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Low fat diet with a high polyunsaturate to saturate ratio.

(See Also: ''Fatty, Acids" below)

A high fat diet impairs the conversion of linoleic acid to proslaglandin E1 (PGEI) (Brenner RR. The oxidative desaturation of unsaturated fatty acids in animals. Mol Cell Biochem 3:41-52 I974). PGE1 levels may have a relationship to disease activity (see Omega-6 Fatty Acids below).

Experimental Study: 144 pts. followed a low-fat diet for 34 years. At each level of severity of disability pts. who adhered to the diet showed significantly less deterioration and much lower death rates than did those who consumed more fat than prescribed (>20g/d) The greatest benefit was seen in those with minimum disability at the start of the trial; in this gp., when those who died from non-MS diseases were excluded, 95% survived and remained physically active. Defaulting from the diet even after 5-10 yrs. was, in almost all cases, followed by reactivation of the disease. Pts. consuming 10-15g/d or less had even better improvement in energy and fatigue levels (Swank RL, Dugan BB. Effect of low saturated fat diet in early and late cases ofmurripre sclerosis Lancer 336:37-39, 1990).

Note: Since pts. who are well are more likely to conrinue on treatment than those who deteriorate "good compllers" are likely to he self-selected from those who do well, giving the predictable "positive" result (Editorial: Lipids and multiple sclerosis Lancet 336:21-26, 1990).

Experimental Study: The pts. in this 36-yr.-oId study all reduced their saturated fat intake markedly from an ave. of 125 g/d prior to the start of the study. Only oils which were fluid at room temperature were allowed as a source of fats. All experienced a marked decrease in exacerbations The best clinical results were in pts. who reduced daily fat intake to <20 g. For this gp.. deterioration was slight, and only 31% died. Above 20 g fat per day, the level of disability was serious, and the death rate increased to 80% Females tended to do better than males. The response to the diet was more marked if made early in the course of the disease. While oil consumption was found to be indirectly beneficial, the authors believe that this was the result of the replacement of saturated fats by unsaturated oils, rather than by a direct benefit from the essential fatty acids in the oils (Swank RL. Grimsgaard A. Multiple sclcrosis: The lipid relationship. Am J. Clin Nwr 48:1387-93, 1988).

Experimental Controlled Study: 83 pts. increased the P:S ratio of the diet from 0.8 to 1.5 after 6 mo. and 1.34 at 36 months. There were significant correlations between linoleic, eicosapentaenoic and docosahexaenoic acid levels and the diet. Not only was there a reduction in the exacerbation rate. but there was also an improvement in the neurological status of compliant pts., while matched controls continued to deteriorate in terms of rate and severity of exacerbations and neurological status Fitzgerald G et al. The effect of nutritional counselling on diet and plasma EFA status In multiple sclerosis parients over 3 years. Hum Nutr Appl Nutr 41(5):297-310, 1987).

Observational Study: On the basis of an examination of the statistical correlations between the main foodstuff and nutrient intakes and the chief causes of mortality in 20 different countries findings suggested a causal interpretation between total fat intake and multiple sclerosis (Knox EG. Foods and diseases. BrJ Prey Soc. Mrd 31(2):71-80, 1977).

Observational Study: Cow's milk contains only 1/5 the linoleic acid (an essential polyunsaturate) of human milt and then is none in skim milk. People who were fed cow's milkas children were found to be more susceptible to MS as as adults than people who were breast fed (Agranoff BW, Goldberg D. Diet and the geographical distribution of multiple sclerosis. Lancet 2:1061-66, 1974).

Experimental Study: 146 pts. were placed on a low fat diet and followed up to an ave. of 17 years. The course of the disease was less rapidly progressive than in untreated cases. If treated before significant disability developed a high percentage of cases remained unchanged for up to 20 years. When treated later, the disease was slowly progressive. Pts. consuming the least fat and the largest amount of fluid (mono- and polyunsaturated) oils deteriorated the least (Swank RL. Multiple Sclerosis: Twenty years on low fat diet. Arch Neurol 23:460-74, 1970),

Observational Study: The brain tissue of pts. was found to have a higher saturated fat content than controls (Baker R. Lancer 1:26, 1963).


Supplementation by injection may be beneficial.

