an overall negative health effect. Increased consumption of red meat and saturated fats has been linked to major disorders such as coronary artery disease, type 2 diabetes, and certain types of cancer. Thus, it is important for patients with gout to limit red meat consumption, as is indicated by the new Healthy Eating Pyramid recommendations for the general public (Fig. 2) [49].

Figure 2
figure 2

Dietary influences on the risk for gout and their implications within a Healthy Eating Pyramid. Data on the relationship between diet and the risk for gout are primarily derived from the recent Health Professionals Follow-Up Study [15,32,33]. Upward solid arrows denote an increased risk for gout, downward solid arrows denote a decreased risk, and horizontal arrows denote no influence on risk. Broken arrows denote potential effect but without prospective evidence for the outcome of gout. Adapted from [48]. Copyright 2005 with permission from American College of Physicians.

For cardiovascular benefit, instead of consuming fish, patients with gout could consider taking plant-derived ω3 fatty acids or eicosapentanoic acid and docosahexanoic acid supplements. Experimental evidence also suggests that diets enriched with γ-linolenic acid and eicosapentaenoic acid significantly reduce urate crystal induced inflammation; however, the effect of such a diet on the clinical course of gout has not yet been studied [55].

The recent recommendations on dairy consumption for the general public may be applicable in most patients with gout or hyperuricemia, and may offer additional benefit to those individuals with hypertension, diabetes, and cardiovascular disorders [32, 56]. Further risk-benefit assessments in specific clinical contexts would be helpful. Daily consumption of nuts and legumes, as recommended by the Harvard Healthy Eating Pyramid [49], may also provide important health benefits without increasing the risk for gout [32]. New data on the incidence of gout suggest that a daily glass of wine might provide health benefits without raising the risk for gout, as opposed to beer or liquor consumption [33, 57]. However, reducing or eliminating alcohol – particularly purine-rich beverages such as beer and certain liquors – is generally recommended due to the significant effect on uric acid levels.

Several studies have suggested that high doses of vitamin C have a uricosuric effect [5862]. For example, one study [61] showed that ingestion of 4.0 g ascorbic acid led to a twofold increase in fractional clearance of uric acid up to 6 hours after ingestion, and that ingestion of 8.0 g ascorbic acid for 3–7 days reduced serum uric acid by up to 3.1 mg/dl as a result of sustained uricosuria. A recent trial indicated that taking 500 mg/day vitamin C for 2 months reduced serum uric acid by 0.5 mg/dl [62]. Because vitamin C is generally considered safe, its uricosuric effect may provide a potentially useful option for the prevention and management of hyperuricemia and gout.


Emerging data on the epidemiology of gout suggest that the prevalence of gout is rising. Advancing age increases the prevalence of gout; this is partly attributable to the increased risk factors for gout – including metabolic syndrome, hypertension, and renal disease – that are associated with age. New data is emerging on risk factors for gout, and of note is the increasingly strong association of hyperuricemia with both hypertension and CVD.

The increasing prevalence of gout worldwide indicates that there is an urgent need for improved efforts to identify patients with hyperuricemia early in the disease process and before the clinical manifestations of gout become apparent. Lifestyle modifications, including weight loss, dietary changes, hypertension control, and changes in medication regimens, may provide adequate control of hyperuricemia in some patients, particularly when they are instituted early in the course of disease; they may also result in better control of gout in other patients when combined with drug therapy.



body mass index


cardiovascular disease


high-density lipoprotein.


  1. Campion E, Glynn R, DeLabry L: Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study. Am J Med. 1987, 82: 421-426. 10.1016/0002-9343(87)90441-4.

    Article  CAS  PubMed  Google Scholar 

  2. Roubenoff R, Klag M, Mead L, Liang K, Seidler A, Hochberg M: Incidence and risk factors for gout in white men. JAMA. 1991, 266: 3004-3007. 10.1001/jama.266.21.3004.

    Article  CAS  PubMed  Google Scholar 

  3. Hochberg M, Thomas J, Thomas D, Mead L, Levine D, Klag M: Racial differences in the incidence of gout: the role of hypertension. Arthritis Rheum. 1995, 38: 628-632.

