Association of dietary preferences with cardiovascular disease: a Mendelian randomization study

IF 1.4 Q3 PERIPHERAL VASCULAR DISEASE
Mia D. Lee , Benjamin F. Voight
{"title":"Association of dietary preferences with cardiovascular disease: a Mendelian randomization study","authors":"Mia D. Lee ,&nbsp;Benjamin F. Voight","doi":"10.1016/j.athplu.2025.04.002","DOIUrl":null,"url":null,"abstract":"<div><h3>Background and aims</h3><div>Susceptibility to cardiovascular disease (CVD) is driven by genetic and environmental risk factors. Diet is a modifiable and largely environmental risk factor for CVD. Genetic factors associated with a variety of dietary preferences revealed via recent genome-wide association studies (GWAS) allow further investigate the role of diet in liability to disease that has been limited to observational and epidemiologic studies with mixed findings.</div></div><div><h3>Method</h3><div>We obtained publicly available genome-wide association data for 38 dietary preference traits and seven common CVDs to investigate causal hypotheses between diet as the exposure to CVD as outcomes using the statistical framework of Mendelian randomization (MR) for hypothesis testing and sensitivity analyses. We also conducted mediation analyses to evaluate the effects of dietary preferences on CVDs to elucidate potential causal graphs and estimate the effects of dietary preferences mediated by potential mediators.</div></div><div><h3>Results</h3><div>Across all methods, we identified 10 significant causal effects, which included eight dietary preferences across three CVD endpoints (Bonferroni-corrected P &lt; 1.88 × 10<sup>−4</sup>). In sensitivity MR and mediation analysis, we observed that obesity - quantified by body mass index (BMI) - was a common mediator that contributed to many of these observed effects. We also found that educational attainment was an exclusive, additional mediator for the effect of preference for muesli with risk to peripheral artery disease (PAD).</div></div><div><h3>Conclusions</h3><div>Our results provide genetic evidence for a link between diet and CVD that aligns with obesity-mediated risk of CVD in individuals in relation to their specific preferences for food.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"60 ","pages":"Pages 43-50"},"PeriodicalIF":1.4000,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Atherosclerosis plus","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2667089525000094","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PERIPHERAL VASCULAR DISEASE","Score":null,"Total":0}
引用次数: 0

Abstract

Background and aims

Susceptibility to cardiovascular disease (CVD) is driven by genetic and environmental risk factors. Diet is a modifiable and largely environmental risk factor for CVD. Genetic factors associated with a variety of dietary preferences revealed via recent genome-wide association studies (GWAS) allow further investigate the role of diet in liability to disease that has been limited to observational and epidemiologic studies with mixed findings.

Method

We obtained publicly available genome-wide association data for 38 dietary preference traits and seven common CVDs to investigate causal hypotheses between diet as the exposure to CVD as outcomes using the statistical framework of Mendelian randomization (MR) for hypothesis testing and sensitivity analyses. We also conducted mediation analyses to evaluate the effects of dietary preferences on CVDs to elucidate potential causal graphs and estimate the effects of dietary preferences mediated by potential mediators.

Results

Across all methods, we identified 10 significant causal effects, which included eight dietary preferences across three CVD endpoints (Bonferroni-corrected P < 1.88 × 10−4). In sensitivity MR and mediation analysis, we observed that obesity - quantified by body mass index (BMI) - was a common mediator that contributed to many of these observed effects. We also found that educational attainment was an exclusive, additional mediator for the effect of preference for muesli with risk to peripheral artery disease (PAD).

Conclusions

Our results provide genetic evidence for a link between diet and CVD that aligns with obesity-mediated risk of CVD in individuals in relation to their specific preferences for food.

Abstract Image

饮食偏好与心血管疾病的关联:一项孟德尔随机研究
背景和目的心血管疾病(CVD)的易感性是由遗传和环境危险因素驱动的。饮食是心血管疾病可改变的主要环境风险因素。最近的全基因组关联研究(GWAS)揭示了与多种饮食偏好相关的遗传因素,从而进一步研究饮食在疾病倾向性中的作用,这些研究仅限于观察性和流行病学研究,结果不一。方法利用公开的38个饮食偏好性状与7种常见心血管疾病的全基因组关联数据,采用孟德尔随机化(Mendelian randomization, MR)的统计框架进行假设检验和敏感性分析,探讨饮食与心血管疾病暴露之间的因果关系。我们还进行了中介分析,评估饮食偏好对心血管疾病的影响,以阐明潜在的因果关系图,并估计饮食偏好在潜在介质中的中介作用。在所有方法中,我们确定了10个显著的因果效应,其中包括3个CVD终点的8种饮食偏好(bonferroni校正P <;1.88 × 10−4)。在敏感性MR和中介分析中,我们观察到肥胖(通过体重指数(BMI)量化)是导致许多观察到的影响的常见中介。我们还发现,受教育程度是外周动脉疾病(PAD)风险偏好muesli影响的唯一额外中介。结论:我们的研究结果为饮食和心血管疾病之间的联系提供了遗传证据,这与肥胖介导的心血管疾病风险与个体特定的食物偏好有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Atherosclerosis plus
Atherosclerosis plus Cardiology and Cardiovascular Medicine
CiteScore
2.60
自引率
0.00%
发文量
0
审稿时长
66 days
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信