This topic was discussed recently on the forum. Today I received my order and started taking 5mg x2 a day of methylcobalamin taken under the tongue in lozenge form. Wish this old white rat good luck
I read again this article (as well as other sources).
http://www.prohealth.com/library/sho....cfm?libid=481
"
Japanese scientists have identified a form of vitamin B-12 that protects against neurological disease and aging by a unique mechanism that differs from current therapies.

Some of the disorders that may be preventable or treatable with this natural vitamin therapy, called methylcobalamin, include chronic fatigue syndrome, Parkinson's disease, peripheral neuropathies, Alzheimer's disease, muscular dystrophy and neurological aging. Americans have immediate access to this unique and new form of vitamin B-12, and, unlike prescription drugs, it costs very little and is free of side effects.

Vitamin B-12 is a general label for a group of essential biological compounds knows as cobalamins.

The cobalamins are structurally related to hemoglobin in the blood, and a deficiency of vitamin B-12 can cause anemia. The primary concern of conventional doctors is to maintain adequate cobalamin status to protect against anemia.

The most common form of vitamin B12 is called cyanocobalamin. However, over the last ten years, a number of central and peripheral neurological diseases have been linked to a deficiency of a very specific cobalamin, the methylcobalamin form, that is required to protect against neurological diseases and aging. The liver converts a small amount of cyanocobalamin into methylcobalamin within the body, but larger amounts of methylcobalamin are necessary to correct neurological defects and protect against aging.

Published studies show that high doses of methylcobalamin are needed to regenerate neurons as well as the myelin sheath that protects nerve axons and peripheral nerves.

CFIDS and B-12
In the Summer 1998 issue of HealthWatch, an important research article reported a fascinating new finding. Over 60% of CFIDS and FM patients' cerebral spinal fluids contained subnormal levels of vitamin B-12. On the other hand, vitamin B-12 levels in the blood did not significantly deviate from normal ranges.

According to Dr. Paul Cheney's treatment pyramid for CFIDS, vitamin B-12 in its non-cyanocobalamin form - the [only type then] commercially available - is a potent detoxifier of the brain. Recent studies in Europe suggest that it needs to be given in large doses in the range of 10 - 20 mg per day, or even more. This supplementation of methylcobalamin might protect the cognitive function of patients with CFIDS by preventing the death of brain cells.

One cause of brain cell death is glutamate toxicity. Brain cells use glutamate as a neurotransmitter, but unfortunately glutamate is a double-edged sword in that it can also kill brain cells. The release of glutamate from the synapses is a usual means by which neurons communicate with each other.

Effective communication means controlled release of glutamate at the right time to the right cells, but when glutamate is released in excessive amounts, intercellular communication ceases. The flood of glutamate into the receiving neurons drives them into hyperactivity, and the excessive activity leads to cellular degradation.

The good news is that it may now be possible to protect brain cells against glutamate toxicity by taking methylcobalamin supplementation. In a study in the European Journal of Pharmacology, it was shown that methylcobalamin protected against glutamate-, aspartate- and nitroprusside- induced neurotoxicity in rat cortical neurons.

Researchers concluded that methylcobalamin protects against neurotoxicity by enhancing brain cell methylation. The CFIDS & Fibromyalgia Health Resource recommends methylation-enhancing therapies such as vitamin B6, vitamin B-12, folic acid and trimethylglycine (TMG), taken together, to protect against heart disease, stroke and other aging-related diseases.

The scientists who conducted the methylcobalamin studies emphasize that ongoing intake of methylcobalamin is necessary to protect against neurotoxicity. Thus for methylcobalamin to be effective in protecting against neurological disease, daily supplementation may be required.

An appropriate dose to protect against neurological aging might be 1 to 5 mg a day taken under the tongue in lozenge form.
"

Please do this on an empty stomach.

Most of it is swallowed in the saliva...and needs absorption
in the intestine as well. If food is present, there will be less absorbed.

