Dietary n-3 alpha-linolenic and n-6 linoleic acids modestly lower serum lipoprotein(a) concentration but differentially influence other atherogenic lipoprotein traits: A randomized trial

Background and aims: Lipoprotein(a) [Lp(a)] is a causal, genetically determined cardiovascular
risk factor. Limited evidence suggests that dietary unsaturated fat may increase serum Lp(a)
concentration by 10-15 %. Linoleic acid may increase Lp(a) concentration through its
endogenous conversion to arachidonic acid, a process regulated by the fatty acid desaturase
(FADS) gene cluster. We aimed to compare the Lp(a) and other lipoprotein trait-modulating
effects of dietary alpha-linolenic (ALA) and linoleic acids (LA). Additionally, we examined
whether FADS1 rs174550 genotype modifies Lp(a) responses. Methods: A genotype-based
randomized trial was performed in 118 men homozygous for FADS1 rs174550 SNP (TT or CC).
After a 4-week run-in period, the participants were randomized to 8-week intervention diets
enriched with either Camelina sativa oil (ALA diet) or sunflower oil (LA diet) 30-50 mL/day based
on their BMI. Serum lipid profile was measured at baseline and at the end of the intervention.
Results: ALA diet lowered serum Lp(a) concentration by 7.3 % (p = 0.003) and LA diet by 9.5 %
(p < 0.001) (p = 0.089 for between-diet difference). Both diets led to greater absolute decreases
in individuals with higher baseline Lp(a) concentration (p < 0.001). Concentrations of LDL
cholesterol (LDL-C), non-HDL-C, remnant-C, and apolipoprotein B were lowered more by the
ALA diet (p < 0.01). Lipid or lipoprotein responses were not modified by the FADS1 rs174550
genotype. Conclusions: A considerable increase in either dietary ALA or LA from vegetable oils
has a similar Lp(a)-lowering effect, whereas ALA may lower other major atherogenic lipids and
lipoproteins to a greater extent than LA. Genetic differences in endogenous PUFA conversion
may not influence serum Lp(a) concentration.