Case Reports: Intraspinal injections led to dramatic, though transient, improvements (Stern EI. The intraspinal injection of vitamin B1 for the relief of intractable pain and for inflamatory ond degenerative diseases of the central nervous system Am J Surg 34:495, 1938).

- with Niacin:

Case Reports: Rs. benefited from N injections containing nicotinic acid 100 mg and thiamine 60 mg in each 10 cc solution (Moore MT. Treatment of multiple sclerosis with nicotinic acid and vitamin B1. Arch Intern Med 65:18, 1940).

Vitamin B6:

Deficiency may predispose to multiple sclerosis.

Theoretical Discussion: Carbon monoxide pollution of the air is the one environmental factor present only in the localities where MS is common. Of 21,000 non-fatal cases of CM poisoning, a number developed a demyelinating condition. Similarly, animals exposed to CM develop CNS degeneration. It has been shown that CM exposure increases the need for pyridoxine, suggesting that a relative B6 deficiency may cause MS in susceptible persons (Mitchell DA, Schandl EK. Am J Clin Nutr August, 1973).

Vitamin B12:

Deficiency may be associated with multiple sclerosis.

Case Report: A 46-year-old woman had painful paresthesias associated with progressive rt. leg weakness Myelography was normal. MS was diagnosed. During the following 15 yrs. she was admitted about every 18 mo. for symptom exacerbation and responded each time to ACTH infusions. In June, 1987, a brain MRI showed bilateral high-signal-intensity white matter abnormalities. About 2 mo. later, a MCV of 100.8 fl was recorded. When evaluated in 1988, she had seven spastic monoparesis of the rt. leg associated with distal wasting. Vibration appreciation was bilaterally absent in the feet, With decreased pinprick appreciation the the mid-thigh on the right. Reflexes were symmetrically depressed with bilateral plantor extensor responses HGb was 1424 g/dL, MCV was 98.3 fl. The blood smear contained rare hypersegmented polymorphonuclear leucocytes. Serum B12 was <100 pg/ml and folic acid wits 8.2 ng/ml. plasma concentrations of vitamin B12-dependent metabolites were normal (total serum homocystine and serum methymalonic acid). Rheumatoid factor was raised with an antinuclear factor titer of 20. Serum intrinsic factor antibodies were present. She was treated with vitamin B12 injections 1000 micrograms daily for 1 wk. followed by weekly injections. Initial improvement was such that she could climb stairs without circumduction of the rt. leg. After 6 mo., she showed evidence of increased rt. leg strength. Blood count was normal with a decreased in MCV to 92.7 fl and no hypersegmented polymorphonuclear cells. Serum B12 was 210 pg/ml. Since pernicious anemia has an autoimmune basis. both ACTH and steroids produce amelioration of the disease with hematological remission. It is suggested that ACTH produced temporary remissions, giving rise to the mistaken impression that she had a classic clinical course for MS (Ransohoff RM ct al. Viramin B12 deficiency and multiple sclerosis. Letter. Lancet 335:1285-86, 1990).

Case reports: 3 pts. with convincing evidence of MS also had vitamin B12 deficiency of an unusual or obscure kind. One had juvenile pernicious anemia which preceded the onset of MS; the other 2 had unexplained deficiency. 2 of the pts., including hte man with juvenile PA, had persistent macrocytosis despite vitamin B12 therapy. None had any of the usually recognized neurological or psychiatric complications of B12 deficiency. While the relationship between vitamin B12 deficiency and MS in these pts. is unclear, depletion of RBC cobalamin levels in one pt. suggests that there is a defect in transport of Bqw into the cells, perhaps due to a disturbance in protein binding (Reynolds EH, Linnell JC. Vitamin B12 deficiency, demyelination, and multiple sclerosis. Letter Lancet 2:920, 1987).

Review Article: During the 1950's and 1960's there were several studies of serum and CSF vitamin B12 levels in MS because of the suspected role ob B12 in myelin formation. Because of equivocal results, the interest waned (Chandarin I. The Megaloblastic Anemias. Oxford, Blackwell, 1982).


- and Vitamin D:

Deficiency during puberty has been theorized to predispose to multiple sclerosis. If so, supplementation during puberty may be preventative.

