High- oleic rapeseed (canola) and flaxseed oils modulate serum lipids and inflammatory biomarkers in hypercholesterolaemic subjects

Recently, novel dietary oils with modified fatty acid profiles have been manufactured to improve fatty acid intakes and reduce CVD risk. Our objective was to evaluate the efficacy of novel high-oleic rapeseed (canola) oil (HOCO), alone or blended with flaxseed oil (FXCO), on circulating lipids and inflammatory biomarkers v. a typical Western diet (WD). Using a randomised, controlled, crossover trial, thirty-six hypercholesterolaemic subjects consumed three isoenergetic diets for 28d each containing approximately 36% energy from fat, of which 70% was provided by HOCO, FXCO or WD. Dietary fat content of SFA, MUFA, PUFA n-6 and n-3 was 6, 23, 5, 1% energy for HOCO; 6, 16, 5, 7.5% energy for FXCO; 11.5, 16, 6, 0.5% energy for WD. After 28d, compared with WD, LDL-cholesterol was reduced 15.1% (P<0.001) with FXCO and 7?4% (P<0.001) with HOCO. Total cholesterol (TC) was reduced 11% (P<0.001) with FXCO and 3?5% (P=0.002) with HOCO compared with WD. Endpoint TC differed between FXCO and HOCO (P<0.05). FXCO consumption reduced HDL-cholesterol by 8?5% (P<0.001) and LDL:HDL ratio by 7.5% (P=0.008) v. WD. FXCO significantly decreased E-selectin concentration compared with WD (P=0.02). No differences were observed in inflammatory markers after the consumption of HOCO compared with WD. In conclusion, consumption of novel HOCO alone or when blended with flaxseed oil is cardioprotective through lipid-lowering effects. The incorporation of flaxseed oil may also target inflammation by reducing plasma E-selectin. (Author's abstract)
Increased consumption of novel dietary oils rich in MUFA and a-linolenic acid (ALA) may improve the fatty acid imbalance typical of modern Western diets (WD), high in SFA and the n-6:n-3 fatty acid ratio. High-oleic rapeseed (canola) oil (HOCO) is rich in MUFA, low in SFA and exhibits a low ratio of n-6:n-3 fatty acids. With enhanced oxidative stability, HOCO is an attractive oil replacement for high SFA high trans oil varieties currently used in the food industry. To date, the efficacy of HOCO consumption in modulating established biomarkers of CVD risk has not been investigated in a human clinical study. Additionally, although a high dose of flaxseed oil consumption has been reported to reduce inflammatory biomarkers in at-risk subjects, the effects of flaxseed oil on serum lipids have been inconsistent. Therefore, the objectives of this human clinical study were to evaluate the efficacy of HOCO and a flaxseed/high-oleic rapeseed oil (FXCO) blend in modulating circulating lipids and inflammatory biomarkers associated with CVD risk as compared with a typical WD. The present results are the first to demonstrate the lipid lowering efficacy of low-SFA diets enriched with novel HOCO alone or blended with ALA-rich flaxseed oil. FXCO diet further reduced TC beyond that of the HOCO diet. Similar reductions in LDL-cholesterol concentrations after the consumption of the HOCO and FXCO diets compared with the WD control were reported. The FXCO diet and WD control, both higher in dietary PUFA content, tended to reduce endpoint TAG concentrations; however, due to large individual variation, there was no difference in percentage change in TAG levels from baseline between the dietary interventions examined. Reports suggest that ALA-rich flaxseed oil interventions fail to modify TC and LDL-cholesterol levels when compared with other dietary interventions. However, these results could be confounded by the use of MUFA and n-6 PUFA dietary controls. FXCO reduced HDL-cholesterol from baseline, resulting in lower endpoint HDL-cholesterol levels than the WD control. Generally, dietary strategies replacing SFA with PUFA result in a reduction in plasma TC and LDL-cholesterol and a parallel decrease in plasma HDL-cholesterol concentrations. Although concern exists that the cardio protection associated with low LDL-cholesterol is diminished with simultaneous reductions in HDL-cholesterol, it has been shown that rates of cholesterol efflux from macrophage cells to serum are not affected. Endpoint LDL:HDL-cholesterol ratios were reduced in response to the HOCO and FXCO diets compared with the WD control. In the present study, after 4-week supplementation of 21g/d (7.5% energy) of ALA in the FXCO diet, a reduction was observed in E-selectin compared with the WD control; however, no reductions in other inflammatory biomarkers were observed. The expression of E-selectin directly associates with dyslipidaemia. In this study, a significant correlation was observed between changes in plasma E-selectin and TC, LDL-cholesterol and non-HDL-cholesterol concentrations when subjects consumed the FXCO diet compared with the WD control.  Although a 4-week intervention is typically sufficient to observe significant alterations in blood lipids, previous studies reporting reductions in inflammatory markers were of 6 to 12 weeks in duration. The limited duration of this study may also explain the absence of treatment effects on carotid IMT.  After consumption of the ALA-rich FXCO diet, an approximate 5-fold increase in plasma ALA (18:3n-3) concentrations and 3-fold increase in EPA (20:5n-3) concentrations were observed compared with the HOCO diet and WD control. However, there were no differences in plasma DHA (20:6n-3) concentrations between the FXCO diet and the WD control. For consumers, an increased compliance with dietary recommendations targeting a reduction in CHD risk would be possible by replacing a proportion of commonly used dietary oils and spreads in the WD with HOCO alone or blended with flaxseed oil. The present study found that the ALA-rich FXCO may target inflammation and atherogenic pathways by reducing plasma E-selectin. (Editors comments)