REVIEW

Update on Importance of Diet in Gout

Randall N. Beyl, Jr, MD, Laura Hughes, MD, MSPH, Sarah Morgan, MD, MS, RD, FADA, CCD
Division of Clinical Immunology and Rheumatology, The University of Alabama at Birmingham.

ABSTRACT

Gout is an inflammatory arthritis caused by deposition of monosodium urate crystals within synovial joints.
Although it is most well-known for its arthritis, gout has an intimate relationship with many other car-
diovascular and metabolic conditions. Current recommendations support aggressive medical therapy to treat
gout, whereas dietary counseling has become less emphasized. This article argues for the absolute
importance of dietary counseling in gout and proves why this counseling may impact the long term well-
being of a patient with gout.
Ó 2016 Elsevier Inc. All rights reserved.
The American Journal of Medicine (2016) 129, 1153-1158

KEYWORDS: Dietary modification; Gout; Hyperuricemia; Metabolic syndrome

Gout is an inflammatory arthritis caused by deposition of
monosodium urate crystals within synovial joints as a result
of elevated serum uric acid (SUA) levels.1 The classic
symptoms described are recurrent “attacks” of severe pain,
swelling, redness, and warmth in one or a few joints; in
some cases it can become chronic and polyarticular.2
In the United States the estimated prevalence of gout is 8
million individuals, which is an increase of approximately
1.2% over the last 20 years.3-5 When comparing 2 incidence
cohorts from 1977-1978 and 1995-1996 in Minnesota, the
incidence of primary gout was shown to have increased
from 42 to 62.3 per 100,000 (P ¼ .1) over the 20-year
period.6 Other studies have shown this trend to be world-
wide. In New Zealand, where gout is especially common,
the prevalence is estimated at 2.69% and rose as high as
25% in elderly men.7
Because of new pharmacotheraputics targeting hyperuri-
cemia, healthcare providers often start medical therapy
sooner and give dietary counseling less emphasis.8 With this
approach comes the inherent risk of drug toxicity, in-
teractions, and polypharmacy in patients who often have
multiple comorbidities. However, if the approach to gout
treatment included dietary therapy and lifestyle modification,
Funding: None.
Conflict of Interest: None.
Authorship: All authors had access to and input in writing this
manuscript.
Requests for reprints should be addressed to Randall N. Beyl, Jr, MD,
Rheumatology, The University of Alabama at Birmingham, 510 20th Street,
Faculty Office Tower Room 851, Birmingham, AL 35210.
E-mail address: rbeyl@uabmc.edu or rbeylj@gmail.com
it could lower uric acid levels as well as potentially mitigate
the long-term consequences of the metabolic syndrome that
often coexist with gout.9,10
GOUT AND METABOLIC SYNDROME
It has been well described that gout affects those who tend
to be overindulgent; hence the name “The Disease of
Kings.” Although gout is not formally included in the
metabolic syndrome definition, they share common condi-
tions, such as obesity, dyslipidemia, insulin resistance, and
hypertension. The prevalence of metabolic syndrome is
62.8% in patients with gout, compared with 25.4% in non-
gout patients.11 Whereas 3.4% of people with weight below
the 20th percentile are hyperuricemic, 11.4% of those above
the 80th percentile have elevated serum urate.10 Hyperten-
sion was shown to be directly related to serum urate levels in
mice treated with uricase inhibitors; their blood pressure
rose proportionally to their uric acid.12 Several recent small
clinical trials have demonstrated that SUA-lowering agents,
such as allopurinol and probenecid, can reduce blood
pressure in adolescents.13,14 Hyperlipidemia has been found
in 25%-60% of gout patients, whereas hypertriglyceridemia
was seen in 53.7% of gout patients versus 35.3% of non-
gout patients.9 Insulin resistance has been found in 48.4%-
76% of patients with gout, with the observed relative risk for
incident type 2 diabetes mellitus in gout patients being 1.34
(95% confidence interval [CI] 1.09-1.64) compared with
those without gout.9,10,15 The prevalence of coronary heart
disease is estimated at 25% of gout patients in the United
Kingdom and 18% in the United States.9 When compared

