A case-control study of the association of diet and obesity with
gout in Taiwan13
Li-Ching Lyu, Chi-Yin Hsu, Ching-Ying Yeh, Meei-Shyuan Lee, Su-Hua Huang, and Ching-Lan Chen
ABSTRACT
Background: Gout has been a significant metabolic disorder for
Chinese men in Taiwan; however, there is insufficient information
on diet and lifestyle risk factors in this population.
Objective: The purpose of this case-control study was to explore
potential dietary and lifestyle risk factors associated with gout in
Chinese men.
Design: Between 1998 and 1999, we recruited and conducted
face-to-face interviews with patients from outpatient clinics in
Taipei who had incident gout (n = 92) and with their healthy
coworkers (controls; n = 92).
Results: Systolic blood pressure, diastolic blood pressure, waist-
to-hip ratio, waist-to-height ratio, and body mass index were signi-
ficantly higher in cases than in controls. Family histories of gout
and diabetes mellitus were strong risk factors for gout. Frequen-
cies of vegetable and fruit consumption were significantly lower
in cases than in controls. Logistic regression analyses showed that
high alcohol intake and low intakes of fiber, folate, and vitamin C
increased the risk of gout, but no association was found with
purine intake. After covariates were controlled for, the adjusted
odds ratios for the middle and highest tertiles of waist-to-height
ratio (0.500.54 and 0.55, respectively) were 3.89 (95% CI: 1.32,
11.46) and 4.37 (1.18, 16.22), respectively, but no linear associa-
tion was found for waist-to-hip ratio and waist circumference.
Conclusions: Consumption of alcohol, but not of purine, may be
a significant dietary risk factor for gout. Food sources rich in
dietary fiber, folate, and vitamin C, such as fruit and vegetables,
protect against gout. Waist-to-height ratio, which indicates central
obesity, has a significant linear effect on gout occurrence, inde-
pendent of body mass index. Am J Clin Nutr 2003;78:690701.
KEY WORDS Gout, case-control study, diet, obesity, waist-
to-height ratio, Taiwan
INTRODUCTION
Gout is a metabolic disorder associated with altered uric acid
metabolism and hyperuricemia. Various epidemiologic studies
have reported effects of modernization and affluence on lifestyle,
which have led to hyperuricemia and an increased prevalence of
gouty arthritis in Asian populations (110). In Taiwan, a high
prevalence of hyperuricemia and gout was observed. In a national
survey from 1986 to 1989, Chou et al (2) reported a prevalence
rate of gout of 0.5%. Moreover, the National Nutrition and Health
Survey (19931996) showed that 22% of men (blood uric acid
concentration > 7.7 mg/dL) and 23% of women (blood uric acid
690 Am J Clin Nutr 2003;78:690701. Printed in USA. 2003 American Society for Clinical Nutrition
concentration > 6.6 mg/dL) in Taiwan who were > 45 y old had
hyperuricemia (3).
Until now, most of these studies were conducted to identify risk
factors for hyperuricemia, including ethnic (46), enzymatic
(1113), and environmental predispositions (1417). Among
acquired factors, reversible lifestyle factors contributed to
Downloaded from ajcn.nutrition.org by guest on August 28, 2015
increased blood uric acid concentrations. These factors were sug-
gested to be a high-purine diet, alcohol consumption, and obesity
(18, 19). However, no case-control studies have examined factors
that are important to the etiology of gout. Thus, this age-matched
case-control study was conducted to explore potential risk factors
and protective lifestyle factors for gout in a Chinese population.
Our primary objectives were to answer the following questions.
First, are purine and alcohol consumption risk factors for gout?
Second, is the pattern of body adiposity a risk factor for gout that
is independent of general obesity?
SUBJECTS AND METHODS
Study subjects
From July 1988 to August 1989, we contacted 236 male
patients who visited the outpatient clinic at the Taipei Municipal
Ho-Ping Hospital mainly for bone and joint problems and were
willing to participate in future in-person lifestyle interviews. Ini-
tial criteria for eligible cases and controls were as follows: Han
ethnicity, age 2070 y, generally good health with no regular
use of medications such as diuretics and aspirin, no change in
diet in the past year, and residency in Taipei city or county in a
household with a full-time worker who had an available home
address and a contact telephone number. We used the diagnos-
tic criteria for gout of Wallace et al (20) and Hart and Fry (21),
1
From the Graduate Program of Nutrition, National Taiwan Normal Uni-
versity, Taipei, Taiwan (L-CL, C-YH, and S-HH); the School of Public Health,
Taipei Medical University, Taipei, Taiwan (C-YY); the School of Public Health,
National Defense Medical College, Taipei, Taiwan (M-SL); and the Clinic of
Gout, Taipei Municipal Ho-Ping Hospital, Taipei, Taiwan (C-LC).
2
Supported by the National Science Council, Taiwan, Republic of China
(grant NSC 88-2314-B-003-001).
3
Address reprint requests to L-C Lyu, Department of Human Development
and Family Studies, National Taiwan Normal University, #162 Section 1, Hop-
ing East Road, Taipei, Taiwan 10610, Republic of China. E-mail: t10010@
cc.ntnu.edu.tw.
Received July 30, 2002.
Accepted for publication April 21, 2003.
 CASE-CONTROL STUDY OF GOUT IN TAIWAN
which follow the guidelines recommended by the American Col-
lege of Rheumatology. A total of 95 episodic cases of diagnosed
gout and 53 nongout controls (as hospital controls) were later
identified and enrolled in the study by C-LC. We also contacted
office coworkers of gout patients and recruited 46 healthy subjects
without gout who were within a 5-y age range (as friend controls)
(22). The 2 groups of controls did not differ from each other in
age range and dietary intake distributions. Three cases and 7 con-
trols did not complete the interviews, and thus the final analyses
consisted of 184 subjects (92 cases and 92 controls). All subjects
signed an informed consent form in accord with the Helsinki Dec-
laration of 1975 as revised in 1983.
Diet history and lifestyle interview
The diet history questionnaire consisted of questions on dietary
habits, one 24-h recall, and a total-diet Chinese food-frequency
questionnaire consisting of questions arranged by meal sequence
on the intake of 493 items during the previous year. A test of rel-
