The effect of single dietary fibre (DF) on lowering uric acid (UA) level has been reported in the literature. However, the potential protective mechanism of DF against potassium oxybate-induced hyperuricaemia (HUA), as modelled by prophylactic administration, remains unclear. The data demonstrate that DF significantly decreased serum and cerebral tissue UA concentrations, inhibited xanthine oxidase expression and activity in the liver and reduced levels of creatinine and urea nitrogen in the serum. Additionally, it mitigated the deposition of amyloid-β in cerebral tissue. Correlation analysis showed that DF modulated the Toll-like receptor 4/NF-κB signalling pathway, attenuating oxidative stress and inflammatory responses in HUA mice. Additionally, DF helps to maintain the composition of the gut microbiota, reducing harmful Desulfovibrio and enriching beneficial Akkermansia and Ruminococcus populations. The results of the faecal metabolomics analysis indicate that DF facilitates the regulation of metabolic pathways involved in oxidative stress and inflammation. These pathways include pyrimidine metabolism, tryptophan metabolism, nucleotide metabolism and vitamin B6 metabolism. Additionally, the study found that DF has a preventive effect on anxiety-like behaviour induced by HUA. In summary, DF shows promise in mitigating HUA and cognitive deficits, primarily by modulating gut microbiota and metabolites.

Two population-based cross-sectional surveys involving randomly selected Chinese adults aged 35–74 years were conducted in Qingdao, China in 2006 and 2009. Nine thousand fifty-five subjects from the two surveys were grouped into four birth groups of fetal/infant exposed (born between 1 January 1959 and 31 December 1962), childhood exposed (born between 1 January 1950 and 31 December 1958), adolescence exposed (born between 1 January 1942 and 31 December 1949) and the unexposed (born before 1941 and after 1963). Multivariate logistic regression models were used to calculate the OR and 95 % CI of hyperuricaemia in different exposed groups. Overall, famine exposure in the fetal/infant period, childhood and adolescence was not associated with adulthood hyperuricaemia (all P > 0·05). In females, childhood exposed group (OR = 1·59, 95 % CI 1·25, 2·02) and adolescence exposed group (OR = 1·74, 95 % CI 1·30, 2·33) both had higher risks to have hyperuricaemia in adult. However, this difference was not found in fetal/infant exposed group. In males, no significant relation was observed in any famine exposed group (all P > 0·05). Exposure to famine in childhood and adolescence is associated with an increased risk of hyperuricaemia for adulthood of females, but not in males. Adequate nutrition during early life appears to be beneficial to prevent hyperuricaemia of adult females.

Seaweeds have numerous biologically active ingredients, such as polysaccharides, polyphenols and carotenoids, that are beneficial to human health. Although these benefits might be related to the synthesis, secretion or reabsorption of uric acid, no studies have explored the relationship between seaweeds consumption and hyperuricaemia (HUA) in the general population. The aim of this study was to investigate whether seaweeds consumption is related to HUA in a large-scale adult population. A cross-sectional study was conducted with 32 365 adults (17 328 men and 15 037 women) in Tianjin, People’s Republic of China. Frequency of seaweeds consumption was assessed by a validated self-administered FFQ. HUA was defined as serum uric acid levels >420 μmol/L in men and >350 μmol/L in women. The association between seaweeds consumption and HUA was assessed by multiple logistic regression analysis. Restricted cubic spline functions were used for non-linearity tests. The prevalence of HUA in men and women was 21·17 % and 5·93 %, respectively. After adjustments for potential confounding factors, the OR (95 % CI) for HUA across seaweed consumption (g/1000 kcal per d) were 1·00 (reference) for level 1, 0·91 (95 % CI 0·81, 1·02) for level 2; 0·90 (95 % CI 0·81, 1·01) for level 3; 0·86 (95 % CI 0·78, 0·97) for level 4 in men and 0·90 (95 % CI 0·73, 1·10) for level 2; 0·82 (95 % CI 0·67, 1·00) for level 3; 0·84 (95 % CI 0·68, 1·03) for level 4 in women, respectively. A negative correlation between seaweeds consumption and HUA in males but not in females was observed. Further studies are needed to explore the causal relationship.

