B 12

[Guest guest]

Al - where do you get the B12 2500 sublingual? Does it dissolve well? Joyce

[Guest guest]

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LEF Magazine August 1998 B-12NEUROLOGICAL DISEASE A Potential

BreakthroughJapanese scientists have identified a form of vitamin

B12

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 Parkinson's disease,

peripheral neuropathies, Alzheimer's disease, muscular dystrophy

and,

neurological aging. Americans have immediate access to this form of

vitamin B12, and unlike prescription drugs, it costs very little and

is free of side effects. Vitamin B12 is a general label for a group

of essential biological compounds known 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 10 years, a number of central and peripheral

neurological diseases have been related 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 axons and

peripheral nerves. Just how effective is methylcobalamin in treating

acute disease? Lets take a look at some neurological diseases and

other disorders where methylcobalamin has shown therapeutic results.

Bell's Palsy

Bell's palsy is non-lethal paralysis of the facial nerve. Any or all

branches of the nerve may be affected, and, in fact, Bell's palsy

victims may not be able to open an eye or close one side of the

mouth. To assess the benefits of methylcobalamin, 60 patients with

Bell's palsy were divided into three groups. One group was given

standard steroid drug therapy, the second group was given

methylcobalamin plus steroid therapy, and the third group was given

methylcobalamin by itself. The comparison among the three groups was

based upon the number of days needed to attain complete recovery of

nerve function, facial nerve scores, and improvement in symptoms.

The

results: It took an average of 7.79 weeks for the group given the

steroid drug to recover completely. In contrast, the group given the

steroid drug and methylcobalamin took just 1.23 weeks to recover,

and

the group receiving the methylcobalamin by itself enjoyed complete

recovery after just 5.1 days. The facial nerve score was

significantly more severe in the steroid group compared with the

methylcobalamin groups, and improvement in symptoms was better in

the

methylcobalamin groups compared with the group treated with the

steroid drug. The results of this study, published in Methods and

Findings of Experimental Clinical Pharmacology (17[8]:539-44 1996

Oct), showed that methylcobalamin was 10 times more effective than

the steroid drug approved by the Food and Drug Administration. For

those debilitated by Bell's palsy, a dose of 40 to 60 mg a day of

methylcobalamin could be a safe and effective therapy.

Brain Aging

Unlike Bell's palsy, it is difficult to demonstrate

methylcobalamin's

rapid results when protecting against aging-related disorders. On

the

other hand, the mechanisms of action of methylcobalamin, however,

are

intriguing. 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 aging

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

onto the receiving neurons drives them into hyperactivity, and the

excessive activity leads to cellular degradation. The Life Extension

Foundation has never recommended glutamine supplements for healthy

people because of concern about glutamine-induced brain cell damage.

The good news is that it may now be possible to protect brain cells

against glutamate toxicity by taking methylcobalamin supplements. In

a study in the European Journal of Pharmacology (1993 Sep.7;7;241

(1):1-6), it was shown that methylcobalamin protected against

glutamate-, aspartate- and nitroprusside- induced neurotoxicity in

rat cortical neurons. This study also showed that S-

adenosylmethionine (SAMe) protected against neurotoxicity. In a

study

in Investigational Ophthalmology Visual Sciences (1997 Apr; 38

(5):848-

854), a combination of methylcobalamin and SAMe was used to protect

against retinal brain-cell toxicity caused by glutamate and

nitroprusside. Researchers concluded that methylcobalamin protects

against neurotoxicity by enhancing brain cell methylation. The Life

Extension Foundation previously has recommended methylation-

enhancing

therapies such as vitamin B6, vitamin B12, folic acid and TMG

(trimethylglycine) 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.

