The B12 should not be cyano version. Cyano has shown to
actually cause a form of optic nerve damage, called Leber's.
These patients cannot metabolize the cyanide portion.
The one to get is methylcobalamin, the active form and you need at least 1000mcg daily to absorb 1% of that. 5000mcg would be better. This is available easily at Amazon, iherb.com, Puritan's.
I use the Puritan's now myself after testing it out by having blood work after 3mon on it...and it is very efficient. When B12 is taken orally it should be on an empty stomach as it is not well absorbed when food is present.
It costs pennies a day... between .20 and .30 cents depending on which sale you take advantage of.
There are studies at PubMed showing poor B12 levels in the spinal fluid of MS patients. Since B12 moves into the CSF
by a concentration gradient, having higher blood levels insure better movement into nerves and the brain.
Quote:
J Neuroimmunol. 1992 Oct;40(2-3):225-30.
Multiple sclerosis and vitamin B12 metabolism.
Reynolds EH.
Source
Maudsley Hospital, London, UK.
Abstract
Multiple sclerosis (MS) is occasionally associated with vitamin B12 deficiency. Recent studies have shown an increased risk of macrocytosis, low serum and/or CSF vitamin B12 levels, raised plasma homocysteine and raised unsaturated R-binder capacity in MS. The aetiology of the vitamin B12 deficiency in MS is often uncertain and a disorder of vitamin B12 binding or transport is suspected. The nature of the association of vitamin B12 deficiency and MS is unclear but is likely to be more than coincidental. There is a remarkable similarity in the epidemiology of MS and pernicious anaemia. Vitamin B12 deficiency should always be looked for in MS. The deficiency may aggravate MS or impair recovery. There is evidence that vitamin B12 is important for myelin synthesis and integrity but further basic studies are required.
PMID:
1430153
[PubMed - indexed for MEDLINE]
|
Quote:
J Neurol Neurosurg Psychiatry. 1990 Nov;53(11):951-4.
Vitamin B12 and folate concentrations in serum and cerebrospinal fluid of neurological patients with special reference to multiple sclerosis and dementia.
Nijst TQ, Wevers RA, Schoonderwaldt HC, Hommes OR, de Haan AF.
Source
Institute of Neurology, University Hospital, Nijmegen, The Netherlands.
Abstract
Vitamin B12 and folate concentrations were measured in serum and cerebrospinal fluid (CSF) in 293 neurological patients. Serum and CSF vitamin B12 concentrations showed a positive correlation. In individual patients CSF B12 concentrations varied considerably for a given serum concentration. The median serum vitamin B12 concentration of the Alzheimer's type dementia group was significantly lower compared with that of a control group. Lower median CSF vitamin B12 concentrations were found in groups of patients with multiple sclerosis and Alzheimer's type dementia. Five patients with heterogeneous clinical pictures had unexplained low serum and CSF B12 concentrations without macrocytosis. Two patients had very high serum B12 and low-normal CSF concentrations which could be explained by a blood-brain barrier transport defect. Serum and CSF folate concentrations did not show significant differences between the various groups.
PMID:
2283525
[PubMed - indexed for MEDLINE]
PMCID:
PMC488275
Free PMC Article
|
These are only two articles of several on PubMed.
Remyelination (which is repair of damaged myelin of nerves),
is accomplished with Omega-3 fats, B12, folate, B6.
B12, folate and B6 now are available as ACTIVE forms inexpensively at many on-line sources. And are preferred.
Active forms in red:
B12 (
methylcobalamin)
B6 (
P5P aka pyridoxal 5 phosphate)
Folate (
methylfolate aka MetaFolin)
All three are over the counter.
There are sites now on the net specifically for MS patients, and the list of supplements on them is much longer. These four
are the CORE nutrients that help myelin regeneration.
Here is one article on cyanide metabolism and optic neuritis:
Quote:
Fundam Appl Toxicol. 1983 Sep-Oct;3(5):397-9.
Cyanide in human disease: a review of clinical and laboratory evidence.
Wilson J.
Abstract
Experimental cyanide exposure in animals causes demyelination and circumstantial clinical and laboratory evidence suggest that there are human parallels. In Leber's hereditary optic atrophy there appears to be a defect in the conversion of cyanide to thiocyanate because of deficient rhodanese activity. For transmitters of the disease smoking carries the risk of blindness and in the most severely affected patients, there is diffuse neurological disease. It is possible that other hereditary optic atrophies (dominant and recessive) may also reflect inborn errors of cyanide metabolism. In the retrobulbar neuritis and optic atrophy of vitamin B12 deficiency there may be a conditional abnormality of cyanide metabolism in smokers, and likewise in so-called tobacco-alcohol amblyopia in which there are more complex nutritional deficiencies. Epidemiological evidence (differing sex ratios, excess of smokers) indicates that defective cyanide metabolism may contribute to the development of sub-acute combined degeneration of the cord in vitamin B12 deficiency. In protein-malnourished populations consuming large amounts of cyanide or cyanogens, viz. in tropical Africa where the staple diet includes cassava containing large amounts of linamarin, similar maladies occur as acquired disorders. There may be a similar explanation for lathyrism. The known pathways of human cyanide metabolism are reviewed and evidence supporting the clinical data is presented.
PMID:
6357925
[PubMed - indexed for MEDLINE]
|
I am including this information today for all MS readers here.
Some of you including Dej may already know this.
__________________
All truths are easy to understand once they are discovered; the point is to discover them.-- Galileo Galilei
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Weezie looking at petunias 8.25.2017
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