Maturitas · 2026
Association of biological aging with gout risk and all-cause mortality: Evidence from NHANES and UK Biobank.
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Zhao Hong, Xu Yangyu, Gao Yuxiang, Liang Ruyi, Han Jiannan, Liu Sumiao, Wu Ruonan, Wu Zewen, Zhao Junkang, Zhang Liyun
Аннотация
OBJECTIVES: To evaluate the associations of biological aging with the prevalence of gout, risk of incident gout, and all-cause mortality among individuals with gout.
STUDY DESIGN: Cross-sectional and prospective cohort studies were conducted using data from the National Health and Nutrition Examination Survey (NHANES) and the UK Biobank (UKB).
MAIN OUTCOME MEASURES: Biological aging was assessed using Klemera-Doubal method biological age (KDMAge) and phenotypic age (PhenoAge). In NHANES, gout cases were identified by self-reported physician diagnosis, and all-cause mortality was determined through linkage with the National Death Index. In UKB, gout cases were identified using International Classification of Diseases, Tenth Revision (ICD-10) code M10 from inpatient records, and mortality data were obtained from official National Health Service death registries.
RESULTS: In NHANES, each 1-year increase in KDMAge or PhenoAge advance was associated with a 4% higher gout risk (odds ratio [OR] 1.04, 95% confidence interval [CI] 1.03-1.05). In the UKB cohort, accelerated biological aging predicted higher risk of incident gout (KDMAge advance: hazard ratio [HR] 1.80, 95% CI 1.71-1.90; PhenoAge advance: HR 1.69, 95% CI 1.60-1.78). Among individuals with gout, accelerated biological aging was associated with a 21%-134% increased risk of all-cause mortality (HR range 1.21-2.34).
CONCLUSIONS: Accelerated biological aging is significantly associated with greater gout prevalence, increased risk of incident gout, and poorer survival outcomes among individuals with gout.
STUDY DESIGN: Cross-sectional and prospective cohort studies were conducted using data from the National Health and Nutrition Examination Survey (NHANES) and the UK Biobank (UKB).
MAIN OUTCOME MEASURES: Biological aging was assessed using Klemera-Doubal method biological age (KDMAge) and phenotypic age (PhenoAge). In NHANES, gout cases were identified by self-reported physician diagnosis, and all-cause mortality was determined through linkage with the National Death Index. In UKB, gout cases were identified using International Classification of Diseases, Tenth Revision (ICD-10) code M10 from inpatient records, and mortality data were obtained from official National Health Service death registries.
RESULTS: In NHANES, each 1-year increase in KDMAge or PhenoAge advance was associated with a 4% higher gout risk (odds ratio [OR] 1.04, 95% confidence interval [CI] 1.03-1.05). In the UKB cohort, accelerated biological aging predicted higher risk of incident gout (KDMAge advance: hazard ratio [HR] 1.80, 95% CI 1.71-1.90; PhenoAge advance: HR 1.69, 95% CI 1.60-1.78). Among individuals with gout, accelerated biological aging was associated with a 21%-134% increased risk of all-cause mortality (HR range 1.21-2.34).
CONCLUSIONS: Accelerated biological aging is significantly associated with greater gout prevalence, increased risk of incident gout, and poorer survival outcomes among individuals with gout.