British Journal of Nutrition

Research Article

The influence of different combinations of γ-linolenic acid, stearidonic acid and EPA on immune function in healthy young male subjects

Elizabeth A. Milesa1 c1, Tapati Banerjeea1, Maaike M. B. W. Doopera2, Laura M'Rabeta2, Yvo M. F. Grausa2 and Philip C. Caldera1

a1 Institute of Human Nutrition, School of Medicine, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, UK

a2 Numico Research BV, P. O. Box 7005, Wageningen NL-6700, The Netherlands


To determine the effects of EPA, stearidonic acid (STA) or γ-linolenic acid (GLA) on immune outcomes, healthy male subjects consumed one of seven oil blends for 12 weeks. EPA consumption increased the EPA content of peripheral blood mononuclear cells (PBMC). Consumption of GLA (2·0 g/d) in the absence of STA or EPA increased di-homo-GLA content in PBMC. Neither STA nor its derivative 20:4n-3 appeared in PBMC when STA (<1·0 g/d) was consumed. However, STA (1·0 g/d), in combination with GLA (0·9 g/d), increased the proportion of EPA in PBMC. None of the treatments altered neutrophil or monocyte phagocytosis or respiratory burst, production of inflammatory cytokines by monocytes, T lymphocyte proliferation or the delayed-type hypersensitivity response. Production of cytokines by T lymphocytes increased in all groups, with no differences among them. The proportion of lymphocytes that were natural killer cells decreased significantly in subjects receiving 2·0 g EPA or GLA/d. There were no other effects on lymphocyte sub-populations. Plasma IgE concentration decreased in most groups, but not in the control group. Plasma IgG2 concentration increased in the EPA group. Thus, EPA or GLA at a dose of 2·0 g/d have little effect on key functions of neutrophils, monocytes and T lymphocytes, although at this dose these fatty acids decrease the number of natural killer cells. At this dose EPA increases IgG2 concentrations. STA can increase immune cell EPA status, but at 1·0 g/d does not affect human immune function.

(Received August 21 2003)

(Revised December 11 2003)

(Accepted February 17 2004)


c1 *Corresponding author: Dr Elizabeth A. Miles, fax + 44 23 8059 4383, email