Regular bilberry consumption may reduce low-grade inflammation indicating decreased cardiometabolic risk in the long term.

Objective: To investigate cholesterol-lowering effects of stanol ester (STAEST) and sterol ester (STEEST)-enriched margarines as part of a low-fat diet. Design: According to a Latin square model randomized double-blind repeated measures design with three test margarines and three periods. Setting: Outpatient clinical trial with free-living subjects. Subjects: Thirty-four hypercholesterolaemic subjects completed the study. Interventions: Subjects consumed three rapeseed oil-based test margarines (STAEST, STEEST and control (no added stanols or sterols)) as part of a low-fat diet each for 4 weeks. Results: Mean daily intake of total plant sterols plus stanols was 2.01 ± 2.04 g during the two test margarine periods. In reference to control, serum total cholesterol was reduced by 9.2 and 7.3% with the STAEST and STEEST margarine, respectively (P`0.001 for both). The respective reductions for low-density lipoprotein (LDL) cholesterol were 12.7 and 10.4% (P`0.001). The cholesterol-lowering effects of the test margarines did not differ signi®cantly. The presence of apolipoprotein E4 allele had a signi®cant effect on LDL cholesterol response during the STAEST margarine only. Serum sitosterol and campesterol increased by 0.83 and 2.77 mgal with the STEEST (P`0.001), respectively and decreased by 1.18 and 2.60 mgal with the STAEST margarine (P`0.001). Increases of serum sitostanol and campestanol were 0.11 and 0.19 mgal with the STAEST margarine (P`0.001), repsectively. No signi®cant changes were found in serum fat-soluble vitamin and carotenoid concentrations when related to serum total cholesterol. Conclusions: STAEST and STEEST margarines reduced signi®cantly and equally serum total and LDL cholesterol concentrations as part of a low-fat diet.

The roles of polymorphisms of the sitosterolemia genes ABCG5 and ABCG8 in the regulation of cholesterol metabolism and insulin sensitivity were studied in mildly hypercholesterolemic noncoronary subjects (n ‫؍‬ 263, 144 men and 119 women) divided into tertiles by baseline serum cholestanol-to-cholesterol ratio ( Յ 118.3 and Ն 147.7 10 2 ؋ mmol/mol cholesterol), a surrogate marker of cholesterol absorption efficiency. The lowest cholestanol tertile was associated with high body mass index (BMI), plasma glucose, serum insulin and triglycerides, and cholesterol synthesis markers (cholestenol, desmosterol, lathosterol) and low HDL cholesterol and cholesterol absorption markers (campesterol, sitosterol) ( P Ͻ 0.01 for all). The 19H allele of the ABCG8 gene accumulated in the lowest cholestanol tertile ( P Ͻ 0.001) and was associated with low total and LDL cholesterol and absorption markers and with high synthesis markers ( P Ͻ 0.05 for all). The 604E allele of the ABCG5 gene in men was associated with high BMI, plasma insulin, low serum sitosterol, and high serum cholestenol levels ( P Ͻ 0.05 for all). In a subgroup of 71 men, the 604E allele was associated with insulin resistance measured with the hyperinsulinemic euglycemic clamp. In conclusion, low cholesterol absorption efficiency was associated with characteristics of the metabolic syndrome. Low serum cholesterol and cholesterol absorption were linked to the D19H polymorphism of the ABCG8 gene, and characteristics of the insulin resistance syndrome in men were linked with the Q604E polymorphism of the ABCG5 gene. Serum cholesterol level is regulated by cholesterol absorption and synthesis. In different study populations (1-3), serum total and LDL cholesterol levels are associated positively with cholesterol absorption efficiency and negatively with cholesterol synthesis, suggesting that the higher the cholesterol absorption level, the higher the serum cholesterol level and the lower cholesterol synthesis. Cholesterol absorption efficiency and cholesterol synthesis are inversely related, and they can reliably be depicted by serum noncholesterol sterol levels (2). However, it is not known which of these variables, cholesterol absorption or synthesis, is the one primarily regulated. It has been shown that both absorption efficiency and synthesis of cholesterol are genetically determined (4, 5), such that in coronary families, the heredity of cholesterol metabolism can be predicted by serum cholestanol-to-cholesterol ratio, a surrogate marker of cholesterol absorption efficiency (4). We have recently shown that cholesterol absorption correlates positively and cholesterol synthesis correlates negatively with insulin sensitivity (6), but the link between insulin action and cholesterol metabolism has remained unknown. Phytosterolemia, an inherited disease with high absorption and low biliary secretion of cholesterol and plant sterols, is caused by a mutation in genes regulating ABCG5 (G5) or ABCG8 (G8) transporter proteins (7,8). Two sequence variations (D19H a...

We conclude that the low-fat, plant stanol ester-containing margarines are effective cholesterol-lowering products in hypercholesterolemic subjects when used as part of a low-fat, low-cholesterol diet. They offer an additional, clinically significant reduction in serum cholesterol concentrations to that obtained with a low-fat diet alone.

The effect of plant stanol ester on serum cholesterol is dose-dependent. However, it is not clear what the dose is beyond which no additional benefit can be obtained. Therefore, we determined the dose-response relationship for serum cholesterol with different doses of plant stanol ester in hypercholesterolemic subjects. In a single-blind design each of 22 men or women consumed five different doses of plant stanol [target (actual) intake 0 (0), 0.8 (0.8), 1.6 (1.6), 2.4 (2.3), 3.2 (3.0) g/d] added as plant stanol esters to margarine for 4 wk. The order of dose periods was randomly determined. Serum total cholesterol concentration decreased (calculated in reference to control) by 2.8% (P = 0.384), 6.8% (P < 0.001), 10.3% (P < 0.001) and 11.3% (P < 0.001) by doses from 0.8 to 3.2 g. The respective decreases for LDL cholesterol were 1.7% (P = 0. 892), 5.6% (P < 0.05), 9.7% (P < 0.001) and 10.4% (P < 0.001). Although the decreases were numerically greater with 2.4 and 3.2 g doses than with the 1.6 g dose, these differences were not significant (P = 0.054-0.516). Serum plant stanols rose slightly, but significantly with the dose (P < 0.001). Apolipoprotein B concentration was decreased significantly already at the dose of 0.8 g (8.7%, P < 0.001). Apolipoprotein E genotype did not affect the lipid responses. We conclude that significant reduction of serum total and LDL cholesterol concentrations is reached with the 1.6-g stanol dose, and increasing the dose from 2.4 to 3.2 g does not provide clinically important additional effect.