Theoretical Discussion: Based on epidemiologic, biochemical and genetic evidence, it is hypothesized that demyelination in MS results froma breakdown due to abnormal lipid composition and structure produced during the period of brain development. Altered lipid concentrations and fatty acid profiles result from genetic deficiencies in enzymes that govern myelin synthesis and membrane assembly which may occur because of inadequate supplies of vitamin D and calcium at times of rapid myelination and growth, especially adolescence. If this theory is correct, it may be possible to suppress the disease by dietary supplementation with vitamin D and calcium during puberty (Goldberg P. Multiple sclerosis: Vitamin D and calcium as environmental determinants of prevalence. Int J Environ Stud 6:19-27 &121-29, 1974).

- and Magnesium, Vitamin D and Cod Liver Oil:
Supplementation may be beneficial.

Experimental Study: 16 pts. aged 22-37 who exhibited unambiguous exacerbations within 12-24 mo. prior to the trial received dolomite sufficient to furnish 16 mg/kg calcium and 10 mg/kg magnesium daily. k Also, in order to promote mineral absorption, they received 20 g/d cod liver oil to furnish 5,000 IU daily of vitamin D. After 1-2 years., the number of exacerbations was (Goldberg P et al. Multiple sclerosis; decrease relapse rate through dietary suplementation with calcium, magnesium and vitamin D. Med Hypotheses 21 (2):193-200, 1986).

Note: Swank and Dugan state that increasing oil intake is normally accompanied by a decrease in saturated fat intake which may be as much as 2 g for every 1 g increase, which suggests that decreased saturated fat intake was another factor contributing to improvement (Swank RL, Dugan BB. Effect of low saturated fat diet in early and late cases of multiple sclerosis. Lancet 336:37-39, 1986).


Deficiency is associated with defects in myelination in animal studies (Underwood EJ. Trace Elements in Human and Animal Nutrition, 4th Ed. New York, Academic Press, 1971).

Serum levels may be normal (Wikstrom J et al. Selenium, vitamin E and copper in multiple sclerosis. Acta Neurol Scand 54(3):287-90, 1976).
Tissue levels may be depressed.

Observational Study: Compared 42 controls, hair copper levels were significantly lower in 40 pts. (Ryan DE et al. Trace elements in scalp-hair of persons with multiple sclerosis and of normal individuals. Clin Chem 24, 1978).

Ceruloplasmin levels may be elevated.

Observational Study: Compared to controls, ceruloplasmin levels of 27 pts. were higher, but not significantly (Smith DK et al. Trace element status in multiple sclerosis. Am J Clin Nutr 50:136-40, 1989).

Observational Study: Ceruloplasmin was found to be increased during acute exacerbations of MS (Becus T et al. Study of serum and cerebrospinal fluid ceruloplasmin in multiple sclerosis and other neurologic diseases. Rev Roum Neurol 8:3-12, 1971).
The prevalence of multiple sclerosis may be inversely related to selenium levels in the soil.

Observational Study: The prevalence of MS is high in Ostrobothnia, a low selenium district in Finland, while in Lapland, a high selenium district, the prevalence is low (Wikstrom J et al. Selenium, vitamin E and copper in Multiple sclerosis. Acta Neurol Scand 54(3):287-90, 1976).

Glutathione peroxidase activity may be reduced.

Observational Study: compared to controls, pts. had lower glutathione peroxidase (GSH-px) activity (Mai J et al. High dose antioxidant supplmentation to MS patients. Biol Trace Element Res 24:109, 1990).

Negative Observational Study: Compared to controls, concentrations of glutathione peroxidase in 27 pts. were similar (Smith DK et al. Trace element status in multiple sclerosis. Am J Clin Nutr 50:136-40, 1989).

Negative Observational Study: Normal activity of glutathione peroxidase (both selenium-dependent and selenium-independent) was found in lymphocytes, granulocytes and platelets of MS patients (Szeinbserg A et al. Glutathione peroxidase activity in various types of blood cells in multiple sclerosis. Acta Neurol Scand 63(1)67-75, 1981).

Observational Study: Lymphocyte and granulocyte glutathione peroxidase activity in Danish pts. was significantly reduced by 3a5-50% compared to controls (Jensen GE et al. Leucocyte glutathione peroxidase activity and selenium level in multiple sclerosis. J Neurol Sci 48(1)61-67, 1980).

