Abstract
While prior research has shown that consuming alcohol may raise the risk of hyperuricemia, little is known about how individual types of alcohol are linked to levels of uric acid in China. Therefore, this study aimed to investigate the independent impact of beer, wine, and liquor on serum uric acid (SUA) levels in the serum of Chinese adults. This study analyzed data from the 2009 China Health and Nutrition Survey and included 7083 participants (3418 men and 3665 women, ≥18 years of age). Multivariable logistic regression was used to analyze the potential association between alcohol intake and hyperuricemia risk, while linear regression analysis and general linear model were performed to examine the impact of alcohol consumption on SUA levels. This study revealed that men who drank alcohol daily had a greater odds ratio (1.68, 95% confidence interval: 1.01, 2.81) of hyperuricemia than those who drank alcohol no more than once a month. SUA levels of men significantly increased by 0.001 mg/dL for per additional gram of liquor consumed weekly. But men who drank ≤ 90.6 g of liquor per week had lower SUA levels compared with those in nondrinkers. SUA levels were inversely associated with wine intake in women (P = .03, P for trend = .02). Overall, consumption of beer, wine, and liquor differentially affected SUA levels in adult Chinese men and women.
Keywords: alcoholic beverage, China Health and Nutrition Survey, drinking, hyperuricemia, uric acid
1. Introduction
The body eliminates uric acid, which is the final product of the breakdown of purines, through urine.[1,2] Hyperuricemia, characterized by high serum uric acid (SUA) levels, may occur due to increased SUA production or reduced excretion.[3] The presence of hyperuricemia can heighten the likelihood of several illnesses including but not limited to gout, diabetes, cardiovascular disease, obesity, chronic kidney disease, metabolic syndrome, hypertension, and other disorders.[4–11]
In recent decades, hyperuricemia has become more prevalent worldwide,[12–15] and China is no exception.[16] There was an increase in the prevalence of hyperuricemia among Chinese adults, with rates rising from 11.1% in 2015-2016 to 14.0% in 2018-2019.[17] Factors implicated in the development of hyperuricemia include diet, genetics, and lifestyle.[18–25] Drinking alcohol has been reported by numerous investigators to increase the risk of hyperuricemia.[20,26–28] The stronger impact of alcohol on gout than hyperuricemia has been confirmed in a meta-analysis (odds ratio [OR]: 2.58 vs 2.06).[20] As for different alcoholic beverages, a cross-sectional study among Americans reported that drinking beer resulted in a greater increase in SUA levels than drinking liquor (0.46 vs 0.29 mg/dL), whereas moderated wine consumption did not increase uric acid levels (–0.42 mg/dL, 95% confidence interval [95% CI]: –0.62, –0.22).[29] Similar findings were observed in a prospective study conducted among American men: higher risk of gout from drinking beer (relative risk [RR]: 1.49, 95% CI: 1.32, 1.70) than from drinking spirits (RR: 1.15, 95% CI: 1.04, 1.28), and wine intake at a moderate level had no effect on gout (RR: 1.04, 95% CI: 0.88, 1.22).[30]
Limited studies have separately evaluated the impact of beer, wine, and liquor on SUA levels among Chinese individuals. Thus, the objective of this study was to investigate how the consumption of beer, wine, and liquor relates to the levels of SUA utilizing data gathered from the 2009 China Health and Nutrition Survey (CHNS).
2. Methods
2.1. Study participants
The CHNS, an ongoing population-based open cohort study covering nine provinces (Henan, Shandong, Liaoning, Hubei, Guangxi, Heilongjiang, Hunan, Jiangsu, and Guizhou), provided the data for this cross-sectional investigation. By 2011, there were more than 30,000 participants in the CHNS, which accounted for 47% of the total population of China as indicated by the 2010 census.[31] The CHNS began in 1989, and 10 surveys have been completed since then.[32] Because data on blood components were collected only in 2009, we used the dataset of the 2009 survey for our analysis.
A total of 10,752 adults (≥18 years) were screened for eligibility. We excluded 3669 participants with incomplete data, including education level, biochemical parameters, smoking and drinking habits, height, weight, blood pressure, alcoholic beverage intake, and physical activity level. The final analytic sample comprised 7083 adults (Fig. 1).
Figure 1.
Flow chart for including and excluding study participants.
2.2. Biochemical and anthropometric measurements
Blood (12 mL) was collected via venipuncture from participants who had refrained from eating for a minimum of 12 hours the night before. After being stored frozen at −86°C, serum and plasma samples were analyzed under quality control guidelines in the national laboratory in Beijing.[33–35] The Hitachi 7600 automated analyzer was utilized to measure SUA concentrations via the enzymatic colorimetric technique. Trained and experienced investigators administered a structured and standardized questionnaire to gather sociodemographic variables including sex, age, physical activity, area of residence (urban or rural), education level, alcohol intake, smoking status, and 3-day average protein, carbohydrate, fat, and energy intake. Trained clinical staff measured waist circumference, weight, blood pressure, and height. To determine the body mass index (BMI), the weight (kg) was divided by the square of the height (m2).
2.3. Physical activity assessment
Types of physical activities and the duration of each activity were collected using self-reported surveys. Physical activity levels were determined by multiplying the metabolic equivalent of task (MET) by the duration of each activity. The MET is a measurement of the intensity of the activity, and one MET is the amount of oxygen required to sit still.[36]
Physical activities included domestic, transportational, occupational, and leisure activities. The following MET values were assigned to the following activities: 1.5, public transportation; 2.15, washing clothes; 2.3, buying food; 3.0, walking; 4.0, bicycling; 4.5, martial arts; 5.0, ping-pong, gymnastics, badminton, and dancing; 6, soccer and basketball; and 7.5, jogging. Occupational activities were rated as low, medium, or high intensity, with values of 2, 4, and 6, respectively.[37]
2.4. Alcohol consumption
Alcohol intake was evaluated using the following questions: “Did you drink alcohol last year?” and “What is the frequency of alcohol intake?” The responses to the latter were “almost every day,” “3–4 times a week,” “once or twice a week,” “once or twice a month,” and “no more than once a month.” Alcohol drinkers were further questioned regarding how frequently they drank three types of alcohol: “How much beer do you drink each week (bottles)?,” “How much wine do you drink each week (liangs)?,” and “How much liquor do you drink each week (liangs).” Liang is a traditional Chinese weight unit, and 1 liang equals 50 g. We created new categories for the consumption of each type of alcohol (beer, liquor, and wine): 0, equal to or below the median of consumption, and above the median of consumption (0: those who answered no to beer, wine, or liquor drinking plus those who reported their consumption of each alcoholic beverage had a value of 0). The consumption of each alcoholic beverage was calculated by the formula below: Amount of alcohol consumption (g) = drink volume (mL) × alcoholic concentration by volume (%) × specific gravity of alcohol (0.79).[38] The total alcohol intake is equal to the sum of the three types of alcohol. 1 bottle = 600 mL, 1 Liang = 50 mL. According to the 2010 China Monitoring Report on Risk Factors for Chronic Disease, the alcohol contents of various alcoholic beverages were within acceptable limits (beer = 4%, wine = 10%, liquor = 38%).[39]
2.5. Definition of hyperuricemia
There was a separate definition of hyperuricemia for men and women owing to the significant difference between the genders in SUA levels. The criteria for hyperuricemia in this study were SUA levels of ≥ 7.0 mg/dL in men and ≥ 6 mg/dL in women.[40,41]
2.6. Statistical analyses
Mean ± standard deviation is the chosen expression method for continuous variables, while categorical data is presented as frequency (n) and percentage (%). To compare categorical and continuous variables, independent chi-square and the t test were utilized, respectively. To evaluate the association between alcohol intake and hyperuricemia, we conducted a multivariate logistic regression analysis to compute ORs, while controlling for covariates such as area of residence, age, smoking, BMI, waist circumference, education level, physical activity, creatinine level, high sensitivity C-reactive protein, average blood pressure (systolic and diastolic), and 3-day average energy, protein, fat, and carbohydrate intake. Linear regression was applied to examine the impact of alcohol consumption on SUA levels. The P value for the trend was determined based on the SUA level in each category of alcohol consumption (beer, wine, and liquor). If the P value obtained from a statistical test is less than .05, it is considered statistically significant. All statistical analyses were performed with the use of SAS 9.4 software (Cary, NC).
