Are B12 Tablets Toxic?
Most of the Vitamin B12 tablets sold at present contain Cyanocobalamin, this is the stable and less expensive form of B12. Since Cyanocobalamin is not biologically active until converted to methylcobalamin, the liver has to release the bound Cyanide, to activate it. Cyanide is toxic because it inactivates the mitochondria enzyme cytochrome oxidase, which is important in cellular respiration. However, the body only absorbs about one percent of ingested cyanocobalamin, and since this is not stored by the liver, it cannot be used to treat B12 deficiency.
Vitamin B12 exists in two active forms in the body. One of these (Methylcobalamin) is central to health because it is required as a co-factor in the conversion of Homocysteine to methionine via the folate pathway. To start with, this conversion is required to recycle folate, without B12 as a co-factor, an ineffective form of folate builds up in tissue. A deficiency of folate then prevents the synthesis of DNA interrupting the development of red blood cells needed to supply oxygen. New evidence now suggests folic acid deficiency also reduces fertility in men and may damage the DNA carried by sperm. One study showed a folate-restricted diet made sperm counts plunge by 90 percent in rats.
The second form of B12 (adeno-sylcobalamin) is required for a reaction in metabolism of fatty acids. If B12 is deficient, methylmalonyl coA and its precursor, propionyl coA, build up in large amounts and are incorporated into abnormal fatty acids with an odd number of carbon atoms. (Normal fatty acids have an even number of carbon atoms.) These in turn are incorporated into abnormal lipids (fats) in nerve cells and this abnormality is the reason for development of neurologic abnormalities in B12 deficiency. There have been recent reports of neurological damage due to B12 deficiency occurring in people without anaemia, this may be due to the folic acid fortification of grain, delayed until 1996 amid fears it would mask signs of B12 deficiency.
The conversion of Homocysteine to methionine by B12 (Methylcobalamin) is also required in the production of S-adenosylmethionine (SAMe). SAMe is a potent antidepressant since it acts to convert tryptophan to serotonin, and is the methyl donor for other neurotransmitters like dopamine, adrenaline and even melatonin used to treat insomnia. In Europe, SAMe is prescribed more often than any other type of antidepressant.
The methylation of proteins with SAMe's methyl group is also required to derive a number of popular nutrients, such as the "fat burner" L-carnitine from lysine, and CoQ10 from tyrosine; Creatine phosphate the main storage of available energy for muscles and nerves; Glucosamine sulphate and Chondroitin sulphate, including the sulfur amino acids Taurine and Cysteine. Supplementing with any of these nutrients like Creatine, effectively reduces the body's requirement for SAMe, which in turn lowers Homocysteine, the remaining component of SAMe after it has donated its Methyl group.
SAMe is also the main methyl donor for the methylation of DNA, Whilst the demethylation of DNA causes cancer. A methyl group-deficient diet (MGDD) has been shown to result in Hypomethylation of DNA and to promote cancer in the liver of rats in as short a period of time as one week, by causing depletion of SAM pools. Although many of the MGDD-induced alterations in methylation and gene expression occur rapidly, they are essentially reversible. In a comparison of B12 vitamins against cancer, Methylcobalamin and adenoxylcobalamin, another form of B12, were both effective at preventing the fast-growth of malignant cells, but cyanocobalamin had no effect in slowing the growth of any tumor cells.
One of the most exciting things about SAMe is that it acts as melatonin's daytime equivalent. SAMe is necessary for the biochemical reaction that converts serotonin into melatonin. Without adequate SAMe during the day, neither melatonin nor serotonin can be synthesized.
Although B12 and folic acid recycle homocysteine, vitamin B6 actively inhibits it, by converting homocysteine to Cysteine. But this pathway also prevents homocysteine being recycled back to form methionine and the antidepressant SAMe, for this reason overdosing on B6 can cause?s similar effects to B12 and folate deficiency.
Researchers from Norway recently released the results of a 3 year trial (NORVIT) into the effects of vitamin B6 and folate. Patients were administered B6 and folate to reduce homocysteine levels that are commonly believed to damaged the lining of arteries. However results showed that despite a 30% reduction in homocysteine, it actually increased the risk of cardiovascular disease by 20%. In the same study using only folate, they found a slight decrease in overall mortality. I found another study showing that B6 also reduced cholesterol in experiments on rats. So neither homocysteine or cholesterol probably caused the increase in cardiovascular disease. But as CoQ10 and Carnitine are used to treat hart disease, maybe B6 causes hart disease by preventing homocysteine from recycling back to form SAMe, thereby lowering CoQ10.