We aimed to evaluate the relationship of plasma Mg with the risk of new-onset hyperuricaemia and examine any possible effect modifiers in hypertensive patients. This is a post hoc analysis of the Uric acid (UA) Sub-study of the China Stroke Primary Prevention Trial (CSPPT). A total of 1685 participants were included in the present study. The main outcome was new-onset hyperuricaemia defined as a UA concentration ≥417 μmol/l in men or ≥357 μmol/l in women. The secondary outcome was a change in UA concentration defined as UA at the exit visit minus that at baseline. During a median follow-up duration of 4·3 years, new-onset hyperuricaemia occurred in 290 (17·2 %) participants. There was a significantly inverse relation of plasma Mg with the risk of new-onset hyperuricaemia (per sd increment; OR 0·85; 95 % CI 0·74, 0·99) and change in UA levels (per sd increment; β −3·96 μmol/l; 95 % CI −7·14, −0·79). Consistently, when plasma Mg was analysed as tertiles, a significantly lower risk of new-onset hyperuricaemia (OR 0·67; 95 % CI 0·48, 0·95) and less increase in UA levels (β −8·35 μmol/l; 95 % CI −16·12, −0·58) were found among participants in tertile 3 (≥885·5 μmol/l) compared with those in tertile 1 (<818·9 μmol/l). Similar trends were found in males and females. Higher plasma Mg levels were associated with a decreased risk of new-onset hyperuricaemia in hypertensive adults.

Previous studies have indicated that some food items and nutrients are associated with uric acid metabolism in humans. However, little is known about the role of dietary patterns in hyperuricaemia. We designed this case–control study to evaluate the associations between dietary patterns and newly diagnosed hyperuricaemia in Chinese adults. A total of 1422 cases and 1422 controls were generated from 14 538 participants using the 1:1 ratio propensity score matching methods. Dietary intake was assessed using a validated self-administered FFQ. Dietary patterns were derived by factor analysis. Hyperuricaemia was defined as concentrations of serum uric acid higher than 7 mg/dl (416·5 μmol/l) for men and 6 mg/dl (357 μmol/l) for women. Three dietary patterns were derived by factor analysis: sweet pattern; vegetable pattern; animal foods pattern. The animal foods pattern characterised by higher intake of an animal organ, seafood and processed meat products was associated with higher prevalence of newly diagnosed hyperuricaemia (Pfor trend<0·01) after adjustment. Compared with the participants in the lowest quartile of the animal foods pattern, the OR of newly diagnosed hyperuricaemia in the highest quartile was 1·50 (95 % CI 1·20, 1·87). The other two dietary patterns were not associated with the prevalence of newly diagnosed hyperuricaemia after adjustment. In conclusion, a diet rich in animal organ, seafood and processed meat products is associated with higher prevalence of newly diagnosed hyperuricaemia in a Chinese population. Further cohort studies and randomised controlled trials are required to clarify these findings.

Elevated plasma uric acid concentration is a risk factor for gout, insulin resistance and type 2 diabetes. Quercetin, a flavonoid found in high levels in onions, tea and apples, inhibits xanthine oxidoreductase in vitro, the final step in intracellular uric acid production, indicating that quercetin might be able to lower blood uric acid in humans. We determined the effects of 4 weeks of oral supplementation of quercetin on plasma uric acid, blood pressure and fasting glucose. This randomised, double-blinded, placebo-controlled, cross-over trial recruited twenty-two healthy males (19–60 years) with baseline plasma uric acid concentration in the higher, but still considered healthy, range (339 (sd 51) µmol/l). The intervention included one tablet containing 500 mg quercetin daily for 4 weeks, compared with placebo, with a 4-week washout period between treatments. The primary outcome was change in concentrations of plasma uric acid after 2 and 4 weeks; secondary outcome measures were changes in fasting plasma glucose, 24-h urinary excretion of uric acid and resting blood pressure. After quercetin treatment, plasma uric acid concentrations were significantly lowered by −26·5 µmol/l (95 % CI, −7·6, −45·5; P=0·008), without affecting fasting glucose, urinary excretion of uric acid or blood pressure. Daily supplementation of 500 mg quercetin, containing the bioavailable amount of quercetin as present in approximately 100 g red onions, for 4 weeks, significantly reduces elevated plasma uric acid concentrations in healthy males.