Evidence for a relationship between fatty acid levels and allergic disease in a founder population

• Published in: Journal of allergy and clinical immunology Vol. 113; no. 2; pp. S206 - S207
• Main Authors: Grant, A., Mathias, R.A., Markakis, D., Nickel, R., Bickel, C., Beaty, T.H., Surette, M.E., Barnes, K.C.
• Format: Journal Article
• Language: English
• Published: St. Louis Mosby, Inc 01.02.2004; Elsevier Limited
• ISSN: 0091-6749; 1097-6825
• DOI: 10.1016/j.jaci.2004.01.189

Several potent inflammatory mediators involved in allergic disease belong to n-6 series polyunsaturated fatty acids (PUFAs). Epidemiological data show an increased prevalence of asthma and atopy that parallels an increase in dietary n-6:n-3 PUFAs. Linkage of allergic disease and several chromosomal loci has been reported. We hypothesize that fasting plasma fatty acid levels may confound such evidence for linkage in populations exhibiting a high prevalence of allergic disease and high dietary PUFA intake. We evaluated linkage of asthma (n=142), atopy (n=58), and total IgE (tIgE) concentrations (n=187) to 38 microsatellite markers and 6 SNPs in 8 chromosomes (5q, 6p, 11q, 12q, 14q, 17q) in affected sib-pairs from Tangier Island, Virginia, using Haesman-Elston regression analysis. Serum PUFA content was determined by gas chromatography with flame ionization detection. Trait prevalence was the following: asthma=14.2%, atopy=55%, mean tIgE=164.5 ng/mL. We found evidence for linkage to asthma and atopy for multiple 12q markers (P<0.001–0.04) and atopy and 11q markers (P<0.001–0.008). After adjusting for 22 fatty acids and two fatty acid ratios, there was significant evidence for linkage for tIgE to many 12q (P<0.001–0.03) and 6p (P<0.05) markers. Evidence for linkage to asthma and FCER1B (11q; P=0.03) was strengthened after adjusting for these covariates (P=0.0006–0.004). These findings suggest that linkage to allergic disease, including asthma, atopy and especially tIgE levels, is confounded by PUFA levels in residents of Tangier Island, which supports a putative role of diet in expression of genes controlling allergic disease.