Association of equol producing status with aortic calcification in middle-aged Japanese men: The ERA JUMP study

日本中年男性雌马酚生成状态与主动脉钙化的关联:ERA JUMP 研究

阅读:1

Abstract

BACKGROUND: Equol, an isoflavone (ISF)-derived metabolite by the gut microbiome in certain individuals termed as equol-producers, might be the key anti-atherogenic component of ISFs. Our objective was to determine the association between equol-producing status and aortic atherosclerosis assessed as aortic calcification (AC). METHODS: This population-based study of 302 Japanese men aged 40-49, free of cardiovascular disease, examined serum levels of equol and ISFs, AC in the entire aorta by electron-beam computed tomography with Agatston method, and cardiovascular risk factors. We defined equol-producers as individuals with serum levels of equol ≥20 nM and prevalent AC as an AC score ≥ 10. We analyzed the association between equol-producing status and AC using Tobit and logistic regressions. We performed age-stratified analyses since age was a significant effect-modifier. RESULTS: The 70th to 90th percentile AC scores were 4 to 243 in equol-producers and 15 to 444 in non-producers, respectively. Overall, equol-producers (41% of the sample) had lower AC scores (-209, [95% confidence interval (CI): -455, 36]) and odds of AC (odds ratio (OR): 0.7 [95% CI: 0.4, 1.3]), although not statistically significant, compared to non-producers after controlling for cardiovascular risk factors. Among men aged 46-49, equol-producers had significantly lower AC scores (-428 [95% CI: -827, -29]). Furthermore, there were null associations between serum levels of ISFs and both AC score and the odds of AC. CONCLUSION: In middle-aged Japanese men, equol-producers had a non-significantly lower burden of aortic atherosclerosis than non-producers whereas ISFs had a null association. Studies with larger sample sizes in both sexes are warranted.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。