Details

Autor(en) / Beteiligte

• Chen, Ling-Wei
• Lyons, Becky
• Navarro, Pilar
• Shivappa, Nitin
• Mehegan, John
• Murrin, Celine M
• Hébert, James R
• Kelleher, Cecily C
• Phillips, Catherine M

Titel

Maternal dietary inflammatory potential and quality are associated with offspring asthma risk over 10-year follow-up: the Lifeways Cross-Generation Cohort Study

Ist Teil von

• The American journal of clinical nutrition, 2020-02, Vol.111 (2), p.440-447

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2020

Quelle

Oxford Journals 2020 Medicine

Beschreibungen/Notizen

• 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. We aimed to elucidate these associations in a prospective cohort study in Ireland. 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. 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. 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. This prospective observational study was registered at the ISRCTN Registry as ISRCTN16537904.