If selenium-dependent glutathione-peroxidase activity is low, selenium supplementation may increase it.

Case Report: A 34 year-old primipara (weight 50 kg) had suffered from MS for 9 yrs. and her condition had deteriorated considerably during the first 5 mo. of lactation. Prior to selenium supplementation she was, due to fatigue and vertigo, unable to lift and carry her baby, or to walk with snow boots due to ataxia. Because of a low glutathione peroxidase level and short Se75 half-life (58 days), it was decided to administer supplemental selenium. l The pt. received oral sodium selenite 0.02 mg/kg body weight for 1 mo. and then 0.04 mg/kg. Plasma and breast mile selenium rose, and RBC glutathione peroxidase levels increased. After 3 mo., her condition clearly improved, and she was able to handle her baby and to walk normally. After about 1 1/2 yrs. of treatment, however, she had a relapse. Because of the natural history of exacerbations and remissions of MS, it is not possible to know whether selenium supplementation was related to her temporary improvement (Westermark T et al. Selenium level in milk during long-term supplementation with sodium selenite to a patient with multiple sclerosis. Nutr Res Suppl 1:S232-34, 1985).

- with vitamin C and vitamin E

Experimental Study: Following 5 wks. of supplementation with sodium selenite 6 mg/d, vitamin C2 g/d and vitamin E 480 g/d, GSH-px levels increased 5-fold in a gp. of pts. with reduced glutathione peroxidase (GSH-px) activity, while side effects were minimal. Also, 2 mg of sodium selenite was shown to increase selenium concentrations by 24% (Mai J et al. High dose antioxidant supplementation to MS patients. Biol Trace Element Res 24(2):109-17, 1990).


May be abnormalities in its compartmentalization.

Observational Study: Compared to controls, plasma and RBC zinc levels were higher in MS patients and, during periods of relapse, RBC zinc levels decreased dramatically. RBC zinc levels were increased specifically in the extracts of the lipid fraction of the erythrocyte membrane. (Ho S-Y et al. k Zinc in multiple sclerosis. II. Correlation with disease activity and elevated plasma membrane-bound zinc in erythrocytes from patients with multiple sclerosis. Ann Neurol 20:712-15, 1986).

Note: Altered levels of cholesterol in plasma and erythrocytes may contribute to the increased RBC membrane zinc (Cunnane SC et al. Essential fatty acid and lipid profiles in plasma and erythrocytes in patients with multiple sclerosis. Am J Clin Nutr 50:801-06, 1989).

Observational Study: Compared to normal controls, plasma zinc levels were slightly increased in pts. with MS (and significantly increased in pts. with other neurological impairments), while albumin-bound and protein-bound zinc were normal. The alpha 2 macroglobulin-bound zinc was significantly lower in pts. than in controls, while RBC-bound zinc was significantly increased (p>0.05) in MS pts. but not in pts. with other neurological impairments. As RBC-bound zinc levels are relatively independent of daily dietary fluctuations, this increase may suggest alterations in the control mechanisms governing zinc compartmentalization. (Dore-Duffy P et al. Zinc in multiple sclerosis. Ann Neurol 14(4):450-54, 1983).


Fatty Acids:

70% of myelin is lipid and the unsaturated lipids, predominately oleic acid, may be subject to peroxidation insult (Norton WT. Formation, structure, and biochemistry of myelin, in GJ Seigel et al, Eds. Basic Neurochemistry, 2nd Edition. Boston, Little Brown, and Company, 1976:74-79).

Note: Nutritional factors capable of influencing lipid peroxidation include vitamins with known antioxidant activity, such as vitamins C and E, and the trace element-dependent enzymes glutathione peroxidase (selenium), ceruloplasmin (copper), and superoxide dismutases (zinc, copper, and manganese) (Halliwell B, Gutteridge JM. Lipid peroxidation: A radical chain reaction, in B Halliwell, JM Gutteridge JM, Eds. Free Radicals in Biology and Medicine. l Oxvord, Clarendon Press, 1985:139-89).

Epidemiologic studies have shown a negative correlation between the prevalence of the disease and the intake of polyunsaturated fatty acids (Alter M et al. Arch Neurol (Chicago) 31:267-72, 1974).