You can swallow the whole thing...as some people get mouth irritations long term. It will work if the stomach is empty for at least an hour.

I've been taking 1 mg daily for a couple of months but I haven't seen an effect yet. Maybe I should increase the dose.

5mg orally on an empty stomach, can raise you to 2000 level in 3 months. The higher the serum level, the better the transfer of it into the brain.

This paper is interesting:
http://www.orthomolecular.org/librar...12n04-p305.pdf

Fascinating and also slightly horrifying study, Mrs D. Thanks for posting this. It was well worth the read.

As someone whose Pernicious Anaemia (PA) was discovered quite by accident following recent blood tests for something completely different I was more than a little surprised to find that B12 levels are not routinely tested. in fact my GP said that nearly all cases were found as the result of a similar 'accident'.

Not to be alarmist at all, but some of the effects of undetected PA/B12 deficiency are severe and are, as this study indicates, possibly hidden in disorders that are put down to psychiatric causes. I found myself reading the bare bones science of this study and also seeing that the subjects represented a widely different group of people going through a lot of suffering, often of 'psychiatric' origin.

In particular there is mention of a group of women with post-natal depression of long duration, and a reflection that possibly doctors were not listening to patients when they blamed their symptoms on pregnancy etc. I know this is not a direct quote, and therefore a subjective interpretation, but a lot of mental and physical suffering for the want of a blood test seems to me to be a failure to understand that B12 deficiency is a serious disorder, something that is borne out by the experiences of PA sufferers, many of whom have difficulty finding out how to help themselves and find that general medical understanding of it to be poor and sometimes rather offhand. This is a little like thinking that high blood pressure is not serious because there are easily available treatments for it!

Mrs D has provided this forum with a lot of valuable info on this, far more than my doctors did! There is also an online group, PAS, which provides info for those with a PA dx. There are also some indications that B12/folate deficiency is increased in people on long-term l-dopa therapy.

Given some of the study's findings and it's emphasis on brain levels of B12 I also wonder about whether there could be a correlation of onset of PD in post-natal women, something that has been discussed before here, and B12 deficiency as a contributory factor. If so this could account for an increase in cases in younger women; in previous times there was a much higher mortality rate.

This is very much conjecture, I know. However the study does raise these questions for me............ along with quite a lot of others to do with AD and other related conditions.

Can anyone share the improvements / changes on PD related symptoms after taking Methyl B-12? I ordered some last night after reading the posts above. From the website I ordered, I saw some good reviews on this supplement from the people with CFS and some minor neuralgic issues including hand tremor. I did not see any complaint on the side effects. I think to give a try…

When I have an especially rough day ahead, I inject 50 IU of methylcobalamin and it makes all the difference in the world. It's an easy in the hip shot and the benefit is very noticeable. My neuro says OK and that any overage just gets flushed out. I wouldn't be without it. It smooths out my movements, gets me an extra 40-45 minutes on time and gives my much more energy without nervousness.

From previous post:

olic acid and B 12
there are a number of studies noting use of supplements Vitamin B 12 and folic acid in instances of B 12 deficiencies to decrease homocysteine levels that result from use of Levodopa. Levodopa reportedly interferes with folate metabolism and B 12 function.

Parkinsonism Relat Disord. 2008;14(4):321-5. Epub 2007 Dec 4.
Folate and vitamin B12 levels in levodopa-treated Parkinson's disease patients: their relationship to clinical manifestations, mood and cognition.