0002-9343/$ -see front matter Ó 2016 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.amjmed.2016.06.040
1154 The American Journal of Medicine, Vol 129, No 11, November 2016

with men without gout or coronary heart disease, men with design of the studies and the large number of variables, there
gout had a relative risk of 1.28 (95% CI 1.15-1.41) for total must be caution in assuming true causation.
mortality and 1.55 (95% CI 1.24-1.93) for fatal coronary
heart disease.16 In the Multiple Risk Factor Intervention Alcohol
Trial (MRFIT), gout patients had an increased risk of The risk of hyperuricemia and gout differ both with amount
myocardial infarction of 26% and a 35% risk of coronary and type of alcohol ingested. National Health and Nutrition
heart disease.9 Although gout is Examination Survey data from
sometimes thought of as just an men show that when compared
inflammatory arthritis, it is not CLINICAL SIGNIFICANCE
with no alcohol ingestion, beer
difficult to illustrate the relation-
Gout is a prevalent disease. was found to increase serum urate
ship with other cardiovascular and 0.46 mg/dL per drink per day
metabolic conditions and long-
Gout has strong associations with many
(95% CI 0.32-0.6) and liquor 0.29
term poor outcomes. comorbid conditions. mg/dL per drink per day (95% CI
Dietary measures likely play a
Diet is the common thread between 0.14-0.45) (P <.001). Wine was
greater role than urate-lowering not found to be associated with
these conditions.
therapy in the long-term manage- increased urate (P <.001). Body
ment of metabolic syndrome
Dietary modifications can impact hyper- mass index was very similar
commonly associated with gout. A uricemia and gout flares, as well as among beer, liquor, and wine
self-reported incident gout trial metabolic syndrome, hypertension, and drinkers in this study. In 2
found that men with a body mass coronary artery disease. different multivariate analyses,
index (BMI) over 27.5 were 16 after adjusting for BMI, the affect
times more likely to report gout
Certain foods and supplementation may
from each type of alcohol on
flares than men with a BMI <20 improve hyperuricemia, gout flare con-
serum urate remained.21 Cross-
kg/m2.17 Compared with men with trol, and prevention. sectional data show similar
a BMI of 21-22.9 kg/m2, the rela- trends in women: each serving of
tive risk of gout for a BMI of beer per week increased serum
25-29.9 kg/m2 was 1.95 (95% CI 1.44-2.65), BMI of 30-34.9 urate by 0.03 mg/dL. 22
A prospective cohort study of men
kg/m2 was 2.33 (95% CI 1.62-3.36), and a BMI of 35 followed for over 12 years showed that compared with
kg/m2 was 2.97 (95% CI 1.73-5.1).18 In a small cohort of nondrinkers, the relative risk of incident gout in drinkers
obese men with gout who were started on a moderate calorie was 1.32 (95% CI 0.99-1.75) for 10-14.9 g/d, 1.49 (95% CI
and carbohydrate restriction diet for 16 weeks, there was an 1.14-1.94) for 15-29.9 g/d, 1.96 (95% CI 0.48-2.6) for 30-
average weight loss of 5.4 kg, an average decrease in 49.9 g/d, and 2.53 (95% CI 1.73-3.7) for at 50 g/d. The
monthly gout flares from 2.1 to 0.7 (P ¼ .002), and a relative risk was 1.49 (95% CI 1.32-1.7) per 12-oz beer per
decrease in serum urate of 0.57 mg/dL to 0.47 mg/dL (P ¼ day, 1.15 (95% CI 1.04-1.28) per shot of liquor per day, and
.001). Of the 12 men who initially had a high serum urate, 7 was found to be unassociated with wine intake, 1.04 (95%
became normalized.19 In the MRFIT trial, when compared CI 0.88-1.22).23 There have been many proposed mecha-
with no weight change, the odds ratio for reaching normal nisms to explain how alcohol affects urate. An early study
urate with a loss of 1-4.9 kg was 1.43 (95% CI 1.33-1.54), 5- proposed that this was from increased adenosine triphos-