This study was reviewed and approved by the Institutional Review Board (IRB) of Inha University on February 4, 2022 (IRB No. 220121-1A).
3. Results
3.1. Characteristics of the participants according to hyperuricemia and sex
A total of 7083 people participated in this study (3418 men and 3665 women). Based on our study’s definition of hyperuricemia, the overall prevalence was 16.6%, with men (21.3%) exhibiting a higher prevalence than women (12.2%). Table 1 displays the participants’ characteristics according to hyperuricemia. Regardless of sex, participants with hyperuricemia had a larger waist circumference and higher BMI, creatinine level, and blood pressure; and have a higher likelihood of living in urban areas than those without hyperuricemia (all P < .05). The group with hyperuricemia exhibited lower levels of physical activity and 3-day average carbohydrate intake compared to the group without hyperuricemia (P < .05). The men group with hyperuricemia had higher levels of education than those without hyperuricemia while the opposite was observed in women (P < .05).
Table 1.
Baseline characteristics of the study population according to hyperuricemia and sex.
| Characteristic | Men (n = 3418) | Women (n = 3665) | ||||
|---|---|---|---|---|---|---|
| Non-hyperuricemia: serum uric acid < 7 mg/dL (n = 26,90) | Hyperuricemia: serum uric acid ≥ 7 mg/dL (n = 728) | P value | Non-hyperuricemia: serum uric acid < 6 mg/dL (n = 3217) | Hyperuricemia: serum uric acid ≥ 6 mg/dL (n = 448) | P value | |
| Age (yr) | 49.6 ± 15.1 | 49.5 ± 15.6 | .87 | 49.6 ± 15.2 | 58.5 ± 14.0 | <.001 |
| BMI (kg/m2) | 23.1 ± 3.3 | 24.5 ± 3.6 | <.001 | 23.3 ± 3.5 | 25.0 ± 3.9 | <.001 |
| Waist circumference (cm) | 83.3 ± 10.1 | 87.4 ± 10.5 | <.001 | 81.0 ± 10.3 | 86.4 ± 10.3 | <.001 |
| High-sensitivity CRP (mg/L) | 3.0 ± 9.1 | 3.2 ± 10.3 | .69 | 2.3 ± 10.2 | 3.8 ± 6.4 | <.001 |
| Creatinine (mg/dL) | 1.1 ± 0.2 | 1.2 ± 0.2 | <.001 | 0.9 ± 0.2 | 1.1 ± 0.4 | <.001 |
| Average blood pressure (mm Hg) | ||||||
| Systolic | 125.2 ± 17.4 | 127.6 ± 17.6 | .001 | 122.8 ± 19.9 | 133.6 ± 22.2 | <.001 |
| Diastolic | 80.9 ± 10.8 | 82.9 ± 11.0 | <.001 | 78.2 ± 11.0 | 82.0 ± 12.4 | <.001 |
| Physical activity (METs/week) | 110.1 ± 119.2 | 95.0 ± 104.0 | .001 | 82.2 ± 94.2 | 53.1 ± 79.9 | <.001 |
| Education | ||||||
| None | 411 (15.3%) | 99 (13.6%) | .001 | 1015 (31.6%) | 178 (39.7%) | .01 |
| Graduated from primary school | 566 (21.0%) | 123 (16.9%) | 641 (19.9%) | 90 (20.1%) | ||
| Lower middle school degree | 1002 (37.3%) | 266 (36.5%) | 965 (30.0%) | 109 (24.3%) | ||
| Upper middle school degree | 405 (15.1%) | 116 (15.9%) | 307 (9.5%) | 37 (8.3%) | ||
| Technical or vocational degree | 176 (6.5%) | 71 (9.8%) | 193 (6.0%) | 25 (5.6%) | ||
| University/college degree and above | 130 (4.8%) | 53 (7.3%) | 96 (3.0%) | 9 (2.0%) | ||
| Area of residence | ||||||
| Urban site | 815 (30.3%) | 294 (40.4%) | <.001 | 1010 (31.4%) | 185 (41.3%) | <.001 |
| Rural site | 1875 (69.7%) | 434 (59.6%) | 2207 (68.6%) | 263 (58.7%) | ||
| Diet (3-d average) | ||||||
| Energy (kcal) | 2314.7 ± 703.3 | 2288.7 ± 650.6 | .35 | 1918.1 ± 667.6 | 1852.8 ± 592.2 | .03 |
| Carbohydrate (g) | 321.9 ± 114.1 | 304.5 ± 104.6 | <.001 | 264.1 ± 96.0 | 245.1 ± 91.9 | <.001 |
| Fat (g) | 77.9 ± 39.6 | 79.7 ± 38.5 | .30 | 68.6 ± 48.3 | 70.4 ± 38.8 | .36 |
| Protein (g) | 71.2 ± 25.1 | 73.3 ± 24.5 | .27 | 60.3 ± 21.1 | 59.3 ± 21.2 | .36 |
| Ever smoke cigarettes? | ||||||
| No | 1005 (37.4%) | 271 (37.2%) | .95 | 3115 (96.8%) | 430 (96.0%) | .35 |
| Yes | 1685 (62.6%) | 457 (62.8%) | 102 (3.2%) | 18 (4.0%) | ||
Data are presented as mean ± standard deviation or number (percentage). P values were calculated using the chi-squared test for categorical variables and t test for continuous variables.
BMI = body mass index, CRP = C-reactive protein, MET = metabolic equivalent of task.
Regarding alcohol intake, men who had hyperuricemia were more likely to drink wine than participants without hyperuricemia (P = .02) in Table 2. We can also found that men with hyperuricemia drank more wine weekly (P = .01), whereas women with hyperuricemia drank less wine (P = .02), compared with their non-hyperuricemia counterparts. In addition, total weekly alcohol consumption in men with hyperuricemia was higher than in men without the condition (P = .01).
Table 2.
Alcohol intake according to hyperuricemia and sex.
