[Link].

com/scientificreports

OPEN Association between vitamin B1

intake and hyperuricemia in adults
Yi‑Ming Li 1,2, Xiao‑Hu Xu 1,2, Xiao‑Fan Xu 1,2, Xia‑Xia Yang 2, Yi‑Long Dai 1,2, Dong‑Xue Song 2,
Cheng‑Qiang Jin 2,4,5* & Yan‑Xia Jia 3,5*

Studies investigating the relationship between dietary vitamin B1 intake and risk of Hyperuricemia
(HU) are scarce, the present study aimed to examine the association of dietary vitamin B1 intake and
HU among adults. This cross-sectional study included 5750 adults whose data derived from National
Health and Nutrition Examination Survey (NHANES) from March 2017 to March 2020. The dietary
intake of vitamin B1 was assessed using 24-h dietary recall interviews. The characteristics of study
participants were grouped into five levels according to the levels of vitamin B1 quintile. Multivariate
logistic regression analysis was used to estimate the odds ratio (OR) and 95% confidence interval (CI)
of HU, according to the vitamin B1 intake quintile for male and female separately. The dose–response
relationship was determined by the restricted cubic spline (RCS). Smoothed curve fitting was used
to assess serum uric acid concentration versus dietary vitamin B1 intake in the study population. The
prevalence of hyperuricemia was 18.90% (20.15% and 17.79% for males and females, respectively) in
the United States from March 2017 to March 2020. Multiple logistic regression analyses showed that
in the male population, the HU ratio (OR) of vitamin B1 intake in Q2 to Q5 compared with the lowest
quintile (Q1) was 0.75 (95% CI 0.52, 1.09), 0.70 (95% CI 0.48, 1.02), 0.66 (95% CI 0.44, 0.99) and 0.55
(95% CI 0.34, 0.90). The P for trend was 0.028. In women, the ORs for vitamin B1 intake Q2 to Q5 were
0.87 (95% CI 0.64, 1.19), 0.97 (0.68–1.38), 1.05 (0.69–1.60) and 0.75 (0.42–1.34), respectively. The P
for trend was 0.876. The RCS curve revealed a linear relationship between vitamin B1 intake and the
risk of hyperuricemia in men (P nonlinear = 0.401). Smoothed curve fitting demonstrated a negative
association between vitamin B1 intake and serum uric acid concentration in men, whereas there was
no significant association between dietary vitamin B1 intake and the risk of hyperuricemia in women.
In the US adult population, dietary vitamin B1 intake was negatively associated with hyperuricemia in
males.

Keywords Hyperuricemia, Vitamin B1, NHANES, Prevalence, Uric acid

Uric acid is the final product of purine metabolism and the main endogenous antioxidant in the body. It plays
bioprotective roles. Hyperuricemia (HU) occurs because of urate overproduction or impaired urate excretion
through the kidney and gastrointestinal t­ ract1. In recent decades, there is strong epidemiological evidence that
the prevalence of hyperuricemia is on the increase w ­ orldwide2. HU is considered as a precursor of gout and
an essential risk factor for cardiovascular diseases, type 2 diabetes, hypertension, and chronic kidney d ­ isease3.
As HU receives more attention, it is necessary to find potentially modifiable factors that inhibit the increase in
serum uric acid concentration.
Vitamin B1 or thiamin, is an essential water-soluble vitamin critical for carbohydrate and amino acid catabo-
lism and gluconeogenesis. Vitamin B1 is essential for the proper function of most tissues and organs. Thus, its
deficiency can have a myriad of clinical effects, most notably on the nervous and cardiovascular s­ ystems4. Dietary
intake of vitamin B1 is closely related to human health. Studies over the past decade have focused on an associa-
tion between thiamine deficiency and glucose metabolism dysfunction in patients with type 1 and type 2 diabetes.
One of these mentioned that high doses of thiamine may improve the vascular complications of the disease, such
as nephropathy, neuropathy and ­retinopathy5. Previous studies have found that HU may be associated with intake
levels of multiple vitamins, such as vitamin C­ 1, ­retinol6, vitamin B
­ 127 and so on. However, studies investigating

1
College of Clinical Medicine, Jining Medical University, Jining, Shandong Province, China. 2Clinical Laboratory,
Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong Province,
China. 3Radiology Department, Jining First People’s Hospital, Jining, Shandong Province, China. 4Clinical
Laboratory Management Teaching and Research Office, College of Forensic Medicine and Medical Laboratory,
Jining Medical University, Jining, Shandong Province, China. 5These authors contributed equally: Cheng-Qiang Jin
and Yan-Xia Jia. *email: jincq2008@[Link]; jingying001002@[Link]

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the relationship between dietary vitamin B1 intake and risk of HU are scarce, only one cross-sectional study has
shown that dietary vitamin B1 intake is negatively associated with HU in men of C ­ hina8.
To date, no known studies have explored the relationship between dietary vitamin B1 intake and HU. There-
fore, the purpose of this cross-sectional study was to investigate this correlation using a large nationally repre-
sentative sample in the US.

