医学
痛风
遗传倾向
危险系数
内科学
单核苷酸多态性
比例危险模型
置信区间
四分位数
生命银行
基因型
遗传学
生物
基因
疾病
作者
Tingjing Zhang,Xin Xu,Qing Chang,Yanling Lv,Yuhong Zhao,Kaijun Niu,Liangkai Chen,Yang Xia
出处
期刊:Rheumatology
[Oxford University Press]
日期:2023-05-02
卷期号:63 (1): 165-173
被引量:2
标识
DOI:10.1093/rheumatology/kead196
摘要
Abstract Objective This study aimed to examine the interactions between ultraprocessed food (UPF) consumption and genetic predisposition with the risk of gout. Methods This prospective cohort study analysed 181 559 individuals from the UK Biobank study who were free of gout at baseline. UPF was defined according to the NOVA classification. Assessment of genetic predisposition for gout was developed from a genetic risk score of 33 single nucleotide polymorphisms. Cox proportional hazards were used to estimate the associations between UPF consumption, genetic predisposition and the risk of gout. Results Among the 181 559 individuals in the study, 1558 patients developed gout over 1 648 167 person-years of follow-up. In the multivariable adjustment model, compared with the lowest quartile of UPF consumption, the hazard ratio (HR) and 95% CI of the highest UPF consumption was 1.16 (1.01, 1.33) for gout risk, and there was a non-linear correlation between UPF consumption and the development of gout. In substitution analyses, replacing 20% of the weight of UPF in the daily intake with an equal amount of unprocessed or minimally processed food resulted in a 13% lower risk of gout (HR: 0.87; 95% CI: 0.79, 0.95). In the joint-effect analysis, the HR (95% CI) for gout was 1.90 (1.39, 2.60) in participants with high genetic predisposition and high UPF consumption, compared with those with low genetic predisposition and low UPF consumption. Conclusion In summary, UPF consumption was found to be associated with a higher risk of gout, particularly in those participants with genetic predisposition to gout. Our study indicated that reducing UPF consumption is crucial for gout prevention.
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