Objective: To investigate the dose-response relationship between cholesterol lowering and three different, relatively low intake levels of plant sterols (0.83, 1.61, 3.24 gad) from spreads. To investigate the effects on lipidsoluble (pro)vitamins. Design: A randomized double-blind placebo controlled balanced incomplete Latin square design using ®ve spreads and four periods. The ®ve study spreads included butter, a commercially available spread and three experimental spreads forti®ed with three different concentrations of plant sterols. Subjects: One hundred apparently healthy normocholesterolaemic and mildly hypercholesterolaemic volunteers participated. Interventions: Each subject consumed four spreads, each for a period of 3.5 week.
Conclusions:The three relatively low dosages of plant sterols had a signi®cant cholesterol lowering effect ranging from 4.9 ± 6.8%, 6.7 ± 9.9% and 6.5 ± 7.9%, for total, LDL-cholesterol and the LDLaHDL cholesterol ratio, respectively, without substantially affecting lipid soluble (pro)vitamins. No signi®cant differences in cholesterol lowering effect between the three dosages of plant sterols could be detected. This study would support that consumption of about 1.6 g of plant sterols per day will bene®cally affect plasma cholesterol concentrations without seriously affecting plasma carotenoid concentrations.
Postprandial response curves of beta-carotene and retinyl esters in a triglyceride-rich lipoprotein (TRL) fraction were evaluated as a potential measure of beta-carotene uptake and cleavage. beta-Carotene, retinyl ester, and triglyceride concentrations in the TRL fraction (density < 1.006 kg/L) and plasma were measured in 10 men for 8 or 16 h after an oral dose of 15 mg beta-carotene. The beta-carotene response, unlike the triglyceride and retinyl ester response, can be evaluated in the TRL fraction but not in plasma. Intraindividual variations in the triglyceride-adjusted response of beta-carotene and retinyl palmitate in TRL fractions were 23% and 20% and interindividual variations were 42% and 36%, respectively. A low beta-carotene response was associated with a high ratio between retinyl palmitate and beta-carotene responses (r = -0.56, P = 0.013). In conclusion, the measurement of beta-carotene and retinyl esters in the TRL fraction after a dose of beta-carotene with a vitamin A-free meal may be an appropriate method to study beta-carotene uptake and cleavage.
Caffeine is partly responsible for the homocysteine-raising effect of coffee. Coffee, but not caffeine, affects homocysteine metabolism within hours after intake, although the effect is still substantial after an overnight fast.
High plasma homocysteine is a risk for cardiovascular disease and can be lowered through supplementation with 6 g/d of betaine. However, dietary intake of betaine is approximately 0.5-2 g/d. Therefore, we investigated whether betaine supplementation in the range of dietary intake lowers plasma homocysteine concentrations in healthy adults. Four groups of 19 healthy subjects ingested three doses of betaine or placebo daily for 6 wk. A methionine loading test was performed during run in, on d 1 of betaine supplementation, and after 2 and 6 wk of betaine supplementation. Fasting plasma homocysteine after 6-wk daily intakes of 1.5, 3 and 6 g of betaine was 12% (P < 0.01), 15% (P < 0.002) and 20% (P < 0.0001) less than in the placebo group, respectively. Furthermore, the increase in plasma homocysteine after methionine loading on the 1st d of betaine supplementation was 16% (P < 0.06), 23% (P < 0.008) and 35% (P < 0.0002) less than in the placebo group, respectively, and after 6 wk of supplementation was 23% (P < 0.02), 30% (P < 0.003) and 40% (P < 0.0002) less, respectively. Thus, doses of betaine in the range of dietary intake reduce fasting and postmethionine loading plasma homocysteine concentrations. A betaine-rich diet might therefore lower cardiovascular disease risk.
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