Essential fatty-acid deficiency is reported to decrease thymus and spleen weight and suppress cell-mediated immune responses and antibody production (for references, see Kelley and Daudu, 1993; Calder 1998a). However, a large number of studies in rats, mice, rabbits, chickens and monkeys have reported lower mitogen-stimulated lymphocyte proliferation and antibody production following the feeding of diets rich in linoleic acid (maize, sunflower or safflower oils), compared with feeding high-fat diets rich in saturated fatty acids (for references, see Kelley and Daudu, 1993; Calder, 1998a, b). These data suggest that linoleic acid has the potential to suppress acquired immune function. However, no difference in blood lymphocyte proliferation, circulating immunoglobulins or the delayed-type hypersensitivity response was seen in volunteers consuming low-fat diets (25% energy as fat) that were rich (12.9% of energy) or poor (3.5% of energy) in linoleic acid (Kelley et al., 1989, 1992). Furthermore, increasing linoleic acid intake by 6 g day-1 did not affect blood lymphocyte proliferation or the production of a range of cytokines by lymphocytes (Yaqoob et al., 2000). Again, the reason for the apparent discrepancy between animal and human studies most probably relates to the amount of linoleic acid in the diets studied.
Similarly to linoleic acid, feeding rodents diets containing very high levels of a-linolenic acid (linseed oil) is reported to decrease lymphocyte proliferation (e.g. Marshall and Johnston, 1985; Jeffery et al., 1996). The precise effect of a-linolenic acid on lymphocyte function appears to depend on both the level of the fatty acid and the total PUFA content of the diet (Jeffery et al., 1997). Feeding linseed oil (providing about 15 g a-linolenic acid day-1) as part of a low-fat diet (total fat provided 29% energy) for 6 weeks resulted in significant decreases in human blood lymphocyte proliferation and in the delayed-type hypersensitivity response (Kelley et al., 1991). Thus, as was the case for linoleic acid, it appears that both a deficiency and an excess of a-linolenic acid can lead to suppressed immune function. However, increasing a-linolenic acid consumption by 2 g day-1 in healthy humans did not affect lymphocyte proliferation or the production of a range of cytokines by lymphocytes (Thies et al., 2001c), suggesting a limited immunological impact of a more moderate increase in a-linolenic acid intake.
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