By Christina Bolander-Gouaille
During the final 10-12 years, the study on homocysteine has develop into very lively. approximately 1500 of articles are actually released every year on homocysteine and the supplements keen on its metabolism. A disturbed homocysteine metabolism may be an underlying issue for being pregnant problems and fetal malformations, heart problems, dementia, psychiatric and neurologic issues and doubtless carcinogenesis. A disturbed homocysteine metabolism can generally be normalised by means of therapy with folate and/or vitamines B12 and B6. a lot of those findings as a result without delay predicament such a lot practitioners. although, if there are sturdy reports overlaying unmarried points of this study, those are released in specialized journals. the writer has realised the problems for the practitioner in maintaining up to date. This moment variation has been completely up to date and in addition bargains extra info at the supplements. Over 1600 references are made available.
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Additional resources for Focus on Homocysteine and the Vitamins: Involved in its metabolism
1997). The tHcy levelwas the strongest predictor of impaired EDD in a study of hyperhomocysteinaemic patients. It was independent of age, sex, BMI, blood pressure, folate, vitamin Bl2> and cholesterollevels (Woo KS et al. 1997). Several studies have shown that an oral methionine load acutely impairs EDD, bothin healthy adults (Bellamy et al. 1998b, Chambers et al. 1998 and 1999a and b, Schädiger 1999, Usui et al. 1999) andin atherosclerotic patients (Krazanowski 1998, Schiaich et al. 2000 ). Chambers et al.
1996), and dase-rlependent acceleration of endothelial cell senescence (Xu et al. 2000) • Inhibition of growth of vascular endothelial cells associated with decreased DNA methylation (Wang H et al. 1997, Chen CY et al. 2000) and specific changes in gene expression (Outinen et al. 1999) • Promotion of smooth muscle cell proliferation (Tsai JC et al. 1994, Carmody et al. 1999, Chen CY et al. 2ooo, Woo DK et al. 2000), an effect counteracted by folic acid (Carmody et al. 1999) • CoUagen accumulation (Majors et al.
Homocysteine decreased carboxyl methylation of p21(ras) (a major GI regulator whose activity is regulated by prenylation and methylation) by 50% in vascular endothelial cells but not in vascular smooth muscle cells. The difference may be explained by the ability of Hcy to increase SAH in vascular endothelial cells but not in vascular smoorh muscle cells (Wang H et al. I997). In a subsequent study of human vascular endothelial cells, 10-50 ~tmol/L of homocysteine (but not cysteine) inhibited progression of the vascular endothelial cell cycle at or before the GI-S junction, and this inhibition appeared to be mediated by decreases in the carboxyl methylation indicated by a substantial increase of the SAH/SAM ratio (Lee and Wang I999).
Focus on Homocysteine and the Vitamins: Involved in its metabolism by Christina Bolander-Gouaille