| Characteristic | Men (n = 3418) | Women (n = 3665) | ||||
|---|---|---|---|---|---|---|
| Non-hyperuricemia: serum uric acid < 7 mg/dL (n = 2690) | Hyperuricemia: serum uric acid ≥ 7 mg/dL (n = 728) | P value | Non-hyperuricemia: Serum uric acid < 6 mg/dL (n = 3217) | Hyperuricemia: serum uric acid ≥ 6 mg/dL (n = 448) | P value | |
| Drank alcohol last year? | ||||||
| No | 1193 (44.4%) | 294 (40.4%) | .06 | 2968 (92.3%) | 413 (92.2%) | .96 |
| Yes | 1497 (55.7%) | 434 (59.6%) | 249 (7.7%) | 35 (7.8%) | ||
| Frequency of alcohol consumption (n = 2213) | ||||||
| Almost every day | 510 (34.1%) | 174 (40.1%) | .06 | 42 (16.9%) | 6 (17.1%) | .52 |
| 1–4 times a week | 572 (38.3%) | 164 (37.8%) | 73 (29.3%) | 11 (31.4%) | ||
| Once or twice a month | 301 (20.1%) | 71 (16.4%) | 64 (25.7%) | 12 (34.3%) | ||
| No more than once a month | 112 (7.5%) | 25 (5.8%) | 70 (28.1%) | 6 (17.1%) | ||
| Drink beer? (n = 2212) | ||||||
| No | 602 (40.3%) | 169 (38.9%) | .61 | 113 (45.4%) | 20 (57.1%) | .19 |
| Yes | 892 (59.7%) | 265 (61.1%) | 136 (54.6%) | 15 (42.9%) | ||
| Drink wine? (n = 2208) | ||||||
| No | 1352 (90.7%) | 377 (86.9%) | .02 | 176 (70.7%) | 25 (71.4%) | .93 |
| Yes | 138 (9.3%) | 57 (13.1%) | 73 (29.3%) | 10 (28.6%) | ||
| Drink liquor? (n = 2213) | ||||||
| No | 287 (19.2%) | 90 (20.7%) | .48 | 105 (42.2%) | 11 (31.4%) | .23 |
| Yes | 1208 (80.8%) | 344 (79.3%) | 144 (57.8%) | 24 (68.6%) | ||
| Beer intake (g/wk) | 37.6 ± 62.7 | 44.2 ± 93.3 | .17 | 25.5 ± 61.9 | 16.8 ± 45.7 | .32 |
| Wine intake (g/wk) | 2.3 ± 15.0 | 5.7 ± 27.4 | .01 | 5.3 ± 19.3 | 2.0 ± 4.1 | .02 |
| Liquor intake (g/wk) | 128.1 ± 181.0 | 146.8 ± 196.5 | .08 | 42.2 ± 75.4 | 69.5 ± 114.7 | .18 |
| Total alcohol intake (g/wk) | 167.9 ± 193.3 | 196.7 ± 220.8 | .01 | 73.3 ± 102.7 | 88.3 ± 115.7 | .43 |
| Beer intake (g/wk) (n = 2207) | ||||||
| 0 | 610 (40.9%) | 172 (38.8%) | .88 | 118 (47.4%) | 22 (62.9%) | .23 |
| ≤37.92 (M)/≤18.96 (W) | 528 (35.4%) | 153 (35.4%) | 78 (13.3%) | 8 (22.9%) | ||
| >37.92 (M)/>18.96 (W) | 353 (23.7%) | 107 (24.8%) | 53 (21.3%) | 5 (14.3%) | ||
| Wine intake (g/wk) (n = 2205) | ||||||
| 0 | 1357 (91.2%) | 378 (87.1%) | .02 | 179 (72.2%) | 26 (74.3%) | .86 |
| ≤11.85 (M)/≤7.90 (W) | 70 (4.7%) | 25 (5.8%) | 40 (16.1%) | 6 (17.1%) | ||
| >11.85 (M)/>7.90 (W) | 61 (4.1%) | 31 (7.1%) | 29 (11.7%) | 3 (8.6%) | ||
| Liquor intake (g/wk) (n = 2207) | ||||||
| No | 296 (19.8%) | 93 (21.6%) | .05 | 106 (42.6%) | 11 (31.4%) | .39 |
| ≤90.60 (M)/≤30.20 (W) | 637 (42.7%) | 156 (36.2%) | 74 (29.7%) | 11 (31.4%) | ||
| >90.60 (M)/>30.20 (W) | 559 (37.5%) | 182 (42.2%) | 69 (27.7%) | 13 (37.1%) | ||
Data are expressed a number (percentage) or mean ± standard deviation. P values were calculated using the chi-squared test for categorical variables and t test for continuous variables.
M = men, W = women.
3.2. Alcohol intake and serum uric acid level
The mean SUA levels of the participants based on their alcohol consumption status are shown in Table 3. There was no significant relationship between the overall frequency of alcohol consumption and SUA levels in women. However, in men, the mean SUA levels increased from 5.81 to 6.22 mg/dL with an increased frequency of alcohol consumption (P = .001). Men who consumed wine had higher SUA levels than those who did not drink (P = .001).
Table 3.
Serum uric acid levels according to alcohol consumption.
| Characteristic | Men (n = 3418) | Women (n = 3665) | ||
|---|---|---|---|---|
| n (%) | Serum uric acid (mg/dL) Mean ± SD | n (%) | Serum uric acid (mg/dL) Mean ± SD | |
| Drank alcohol last year? | ||||
| No | 1487 (43.5%) | 5.95 ± 2.01 | 3381 (92.3%) | 4.50 ± 1.36 |
| Yes | 1931 (56.5%) | 6.00 ± 1.78 | 284 (7.8%) | 4.52 ± 1.35 |
| P value | .44 | .83 | ||
| Frequency of alcohol consumption (n = 2213) | ||||
| Almost every day | 684 (35.5%) | 6.22 ± 1.93 | 48 (16.9%) | 4.51 ± 1.11 |
| 1–4 times a week | 736 (38.2%) | 5.92 ± 1.71 | 84 (29.6%) | 4.52 ± 1.32 |
| Once or twice a month | 372 (19.3%) | 5.86 ± 1.65 | 76 (26.8%) | 4.44 ± 1.39 |
| No more than once a month | 137 (7.1%) | 5.81 ± 1.62 | 76 (26.8%) | 4.62 ± 1.50 |
| P value | .001 | .88 | ||
| Drink beer? (n = 2212) | ||||
| No | 771 (40.0%) | 5.97 ± 1.78 | 133 (46.8%) | 4.56 ± 1.38 |
| Yes | 1157 (60.0%) | 6.03 ± 1.78 | 151 (53.2%) | 4.49 ± 1.33 |
| P value | .44 | .63 | ||
| Drink wine? (n = 2208) | ||||
| No | 1729 (89.9%) | 5.96 ± 1.77 | 201 (70.8%) | 4.55 ± 1.35 |
| Yes | 195 (10.1%) | 6.40 ± 1.81 | 83 (29.2%) | 4.47 ± 1.37 |
| P value | .002 | .66 | ||
| Drink liquor | ||||
| No | 377 (19.5%) | 6.20 ± 1.86 | 116 (40.9%) | 4.42 ± 1.27 |
| Yes | 1552 (80.5%) | 5.96 ± 1.76 | 168 (59.2%) | 4.59 ± 1.41 |
| P value | .02 | .29 | ||
| Beer intake (g/wk) (n = 2207) | ||||
| 0 | 782 (40.7%) | 5.97 ± 1.77 | 140 (49.3%) | 4.61 ± 1.43 |
| ≤37.92 (M)/≤18.96 (W) | 681 (35.4%) | 6.00 ± 1.73 | 86 (30.3%) | 4.44 ± 1.33 |
| >37.92 (M)/>18.96 (W) | 460 (23.9%) | 6.06 ± 1.88 | 58 (20.4%) | 4.44 ± 1.19 |
| P value | .70 | .58 | ||
| Wine intake (g/wk) (n = 2205) | ||||
| 0 | 1735 (90.3%) | 5.96 ± 1.77 | 205 (72.4%) | 4.57 ± 1.38 |
| ≤11.85 (M)/≤7.90 (W) | 95 (4.9%) | 6.38 ± 1.87 | 46 (16.3%) | 4.55 ± 1.37 |
| >11.85 (M)/>7.90 (W) | 92 (4.8%) | 6.43 ± 1.82 | 32 (11.3%) | 4.19 ± 1.12 |
| P value | .001 | .33 | ||
| Liquor intake (g/wk) (n = 2207) | ||||
| 0 | 389 (20.2%) | 6.20 ± 1.84 | 117 (41.2%) | 4.43 ± 1.27 |
| ≤90.60 (M)/≤30.20 (W) | 793 (41.2%) | 5.79 ± 1.63 | 85 (29.9%) | 4.50 ± 1.40 |
| >90.60 (M)/>30.20 (W) | 741 (38.5%) | 6.12 ± 1.89 | 82 (28.9%) | 4.68 ± 1.42 |
| P value | <.001 | .43 | ||
P values were calculated using the t test and analysis of variance for continuous variables and the chi-square test for categorical variables.