Results
A total of 5750 individuals (2725 males, 3025 females) participated in our study. The characteristics of study
participants were grouped into five levels according to the levels of vitamin B1 quintile, as shown in Table 1.
Significant differences were detected across all quintiles of vitamin B1 intake for age, gender, race, educational
background, BMI, HU prevalence, vitamin C intake, vitamin B6 intake, folate intake, retinol intake, energy intake,
protein intake, carbohydrate intake, serum cholesterol, and TG levels. Subjects with higher levels of vitamin B1
intake were younger, more non-Hispanic whites, and more males than females, had higher intakes of vitamin
C, dietary vitamin B6, folic acid, retinol, and energy, protein, and carbohydrate intakes, were also likely to have
lower BMI, serum cholesterol, and TG, and were less likely to have hypertension, diabetes, and HU.

Vitamin B1 intake (mg/Day)

Characteristics Q1 (n = 1150) Q2 (n = 1149) Q3 (n = 1148) Q4 (n = 1152) Q5 (n = 1151) P-value
Age (years) 50.93 ± 16.61 51.06 ± 17.72 50.92 ± 16.88 51.48 ± 17.31 48.75 ± 16.41 0.001
Gender (n, %) < 0.001
Male 332 (28.87%) 439 (38.21%) 503 (43.82%) 630 (54.69%) 821 (71.33%)
Female 818 (71.13%) 710 (61.79%) 645 (56.18%) 522 (45.31%) 330 (28.67%)
Race/ethnicity (n,%) < 0.001
Mexican American 115 (10.00%) 144 (12.53%) 142 (12.37%) 128 (11.11%) 137 (11.90%)
Other Hispanic 136(11.83%) 111 (9.66%) 104 (9.06%) 115 (9.98%) 114 (9.90%)
Non-Hispanic White 367 (31.91%) 427 (37.16%) 449 (39.11%) 450 (39.06%) 462 (40.14%)
Non-Hispanic Black 387 (33.65%) 324 (28.20%) 279 (24.30%) 268 (23.26%) 236 (20.50%)
Non-Hispanic Asian 80 (6.96%) 95 (8.27%) 122(10.63%) 128(11.11%) 147(12.77%)
Other Race 65 (5.65%) 48 (4.18%) 52 (4.53%) 63 (5.47%) 55 (4.78%)
Education < 0.001
< High school graduate 213 (18.52%) 169 (14.71%) 190 (16.55%) 170 (14.76%) 172 (14.94%)
High school graduate/
317 (27.57%) 253 (22.02%) 264 (23.00%) 251 (21.79%) 264 (22.94%)
GED or equivalent
> High school graduate 620 (53.91%) 727 (63.27%) 694 (60.45%) 731 (63.45%) 715 (62.12%)
Drinking status (n,%) 0.009
Never 348 (30.26%) 309 (26.89%) 319 (27.79%) 338 (29.34%) 280 (24.33%)
Moderate consumption 682 (59.30%) 685 (59.62%) 670 (58.36%) 650 (56.42%) 706 (61.34%)
Excessive consumption 120 (10.43%) 155 (13.49%) 159 (13.85%) 164 (14.24%) 165 (14.34%)
Smoking status (n,%) 0.009
Yes 490 (42.61%) 438 (38.12%) 477 (41.55%) 480 (41.67%) 525 (45.61%)
No 660 (57.39%) 711 (61.88%) 671 (58.45%) 672 (58.33%) 626 (54.39%)
Diabetes status (n,%) 174 (15.13%) 163 (14.19%) 173 (15.07%) 170 (14.76%) 148 (12.86%) 0.639
Hypertension status (n,%) 467(40.61%) 421(36.64%) 444(38.68%) 451(39.15%) 404(35.10%) 0.109
BMI (kg/m2) 30.90 ± 7.70 30.37 ± 7.69 30.13 ± 6.81 30.06 ± 7.72 29.99 ± 8.06 0.027
HU (n,%) 245 (21.30%) 208 (18.10%) 217 (18.90%) 221 (19.18%) 196 (17.03%) < 0.001
Vitamin C intake (mg/day) 33.10 (13.65–68.75) 50.80 (24.45–92.20) 59.85 (29.27–109.03) 66.47 (34.99–118.26) 87.05 (44.45–143.07) < 0.001
Vitamin B6 intake (mg/
1.04 (0.75–1.37) 1.41 (1.11–1.80) 1.69 (1.34–2.12) 1.96 (1.60–2.44) 2.67 (2.10–3.36) < 0.001
day)
Folate intake (mcg/day) 174.50 (136.50–217.50) 259.50 (217.50–309.50) 323.25 (275.38–380.50) 398.00 (331.00–476.00) 538.00 (436.75–667.00) < 0.001
Retinol intake(mcg/day) 173.75 (94.62–269.75) 255.00 (158.50–373.50) 314.25 (197.75–459.75) 392.50 (253.38–571.38) 501.50 (323.25–737.25) < 0.001
Energy intake(kcal/day) 1242.50 (971.56–1526.50) 1640.00 (1373.50–1950.00) 1957.25 (1627.00–2305.62) 2254.25 (1896.38–2684.50) 2779.50 (2333.50–3323.75) < 0.001
Protein intake(gm/day) 46.48 (34.62–59.99) 62.16 (51.17–75.59) 72.40 (59.45–87.97) 84.39 (70.13–100.85) 105.56 (85.59–129.33) < 0.001
Carbohydrate intake(gm/
136.98 (103.75–175.88) 185.74 (155.10–225.55) 223.85 (184.63–264.59) 260.44 (215.45–314.24) 327.25 (267.43–393.55) < 0.001
day)
Glucose (mg/dL) 93.00 (86.00–103.00) 93.00 (87.00–101.00) 93.00 (86.00–103.00) 93.00 (87.00–102.00) 93.00 (87.00–101.00) 0.575
Cholesterol (mg/dL) 186.00 (160.00–216.00) 183.00 (159.00–211.00) 185.00 (160.00–212.00) 181.00 (156.00–207.00) 181.00 (156.00–208.00) < 0.001
TG (mg/dL) 105.00 (79.00–147.00) 107.00 (77.00–158.00) 116.00 (81.00–168.00) 115.00 (81.00–168.00) 119.00 (80.00–179.00) < 0.001