    Article  CAS  PubMed  Google Scholar 

  4. Arromdee E, Michet C, Crowson C, O'Fallon M, Gabriel S: Epidemiology of gout: is the incidence rising?. J Rheumatol. 2002, 29: 2403-2406.

    PubMed  Google Scholar 

  5. Adams PF, Hendershot GE, Marano MA, Centers for Disease Control and Prevention/National Center for Health Statistics: Current estimates from the National Health Interview Survey, 1996. Vital Health Stat. 1999, 10: 1-203.

    Google Scholar 

  6. Harris CM, Lloyd DC, Lewis J: The prevalence and prophylaxis of gout in England. J Clin Epidemiol. 1995, 48: 1153-1158. 10.1016/0895-4356(94)00244-K.

    Article  CAS  PubMed  Google Scholar 

  7. Mikuls T, Farrar J, Bilker W, Fernandes S, Saag K: Suboptimal physician adherence to quality indicators for the management of gout and asymptomatic hyperuricaemia: results from the UK General Practice Research Database (GPRD). Rheumatology. 2005, 44: 1038-1042. 10.1093/rheumatology/keh679.

    Article  CAS  PubMed  Google Scholar 

  8. Klemp P, Stansfield S, Castle B, Robertson M: Gout is on the increase in New Zealand. Ann Rheum Dis. 1997, 56: 22-26.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  9. Prior I, Rose B: Uric acid, gout and public health in the South Pacific. NZ Med J. 1966, 65: 295-300.

    CAS  Google Scholar 

  10. Kim KY, Ralph Schumacher H, Hunsche E, Wertheimer AI, Kong SX: A literature review of the epidemiology and treatment of acute gout. Clin Ther. 2003, 25: 1593-1617. 10.1016/S0149-2918(03)80158-3.

    Article  PubMed  Google Scholar 

  11. O'Sullivan J: Gout in a New England town: a prevalence study in Sudbury, Massachusetts. Ann Rheum Dis. 1972, 31: 166-169.

    Article  PubMed Central  PubMed  Google Scholar 

  12. American Heart Association: Heart Disease and Stroke Statistics, 2004 Update. 2003, Dallas: AHA

    Google Scholar 

  13. Hajjar I, Kotchen TA: Trends in prevalence, awareness, treatment, and control of hypertension in the United States, 1988–2000. JAMA. 2003, 290: 199-206. 10.1001/jama.290.2.199.

    Article  PubMed  Google Scholar 

  14. Rathmann W, Funkhouser E, Dyer AR, Roseman JM: Relations of hyperuricemia with the various components of the insulin resistance syndrome in young black and white adults: The CARDIA study. Ann Epidemiol. 1998, 8: 250-261. 10.1016/S1047-2797(97)00204-4.

    Article  CAS  PubMed  Google Scholar 

  15. Choi H, Atkinson K, Karlson E, Curhan G: Obesity, weight change, hypertension, diuretic use, and risk of gout in men. Arch Intern Med. 2005, 165: 742-748. 10.1001/archinte.165.7.742.

    Article  PubMed  Google Scholar 

  16. Tykarski A: Evaluation of renal handling of uric acid in essential hypertension: hyperuricemia related to decreased urate secretion. Nephron. 1991, 59: 364-368.

    Article  CAS  PubMed  Google Scholar 

  17. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL, Jones DW, Materson BJ, Oparil S, Wright JT, National Heart, Lung, and Blood Institute Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National High Blood Pressure Education Program Coordinating Committee, et al: The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. JAMA. 2003, 289: 2560-2572. 10.1001/jama.289.19.2560.

    Article  CAS  PubMed  Google Scholar 

  18. Kim C, Beckles GL: Cardiovascular disease risk reduction in the Behavioral Risk Factor Surveillance System. Am J Prev Med. 2004, 27: 1-7. 10.1016/j.amepre.2004.03.008.

