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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #217420

Title: Folic acid, homocysteine and cardiovascular disease: Are the dots connecting?

Author
item Ordovas, Jose

Submitted to: Current Cardiovascular Risk Reports
Publication Type: Review Article
Publication Acceptance Date: 10/17/2007
Publication Date: 1/1/2008
Citation: Ordovas, J.M. 2008. Folic acid, homocysteine and cardiovascular disease: Are the dots connecting?. Current Cardiovascular Risk Reports. 2(1):7-8.

Interpretive Summary:

Technical Abstract: For many decades, atherosclerosis research has been dominated by the lipid hypothesis. Even when new concepts were brought to the table (i.e., oxidation hypothesis); efforts were made to fit them into the lipid context (i.e., oxidized LDL). This dominance provided the right environment for the development of the diet-heart hypothesis, which proposed a sequence of etiological relationships between the saturated fat content of the diet, the level of serum cholesterol and the development of the disease. However, the driving force of the atherosclerotic process cannot be restricted exclusively to lipid disorders but rather to a constellation of risk factors, which also brings a parallel constellation of potential therapeutic approaches. In this regard, during 1970’s several other risk factors [i.e., homocysteine and C-reactive Protein (CRP)] started to be seriously considered by the scientific community and CVD researchers began to look "Beyond Cholesterol." The case against homocysteine appeared almost fool-proof and the solution evident and even inexpensive. However, several randomized controlled trials have been published evaluating the effects of supplemental folic acid and B vitamins on the risk of CVD. These were conducted among patients with preexisting vascular disease. The results emerging from those trials did not provide the expected strength or the consistency on the pattern of protection against CVD. It became evident that these trials may have been designed with insufficient statistical power on their own and thus, their inconsistent findings.