M = men, SD = standard deviation, W = women.
Men who drank alcohol almost every day had higher levels of SUA (difference: 0.48 mg/dL, 95% CI: 0.16, 0.80) than did those who drank alcohol no more than once a month (the reference group) in Table 4. After adjusting for covariates, higher wine consumption in women was associated with decreased SUA levels (P = .03, P for trend = .02). SUA levels were 0.66 mg/dL lower in women who consumed > 7.9g of wine per week than in those who did not consume wine (95% CI: –1.16, –0.17). SUA levels were lower (by 0.32 mg/dL) in men who consumed ≤ 90.6 g per week of liquor than those in men who did not consume liquor after adjusting for covariates (P < .001, P for trend = .02).
Table 4.
Differences in serum uric acid levels (mg/dL) according to alcoholic beverage intake.
| Characteristic | Men (n = 3418) | Women (n = 3665) | ||||
|---|---|---|---|---|---|---|
| n (%) | Non-adjusted difference (95% CI) | Multivariable difference (95% CI) | n (%) | Non-adjusted difference (95% CI) | Multivariable difference (95% CI) | |
| Drank alcohol last year? | ||||||
| No | 1487 (43.5%) | 0 (reference) | 0 (reference) | 3381 (92.3%) | 0 (reference) | 0 (reference) |
| Yes | 1931 (56.5%) | 0.05 (–0.08, 0.18) | –0.003 (–0.14, 0.13) | 284 (7.8%) | 0.02 (–0.15, 0.18) | 0.04 (–0.11, 0.20) |
| P value | .44 | .95 | .83 | .59 | ||
| Frequency of alcohol consumption (n = 2213) | ||||||
| Almost every day | 684 (35.5%) | 0.41 (0.08, 0.74) | 0.48 (0.16, 0.80) | 48 (16.9%) | –0.10 (–0.60, 0.39) | –0.31 (–0.80, 0.17) |
| 1–4 times a week | 736 (38.2%) | 0.11 (–0.22, 0.43) | 0.12 (–0.18, 0.43) | 84 (29.6%) | –0.10 (0.52, 0.33) | –0.13 (–0.53, 0.27) |
| Once or twice a month | 372 (19.3%) | 0.04 (–0.30, 0.40) | 0.10 (–0.23, 0.43) | 76 (26.8%) | –0.18 (–0.61, 0.26) | –0.31 (–0.71, 0.10) |
| No more than once a month | 137 (7.1%) | 0 (reference) | 0 (reference) | 76 (26.8%) | 0 (reference) | 0 (reference) |
| P value | .001 | <.001 | .88 | .41 | ||
| Drink beer? (n = 2212) | ||||||
| No | 771 (40.0%) | 0 (reference) | 0 (reference) | 133 (46.8%) | 0 (reference) | 0 (reference) |
| Yes | 1157 (60.0%) | 0.06 (–0.10, 0.23) | –0.02 (–0.19, 0.15) | 151 (53.2%) | –0.08 (–0.39, 0.24) | 0.08 (–0.24, 0.41) |
| P value | .44 | .82 | .64 | .62 | ||
| Drink wine? (n = 2208) | ||||||
| No | 1729 (89.9%) | 0 (reference) | 0 (reference) | 201 (70.8%) | 0 (reference) | 0 (reference) |
| Yes | 195 (10.1%) | 0.43 (0.17, 0.70) | 0.20 (–0.06, 0.46) | 83 (29.2%) | –0.08 (–0.43, 0.27) | –0.22 (–0.57, 0.13) |
| P value | .001 | .13 | .66 | .22 | ||
| Drink liquor? (n = 2213) | ||||||
| No | 377 (19.5%) | 0 (reference) | 0 (reference) | 116 (40.9%) | 0 (reference) | 0 (reference) |
| Yes | 1552 (80.5%) | –0.24 (–0.44,–0.04) | –0.17 (–0.37, 0.03) | 168 (59.2%) | 0.17 (–0.15, 0.49) | 0.12 (–0.19, 0.44) |
| P value | .02 | .09 | .29 | .45 | ||
| Beer intake (g/wk) (n = 2207) | ||||||
| 0 | 782 (40.7%) | 0 (reference) | 0 (reference) | 140 (49.3%) | 0 (reference) | 0 (reference) |
| ≤37.92 (M)/≤18.96 (W) | 681 (35.4%) | 0.03 (–0.16, 0.21) | –0.02 (–0.20, 0.17) | 86 (30.3%) | –0.17 (–0.54, 0.19) | 0.02 (–0.34, 0.38) |
| >37.92 (M)/>18.96 (W) | 460 (23.9%) | 0.09 (–0.12, 0.29) | –0.05 (–0.26, 0.16) | 58 (20.4%) | –0.17 (–0.58, 0.25) | –0.06 (–0.47, 0.35) |
| P value | .70 | .89 | .58 | .93 | ||
| P for trend | .40 | .61 | .42 | .88 | ||
| Wine intake (g/wk) (n = 2205) | ||||||
| 0 | 1735 (90.3%) | 0 (reference) | 0 (reference) | 205 (72.4%) | 0 (reference) | 0 (reference) |
| ≤11.85 (M)/≤7.90 (W) | 95 (4.9%) | 0.42 (0.05, 0.78) | 0.22 (–0.13, 0.58) | 46 (16.3%) | –0.03 (–0.46, 0.41) | –0.05 (–0.46, 0.37) |
| >11.85 (M)/>7.90 (W) | 92 (4.8%) | 0.47 (0.10, 0.84) | 0.17 (–0.19, 0.53) | 32 (11.3%) | –0.38 (–0.89, 0.12) | –0.66 (–1.16,–0.17) |
| P value | .006 | .33 | .33 | .03 | ||
| P for trend | .005 | .25 | .10 | .02 | ||
| Liquor intake (g/wk) (n = 2207) | ||||||
| 0 | 389 (20.2%) | 0 (reference) | 0 (reference) | 117 (41.2%) | 0 (reference) | 0 (reference) |
| ≤90.60 (M)/≤30.20 (W) | 793 (41.2%) | –0.40 (–0.62,–0.19) | –0.32 (–0.53,–0.11) | 85 (29.9%) | 0.07 (–0.31, 0.45) | –0.02 (–0.38, 0.34) |
| >90.60 (M)/>30.20 (W) | 741 (38.5%) | –0.07 (–0.29, 0.15) | 0.03 (–0.19, 0.25) | 82 (28.9%) | 0.25 (–0.13, 0.63) | 0.28 (–0.10, 0.67) |
| P value | <.001 | <.001 | .43 | .25 | ||
| P for trend | .09 | .02 | .20 | .19 | ||
Adjusted for age, area, smoking, body mass index, waist circumference, education level, physical activity, creatinine level, high sensitivity, average systolic blood pressure, average diastolic blood pressure, energy intake, protein intake, fat intake, and carbohydrate intake. The P value for a trend was calculated using the median of weekly beer, wine, or liquor consumption.
CI = confidence interval, M = men, W = women.
The findings of linear regression analysis for the effect of alcohol intake on SUA levels are shown in Table 5. No statistically significant relationship was discovered between beer and SUA levels in either men or women. In women, SUA levels were decreased by 0.008 mg/dL for one gram increase in weekly wine consumption in the adjusted model (P = .047) while a weak positive association was shown among men only in the age-adjusted model. SUA levels of men significantly increased by 0.001 mg/dL for per additional gram of liquor consumed in all three models (unadjusted, age-adjusted, adjusted). This positive relationship for the total alcohol intake was also seen among men (β = 0.001).