ative validity showed strong correlations of macro- and micronu-
trient intakes with 7-d records (r = 0.38, P < 0.05), and repro-
ducibility was consistently high for most nutrients, with Spearman
correlation coefficients between 0.42 for vitamin A and 0.79 for
vitamin B-12. When we designed this Chinese food-frequency
questionnaire, we took particular care to include all foods high in
purines so that our primary research hypotheses could be ade-
quately tested. To collect more specific information on dietary pat-
terns, this questionnaire was supplemented with questions on fam-
ily and individual eating habits. Lifestyle questions, including
questions on drinking, smoking, and betel nut chewing, and ques-
tions on the use of dietary supplements were also asked during the
interview. Abstention from drinking was defined as having < 1
alcoholic drink/mo. Visual aids for showing 3 portion sizes were
developed to facilitate accuracy in reporting long-term dietary
intakes on the food-frequency questionnaire and actual intakes on
the 24-h recall. A similar methodology was used by Lyu et al (23).
Intakes of total fat; animal and plant protein; dietary purine
(2426); cholesterol; fat-soluble vitamins such as vitamins A, D,
and E; dietary fiber; and water-soluble vitamins including thiamin,
riboflavin, niacin, vitamin C, and folate were assessed in this
study. The completeness rates of selective nutrient databases were
75% for folate, 85% for purine, 94% for vitamin C, 97% for
dietary fiber, and 98% for alcohol.
Physical activity level was assessed with the use of structured
questionnaires on the basis of 3 categories (work, leisure time, and
house work). The duration and intensity of physical activity were
considered in evaluating overall physical activity levels (27).
Three types of anthropometric measurements were included in this
study: body size (height and weight), body girth (waist and hip),
and body skinfold thicknesses (triceps). In addition, information
on personal medical history, medication use, and medical history
of first-degree relatives (parents and siblings) were collected in
the in-person interviews. Most of the subjects who were inter-
viewed took 1.52.5 h to complete the interview.
Statistical analysis
We performed all univariate and multivariate analyses by
using SAS, version 6.12 (SAS Institute Inc, Cary, NC). For uni-
variate analysis, comparisons between means were made with
the use of Students t test, and comparisons between values for
categorical variables were made with the use of the chi-square
test. Average daily nutrient intakes were calculated from the
691
total-diet food-frequency questionnaire and were expressed as
nutrient density [amount per 1000 calories (4.185 MJ)] in the
analyses. Moreover, nutrient intakes from 24-h recalls were also
used for verification of possible dietary associations; however,
alcohol intake was not used because of the limited amounts con-
sumed in the short time period. Dietary variables in the analyses
included protein, animal protein, plant protein, fat, animal fat,
plant fat, carbohydrates, dietary fiber, soluble fiber, insoluble
fiber, sodium, phosphorus, calcium, iron, -carotene, -carotene,
retinal, total vitamin A, vitamin E, thiamin, riboflavin, niacin, vita-
min B-6, vitamin B-12, vitamin C, folate, saturated fat, monoun-
saturated fat, polyunsaturated fat, cholesterol, and purine. Nutri-
ent intakes were categorized into upper, middle, and lower thirds
of the range for all subjects including cases and controls. Spear-
man correlation coefficients were calculated between anthropo-
metric measures and dietary variables. Potential confounding fac-
tors were identified and adjusted for in multivariate analyses.
Adjustment variables included age and educational level as con-
tinuous variables. The unconditional logistic regression model
produced odds ratios and 95% CIs, and all results, including
trends, were considered significant if P < 0.05.
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RESULTS
The basic characteristics of the 92 cases and the 92 controls are
shown in Table 1. There was no significant difference in age distri-
bution between the cases and the controls. The educational level of
the controls was significantly higher than that of the cases. Even
though triceps skinfold thicknesses were not significantly different
between the cases and the controls, the cases had significantly higher
body mass index (BMI), waist circumference, hip circumference,
waist-to-hip ratio, and waist-to-height ratio than did the controls. Rel-
ative to the respective lowest tertile, the odds ratio for the highest
tertile was 2.62 for BMI (95% CI: 1.26, 5.42), 3.21 for waist circum-
ference (95% CI: 1.53, 6.73), and 2.54 for hip circumference (95%
CI: 1.23, 5.28); all had significant trends (P < 0.05). However, the
trend for waist-to-hip ratio was not linear: relative to the lowest tertile,
the odds ratio for the middle tertile was 3.10 (95% CI: 1.47, 6.58),
whereas the odds ratio for the upper tertile was 2.13 (95% CI: 1.05,
4.31). The trend for waist-to-height ratio was linear, with odds ratios
of 2.87 (95% CI: 1.37, 6.00) and 3.65 (95% CI: 1.73, 7.73) for the
middle and upper tertiles relative to the lower tertile. Both systolic
and diastolic blood pressures were significant risk factors for gout.
Lifestyle factors, such as smoking history, abstention from drinking,
and vegetarian status, were not significantly different between the
cases and the controls, although the number of vegetarians was too
small to draw a firm conclusion.
The medical histories of the subjects and their first-degree fam-
ily members (parents and siblings) are shown in Table 2. There
were no significant differences between the cases and the controls
in the numbers having diabetes, hypertension, hyperlipidemia,
liver disease, renal disease, lung disease, and other arthritis. How-
ever, the number of subjects who had a family history of diabetes
or gout was significantly higher among the cases than among the
controls (P < 0.05). Therefore, family histories of diabetes and
gout are suggestive potential risk factors for gout. Regarding
energy expenditure assessments, overall physical activity levels
were not significantly different between the cases and the controls
(data not shown).
Associations between the risk of gout and nutrient intakes from
a Chinese food-frequency questionnaire and a 24-h recall are shown
692 LYU ET AL

