There are several potential mechanisms that are associated with elevated homocysteine levels. The most common is probably an insufficient intake of folic acid or of vitamin B-6, as demonstrated by Dr. Selhub and his colleagues in subjects from the Framingham Study (Selhub, et al, JAMA 1993;270:2693-98). Moreover, many investigators have demonstrated that folic acid supplementation lowers homocyst(e)ine levels in most individuals, sometimes requiring additional supplementation of vitamins B-6 and B-12. We have demonstrated that the decrease of blood homocyst(e)ine by folic acid supplementation depends in part on the individual's genetic background (shown in Figure 4).
Much is known on potential mechanisms on how homocyst(e)ine damages arteries and favors thrombosis, as well as on the fact that elevated levels of homocyst(e)ine are usually corrected with vitamin supplementation. However, it is not known whether adequate diet, diet fortification or vitamin supplementation may prevent or beneficially affect the evolution of atherosclerotic diseases.
The National Institutes of Health is supporting a current study that may determine whether vitamin supplementation will alter the course of atherosclerotic diseases; results are expected to be available probably within the next 5 years. Until this pivotal study is completed, it would be advisable that the population consumes a diet rich in green-leaf vegetables, fruits and legumes in order to increase folate intake and lower homocyst(e)ine levels. Legends for figures:
Figure 1. Shows the annual rate of publications listed in MedLine under "Homocysteine/blood." The rate in the last period is 168-fold higher than in the initial period (data up to December 1997).
Figure 2. Results of a prospective study conducted in Norwa
'"/>
Contact: Cathy Yarbrough
cathyy@amhrt.org
214-706-1340
American Heart Association
14-Feb-1998