Parkinson's Disease

At its current rate, Parkinson's disease strikes one in every 100

people over the age of 65. Almost every human suffers Parkinson's-

like symptoms as they age. Methylcobalamin may help to prevent

Parkinson's disease and slow the progression in those who already

have it. Here's how: Dopamine is a neurotransmitter that controls

motor functions. Dopamine transmits messages through different

regions of the brain and along nerve pathways in order to coordinate

muscle movement. Proper dopamine metabolism also is required to

maintain a state of psychological well-being. Aging humans suffer a

progressive disruption of dopamine metabolism that can cause muscle

weakness, loss of coordination, and depression. Parkinson's disease

is caused by the premature destruction of specialized brain cells

that produce dopamine. When 80 percent of dopamine-producing brain

cells have died, Parkinson's disease is usually diagnosed. It is

therefore desirable to protect dopamine-producing brain cells and

maintain youthful dopamine metabolism throughout life. Dopamine is

formed from the amino acid L-dopa. The more L-dopa that enters the

brain, the more dopamine is produced, but the problem is that L-dopa

itself is toxic to brain cells and is a direct cause of cell death.

The mechanism of L-dopa toxicity is excessive release of glutamate

from neurons (Brain Research 1997 Oct 10; 771[1]: 159-162), which

injures and kills brain cells. This could be why the drug Sinemet,

which provides significant amounts of L-dopa to the brain, only

works

for several years before its effects wear off and the Parkinson's

patient deteriorates rapidly. The types of brain cells that are most

vulnerable to glutamate-induced toxicity are the very cells involved

in dopamine metabolism and neural-motor control. Methylcobalamin has

been shown specifically to protect against glutamate- induced neural

toxicity caused by L-dopa. This means that supplementation with

methylcobalamin could protect thos patients with Parkinson's disease

from glutamate-induced toxicity caused by the high amount of L-dopa

they are putting into their brains by taking Sinemet. If brain cells

that control motor function were protected against L-dopa-induced

glutamate toxicity, it could mean that Parkinson's patients who take

methylcobalamin could continue benefitting from the dopamine-

enhancing effects of Sinemet for a much longer period of time. Late-

stage Parkinson's patients for whom Sinemet therapy no longer works

may have already suffered too much glutamate-induced brain cell

damage to benefit from methylcobalamin. The Parkinson's patients who

are still benefitting from Sinemet may be able to protect their

striatal neurons by taking 5 to 20 mg a day of methylcobalamin

sublingually (under the tongue), along with Sinemet. (Additional

therapies are outlined in the Foundation's Parkinson's Disease

Protocol. Call the Foundation at 1-800-544-4440 for a free copy, or

refer to the Foundation's book, Disease Prevention and Treatment

Protocols. The combination of methylcobalamin and Sinemet therapy

could be a medical breakthrough, but this can only be proven by

controlled studies. Today's Parkinson's patients cannot wait for the

completion of clinical studies and may want to start sublingual

intake of 5 to 20 mg a day of methylcobalamin immediately. For

Parkinson's disease prevention, 1 to 5 mg a day of sublingually

administered methylcobalamin may be sufficient.

Alzheimer's Disease

A study in Clinical Therapeutics (1992 May;14(3):426-437) showed

that

the intravenous administration of large doses of methylcobalamin to

Alzheimer's patients improved the patients' intellectual functions

such as memory, emotions and communication with other people. The

scientists concluded that methylcobalamin is a safe and effective

treatment for psychiatric disorders in patients with Alzheimer-type

dementia. This is the only clinical study the Foundation could find

on using methylcobalamin to treat Alzheimer's disease. It could be

that 40 to 80 mg a day of sublingually administered methylcobalamin

would be an effective adjuvant (assisting) Alzheimer's therapy. To

obtain a referral to sources of intravenous methylcobalamin drugs,

Foundation members should call our technical support line at 1-800-

226-2370.

Multiple Sclerosis

A study in the journal Internal Medicine (1994 Feb. 33(2):82-86)

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 features widespread demyelination in

the central nervous system. Although motor disability did not

improve, there were clinical improvements in visual and auditory MS-

related disabilities. The scientists 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 Letters

(1994 Mar 28; 170[1] 195-197), looked at the degeneration of axon

motor terminals. In mice receiving methylcobalamin, nerve sprouts

were more frequently observed and regeneration of motor nerve

terminals occurred in sites that had previously been degenerating.