Table 1.  Characteristics of the participants according to intake of vitamin B1.

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The prevalence of hyperuricemia was 18.90% (20.15% and 17.79% for males and females, respectively). The
results comparing vitamin B1 status and other indicators between hyperuricemia and non-hyperuricemia are
shown in Table 2. For men, race, drinking status, BMI, hypertension status, vitamin B1 intake, carbohydrate
intake, retinol intake, serum glucose, serum cholesterol and TG level indicators were significantly different
between hyperuricemia and non-hyperuricemia. Compared to the participants without hyperuricemia, those
with hyperuricemia were more likely to be non-Hispanic white, have hypertension, have higher BMI levels,
serum glucose, serum cholesterol, and TG levels, and have lower dietary vitamin B1 intake, carbohydrate intake,
retinol intake. In women, patients with hyperuricemia tended to be older, had a higher prevalence of diabetes,
hypertension, and higher blood glucose, serum cholesterol, and TG levels, in addition to a lower dietary carbo-
hydrate intake and vitamin C intake (All P < 0.05).
A multivariate model was used to investigate the association between vitamin B1 intake and hyperurice-
mia, as shown in Table 3. In this cross-sectional study, the association between dietary vitamin B1 intake and

Male Female
Non-HU HU Non-HU HU
Characteristics (n = 2176) (n = 549) P-value (n = 2487) (n = 538) P-value
52.00 49.00 60.00
Age(years) 52.00 (36.00–65.00) 0.781 < 0.001
(36.00–64.00) (35.00–62.00) (48.00–69.00)
Race/ethnicity
0.003 < 0.001
(n,%)
Mexican American 260 (11.95%) 47 (8.56%) 320 (12.87%) 39 (7.25%)
Other Hispanic 224 (10.29%) 63 (11.48%) 261 (10.49%) 32 (5.95%)
Non-Hispanic White 850(39.06%) 190(34.61%) 903 (36.31%) 212(39.41%)
Non-Hispanic Black 533(24.49%) 138(25.14%) 637 (25.61%) 186(34.57%)
Non-Hispanic Asian 194 (8.92%) 73 (13.30%) 262 (10.53%) 43 (7.99%)
115 38 104 26
Other Race—Including Multi-Racial
(5.28%) (6.92%) (4.18%) (4.83%)
Education level (n, %) 0.252 0.112
< High school graduate 388 (17.83%) 82 (14.94%) 378 (15.20%) 66 (12.27%)
High school graduate/GED or
531(24.40%) 134(24.41%) 549(22.07%) 135(25.09%)
equivalent
> High school graduate 125(57.77%) 333(60.66%) 1560(62.73%) 337(62.64%)
Drinking status (n, %) 0.001 0.056
never 559(25.69%) 113(20.58%) 735 (29.55%) 187(34.76%)
moderate consumption 1245(57.22%) 309(56.28%) 1530(61.52%) 309(57.43%)
excessive consumption 372 (17.10%) 127(23.13%) 222 (8.93%) 42 (7.81%)
Smoking status (n, %) 0.503 0.001
1105 270 819 216
Yes
(50.78%) (49.18%) (32.93%) (40.15%)