9.9 kg was 2.17 (95% CI 1.95-2.4), and 10 kg was 3.9 phate consumption, causing eventual increased uric acid
(95% CI 3.31-4.61). The decrease in serum urate levels for production.24 Serum lactate was also recorded here and
each bracket of weight loss was 0.12, 0.31, and 0.62 found to be elevated, which although since unproven, was
mg/dL, respectively.20 Therefore, obesity is associated with postulated to decrease uric acid excretion.24,25 Others have
gouty flares and hyperuricemia, and weight loss is one of the proposed that increased purine loads in beer cause increased
most important modifiable risk factors for gout. uric acid production.26 In a study of alcoholic versus
nonalcoholic beer, both were found to increase serum urate
levels, 6.5% versus 4.4% respectively, arguing that the
SINGLE FOOD/SUPPLEMENTS EFFECTS ON
ingestion of the purine load alone can increase uric acid
HYPERURICEMIA AND GOUT levels.27
The National Health and Nutrition Examination Survey
studies were designed to assess the health and nutritional
status of citizens in the United States. Questionnaires, Purine-Rich Foods
examinations, vital signs, and laboratory data were collected Purine-containing foods (such as meats, organ meat,
over time, to assess risk factors for certain diseases. Much of seafood, legumes, yeast, mushrooms, and gravies) have
the data on diet and gout come from these studies. For each been the target of many early gout diets, mainly on the basis
of the following foods for which National Health and of the concept that the biochemical degradation end product
Nutrition Examination Survey data are used there will be a of purines is urate. More recent studies have found that this
description of certain associations found, but given the is not necessarily true. National Health and Nutrition
Beyl et al Update on Diet in Gout
Examination Survey data show that the age-adjusted
differences in serum urate between the lowest and highest
intake of meat was 0.48 mg/dL (95% CI 0.34-0.61 mg/dL,
P <.001) and 0.16 mg/dL for seafood (95% CI 0.06-0.27
mg/dL, P ¼ .005). Total protein intake was not found to be
related to increasing urate levels.28 In a similar prospective
study, the relative risk for gout in men with the highest meat
intake compared with the lowest was 1.41 (95% CI 1.07-
1.8), whereas seafood was 1.51 (95% CI 1.17-1.95). Each
additional serving of meat per day increased the risk of gout
by 21%, whereas each additional weekly seafood serving
increased risk by 7%. The intake of dried beans and greens
is not associated with gouty flares, as shown by a relative
risk of 0.73 (95% CI 0.56-0.96).29
High-Fructose Corn Syrup (HFCS)-Sweetened
Soft Drinks
Fructose is the only carbohydrate known to increase urate.
Fructose and sugar intake also predispose to insulin resis-
tance and metabolic syndrome, which further increase the
risk of hyperuricemia.3 National Health and Nutrition Ex-
amination Survey data show a correlation between
increasing HFCS-sweetened soft drink intake and serum
urate levels. Compared with none, soft drink intake of <0.5,
0.5-0.9, 1-3.9, and 4 servings per day lead to serum urate
increases of 0.08, 0.15, 0.33, and 0.42 mg/dL (95% CI 0.11-
0.73 mg/dL, P <.001) and relative risks of gout of 1.01,
1.34, 1.51, and 1.82, respectively. This correlation was not
found to be significant with diet soft drinks. Body mass
index was similar between the sugar-sweetened and diet soft
drink groups. Elevated BMI did not seem to be the cause of
increased serum urate in the sweetened soft drink group
because serum urate was elevated similarly in individuals
with both high and low BMI.30 In a prospective cohort of
women similar findings were reported. The relative risk of
gout for 1 serving of HFCS-sweetened soft drink per day
was 1.74 (95% CI 1.19-2.55) and for at least 2 servings per
