Dietary Alpha-Linolenic Acid and Immunocompetence in Humans.

January 1, 1991 Human Health and Nutrition Data 0 Comments

Dietary Alpha-Linolenic Acid and Immunocompetence in Humans.

Year: 1991
Authors: D S Kelley, L B Branch, J E Love, P C Taylor, Y M Rivera, J M Iacono.
Publication Name: Amer. J. Clin. Nutr.
Publication Details: Volume 53; 40.


Research to ascertain the influence of n-3 PUFAs on immune status has lead to inconsistent results and only a few studies in humans have been performed. In previous a previous study by these investigators in rabbits, flaxseed oil feeding led to significant enhancement of several indices of the immune system. The proliferation of peripheral blood mononuclear cells (PBMNCs) in response to phytohemagglutinin-P (PHA), concanavalin A (Con A) and pokeweed was suppressed in three ALA-deficient patients upon supplementation of their diet with ALA followed by EPA. The n-3 PUFA supplementation also resulted in increased T-cell numbers in the blood. Feeding EPA to a healthy human subject suppressed serum concentrations of immunoglobulin G (IgG) and IgM. Feeding fish oil to humans has also been reported to suppress macrophage and neutrophil functions. In this study, the effect of ALA on several indices of immunocompetence in 10 healthy free-living men (age 21-37 years) was examined. Subjects consumed all meals in a metabolic laboratory unit for 126 days. A stabilization period of 14 days in which all subjects consumed a basal diet (BD) preceded two intervention periods of 56 days each. The BD consisted of 16.5 % protein, 60% carbohydrate and 23% fat (7% SFA, 9%, MUFA, 6% PUFA of which 25% was LA and 1.1% ALA). Five of the subjects consumed the basal diet and the other five consumed flaxseed oil diet during each intervention period. The flaxseed oil diet consisted of 16 % protein, 55% carbohydrate and 29% fat (7% SFA, 10%, MUFA, 10.5% PUFA of which 15% was LA and 21.2% ALA). Indices of immune status dependent on both T-cell functions (cell-mediated immunity) and B-cell functions (humoral immunity) were examined. Overall, the flaxseed oil tended to suppress the cell-mediated immunity without affecting the humoral immunity. Feeding of flaxseed oil significantly suppressed the proliferation of PBMNCs cultured with the T-cell mitogens PHA and Con A. The flaxseed oil also suppressed the delayed hypersensitivity response of the skin when exposed to seven recall antigens. The concentrations of immunoglobulins C3 and C4 in serum, salivary IgA, the numbers of helper cells, suppressor cells, and total T and B cells in the peripheral blood were not affected by the diets. The mechanisms involved in the suppression of T-cell function by ALA were not examined in this study. The authors hypothesize that the effects may be mediated through alterations in lymphocyte membrane fatty acid composition, physical properties of the lipoproteins, or prostaglandin synthesis. Further work is planned to address this question. The authors indicate that the suppressive effect of flaxseed oil on several indices of cell-mediated immunity may be of benefit in the treatment of individuals with autoimmune disorders or chronic inflammation such as arthritis, lupus and allergies. Further research is necessary prior to making recommendations in this regard.

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