I can't read all this stuff about m.s. since I don't have it but I read the first posting and did not see the things I know about m.s. so here goes for those who are interested:
(1) on the radio about 5 years ago was reported a study that said tetanus shots confer immunity to m.s.
(2) The web states that those with m.s. have low uric acid. uric acid is a cellular level antioxidant which appears to be very important to fending off m.s. Those with gout (my family) do not get m.s. This is an EXTREMELY INTERESTING article:
http://en.wikipedia.org/wiki/Uric_acid And here is the bit about causes of low uric acid and m.s.:
Causes of low uric acid
Low dietary zinc intakes cause lower uric acid levels. This effect can be even more pronounced in women taking oral contraceptive medication.[34]
Xanthine oxidase is a copper, iron, and molybdenum-containing enzyme, so people with iron deficiency (the most common cause of anemia in young women) or molybdenum deficiency can experience low uric acid
Xanthine oxidase loses its function and gains ascorbase function when some of the Fe atoms in XO are replaced with Cu atoms. Accordingly, people with high Cu/Fe can experience low uric acid and vitamin C deficiency, resulting in oxidative damage. Since estrogen increases the half life of Cu, women with very high estrogen levels and intense blood loss during menstruation are likely to have a high Cu/Fe and present with low uric acid
Sevelamer, a drug indicated for prevention of hyperphosphataemia in patients with chronic renal failure, can significantly reduce serum uric acid.[35]
Multiple sclerosis
Lower serum values of uric acid have been associated with multiple sclerosis (MS). MS patients have been found to have serum levels ~194 mol/L, with patients in relapse averaging ~160 mol/L and patients in remission averaging ~230 mol/L. Serum uric acid in healthy controls was ~290 mol/L.[36] Conversion factor: 1 mg/dL=59.48 mol/L[17]
A 1998 study completed a statistical analysis of 20 million patient records, comparing serum uric acid values in patients with gout and patients with multiple sclerosis. Almost no overlap between the groups was found.[37]
Uric acid has been successfully used in the treatment and prevention of the animal (murine) model of MS. A 2006 study found elevation of serum uric acid values in multiple sclerosis patients, by oral supplementation with inosine, resulted in lower relapse rates, and no adverse effects.[38]
Normalizing low uric acid
Correcting low or deficient zinc levels can help elevate serum uric acid.[39]
Inosine can be used to elevate uric acid levels.[36]
Zn inhibits Cu absorption, helping to reduce the high Cu/Fe in some people with hypouricemia.
Fe supplements can ensure adequate Fe reserves (ferritin above 25 ng/dl), also correcting the high Cu/Fe.
Oxidative stress
Uric acid may be a marker of oxidative stress,[40] and may have a potential therapeutic role as an antioxidant.[41] On the other hand, like other strong reducing substances such as ascorbate, uric acid can also act as a prooxidant,[42] particularly at elevated levels. Thus, it is unclear whether elevated levels of uric acid in diseases associated with oxidative stress such as stroke and atherosclerosis are a protective response or a primary cause.[43][44]
For example, some researchers propose hyperuricemia-induced oxidative stress is a cause of metabolic syndrome.[32][45] On the other hand, plasma uric acid levels correlate with longevity in primates and other mammals.[46] This is presumably a function of urate's antioxidant properties.[47]
(3) I have always known that m.s. is caused by destruction of the myelin sheath and myelin is fat and so I have always reasoned that antioxidants which prevent rancidity of fat would be protective. I do not know which antioxidants work where but it is a good guess that the ones which are fat soluble are important. For instance Vitamin E is oil soluble and can cross the lipid wall of the cell. Vitamin C is water soluble and cannot. Alpha Lipoic acid is soluble in fat AND water and can work in both places. Some cellular antioxidants like apparently glutathione and uric acid are more important than these because they are there where they are needed. I think also SOD is one of those super-important anti-oxidants.
(4) When the myelin sheath which insulates the nerve from other nearby nerves is damaged this allows "cross-talk" between the nerves which is what causes the overstimulation and pain.
