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Lowering homocysteine and modifying nutritional status with folic acid and vitamin B(12) in Indian patients of vascular disease
Hyperhomocysteinemia is more commonly associated with vascular disease in Indians than in the western populations. It is caused by genetic polymorphisms or dietary deficiencies of the B vitamins. We attempted to identify the association of hyperhomocysteinemia with vitamin B(12) and folate in Indian...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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the Society for Free Radical Research Japan
2012
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3334376/ https://www.ncbi.nlm.nih.gov/pubmed/22573925 http://dx.doi.org/10.3164/jcbn.11-72 |
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author | Bhargava, Seema Ali, Arif Bhargava, Eishaan Kamta Manocha, Anjali Kankra, Mamta Das, Sabari Mohan Srivastava, Lalit |
author_facet | Bhargava, Seema Ali, Arif Bhargava, Eishaan Kamta Manocha, Anjali Kankra, Mamta Das, Sabari Mohan Srivastava, Lalit |
author_sort | Bhargava, Seema |
collection | PubMed |
description | Hyperhomocysteinemia is more commonly associated with vascular disease in Indians than in the western populations. It is caused by genetic polymorphisms or dietary deficiencies of the B vitamins. We attempted to identify the association of hyperhomocysteinemia with vitamin B(12) and folate in Indian patients of vascular disease. Homocysteine, vitamin B(12) and folate levels were estimated in 100 controls and 100 patients of vascular disease. Homocysteine estimation was repeated in 73 patients on different vitamin supplements for 6 months. Homocysteine exhibited a significant negative correlation with B(12) only in cerebrovascular disease and peripheral vascular diseasepatients, and with folate in coronary artery disease and cerebrovascular disease patients as well as controls. Single daily dose of folate was as effective as a combination of folate and cobalamin in reducing plasma homocysteine concentrations. Low levels of B(12) contribute to the higher incidence of cerebrovascular disease and peripheral vascular disease, and low folate levels account for higher prevalence of hyperhomocysteinemia in coronary artery disease and cerebrovascular disease. Moreover, irrespective of the cause of hyperhomocysteinemia, folate is known to ameliorate it. Hence, large-scale corrective measures like food fortification or dietary supplementation with folate might benefit the Indian population and reduce the incidence and morbidity of vascular disease. |
format | Online Article Text |
id | pubmed-3334376 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | the Society for Free Radical Research Japan |
record_format | MEDLINE/PubMed |
spelling | pubmed-33343762012-05-09 Lowering homocysteine and modifying nutritional status with folic acid and vitamin B(12) in Indian patients of vascular disease Bhargava, Seema Ali, Arif Bhargava, Eishaan Kamta Manocha, Anjali Kankra, Mamta Das, Sabari Mohan Srivastava, Lalit J Clin Biochem Nutr Original Article Hyperhomocysteinemia is more commonly associated with vascular disease in Indians than in the western populations. It is caused by genetic polymorphisms or dietary deficiencies of the B vitamins. We attempted to identify the association of hyperhomocysteinemia with vitamin B(12) and folate in Indian patients of vascular disease. Homocysteine, vitamin B(12) and folate levels were estimated in 100 controls and 100 patients of vascular disease. Homocysteine estimation was repeated in 73 patients on different vitamin supplements for 6 months. Homocysteine exhibited a significant negative correlation with B(12) only in cerebrovascular disease and peripheral vascular diseasepatients, and with folate in coronary artery disease and cerebrovascular disease patients as well as controls. Single daily dose of folate was as effective as a combination of folate and cobalamin in reducing plasma homocysteine concentrations. Low levels of B(12) contribute to the higher incidence of cerebrovascular disease and peripheral vascular disease, and low folate levels account for higher prevalence of hyperhomocysteinemia in coronary artery disease and cerebrovascular disease. Moreover, irrespective of the cause of hyperhomocysteinemia, folate is known to ameliorate it. Hence, large-scale corrective measures like food fortification or dietary supplementation with folate might benefit the Indian population and reduce the incidence and morbidity of vascular disease. the Society for Free Radical Research Japan 2012-05 2012-02-10 /pmc/articles/PMC3334376/ /pubmed/22573925 http://dx.doi.org/10.3164/jcbn.11-72 Text en Copyright © 2012 JCBN This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Bhargava, Seema Ali, Arif Bhargava, Eishaan Kamta Manocha, Anjali Kankra, Mamta Das, Sabari Mohan Srivastava, Lalit Lowering homocysteine and modifying nutritional status with folic acid and vitamin B(12) in Indian patients of vascular disease |
title | Lowering homocysteine and modifying nutritional status with folic acid and vitamin B(12) in Indian patients of vascular disease |
title_full | Lowering homocysteine and modifying nutritional status with folic acid and vitamin B(12) in Indian patients of vascular disease |
title_fullStr | Lowering homocysteine and modifying nutritional status with folic acid and vitamin B(12) in Indian patients of vascular disease |
title_full_unstemmed | Lowering homocysteine and modifying nutritional status with folic acid and vitamin B(12) in Indian patients of vascular disease |
title_short | Lowering homocysteine and modifying nutritional status with folic acid and vitamin B(12) in Indian patients of vascular disease |
title_sort | lowering homocysteine and modifying nutritional status with folic acid and vitamin b(12) in indian patients of vascular disease |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3334376/ https://www.ncbi.nlm.nih.gov/pubmed/22573925 http://dx.doi.org/10.3164/jcbn.11-72 |
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