TABLE 1 TABLE 1 (Continued)

Basic characteristics of the cases and the controls1
Cases Controls P for
Cases Controls P for (n = 92) (n = 92) OR (95%CI) trend
(n = 92) (n = 92) OR (95% CI) trend n n
n n Drinker
Yes 59 48
Age (y)
No 33 44 1.56 (0.87, 2.82)
< 36 33 28
Alcohol type
3645 29 32 0.77 (0.38, 1.57)
Beer 22 31
46 30 32 0.80 (0.39, 1.62) 0.53
Wine 11 5 3.07 (1.39, 6.78)
Education
Liquor 26 12 1.06 (0.52, 2.15) 0.86
High school 27 11
Poultry skin eaten
College 26 20 0.53 (0.21, 1.32)
Always 17 14
Graduate school 39 61 0.26 (0.12, 0.58) < 0.01
Occasionally 15 16 0.89 (0.34, 2.33)
Height (cm)
Never 60 62 0.94 (0.44, 2.01) 0.93
< 165 32 21
Fish skin eaten
165169 31 30 0.68 (0.32, 1.43)
Always 6 15
170 29 41 0.46 (0.22, 0.96) 0.04
Occasionally 9 14 1.65 (0.49, 5.54)
Weight (kg)
Never 77 63 3.26 (1.28, 8.31) < 0.01
< 64 23 31
1
6474 31 35 1.23 (0.60, 2.54) OR, odds ratio.
75 38 26 2.12 (1.01, 4.42) 0.04

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Triceps skinfold thickness
(mm)
in Tables 3 and 4, respectively. As shown in Table 3, dietary fiber,
< 16 25 34 soluble fiber, vitamin C, and folate were protective dietary factors
1621 32 31 1.40 (0.69, 2.87) against gout, and alcohol was a risk factor. Relative to the respec-
22 35 27 1.76 (0.86, 3.62) 0.12 tive lowest intake tertile, the odds ratios for the highest tertile were
BMI (kg/m2) 3.27 for alcohol, 0.38 for dietary fiber, 0.44 for soluble fiber, 0.31
< 23.24 24 37 for vitamin C, and 0.33 for folate. Moreover, the intakes of dietary
23.2426.48 30 31 1.58 (0.77, 3.27) fiber, iron, vitamin A, riboflavin, and folate calculated from the 24-h
26.49 38 24 2.62 (1.26, 5.42) < 0.01 recall showed protective effects against gout (Table 4). From both
Waist circumference (cm) dietary assessment methods, consumption of dietary fiber and
< 84 18 41 folate seemed to be consistent protective factors against gout.
8490 36 24 3.42 (1.60, 7.29)
Average nutrient intakes calculated by using the 24-h recall
91 38 27 3.21 (1.53, 6.73) < 0.01
Hip circumference (cm)
method did not differ significantly between the cases and the con-
< 95 24 36 trols, except for the intakes of dietary fiber, folate, calcium, and
95100 29 33 1.32 (0.64, 2.70) iron, which were significantly (P < 0.05) higher in the controls
101 39 23 2.54 (1.23, 5.28) 0.01 than in the cases (Table 4). In the controls, the average daily
Waist-to-hip ratio energy intake was 2305 kcal (9.653 MJ), and the average
< 0.87 20 41 macronutrient energy distribution was as follows: 14% of total
0.870.91 40 21 3.10 (1.47, 6.58) energy from protein, 33% from fat, and 51% from carbohydrates.
0.92 32 30 2.13 (1.05, 4.31) 0.04 Average daily purine intakes did not differ significantly between
Waist-to-height ratio the 2 groups, with a mean ( SD) of 374 208 mg for the cases
< 0.5 19 42
and of 378 221 mg for the controls. Monthly frequencies of
0.50.54 35 27 2.87 (1.37, 6.00)
selected dietary habits pertaining to gout among the cases and the
0.55 38 23 3.65 (1.73, 7.73) < 0.01
Systolic blood pressure controls are shown in Table 5. Vegetable and fruit consumption
(mm Hg) was significantly higher in the controls than in the cases, although
< 121.5 23 37 the frequency of social dining was significantly lower in the con-
121.5131 28 33 1.37 (0.66, 2.82) trols (P < 0.05). The frequency of consumption of foods with a
132 41 22 3.00 (1.44, 6.25) < 0.01 high purine content, such as seafood and organ meat, did not dif-
Diastolic blood pressure fer significantly between the cases and the controls.
(mm Hg) Six multivariable models of gout occurrence consisting of vari-
< 78.5 23 37 ables for family history, obesity, and dietary factors after adjust-
78.587 31 30 1.66 (0.81, 3.43)
ment for age and education level are shown in Table 6. Consis-
88 38 25 2.45 (1.18, 5.05) 0.02
tently, the risk of gout among the subjects with family histories of
Smoking history
No smoking 41 46 diabetes or gout was > 3-fold (odds ratio: 3.554.17) and > 6-fold
15 y 9 8 1.26 (0.45, 3.58) (odds ratio: 6.959.54), respectively, that of the subjects without
610 y 13 10 1.46 (0.58, 3.68) such family histories. Obesity indexes including BMI, triceps
> 10 y 29 28 1.16 (0.60, 2.27) 0.58 skinfold thickness, waist circumference, hip circumference, waist-
Vegetarian to-hip ratio, and waist-to-height ratio were highly correlated, and
No 85 83 the central obesity index, the waist-to-height ratio (model 4),
Yes 7 9 0.76 (0.27, 2.13) seemed to have more stable effects on gout than did general obe-
(Continued) sity (trend P < 0.05). After adjustment for the general obesity
 CASE-CONTROL STUDY OF GOUT IN TAIWAN 693

TABLE 2 TABLE 3
Personal medical histories of the cases and the controls and medical Associations of nutrient densities from a Chinese food-frequency
histories of their first-degree family members1 questionnaire with the risk of gout1
Cases Controls Cases Controls P for
(n = 92) (n = 92) OR (95% CI) (n = 92) (n = 92) OR (95% CI) trend
Personal n n n n
Diabetes
Protein (g)
Yes 0 0
No 92 92 < 38.20 30 31
Hypertension 38.2044.35 32 29 1.14 (0.56, 2.32)
Yes 9 12 44.36 30 32 0.97 (0.48, 1.97) 0.93
No 83 80 0.72 (0.29, 1.81) Animal protein (g)
Hyperlipidemia < 23.56 31 30
Yes 12 8 23.5630.33 27 34 0.77 (0.38, 1.57)
No 80 84 1.58 (0.61, 4.05) 30.34 34 28 1.18 (0.58, 2.39) 0.65
Liver disease Plant protein (g)
Yes 11 10 < 12.74 33 28
No 81 82 1.11 (0.45, 2.77) 12.7415.53 31 30 0.88 (0.43, 1.79)
Renal disease 15.54 28 34 0.70 (0.34, 1.42) 0.32
Yes 7 3 Fat (g)
No 85 89 2.44 (0.61, 9.76) < 35.74 33 28
Lung disease 35.7442.63 24 37 0.55 (0.27, 1.13)