day was 2.39 (95% CI 1.34-4.26, P <.001), whereas diet
soda was not found to be correlated to risk of gout.31
Low-Fat Dairy Intake
National Health and Nutrition Examination Survey data
show that those who consumed at least 1 serving of milk per
day had a lower serum urate, with a difference of 0.25 mg/
dL versus those who did not (95% CI 0.4 to 0.09, P
<.001). One serving of yogurt every other day had a dif-
ference of 0.26 (95% CI 0.41 to 0.12, P <.001)
compared with none.28 The incidence of gout seems to be
inversely related to the intake of dairy products. The relative
risk in men who took in the highest quintile of dairy
compared with the lowest quintile was 0.56 (95% CI 0.42-
0.74, P <.001).28 A randomized, controlled trial showed
that each type of skim milk studied decreased serum uric
acid by approximately 10% (P <.001).32 Another random-
ized, controlled proof of concept trial compared lactose
1155
powder control, skim milk powder control, and skim milk
enriched with a whey protein, glycomacropeptide, and a fat
extract, G600, that are naturally found in milk.
Glycomacropeptide and G600 were hypothesized to be the
active components of milk that decrease urate levels. There
were significantly fewer gout flares over 3 months in the
glycomacropeptide/G600 skim milk group than in the
lactose powder group; interestingly, there was no difference
between the lactose and skim milk powder control groups,
suggesting these supplemental compounds may actually
reduce gout flares.33 The presumed mechanism behind
decreased urate levels is the uricosuric effect of the protein
in dairy products.3
Coffee/Tea
Coffee may affect serum urate in many ways, but few have
been proven. National Health and Nutrition Examination
Survey data show that serum urate seemed to decrease with
increasing levels of coffee intake. Compared with no coffee
intake, 4-5 cups and 6 cups per day resulted in reductions
of urate of 0.26 mg/dL (95% CI 0.11-0.41 mg/dL) and 0.43
mg/dL (95% CI 0.23-0.65 mg/dL, P <.001), respectively.
Body mass index was similar in all levels of coffee con-
sumption. After adjusting for many variables, including
BMI, higher levels of coffee intake still led to lower SUA
levels. There was a similar inverse relationship between
decaffeinated coffee and urate. Total caffeine levels were
not associated with urate levels, suggesting that something
besides caffeine in coffee is driving this relationship. The
odds ratio for hyperuricemia in those who took in 6 cups
of coffee per day compared with none was 0.57 (95% CI
0.35-0.94, P ¼ .001). Increasing coffee intake decreased the
relative risk for gout in a prospective trial. Relative risk for
0, <1, 1-3, 4-5, and 6 cups of coffee daily were 1, 0.97,
0.92, 0.6 (95% CI 0.41-0.87), and 0.41, respectively (95%
CI 0.46-1.17, P ¼ .002). Again total caffeine consumption
did not affect gout risk.34 Tea has not been shown to affect
serum urate.35
Vitamin C
A randomized control trial supplemented the intervention
arm with 500 mg/d vitamin C for 2 months. At the
completion of the study the vitamin C group had reduced
urate, with a mean change of 0.5 mg/dL (0.6 mg/dL
to 0.3 mg/dL), whereas there was no change in the control
group.36 Later, a prospective trial found that when compared
with men with vitamin C intake <250 mg/dL, men with
intake of 500-999 mg/dL, 1000-1499 mg/dL, and 1500
mg/dL had a relative risk of gout of 0.83 (95% CI 0.71-
0.97), 0.66 (95% CI 0.52-0.86), and 0.55, respectively (95%
CI 0.38-0.80, P <.001).37 An observational study supported
this by showing an inverse relationship between vitamin C
dose and serum urate plateauing at 500 mg/d.38 A recent
meta-analysis of the 13 known randomized, controlled trials
studying the effects of vitamin C on serum urate showed
1156 The American Journal of Medicine, Vol 129, No 11, November 2016

