Tags

Type your tag names separated by a space and hit enter

Fatty acid composition abnormalities in atopic disease: evidence explored and role in the disease process examined.
Clin Exp Allergy. 2008 Sep; 38(9):1432-50.CE

Abstract

Summary There is a hypothesis causally linking excess intake of n-6 polyunsaturated fatty acids (PUFAs) to atopic disease. Under most dietary conditions, the main precursor of eicosanoids is the n-6 PUFA arachidonic acid (AA). AA-derived eicosanoids play many roles in sensitization to allergens and in allergic inflammation. Long chain n-3 PUFAs inhibit AA incorporation into cell membranes and inhibit AA metabolism to eicosanoids. It is hypothesized that atopy is associated with a higher n-6 PUFA status and with a low n-3 PUFA status. However, measurements of fatty acid composition do not provide a clear picture that such fatty acid abnormalities exist in atopy with no really clear pattern of altered status of a particular fatty acid or a particular fatty acid family. There are few reports of elevated linoleic acid in atopy. Some studies report lower amounts of the n-6 PUFAs, including AA, and of long chain n-3 PUFAs in atopy, although observations on this are not consistent. Taken together these data clearly do not support the hypothesis that atopy is somehow associated with a high exposure to, and status of, n-6 PUFAs. Intervention studies with n-3 PUFAs in pregnant women, infants and children suggest some clinical benefits, although how long lasting these are remains to be determined. The observation that there may be low AA status in atopy suggests that fish oil intervention, which targets AA status and metabolism, may not be ideal and that a combination of fish oil with some longer chain n-6 PUFAs may be more efficacious.

Authors+Show Affiliations

Institute of Human Nutrition, School of Medicine, University of Southampton, Southampton General Hospital, Southampton, UK. E.A.Miles@soton.ac.ukNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

18665842

Citation

Sala-Vila, A, et al. "Fatty Acid Composition Abnormalities in Atopic Disease: Evidence Explored and Role in the Disease Process Examined." Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, vol. 38, no. 9, 2008, pp. 1432-50.
Sala-Vila A, Miles EA, Calder PC. Fatty acid composition abnormalities in atopic disease: evidence explored and role in the disease process examined. Clin Exp Allergy. 2008;38(9):1432-50.
Sala-Vila, A., Miles, E. A., & Calder, P. C. (2008). Fatty acid composition abnormalities in atopic disease: evidence explored and role in the disease process examined. Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, 38(9), 1432-50. https://doi.org/10.1111/j.1365-2222.2008.03072.x
Sala-Vila A, Miles EA, Calder PC. Fatty Acid Composition Abnormalities in Atopic Disease: Evidence Explored and Role in the Disease Process Examined. Clin Exp Allergy. 2008;38(9):1432-50. PubMed PMID: 18665842.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fatty acid composition abnormalities in atopic disease: evidence explored and role in the disease process examined. AU - Sala-Vila,A, AU - Miles,E A, AU - Calder,P C, Y1 - 2008/07/28/ PY - 2008/7/31/pubmed PY - 2009/1/23/medline PY - 2008/7/31/entrez SP - 1432 EP - 50 JF - Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology JO - Clin. Exp. Allergy VL - 38 IS - 9 N2 - Summary There is a hypothesis causally linking excess intake of n-6 polyunsaturated fatty acids (PUFAs) to atopic disease. Under most dietary conditions, the main precursor of eicosanoids is the n-6 PUFA arachidonic acid (AA). AA-derived eicosanoids play many roles in sensitization to allergens and in allergic inflammation. Long chain n-3 PUFAs inhibit AA incorporation into cell membranes and inhibit AA metabolism to eicosanoids. It is hypothesized that atopy is associated with a higher n-6 PUFA status and with a low n-3 PUFA status. However, measurements of fatty acid composition do not provide a clear picture that such fatty acid abnormalities exist in atopy with no really clear pattern of altered status of a particular fatty acid or a particular fatty acid family. There are few reports of elevated linoleic acid in atopy. Some studies report lower amounts of the n-6 PUFAs, including AA, and of long chain n-3 PUFAs in atopy, although observations on this are not consistent. Taken together these data clearly do not support the hypothesis that atopy is somehow associated with a high exposure to, and status of, n-6 PUFAs. Intervention studies with n-3 PUFAs in pregnant women, infants and children suggest some clinical benefits, although how long lasting these are remains to be determined. The observation that there may be low AA status in atopy suggests that fish oil intervention, which targets AA status and metabolism, may not be ideal and that a combination of fish oil with some longer chain n-6 PUFAs may be more efficacious. SN - 1365-2222 UR - https://www.unboundmedicine.com/medline/citation/18665842/Fatty_acid_composition_abnormalities_in_atopic_disease:_evidence_explored_and_role_in_the_disease_process_examined_ L2 - https://doi.org/10.1111/j.1365-2222.2008.03072.x DB - PRIME DP - Unbound Medicine ER -