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Yes 2 2 42.64 35 27 1.10 (0.54, 2.24) 0.79
No 90 90 1.00 (0.14, 7.25) Animal fat (g)
Other arthritis < 13.25 33 28
Yes 2 2 13.2517.88 29 32 0.77 (0.38, 1.57)
No 90 90 1.00 (0.06, 16.23) 17.89 30 32 0.80 (0.39, 1.62) 0.53
Family Plant fat (g)
Diabetes
< 20.06 31 30
Yes 31 14
2 20.0625.43 28 33 0.82 (0.40, 1.67)
No 61 78 2.83 (1.39, 5.79)
25.44 33 29 1.10 (0.54, 2.24) 0.79
Hypertension
Carbohydrate (g)
Yes 32 33
< 110.87 31 30
No 60 59 0.95 (0.52, 1.75)
Hyperlipidemia 110.87128.13 30 31 0.94 (0.46, 1.91)
Yes 9 7 128.74 31 31 0.97 (0.48, 1.96) 0.93
No 83 85 1.32 (0.47, 3.70) Dietary fiber (g)
Liver disease < 6.16 39 22
Yes 4 5 6.167.94 28 33 0.48 (0.23, 0.99)
No 88 87 0.79 (0.21, 3.04) 7.95 25 37 0.38 (0.18, 0.79) < 0.01
Renal disease Soluble fiber (g)
Yes 8 7 < 0.90 37 24
No 84 85 1.16 (0.40, 3.33) 0.901.31 30 31 0.63 (0.31, 1.29)
Lung disease 1.32 25 37 0.44 (0.21, 0.90) 0.03
Yes 3 0 Insoluble fiber (g)
No 89 92 0.16 (0.12, 3.27) < 1.45 35 26
Gout 1.452.02 29 32 0.67 (0.33, 1.38)
Yes 24 6 2.03 28 34 0.61 (0.30, 1.25) 0.18
No 68 86 5.06 (1.96, 13.07)2 Sodium (mg)
Other arthritis < 5106.13 29 32
Yes 3 4 5106.136742.83 32 29 1.22 (0.60, 2.48)
No 89 88 0.74 (0.16, 3.41) 6742.84 31 31 1.10 (0.54, 2.24) 0.79
1 Phosphorous (mg)
OR, odds ratio.
2
P < 0.05 (Wald chi-square test). < 992.74 32 29
992.741218.07 32 29 1.00 (0.49, 2.04)
1218.08 28 34 0.75 (0.37, 1.52) 0.42
index (BMI) and alcohol intake, we found that the adjusted odds Calcium (mg)
ratios for the middle (0.500.54) and highest ( 0.55) tertiles of < 181.66 34 27
waist-to-height ratio were 3.89 (95% CI: 1.32, 11.46) and 4.37 181.66237.19 30 31 0.77 (0.38, 1.57)
(95% CI: 1.18, 16.22), respectively, but no linear association was 237.20 28 34 0.65 (0.32, 1.33) 0.24
found for waist-to-hip ratio and waist circumference. Model 4 Iron (mg)
explained 25.8% of variability with 80.8% concordance. < 5.86 32 29
Because of the high correlations between the intakes of dietary 5.867.33 32 29 1.00 (0.49, 2.04)
fiber, vitamin C, and folate (r = 0.67 for dietary fiber and vitamin C, 7.34 28 34 0.75 (0.37, 1.52) 0.42
r = 0.57 for dietary fiber and folate, r = 0.64 for vitamin C and (Continued)
694 LYU ET AL

TABLE 3 (Continued) TABLE 3 (Continued)

Cases Controls P for Cases Controls P for
(n = 92) (n = 92) OR (95% CI) trend (n = 92) (n = 92) OR (95% CI) trend
n n n n
-Carotene (g) Cholesterol (mg)
< 77.92 29 32 < 179.81 29 32
77.92171.53 31 30 1.14 (0.56, 2.32) 179.81232.71 33 28 1.30 (0.64, 2.65)
171.54 32 30 1.18 (0.58, 2.39) 0.65 232.72 30 32 1.03 (0.51, 2.10) 0.93
-Carotene (g) Alcohol (g)
< 1239.62 36 25 0.00 36 46
1239.621882.39 26 35 0.52 (0.25, 1.06) 0.012.99 33 37 1.14 (0.60, 2.16)
1882.40 30 32 0.65 (0.32, 1.33) 0.24 3.00 23 9 3.27 (1.35, 7.92) 0.02
Retinol (g) Purine (mg)
< 70.85 34 27 < 227.75 29 32
70.85137.03 26 35 0.59 (0.29, 1.21) 227.75297.86 34 27 1.39 (0.68, 2.83)
137.04 32 30 0.85 (0.42, 1.72) 0.65 297.87 29 33 0.97 (0.48, 1.97) 0.93
Vitamin A (g RE) 1
All nutrient intake amounts are per 1000 kcal. OR, odds ratio; RE,
< 355.96 30 31 retinol equivalents.
355.96527.21 27 34 0.82 (0.40, 1.67)
527.22 35 27 1.34 (0.66, 2.72) 0.42
Vitamin E (mg) folate, P < 0.01), we decided to put dietary fiber in model 5 and
< 12.25 28 33 folate in model 6. From model 5, the protective effect from dietary