Polyunsaturates may be deficient in the brain, serum and erythrocytes of patients (gul S et al. J Neurol Neurosurg Psychiatry 33:506-10, 1970; Baker RWR et al. J Neurol Neurosurg Psychiatry 33:506, 1970; Gerstl B et al. Brain 84:310-19, 1961).
-Omega-3 Fatty Acids (Fish Oils):
Example: 'Max EPA' 3 capsules three times daily (9 gms)

WARNING: Supplementation may require additional vitamin E intake to prevent increased membrane perxidation and cellular damage (Laganiere S, Fernandes G. High peroxidizability of subcellular membrane induced by high fish oil diet is reversed by vitamin E. Clin Res 35:A565, 1987).

May be reduced.

Observational Study: Although levels of omega-3 fatty acids in the total phospholipids in plasma were not different from those of 14 healthy controls, the sum of the omega-3 fatty acids derived from alpha-linolenic acid was 19% lower in 12 MS pts. (p<0.01) (Cuanne SC et al. Essential fatty acid and lipid profiles in plasma and erythrocytes in patients with multiple sclerosis. Am J Clin Nutr 50:801-06, 1989).

Review Article: Of the 2 essential fatty acids, linoleid (omega-6) and alpha-linolenic (omega-3), the evidence points more to a dietary deficiencyof alpha-linolenic acid as an etiologic factor. Epidemiologic information seems to indicate that the geographical distribution of MS is inversely related to the intake of foods such as fish which are rich in alpha-linolenic acid and its derivatives. For example, there is a relatively low incidence of MS in the Faroe Islands, compred to the Shetlands. The Islanders come from teh same Danish genetic backgrounds but the Faroe Islanders remained fishermen while the Shetlanders adopted a British agricultural practice. Similar contrasts are apparent in Scandinavia (Bernsohn J, Stephandies LM. Aetiology of multiple sclerosis. Nature 215:821-23, 1967).
Supplementation may be beneficial.

Experimental Study: 12 pts. with clinically definite MS according to the criteria of MdAlpine received Max EPA (R.P. Scherer) 25 ml/d (4.2 g EPA, 2.8 g DHA) ( range 20-30 ml) with 1/3 of the daily dose taken with each meal. Pts. continued on vitamins and rehabilitation services; 2 pts. also supplemented their diets with sunflower seed oil. After 1-4 mo., 5 pts. with acute remitting MS, showed evidence of a slight, but significant reduction of total neurologic score from Kurtzke's Expanded Disability Status Scale (EDSS) of 16.5 to 13.5, mean EDSS degree from 3.7 to 2.7, and of Cendrowski's progression index from 0.59 to 0.44. In 7 pts. with slowly progressive MS, clinical parameters continued to deteriorate. Results suggest that, with a longer peroiod of treatment, it may be possible to demonstrate clearly that the differences observed did not arise by chance. (Cendrowski @. Multiple sclerosis and Max EPA. Br J Clin Prac 40:365-67, 1986).

Omega-6 Fatty Acids:

	linoleic acid -->GLA -->DGLA -->PGE1

Linoleic acid, a polyunsaturate which is the main essential fatty acid in the diet, tends to be low in the blood of patients and to fall further during relapses (Mertin H, Meade CJ. Relevance of fatty acids in MS. Br Med Bull 33:67-71, 1977; Sanders H et al. Further studies on platelet adhesiveness and serum cholesteryl linoleate levels in MS. J Neurol Neurosurg Psychiatry 31:321l-5, 1968; Thompson RHS. Proc Roy Soc Med 59:269, 1966).

Negative Observational Study: Compared to 33 controls, 30 pts. showed no significant decrease in serum linoleic acid, suggesting that a disturbance in linoleic acid metablolism is not inevitably associated with this disease (Wolfgram F et al. Serum linoleic acid in multiple sclerosis. Neurology 25 (8):786-88, 1975).

Epidemiologic studies of the relationship between the prevalence of MS and diet are consistent with the hypothesis that linoleic acid intake is negatively associated with MS (Alter M et al. Multiple sclerosis and nutrition. Arch Neurol 31:267-72, 1974; Agranoff BW, Goldberg D. Diet and geographical distribution of multiple sclerosis. Lancet 2:1061-66, 1974).

Supplementation with linoleic acid may be beneficial.