that even though these studies were very heterogenic in

design, there was a significant decrease in urate with vitamin Plenty
Most meals: Whole grains, plant protein, fresh vegetables
C supplementation. The combined effect was reduction 2-3 servings a day: fresh fruits (less sweet when possible)
of 0.35 mg/dL (0.66 mg/dL to 0.03 mg/dL, P ¼ 1-3 servings a day: legumes, nuts

.032).39 In vitro and animal studies show that vitamin C has 1-2 servings a day: low fat dairy

uricosuric effects, decreases urate production, and lowers ModeraƟon (0-3 servings of each daily)
Oily fish (tuna, salmon, trout) , Chicken,
serum urate levels.40 eggs
Rare / Avoid
-Red meat / Shell fish, HFCS, Refined Sugar,
Liquor, Beer
Cherry/Cherry Extract
Small human and animal studies suggest that cherry extract
can decrease serum urate. A recent case-crossover observa-
tional study showed that patients who ingested cherries over
a 2-day hazard period had 35% lower risk of gout flares than
those not taking cherry products. An inverse relationship
between cherry intake and risk for flare was also found for up
to 3 servings (12 whole raw or ½ cup unsweetened canned Figure 2 Gout inverse food pyramid. HFCS ¼ high-
per serving) in 2 days.41 Although these data may suggest a fructose corn syrup.
benefit with cherry intake, there is a paucity of data needed to
make this a strong recommendation to patients. Cherry use
remains an area of potential interest in future studies. levels.20 In the Dietary Approaches to Stop Hypertension
(DASH) trial patients were randomized to 1 of 3 diets:
control, healthy choice weight loss, and the DASH diet.
DIET THERAPY FOR GOUT
Compared with the control group, the DASH diet resulted in
Past guidelines recommended a rigid avoidance of purine-
increased high-density lipoprotein, with decreased tri-
rich foods. Challenges existed with this approach,
glycerides, systolic and diastolic blood pressures, and
including limited food choices and heightened long-term
weight, whereas the healthy choice group only reduced tri-
metabolic risk with increased carbohydrate intake. Our
glycerides, systolic blood pressure, and weight. It appeared
proposed dietary strategy (Figure 1) places less emphasis on
that the addition of fresh fruits and vegetables improved
high purine avoidance while supporting choices that benefit
certain components of metabolic syndrome in addition to
the entire metabolic syndrome. Clinicians should emphasize
weight loss.42 The ATTICA study, a trial in the Grecian
strategies that help increase insulin sensitivity, decrease
Province of Attica, investigated benefits of the Mediterra-
triglycerides, improve blood pressure, and lower the risk
nean diet in non-gout patients. Those with better
for coronary heart disease.9
self-reported compliance had lower serum uric acid levels.
Several specific diet plans have been well documented
Serum urate positively correlated with meat intake, sugar-
with the above approach in mind. In MRFIT compared with
sweetened soft drinks, and legumes, whereas urate was
no weight change, the odds ratio of achieving normal urate
inversely related to fruit and dairy consumption. Adherence
for weight loss of 1-4.9 kg was 1.43 (95% CI 1.33-1.54), for
was inversely related to serum urate, and those with the
5-9.9 kg was 2.17 (95% CI 1.95-2.4), and for 10 kg was
highest level of compliance had a 70% lower chance of
3.9 (95% CI 3.31-4.61) (P <.001). The associated decrease
hyperuricemia than those with the lowest compliance.
in serum urate was 0.12, 0.31, and 0.62 mg/dL,
Weight change according to compliance was not specifically
respectively, suggesting weight loss alone can improve urate
assessed, nor was the effect of weight change on serum urate
levels. Thus, weight loss could be an explanation for the
improved serum urate levels in the ATTICA study.43
Diet Goals for Flares Long Term Diet Principles

