International journal of surgery (London, England) · 2025
Biological aging and gout risk in hyperuricemia: a UK Biobank cohort study.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Li Ningfei, Chen Zeqi, Han Man, Shang Ao, Zhou Jiayan, Sun Ya Xuan, Li Yige, Sun Jigao, Shen Aling, Yang Yanyu, Wei Benjun, Lin Fei, Zhou Fang, Zhu Xiaoxia, Yu Jing, Zhang Hui, Teng Yuke, Bai Litao, Yin Xiangjun, Wu Ying, Li Jinlin, Ayad Nardeen, Cheng Zhiang, Assimes Themistocles L, Chen Guang
Аннотация
OBJECTIVE: To investigate the role of biological aging in the progression from hyperuricemia to gout and to evaluate whether an antiaging diet can prevent this progression.
METHODS: This prospective study involved 412 493 participants from the UK Biobank. Multiple regression models were employed to assess the associations, while Mendelian Randomization was utilized to explore causality. Additionally, the composite dietary antioxidant index (CDAI) was evaluated to examine its preventive effects.
RESULTS: Biological aging acceleration was associated with higher level of serum uric acid by an average of 8.1 μmol/l (95% CI: 7.6-8.7, P < 0.001), 40% increased odds of developing hyperuricemia (OR 1.4, 95% CI: 1.36-1.43, P < 0.001), and 39% increased odds of gout (OR 1.39, 95% CI: 1.32-1.46, P < 0.001). Among the hyperuricemia population, accelerated biological aging participants had a 14% increased odds of developing gout compared with participants with delayed biological aging (OR 1.14, 95% CI 1.06-1.22, P < 0.001). Genetically determined delayed biological aging traits remained significantly causally associated with a decreased risk of gout. Among patients with hyperuricemia, those with positive CDAI had a marginally significant 68% reduction in the odds of developing gout compared to those with negative CDAI (OR 0.32, 95% CI = 0.09-0.96, P = 0.055).
CONCLUSIONS: These findings suggest that biological aging acceleration represents a risk factor for the progression from hyperuricemia to gout, thus highlighting a new strategy and approach to manage hyperuricemia and prevent gout through healthy aging approaches.
METHODS: This prospective study involved 412 493 participants from the UK Biobank. Multiple regression models were employed to assess the associations, while Mendelian Randomization was utilized to explore causality. Additionally, the composite dietary antioxidant index (CDAI) was evaluated to examine its preventive effects.
RESULTS: Biological aging acceleration was associated with higher level of serum uric acid by an average of 8.1 μmol/l (95% CI: 7.6-8.7, P < 0.001), 40% increased odds of developing hyperuricemia (OR 1.4, 95% CI: 1.36-1.43, P < 0.001), and 39% increased odds of gout (OR 1.39, 95% CI: 1.32-1.46, P < 0.001). Among the hyperuricemia population, accelerated biological aging participants had a 14% increased odds of developing gout compared with participants with delayed biological aging (OR 1.14, 95% CI 1.06-1.22, P < 0.001). Genetically determined delayed biological aging traits remained significantly causally associated with a decreased risk of gout. Among patients with hyperuricemia, those with positive CDAI had a marginally significant 68% reduction in the odds of developing gout compared to those with negative CDAI (OR 0.32, 95% CI = 0.09-0.96, P = 0.055).
CONCLUSIONS: These findings suggest that biological aging acceleration represents a risk factor for the progression from hyperuricemia to gout, thus highlighting a new strategy and approach to manage hyperuricemia and prevent gout through healthy aging approaches.