Two studies find supplementation and moderation are keys to lowering homocysteine

Growing evidence has identified serum levels of homocysteine as an independent risk factor for vascular disease. Two different studies in the American Journal of Clinical Nutrition examined modifiable lifestyle choices, which can have a significant effect on homocysteine levels. Vitamin supplementation—especially with folic acid—emerged as a strong influence on homocysteine levels, taking into consideration that the data for both studies were obtained before the implementation of folic acid fortification of the U.S. grain supply. Alcohol consumption, coffee, and smoking, and individual decisions on how much to moderate consumption of these items were all potential determinants of homocysteine levels.

The first study, by Jacques et al., consisted of offspring (and their spouses) aged 28-82 years old, of the original Framingham Heart Study, which was initiated in 1950. In this group, the consumption of more than one drink per day of liquor or red wine was associated with higher homocysteine levels, whereas white wine and beer were not. Heavy smokers (more than 26 cigarettes per day) had 16% higher homocysteine levels than nonsmokers, with a similar difference occurring in consumers of caffeine in the form of coffee or cola, but not tea. Significantly lower homocysteine levels were evident in those who regularly took vitamin B supplements, as opposed to those who did not.

A smaller study of 278 elderly subjects, the New Mexico Aging Process Study by Koehler et al., echoed the benefits of supplementation and moderation found in the Framingham Offspring Study. In comparison to nonusers, coffee and tea drinkers had higher homocysteine levels, but only at high consumption levels of >3 servings per day. The varying effects of alcohol consumption on homocysteine were a focus of the research among these elderly subjects, whose homocysteine levels were higher due to their age and whose cardiovascular risk was more immediate. Thirty-nine percent higher homocysteine levels were seen among those who drank more than 60 alcoholic beverages per month when compared to moderate drinkers who drank 30 to 60 drinks per month. On the other hand, homocysteine was 23% higher among nondrinkers, and was lowest among moderate drinkers who consumed < 2 drinks per day.

In the accompanying editorials, Vollset et al. comment that the Framingham Offspring Study is the most comprehensive epidemiological study on homocysteine to date, and that standard statistical methods may not be able to fully capture the complexity of its data. Dr. Charles Halsted, Editor-in-Chief of The American Journal of Clinical Nutrition, highlights the alcohol-homocysteine paradox in the New Mexico Study, whereby alcohol consumption, known to be cardioprotective, elevates homocysteine when more than 2 drinks per day are consumed, thus becoming a cardiovascular risk factor. The opposing effects of alcohol on homocysteine--decreasing with low alcohol and increasing with high alcohol consumption--should be interpreted in light of multiple other factors, including gender and increasing age, which also influence homocysteine metabolic levels.

Jacques, Paul F., et al. Determinants of plasma total homocysteine concentration in the Framingham Offspring cohort. Am J Clin Nut 2001;73:613-21

Vollset, Emil, et al. Population determinants of homocysteine. Am J. Clin Nut 2001;73:499-501.

Koehler, Kathleen M., et al. Association of folate intake and serum homocysteine in elderly persons according to vitamin supplementation and alcohol use. Am J Clin Nut 2001;73:628-37.

Halsted, Charles H. Lifestyle effects on homocysteine and an alcohol paradox. Am J Clin Nut 2001;73:501-2.

This media release is provided by The American Society for Clinical Nutrition, to provide current information on nutrition-related research. This information should not be construed as medical advice. If you have a medical concern, consult your doctor. To see the complete text of these articles, please go to: http://www.faseb.org/ajcn/March/11813-Jacques.pdf
http://www.faseb.org/ajcn/March/11897-Koehler.pdf
http://www.faseb.org/ajcn/March/12495-Vollset.pdf
http://www.faseb.org/ajcn/March/12484-Halsted.pdf

For more information please contact: paul@hnrc.tufts.edu, stein.vollset@uib.no, kathleen.koehler@cfsan.fda.gov, or chhalsted@ucdavis.edu.