1071 279 1668 322
No
(49.22%) (50.82%) (67.07%) (59.85%)
28.10 31.00 28.60 34.00
BMI (kg/m2) < 0.001 < 0.001
(24.80–32.30) (27.30–36.10) (24.30–33.60) (28.72–40.18)
Diabetes status (n, %) 373 (17.14%) 75 (13.66%) 0.114 263 (10.57%) 117(21.75%) < 0.001
780 254 798 355
Hypertension status (n, %) < 0.001 < 0.001
(35.85%) (46.27%) (32.09%) (65.99%)
VitaminB1 1.62 1.54 1.24 1.22
0.015 0.158
intake (mg/day) (1.20–2.14) (1.11–2.03) (0.92–1.61) (0.88–1.58)
Energy intake(kcal/day) 2239.50 (1723.50–2796.62) 2196.50 (1653.50–2755.25) 0.333 1708.50 (1327.50–2163.75) 1679.00 (1306.00–2081.25) 0.113
84.43 63.43 63.58
Protein intake(gm/day) 82.84 (64.77–108.20) 0.570 0.169
(64.56–108.16) (48.95–82.40) (50.03–79.08)
Carbohydrate intake(gm/day) 252.29 (187.64–327.27) 239.15 (179.44–325.13) 0.108 199.86 (153.30–258.44) 190.52 (145.80–248.37) 0.008
Retinol intake(mcg/day) 346.50 (199.88–546.12) 306.50 (177.00–499.50) < 0.001 288.00 (170.50–446.25) 277.75 (164.12–445.12) 0.227
60.38 58.00 52.80
Vitamin C intake(mg/day) 56.15 (26.85–107.45) 0.628 0.020
(26.60–112.19) (27.20–104.15) (25.59–93.61)
1.96 1.95 1.49 1.49
Vitamin B6 intake(mg/day) 0.467 0.312
(1.43–2.72) (1.44–2.73) (1.08–2.04) (1.10–1.95)
Folate intake(mcg/day) 361.50 (268.88–501.50) 353.50 (251.50–487.00) 0.304 291.50 (210.00–392.00) 277.00 (196.00–381.25) 0.091
94.00 91.00 96.00
Glucose (mg/dL) 95.00 (89.00–106.00) 0.022 < 0.001
(88.00–104.00) (85.00–99.00) (89.00–110.00)
Cholesterol (mg/dL) 177.00 (152.00–205.00) 187.00 (160.00–220.00) < 0.001 185.00 (162.00–213.00) 188.00 (160.25–223.00) 0.021
TG (mg/dL) 114.50 (80.00–172.25) 137.00 (98.00–213.00) < 0.001 102.00 (74.00–146.00) 132.00 (96.00–177.75) < 0.001

Table 2.  Characteristics of the participants with or without hyperuricemia.

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Dietary vitamin B1 intake (mg/day)

Q1 Q2 Q3 Q4 Q5
(< 0.94) (0.94–1.24) (1.25–1.55) (1.56–1.99) (> 2.00)
(n = 1150) (n = 1149) (n = 1148) (n = 1152) (n = 1151) P for tend
Male 0.76 0.76 0.69 0.64
Model ­Ia
Reference 0.007
(n = 2725) (0.54, 1.06) (0.54, 1.06) (0.50, 0.95) (0.47, 0.87)
0.74 0.72 0.68 0.57
Model ­IIb Reference 0.028
(0.52, 1.06) (0.50, 1.04) (0.46, 1.00) (0.35, 0.91)
0.75 0.70 0.66 0.55
Model ­IIIc Reference 0.028
(0.52, 1.09) (0.48, 1.02) (0.44, 0.99) (0.34, 0.90)
Female 0.82 0.91 0.96 0.80
Model ­Ia Reference 0.503
(n = 3025) (0.63, 1.08) (0.69, 1.20) (0.72, 1.28) (0.56, 1.16)
0.89 1.00 1.10 0.78
Model ­IIb Reference 0.989
(0.66, 1.22) (0.70, 1.41) (0.72, 1.68) (0.44, 1.39)
0.87 0.97 1.05 0.75
Model ­IIIc Reference 0.876
(0.64, 1.19) (0.68, 1.38) (0.69, 1.60) (0.42, 1.34)