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12.2516.29 29 32 1.07 (0.52, 2.18) fiber was borderline (P for trend = 0.09) after adjustment for
16.30 35 27 1.53 (0.75, 3.11) 0.24 covariates. Because intakes of dietary fiber and alcohol were cor-
Thiamine (mg) related (r = 0.21, P < 0.01), when we removed alcohol from the
< 0.44 33 28 model, dietary fiber showed a protective effect (P for trend = 0.05),
0.440.60 28 33 0.72 (0.35, 1.47) with odds ratios of 0.43 (95% CI: 0.17, 1.08) and 0.41 (95% CI:
0.61 31 31 0.85 (0.42, 1.72) 0.65
0.17, 1.00) for the middle and upper tertiles, respectively (data not
Riboflavin (mg)
shown). In model 6, folate intake also showed a protective effect
< 0.51 32 29
0.510.64 30 31 0.88 (0.43, 1.78) against gout, with adjusted odds ratios of 0.30 (95% CI: 0.12,
0.65 30 32 0.85 (0.42, 1.72) 0.65 0.77) and 0.37 (95% CI: 0.15, 0.92) for the middle and upper ter-
Niacin (mg) tiles, respectively. This model explained 28.8% of variability with
< 8.00 35 26 82.8% concordance. The nonsignificant results for alcohol from
8.0010.22 28 33 0.63 (0.31, 1.29) multivariate analyses could be explained on the basis that alcohol
10.23 29 33 0.65 (0.32, 1.33) 0.24 intake was significantly correlated with education level in this
Vitamin B-6 (g) population (r = 0.20, P < 0.01). When we removed education
< 386.13 32 29 level from the models, alcohol intake showed significant odds
386.13522.84 33 28 1.07 (0.52, 2.18) ratios in the upper tertiles (95% CI: 1.13, 7.62) for models 14
522.85 27 35 0.70 (0.34, 1.42) 0.32
(P for trend = 0.020.03); the attenuation of effects by adjustment
Vitamin B-12 (g)
for education level was also shown for dietary fiber in model 5
< 3.92 30 31
3.929.12 30 31 1.00 (0.49, 2.03)
(P for trend = 0.03) and weight-to-height ratio (P for trend = 0.02)
9.13 32 30 1.10 (0.54, 2.24) 0.79 and folate (P for trend = 0.01) in model 6 when education level
Vitamin C (mg) was removed from the models (data not shown). The consistently
< 52.23 39 22 higher odds ratios in a dose-response fashion and the significant
52.2377.54 31 30 0.58 (0.28, 1.20) trends without adjustment for education level in the models sug-
77.55 22 40 0.31 (0.15, 0.65) < 0.01 gested that alcohol was a risk factor for gout and that dietary fiber
Folate (g) and folate were protective factors against gout.
< 51.53 42 19
51.5362.47 24 37 0.29 (0.14, 0.62)
62.48 26 36 0.33 (0.16, 0.69) < 0.01 DISCUSSION
Saturated fat (g)
The objective of this case-control study was to determine
< 9.16 33 28
whether dietary intakes and related lifestyle factors are associated
9.1610.99 26 35 0.63 (0.31, 1.29)
> 10.99 33 29 0.97 (0.48, 1.96) 0.93 with the development of gout. Although the medical community
Monounsaturated fat (g) generally agrees that gout prevention can be achieved through
< 11.07 32 29 lifestyle changes including weight loss, restricting protein and
11.0713.62 27 34 0.72 (0.35, 1.47) calorie intake, limiting alcohol consumption, and avoiding the use
> 13.62 33 29 1.03 (0.51, 2.09) 0.93 of diuretics (18, 19, 28), supporting quantitative data are not avail-
Polyunsaturated fat (g) able from any dietary case-control studies. Our study was the first
< 14.42 28 33 to identify potential dietary factors affecting gout occurrence in a
14.4217.41 32 29 1.30 (0.64, 2.65) Chinese sample, and surprisingly, we did not find that the intakes
> 17.41 32 30 1.26 (0.62, 2.55) 0.53 of fat, total protein, animal protein, and purine are related to gout
(Continued) occurrences, as we had previously assumed.
 CASE-CONTROL STUDY OF GOUT IN TAIWAN 695

TABLE 4
Associations of nutrient intakes from a 24-h recall with the risk of gout1
Cases (n = 92) Controls (n = 92) OR (95% CI) P for trend
Energy
x SD (kcal) 2327 636 2305 618
Tertile (n)
< 2018.50 kcal 31 30
2018.502502.69 kcal 29 32 0.88 (0.43, 1.78)
2502.70 kcal 32 30 1.03 (0.51, 2.09) 0.93
Protein
x SD (% of energy) 13 3 14 4
Tertile (n)
< 11.90% of energy 34 27
11.9014.80% of energy 33 28 0.94 (0.46, 1.91)
14.81% of energy 25 37 0.54 (0.26, 1.10) 0.09
Protein
x SD (g) 76 27 80 27
Tertile (n)
< 65.48 g 30 31
65.4885.52 g 31 30 1.07 (0.53, 2.17)
85.53 g 31 31 1.03 (0.51, 2.10) 0.93

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Animal protein
x SD (g) 44 25 44 23
Tertile (n)
< 31.46 g 32 29
31.4653.59 g 27 34 0.72 (0.35, 1.47)
53.60 g 33 29 1.03 (0.51, 2.09) 0.93
Plant protein
x SD (g) 31 12 35 16
Tertile (n)
< 27.01 g 35 26
27.0136.93 g 31 30 0.77 (0.38, 1.57)
36.94 g 26 36 0.54 (0.26, 1.10) 0.09
Fat
x SD (% of energy) 33 11 33 10
Tertile (n)
< 29.72% of energy 31 30
29.7236.98% of energy 29 32 0.88 (0.43, 1.78)
> 36.98% of energy 32 30 1.03 (0.51, 2.09) 0.93
Fat
x SD (g) 86 37 84 35
Tertile (n)
< 66.64 g 27 34
66.6495.08 g 34 27 1.59 (0.78, 3.24)
95.09 g 31 31 1.26 (0.62, 2.56) 0.53
Animal fat
x SD (g) 39 32 36 26
Tertile (n)
< 22.44 g 31 30
22.4442.57 g 25 36 0.67 (0.33, 1.38)
42.58 g 36 26 1.34 (0.66, 2.73) 0.42
Plant fat
x SD (g) 46 19 48 22
Tertile (n)
< 38.28 g 31 30
38.2854.84 g 30 31 0.94 (0.46, 1.91)
54.85 g 31 31 0.97 (0.48, 1.96) 0.93
Carbohydrate
x SD (%) 50 12 51 10
Tertile (n)
< 46.94% of energy 29 32
46.9454.39% of energy 36 25 1.59 (0.78, 3.25)
54.40% of energy 27 35 0.85 (0.42, 1.73) 0.65
(Continued)
696 LYU ET AL

