{"id":854,"date":"2017-10-26T16:43:50","date_gmt":"2017-10-26T16:43:50","guid":{"rendered":"https:\/\/courses.lumenlearning.com\/sunynutrition\/?post_type=chapter&p=854"},"modified":"2017-11-14T16:54:46","modified_gmt":"2017-11-14T16:54:46","slug":"11-3-b-vitamins-homocysteine-cardiovascular-disease","status":"publish","type":"chapter","link":"https:\/\/courses.lumenlearning.com\/suny-herkimer-nutritionflex\/chapter\/11-3-b-vitamins-homocysteine-cardiovascular-disease\/","title":{"raw":"11.3 B Vitamins, Homocysteine & Cardiovascular Disease","rendered":"11.3 B Vitamins, Homocysteine & Cardiovascular Disease"},"content":{"raw":"
\r\n\r\nHomocysteine is a sulfur containing, non-proteinogenic (not used for making proteins) amino acid whose structure is shown in the figure below.\r\n
\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"800\"]\"\" Figure 11.31 Structure of homocysteine1<\/sup>[\/caption]\r\n\r\n<\/div>\r\nElevated circulating homocysteine levels have been found in people with cardiovascular disease. Folate, vitamin B6, and vitamin B12 contribute to the conversion of homocysteine to methionine by providing methyl groups, thereby decreasing homocysteine levels, as illustrated in the figure below. Thus, based on these facts, it was hypothesized that intake of these B vitamins may decrease the risk of cardiovascular disease.\r\n
\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"981\"]\"\" Figure 11.32 One-carbon metabolism[\/caption]\r\n\r\n<\/div>\r\nResearch has found that intake of these B vitamins does decrease circulating homocysteine levels. However, most studies have not found that it results in improved cardiovascular disease outcomes2-4<\/sup>. It is debated why B vitamin intake has not resulted in improved outcomes. Some think it is because the studies have not focused on individuals with elevated homocysteine levels2<\/sup>, while others believe that homocysteine is a biomarker or indicator of cardiovascular disease, not a causative or contributing factor to cardiovascular disease development3<\/sup>.\r\n\r\nReferences & Links<\/b>\r\n\r\n1. http:\/\/en.wikipedia.org\/wiki\/File:Homocysteine_racemic.png\r\n\r\n2. Abraham J, Cho L. (2010) The homocysteine hypothesis: Still relevant to the prevention and treatment of cardiovascular disease? Cleve Clin J Med 77(12): 911-918.\r\n\r\n3. Cacciapuoti F. (2011) Hyper-homocysteinemia: A novel risk factor or a powerful marker for cardiovascular diseases? pathogenetic and therapeutical uncertainties. J Thromb Thrombolysis 32(1): 82-88.\r\n\r\n4. Martai-Carvajal AJ, Sola J, Lathyris D. (2015) Homocysteine-lowering interventions for preventing cardiovascular events. Cochrane Database Syst Rev. 1:CD006612.\r\n\r\n<\/div>","rendered":"
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Homocysteine is a sulfur containing, non-proteinogenic (not used for making proteins) amino acid whose structure is shown in the figure below.<\/p>\n

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\"\"<\/p>\n

Figure 11.31 Structure of homocysteine1<\/sup><\/p>\n<\/div>\n<\/div>\n

Elevated circulating homocysteine levels have been found in people with cardiovascular disease. Folate, vitamin B6, and vitamin B12 contribute to the conversion of homocysteine to methionine by providing methyl groups, thereby decreasing homocysteine levels, as illustrated in the figure below. Thus, based on these facts, it was hypothesized that intake of these B vitamins may decrease the risk of cardiovascular disease.<\/p>\n

\n
\"\"<\/p>\n

Figure 11.32 One-carbon metabolism<\/p>\n<\/div>\n<\/div>\n

Research has found that intake of these B vitamins does decrease circulating homocysteine levels. However, most studies have not found that it results in improved cardiovascular disease outcomes2-4<\/sup>. It is debated why B vitamin intake has not resulted in improved outcomes. Some think it is because the studies have not focused on individuals with elevated homocysteine levels2<\/sup>, while others believe that homocysteine is a biomarker or indicator of cardiovascular disease, not a causative or contributing factor to cardiovascular disease development3<\/sup>.<\/p>\n

References & Links<\/b><\/p>\n

1. http:\/\/en.wikipedia.org\/wiki\/File:Homocysteine_racemic.png<\/p>\n

2. Abraham J, Cho L. (2010) The homocysteine hypothesis: Still relevant to the prevention and treatment of cardiovascular disease? Cleve Clin J Med 77(12): 911-918.<\/p>\n

3. Cacciapuoti F. (2011) Hyper-homocysteinemia: A novel risk factor or a powerful marker for cardiovascular diseases? pathogenetic and therapeutical uncertainties. J Thromb Thrombolysis 32(1): 82-88.<\/p>\n

4. Martai-Carvajal AJ, Sola J, Lathyris D. (2015) Homocysteine-lowering interventions for preventing cardiovascular events. Cochrane Database Syst Rev. 1:CD006612.<\/p>\n<\/div>\n\n\t\t\t

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Candela Citations<\/h3>\n\t\t\t\t\t
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