Table 5.
Association between 3 types of alcohol and serum uric acid levels in men and women.
| Characteristic | Unadjusted model | Age-adjusted model | Adjusted model | |||
|---|---|---|---|---|---|---|
| Beta | P value | Beta | P value | Beta | P value | |
| Men (n = 3418) | ||||||
| Beer intake (g/wk) | 0.001 | .04 | 0.001 | .09 | 0.001 | .60 |
| Wine intake (g/wk) | 0.006 | .007 | 0.006 | .005 | 0.002 | .16 |
| Liquor intake (g/wk) | 0.001 | .007 | 0.001 | .002 | 0.001 | .002 |
| Total alcohol intake (g/wk) | 0.001 | <.001 | 0.001 | <.001 | 0.001 | .002 |
| Women (n = 3665) | ||||||
| Beer intake (g/wk) | –0.001 | .53 | –0.0002 | .86 | –0.0004 | .76 |
| Wine intake (g/wk) | –0.009 | .03 | –0.010 | .02 | –0.008 | .047 |
| Liquor intake (g/wk) | 0.002 | .08 | 0.002 | .13 | 0.002 | .06 |
| Total alcohol intake (g/wk) | 0.0005 | .55 | 0.001 | .50 | 0.001 | .36 |
Adjusted for age, area, smoking, body mass index, waist circumference, education level, physical activity, creatinine, high-sensitivity, average systolic blood pressure, average diastolic blood pressure, energy intake, protein intake, fat intake, and carbohydrate intake.
3.3. Association of alcohol intake and hyperuricemia
Table 6 presents the multivariable analyses for the risk of hyperuricemia due to alcohol intake are presented. The analysis did not reveal any significant association between total alcohol intake and hyperuricemia risk in women. However, among men who consumed alcohol almost every day, the adjusted OR was 1.68 (95% CI: 1.01, 2.81, P = .047) for hyperuricemia when compared to the reference group (no more than once a month).
Table 6.
Association between alcohol intakes and hyperuricemia: crude and adjusted odd ratios and 95% confidence intervals.
| Men (n = 3418) | Women (n = 3665) | |||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| n | Crude OR (95% CI) | P value | P for trend | Adjusted OR (95% CI) | P value | P for trend | n | Crude OR (95% CI) | P value | P for trend | Adjusted OR (95% CI) | P value | P for trend | |
| Drank alcohol last year? | ||||||||||||||
| No | 1487 (43.5%) | 1.00 | 1.00 | 3381 (92.3%) | 1.00 | 1.00 | ||||||||
| Yes | 1931 (56.5%) | 1.18 (1.00, 1.39) | .06 | 1.16 (0.96, 1.40) | .13 | 284 (7.8%) | 0.97 (0.67, 1.42) | .88 | 1.06 (0.69, 1.61) | .80 | ||||
| Frequency of alcohol consumption (n = 2213) | ||||||||||||||
| Almost every day | 684 (35.5%) | 1.42 (0.96, 2.44) | .08 | 1.68 (1.01, 2.81) | .047 | 48 (16.9%) | 1.67 (0.51, 5.50) | .40 | 1.32 (0.31, 5.57) | .70 | ||||
| 1–4 times a week | 736 (38.2%) | 1.28 (0.81, 2.05) | .29 | 1.35 (0.83, 2.21) | .23 | 84 (29.6%) | 1.76 (0.62, 0.01) | .29 | 1.97 (0.55, 0.12) | .30 | ||||
| Once or twice a month | 372 (19.3%) | 1.06 (0.64, 1.75) | .83 | 1.15 (0.68, 1.95) | .61 | 76 (26.8%) | 2.19 (0.78, 6.17) | .14 | 2.10 (0.60, 7.41) | .25 | ||||
| No more than once a month | 137 (7.1%) | 1.00 | 1.00 | 76 (26.8%) | 1.00 | |||||||||
| Drink beer? (n = 2212) | ||||||||||||||
| No | 771 (40.0%) | 1.00 | 1.00 | 133 (46.8%) | 1.00 | 1.00 | ||||||||
| Yes | 1157 (60.0%) | 1.06 (0.85, 1.32) | .61 | 1.00 (0.77, 1.28) | .97 | 151 (53.2%) | 0.62 (0.31, 1.27) | .20 | 0.81 (0.33, 2.02) | .65 | ||||
| Drink wine? (n = 2208) | ||||||||||||||
| No | 1729 (89.9%) | 1.00 | 1.00 | 201 (70.8%) | 1.00 | 1.00 | ||||||||
| Yes | 195 (10.1%) | 1.48 (1.07, 2.06) | .02 | 1.18 (0.83, 1.67) | .36 | 83 (29.2%) | 0.97 (0.44, 2.11) | .93 | 0.86 (0.33, 2.26) | .77 | ||||
| Drink liquor? (n = 2213) | ||||||||||||||
| No | 377 (19.5%) | 1.00 | 1.00 | 116 (40.9%) | 1.00 | 1.00 | ||||||||
| Yes | 1552 (80.5%) | 0.91 (0.70, 1.18) | .48 | 0.98 (0.73, 1.30) | .87 | 168 (59.2%) | 1.59 (0.75, 3.39) | .23 | 1.35 (0.55, 3.37) | .51 | ||||
| Beer intake (g/wk) (n = 2207) | ||||||||||||||
| 0 | 782 (40.7%) | 1.00 | .61 | 1.00 | .66 | 140 (49.3%) | 1.00 | .15 | 1.00 | .54 | ||||
| ≤37.92 (M)/≤18.96 (W) | 681 (35.4%) | 1.03 (0.80, 1.32) | .83 | 1.00 (0.76, 1.33) | .99 | 86 (30.3%) | 0.55 (0.23, 1.30) | .17 | 0.68 (0.24, 1.90) | .46 | ||||
| >37.92 (M)/>18.96 (W) | 460 (23.9%) | 1.08 (0.82, 1.42) | .61 | 0.96 (0.71, 1.31) | .80 | 58 (20.4%) | 0.51 (0.18, 1.41) | .19 | 0.64 (0.18, 2.22) | .48 | ||||
| Wine intake (g/wk) (n = 2205) | ||||||||||||||
| 0 | 1735 (90.3%) | 1.00 | .005 | 1.00 | .17 | 205 (72.4%) | 1.00 | .61 | 1.00 | .47 | ||||
| ≤11.85 (M)/≤7.90 (W) | 95 (4.9%) | 1.28 (0.80, 2.05) | .30 | 1.05 (0.64, 1.73) | .84 | 46 (16.3%) | 1.03 (0.40, 2.67) | .95 | 0.97 (0.31, 3.06) | .96 | ||||
| >11.85 (M)/>7.90 (W) | 92 (4.8%) | 1.82 (1.17, 2.85) | .008 | 1.37 (0.85, 2.19) | .19 | 32 (11.3%) | 0.71 (0.20, 2.51) | .60 | 0.71 (0.17, 2.99) | .64 | ||||
| Liquor intake (g/wk) (n = 2207) | ||||||||||||||
| 0 | 389 (20.2%) | 1.00 | .15 | 1.00 | .08 | 117 (41.2%) | 1.00 | .21 | 1.00 | .27 | ||||
| ≤90.60 (M)/≤30.20 (W) | 793 (41.2%) | 0.78 (0.58, 1.04) | .09 | 0.83 (0.61, 1.14) | .25 | 85 (29.9%) | 1.43 (0.59, 3.48) | .43 | 1.00 (0.35, 2.87) | >.99 | ||||
| >90.60 (M)/>30.20 (W) | 741 (38.5%) | 1.04 (0.78, 1.38) | .81 | 1.15 (0.84, 1.58) | .39 | 82 (28.9%) | 1.82 (0.77, 4.28) | .17 | 2.22 (0.75, 6.61) | .15 | ||||
Adjusted for age, area, smoking, body mass index, waist circumference, education level, physical activity, creatinine, high-sensitivity, average systolic blood pressure, average diastolic blood pressure, energy intake, protein intake, fat intake, and carbohydrate intake. The P value for the trend was calculated using the median of weekly alcohol consumption in each category (beer, wine, liquor).
