scholarly journals Elevated Plasma Homocysteine and Diabetic Vascular Disease

Diabetes Care ◽  
1997 ◽  
Vol 20 (12) ◽  
pp. 1805-1806 ◽  
Author(s):  
J. A. Colwell
2007 ◽  
Vol 17 (1) ◽  
pp. 33-38
Author(s):  
K Zaw ◽  
M T Hasan ◽  
B Bhowmick ◽  
P B Khanna ◽  
E A Freeman

Interest in homocysteine's role in vascular disease was stimulated by the paper of McCully (1969) in which, based on autopsy evidence of extensive arterial thrombosis in two children with elevated plasma homocysteine concentrations and homocystinuria, he proposed that elevated plasma homocysteine (hyperhomocysteinaemia) can cause atherosclerotic vascular disease. A meta-analysis of subsequent prospective observational studies concluded that elevated homocysteine is indeed a modest independent predictor of ischaemic heart disease and stroke risk in healthy populations with a 25% reduction in serum homocysteine concentration, a reduction of approximately 3 micromol per litre (μmol/l) being associated with a 19% lower risk of stroke (odds ratio, 0.81; 95% confidence interval (CI), 0.69 – 0.95). In the nationally representative sample of US adults, elevated homocysteine concentration was independently associated with an increased likelihood of non-fatal stroke in both black and white adults. In this article, the current concepts relating homocysteine to ischaemic stroke are reviewed.


2004 ◽  
Vol 175 (1) ◽  
pp. 69-75 ◽  
Author(s):  
Rocio Riba ◽  
Anna Nicolaou ◽  
Max Troxler ◽  
Shervanthi Homer-Vaniasinkam ◽  
Khalid.M. Naseem

Metabolism ◽  
1988 ◽  
Vol 37 (7) ◽  
pp. 697-701 ◽  
Author(s):  
David E.L. Wilcken ◽  
Nicholas P.B. Dudman ◽  
Pauline A. Tyrrell ◽  
Malcolm R. Robertson

2003 ◽  
Vol 83 (3) ◽  
pp. 601-604 ◽  
Author(s):  
S. E. Samuels

The aim of this study was to determine if total plasma homocysteine (HCY) concentrations and mortality rates due to ascites syndrome and (AS) sudden death syndrome (SDS) in broiler chickens could be lowered by diet. Elevated plasma HCY is an independent risk factor for cardiovascular disease in humans. A total of 828 day-old male broiler chickens (Arbor Acre) were fed, for 6 wk, either a basal practical diet or one supplemented with excess vitamins B6 and B12, folic acid and betaine to stimulate the degradation of HCY. The supplemented diet decreased plasma HCY by 17% (P < 0.05; n = 16 per diet). Total mortality due to AS and SDS was 18% lower in the supplemented diet but this difference was not statistically significant. Key words: Homocysteine, folate, chickens, cardiovascular disease, ascites, sudden death syndrome


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