Apolipoprotein E Genotype in Dyslipidemic Patients and Response of Blood Lipids and Inflammatory Markers to Alpha-Linolenic Acid

Abstract

The objective of this study was to determine the effect of alpha-linolenic acid (ALA) supplementation on blood lipids and inflammatory markers, in relation to apolipoprotein (apo) E genotype. The diets of 50 dyslipidemic male patients were supplemented with 15 mL of flaxseed oil per day for 12 weeks. Retrospectively, 3 apo E genotype variants were found (epsilon2/epsilon3, n=7; epsilon3/epsilon3, n=33; epsilon3/epsilon4, n=10). No significant differences were found among apo E genotypes in any variables at baseline. ALA supplementation produced a small but significant decrease in high-density lipoprotein cholesterol (from 1.12 to 1.08 mmol/L, 43 to 42 mg/dL; p=0.008) and apo A-I levels (from 1.28 to 1.24 g/L, p=0.036) in the epsilon3/epsilon3 homozygotes. In addition, ALA supplementation resulted in a significant decrease in the serum concentration of serum amyloid A (SAA) (p=0.014), C-reactive protein (CRP) (p=0.013), macrophage colony-stimulating factor (MCSF) (p<0.001), and interleukin (IL)-6 (p=0.028). Serum SAA and MCSF were also significantly decreased in the epsilon3/epsilon4 group (p=0.005 and p=0.017, respectively). In contrast, ALA produced no effects on any of the inflammatory markers in the epsilon2/epsilon3 group. ALA may have beneficial effects on inflammation in dyslipidemic carriers of the apo epsilon3/epsilon3 and epsilon3/epsilon4 genotypes, but not in carriers of the epsilon2 allele.

Systemic Inflammation in Morbidly Obese Subjects: Response to Oral Supplementation with Alpha-Linolenic Acid

“…Recently, alpha-linolenic acid has been advocated as well, as an antagonist for groups with increased cardiovascular risk. 9 No study in obese populations has been found in the literature.…”

Heritability of serum hs-CRP concentration and 5-year changes in the Stanislas family study: association with apolipoprotein E alleles

“…16,17 Moreover, some other gene polymorphisms were associated with circulating levels of the hs-CRP, the most studied being the common polymorphisms of the apolipoprotein E gene (APOE) (e2, e3, e4) for which an association was confirmed by many authors in adults and elderly. 12,[18][19][20][21][22][23][24] However, no data exist either about APOE genotype-hs-CRP concentration association in children or about effect of these polymorphisms in combination with estimate of heritability component. 12 Thus, in the present analysis, we aimed at reporting on (i) the association between the APOE gene alleles with the serum hs-CRP concentration in adults and also in children, (ii) the familial aggregation of the serum hs-CRP concentration on a sample of French nuclear families and on (iii) the variance-component genetic linkage of this inflammatory factor with the alleles of the APOE gene.…”

Omega-3 fatty acids: How can they be used in secondary prevention?

“…In some studies, increased intake of ALA reduced CRP [29,31,35], IL-6 [31], and sVCAM-1 levels [29], but this did not occur in all studies [30]. Increased intake of ALA reduced sICAM-1 and E-selectin levels in some studies [29] but not in others [35].…”

“…In some studies, ALA reduced TC, LDL-C, TG [29], and lipoprotein(a) levels [30]. However, in other studies, ALA had no effect on these variables [30,31]. Unfavorable actions, including an increase in TC [32] and TG levels, were also reported [33].…”