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Nutritional Evidence in Asthma and Allergy Pathogenesis

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutritional Immunology".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 2496

Special Issue Editors


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Guest Editor
Division of Respiratory Medicine, University of British Columbia, Vancouver, BC, Canada
Interests: airway diseases; air pollution; diet; obesity; health equity

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Guest Editor
St. Michael’s Hospital, Unity Health Toronto, Toronto, ON, Canada
Interests: malnutrition; food insecurity; diet; dietary intervention; respiratory infections; asthma; COPD

Special Issue Information

Dear Colleagues,

Nutritional exposures have the potential to impact health through a variety of biologic mechanisms, including the influence on inflammation and oxidant balance, alteration of the gut microbiome, and epigenetic change. Indeed, the World Health Organization recognized an unhealthy diet as a prominent risk factor for the development of chronic disease. There is a growing body of evidence suggesting that nutrition may contribute more specifically to the pathogenesis and severity of asthma and allergic disease, affecting hundreds of millions of individuals globally. A thorough understanding of which nutritional factors may contribute to disease, and how, is critical to achieving progress in the goal of reducing disease incidence and morbidity. This Special Issue aims to collect original research articles, reviews, and short papers on the topic of evidence (including interventions) in the prevention or management of asthma and allergy.

Dr. Emily Brigham
Dr. Banafshe Benita Hosseini
Guest Editors

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Keywords

  • asthma
  • allergy
  • wheeze
  • diet
  • nutrition
  • vitamin
  • antioxidant
  • inflammation
  • nutraceuticals

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Published Papers (1 paper)

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Research

14 pages, 1721 KiB  
Article
Omega-3 Fatty Acids Interact with DPP10 Region Genotype in Association with Childhood Atopy
by Kathleen A. Lee-Sarwar, Kasper Fischer-Rasmussen, Klaus Bønnelykke, Hans Bisgaard, Bo Chawes, Rachel S. Kelly, Jessica Lasky-Su, Robert S. Zeiger, George T. O’Connor, Leonard B. Bacharier, Vincent J. Carey, Nancy Laranjo, Augusto A. Litonjua and Scott T. Weiss
Nutrients 2023, 15(10), 2416; https://doi.org/10.3390/nu15102416 - 22 May 2023
Cited by 1 | Viewed by 1996
Abstract
Associations of omega-3 fatty acids (n-3) with allergic diseases are inconsistent, perhaps in part due to genetic variation. We sought to identify and validate genetic variants that modify associations of n-3 with childhood asthma or atopy in participants in the [...] Read more.
Associations of omega-3 fatty acids (n-3) with allergic diseases are inconsistent, perhaps in part due to genetic variation. We sought to identify and validate genetic variants that modify associations of n-3 with childhood asthma or atopy in participants in the Vitamin D Antenatal Asthma Reduction Trial (VDAART) and the Copenhagen Prospective Studies on Asthma in Childhood 2010 (COPSAC). Dietary n-3 was derived from food frequency questionnaires and plasma n-3 was measured via untargeted mass spectrometry in early childhood and children aged 6 years old. Interactions of genotype with n-3 in association with asthma or atopy at age 6 years were sought for six candidate genes/gene regions and genome-wide. Two SNPs in the region of DPP10 (rs958457 and rs1516311) interacted with plasma n-3 at age 3 years in VDAART (p = 0.007 and 0.003, respectively) and with plasma n-3 at age 18 months in COPSAC (p = 0.01 and 0.02, respectively) in associationwith atopy. Another DPP10 region SNP, rs1367180, interacted with dietary n-3 at age 6 years in VDAART (p = 0.009) and with plasma n-3 at age 6 years in COPSAC (p = 0.004) in association with atopy. No replicated interactions were identified for asthma. The effect of n-3 on reducing childhood allergic disease may differ by individual factors, including genetic variation in the DPP10 region. Full article
(This article belongs to the Special Issue Nutritional Evidence in Asthma and Allergy Pathogenesis)
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