Jump to content
RemedySpot.com

Methylcobalamin: A Potential Breakthrough in Neurological Disease

Rate this topic


Guest guest

Recommended Posts

Guest guest

This is what I use 2 to 3 times a week, IM....good stuff

Angel huggzz

or angel

=================================================

_http://www.immunesupport.com/message/neurob12.htm_

(http://www.immunesupport.com/message/neurob12.htm)

Methylcobalamin: A Potential Breakthrough in Neurological Disease

Japanese scientists have identified a form of _vitamin B12_

(http://www.immunesupport.com/coderedirect.cfm?Product__Code=PH19) 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_

(http://www.immunesupport.com/coderedirect.cfm?Product__Code=P278) , 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 B12, and, unlike prescription drugs, it costs

very

little and is free of side effects.

_vitamin B12_

(http://www.immunesupport.com/coderedirect.cfm?Product__Code=PH19) 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 B12 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_

(http://www.immunesupport.com/coderedirect.cfm?Product__Code=P278)

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_

(http://www.immunesupport.com/coderedirect.cfm?Product__Code=P278) 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 B12. On the other hand,

vitamin B12 levels in the blood did not significantly deviate from normal

ranges.

According to Dr. Cheney's treatment pyramid for CFIDS, vitamin B12 in

its non-cyanocobalamin form (the type 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_

(http://www.immunesupport.com/coderedirect.cfm?Product__Code=P278) protects

against neurotoxicity by

enhancing brain cell methylation. The CFIDS & Fibromyalgia Health Resource

recommends methylation-enhancing therapies such as vitamin B6, vitamin B12,

folic acid

and trimethylglycine (TMG), taken together, to protect against heart

disease, stroke and other aging-related diseases.

The scientists who conducted the _methylcobalamin_

(http://www.immunesupport.com/coderedirect.cfm?Product__Code=P278) 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.

Sleep

A recent German study appearing in Neuropharmacology showed methylcobalamin

reduced the amount of time subjects slept; sleep quality was better and

subjects awoke feeling refreshed, with better alertness and concentration. Part

of

this effect was apparently due to melatonin suppression during the daytime

because morning methylcobalamin supplementation reduces drowsiness by

decreasing daytime melatonin levels.

Multiple Sclerosis

According to a recent study at Vanderbilt University, chlamydia pneumoniae

might link multiple sclerosis (MS) to CFIDS. This makes the published effect

of methylcobalamin treatment on MS of great importance to those who suffer

from CFIDS.

A study in the Journal of Internal Medicine investigated the daily

administration of 60 mg of methylcobalamin to patients with chronic progressive

multiple sclerosis (MS), a disease that has a poor prognosis and feature side

spread demyelination in the central nervous system.

Although motor disability did not improve, there were clinical improvements

in visual and auditory MS related disabilities. The scientist stated that

methylcobalamin might be an effective adjunct to immunosuppressive treatment

for

chronic, progressive MS. Those with less serious forms of MS may consider

adding methylcobalamin to their daily treatment regimen.

The effects of methylcobalamin were studied on an animal model of muscular

dystrophy. This study, published in Neuroscience Letter looked at

degeneration of axon motor terminals. In mice receiving _methylcobalamin_

(http://www.immunesupport.com/coderedirect.cfm?Product__Code=P278) , nerve

sprouts were more

frequently observed and regeneration of motor nerve terminals occurred in

sites that had been previously degenerating.

Regenerating Nerves

Few substances have been shown to regenerate nerves in humans with

peripheral neuropathies. However, a study in the Journal of Neurological

Science

postulated that methylcobalamin could increase protein synthesis and help

regenerate nerves. The scientists showed that very high doses of

methylcobalamin

produce nerve regeneration in laboratory rats.

The scientists stated that ultra-high doses of _methylcobalamin_

(http://www.immunesupport.com/coderedirect.cfm?Product__Code=P278) might be of

clinical

use for patients with peripheral neuropathies. The human equivalent dose the

scientists used is about 40 mg of sublingually administered methylcobalamin

on a daily basis.

Those suffering from peripheral neuropathies often take alpha lipoic acid.

Based on our new understanding of peripheral neuropathy, it may be prudent

that anyone using alpha lipoic acid also take at least 5 mg a day of

sublingually administered methylcobalamin to ensure that alpha lipoic acid will

be

bioavailable to the peripheral nerves.

Cancer/Immune Function

A study in the journal Oncology examined the effects of _methylcobalamin_

(http://www.immunesupport.com/coderedirect.cfm?Product__Code=P278) on several

different kinds of tumors in mice. The administration of methylcobalamin for

seven days suppressed liver, lung and ascites tumor growth. Mice receiving

methylcobalamin survived longer than control mice did. In mice irradiated

before tumor cell inoculation, methylcobalamin did not improve survival.

The effects of _methylcobalamin_

(http://www.immunesupport.com/coderedirect.cfm?Product__Code=P278) on human

immune function was investigated in the

Journal of Clinical Immunology. The study showed that methylcobalamin

demonstrated remarkable T cell-enhancing effects when the T cells were exposed

to

certain antigens.

The scientists also showed that methylcobalamin improved the activity of T

helper cells. The scientists concluded that methylcobalamin could modulate

lymphocyte function by augmenting regulatory T cell activities.

Americans need to know about this important natural therapy that could

extend the healthy human life span. A search of the scientific literature

reveals

334 published studies on methylcobalamin. However, it would not be an

exaggeration to say that virtually no doctors know of it or are recommending

it.

Methylcobalamin should be considered for the treatment of any neurological

disease. For example, based on its unique mechanisms of action,

methylcobalamin could be effective in slowing the progression of " untreatable "

diseases

such as ALS (Lou Gerhig's disease).

Since _methylcobalamin_

(http://www.immunesupport.com/coderedirect.cfm?Product__Code=P278) is not a

drug, there is little economic incentive to conduct

expensive clinical studies on it, so it may be a long time before we know just

how effective this unique form of vitamin B12 is in slowing the progression

of common diseases like Parkinson's disease.

The sublingual intake of _methylcobalamin_

(http://www.immunesupport.com/coderedirect.cfm?Product__Code=P278) is an

affordable and effective natural

therapy, and has proven even safe when given in large doses.

(euro-journ-pharm; 1993 Sep.7;7;241 (1):1-6) (Experientia; 1992

Aug;48[8]:716-720)

(Neuropharmacology; 1996;15[5]:456-464)

(journ-int-med; 1994 Feb. 33(2):82-86)

(Neuroscience Letter; 1994 Mar 28; 170[1] 195-197)

(journ-neuro-sci 1994 Apr. 122[2]:140-143)

(journ-inherited-meta-dis 1993;16[4]:762-770) (Oncology; 1987;44[3]:169-173)

(journ-clin-immuno 1982 Apr 2;[2]:101-109)

Link to comment
Share on other sites

Join the conversation

You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.

Guest
Reply to this topic...

×   Pasted as rich text.   Paste as plain text instead

  Only 75 emoji are allowed.

×   Your link has been automatically embedded.   Display as a link instead

×   Your previous content has been restored.   Clear editor

×   You cannot paste images directly. Upload or insert images from URL.

Loading...
×
×
  • Create New...