MS

patients can obtain a copy of the Life Extension Foundation's

Multiple Sclerosis Protocol on-line. (Also, refer to Disease

Prevention and Treatment Protocols).

Regenerating Nerves

Few substances have been shown to regenerate nerves in humans with

peripheral neuropathies. However, a study in the Journal of

Neurological Science (1994 Apr. 122[2]:140-143) 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 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. In humans, subacute degeneration of the brain and

spinal cord can occur through the demyelination of nerve sheaths

caused by a folic acid or vitamin B12 deficiency. In a study in the

Journal of Inherited Metabolic Diseases (1993;16[4]:762-770), it was

shown that some people have genetic defects that preclude them from

naturally producing methylcobalamin. The scientists stated that a

deficiency of methylcobalamin causes demyelination disease in people

with this in-born defect. An early study published in the Russian

journal Farmakol Toksikol (1983 Nov; 46[6]: 9-12) Nov 1983) showed

that the daily administration of methylcobalamin in rats markedly

activated the regeneration of mechanically damaged axons of motor

neurons. An even more-pronounced effect was observed in laboratory

rats whose sciatic nerves were crushed mechanically. Two studies

published in the Japanese journal Nippon Yakurigaku Zasshi (1976,

Mar, 72,[2]: 269-278) showed that the administration of

methylcobalamin caused significant increases in the in vivo

incorporation of the amino acid leucine into crushed sciatic nerves,

resulting in a stimulating effect on protein synthesis repair and

neural regeneration. Those suffering from peripheral neuropathies

often take alpha lipoic acid. Based on our new understandings of

peripheral neuropathy, we suggest 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 (1987; 44[3]:169-173) examined the

effects of methylcobalamin 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. In mice irradiated before tumor

cell inoculation, methylcobalamin did not improve survival. The

effects of methylcobalamin on human immune function was investigated

in the Journal of Clinical Immunology (1982 Apr 2; [2]:101-109). The

study showed that methylcobalamin showed 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.

Sleep

A study in the journal Experientia (1992 Aug;48[8]:716-720)

indicates

that those taking methylcobalamin also might want to take melatonin.

In the study, it was detailed how nine healthy humans were given 3

mg

of methylcobalamin a day for four weeks. Among the results, it was

found that melatonin levels were significantly lower in the group

receiving methylcobalamin compared with placebo, although

methylcobalamin did not adversely effect sleep patterns. On the

contrary, previous reports of experiments show that vitamin B12

improves sleep patterns. The Life Extension Foundation suggests that

those taking methylcobalamin take at least 500 micrograms (½ mg) of

melatonin at bedtime. In addition to its sleep-enhancing

capabilities, melatonin has shown potent anti-cancer and immune-

enhancing benefits. A more recent German study appearing in

Neuropharmacology (15[5]:456-464, 1996) showed that while

methylcobalamin reduced the amount of time subjects slept, that

sleep

quality was better and subjects awoke feeling refreshed, and with

better alertness and concentration. Part of this effect was

apparently due to melatonin suppression during the daytime because

methylcobalamin reduced drowsiness. Most of the scientific studies

cited in this article were conducted in Japan. 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

exageration to say that virtually no American 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

Gehrig's disease). Since methylcobalamin 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

form of vitamin B12 is in slowing the progression of common

disorders

like Parkinson's disease. The sublingual intake of methylcobalamin

is

an affordable and effective natural therapy, and it is safe even

when

given in large doses. For prevention purposes, just 1 mg of

methylcobalamin taken under the tongue every day could produce

enormous anti-aging benefits at a very low price.

--- End forwarded message ---

[Guest guest]

Just checked the Swanson Vitamins website and they say this about B 12: featuring methylcobalamin, the preferred form of B-12. It goes to work immediately, without having to undergo a conversion process in the body like other forms of B-12.  

So now what to believe?

Rod