Vitamin B12: Surprising New FindingsDecember 2000
By Terri Mitchell
Protect your nerves
Methylcobalamin is terrific for protecting neurons. It saves the brain from the damaging effects of glutamate, nitric oxide, low blood sugar and low oxygen. Low oxygen occurs during stroke or heart attack. Low blood sugar is a chronic problem in diabetes. Glutamate and nitric oxide toxicity are features of Alzheimer’s and Parkinson’s diseases.
Taking methylcobalamin everyday may provide immediate protection should a person be suddenly injured or have a stroke. Researchers in Japan demonstrated that chronic application of methylcobalamin to neurons protects them, but in order for the vitamin to work, it has to be ready and available before the injury occurs.
Myelin sheath, the “insulation” around nerve cells, is critical for nerve conduction. Degeneration of this protein causes serious neurological diseases. Myelin is created and maintained by methylation reactions that depend on vitamin B12.
Recently, researchers in France succeeded in creating for the first time a model of vitamin B12 deficiency in oligodendrocytes, the cells that produce myelin sheath. This will enable the in-depth study of the effects of vitamin B12 on the synthesis of myelin for the first time. Data from this new model could lead to new insight into muscular dystrophy, amyotrophic lateral sclerosis, subacute combined degeneration of the spinal cord, multiple sclerosis and other neuro-degenerative diseases.
Methylcobalamin has been used in animal studies on neurodegenerative diseases. The methyl form of vitamin B12 clearly promotes nerve regeneration and slows the progression of neurodegenerative diseases.
Neuropathies are strange and sometimes painful sensations caused by degeneration of nerves. Methylcobalamin is effective for this condition. In a study on diabetic rats, methylcobalamin reduced demyelination. In a study on humans undergoing hemodialysis, 500 micrograms of methylcobalamin by injection three times a week, lessened neuropathies.
Heart attack and stroke
Vitamin B12 has an important role in reducing levels of homocysteine to prevent heart attack and stroke. Homocysteine is a by-product of methionine metabolism that can damage blood vessels. B12 and folate are critical for the production of the tongue-twisting enzyme, methylenetetrahydrofolatereductase, which helps convert homocysteine to methionine. Dozens of studies show that the most common cause of elevated homocysteine is inadequate folate or vitamin B12. Supplementation with these vitamins lowers homocysteine levels, but vitamin B6 and trimethylglycine (TMG) are usually also required to lower homocysteine to a healthy range.
Vitamin B12 deficiency has another effect on the heart as well. Turkish researchers recently reported that people with megalobastic anemia have abnormal electrical conductivity of the heart. The problem originates in the nerves that control heart rate. When the anemic volunteers took supplemental B12, heart rate returned to normal.
Elevated homocysteine is rightfully considered a risk factor for cancer. High levels of homocysteine are consistently linked with DNA damage. The connection was shown recently in a study from Australia where the micro-nucleus index (a measure of DNA damage) increased as levels of homocysteine increased. This held true for both younger (18-32) and older (50-70) people.
Fifty-six percent of the men in the older bracket either tested below par for B12 or folate, or abnormally high for homocysteine. Men with homocysteine levels greater than 10 micromoles per liter had significantly more DNA damage than those with lower homocysteine, even if they had normal levels of B12 and folate. Despite no folate deficiency, supplementation with 3.5 times the recommended allowance of folate and B12 still significantly reduced the micronucleus index in people where it was initially elevated above the 50th percentile. (Note: in this study, taking 10 times the recommended amount of folate and B12 did not have any added benefit).
One of the implications of this study is that “normal” levels of these vitamins—standard blood levels—are probably not adequate to prevent DNA damage. It also indicates that high homocysteine levels are a red flag that DNA damage is occurring whether or not homocysteine-lowering vitamins are adequate by blood measurements. Men with low, but still “normal”, levels of B12 had significantly more damage. According to Dr. Michael Fenech, author of the study, “the accepted standard for vitamin B12 sufficiency (i.e., plasma concentration <150 pmol/L) may not be adequate to minimize chromosome damage rates.”