The long chain polyunsaturated fatty acids (PUFA) eicosapentanoic acid (EPA, C20:5 (n-3)) and docosahexanoic acid (DHA, C22:6 (n-3)) accumulate in cell membranes where they provide protection against cardiovascular disease. This is because they are converted to eicosanoid hormones that regulate inflammation, thrombosis, cell aggregation and immune system function. Increasing cellular levels of EPA and DHA by increasing their precursor fatty acid α-linolenic acid (ALA, C18:3 (n-3)) is not straightforward because the conversion can be inhibited by other PUFA. In particular, linoleic acid (LA, C18:2 (n-6)) is know to reduce the conversion of ALA to EPA via competition for the elongase and desaturase enzymes. In addition, LA can be converted to either dihomo-γ-linolenic acid (DGLA, C20:3 (n-6)) or arachidonic acid (AA, C20:4 (n-6)) which can subsequently be converted to anti-inflammatory or pro-inflammatory eicosanoids, respectively.
Researchers1 have investigated the interaction of n-3 and n-6 fatty acids in 30 healthy male volunteers. Fifteen of these subjects were administered a high ALA diet, that avoided all sources of LA and was supplemented with flaxseed in order to maintain a high n-3:n-6 ratio. The other 15 subjects acted as a control group and were instructed to maintain a typical Western diet with a naturally high n-6:n-3 ratio. Study participants had intakes of LA that ranged from 2.9 to 41.4g/d and intakes of ALA that ranged from 0.3 to 22.0g/d, with the treatment group having intakes of ALA >50% higher than the control group. Dietary levels of LA and ALA correlated with the concentrations in plasma phospholipids of neutrophils, erythrocytes, platelets and mononuclear cells. In addition, dietary ALA showed positive association, and LA negative association, with the EPA concentration in plasma phospholipids.
Dietary intakes of ALA and LA increase their concentrations in the plasma phospholipids, but in this study there was a 10-fold difference in the percentage of each in the tissues. For example, 20g/d LA resulted in a 11% increase in LA in neutrophil phospholipid membranes, but the same intake of ALA only resulted in a 0.8% increase. However, the reasons for this are not clear. High levels of ALA accumulation were associated with reductions in the DHA concentration in plasma phospholipids, suggesting an inhibitory action of ALA on DHA synthesis. Interestingly, the AA content of phospholipid membranes was not affected by the LA content of the diet. This may be due to adipose tissue containing 10 to 15% LA, with continual release maintaining AA concentrations despite changing dietary intakes. Rats studies suggest that intakes of LA above 0.33% of energy result in no further increase in AA concentrations.
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