Table 3.  Adjusted odds ratios of hyperuricemia among participants associated with vitamin B1 intake.
a
Adjusted for age, race/ethnicity; b Adjusted for age, race/ethnicity, hypertension status, BMI, protein intake,
carbohydrate intake, vitamin B6 intake, folate intake, and retinol intake; c Adjusted for age, race/ethnicity,
smoking status, drinking status, education background, hypertension status, diabetes status, protein intake,
carbohydrate intake, retinol intake, vitamin B6 intake, folate intake, BMI, cholesterol and TG.

hyperuricemia was revealed based on analysis stratified by gender. In the male population, a significant negative
association between vitamin B1 intake and HU prevalence was found in models 1, 2 and 3, with linear trend
tests showing a statistically significant difference (P values are 0.007, 0.028 and 0.028, respectively). In model 3,
after controlling for age, race/ethnicity, smoking status, alcohol consumption status, educational background,
hypertension status and diabetes status, protein intake, carbohydrate intake, retinol intake, vitamin B6 intake,
folate intake, BMI, cholesterol, and TG, an inverse trend was also observed for higher vitamin B1 intake and HU
risk. When compared to those consuming less than 0.94 mg Vitamin B1 daily, the relative odds of hyperuricemia
were significantly decreased by 0.75 times among those that were consuming 0.94–1.24 mg of vitamin B1 daily
(OR = 0.75, 95% CI 0.52, 1.09), 0.70 times among participants who consumed 1.25–1.55 mg daily (OR = 0.70,
95% CI 0.48, 1.02), 0.66 times among those consuming 1.56–1.99 mg daily (OR = 0.66, 95% CI 0.44, 0.99), and
by 0.55 times among those consuming 2.00 mg or more daily (OR = 0.55, 95% CI 0.34, 0.90). However, no sig-
nificant differences were found between dietary vitamin B1 intake and risk of hyperuricemia in women. Among
the women, after adjustment for multiple covariates, compared to Q1, the adjusted ORs of HU are 1.05 (95%
CI 0.69, 1.60) for Q4 (those consuming 1.56–1.99 mg vitamin B1 daily), 0.75 (95% CI 0.42, 1.34) for Q5 (those
consuming 2.00 mg or more), and the P for trend is 0.876.
This study will further stratify the study population to explore the relationship between vitamin B1 and
hyperuricemia among subgroups, as shown in Table 4. First, the vitamin B1 five groups Q1-Q5 of Non-Hispanic
White were observed in race, and the OR values were 0.79, 0.80, 0.65, 0.43, respectively, and P for tend was 0.017.
No significant OR values were observed among the other [Link] the Middle age group (42–60 years old),
with the increase of vitamin B1 intake (Q1–Q5), the OR values were 0.72, 0.64, 0.64 and 0.44, respectively. The
P value was 0.023. However, no relationship between vitamin B1 intake and HU was demonstrated in BMI and
alcohol consumption status groups.
Following multiple regression, we used the restricted cubic spline curve (RCS) to analyze the dose–response
relationship between vitamin B1 and HU. As shown in Fig. 1a, our results indicated a linear relationship between
dietary vitamin B1 intake and HU risk in men (P = 0.401), with the prevalence of hyperuricemia decreasing with
increasing dietary vitamin B1 concentrations. However, this trend was not observed in women (Fig. 1b). In
addition, a smoothed curve-fitting analysis was performed to compare the serum uric acid concentration with
vitamin B1 intake of the study participants. The results are shown in Fig. 2, which indicates that in men, vitamin
B1 intake was inversely related to serum uric acid concentration, meaning that the higher the vitamin B1 intake,
the lower the serum uric acid concentration in men. Meanwhile, we plotted no significant relationship between
vitamin B1 intake and serum uric acid concentration in women.

Discussion
In this large population-based study of US adults, we observed a negative association between dietary vitamin
B1 intake and HU in men. After adjustment for multiple covariates (age, race/ethnicity, BMI, smoking status,
etc.), this association remained significant in men, but no significant association was observed among women.
To the best of our knowledge, this is the first study to show an association between dietary vitamin B1 intake
and hyperuricemia in an adult US population. In this study, we used data from nhanes 2017 to 2020 to investigate
this association, using a nationally representative sample of US adults, to reveal the association between dietary
vitamin B1 intake and hyperuricemia in men and women. A preclinical study has shown the effect of thiamine
in reducing uric acid levels in diabetic r­ ats9. Thiamin reduces the substrates of the upregulated catabolic pathway
involved in uric acid synthesis. One study suggested that treatment with thiamine as a therapeutic agent can
alleviate serum uric acid levels in patients with AUD (alcohol use disorder), whether or not they exhibit liver

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Dietary vitamin B1 intake (mg/day)

