Role of polyunsaturated fatty acids in lung disease.
DF Horrobin hypothesized that the low prevalence of lung disease among Eskimos is the result of their diet, which is high in n-3 fatty acids. The n-3 and n-6 fatty acids shunt eicosanoid production away from the arachidonic acid pathway, and hence decrease the production of bronchoconstrictive leukotrienes. Animal studies showed that eicosapentaenoic acid or gamma-linolenic acid supplementation of animals exposed to endotoxins results in decreased effects on thromboxane B(2) and pulmonary vascular resistance. Small human trials confirmed that supplementation with eicosapentaenoic acid results in increased eicosapentaenoic acid in phospholipids and decreased generation of leukotrienes by neutrophils. Hence, a protective effect of such fatty acids in lung disease is biologically plausible. The results of human intervention studies looking at respiratory outcomes have been mixed, but they do suggest a possible difference between long-term and short-term effects. Epidemiologic studies showed possible protective effects against asthma in children, but weak to no evidence of such effects in adults. Results for bronchitis are more positive, although intervention trials are lacking. Recently, a cross-sectional analysis of data from the first National Health and Nutrition Examination Survey reported an approximately 80-mL difference in forced expiratory volume at 1 s between adults with high compared with low fish consumption. This response was not limited to asthmatic subjects. Others found that both fish consumption and n-3 fatty acid consumption (as estimated from food-frequency questionnaires) were protective against physician-diagnosed emphysema and chronic bronchitis and low spirometry values. Only smokers were included in this analysis. These results suggest that dietary fatty acids may play a role in lung disease; further work is needed to elucidate that role.
Schwartz
J
J
Environmental Epidemiology Program, Department of Environmental Health, Harvard School of Public Health, Channing Laboratory, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA. joel@tiamat.harvard.edu
D000328:Adult; D000818:Animals; D001249:Asthma / Q000178:diet therapy; D001991:Bronchitis / Q000178:diet therapy; D002648:Child; D003550:Cystic Fibrosis / Q000178:diet therapy; D004042:Dietary Fats, Unsaturated / Q000378:metabolism*; D015118:Eicosapentaenoic Acid / Q000378:metabolism; D005231:Fatty Acids, Unsaturated / Q000378:metabolism*; D006801:Humans; D008171:Lung Diseases / Q000178:diet therapy / Q000517:prevention & control*; D008173:Lung Diseases, Obstructive / Q000178:diet therapy; D011817:Rabbits; D012129:Respiratory Function Tests; D013552:Swine; D017965:gamma-Linolenic Acid / Q000378:metabolism
D004042:Dietary Fats, Unsaturated; D005231:Fatty Acids, Unsaturated; D017965:gamma-Linolenic Acid; D015118:Eicosapentaenoic Acid