TABLE 4 (Continued)
Cases (n = 92) Controls (n = 92) OR (95% CI) P for trend

Carbohydrate
x SD (g) 291 99 290 91
Tertile (n)
< 251.20 g 31 30
251.20317.66 g 27 34 0.77 (0.38, 1.57)
317.67 g 34 28 1.18 (0.58, 2.39) 0.65
Dietary fiber
x SD (g) 13 62 15 7
Tertile (n)
< 11.09 g 38 23
11.0915.93 g 30 31 0.59 (0.29, 1.21)
15.94 g 24 38 0.38 (0.19, 0.79) 0.01
Soluble fiber
x SD (g) 22 22
Tertile (n)
< 1.03 g 33 28
1.032.31 g 30 31 0.82 (0.40, 1.67)
2.32 g 29 33 0.75 (0.37, 1.52) 0.42

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Insoluble fiber
x SD (g) 32 43
Tertile (n)
< 1.85 g 33 28
1.853.99 g 31 30 0.88 (0.43, 1.79)
4.00 g 28 34 0.70 (0.34, 1.42) 0.32
Sodium
x SD (mg) 1363 865 1633 1089
Tertile (n)
< 974.5 mg 35 26
974.51670.09 mg 30 31 0.72 (0.35, 1.47)
1670.10 mg 27 35 0.57 (0.28, 1.17) 0.13
Phosphorous
x SD (mg) 1944 719 2027 742
Tertile (n)
< 1630.35 mg 34 27
1630.352183.75 mg 28 33 0.67 (0.33, 1.38)
2183.76 mg 30 32 0.74 (0.37, 1.51) 0.42
Calcium
x SD (mg) 445 3392 551 380
Tertile (n)
< 295.10 mg 34 27
295.10534.09 mg 33 28 0.94 (0.46, 1.91)
534.10 mg 25 37 0.54 (0.26, 1.10) 0.09
Iron
x SD (mg) 10 62 12 6
Tertile (n)
< 7.34 mg 41 20
7.3411.72 mg 30 31 0.47 (0.23, 0.98)
11.73 mg 21 41 0.25 (0.12, 0.53) < 0.01
-Carotene
x SD (g) 259 506 349 528
Tertile (n)
< 13.20 g 34 27
13.20187.99 g 31 30 0.82 (0.40, 1.67)
188.00 g 27 35 0.61 (0.30, 1.25) 0.18
-Carotene
x SD (g) 3314 3942 4184 4631
Tertile (n)
< 1177.50 g 36 25
1177.504034.99 g 27 34 0.55 (0.27, 1.13)
4035.00 g 29 33 0.61 (0.30, 1.25) 0.18
(Continued)
 CASE-CONTROL STUDY OF GOUT IN TAIWAN 697

TABLE 4 (Continued)
Cases (n = 92) Controls (n = 92) OR (95% CI) P for trend
Retinol
x SD (g) 952 7510 356 1263
Tertile (n)
< 120.40 g 34 27
120.40217.99 g 33 28 0.94 (0.46, 1.91)
218.00 g 25 37 0.54 (0.26, 1.10) 0.09
Vitamin A
x SD (g RE) 1526 7644 1083 1421
Tertile (n)
< 406.43 g RE 39 22
406.43941.87 g RE 29 32 0.51 (0.25, 1.06)
941.88 g RE 24 38 0.36 (0.17, 0.74) < 0.01
Vitamin E
x SD (mg) 24 11 24 14
Tertile (n)
< 19.62 mg 29 32
19.6227.57 mg 31 30 1.14 (0.56, 2.32)
27.58 mg 32 30 1.18 (0.58, 2.39) 0.65
Thiamine

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x SD (mg) 1.14 1.80 1.02 0.80
Tertile (n)
< 0.69 mg 30 31
0.691.13 mg 31 30 1.07 (0.53, 2.17)
1.14 mg 31 31 1.03 (0.51, 2.10) 0.93
Riboflavin
x SD (mg) 1.20 1.12 1.26 0.64
Tertile (n)
< 0.86 mg 37 23
0.861.26 mg 32 29 0.72 (0.35, 1.47)
1.27 mg 23 39 0.38 (0.19, 0.79) 0.01
Niacin
x SD (mg) 18 10 20 12
Tertile (n)
< 12.22 mg 32 29
12.2220.37 mg 31 30 0.94 (0.46, 1.91)
20.38 mg 29 33 0.80 (0.39, 1.62) 0.53
Vitamin B-6
x SD (g) 645 411 763 528
Tertile (n)
< 429.39 g 34 27
429.39828.12 g 30 31 0.77 (0.38, 1.57)
828.13 g 28 34 0.65 (0.32, 1.33) 0.24
Vitamin B-12
x SD (g) 67 78
Tertile (n)
< 2.75 g 31 30
2.755.75 g 28 33 0.82 (0.40, 1.67)
5.76 g 33 29 1.10 (0.54, 2.24) 0.79
Vitamin C
x SD (mg) 176 346 141 132
Tertile (n)
< 73.70 mg 34 27
73.70141.76 mg 25 36 0.55 (0.27, 1.13)
141.77 mg 33 29 0.90 (0.44, 1.84) 0.79
Folate
x SD (g) 113 512 144 74
Tertile (n)
< 99.02 g 38 23
99.02134.34 g 32 28 0.69 (0.34, 1.43)
134.35 g 22 41 0.33 (0.16, 0.68) < 0.01
(Continued)
698 LYU ET AL