    Article  CAS  PubMed  Google Scholar 

  19. Caspi D, Lubart E, Graff E, Habot B, Yaron M, Segal R: The effect of mini-dose aspirin on renal function and uric acid handling in elderly patients. Arthritis Rheum. 2000, 43: 103-108. 10.1002/1529-0131(200001)43:1<103::AID-ANR13>3.0.CO;2-C.

    Article  CAS  PubMed  Google Scholar 

  20. Wallace K, Riedel A, 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: 1582-1587.

    PubMed  Google Scholar 

  21. Mikkelsen W, Dodge H, Valkenburg H: The distribution of serum uric acid values in a population unselected as to gout or hyperuricemia, Tecumseh, Michigan 1959–1960. Am J Med. 1965, 39: 242-251. 10.1016/0002-9343(65)90048-3.

    Article  CAS  PubMed  Google Scholar 

  22. Lin KC, Lin HY, Chou P: Community based epidemiological study on hyperuricemia and gout in Kin-Hu, Kinmen. J Rheumatol. 2000, 27: 1045-1050.

    CAS  PubMed  Google Scholar 

  23. Yu TF, Gutman AB: Study of the paradoxical effects of salicylate in low, intermediate and high dosage on the renal mechanisms of excretion of urate in man. J Clin Invest. 1959, 38: 1298-1313.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  24. Burack DA, Griffith BP, Thompson ME, Kahl LE: Hyperuricemia and gout among heart transplant recipients receiving cyclosporine. Am J Med. 1992, 92: 141-146. 10.1016/0002-9343(92)90104-J.

    Article  CAS  PubMed  Google Scholar 

  25. Abdelrahman M, Rafi A, Ghacha R, Youmbissi JT, Qayyum T, Karkar A: Hyperuricemia and gout in renal transplant recipients. Ren Fail. 2002, 24: 361-367. 10.1081/JDI-120005370.

    Article  PubMed  Google Scholar 

  26. Better OS: Tubular dysfunction following kidney transplantation. Nephron. 1980, 25: 209-213.

    Article  CAS  PubMed  Google Scholar 

  27. Baroletti S, Bencivenga GA, Gabardi S: Treating gout in kidney transplant recipients. Prog Transplant. 2004, 14: 143-147.

    Article  PubMed  Google Scholar 

  28. Hollander AA, van Saase JL, Kootte AM, van Dorp WT, van Bockel HJ, van Es LA, van der Woude FJ: Beneficial effects of conversion from cyclosporin to azathioprine after kidney transplantation. Lancet. 1995, 345: 610-614. 10.1016/S0140-6736(95)90520-0.

    Article  CAS  PubMed  Google Scholar 

  29. Peeters P, Sennesael J: Low-back pain caused by spinal tophus: a complication of gout in a kidney transplant recipient. Nephrol Dial Transplant. 1998, 13: 3245-3247. 10.1093/ndt/13.12.3245.

    Article  CAS  PubMed  Google Scholar 

  30. Lin HY, Rocher LL, McQuillan MA, Schmaltz S, Palella TD, Fox IH: Cyclosporin-induced hyperuricemia and gout. N Engl J Med. 1989, 321: 287-292.

    Article  CAS  PubMed  Google Scholar 

  31. Pilmore HL, Faire B, Dittmer I: Tacrolimus for the treatment of gout in renal transplantation: two case reports and review of the literature. Transplantation. 2001, 72: 1703-1705. 10.1097/00007890-200111270-00024.

    Article  CAS  PubMed  Google Scholar 

  32. Choi H, Atkinson K, Karlson E, Willett W, Curhan G: Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med. 2004, 350: 1093-1103. 10.1056/NEJMoa035700.

    Article  CAS  PubMed  Google Scholar 

  33. Choi H, Atkinson K, Karlson E, Willett W, Curhan G: Alcohol intake and risk of incident gout in men: a prospective study. Lancet. 2004, 363: 1277-1281. 10.1016/S0140-6736(04)16000-5.

    Article  PubMed  Google Scholar 

  34. Choi H, Curhan G: Beer, liquor, and wine consumption and serum uric acid level: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2004, 51: 1023-1029. 10.1002/art.20821.

