母亲过多促炎饮食,或增加后代哮喘风险
创作:小笋干儿 审核:小笋干儿
  • 纳入862对母婴,在妊娠早期评估母亲饮食HEI指数(评估饮食质量)和EDII指数(评估促炎饮食),并随访后代儿童10年,记录哮喘患病情况;
  • 随访期间,儿童累积哮喘患病率在21%;
  • EDII指数越高,促炎饮食越多,后代哮喘风险越高;
  • 而HEI指数越高,饮食质量越健康,后代哮喘风险越低;
  • 在调整EDII指数以后,HEI指数与后代哮喘关联减弱,表明炎症饮食途径在此关联中的重要作用;
  • 上述关联在调整了潜在混杂因素后,仍稳定存在。
主编推荐语
小笋干儿
何为促炎饮食(Dietary inflammatory)?这个概念在汉语中较少提及,其指饮食所具有的潜在的引起炎症反应的能力。在我们生活中,最常见促炎食物可能包括反式脂肪、精炼种子油、糖以及引起过敏或不耐受的食物。本研究发现,孕早期母亲摄入较多的促炎饮食,其后代儿童在10年内患哮喘的风险将增加。
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Maternal dietary inflammatory potential and quality are associated with offspring asthma risk over 10-year follow-up: the Lifeways Cross-Generation Cohort Study

母亲炎症饮食及膳食质量与后代10年内哮喘风险的关联:跨代队列研究

10.1093/ajcn/nqz297

2019-12-11, Article

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Background: Asthma is the most common childhood chronic health condition. Maternal antenatal diet has been associated with offspring asthma risk, but studies investigating maternal whole diet quality and inflammatory potential with long-term offspring follow-up (>5 y) are rare.
Objectives: We aimed to elucidate these associations in a prospective cohort study in Ireland.
Methods: Early pregnancy diets were assessed using a validated FFQ from which energy-adjusted Dietary Inflammatory Index (E-DII) and Healthy Eating Index (HEI)-2015 scores were computed. Doctor-diagnosed offspring asthma status (general practitioner or parent reports) for the first 10 y of life was collected at 3-y, 5-y, and 9-y follow-up. A total of 862 mother–child pairs with information on maternal diet and ≥1 offspring asthma data points were included. The longitudinal associations between maternal E-DII and HEI scores and offspring asthma status were assessed using generalized estimating equations.
Results: Cumulative offspring asthma incidence was 21% over the 10-y period. In the main models, adjusted for maternal lifestyle and sociodemographic factors, a higher E-DII score, indicating a more proinflammatory diet, was associated with higher risk of offspring asthma (OR: 1.35; 95% CI: 1.10, 1.65; per 1-SD score increment), whereas a higher HEI-2015 score, indicating better dietary quality, was associated with lower risk (OR: 0.77; 95% CI: 0.64, 0.93) (both P < 0.01). Results persisted with further adjustment for childhood factors (e.g., breastfeeding, diet, and childcare attendance) and parental asthma history. Similar associations were observed when E-DII and HEI-2015 scores were modeled in quartiles (both P-trend < 0.05). Associations for HEI-2015 were attenuated after adjustment for E-DII, suggesting the importance of anti-inflammatory pathways.
Conclusions: Our results suggest that a proinflammatory and low-quality diet during pregnancy is associated with a higher risk of offspring asthma. Pending confirmation from other studies, optimizing these aspects of maternal diet can be a promising strategy for reducing childhood asthma risk.

First Authors:
Ling-Wei Chen

Correspondence Authors:
Catherine M Phillips

All Authors:
Ling-Wei Chen,Becky Lyons,Pilar Navarro,Nitin Shivappa,John Mehegan,Celine M Murrin,James R Hébert,Catherine M Phillips

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