AbstractLinoleic acid is metabolised to arachidonic acid via gamma-linolenic acid (GLA) and dihomogammalinolenic acid (DGLA). It is commonly assumed that in humans linoleic acid is easily converted along this route. However, several reports indicate that very large increases in daily linoleate intake (10-40g/day) are unable to modify plasma levels of DGLA and arachidonic acid. We now report the effects of 14 days treatment with modest doses (4-6g/day) of safflower oil (82% linoleic), Efamol evening primrose oil (72% linoleic, 9% GLA), fish oil (18% EPA, 12% DHA), Efamol Marine (80% Efamol + 20% fish oil) and an inert placebo, liquid paraffin. The only agent which had no significant effect on any essential fatty acid (EFA) in plasma phospholipids was the paraffin. This is therefore an appropriate inert placebo when modest doses of oil supplements are given. Efamol caused a significant rise in DGLA with no change in linoleic or arachidonic acids, consistent with previous reports of slow conversion of DGLA to arachidonic acid. Fish oil elevated EPA and DHA and reduced linoleic acid and DGLA while leaving arachidonic acid unchanged. Efamol Marine significantly raised both EPA and DGLA but had no effects on linoleic or arachidonic acids. The surprise was the effect of safflower oil. This significantly raised levels of both linoleic and arachidonic acids without any effect on GLA or DGLA. This is consistent with recent in vitro observations suggesting that linoleic acid can be converted to arachidonic acid without mixing with GLA or DGLA pools (Voss & Sprecher, Lipids 23: 660-5, 1988). Safflower oil is therefore not an appropriate placebo for studies with GLA-rich oils. A truly inert placebo such as liquid paraffin should be compared with both GLA-containing oils and oils which contain linoleic acid as their only EFA.
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