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Obesity, dietary arachadonic acid and risk of allergic disease in women
Author(s) -
Tagliaferro Anthony Richard,
Windt Mark R,
Ronan Anne M,
Vieira Victoria J
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a603-c
Subject(s) - obesity , medicine , disease , environmental health
Research evidence strongly suggests that obesity and the dietary polyunsaturated fatty acid, arachadonic acid (AA), are proinflammatory factors in the etiology and/or exacerbation of asthma and related allergic diseases. The present cross‐sectional study examined the relationship between fat mass, insulin sensitivity and dietary polyunsaturated fatty acids in relation to circulating specific IgE antibodies (SpIgE) and pulmonary function. Fifty‐nine non‐asthmatic (NA=42), asthmatic (A=17), obese (OB) and non‐obese women (NO), ages 18–45 yr were studied. Asthma was diagnosed by medical history and ≥20% reduction in forced expiratory volume in one second (FEV1) to a methacholine challenge, or a ≥12% increase in FEV1 to a bronchodilator. Ventilatory function was by FEV1, pre and post bronchodilator, Obesity was body fat ≥30%, measured by air displacement plethysmography; plasma concentration of SpIgE measured by automated immunosorbent analysis (Pharmacia Diagnostics). Insulin resistance was measured using Fasting Insulin Resistance Index; dietary intake measured by Food Frequency Questionnaire. SpIgE was greater among OB vs NO and A vs NA (P<0.05). FIRI was greater among OB vs NO (P<0.001), A vs NA (P<0.1). Dietary intake of AA was greater among OB vs NO (P<0.1), A vs NA (P<0.05). Multiple regression analyses indicated AA and fat mass were independent positive predictors of SpIgE (P<0.05), AA and FIRI were independent positive predictors of change in FEV1, pre vs post bronchodilator (P<0.05). Findings indicate obesity and dietary AA are promoters of allergic disease in women. Funded by NHAES H285, NHALA.