TABLE 4 (Continued)
Cases (n = 92) Controls (n = 92) OR (95% CI) P for trend

Saturated fat
x SD (g) 25 15 23 11
Tertile (n)
< 16.55 g 30 31
16.5526.47 g 30 31 1.00 (0.49, 2.03)
> 26.47 g 32 30 1.10 (0.54, 2.24) 0.79
Monounsaturated fat
x SD (g) 28 14 27 13
Tertile (n)
< 20.30 g 29 32
20.3031.83 g 29 32 1.00 (0.49, 2.04)
> 31.83 g 34 28 1.34 (0.66, 2.72) 0.42
Polyunsaturated fat
x SD (g) 31 14 31 14
Tertile (n)
< 24.89 g 31 30
24.8935.49 g 28 33 0.82 (0.40, 1.67)
> 35.49 g 33 29 1.10 (0.54, 2.24) 0.79
Cholesterol

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x SD (mg) 316 217 358 204
Tertile (n)
< 242.90 mg 34 27
242.90387.99 mg 33 28 0.94 (0.46, 1.91)
388.00 mg 25 37 0.54 (0.26, 1.10) 0.09
Purine
x SD (mg) 374 208 378 221
Tertile (n)
< 259.22 mg 32 31
259.22435.91 mg 29 31 0.82 (0.40, 1.67)
435.92 mg 31 30 0.91 (0.45, 1.84) 0.79
1
OR, odds ratio; RE, retinol equivalents.
2
Significantly different from controls, P < 0.05 (Students t test).

Besides animal sources, plant foods including whole grains, Our findings agree with many other findings that alcohol
beans, peas, lentils, asparagus, cauliflower, sprouts, spinach, and intake is strongly associated with gout occurrence. The ethanol
mushrooms are high in purines (18, 24, 26). Soy products such as and purine content in alcoholic beverages may account for the
soy milk, tofu, and pressed tofu are predominant plant sources of association with hyperuricemia and gout. For example, beer is
protein in Taiwan, and the intake of soy products contributed a fair reported to have a high guanosine content from yeast and barley
amount to the purine intake in our study population. We estimated fermentation (33). A possible mechanism for the association of
that 20% of purine intake in this population was from soy prod- alcohol intake with gout includes the overproduction of lactic
ucts. A misleading nutrition claim that soy products cause gout is acid and fatty acids, which affect the pH values of body fluids
a popular health belief among Asian populations with high soy and alter the renal excretion of uric acid (18, 32, 33). In addition,
consumption (14, 29). Yamakita et al (29) conducted a study in nucleotide overproduction occurs after injection of ethanol, and
Japan to examine the effect of tofu on uric acid metabolism in
healthy subjects and subjects with gout and found no significant
increase in plasma or urine uric acid concentrations or in uric acid
clearance in gout patients with normal uric acid clearance. In Tai- TABLE 5
Frequencies of selected dietary habits pertaining to gout among the cases
wan, one study compared the blood uric acid concentrations in
and the controls
vegetarians who usually consumed a fairly large amount of soy
products as protein sources with those in nonvegetarians and Cases (n = 92) Controls (n = 92)
found lower blood uric acid concentrations in the vegetarians (30). times/mo
Our data support the observation that increased consumption of Social dining 2.54 5.471 1.26 2.49
foods from plant sources, especially fruit and vegetables, reduce Vegetable intake 26.34 8.152 28.72 4.79
the risk of gout development, but probably not in the way sug- Fruit intake 17.07 10.521 20.35 10.45
gested by the purine content theory. The complexity of human Snack intake 4.59 7.11 3.68 5.77
uric acid metabolism and the difficulties of human diet assessment All-you-can-eat dining 0.78 3.76 0.33 1.04
may account for the uncertain causal relation of dietary purine and Seafood intake 12.09 10.48 14.99 11.81
nucleoprotein intakes, as well as amino acid and protein intakes, Organ meat intake 3.33 5.16 2.70 3.63
1,2
with gout (31, 32). Significantly different from controls: 1 P = 0.04, 2 P = 0.02.
 CASE-CONTROL STUDY OF GOUT IN TAIWAN 699

TABLE 6
Odds ratios and 95% CIs for gout of multivariable models consisting of variables for family history, obesity, and dietary factors after adjustment for age
and education level
Model 1 Model 2 Model 3 Model 4 Model 5 Model 6
Family history of diabetes
No 1.00 1.00 1.00 1.00 1.00 1.00
Yes 3.77 (1.61, 8.80) 3.55 (1.47, 8.55) 3.87 (1.61, 9.29) 4.12 (1.71, 9.95) 4.17 (1.71, 10.19) 3.70 (1.52, 9.02)
Family history of gout
No 1.00 1.00 1.00 1.00 1.00 1.00
Yes 6.95 (2.40, 20.13) 7.51 (2.54, 22.18) 6.69 (2.28, 19.68) 7.19 (2.40, 21.58) 8.43 (2.73, 26.04) 9.54 (3.03, 30.11)
BMI (kg/m2)
< 23.24 1.00 1.00 1.00 1.00 1.00 1.00
23.2426.48 1.11 (0.47, 2.61) 0.43 (0.14, 1.36) 0.99 (0.40, 2.47) 0.56 (0.20, 1.59) 0.61 (0.21, 1.77) 0.63 (0.21, 1.86)
26.49 2.04 (0.90, 4.62) 0.91 (0.25, 3.32) 1.65 (0.62, 4.39) 0.760 (0.23, 2.54) 0.85 (0.25, 2.97) 0.78 (0.22, 2.75)
P for trend 0.09 0.99 0.31 0.68 0.85 0.74
Alcohol (g/1000 kcal)
0.00 1.00 1.00 1.00 1.00 1.00 1.00
0.012.99 1.40 (0.65, 3.02) 1.42 (0.64, 3.16) 1.40 (0.64, 3.04) 1.40 (0.64, 3.09) 1.48 (0.66, 3.34) 1.45 (0.64, 3.26)
3.00 2.12 (0.82, 5.45) 2.00 (0.74, 5.41) 2.15 (0.82, 5.64) 2.09 (0.76, 5.72) 1.72 (0.61, 4.80) 1.83 (0.64, 5.23)
P for trend 0.11 0.16 0.12 0.14 0.25 0.22
Waist circumference (cm)

