ABSTRACT
Brachial artery flow-mediated dilation (BAFMD) has been proposed as a measurement of the degree and severity of cardiovascular disease. The purpose of this study was to (1) evaluate the associations between BAFMD and homocysteine, folate, vitamin B(12), vitamin B(6); (2) examine the influence of 5,10-methylenetetrahydrofolate reductase (MTHFR) genotypes on homocysteine levels and BAFMD; and (3) evaluate the effect of homocysteine on the baseline diameter of the vessel vs BAFMD. A total of 174 healthy research subjects were examined for BAFMD, homocysteine, folate, vitamin B(12), vitamin B(6), and MTHFR genotype, nucleotide 677 C-->T. The data indicated a significant inverse correlation between homocysteine and BAFMD (r = -0.1763, P = .02). There was a significant difference in BAFMD between MTHFR genotype groups (P = .01) (T/T vs C/C, P = .042; C/C vs C/T, P = .13; T/T vs C/T, P = .003). Homocysteine was significantly associated with the baseline brachial artery diameter (r = 0.1878, P = .013). The data confirmed a significant inverse correlation between baseline diameter and BAFMD (r = -0.3321, P = .0001). Regression analysis indicated that the MTHFR genotype, homocysteine, and age were significant predictors of BAFMD (P = .0001, r(2) = 0.118). When the baseline brachial diameter was incorporated into the model, the effect of homocysteine on BAFMD disappeared. The present data indicate an association between homocysteine and BAFMD and reduced BAFMD in individuals with the MTHFR nucleotide 677 T/T genotype, despite similar blood values for folate and homocysteine. Finally, the data suggest that the effect of homocysteine on vascular reactivity is in part a consequence of its influence on baseline brachial artery diameter.
Subject(s)
Brachial Artery/physiology , Cardiovascular Diseases/blood , Homocysteine/blood , 5,10-Methylenetetrahydrofolate Reductase (FADH2)/genetics , Aged , Brachial Artery/diagnostic imaging , Brachial Artery/pathology , Cardiovascular Diseases/diagnosis , Cardiovascular Diseases/diagnostic imaging , Cardiovascular Diseases/pathology , DNA/chemistry , DNA/genetics , Dilatation, Pathologic , Female , Folic Acid/blood , Humans , Male , Middle Aged , Multivariate Analysis , Point Mutation , Polymerase Chain Reaction , Ultrasonography , Vitamin B 12/blood , Vitamin B 6/bloodABSTRACT
The objective of this study was to determine whether vitamin supplementation during long-term (36 wk) ingestion of olestra supplemented with vitamin E could prevent decreases in vitamin E, vitamin A, and carotenoids. This was a 36-wk study of 37 healthy males randomly assigned to consume a control diet composed of 33% energy from fat, a similar diet in which one third of the energy from fat had been replaced with olestra, or a fat-reduced (25% of energy from fat) diet. Subjects also ingested a daily multivitamin (Centrum). Serum concentrations of alpha-tocopherol, retinol, beta-carotene, lycopene, and lutein + zeaxanthin were analyzed by HPLC. Subjects eating the olestra-containing diet had substantial decreases in serum beta-carotene, lycopene, and lutein + zeaxanthin, which occurred by 12 wk; these changes were found despite correcting for serum total cholesterol or BMI. Serum beta-carotene and lycopene concentrations were below the lower limit of the reference range (<0.186 and <0.298 mumol/L, respectively) at one or more time points. The slight decline in serum alpha-tocopherol concentration, significant at 24 wk, was caused by the decline in serum cholesterol. Retinol concentrations decreased with time in all 3 groups, but were not affected by olestra. We conclude that supplementation with a multivitamin containing vitamins A and E was adequate to prevent olestra-induced decrease in serum alpha-tocopherol and retinol. Olestra-induced decreases in serum beta-carotene, lycopene, and lutein + zeaxanthin were not prevented by the vitamin supplement used in this study.
