Cumulative exposure to AHA Life's Essential 8 is associated with nonalcoholic fatty liver disease: a large cohort study.

IF 3.9 2区医学 Q2 NUTRITION & DIETETICS Nutrition & Metabolism Pub Date : 2024-06-27 DOI:10.1186/s12986-024-00821-z

Wang Yaqin, Deng Shuwen, Yuan Ting, Zhu Xiaoling, Deng Yuling, Liu Lei, Wang Changfa

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Abstract

Background and aim: We aimed to explore the associations of baseline and cumulative cardiovascular health with nonalcoholic fatty liver disease (NAFLD) development and regression using the new Life's Essential 8 score.

Methods: From a health screening database, participants who underwent at least 4 health examinations between 2012 and 2022 were recruited and categorized into two cohorts: (a) the NAFLD development cohort with no history of NAFLD prior to Exam 4 and (b) the NAFLD regression cohort with diagnosed NAFLD prior to Exam 4. The LE8 score was calculated from each component. The outcomes were defined as newly incident NAFLD or regression of existing NAFLD from Exam 4 to the end of follow-up.

Results: In the NAFLD development cohort, of 21,844 participants, 3,510 experienced incident NAFLD over a median follow-up of 2.3 years. Compared with the lowest quartile of cumulative LE8, individuals in the highest quartile conferred statistically significant 76% lower odds (hazard ratio [HR] 0.24, 95% confidence interval [CI], 0.21-0.28) of NAFLD incidence, and corresponding values for baseline LE8 were 42% (HR 0.58, 95% CI 0.53-0.65). In the NAFLD regression cohort, of 6,566 participants, 469 experienced NAFLD regression over a median follow-up of 2.4 years. Subjects with the highest quartile of cumulative LE8 had 2.03-fold (95% CI, 1.51-2.74) higher odds of NAFLD regression, and corresponding values for baseline LE8 were 1.61-fold (95% CI, 1.24-2.10).

Conclusion: Cumulative ideal cardiovascular health exposure is associated with reduced NAFLD development and increased NAFLD regression. Improving and preserving health behaviors and factors should be emphasized as an important part of NAFLD prevention and intervention strategies.

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累积接触 AHA 生命必需 8 与非酒精性脂肪肝的关系：一项大型队列研究。

背景和目的：我们的目的是利用新的 "生活必备 8 项评分"，探讨基线和累积心血管健康状况与非酒精性脂肪肝（NAFLD）的发展和消退之间的关系：从健康检查数据库中招募了在 2012 年至 2022 年期间接受过至少 4 次健康检查的参与者，并将其分为两个队列：(a) 非酒精性脂肪肝发展队列，在第 4 次体检前无非酒精性脂肪肝病史；(b) 非酒精性脂肪肝回归队列，在第 4 次体检前已确诊非酒精性脂肪肝。LE8评分由每个组成部分计算得出。结果定义为从第4次检查到随访结束期间新发生的非酒精性脂肪肝或现有非酒精性脂肪肝的消退：在非酒精性脂肪肝发展队列的21844名参与者中，有3510人在2.3年的中位随访期间发生了非酒精性脂肪肝。与累积LE8最低四分位数相比，处于最高四分位数的个体发生非酒精性脂肪肝的几率在统计学上显著降低了76%（危险比[HR]0.24，95%置信区间[CI]，0.21-0.28），基线LE8的相应值为42%（HR 0.58，95% CI 0.53-0.65）。在非酒精性脂肪肝消退队列中，6566名参与者中有469人在中位随访2.4年期间出现非酒精性脂肪肝消退。累积LE8值最高四分位数的受试者发生非酒精性脂肪肝的几率要高出2.03倍（95% CI，1.51-2.74），而基线LE8的相应值为1.61倍（95% CI，1.24-2.10）：结论：累积的理想心血管健康暴露与减少非酒精性脂肪肝的发生和增加非酒精性脂肪肝的消退有关。非酒精性脂肪肝预防和干预策略的一个重要部分是强调改善和保护健康行为和因素。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Nutrition & Metabolism 医学-营养学

CiteScore

8.40

自引率

0.00%

发文量

审稿时长

4-8 weeks

期刊介绍： Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects. The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases. Key areas we wish to encourage submissions from include: -how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes; -the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components; -how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved; -how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.