Dietary polyunsaturated fatty acid intake and all-cause and cardiovascular mortality in patients with COPD.

IF 4.1 2区 医学 Q2 NUTRITION & DIETETICS
Yang Zhang, Xiao Liang, Shuai Luo, Zhizhe Zhang, Pinglang Zhou, Zhiyang Zhou, Yihan Yang
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引用次数: 0

Abstract

Background: Chronic obstructive pulmonary disease (COPD) patients face increased mortality risk, particularly from cardiovascular causes. While polyunsaturated fatty acids (PUFAs) have shown cardiovascular benefits in general populations, their impact on COPD mortality remains unexplored.

Methods: This prospective cohort study analyzed 2,102 COPD patients from NHANES (1999-2018). PUFA intake was assessed through 24-hour dietary recalls and categorized into tertiles. Associations with all-cause and cardiovascular mortality were evaluated using Cox regression models, restricted cubic splines (RCS), and weighted quantile sum (WQS) regression. Comprehensive subgroup and sensitivity analyses confirmed result robustness.

Results: During 9.08 years of follow-up, 603 deaths (28.7%) occurred, including 190 (9.0%) from cardiovascular disease. Compared to the lowest tertile, the highest tertile of total PUFA (HR: 0.70, 95% CI: 0.53-0.91), N-3 PUFA (HR: 0.67, 95% CI: 0.52-0.87), and N-6 PUFA (HR: 0.74, 95% CI: 0.57-0.97) intake was associated with lower all-cause mortality. For cardiovascular mortality, higher intake of total PUFA (HR: 0.55, 95% CI: 0.33-0.90), N-3 PUFA (HR: 0.56, 95% CI: 0.36-0.89), and N-6 PUFA (HR: 0.57, 95% CI: 0.34-0.93) showed significant protective effects. RCS analyses revealed non-linear associations with significant threshold effects. WQS analysis identified two plant-derived PUFA-α-linolenic acid (ALA) and linoleic acid (LA) as the primary contributors to mortality reduction. All sensitivity analyses confirmed the stability and consistency of our main findings.

Conclusions: Higher dietary PUFA intake is associated with lower all-cause and cardiovascular mortality among COPD patients, suggesting that increasing dietary PUFA, particularly from plant sources, may help reduce COPD-related mortality risk.

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COPD患者饮食多不饱和脂肪酸摄入与全因死亡率和心血管死亡率的关系
背景:慢性阻塞性肺疾病(COPD)患者面临更高的死亡风险,尤其是心血管疾病。虽然多不饱和脂肪酸(PUFAs)在一般人群中显示出心血管益处,但其对COPD死亡率的影响仍未被探索。方法:这项前瞻性队列研究分析了NHANES(1999-2018)的2102例COPD患者。通过24小时饮食回顾评估PUFA摄入量,并将其分类。使用Cox回归模型、限制性三次样条(RCS)和加权分位数和(WQS)回归评估全因死亡率和心血管死亡率的相关性。综合亚组分析和敏感性分析证实了结果的稳健性。结果:在9.08年的随访中,共发生603例死亡(28.7%),其中190例(9.0%)死于心血管疾病。与最低分位数相比,总PUFA (HR: 0.70, 95% CI: 0.53-0.91)、N-3 PUFA (HR: 0.67, 95% CI: 0.52-0.87)和N-6 PUFA (HR: 0.74, 95% CI: 0.57-0.97)摄入量最高的分位数与较低的全因死亡率相关。对于心血管疾病死亡率,较高的总PUFA (HR: 0.55, 95% CI: 0.33-0.90)、N-3 PUFA (HR: 0.56, 95% CI: 0.36-0.89)和N-6 PUFA (HR: 0.57, 95% CI: 0.34-0.93)的摄入显示出显著的保护作用。RCS分析显示非线性关联与显著的阈值效应。WQS分析发现,两种植物源PUFA-α-亚麻酸(ALA)和亚油酸(LA)是降低死亡率的主要因素。所有敏感性分析都证实了我们主要发现的稳定性和一致性。结论:在COPD患者中,较高的膳食PUFA摄入量与较低的全因死亡率和心血管死亡率相关,这表明增加膳食PUFA,特别是植物来源的PUFA,可能有助于降低COPD相关的死亡风险。
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来源期刊
Nutrition & Metabolism
Nutrition & Metabolism 医学-营养学
CiteScore
8.40
自引率
0.00%
发文量
78
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.
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