CI = confidence interval, M = men, OR = odds ratio, W = women.
4. Discussion
This cross-sectional study included 7083 adult participants. The OR of hyperuricemia was greater in men who drank alcohol almost every day than that in men who drank alcohol no more than once a month. Liquor consumption showed a positive association with SUA levels both in men while wine consumption was found to have a negative association with SUA levels only in women.
Alcohol (specifically ethanol) intake can elevate the SUA by stimulating its production and impeding its elimination from the body.[29] Alcohol consumption accelerates the rate of ATP degradation, causing the formation of adenosine and adenine.[42] Adenosine can subsequently undergo further degradation into hypoxanthine and inosine.[42] The enzyme xanthine oxidase then converts hypoxanthine into xanthine, which ultimately transforms into uric acid.[42] Therefore, an increase in the breakdown of ATP would result in an increase in the production of purines and uric acid. Additionally, alcohol metabolism increases lactic acid levels in the blood, and lactic acid prevents uric acid excretion through the renal tubules.[43]
Our findings demonstrated that men who drank alcohol daily had a 1.68 times greater likelihood of developing hyperuricemia than those who drank alcohol no more than once a month (95% CI: 1.01, 2.81, P = .05). Likewise, a prior investigation suggested that SUA levels were higher (by 42.6 μmol/L) in middle-aged and older Singaporean Chinese adults who consumed alcoholic drinks every day than in those who did not drink alcohol.[44] In another investigation, adults who drank over 30 g or 2 alcoholic drinks per day had a risk of hyperuricemia that was over 65% higher than that of individuals who did not drink alcohol.[45] In the study by Nishimura et al,[46] the ingestion of 0.5 g ethanol per kilogram of body weight per day was found to raise SUA concentrations by 0.8 ± 0.4 mg/dL. Collectively, these findings associate daily drinking of alcoholic beverages with increased levels of SUA. The finding in our study that no significant association was observed between alcohol consumption frequency and hyperuricemia in women could be attributed to the limited number of female participants who reported drinking alcohol.
Our study found that the consumption of beer, wine, and liquor had varying impacts on SUA levels. Beer consumption and SUA levels were not shown to be statistically significantly associated in either men or women. A previous study found a weak link between beer intake and SUA.[47] This research and ours have a common feature, which is the small amount of beer consumed by the participants. Because the alcohol content of beer is lower than wine and liquor, generally between 4% and 5%, it may be difficult to observe a significant rise in uric acid when the intake is low.[48] Another research reported that SUA levels increased in five healthy men who consumed beer for 1 month (369 ± 71 vs 315 ± 58 μmol/L in the reference group, P < .05).[49] According to the CARDIA cohort study, which tracked participants over a 20-year period, there appears to be a correlation between increased beer consumption and higher SUA concentrations in both men and women.[50] Beer contains ethanol and the purine guanosine, both of which can promote uric acid synthesis.[51] The large amounts of guanosine in beer are more easily absorbed by the body than are other nucleosides or nucleotides.[52] Purine nucleoside phosphorylase converts guanosine to guanine, which is then deaminated by guanine deaminase to xanthine and finally converted to uric acid.[53]
Our data showed reductions in uric acid levels of 0.05 and 0.66 mg/dL in women who drank ≤ 7.9 and > 7.9g of wine per week, respectively, relative to those who did not drink wine. SUA levels decreased as wine consumption increased weekly in women (β = −0.008 mg/dL, P = .047) while a weak positive relationship was observed among men. Similarly, in a cross-sectional study with 14,809 individuals aged ≥ 20 years, SUA levels decreased as wine consumption increased from 0.01 to 0.99 servings per day.[29] According to a study conducted on middle-aged and older Koreans, it was found that consuming wine did not have any significant impact on SUA levels.[54] The conclusion that drinking wine decreases or does not affect SUA levels may partially be attributed to the antioxidant properties of polyphenols present in wine.[55] Wine has a more complex fermentation process than do beer and liquor.[56] Alcohol increases oxidative stress; thus, polyphenols may counteract its ability to do so. Since SUA is considered a potential marker of oxidative stress, decreased SUA levels indicate that the antioxidants in red wine help to improve the antioxidant capability of serum.[57–60] In our study, the finding that wine intake is only associated with lower SUA in women may be due to differences in the way that men and women metabolize alcohol.[61] Research suggests that women tend to have lower levels of alcohol dehydrogenase, which is responsible for metabolizing alcohol in the liver.[62,63] This can lead to higher blood alcohol levels and slower clearance of alcohol from the body in women, which may prolong the exposure to polyphenols from wine.
In the results of the linear regression analysis, we observed that liquor intake was positively related to SUA levels in men. However, in the general linear model, we observed that men who drank ≤ 90.6 g of liquor per week have lower SUA levels compared with those in nondrinkers. The 2016 Chinese Dietary Guidelines recommend the intake of < 25 g of liquor per day for men.[64] Because drinking frequency in our study was grouped according to the median amount of alcohol consumed, exact determination of the threshold amount of alcohol intake required for elevation of uric acid concentration was difficult. It is worth mentioning that excessive alcohol consumption, even from wine, can still have negative effects on health.[29,65,66]
Our study has several limitations. First, we did not determine whether drug use affected SUA levels. Medications such as diuretics, antitubercular drugs, immunosuppressants, nicotinic acid, and aspirin may have caused variations in SUA levels.[67] Drug usage was not examined in the CHNS. Second, because our study was cross-sectional, with exposure and outcome measured simultaneously, causal relationships could not be established. Finally, we could not obtain dietary data from the CHNS owing to its unavailability.
Although our study has some limitations, there are also several strengths worth noting. First, the CHNS database contains a substantial amount of data from nationally representative samples, covering diverse demographic and geographic regions including urban and rural communities. Second, all collected blood samples were examined by trained personnel in accordance with clinical laboratory standards in the same laboratory. Consequently, deviations in measurements were unlikely and the quality of the data was guaranteed.
Our study provided new information on the independent effects of beer, wine, and liquor on SUA levels in the Chinese population. In conclusion, beer, wine, and liquor have different effects on SUA levels in both men and women. Specifically, liquor consumption was positively related to SUA levels in men but moderate consumption of liquor was not associated with elevated SUA levels among men. In women, wine consumption was found to have a negative association with SUA levels while a weak positive relationship was observed among men. Replication studies in other ethnic groups or other study groups in China are warranted. Further research is necessary to confirm whether there is a causal connection between beer, liquor, or wine intake and SUA levels. Additionally, more research is required to determine whether moderate drinking is associated with elevated SUA levels for each type of alcoholic beverage.
Author contributions
Conceptualization: Yueying Wu, Dayeon Shin.
Data curation: Yueying Wu, Dayeon Shin.
Funding acquisition: Dayeon Shin.
Investigation: Yueying Wu, Dayeon Shin.
Methodology: Yueying Wu, Dayeon Shin.
Supervision: Dayeon Shin.
Writing – original draft: Yueying Wu.
Writing – review & editing: Yueying Wu, Dayeon Shin.
