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Background and Objectives: Overconsumption of drinks containing fructose increases the risk for hyperuricemia and gout. Comparative analysis evaluating the indicators of serum uric acid (SUA) load caused by natural food-derived fructose and pure fructose in sweeteners is lacking. We aimed to uncover the effect of fructose from apple and honey and pure fructose powder on the SUA concentration of healthy young Chinese individuals.Methods and Study Design: Two randomized crossover trials were performed. The participants were randomly assigned to consume apple or honey (test food) or pure fructose powder (reference food); one week later, the groups' dietary intervention was switched. Blood samples were collected at 0, 30, 60, and 120 min after meal to measure the SUA and blood glucose concentrations.Results: At 30 and 60 min, the SUA concentration in participants consuming apple or honey was lower than in those consuming fructose powder. At 120 min, the SUA concentration of participants consuming apple returned to baseline. The areas under the curve (AUC) within 2 h (2h- AUCs) of SUA exhibited the trend of fructose >honey >apple. The 2h-AUC ratio between test food and reference food was determined using the uric acid index to assess the efficiency of food-derived fructose in increasing the SUA concentration. The uric acid index of honey was higher than that of apple. Men had higher postprandial SUA concentration than women.Conclusions: Food-derived fructose caused a lighter load on uric acid metabolism than pure fructose. Uric acid index can be useful for distinguishing fructose-containing foods. [ABSTRACT FROM AUTHOR]

Background and Objectives: To assess the causality of potentially modifiable factors, including lifestyle, nutrients, lipids, anthropometric traits, and inflammatory factors of Parkinson's disease (PD), genetic instruments for modifiable factors were identified from genome-wide association studies (GWAS).Methods and Study Design: Genetic associations for PD (1,239 cases and 451,025 matched controls) were extracted from the UK Biobank GWAS summary statistics. The causal effects of modifiable factors on the risk of PD were estimated using the multiplicative random-effects inverse variance weighted method (IVW).Results: In the IVW analysis, a decreased risk for PD was causally associated with genetically predicted smoking cessation (odds ratio 0.41, [95% confidence interval] 0.32-0.78; p<0.001), and higher bone mineral density (0.43, 0.38 -0.71; p<0.001), higher concentrations of vitamin B-12 (0.56, 0.43-0.91; p<0.001), docosahexenoic acid (0.52, 0.37-0.71; p<0.001), and sIL-6R (0.69, 0.58-0.75; p<0.001). Instead, analysis further supported the role of apolipoprotein (a) isoform size(1.67, 1.36-1.71; p<0.001), being a genetically morning person (2.18, 1.12-4.72; p<0.001), and number of cigarette smoking (1.05, 1.01-1.08; p<0.001) in contributing to the risk of developing PD.Conclusions: Our findings provide new evidence for the potential positive causal association of cigarette smoking number and apolipoprotein (a) isoform size and the inverse causal association of vitamin B-12, docosahexaenoic acid, smoking cessation, and soluble interleukin-6 receptor with PD, which contributes to the development of new interventions for PD. [ABSTRACT FROM AUTHOR]