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.)
Atherosclerosis-related diseases are a leading cause of death and impairment in the United States, affecting over 60 million people. Additionally, 50% of Americans have levels of cholesterol that place them at high risk for developing coronary artery disease. However, cholesterol is only one factor that causes the occlusion of arteries that is technically known as atherosclerosis.
Precisely what causes atherosclerosis is not known, but several theories have been proposed. Scientists think atherosclerosis begins with damage to the endothelium (the inner layer of an artery). Possible causes of damage to the arterial wall are free-radical reactions; elevated levels of oxidized serum cholesterol, triglycerides, fibrinogen, homocysteine, insulin; high blood pressure; obesity; chronic inflammation, lifestyle factors (physical inactivity and tobacco smoking); and diabetes (AHA 2002b).
The Life Extension Foundation recommends using four different approaches to reduce elevated homocysteine levels. One approach is to supply supplements such as folic acid, vitamin B12, and trimethylglycine (TMG) to increase the remethylation of homocysteine back to methionine. The second approach employs the detoxification method using vitamin B6 to enhance the transsulfuration pathway to convert homocysteine into cysteine, which can be used to synthesize such beneficial amino acids such as glutathione and taurine. The third approach entails addition to the diet of ‘methylated nutrients’, such as creatine and various choline-containing supplements. More than half of the body’s S-adenosylmethionine (SAMe) is used to synthesize creatine alone (Devlin 2002), which generates most of the homocysteine that must be either remethylated or detoxified. The fourth approach is to cut down or eliminate ingestion of foods containing high amounts of methionine such as red meat.
Life Extension has long warned members about the dangers of high homocysteine and has advised taking vitamin B6, folic acid, and vitamin B12 to help maintain healthy arteries.
Not only have large human trials linked high homocysteine with a dramatically greater risk of heart problems, but more recent studies associate high homocysteine with an increased incidence of neurodegenerative issues.
For those seeking to lower their homocysteine, Homocysteine Resist provides a potent dose of 750 mg vitamin B6 along with 800 micrograms folic acid and 500 micrograms vitamin B12.
Methylcobalamin is the form of vitamin B12 active in the central nervous system. It is an active coenzyme of the vitamin B12 analogs, that are essential for cell growth and replication. The liver may not convert cyanocobalamin, the common supplemental form of vitamin B12, into adequate amounts of methylcobalamin the body may need for proper neuronal functioning. Methylcobalamin may exert its neuroprotective effects through enhanced methylation, acceleration of nerve cell growth or its ability to promote healthy homocysteine levels.
This supplement should be taken in conjunction with a healthy diet and regular exercise program. Individual results are not guaranteed and results may vary.
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