Abbreviations:
- BMI
- body mass index
- CHNS
- China Health and Nutrition Survey
- CI
- confidence interval
- MET
- metabolic equivalent of task
- OR
- odds ratio
- SUA
- serum uric acid
This work was supported by Inha University Research Grant.
This study was reviewed and approved by the Institutional Review Board (IRB) of Inha University on February 4, 2022 (IRB No. 220121-1A).
Written informed consent for CHNS was reviewed by the University of Chapel Hill, NC, USA and the National Institute of Nutrition and Health of the Chinese Center for Disease Control and Prevention, Beijing, China. Informed consent was obtained from all the participants.
The authors have no conflicts of interest to disclose.
The datasets generated during and/or analyzed during the current study are publicly available.
How to cite this article: Wu Y, Shin D. Association between alcoholic beverage intake and hyperuricemia in Chinese adults: Findings from the China Health and Nutrition Survey. Medicine 2023;102:22(e33861).
References
- [1].Sachs L, Batra KL, Zimmermann B. Medical implications of hyperuricemia. Med Health R I. 2009;92:353. [PubMed] [Google Scholar]
- [2].Jin M, Yang F, Yang I, et al. Uric acid, hyperuricemia and vascular diseases. Front Biosci. 2012;17:656. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [3].George C, Minter DA. Hyperuricemia. Treasure Island, FL: StatPearls Publishing; 2022. [PubMed] [Google Scholar]
- [4].Yokokawa H, Fukuda H, Suzuki A, et al. Association between serum uric acid levels/hyperuricemia and hypertension among 85,286 Japanese workers. J Clin Hypertens. 2016;18:53–9. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [5].Krishnan E, Pandya BJ, Chung L, et al. Hyperuricemia in young adults and risk of insulin resistance, prediabetes, and diabetes: a 15-year follow-up study. Am J Epidemiol. 2012;176:108–16. [DOI] [PubMed] [Google Scholar]
- [6].Braga F, Pasqualetti S, Ferraro S, et al. Hyperuricemia as risk factor for coronary heart disease incidence and mortality in the general population: a systematic review and meta-analysis. Clin Chem Lab Med. 2016;54:7–15. [DOI] [PubMed] [Google Scholar]
- [7].Wei CY, Sun CC, Wei JCC, et al. Association between hyperuricemia and metabolic syndrome: an epidemiological study of a labor force population in Taiwan. Biomed Res Int. 2015;2015:1–7. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [8].Kuwata H, Okamura S, Hayashino Y, et al. Serum uric acid levels are associated with a high risk of rapid chronic kidney disease progression among patients with type 2 diabetes: a prospective cohort study [Diabetes Distress and Care Registry at Tenri (DDCRT 12)]. Diabetol Int. 2016;7:352–60. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [9].Gustafsson D, Unwin R. The pathophysiology of hyperuricaemia and its possible relationship to cardiovascular disease, morbidity and mortality. BMC Nephrol. 2013;14:1–9. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [10].Tsumuraya Y, Hirayama T, Tozuka E, et al. Impact of hyperuricaemia on the chronic kidney disease‐associated risk factors in a community‐based population. Nephrology (Carlton). 2015;20:399–404. [DOI] [PubMed] [Google Scholar]
- [11].Yan D, Tu Y, Jiang F, et al. Uric acid is independently associated with diabetic kidney disease: a cross-sectional study in a Chinese population. PLoS One. 2015;10:e0129797. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [12].Zhu Y, Pandya BJ, Choi HK. Prevalence of gout and hyperuricemia in the US general population: the National Health and Nutrition Examination Survey 2007–2008. Arthritis Rheum. 2011;63:3136–41. [DOI] [PubMed] [Google Scholar]
- [13].Uaratanawong S, Suraamornkul S, Angkeaw S, et al. Prevalence of hyperuricemia in Bangkok population. Clin Rheumatol. 2011;30:887–93. [DOI] [PubMed] [Google Scholar]
- [14].Robinson P, Taylor W, Merriman T. Systematic review of the prevalence of gout and hyperuricaemia in Australia. Intern Med J. 2012;42:997–1007. [DOI] [PubMed] [Google Scholar]
- [15].Trifirò G, Morabito P, Cavagna L, et al. Epidemiology of gout and hyperuricaemia in Italy during the years 2005–2009: a nationwide population-based study. Ann Rheum Dis. 2013;72:694–700. [DOI] [PubMed] [Google Scholar]
- [16].Li Y, Shen Z, Zhu B, et al. Demographic, regional and temporal trends of hyperuricemia epidemics in mainland China from 2000 to 2019: a systematic review and meta-analysis. Glob Health Action. 2021;14:1874652. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [17].Zhang M, Zhu X, Wu J, et al. Prevalence of hyperuricemia among Chinese adults: findings from two nationally representative cross-sectional surveys in 2015–16 and 2018–19. Front Immunol. 2022;12:791983. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [18].Wang W, Zhang D, Xu C, et al. Heritability and genome-wide association analyses of serum uric acid in middle and old-aged Chinese twins. Front Endocrinol. 2018;9:75. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [19].Multidisciplinary Expert Task Force on Hyperuricemia Related Diseases. Chinese multidisciplinary expert consensus on the diagnosis and treatment of hyperuricemia and related diseases. Chin Med J. 2017;130:2473–88. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [20].Li R, Yu K, Li C. Dietary factors and risk of gout and hyperuricemia: a meta-analysis and systematic review. Asia Pac J Clin Nutr. 2018;27:1344–56. [DOI] [PubMed] [Google Scholar]
- [21].Qiu L, Cheng XQ, Wu J, et al. Prevalence of hyperuricemia and its related risk factors in healthy adults from Northern and Northeastern Chinese provinces. BMC Public Health. 2013;13:1–9. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [22].Xiong X, He F, Sun G, et al. The relationship between self-reported habitual snoring and hyperuricemia among Chinese urban adults: a cross-sectional study. Sleep Med. 2020;68:207–12. [DOI] [PubMed] [Google Scholar]
- [23].Tang YX, Bloom MS, Qian Z, et al. Association between ambient air pollution and hyperuricemia in traffic police officers in China: a cohort study. Int J Environ Health Res. 2021;31:54–62. [DOI] [PubMed] [Google Scholar]
- [24].Hollis-Moffatt JE, Xu X, Dalbeth N, et al. Role of the urate transporter SLC2A9 gene in susceptibility to gout in New Zealand Māori, Pacific Island, and Caucasian case–control sample sets. Arthritis Rheumatol. 2009;60:3485–92. [DOI] [PubMed] [Google Scholar]
- [25].Cheng LS, Chiang SL, Tu HP, et al. Genomewide scan for gout in Taiwanese aborigines reveals linkage to chromosome 4q25. Am J Hum Genet. 2004;75:498–503. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [26].Piao W, Zhao L, Yang Y, et al. The prevalence of hyperuricemia and its correlates among Adults in China: Results from CNHS 2015–2017. Nutrients. 2022;14:4095. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [27].Kakutani Hatayama M, Kadoya M, Okazaki H, et al. Nonpharmacological management of gout and hyperuricemia: hints for better lifestyle. Am J Lifestyle Med. 2017;11:321–9. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [28].Maksimov SA, Shalnova SA, Deyev A, et al. Hyperuricemia versus lifestyle in men and women of the Russian Federation population. Russ Open Med J. 2020;9:214. [Google Scholar]
- [29].Choi HK, Curhan G. Beer, liquor, and wine consumption and serum uric acid level: the Third National Health and Nutrition Examination Survey. Arthritis Care Res. 2004;51:1023–9. [DOI] [PubMed] [Google Scholar]