Q1 Q2 Q3 Q4 Q5
(< 0.94) (0.94–1.24) (1.25–1.55) (1.56–1.99) (> 2.00)
Covariates (n = 1150) (n = 1149) (n = 1148) (n = 1152) (n = 1151) P for tend
Race/ethnicitya
Mexican American Reference 0.62 (0.29, 1.33) 0.58 (0.25, 1.38) 1.09 (0.44, 2.68) 0.62 (0.18, 2.08) 0.936
Other Hispanic Reference 0.89 (0.41, 1.94) 0.71 (0.31, 1.64) 0.53 (0.21, 1.29) 0.35 (0.11, 1.15) 0.068
Non-Hispanic
Reference 0.79 (0.54, 1.17) 0.80 (0.53, 1.20) 0.65 (0.41, 1.04) 0.43 (0.24, 0.80) 0.017
White
Non-Hispanic Black Reference 0.83 (0.55, 1.25) 1.01 (0.64, 1.59) 0.85 (0.49, 1.45) 0.92 (0.46, 1.85) 0.823
Non-Hispanic Asian Reference 0.86 (0.36, 2.03) 0.75 (0.31, 1.80) 1.42 (0.56, 3.62) 0.70 (0.23, 2.18) 0.986
Other Race—
Including Multi- Reference 1.15 (0.39, 3.35) 0.96 (0.32, 2.87) 1.17 (0.37, 3.69) 2.25 (0.55, 9.28) 0.413
Racial
Ageb
Low
Reference 0.69 (0.43, 1.09) 0.88 (0.54, 1.43) 0.90 (0.53, 1.53) 0.77 (0.39, 1.50) 0.814
(21–41 years)
Middle
Reference 0.72 (0.47, 1.11) 0.64 (0.41, 1.00) 0.64 (0.40, 1.05) 0.44 (0.24, 0.83) 0.023
(42–60 years)
High
Reference 0.93 (0.66, 1.31) 0.94 (0.65, 1.38) 0.88 (0.57, 1.36) 0.71 (0.40, 1.29) 0.388
(> 60 years)
c
BMI
Low
Reference 0.90 (0.54, 1.50) 0.80 (0.45, 1.40) 0.99 (0.54, 1.80) 0.76 (0.36, 1.64) 0.681
(14.6–26.3)
Middle
Reference 0.98 (0.66, 1.46) 1.03 (0.68, 1.57) 0.89 (0.55, 1.44) 0.66 (0.35, 1.25) 0.316
(26.4–32.0)
High
Reference 0.67 (0.48, 0.93) 0.66 (0.46, 0.93) 0.67 (0.45, 0.99) 0.58 (0.35, 0.97) 0.066
(> 32.1)
Drinking ­statusd
Never Reference 0.93 (0.60, 1.43) 0.65 (0.40, 1.05) 0.82 (0.48, 1.41) 0.67 (0.33, 1.36) 0.244
Moderate consump-
Reference 0.77 (0.57, 1.04) 0.90 (0.65, 1.24) 0.87 (0.60, 1.25) 0.66 (0.41, 1.05) 0.303
tion
Excessive consump-
Reference 0.65 (0.35, 1.22) 0.73 (0.38, 1.40) 0.50 (0.24, 1.04) 0.46 (0.18, 1.19) 0.098
tion

Table 4.  Participants’ data on vitamin B1 intake were analyzed by stratified subgroups. a Adjusted for age,
hypertension status, BMI, protein intake, carbohydrate intake, vitamin B6 intake, folate intake, and retinol
intake. b Adjusted for race/ethnicity, hypertension status, BMI, protein intake, carbohydrate intake, vitamin B6
intake, folate intake, and retinol intake. c Adjusted for age, race/ethnicity, hypertension status, protein intake,
carbohydrate intake, vitamin B6 intake, folate intake, and retinol intake. d Adjusted for age, race/ethnicity,
hypertension status, BMI, protein intake, carbohydrate intake, vitamin B6 intake, folate intake, and retinol
intake.