(5) Fredd says that omega-3 is needed to regenerate nerves as well as the B12 methylation supplements and this makes sense as the myelin sheath is fat.
(6) This is the most interesting info I have learned in the past year on nerves -- it is extremely interesting.
www.lef.org says that the nerve cell does not use insulin to gate sugar entry (and thereby fend it off when undesireable) like the non-nerve cell does. The normal method it is supposed to gate and fend off sugar is via carnitine. It requires adequate methylation to make carnitine. If you do not have enough carnitine, sugar gets into the nerve cell and the nerve cell cannot get rid of it and it turns to sorbitol and damages the cell. This has to do with the polyol pathway. I read this in Life EXtensions compendium book which explains it better than the online references I can find, but here they are (which I retrieve with search string "polyol pathway"):
(p.s. I believe neuropathy is neuropathy whatever the cause so I think this applies despite that it was studied in the context of diabetes - for instance doctors in India are treating neuropathies caused by tropical diseases (chagas I believe?) with b12 therapies successfully)
Polyol pathway hyperactivity is closely related to carnitine deficiency in the pathogenesis of diabetic neuropathy of streptozotocin-diabetic rats.
Nakamura J, Koh N, Sakakibara F, Hamada Y, Hara T, Sasaki H, Chaya S, Komori T, Nakashima E, Naruse K, Kato K, Takeuchi N, Kasuya Y, Hotta N. The Third Department of Internal Medicine, Nagoya University School of Medicine, Nagoya, Japan.
J Pharmacol Exp Ther 1998 Dec;287(3):897-902
To investigate the relationship between polyol pathway hyperactivity and altered carnitine metabolism in the pathogenesis of diabetic neuropathy, the effects of an aldose reductase inhibitor, [5-(3-thienyl) tetrazol-1-yl]acetic acid (TAT), and a carnitine analog, acetyl-L-carnitine (ALC), on neural functions and biochemistry and hemodynamic factors were compared in streptozotocin-diabetic rats. Significantly delayed motor nerve conduction velocity, decreased R-R interval variation, reduced sciatic nerve blood flow and decreased erythrocyte 2, 3-diphosphoglycerate concentrations in diabetic rats were all ameliorated by treatment with TAT (administered with rat chow containing 0.05% TAT, approximately 50 mg/kg/day) or ALC (by gavage, 300 mg/kg/day) for 4 weeks. Platelet hyperaggregation activity in diabetic rats was diminished by TAT but not by ALC. TAT decreased sorbitol accumulation and prevented not only myo-inositol depletion but also free-carnitine deficiency in diabetic nerves. On the other hand, ALC also increased the myo-inositol as well as the free-carnitine content without affecting the sorbitol content. These observations suggest that there is a close relationship between increased polyol pathway activity and carnitine deficiency in the development of diabetic neuropathy and that an aldose reductase inhibitor, TAT, and a carnitine analog, ALC, have therapeutic potential for the treatment of diabetic neuropathy.
The role of taurine in diabetes and the development of diabetic complications.
Hansen SH. Department of Clinical Biochemistry, Rigshospitalet, Copenhagen University Hospital, Denmark.
shhansen@rh.dk
Diabetes Metab Res Rev 2001 Sep-Oct;17(5):330-46
The ubiquitously found beta-amino acid taurine has several physiological functions, e.g. in bile acid formation, as an osmolyte by cell volume regulation, in the heart, in the retina, in the formation of N-chlorotaurine by reaction with hypochlorous acid in leucocytes, and possibly for intracellular scavenging of carbonyl groups. Some animals, such as the cat and the C57BL/6 mouse, have disturbances in taurine homeostasis. The C57BL/6 mouse strain is widely used in diabetic and atherosclerotic animal models. In diabetes, the high extracellular levels of glucose disturb the cellular osmoregulation and sorbitol is formed intracellularly due to the intracellular polyol pathway, which is suspected to be one of the key processes in the development of diabetic late complications and associated cellular dysfunctions. Intracellular accumulation of sorbitol is most likely to cause depletion of other intracellular compounds including osmolytes such as myo-inositol and taurine. When considering the clinical complications in diabetes, several links can be established between altered taurine metabolism and the development of cellular dysfunctions in diabetes which cause the clinical complications observed in diabetes, e.g. retinopathy, neuropathy, nephropathy, cardiomyopathy, platelet aggregation, endothelial dysfunction and atherosclerosis. Possible therapeutic perspectives could be a supplementation with taurine and other osmolytes and low-molecular compounds, perhaps in a combinational therapy with aldose reductase inhibitors. Copyright 2001 John Wiley & Sons, Ltd.