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< 84 1.00
8490 6.44 (2.08, 19.99)
91 3.28 (0.85, 12.63)
P for trend 0.12
Waist-to-hip ratio
< 0.87 1.00
0.870.91 2.35 (0.94, 5.91)
0.92 1.44 (0.52, 3.95)
P for trend 0.52
Waist-to-height ratio
< 0.50 1.00 1.00 1.00
0.500.54 3.89 (1.32, 11.46) 3.46 (1.15, 10.35) 3.81 (1.22, 11.84)
0.55 4.37 (1.18, 16.22) 3.87 (1.02, 14.68) 3.92 (1.01, 15.19)
P for trend 0.04 0.05 0.07
Dietary fiber (g/1000 kcal)
< 6.16 1.00
6.167.94 0.44 (0.17, 1.13)
7.95 0.43 (0.17, 1.09)
P for trend 0.09
Folate (g/1000 kcal)
< 51.53 1.00
51.5362.48 0.30 (0.12, 0.77)
62.48 0.37 (0.15, 0.92)
P for trend 0.04
R2 (%) 22.93 27.83 24.42 25.83 27.44 28.84

one study in Japan showed that this effect occurred via a distur-
bance of ATP metabolism (34).
Fruit and vegetables, which are rich in micronutrients includ-
ing folate, vitamin C, and dietary fiber, were found to have a
significant protective role in our study. Previous research has
shown that approximately two-thirds of the uric acid produced
each day is excreted in urine and that one-third is eliminated
directly in intestinal secretions and saliva (35, 36). This may
explain the possible protective effect against gout of the intake
of dietary fiber and soluble fiber that was shown in the estima-
tion of usual diets with the Chinese food-frequency question-
naire. Fiber has been recognized as being beneficial for intes-
tinal motility and as having a potential role in binding uric acid
in the gut for excretion, and thus the intake of fiber has been sug-
gested to result in a lower risk of gout, as was observed in the
present study. The hypouricemic effect of folate was suggested
by Oster in 1977 (37), and the mechanism was presumed to be
mediated through the inhibition of xanthine oxidase. However,
one intervention study conducted by Boss et al (38) using
folate supplementation failed to lower blood uric acid con-
centrations. The results of the present study show high corre-
lations (r = 0.570.67) of the consumption of dietary fiber,
folate, and vitamin C in this population with fruit and vegetable
intake, which may account for the protective effects.
We found that hypertension and obesity are strong risk fac-
tors for gout. In 1997 Li et al (7) reported a population study
from Beijing that showed strong associations of serum uric
acid concentrations with triacylglycerol and glucose concen-
trations and BMI (7). A cross-sectional population study of 910
men and 603 women in Hong Kong showed positive associations
700 LYU ET AL
of serum uric acid with BMI, waist-to-hip ratio, systolic and
diastolic blood pressure, fasting glucose, triacylglycerol, and
apolipoprotein B, as well as a negative association with HDL
cholesterol (39). The authors suggested that serum uric acid
may be a marker for the presence of an adverse cardiovascular
disease risk, which is strongly related to hypertension, hyper-
lipidemia, and diabetes mellitus. The inclusion of hyperuricemia
as a part of syndrome X, which is associated with insulin resist-
ance and coronary artery disease risk factors, was also sug-
gested by some clinicians (19, 40).
Obese people often have hyperuricemia, which frequently leads
to painful attacks of gout. It has been suggested that increased
serum uric acid (41) and gout occurrence (42) are closely associ-
ated with an increase in visceral fat accumulation. The significance
of visceral fat obesity has been noticed for many interrelated
chronic metabolic disorders (43). Many studies have compared the
associations of these proxy measures of abdominal obesity, includ-
ing waist circumference, waist-to-hip ratio, and waist-to-height
ratio, with coronary artery disease risk factors (4446). As our
multivariable models suggest, indexes of central obesity, espe-
cially waist-to-height ratio, are better linear indexes for identify-
ing the risk of gout in this population than are waist circumference
and waist-to-hip ratio. In a Japanese population study, waist-to-height
ratio was also proposed to be a better predictor of multiple coro-
nary risk levels than was waist-to-hip ratio (47).
Many physiologic studies suggested a strong association
between hyperuricemia and gout (19, 48). However, as with
other blood biochemical disorders, only 5% of hyperuricemic
subjects developed clinical symptoms of gout (19, 48). Gout has
been recognized as a disorder of altered uric acid metabolism
(either overproduction or underexcretion of uric acid) that
results in high blood uric acid concentrations (18, 19, 48).
Besides diet, the other factors that are related to reductions in
uric acid excretion include renal dysfunction, lead toxicity, and
medication side effects (19, 21). Also, various genetic metabolic
factors affecting uric acid production and excretion complicate
the scenario for gout occurrence. In the present study, the aver-
age uric acid concentration in the 92 patients with gout was
9.22 mg/dL, with 62 subjects having the underexcretion type
(24-h urinary excretion of uric acid < 600 mg) and 30 subjects
having the overproduction type (> 600 mg uric acid/d). Poten-
tial lifestyle risk factors were not found to differ between these
subgroups in the present study.
The strength of this study was that we recruited incident
cases of gout rather than patients with long-term gout; there-
fore, selection bias was limited. The weakness of this study was
that only male patients were included in the analysis. Sex dif-
ferences have often been observed, and the differences are
reported to result from differences in sex hormones (49). In
conclusion, we confirmed that alcohol intake, but not purine
intake, is a strong risk factor for developing gout. Fruit and veg-
etables, which are rich in dietary fiber, folate, and vitamin C,
are protective against gout.
We thank Feng-Hsin Chang for typing assistance and Jeng-Long Feng for
valuable advice on energy expenditure and exercise physiology.
C-YH and S-HH contributed to data collection and database management,
C-YY and M-SL assisted in the statistical analyses and contributed to data analy-
ses, and C-LC was responsible for the diagnosis and recruitment of participants.
L-CL designed and oversaw this project and contributed to the writing of the man-
uscript. None of the authors of this manuscript had any conflicts of interest.
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