- [30].Choi HK, Atkinson K, Karlson EW, et al. Alcohol intake and risk of incident gout in men: a prospective study. Lancet. 2004;363:1277–81. [DOI] [PubMed] [Google Scholar]
- [31].Zhang B, Zhai F, Du S, et al. The China Health and Nutrition Survey, 1989–2011. Obes Rev. 2014;15:2–7. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [32].Popkin BM, Du S, Zhai F, et al. Cohort profile: the China Health and Nutrition Survey—monitoring and understanding socio-economic and health change in China, 1989–2011. Int J Epidemiol. 2010;39:1435–40. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [33].Zhan Y, Chen R, Zheng W, et al. Association between serum magnesium and anemia: China health and nutrition survey. Biol Trace Elem Res. 2014;159:39–45. [DOI] [PubMed] [Google Scholar]
- [34].Yan S, Li J, Li S, et al. The expanding burden of cardiometabolic risk in China: the China Health and Nutrition Survey. Obes Rev. 2012;13:810–21. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [35].Han LL, Wang YX, Li J, et al. Gender differences in associations of serum ferritin and diabetes, metabolic syndrome, and obesity in the China Health and Nutrition Survey. Mol Nutr Food Res. 2014;58:2189–95. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [36].Ainsworth BE, Haskell WL, Herrmann SD, et al. 2011 Compendium of Physical Activities: a second update of codes and MET values. Med Sci Sports Exerc. 2011;43:1575–81. [DOI] [PubMed] [Google Scholar]
- [37].Ainsworth BE, Haskell WL, Whitt MC, et al. Compendium of physical activities: an update of activity codes and MET intensities. Med Sci Sports Exerc. 2000;32(9; SUPP/1):S498–504. [DOI] [PubMed] [Google Scholar]
- [38].Babor TF, Higgins-Biddle JC, Saunders JB, et al. The Alcohol Use Disorders Identification Test. Geneva, Switzerland: World Health Organization; 2001. [Google Scholar]
- [39].Chinese Center for Disease Control Prevention. Surveillance Report on Chronic Diseases and Its Risk Factors in China. Beijing, China: Military Medical Science Press; 2010. [Google Scholar]
- [40].Bardin T, Richette P. Definition of hyperuricemia and gouty conditions. Curr Opin Rheumatol. 2014;26:186–91. [DOI] [PubMed] [Google Scholar]
- [41].Li X, He T, Yu K, et al. Markers of iron status are associated with risk of hyperuricemia among Chinese adults: nationwide population-based study. Nutrients. 2018;10:191. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [42].Yamamoto T, Moriwaki Y, Takahashi S. Effect of ethanol on metabolism of purine bases (hypoxanthine, xanthine, and uric acid). Clin Chim Acta. 2005;356:35–57. [DOI] [PubMed] [Google Scholar]
- [43].Nieradko Iwanicka B. The role of alcohol consumption in pathogenesis of gout. Crit Rev Food Sci Nutr. 2022;62:7129–37. [DOI] [PubMed] [Google Scholar]
- [44].Teng GG, Tan CS, Santosa A, et al. Serum urate levels and consumption of common beverages and alcohol among Chinese in Singapore. Arthritis Care Res (Hoboken). 2013;65:1432–40. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [45].Sun SZ, Flickinger BD, Williamson-Hughes PS, et al. Lack of association between dietary fructose and hyperuricemia risk in adults. Nutr Metab. 2010;7:1–12. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [46].Nishimura T, Shimizu T, Mineo I, et al. Influence of daily drinking habits on ethanol-induced hyperuricemia. Metabolism. 1994;43:745–8. [DOI] [PubMed] [Google Scholar]
- [47].Zhu B, Li Y, Shi Y, et al. Long-term drinking behavior change patterns and its association with hyperuricemia in Chinese adults: evidence from China Health and Nutrition Survey. BMC Public Health. 2022;22:1–11. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [48].World Health Organization. International Guide for Monitoring Alcohol Consumption and Related Harm. Geneva: World Health Organization; 2000. [Google Scholar]
- [49].Moriwaki Y, Ka T, Takahashi S, et al. Effect of beer ingestion on the plasma concentrations and urinary excretion of purine bases: one-month study. Nucleosides Nucleotides Nucleic Acids. 2006;25:1083–5. [DOI] [PubMed] [Google Scholar]
- [50].Gaffo AL, Roseman JM, Jacobs DR, et al. Serum urate and its relationship with alcoholic beverage intake in men and women: findings from the Coronary Artery Risk Development in Young Adults (CARDIA) cohort. Ann Rheum Dis. 2010;69:1965–70. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [51].Ekpenyong CE, Daniel N. Roles of diets and dietary factors in the pathogenesis, management and prevention of abnormal serum uric acid levels. PharmaNutrition. 2015;3:29–45. [Google Scholar]
- [52].Gibson T, Rodgers A, Simmonds H, et al. Beer drinking and its effect on uric acid. Rheumatology. 1984;23:203–9. [DOI] [PubMed] [Google Scholar]
- [53].Danve A, Sehra ST, Neogi T. Role of diet in hyperuricemia and gout. Best Pract Res Clin Rheumatol. 2021;35:101723. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [54].Shin D, Lee KW. Dietary acid load is positively associated with the incidence of hyperuricemia in middle-aged and older Korean adults: findings from the Korean Genome and epidemiology study. Int J Environ Res Public Health. 2021;18:10260. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [55].Fernández Pachón M, Villano D, Garcia Parrilla M, et al. Antioxidant activity of wines and relation with their polyphenolic composition. Anal Chim Acta. 2004;513:113–8. [Google Scholar]
- [56].Pillinger MH, Keenan RT. Update on the management of hyperuricemia and gout. Bull NYU Hosp Jt Dis. 2008;66:231–9. [PubMed] [Google Scholar]
- [57].Bertelli AA. Wine, research and cardiovascular disease: instructions for use. Atherosclerosis. 2007;195:242–7. [DOI] [PubMed] [Google Scholar]
- [58].Maxwell S, Cruickshank A, Thorpe G. Red wine and antioxidant activity in serum. Lancet. 1994;344:193–4. [DOI] [PubMed] [Google Scholar]
- [59].Covas MI, Gambert P, Fitó M, et al. Wine and oxidative stress: up-to-date evidence of the effects of moderate wine consumption on oxidative damage in humans. Atherosclerosis. 2010;208:297–304. [DOI] [PubMed] [Google Scholar]
- [60].Huisman H, Schutte A, van Rooyen J, et al. P1. 08 effects of antioxidants on serum uric acid as a marker of vascular function. Artery Res. 2008;2:94–94. [Google Scholar]
- [61].Soldin OP, Mattison DR. Sex differences in pharmacokinetics and pharmacodynamics. Clin Pharmacokinet. 2009;48:143–57. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [62].Meier P, Seitz HK. Age, alcohol metabolism and liver disease. Curr Opin Clin Nutr Metab Care. 2008;11:21–6. [DOI] [PubMed] [Google Scholar]
- [63].Shankar K, Ronis MJ, Badger TM. Effects of pregnancy and nutritional status on alcohol metabolism. Alcohol Res Health. 2007;30:55–9. [PMC free article] [PubMed] [Google Scholar]
- [64].Wang S, Lay S, Yu H, et al. Dietary guidelines for Chinese residents (2016): comments and comparisons. J Zhejiang Univ Sci B. 2016;17:649–56. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [65].Minzer S, Losno RA, Casas R. The effect of alcohol on cardiovascular risk factors: is there new information? Nutrients. 2020;12:912. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [66].Fradera U, Hammer C. Moderate wine consumption and cancer risk in context. BIO Web Conf. 2023;56:04002. [Google Scholar]
- [67].Ben Salem C, Slim R, Fathallah N, et al. Drug-induced hyperuricaemia and gout. Rheumatology. 2017;56:679–88. [DOI] [PubMed] [Google Scholar]