    Article  PubMed  Google Scholar 

  35. St-Onge MP, Keller KL, Heymsfield SB: Changes in childhood food consumption patterns: a cause for concern in light of increasing body weights. Am J Clin Nutr. 2003, 78: 1068-1073.

    CAS  PubMed  Google Scholar 

  36. Dessein P, Shipton E, Stanwix A, Joffe B, 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: 539-543. 10.1136/ard.59.7.539.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  37. Glynn RJ, Campion EW, Silbert JE: Trends in serum uric acid levels 1961–1980. Arthritis Rheum. 1983, 26: 87-93.

    Article  CAS  PubMed  Google Scholar 

  38. Yamashita S, Matsuzawa Y, Tokunaga K, Fujioka S, Tarui S: Studies on the impaired metabolism of uric acid in obese subjects: marked reduction of renal urate excretion and its improvement by a low-calorie diet. Int J Obes. 1986, 10: 255-64.

    CAS  PubMed  Google Scholar 

  39. Bieber J, Terkeltaub R: On the brink of novel therapeutic options for an ancient disease. Arthritis Rheum. 2004, 50: 2400-2414. 10.1002/art.20438.

    Article  PubMed  Google Scholar 

  40. Ford ES, Giles WH, Dietz WH: Prevalence of the metabolic syndrome among U.S. adults. Findings from the Third National Health and Nutrition Examination Survey. JAMA. 2002, 287: 356-359. 10.1001/jama.287.3.356.

    Article  PubMed  Google Scholar 

  41. Meigs JB, Wilson PW, Nathan DM, D'Agostino Sr RB, Williams K, Haffner SM: Prevalence and characteristics of the metabolic syndrome in the San Antonio Heart and Framingham Offspring Studies. Diabetes. 2003, 52: 2160-2167.

    Article  CAS  PubMed  Google Scholar 

  42. Sanchez-Lozada LG, Tapia E, Avila-Casado C, Soto V, Franco M, Santamaria J, Nakagawa T, Rodriguez-Iturbe B, Johnson RJ, Herrera-Acosta J: Mild hyperuricemia induces glomerular hypertension in normal rats. Am J Physiol Renal Physiol. 2002, 283: F1105-1110.

    Article  PubMed  Google Scholar 

  43. Culleton BF, Larson MG, Kannel WB, Levy D: Serum uric acid and risk for cardiovascular disease and death: the Framingham Heart Study. Ann Intern Med. 1999, 131: 7-13.

    Article  CAS  PubMed  Google Scholar 

  44. Fang J, Alderman M: Serum uric acid and cardiovascular mortality: NHANES I epidemiologic follow-up study, 1971–1992. JAMA. 2000, 283: 2404-2410. 10.1001/jama.283.18.2404.

    Article  CAS  PubMed  Google Scholar 

  45. Høieggen A, Alderman MH, Kjeldsen SE, Julius S, Devereux RB, De Faire U, Fyhrquist F, Ibsen H, Kristianson K, Lederballe-Pedersen O, Lindholm LH, Nieminen MS, Omvik P, Oparil S, Wedel H, Chen C, Dahlöf B, for the LIFE Study Group: The impact of serum uric acid on cardiovascular outcomes in the LIFE study. Kidney Int. 2004, 65: 1041-1049. 10.1111/j.1523-1755.2004.00484.x.

    Article  PubMed  Google Scholar 

  46. August P: Initial treatment of hypertension. N Engl J Med. 2003, 348: 610-617. 10.1056/NEJMcp010357.

    Article  PubMed  Google Scholar 

  47. Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL: Harrison's Principles of Internal Medicine. 2004, New York: McGraw-Hill Professional Publishing, 16

    Google Scholar 

  48. Choi HK, Mount DB, Reginato AM: Pathogenesis of gout. Ann Intern Med. 2005, 143: 499-516.

    Article  CAS  PubMed  Google Scholar 

  49. Willett WC, Stampfer MJ: Rebuilding the food pyramid. Sci Am. 2003, 288: 64-71.

    Article  PubMed  Google Scholar 

  50. Griebsch A, Zollner N: Effect of ribomononucleotides given orally on uric acid production in man. Adv Exp Med Biol. 1974, 41: 443-449.