Abstract
We tested the hypothesis that mood, clinical manifestations and cognitive impairment of levodopa-treated Parkinson's disease (PD) patients are associated with vitamin B12 and folate deficiency...Levodopa-treated PD patients showed significantly lower serum levels of folate and vitamin B12 than neurological controls, while depressed patients had significantly lower serum folate levels as compared to non-depressed. Cognitively impaired PD patients exhibited significantly lower serum vitamin B12 levels as compared to cognitively non-impaired. In conclusion, lower folate levels were associated with depression, while lower vitamin B12 levels were associated with cognitive impairment. The effects of vitamin supplementation merit further attention and investigation.
PMID: 18055246 [PubMed - indexed for MEDLINE]


The influence of levodopa and the COMT inhibitor on serum vitamin B12 and folate levels in Parkinson's disease patients.
...Our findings show that levodopa-treated Parkinson's disease patients have low folate (p < 0.0007) and vitamin B12 levels (p < 0.0003). They also demonstrate that the addition of a COMT-i to levodopa + DDC-i treatment causes lower serum vitamin B12 (p < 0.03) and folate levels (p < 0.005) than levodopa + DDC-i treatment alone. We suggest supplementary treatment with vitamin B12 and folic acid in these situations.
http://www.ncbi.nlm.nih.gov/pubmed/17565222

Neurol Neurosurg Psychiatry 2003;74:549 doi:10.1136/jnnp.74.4.549
Correspondence
Benefit of folic acid supplementation in parkinsonian patients treated with levodopa
T Müller, D Woitalla, W Kuhn
+ Author Affiliations

Department of Neurology, St Josef Hospital, Ruhr University Bochum, Gudrunstrasse 56, 44791 Bochum, Germany
Correspondence to:
 Dr T Müller; 
 thomas.mueller@ruhr-uni-bochum.de
We read with interest the recent excellent review by Reynolds on the role of folic acid and the risks and benefits of its supplementation in the nervous system.1 It emphasises the beneficial importance of folate on the numerous methylation processes in combination with S-adenosylmethionine (SAM), which donates its methyl group to prevent hyperhomocysteinaemia.1 However SAM deficiency, which is associated with, for example, cognitive decline and/or mood disturbances, and increased total homocysteine levels, which support onset of vascular disease, may also caused by drugs, for example, levodopa.2,3 Levodopa is administered with dopa decarboxylase inhibitors (DDI) to prevent its peripheral degradation. This increases conversion of levodopa to 3-O-methyldopa (3-OMD) by the ubiquitious enzyme catechol-O-methyltransferase (COMT) in blood, peripheral tissues and in nigrostriatal neurons.2,3 COMT requires Mg2+ as cofactor and SAM as methyl donor. Thus O-methylation of levodopa to 3-OMD is associated with conversion of SAM to S-adenosylhomocysteine and subsequently homocysteine.

http://jnnp.bmj.com/content/74/4/549.1.full


For those individuals who have had DNA profiling, check for polymorphisms of the methylenetetrahydrofolate reductase (MTHFR C677T), methyltetrahydrofolate-homocysteine methyltransferase (MTR A2756G), and 5-methyltetrahydrofolate-homocysteine methyltransferase reductase both associated with folate metabolism and in addition, check (MTRR A1049G and C1783T) associated with processing of B12 in the bodY. If you have mutations in the MTHFR gene, must use a breakdown product of folic acid, methyl folate, and folinic acid if one has the other mutation. Mutations in MTRR requires a B 12 supplement.

madamlash,

did you ever try the liquid or tablet form ? what is the 50 IU dosage in grams? is yours a prescription?
thanks for posting!
sharilyn

Here are two very useful reference sites:

http://b12d.org/

and

http://www.pernicious-anaemia-society.org/

Dr Chandy's work on PA is now filtering into the system in the UK, and gaining recognition, and informing the NICE guidelines people. It will take a little longer to filter down to GP level, where there is little awareness. Like PD it is a B12 deficiency is little understood in terms of it's effect on the patient though the science of why it happens seems to be fairly sound, unlike PD it is only now gaining attention. As the long term effects of late diagnosis, and poor management are starting to come to light it is clear that a lot of people find it impacting on their lives in a major way.

If there are people in the US working on this and making a difference it would be useful to know.......especially for those of us on longterm ldopa treatment. It would also be useful to know how many of us here have diagnosed B12 deficiency and PD......