• 8-16 cups of water a day • Weight loss and daily exercise

• No Alcohol • Increase plant protein, nuts, GENERAL RECOMMENDATIONS AND CONCLUSION
• Meat < 4-6oz / day fruit, whole grains Although the current teaching is that health care
• Protein from • 1-2 servings low fat dairy daily
• Decrease / eliminate beer,
professionals should concentrate on urate-lowering therapy,
• Low fat dairy
• Tofu liquor and HFCS sweetend diet remains a very important part of gout management.
drinks
• Eggs More importantly than improving the arthritis associated
• Consider Vitamin C 500mg/day
• Nut Buers with gout, diet gives the practitioner the opportunity to
• If drinking coffee, connue up
to 6 cups daily impact patients’ risk for morbidity and mortality from
consequences of metabolic syndrome.
Figure 1 General dietary recommendations for gout pa- Strong evidence supports weight loss through diet as a
tients. HFCS ¼ high-fructose corn syrup. foundation of lifestyle changes needed in gout patients.
Liberal intake of plant proteins, nuts, vegetables, legumes,
Beyl et al Update on Diet in Gout
whole grains, lower-sugar fruits, and plant oils is supported,
and up to 2 servings daily of low-fat dairy products is rec-
ommended (Figure 2). Although fish intake can increase
serum urate, there may be greater overall cardiovascular
benefit from the addition of moderate amounts of cold
water, oily fish such as tuna, salmon, and trout, which are
high in omega-3 fatty acids.9 Eggs and poultry are lower-
risk protein sources when used in moderation. One or less
serving(s) of red meat or shellfish per week may be rec-
ommended. Avoidance of fructose-sweetened food, beer,
liquor, and starchy carbohydrates is highly recommended.
Wine in moderation is acceptable. Up to 6 cups of coffee
daily has been shown beneficial but warn that new initiation
of coffee may exacerbate gout flares.9 Supplementation with
vitamin C may be useful, but a dosing range and long-term
safety recommendations have not been made. Cherry
products may be beneficial, but better data are needed before
making this a recommendation to patients. During an acute
flare it is recommended to increase water intake to at least 8-
16 cups per day and avoid alcohol or meat.
References
1. Eggebeen AT. Gout: an update. Am Fam Physician. 2007;76(6):
801-808.
2. Lee SJ, Terkeltaub RA, Kavanaugh A. Recent developments in diet
and gout. Curr Opin Rheumatol. 2006;18(2):193-198.
3. MacFarlane LA, Kim SC. Gout: a review of nonmodifiable and
modifiable risk factors. Rheum Dis Clin North Am. 2014;40(4):
581-604.
4. Torralba KD, De Jesus E, Rachabattula S. The interplay between diet,
urate transporters and the risk for gout and hyperuricemia: current and
future directions. Int J Rheum Dis. 2012;15(6):499-506.
5. Roddy E, Choi HK. Epidemiology of gout. Rheum Dis Clin North Am.
2014;40(2):155-175.
6. Arromdee E, Michet CJ, Crowson CS, O’Fallon WM, Gabriel SE.
Epidemiology of gout: is the incidence rising? J Rheumatol.
2002;29(11):2403-2406.
7. Winnard D, Wright C, Taylor WJ, et al. National prevalence of gout
derived from administrative health data in Aotearoa New Zealand.
Rheumatology (Oxford). 2012;51(5):901-909.
8. Holland R, McGill NW. Comprehensive dietary education in treated
gout patients does not further improve serum urate. Intern Med J.
2015;45(2):189-194.
9. Choi HK. A prescription for lifestyle change in patients with hyper-
uricemia and gout. Curr Opin Rheumatol. 2010;22(2):165-172.
10. Fam AG. Gout, diet, and the insulin resistance syndrome. J Rheumatol.
2002;29(7):1350-1355.
11. Choi HK, Ford ES, Li C, Curhan G. Prevalence of the metabolic
syndrome in patients with gout: the Third National Health and Nutri-
tion Examination Survey. Arthritis Rheum. 2007;57(1):109-115.
12. Volterrani M, Iellamo F, Sposato B, Romeo F. Uric acid lowering
therapy in cardiovascular diseases. Int J Cardiol. 2016;213:20-22.
13. Feig DI, Soletsky B, Johnson RJ. Effect of allopurinol on blood
pressure of adolescents with newly diagnosed essential hypertension: a
randomized trial. JAMA. 2008;300(8):924-932.
14. Soletsky B, Feig DI. Uric acid reduction rectifies prehypertension in
obese adolescents. Hypertension. 2012;60(5):1148-1156.
15. Choi HK, De Vera MA, Krishnan E. Gout and the risk of type 2
diabetes among men with a high cardiovascular risk profile. Rheuma-
tology (Oxford). 2008;47(10):1567-1570.
