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Gao, X. B. et al. Intake of added sugar and sugar-sweetended drink and serum uric acid concentration in U. S. men and women. Hypertension 50, 306-312

Department of Nutrition , Harvard University, Cambridge, Massachusetts, United States
Hypertension (Impact Factor: 7.63). 08/2007; 50(2):306-12. DOI: 10.1161/HYPERTENSIONAHA.107.091041
Source: PubMed

ABSTRACT Fructose-induced hyperuricemia might have a causal role in metabolic syndrome, hypertension, and other chronic disease. However, no study has investigated whether sugar added to foods or sugar-sweetened beverages, which are major sources of fructose, are associated with serum uric acid concentration in free-living populations. We examined the relationship between the intakes of added sugars and sugar-sweetened beverages and serum uric acid concentrations in the National Health and Nutrition Examination Survey 2001-2002, a nationally representative sample of men and women. We included 4073 subjects (1988 men and 2085 women) >18 years of age in the current study. Dietary intake was assessed by a single 24-hour recall. We used multivariate linear regression to adjust for age, gender, intake of energy and alcohol, body mass index, use of diuretics, beta-blockers, and other covariates. Male subjects in the highest intake quartile of estimated intake of added sugars or sugar-sweetened drinks had higher plasma uric acid concentrations than those in the lowest intake quartiles (P<0.001 for both) after adjusting for potential confounders, whereas we did not observe significant associations for females (P for trend>0.2; P for interaction <0.01). Further research is needed to confirm causality of these associations and the observed difference by gender.

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    • "This finding is compatible with data from NHANES (1988–1994) showing a higher risk for hyperuricemia with increased orange juice intake compared to subjects not consuming orange juice (p for trend ¼ 0.005) [7]. However, Gao et al. [8] reported no association of apple and pear or fruit juice intake with serum uric acid level. Interestingly, we also observed a close association between orange or orange juice intake and serum uric acid level in male subjects but not with apple or apple juice intake in linear regression analysis, whereas females showed no association of fruit or fruit juice consumption with serum uric acid level. "
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    ABSTRACT: The clinical implication of sugar-sweetened soft drinks on the risk of hyperuricemia has increased, especially in Western population studies. The aim of this study is to clarify the association between sugar-sweetened soft drinks and fruit drinks made from oranges and apples and the risk of hyperuricemia in the Korean Multi-Rural Communities Cohort. A total of 9400 subjects were enrolled in the Korean Multi-Rural Communities Cohort Study, and a cross-sectional analysis was performed. Five quintiles (Q1-Q5) according to consumption of soft drinks and other fruit/fruit juices were classified and then categorized into three groups (Q1-Q3, Q4, and Q5) to assess the risk of hyperuricemia. Information on dietary intake was collected by well-trained interviewers using validated food frequency questionnaires. Higher consumption of sugar-sweetened soft drinks (Q5) increased the risk of hyperuricemia in males (adjusted OR = 1.35, 95% CI: 1.07-1.71) with a linear trend (p for trend = 0.01) and in females (adjusted OR = 1.40, 95% CI: 1.03-1.90) with no linear trend (p for trend = 0.09), compared to lower consumption (Q1-Q3). However, there were no significant differences of serum uric acid level according to the three categories of soft drink consumption, Q1-Q3, Q3, and Q5, in males (p = 0.21) or in females (p = 0.16), whereas all subjects showed statistical significance of serum uric acid level within the categories (p < 0.001). Estimated amount of soft drink intake was associated with serum uric acid level in males (β = 0.001; p = 0.01) but not in females (β = 0.0005; p = 0.10). Higher consumption of sugar-sweetened soft drinks increased the risk of hyperuricemia in the Korean population, showing a differential linear trend for hyperuricemia according to gender.
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    • "Preventing oxidative damage may delay onset and improve the prognosis of these common CNS disorders. Uric acid (UA) is an endogenously produced watersoluble antioxidant that is modified by both drug and diet [4] [5] [6]. UA accounts for over half of the free radical scavenging activity in human blood [7] by quenching superoxide and singlet oxygen, and protecting oxidation of vitamin C (ascorbic acid; AA) through the chelation of iron [8] [9] [10]. "
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    ABSTRACT: Oxidative damage is a consistent finding in a number of central nervous system (CNS) disorders. Uric acid (UA) is a potent hydrophilic antioxidant that is modified by diet and drug. Several lines of evidence suggest that plasma UA may modulate outcomes in neurologic disease, but little attention has been paid to CNS levels of UA. Our objective was to test the hypothesis that cerebrospinal fluid (CSF) UA is determined by plasma UA, modified by blood-brain barrier (BBB) integrity and associated with rate of cognitive decline in Alzheimer's disease (AD). Also, since UA and ascorbic acid may act as antioxidants for one another, we also explored a potential interaction between them in the brain. Thirty-two patients with mild to moderate AD (Mini-Mental Status Exam 19 +/- 5) participated in a longitudinal biomarker study for one year involving standardized clinical assessments. CSF and blood were collected at baseline for UA, ascorbic acid, and albumin. Cognitive measures were collected at baseline and again one year later. CSF UA was independent of age, gender, and AD severity. CSF and plasma UA were positively correlated (r=0.669, p=0.001) and BBB impairment was associated with higher CSF levels of UA (p=0.028). Neither plasma nor CSF UA reached significant association with rates of cognitive decline over 1 year. CSF UA and CSF ascorbic acid were positively correlated (r=0.388, p=0.001). The hypothesis that CSF UA is determined by plasma UA and BBB integrity is supported, as is the hypothesis that UA and ascorbic acid are associated in CSF but not plasma. Adequately powered prospective studies would help assess any role for UA in primary and secondary prevention of AD.
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