Immunomodulatory effects of Flaxseed and Other Oils rich in Alpha-linolenic acid. In: Flaxseed in Human Nutrition.
Immunomodulatory effects of Flaxseed and Other Oils rich in Alpha-linolenic acid. In: Flaxseed in Human Nutrition.
Year: 1995
Authors: D S Kelley.
Publication Name: AOCS Press, Champaign, Ill.
Publication Details: 147. 163.
Abstract:
The immune system protects the body against foreign invaders through a complex interaction between immune cells and the numerous factors they produce. The immune status of an individual is regulated by several physiological factors, including nutritional intake. Epidemiological and clinical research has shown a lower incidence of inflammatory and autoimmune diseases in populations and subjected consuming high intakes of n-3 PUFAs. Studies assessing the effects of dietary ALA on indices of immune status have reported inconsistent results. ALA has been shown to inhibit lymphocyte proliferation when fed to rats and chickens and simulated this index when fed to rabbits. In rat splenocytes, ALA did not alter natural killer cell (NK) activity, but it stimulated this fraction in mouse splenocytes. ALA stimulated TNF production by rat and mouse peritoneal macrophages. Limited data from human studies indicated that flaxseed oil inhibited peripheral blood mononuclear cells (PBMNC) proliferation and DHS response, but several other indices were not affected. Mechanisms by which ALA might alter immune response are poorly understood. ALA may act via modifications in the FA composition of immune cells and platelets which secrete compounds that affect immune responses. ALA has been shown to reduce the synthesis of PGE2, PGF1, PGI2, TXA2, TXB2 and LTE5. ALA may also have an inhibitory effect on some immune indices through pro-oxidation mechanisms. Incorporation of ALA into membrane lipids can alter membrane fluidity, which can affect receptor expression, signal transduction, nutrient transport, and cell to cell interactions. Since3 the effects of ALA vary in different species and in different cell types, several mechanisms may be operative. The author speculates that several factors may have contributed to the lack of consistent effects of ALA on immune response. Differences in the concentration and duration of ALA fed, total fat content and composition of the control diets, concentration of antioxidants, and lack of uniformity of assay techniques may have led to the differences in results between studies. The author indicates that relatively high intakes of ALA could have an adverse effect in individuals with compromised immune status, but may be of benefit to individuals with autoimmune disorders. He suggests further studies be performed to evaluate the clinical implications of ALA diets in humans.
