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Clin Chem Lab Med. 2005;43(10):1048-51.

Vitamin B12 deficiency is the dominant nutritional cause of hyperhomocysteinemia in a folic acid-fortified population.

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  • 1Department of Medical Pathology and Laboratory Medicine, University of California, Davis, Sacramento, CA 95817, USA.


Prevalence rates for folate deficiency and hyperhomocysteinemia have been markedly reduced following the introduction of folic acid fortification in the United States. We report the prevalence of hyperhomocysteinemia in a population of community-dwelling elderly Latinos in the post-folic acid fortification era. We measured homocysteine, total vitamin B12, holotranscobalamin, red blood cell folate, and serum creatinine in 1096 subjects aged > or =60 years. Hyperhomocysteinemia (>13 micromol/L) was observed in 16.5% of the subjects. The population attributable risk percentages for hyperhomocysteinemia were 29.7% for total B12 <148 pmol/L, 36.4% for holotranscobalamin <35 pmol/L, and 41.4% for creatinine >115 micromol/L. In contrast, the population attributable risk percentage for hyperhomocysteinemia was only 0.3% for red blood cell folate <365 nmol/L. We conclude that in the post-folic acid fortification era, low vitamin B12 status has become the dominant nutritional determinant of hyperhomocysteinemia. Steps to either reduce the prevalence of vitamin B12 deficiency or to identify and treat individuals with vitamin B12 deficiency could further reduce the prevalence of hyperhomocysteinemia.

[PubMed - indexed for MEDLINE]
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