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来自PREDIMED-NAVARRA研究的心血管疾病高风险受试者的饮食炎症指数与端粒长度:5年的横断面和纵向分析

Dietary inflammatory index and telomere length in subjects with a high cardiovascular disease risk from the PREDIMED-NAVARRA study: cross-sectional and longitudinal analyses over 5 y.

作者信息

García-Calzón Sonia, Zalba Guillermo, Ruiz-Canela Miguel, Shivappa Nitin, Hébert James R, Martínez J Alfredo, Fitó Montserrat, Gómez-Gracia Enrique, Martínez-González Miguel A, Marti Amelia

机构信息

Departments of Nutrition, Food Science and Physiology, Navarra Institute for Health Research, Pamplona, Spain;

Biochemistry and Genetics, and Navarra Institute for Health Research, Pamplona, Spain;

出版信息

Am J Clin Nutr. 2015 Oct;102(4):897-904. doi: 10.3945/ajcn.115.116863. Epub 2015 Sep 9.

Abstract

BACKGROUND

Dietary factors can affect telomere length (TL), a biomarker of aging, through oxidation and inflammation-related mechanisms. A Dietary Inflammatory Index (DII) could help to understand the effect of the inflammatory potential of the diet on telomere shortening.

OBJECTIVE

This study aimed to determine the association of the DII with TL and to examine whether diet-associated inflammation could modify the telomere attrition rate after a 5-y follow-up of a Mediterranean dietary intervention.

DESIGN

This was a prospective study of 520 participants at high cardiovascular disease risk (mean ± SD age: 67.0 ± 6.0 y, 45% males) from the PREDIMED-NAVARRA (PREvención con DIeta MEDiterránea-NAVARRA) trial. Leukocyte TL was measured by quantitative real-time polymerase chain reaction at baseline and after 5 y of follow-up. The DII was calculated from self-reported data by using a validated 137-item food-frequency questionnaire.

RESULTS

Longer telomeres at baseline were found in participants who had a more anti-inflammatory diet (lowest DII score) (P-trend = 0.012). Longitudinal analyses further showed that a greater anti-inflammatory potential of the diet (i.e., a decrease in the DII) could significantly slow down the rate of telomere shortening. Moreover, the multivariable-adjusted OR for short telomeres (z score ≤20th percentile) was 1.80 (95% CI: 1.03, 3.17) in a comparison between the highest (proinflammatory) and the lowest (anti-inflammatory) DII tertiles. Similarly, a greater DII (greatest proinflammatory values) after a 5-y follow-up was associated with almost a 2-fold higher risk of accelerated telomere attrition compared with the highest decrease in DII (greatest anti-inflammatory values) during this period (P-trend = 0.025).

CONCLUSIONS

This study showed both cross-sectional and longitudinal associations between the inflammatory potential of the diet and telomere shortening in subjects with a high cardiovascular disease risk. Our findings are consistent with, but do not show, a beneficial effect of adherence to an anti-inflammatory diet on aging and health by slowing down telomere shortening. These results suggest that diet might play a key role as a determinant of TL through proinflammatory or anti-inflammatory mechanisms. This trial was registered at controlled-trials.com as ISRCTN35739639.

摘要

背景

饮食因素可通过氧化和炎症相关机制影响端粒长度(TL),端粒长度是衰老的生物标志物。饮食炎症指数(DII)有助于了解饮食的炎症潜能对端粒缩短的影响。

目的

本研究旨在确定DII与TL之间的关联,并检验在对地中海饮食干预进行5年随访后,与饮食相关的炎症是否会改变端粒磨损率。

设计

这是一项对来自PREDIMED-NAVARRA(地中海饮食预防-纳瓦拉)试验的520名心血管疾病高风险参与者(平均±标准差年龄:67.0±6.0岁,45%为男性)进行的前瞻性研究。在基线和随访5年后,通过定量实时聚合酶链反应测量白细胞TL。DII通过使用经过验证的137项食物频率问卷从自我报告数据中计算得出。

结果

饮食具有更强抗炎性(DII得分最低)的参与者在基线时端粒更长(P趋势=0.012)。纵向分析进一步表明,饮食具有更大的抗炎潜能(即DII降低)可显著减缓端粒缩短率。此外,在最高(促炎)和最低(抗炎)DII三分位数的比较中,短端粒(z评分≤第20百分位数)的多变量调整OR为1.80(95%CI:1.03,3.17)。同样,与在此期间DII下降最大(抗炎性最强)相比,5年随访后更高的DII(促炎值最高)与端粒加速磨损风险几乎高出2倍相关(P趋势=0.025)。

结论

本研究显示了饮食的炎症潜能与心血管疾病高风险受试者端粒缩短之间的横断面和纵向关联。我们的研究结果与通过减缓端粒缩短对衰老和健康产生抗炎饮食依从性的有益作用一致,但未显示出这种作用。这些结果表明,饮食可能通过促炎或抗炎机制作为TL的决定因素发挥关键作用。本试验在controlled-trials.com上注册,注册号为ISRCTN35739639。

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