    Article  CAS  PubMed  Google Scholar 

  51. Coe FL, Moran E, Kavalich AG: The contribution of dietary purine over-consumption to hyperpuricosuria in calcium oxalate stone formers. J Chronic Dis. 1976, 29: 793-800. 10.1016/0021-9681(76)90053-9.

    Article  CAS  PubMed  Google Scholar 

  52. Emmerson BT: The management of gout. N Engl J Med. 1996, 334: 445-451. 10.1056/NEJM199602153340707.

    Article  CAS  PubMed  Google Scholar 

  53. Christiansen E, Schnider S, Palmvig B, Tauber-Lassen E, Pedersen O: Intake of a diet high in trans monounsaturated fatty acids or saturated fatty acids. Effects on postprandial insulinemia and glycemia in obese patients with NIDDM. Diabetes Care. 1997, 20: 881-887.

    Article  CAS  PubMed  Google Scholar 

  54. Feskens EJ, Kromhout D: Habitual dietary intake and glucose tolerance in euglycaemic men: the Zutphen Study. Int J Epidemiol. 1990, 19: 953-959.

    Article  CAS  PubMed  Google Scholar 

  55. Tate GA, Mandell BF, Karmali RA, Laposata M, Baker DG, Schumacher HR, Zurier RB: Suppression of monosodium urate crystal-induced acute inflammation by diets enriched with gamma-linolenic acid and eicosapentaenoic acid. Arthritis Rheum. 1988, 31: 1543-1551.

    Article  CAS  PubMed  Google Scholar 

  56. Choi HK, Curhan G: Dairy consumption and risk of incident gout in women: The Nurses Health Study [abstract]. Arthritis Rheum. 2005, 52 (suppl 9): S31-S41.

    Google Scholar 

  57. Choi HK: Diet, alcohol, and gout: how do we advise patients given recent developments?. Curr Rheumatol Rep. 2005, 7: 220-226.

    Article  CAS  PubMed  Google Scholar 

  58. Mitch WE, Johnson MW, Kirshenbaum JM, Lopez RE: Effect of large oral doses of ascorbic acid on uric acid excretion by normal subjects. Clin Pharmacol Ther. 1981, 29: 318-321.

    Article  CAS  PubMed  Google Scholar 

  59. Berger L, Gerson CD, Yu TF: The effect of ascorbic acid on uric acid excretion with a commentary on the renal handling of ascorbic acid. Am J Med. 1977, 62: 71-76. 10.1016/0002-9343(77)90351-5.

    Article  CAS  PubMed  Google Scholar 

  60. Sutton JL, Basu TK, Dickerson JW: Effect of large doses of ascorbic acid in man on some nitrogenous components of urine. Hum Nutr Appl Nutr. 1983, 37: 136-140.

    CAS  PubMed  Google Scholar 

  61. Stein HB, Hasan A, Fox IH: Ascorbic acid-induced uricosuria. A consequency of megavitamin therapy. Ann Intern Med. 1976, 84: 385-388.

    Article  CAS  PubMed  Google Scholar 

  62. Huang HY, Appel LJ, Choi MJ, Gelber AC, Charleston J, Norkus EP, Miller ER: The effects of vitamin C supplementation on serum concentrations of uric acid: results of a randomized, controlled trial. Arthritis Rheum. 2005, 52: 1843-1847. 10.1002/art.21105.

    Article  CAS  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations


Corresponding author

Correspondence to Kenneth G Saag.

Additional information

Competing interests

KGS is a consultant for TAP Pharmaceuticals and Servier and has received a grant from TAP Pharmaceuticals.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Saag, K.G., Choi, H. Epidemiology, risk factors, and lifestyle modifications for gout. Arthritis Res Ther 8 (Suppl 1), S2 (2006).

Download citation

  • Published:

  • DOI: