CAN METHYLCOBALAMIN PROTECT AGAINST NEUROLOGICAL DISEASE AND CHRONIC FATIGUE SYNDROME ?
Methylcobalamin is a form of vitamin B12 that is known to protect cognitive function, combat Chronic Fatigue Syndrome and promote healthy sleep patterns. As a vitamin, methylcobalamin is essential and must be taken in the diet. Methylcobalamin is the active form and coenzyme form of vitamin B12 that is responsible for transferring methyl groups to an inactive form of folic acid to homocysteine forming methionine. Elevated levels of homocysteine are associated with a decrease in cognitive function, memory loss and brain vascular complications. Vascular problems involve the decreased production of nitric oxide and the inability to vasodilate properly in the brain and may occur with a B12 deficiency.
B12 and Sleep
This B12 coenzyme has also been reported to effect melatonin levels decreasing sleep requirements by suppressing melatonin release during the day. B12 acts directly on the pineal gland in the brain which contains melatonin. This causes melatonin to be released faster at night which has the effect of resetting the sleep cycle. This new cycle causes melatonin release to drop off faster in the morning. Last but not least methylcobalamin is important for the generation of red blood cells and a deficiency of this B12 coenzyme generates anemia and fatigue.
The most common form of B12 is known as cyanocobalamin which has been used as a source of vitamin B12 in multivitamins. The body doesn’t make much use of that form however, the liver will convert small amounts of cyanocobalamin into methylcobalamin. This small amount is insufficient to to prevent neurological and aging problems therefore foods rich in methylcobalamin need to be taken in or supplementation may be required.
Remove brain damaging levels of the neurotransmitter glutamate
One of the medical benefits of methylcobalamin are thought to come from the fact that this vitamin helps to remove brain damaging levels of the neurotransmitter glutamate. This reduces fatigue, prevents moods swings and improves memory. Other neurological benefits appear to be from the increased production of SAM (S-adenosyl-L-methionine) which is known to be a mood-affecting molecule. Studies indicate that there is a correlation between hypertension and coronary artery disease (CAD) and high levels of the amino acid homocysteine. Researchers reported high levels of homocysteine and low concentrations of vitamin B12, SAMe and folic acid in cerebral spinal fluid. Interestingly, serum levels of homocysteine, folic acid and B12 were well within normal ranges. This indicates that a problem with homocysteine metabolism was occurring in the brain only. This suggests that there is a transport problem of B12 across the blood-brain-barrier. It had been reported that healthcare providers had to use high doses of B12 in their patients suffering from Chronic Fatigue Syndrome to see some effect.
The bad molecule homocysteine is broken down by transsulfuration and remethylation which requires folic acid (vitamin B9), vitamin B6 (pyridoxine) and B12 (cobolamin) as cofactors. If this goes off without a hitch homocysteine turns into methionine which can then be converted to S-adenosyl-methionine (SAM). SAM in turn is another important cofactor in the metabolism of monoamine transmitters such as dopamine, norepinephrine and serotonin. A lack of methylcobalamin causes this pathway to slow down and leave harmful levels of homocysteine and neurotransmitters around leading to loss of cognitive function and generating Chronic Fatigue Syndrome.
Chronic Fatigue Syndrome and nitrix oxide buildup
Chronic Fatigue Syndrome is also associated with excess nitric oxide buildup. Nitric oxide is used by blood vessels to dilate. This oxide is also known to be an inhibitor of the enzyme that converts homocysteine into methionine. Excess nitric oxide has been reported to allow homocysteine levels to rise. High nitric oxide levels can be due to low methylcobalamin levels and/or a bacterial or viral infection. It turns out that methylcobalamin is a powerful nitric oxide free radical scavenger and so a deficiency in this form of B12 can lead oxide to accumulate if nitric oxide is being produced. These metabolic pathways are very complex and have many branching points and intermediate products. A change in any one of the substrates may affect the outcome down the road in different ways. In fact, the end result can appear to be contradictory. This is best left to biochemists. Keep in mind that all metabolic pathways have not been elucidated.
What it boils down to is that it appears that high levels of homocysteine in cerebrospinal fluid is an important aspect of Chronic Fatigue Syndrome and loss of cognitive function along with low cerebrospinal fluid levels of B12, SAM and folic acid. Serum levels of all components have been reported to be normal so a blood test can not diagnose this problem. Cerebrospinal spinal fluid needs to be taken to get a proper measurement.