damage. Abstinence and treatment with thiamine could alleviate hyperuricemia in heavy drinkers with mild or
no ­ALD10. In addition, benfotiamine which is a derivative of thiamine reduces the effect of uric acid by increasing
the serum concentration of nitrite/nitrate at a 4-week low-dose (70 mg/kg/day) ­regimen11. A cross-sectional study
in China showed that dietary vitamin B1 income levels were negatively associated with hu prevalence in the male
population and not in the female p ­ opulation8. This is consistent with our findings. The potential mechanisms
between vitamin B1 intake and HU are still largely unknown, but may be related through antioxidant proper-
ties and inflammatory mechanisms. Uric acid is an important endogenous antioxidant with physiologically
appropriate concentrations that may be required to reduce oxidative stress in cells of the central nervous system.
Uric acid provides up to 55% of the free radical scavenging antioxidant capacity of human ­plasma12, making
it one of the major antioxidants in the b­ ody13. In addition, uric acid itself and/or downstream radicals can act
as a biologically active proinflammatory factor involved in the production of intracellular oxidants through
the ubiquitous NADPH oxidase-dependent pathway, leading to oxidative s­ tress14. HU is most often caused by
decreased renal uric acid excretion, and excessive serum uric acid levels can lead to precipitation of uric acid
crystals in the connective tissue of joints, leading to gouty arthritis and precipitation in the renal tubules, lead-
ing to acute tubular ­necrosis15. Thiamine has antioxidative effects. It protects the neutrophil sulfhydryl groups
from oxidation by the s­ ystem16 and shows significant inhibition of oxygen radicals produced by n ­ [Link]
soluble form of vitamin B1 could modulate the macrophage inflammatory response against the bacterial toxin-
induced inflammation by regulating signaling intermediates such as MAPK/PKC/IΚB leading to the expression
of NF-ΚB-dependent inflammatory ­markers18. Therefore, vitamin B1 supplementation could be beneficial in the
prevention of inflammation as well as pathological conditions caused by oxidative stress.
Hyperuricemia needs more attention as an early and major cause of gout. Diet has also been hypothesized to
be a contributing factor to hyperuricemia, with increased dietary purines leading to increased urate ­production19.
Due to the interventional nature of diet, there will be an increasing emphasis on the management of various
nutrient intakes in hyperuricemia. A large body of literature focuses on assessing the association between diet

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Figure 1.  RCS analysis of vitamin B1 intake and risk of hyperuricemia. (a) RCS analysis of vitamin B1 in the
male population. (b) RCS analysis of vitamin B1 in female population. The red line represents the trend, and the
light pink area is the 95% confidence interval.

Figure 2.  Smooth curve fitting of serum uric acid concentration and dietary vitamin B1 intake of participants.

and hyperuricemia. For example, red meat, seafood, sugary beverages, alcohol and animal protein have been
identified to be associated with an increased risk of ­hyperuricemia20. One study indicated that after adjusting
­ yperuricemia21. Similarly, our study
for all covariates, only the vitamin B group had a significant total effect on h
suggests that increased intake of dietary vitamin B1 from food sources may reduce the risk of HU in men.
There was no negative association between dietary vitamin B1 intake levels and HU prevalence in the female
population, which may be related to gender differences in uric acid metabolism. The level of uric acid metabolism

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is affected by factors such as sex hormones, visceral obesity and muscle m ­ ass22. Serum urate concentrations on
average about 1 mg/dl higher in men than in women in adulthood, but serum uric acid levels in women were
significantly higher around the age of natural ­menopause23. In a clinical study of alcohol-related liver disease
(ALD), it was noted that uric acid levels were significantly lower in males than in females in hospitalised patients
treated with vitamin ­B110. Furthermore, for men, one study reported that low testosterone levels were associated
with elevated uric acid levels. In postmenopausal women, a significant increase in serum uric acid concentra-
tion was observed. After hormone replacement therapy, uric acid decreased ­significantly24. The above studies all
indicate the effect of gender differences on uric acid levels.
Our study has several highlights. First, we used a large nationally representative sample in the general U.S.
population, increasing the reliability of the results. This is the first study to assess the association between vitamin
B1 intake and the risk of hyperuricemia in US adults. Second, we adjusted for a number of important confound-
ers. Third, a standardized protocol was followed, and trained staff were used to obtain basic information about
the study population. In particular, a standardized assessment instrument was used for dietary nutrient intake
to improve the accuracy and validity of the data obtained.
However, our study has some limitations. First, this was a cross-sectional study, limiting the definition of
direct causality of vitamin B1 and HU, and further prospective longitudinal studies are important to support the
conclusions. Second, the study used 24-h dietary recall to estimate dietary intake levels, which may be subject
to recall bias, and also does not accurately describe long-term vitamin B1 intake. Although we controlled for
several confounding factors, we cannot get rid of the possibility of residual confusion caused by unmeasured
confounding factors.
Our study suggests that that dietary vitamin B1 intake is negatively associated with hyperuricemia in men
among US adults. Further-more, large prospective cohort studies need to be performed to support our findings.

Conclusions
Our study suggests that that dietary vitamin B1 intake is negatively associated with hyperuricemia in men
among US adults after adjusting for major confounders. Further-more, large prospective cohort studies need to
be performed to support our findings.

