背景:证据表明,生活基本8(LE8)中的个体指标,美国心脏协会提出的最新心血管健康(CVH)概念,在炎症性肠病(IBD)的发展中发挥作用。然而,关于LE8对IBD风险的总体流行病学证据仍然有限.我们旨在评估LE8定义的CVH与IBD及其亚型风险的纵向关联,溃疡性结肠炎(UC)和克罗恩病(CD)。我们还测试了遗传易感性是否可以改变这些关联。
方法:共纳入了来自英国生物库的260,836名参与者。LE8评分由8个指标确定(体力活动,饮食,尼古丁暴露,睡眠,身体质量指数,血压,血糖,和血脂),分为三个级别:低CVH(0-49),中等CVH(50-79),和高CVH(80-100)。Cox比例风险模型用于计算与CVH状态相关的IBD风险的风险比(HR)和置信区间(CI)。
结果:中位随访12.3年,我们记录了1,500例IBD病例(包括1,070UC和502CD)。与低CVH的参与者相比,IBD高CVH者的HR(95%CI),UC,CD为0.67(0.52,0.83),0.70(0.52,0.93),和0.55(0.38,0.80),分别。这些关联没有被遗传易感性改变(所有的相互作用P>0.05)。在高CVH和低遗传风险的参与者中观察到最低的HR(UC:0.30,95%CI:0.20-0.45;CD:0.33,95%CI:0.20-0.57)。
结论:更好的CVH,由LE8定义,与IBD的风险显着降低相关,UC,CD,不管遗传倾向。我们的结果强调了坚持LE8指南对维持CVH作为预防IBD的潜在策略的重要性。
BACKGROUND: Evidence has shown that the individual metrics in Life\'s Essential 8 (LE8), an updated cardiovascular health (CVH) concept proposed by the American Heart Association, play a role in the development of inflammatory bowel disease (IBD). However, epidemiological evidence on the overall LE8 on IBD risk remains limited. We aimed to assess the longitudinal associations of LE8-defined CVH and the risks of IBD and its subtypes, ulcerative colitis (UC) and Crohn\'s disease (CD). We also tested whether genetic susceptibility could modify these associations.
METHODS: A total of 260,836 participants from the UK Biobank were included. LE8 scores were determined by 8 metrics (physical activity, diet, nicotine exposure, sleep, body mass index, blood pressure, blood glucose, and blood lipids), and were divided into three levels: low CVH (0-49), moderate CVH (50-79), and high CVH (80-100). Cox proportional hazards models were used to calculate the hazard ratios (HRs) and confidence intervals (CIs) of the risk of IBD in relation to CVH status.
RESULTS: Over a median follow-up 12.3 years, we documented 1,500 IBD cases (including 1,070 UC and 502 CD). Compared to participants with low CVH, the HRs (95% CIs) of those with high CVH for IBD, UC, and CD were 0.67 (0.52, 0.83), 0.70 (0.52, 0.93), and 0.55 (0.38, 0.80), respectively. These associations were not modified by genetic susceptibility (all P for interactions > 0.05). The lowest HR (UC: 0.30, 95% CI: 0.20-0.45; CD: 0.33, 95% CI: 0.20-0.57) was observed in participants with both high CVH and low genetic risk.
CONCLUSIONS: Better CVH, defined by LE8, was associated with significantly lower risks of IBD, UC, and CD, irrespective of genetic predisposition. Our results underscore the importance of adherence to LE8 guidelines for maintaining CVH as a potential strategy in the prevention of IBD.