~ Vitamin B12 Emerges as Strong Determinant of Homocysteine Levels
Despite fortification of flour with folic acid, homocysteine levels in North America are still elevated in many individuals, leading researchers to investigate vitamin B12 levels as an important determinant of homocysteine values. Elevated homocysteine has been identified as a risk factor for atherosclerosis, and can result from deficient intake of folic acid and vitamin B12.
In a study published in the June 7 2005 Canadian Medical Association Journal (http://www.cmaj.ca/), J. David Spence, MD of the University of Western Ontario in London, Ontario and colleagues measured serum levels of homocysteine and vitamin B12 in 215 men and 206 women who were referred to vascular disease prevention clinics. Methylmalonic acid, an indictor of insufficient vitamin B12, was measured in a subset of 50 patients, and creatinine, a measure of kidney function, was determined in 224 participants. Carotid plaque area was evaluated in all participants by ultrasound examination.
Seventeen percent of the patients were determined to have a vitamin B12 deficiency, defined as serum B12 levels of less than 258 picomoles per liter (found in half the patients) with homocysteine greater than 14 micromoles per liter or methylmalonic acid levels greater than 271 nanomoles per liter.
Total homocysteine levels had a strong inverse association with vitamin B12 levels, and a positive association with plaque area. Carotid plaque area was negatively correlated with vitamin B12 levels. Additionally, in 224 patients in whom serum creatinine levels were measured, creatinine levels appeared to be predictors of homocysteine levels. In their discussion of the findings, the authors note “the possibility of a threshold or ceiling effect of homocysteine on carotid plaque, which may indicate that target levels for homocysteine should be lower.” They write that the failure of the VISP trial, which used B vitamin supplements to modestly lower homocysteine levels in an attempt to prevent recurrent cardiovascular events in stroke patients, could be partly explained by an insufficient reduction in homocysteine levels.
In this era of folic acid fortification in which many cases of folic acid deficiency have been corrected, low vitamin B12 levels have become a major determinant of elevated homocysteine and increased atherosclerotic plaque. (Robertson J et al. Vitamin B12, homocysteine and carotid plaque in the era of folic acid fortification of enriched cereal grain products. CMAJ, June 7 2005;172(12): 1569-1573.)
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