Methods
Study population
Data from National Health and Nutrition Examination Survey (NHANES). NHANES is a national survey that
monitors the health and nutritional status of adults and children across the United States. The survey is unique
in that it combines interviews and physical examinations. NHANES is run by the National Center for Health
Statistics (NCHS). The data including interviews, physical and laboratory examination can be downloaded from
the NHANES website ([Link] The information collected is used to provide
important health statistics. The NHANES protocol was approved by the ethical review board of the National
Center for Health Statistics Research, written informed consent was obtained from all subjects. Only publicly
available data was used in the analysis, and no ethical approval was needed in this study.
A total of 9232 participants aged ≥ 20 years were selected from 15,660 participants in the NHANES from
March 2017 to March [Link] excluded pregnant women (n = 87) and participants lacking information or
unreliable 24-h recall data on dietary vitamin B1 intake (n = 2161); those participants with missing information
on uric acid level (n = 710); and those with serum creatinine > 1.5 mg/dL25 were also excluded for considering
renal dysfunction(n = 238); and those with missing or incomplete essential information on demographic or total
nutrient intakes dietary interviews (n = 286). After exclusion, the total subjects in our study included 5750 adults
(2725 men, 3025 women). The filtering process is shown in Fig. 3.

Measures
The dietary intake of vitamin B1 was assessed using 24-h dietary recall interviews. The dietary intake data were
used to estimate the types and amounts of foods and beverages (including all types of water) consumed during
the 24-h period prior to the interview (midnight to midnight). Daily aggregates of energy, nutrients, and other
food components from foods and beverages were calculated using the US Department of Agriculture Food and
Nutrient Database for Dietary Studies (FNDDS 2017–2018 and FNDDS 2019–2020). We used two 24-h dietary
recalls to obtain total nutrient intakes. It is important to note that dietary vitamin B1 intake was derived from
food intake data and included supplement use. Serum concentrations of UA were measured on a Roche Cobas
6000 Chemistry Analyzer (Roche Diagnostics Corporation, Indianapolis, IN 46,250), where UA is oxidized by
allantoin and ­H2O2 by the enzyme allantoin. Hyperuricemia was defined as serum uric acid level ≥ 7.0 in men
and ≥ 6.0 mg/dl in ­women26.

Covariates
Sociodemographic characteristics included age, gender, ethnicity (Mexican American, other Hispanic, Non-
Hispanic White, Non-Hispanic Black, Non-Hispanic Asian and other race), and educational level. Educational
level was divided into less than high school graduate, high school graduate/GED or equivalent and above high
school. Other covariates included smoking status (smoking at least 100 cigarettes in life or not), and alcohol
consumption (never, moderate consumption and excessive consumption). A history of hypertension or diabetes
was defined as a self-reported physician’s diagnosis of hypertension or diabetes.

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Figure 3.  Flow chart of the screening process for the selection of eligible participants.

Statistical analyses
The continuous variables were described by median and interquartile spacing (skewed distributed data), and
categorical variables were presented as percentages. Differences between continuous variables were assessed by
Kruskal–Wallis H test. Differences between categorical variables were evaluated by the chi-square test. Multi-
variate logistic regression analysis was used to estimate the odds ratio (OR) and 95% confidence interval (CI) of
HU, according to the vitamin B1 intake quintile for male and female separately, with the lowest quintile being
considered as the references, respectively. Covariates were selected based on a number of published studies.
Indicators collinearity check was performed using the variance inflation factor (VIF). Model 1 is controlled by
age and race/ethnicity. On the basis of model 1, Model 2 was adjusted for age, BMI, hypertension status, protein
intake, carbohydrate intake, vitamin B6 intake, folic acid intake, retinol intake and TG. On the basis of model
2, Model 3 was further adjusted for smoking status, education background, diabetes status and cholesterol. On
the basis of multiple logistic regression analysis, the linear trend test was conducted for the median intake of
dietary vitamin B1. The dose–response relationship was determined by the restricted cubic spline(RCS) method.
Smooth curve fitting was used to show the relationship between participants’ serum uric acid concentration and
vitamin B1 intake.
For all statistical analyses, data were analyzed with the use of the statistical packages R (The R Foundation;
[Link]
​ ww.r-p​ rojec​ t.o
​ rg; version 4.2.0) and EmpowerStats (www.e​ mpowe​ rstat​ s.n
​ et, X&Y solutions, Inc. Boston,
Massachusetts). A two-sided P value < 0.05 was considered to be statistically significant.

Data availability
The datasets generated during and/or analysed during the current study are available in the [NHANES] reposi-
tory, [[Link]

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Received: 15 February 2024; Accepted: 1 July 2024

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Author contributions
Yi-Ming Li, Xiao-Hu Xu, Xiao-Fan Xu wrote the paper, Xia-Xia Yang, Yi-Long Dai, Dong-Xue Song analyzed
data, Cheng-Qiang Jin and Yan-Xia Jia designed research. All authors reviewed the manuscript.

Competing interests
The authors declare no competing interests.

Additional information
Correspondence and requests for materials should be addressed to C.-Q.J. or Y.-X.J.
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