16. Choi HK, Curhan G. Independent impact of gout on mortality and risk
for coronary heart disease. Circulation. 2007;116(8):894-900.
1157
17. Williams PT. Effects of diet, physical activity and performance, and
body weight on incident gout in ostensibly healthy, vigorously active
men. Am J Clin Nutr. 2008;87(5):1480-1487.
18. Choi HK, Atkinson K, Karlson EW, Curhan G. Obesity, weight
change, hypertension, diuretic use, and risk of gout in men: the health
professionals follow-up study. Arch Intern Med. 2005;165(7):742-748.
19. Dessein PH, Shipton EA, Stanwix AE, Joffe BI, Ramokgadi J. Bene-
ficial effects of weight loss associated with moderate calorie/carbohy-
drate 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(7):539-543.
20. Zhu Y, Zhang Y, Choi HK. The serum urate-lowering impact of weight
loss among men with a high cardiovascular risk profile: the Multiple
Risk Factor Intervention Trial. Rheumatology (Oxford). 2010;49(12):
2391-2399.
21. 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(6):1023-1029.
22. Gaffo AL, Roseman JM, Jacobs DR Jr, et al. Serum urate and its
relationship with alcoholic beverage intake in men and women: find-
ings from the Coronary Artery Risk Development in Young Adults
(CARDIA) cohort. Ann Rheum Dis. 2010;69(11):1965-1970.
23. 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(9417):1277-1281.
24. Faller J, Fox IH. Ethanol-induced hyperuricemia: evidence for
increased urate production by activation of adenine nucleotide turn-
over. N Engl J Med. 1982;307(26):1598-1602.
25. Faller J, Fox IH. Ethanol induced alterations of uric acid metabolism.
Adv Exp Med Biol. 1984;165 Pt A:457-462.
26. Gibson T, Rodgers AV, Simmonds HA, Toseland P. Beer drinking and
its effect on uric acid. Br J Rheumatol. 1984;23(3):203-209.
27. Yamamoto T, Moriwaki Y, Takahashi S, et al. Effect of beer on the
plasma concentrations of uridine and purine bases. Metabolism.
2002;51(10):1317-1323.
28. 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(1):283-289.
29. 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(11):1093-1103.
30. 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(1):109-116.
31. Choi HK, Willett W, Curhan G. Fructose-rich beverages and risk of
gout in women. JAMA. 2010;304(20):2270-2278.
32. Dalbeth N, Wong S, Gamble GD, et al. Acute effect of milk on serum
urate concentrations: a randomised controlled crossover trial. Ann
Rheum Dis. 2010;69(9):1677-1682.
33. Dalbeth N, Ames R, Gamble GD, et al. Effects of skim milk powder
enriched with glycomacropeptide and G600 milk fat extract on fre-
quency of gout flares: a proof-of-concept randomised controlled trial.
Ann Rheum Dis. 2012;71(6):929-934.
34. Choi HK, Willett W, Curhan G. Coffee consumption and risk of incident
gout in men: a prospective study. Arthritis Rheum. 2007;56(6):2049-2055.
35. 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(5):816-821.
36. Huang HY, Appel LJ, Choi MJ, et al. The effects of vitamin C sup-
plementation on serum concentrations of uric acid: results of a ran-
domized controlled trial. Arthritis Rheum. 2005;52(6):1843-1847.
37. Choi HK, Gao X, Curhan G. Vitamin C intake and the risk of gout in
men: a prospective study. Arch Intern Med. 2009;169(5):502-507.
38. Gao X, Curhan G, Forman JP, Ascherio A, Choi HK. Vitamin C intake and
serum uric acid concentration in men. J Rheumatol. 2008;35(9):1853-1858.
39. Juraschek SP, Miller ER 3rd, Gelber AC. Effect of oral vitamin C
supplementation on serum uric acid: a meta-analysis of randomized
1158 The American Journal of Medicine, Vol 129, No 11, November 2016

controlled trials. Arthritis Care Res (Hoboken). 2011;63(9):
1295-1306.
40. Holick M, Shils M, Shike M, Ross A, Caballero B, Cousins R. Modern
nutrition in health and disease. OJME 10th edition, 2006:329-345.
41. Zhang Y, Neogi T, Chen C, Chaisson C, Hunter DJ, Choi HK. Cherry
consumption and decreased risk of recurrent gout attacks. Arthritis
Rheum. 2012;64(12):4004-4011.
42. Azadbakht L, Mirmiran P, Esmaillzadeh A, Azizi T, Azizi F. Beneficial
effects of a Dietary Approaches to Stop Hypertension eating plan on
features of the metabolic syndrome. Diabetes Care. 2005;28(12):
2823-2831.
43. Kontogianni MD, Chrysohoou C, Panagiotakos DB, et al. Adherence
to the Mediterranean diet and serum uric acid: the ATTICA study.
Scand J Rheumatol. 2012;41(6):442-449.