Hyperlipidemias: Paschos GK

Paschos GK, Rallidis LS, Liakos GK, Panagiotakos D, Anastasiadis G, Votteas V, Zampelas A. · Department of Nutrition and Dietetics, Harokopio University, 70 El Venizelou Street, Athens 17671, Greece. · Br J Nutr. · Pubmed #15522134 No free full text.

Abstract: Long-chain n-3 PUFA from fish oils are known to have anti-inflammatory effects. We evaluated the effect of alpha-linolenic acid (ALA), precursor of n-3 fatty acids, on serum inflammatory markers and soluble cellular adhesion molecules (sCAM) of dyslipidaemic males, relative to their background diet. Participants were assigned to two groups, based upon food intake patterns: (a) twenty-one dyslipidaemic subjects who habitually ate a Mediterranean-Cretan-type diet; (b) nineteen dyslipidaemic subjects who normally ate a Westernised Greek diet. All were supplemented with 8.1 g ALA/d for 12 weeks. We determined serum amyloid A (SAA), C-reactive protein (CRP), macrophage colony-stimulating factor (MCSF), IL-6, soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 and soluble E-selectin concentrations at the beginning and the end of the ALA supplementation period. Serum baseline concentrations of inflammatory markers and sCAM were similar across the diet groups. Type of diet had a significant impact on the response of inflammatory markers to ALA supplementation. The Westernised Greek diet group showed a reduction in SAA (P<0.001), CRP (P=0.002), MCSF (P=0.005) and IL-6 (P=0.04) concentrations. The Mediterranean-Cretan-type background diet group showed a significant reduction only in MCSF concentrations (P=0.003). The sVCAM-1 concentrations were significantly reduced in both the Westernised Greek diet group (P=0.001) and the Mediterranean-Cretan-type diet group (P<0.001). The present study demonstrated that ALA supplementation lowered the serum concentrations of inflammatory markers more profoundly when the background diet was rich in saturated fatty acids and poor in MUFA.

Paschos GK, Zampelas A, Panagiotakos DB, Katsiougiannis S, Griffin BA, Votteas V, Skopouli FN. · Department of Nutrition and Dietetics, Harokopio University, Athens, Greece. · Eur J Nutr. · Pubmed #17623225 No free full text.

Abstract: BACKGROUND: Dietary alpha-linolenic acid (ALA) has been associated with reduced risk of development of atherosclerosis. Adiponectin is a hormone specifically secreted by adipocytes and considered to have anti-atherogenic properties. AIM OF THE STUDY: We examined the effect of increased dietary intake of ALA on plasma concentration of adiponectin. METHODS: Thirty-five non-diabetic, dyslipidemic men, 38-71 years old, were randomly allocated to take either 15 ml of flaxseed oil rich in ALA (8.1 g/day; n = 18), or 15 ml of safflower oil per day, containing the equivalent n-6 fatty acid (11.2 g/day linoleic acid, LA; n = 17) (control group). The intervention period lasted for 12 weeks. RESULTS: Plasma levels of adiponectin did not change after the increase in dietary intake of ALA in the flaxseed oil supplementation group, compared to the control group. No changes in body mass index, serum lipid concentrations, LDL density, or plasma TNF-alpha were found in the flaxseed oil versus the control group. CONCLUSIONS: Dietary ALA has no effect on plasma adiponectin concentration in dyslipidemic men.

Paschos GK, Yiannakouris N, Rallidis LS, Davies I, Griffin BA, Panagiotakos DB, Skopouli FN, Votteas V, Zampelas A. · Department of Nutrition and Dietetics, Harokopio University, Athens, Greece. · Angiology. · Pubmed #15678256 No free full text.

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.