Hussein · Journal of lipid research 2005 · controlled dietary intervention trial · n=38

Long-chain conversion of [13C]linoleic acid and alpha-linolenic acid in response to marked changes in their dietary intake in men.

Cited 370 times in the scientific literature.

Level 3 - non-randomized controlled study

Controlled dietary trial with stable isotope tracer substudy (randomization not specified in abstract)

PubMed 15576848 · doi:10.1194/jlr.M400225-JLR200 · record verified 2026-08-28

What was done

Thirty-eight moderately hyperlipidemic men consumed diets enriched for 12 weeks with either flaxseed oil (17 g/day alpha-linolenic acid [ALA], n=21) or sunflower oil (17 g/day linoleic acid [LA], n=17). Long-chain conversion was quantified in subsets (n=6 flaxseed oil, n=5 sunflower oil) using [U-13C]ALA and [U-13C]LA stable isotope tracers with kinetic dilution modeling. Erythrocyte phospholipid fatty acid composition was measured and compared against a reference group receiving sunflower oil supplemented with 3 g/day of EPA plus DHA from fish oil (n=19).

What was found

Flaxseed oil supplementation increased erythrocyte phospholipid ALA (>3-fold), eicosapentaenoic acid (EPA, >2-fold), and docosapentaenoic acid (DPA, 50%), but caused no change in docosahexaenoic acid (DHA), LA, or arachidonic acid (AA). The sunflower oil diet caused a small increase in LA and no change in AA. Fractional tracer conversion from peak plasma 13C concentrations was 0.3% for EPA, 0.02% for DPA, and 0.2% for AA. Conversion to [13C]DHA was <0.01% with no dietary influence.

Why it matters

This study demonstrates that while high dietary ALA intake effectively raises circulating EPA and DPA, endogenous synthesis of DHA in humans is functionally negligible and cannot substitute for preformed dietary DHA.

Limits

The abstract does not state whether treatment allocation was randomized. Tracer kinetics were evaluated in very small subsets (n=5 to 6 per group). The study included only moderately hyperlipidemic men, limiting generalizability to women and normolipidemic individuals. Long-term clinical endpoints were not measured.

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