scholarly journals Plasma total homocysteine in a representative sample of 972 British men and women aged 65 and over

1997 ◽  
Vol 51 (10) ◽  
pp. 691-697 ◽  
Author(s):  
CJ Bates ◽  
MA Mansoor ◽  
J van der Pols ◽  
A Prentice ◽  
TJ Cole ◽  
...  
2003 ◽  
Vol 133 (2) ◽  
pp. 418-420 ◽  
Author(s):  
Bernard J. Venn ◽  
Andrea M. Grant ◽  
Christine D. Thomson ◽  
Timothy J. Green

1999 ◽  
Vol 69 (3) ◽  
pp. 187-193 ◽  
Author(s):  
Brönstrup ◽  
Hages ◽  
Pietrzik

B-vitamin supplementation has previously been shown to lower the concentration of plasma total homocysteine, a risk factor for cardiovascular disease. Little is known about the homocysteine-lowering effects of low-dose B-vitamins in elderly individuals, who are prone to higher homocysteine levels due to advanced age and a greater frequency of impaired vitamin status. We aimed to identify if and to what extent B-vitamins lower total homocysteine and its subfractions in elderly individuals. Men and women (>= 60 years) received either B-vitamins (400 mug folic acid +1.65 mg pyridoxine +3 mug cyanocobalamin) or a placebo daily for 4 weeks. Subjects in the vitamin group showed a significant decrease in plasma total homocysteine during the first 2 weeks; thereafter, total homocysteine only slightly decreased further resulting in a geometric mean reduction of –16.3% (95% CI: –11.3% to –21.0%) over the entire treatment period. Free homocysteine decreased as well. However, the observed higher ratio of free/total homocysteine after 4 weeks of supplementation suggest a more pronounced reduction in protein-bound homocysteine. Low-dose B-vitamin supplementation is effective in lowering homocysteine in elderly individuals. Further studies are needed to be able to depict the effect of B-vitamin supplementation on different homocysteine subfractions in plasma.


1999 ◽  
Vol 159 (10) ◽  
pp. 1077 ◽  
Author(s):  
Andrew G. Bostom ◽  
Halit Silbershatz ◽  
Irwin H. Rosenberg ◽  
Jacob Selhub ◽  
Ralph B. D'Agostino ◽  
...  

1999 ◽  
Vol 131 (5) ◽  
pp. 321 ◽  
Author(s):  
Jeremy D. Kark ◽  
Jacob Selhub ◽  
Bella Adler ◽  
Jaime Gofin ◽  
Joseph H. Abramson ◽  
...  

Author(s):  
Per Magne Ueland ◽  
Pål I. Holm ◽  
Steinar Hustad

AbstractBetaine serves as a methyl donor in a reaction converting homocysteine to methionine, catalysed by the enzyme betaine-homocysteine methyltransferase. It has been used for years to lower the concentration of plasma total homocysteine (tHcy) in patients with homocystinuria, and has recently been shown to reduce fasting and in particular post-methionine load (PML) tHcy in healthy subjects.Betaine exists in plasma at concentrations of about 30μmol/L; it varies 10-fold (from 9 to 90μmol/L) between individuals, but the intra-individual variability is small. Major determinants are choline, dimethylglycine and folate in plasma, folic acid intake and gender.Recent studies have demonstrated that plasma betaine is a stronger determinant of PML tHcy than are vitamin BTo conclude, betaine status is a component of an individual's biochemical make-up with ramifications to one-carbon metabolism. Betaine status should be investigated in pathologies related to altered metabolism of homocysteine and folate, including cardiovascular disease, cancer and neural tube defects.


2003 ◽  
Vol 168 (1) ◽  
pp. 139-146 ◽  
Author(s):  
Erik J. Giltay ◽  
Petra Verhoef ◽  
Louis J.G. Gooren ◽  
Johanna M. Geleijnse ◽  
Evert G. Schouten ◽  
...  

2007 ◽  
Vol 97 (5) ◽  
pp. 842-846 ◽  
Author(s):  
Jonathan M. Hodgson ◽  
Ian B. Puddey ◽  
Frank M. van Bockxmeer ◽  
Valerie Burke

Plasma total homocysteine concentrations (tHcy) are a putative risk factor for CVD. Tea is a rich dietary source of polyphenols and caffeine, both of which may raise tHcy. However, it is possible that much of any effect is transitory and may be influenced by the consumption of food. Our objective was to investigate the acute effect of tea, at a dose representative of ordinary population intakes, on tHcy and to determine whether consumption of a meal influences the magnitude of any effect. Measurements of tHcy were performed in twenty participants at baseline and 3.5 h after drinking three cups of black tea or hot water (consumed at time 0, 1.5 and 3 h) with and without a meal: a total of four treatments administered in random order. Drinking tea resulted in an acute increase in tHcy (0·30 (95 % CI 0·04, 0·56) μmol/l, P = 0·022). The meal resulted in an acute decrease in tHcy ( − 0·42 (95 % CI − 0·68, − 0·16) μmol/l, P = 0·002). There was no interaction between tea and meal on tHcy (P = 0·40); that is, the effect of tea on tHcy was not different in the fasting and non-fasting state. Our results suggest that drinking black tea can cause a small acute increase in tHcy and that this effect is not enhanced in the non-fasting state. Given that results of population studies have generally shown a negative association between tea intake and tHcy, the significance of these findings to CVD risk remains uncertain.


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