Oh, here I find this is their newsletter:
http://www.lef.org/newsletter/2004/2004_12_30.htm?source=search&key=polyol pathway
One predominant theory of neuropathy in diabetic rats involves abnormalities in what is called the polyol pathway. Polyol stands for polyhydroxy alcohols. While most of the cells in the body require insulin in order to transport glucose across the cell membrane, nerve cells are different. Membranes of nerve cells and their capillaries have insulin-independent glucose transport; that is, insulin is not required for glucose to pass into the cells. Since there is an excess of glucose in the bloodstream of diabetics, this glucose can easily be absorbed into nerve cells. In nerve cells, this glucose gets converted to sorbitol (a sugar alcohol) by an enzyme known as aldose reductase. The sorbitol cannot easily get out of the cell and consequently it accumulates, causing free-radical damage to nerves and blood vessels. This causes a decrease in an intracellular nutrient known as myo-inositol that is partly responsible for nerve conduction.
There is also an increase in free radicals such as peroxides and decreased nitric oxide production (a blood vessel-relaxing messenger), which, of course, leads to increased oxidative stress and the need for increased antioxidants. The amino acid taurine is also depleted (Hansen 2000). Terada et al. (1998) suggest that there is a close relationship between increased polyol pathway activity and carnitine deficiency in the development of diabetic neuropathy and that an aldose reductase inhibitor, a carnitine analog, and alpha-lipoic acid have therapeutic potential for the treatment of diabetic neuropathy (Terada et al. 1998).
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So y'all with m.s. may not be diabetic but I think y'all are coming at the polyol pathway problem from the other direction -- a deficiency of carnitine rather than an overabundance of glucose. That's my uneducated but firm opinion. I think the way out is this: YOU CANNOT CONTROL WHAT YOU CANNOT MEASURE. Follow whichever methylation protocol you think best for you and measure your homocysteine and your carnitine. Your homocysteine should be 6.3. EVery 3 points above that is a 35% greater risk of stroke. If your homocysteine is right, you probably have the methylation cycle working in most of your body (not necessarily the brain since the methylation cycle is GREATLY ABBREVIATED in the brain (there are no workarounds for blocked paths there!). Once you get the homocysteine right (it is $60/test) then check your carnitine. The protocol you are taking is NOT RIGHT FOR YOU if you cannot get these numbers in range, so try again. Measure and adjust - that is how you get control. All along make sure you are taking omega-3. I do not know how much - I think maybe 3 g, which to me is measly since I have to take 7-9g/day to fend off NF-kB due to allergies. You can take carnitine directly of course but it will mean you have not gotton your methylation right, which will cause other issues for you. In addition, take the steps above to raise uric acid and you can measure that too! Get yourself in the sweet spot in these measures and take oil soluble antooxidants for good measure. I think that may do the trick. If not, I think these are all key steps on the way to recovery, and maybe additional research will turn up a few more steps.
So in case you missed it, I think m.s. may be caused by a virus in genetically sensitive or for other reason methyl compromised individuals who do not happen to have the genes and or diet that causes gout. If you make your body stronger with methylation and antioxidants the virus won't make any difference. I am not sure a tetanus shot would be a good idea if you already have m.s. I guess you could try Olive Leaf Extract and Oil of Oregano against the virus. I think we make too much of virusses instead of strengthening the organism against it. So for instance there are always weed seeds about, but if you have a healthy lawn, it crowds out the weeds.