Review Article: Data from 3 double-blind trials of linoleic acid in pts. with a remitting-relapsing course were analyzed to determine whether inconsistency in the results was due to a relationship between pt. characteristics and treatment response. The combined data consisted of neurologic assessments over 2 1/2-year trials for 87 treated pts. and 85 control patients. Treated pts. with minimal or no disability at entry had a smaller increase in disability than did controls (p>0.05). In addition, treatment reduced the severity and duration of relapses at all levels of diasability and duration of illness at entry to the trials. The authors suggest that treatment benefits compared to controls may have failed to demonstrate the full extenf of potential benefits as oleic acid, the placebo used, may itself ameliorate MS-like illness (Dworkin RH et al. Linoleic acid and multiple sclerois; A reanalysis of three double-blind trials, Neurology 34:1441-45, 1984; Dworkin RH. Linoleic acid and multiple sclerosis. Lancet 1:1153-4, 1981).

Note: David Horrobin has suggested that the results of these studies were not optimal due to inadequate dosages and the use of dyes which his group has shown to block the conversion of EFA's to prostaglandins (Horrobin D. Multiple sclerosis; The rational basis for treatment with colchicine and evening primrose oil. Med Hypotheses 5:365-78, 1979).

Supplementation with safflower oil (high in linoleic acid) may be beneficial.

Experimental Double-blind Crossover Study: 20pts. received daily doses of safflower oil (high in plyunsaturates) for 5 wks. and daily doses of olive oil (low in oplyunsaturates) for 5 weeks. Only the safflower oil diet appeared to help some of the pts. (Utermohlen, Virginia, nutrition scientist at Cornell University - reported in Science 9/4/82).

In the event that there is a block in the conversion of linoleic acid to GLS, supplementation with evening primrose oil, which has a high concentration of GLA, may be beneficial.

Experimental and Observational Study: 16 pts. were found to have abnormal blood theology (whole blood filterability) and were supplemented with primrose oil 4 gm daily. After 3 wks., both blood rheologyand hand grip strength were improved, suggesting that there was improved capillary perfusion in muscles (Simpson LO et al. Dietary supplementation with Efamol and multiple sclerosis. N Z Med J 98 (798):1053-54, 1985).

Experimental Study: Electrophoretic mobility studies of red cells from MS pts. indicate that treatment with unsaturated fatty acids must continue for at least 2 yrs. before normal reactivity is restored. Assuming htis also applies to myelin, clinical trials need to last longer than 2 yrs. if treatment is to be effective (Field EJ, Joyce G. Multiple sclerosis; Effect of gamma-linolenate administration upon membranses and the need for extended clinical trials of unsaturated fatty acids. Eur Neurol 22:78, 1983).

Experimental Study: 8 seriously disabled pts. were assessed using the Kurtzke disability score, the B-M manual dexterity test and a dynamometer and were treated with undyed EPO in capsules. After 6 mo., 3 showed some improvement onthe Kurtzke score. While there was no improvement in grip strength, there was a significant improvement in manual dexterity (Horrobin DF. Multiple sclerosis; The rational basis for treatment with colchicine and evening primrose oil. Med Hyporheses 5:365-78, 1979).


Supplementation may be beneficial.

Experimental Double-blind Study: 12 men and 38 women were treated with DPA and TENS (transcutaneous electrical nerve stimulation). 49/50 improved. Improvements included better bladder control, greater mobility and less depression (Winter A. New treatment for multiple sclerosis. Neurol Orthoped J Med Surg 5:1, April 1984).


Suplementation may be beneficial.

Experimental Study: 12 pts. received tryptophan. After 30 days, there was a modest improvement in mood and neurological symptoms (Hyyppa MT et al. Effect of L-tryptophan treatment on central indoleamine metabolism and short-lasting neurologic disturbances in multiple sclerosis. J Neural Trans 37:297-304, 1975).


Case Reports: Pts. improved following daily supplementation (much of it by injection) of massive doses of various B compex vitamins, vitamin C, vitamin E, choline, lecithin, magnesium, calcium gluconate and pantothenate, aminoacetic acid-glycine, adenosine-5-monophosphoric acid and crude liver (Klenner FR. Response of peripheral and central nerve pathology to mega-doses of the vitamin B-complex and other metabolites. J Appl Nutr 25:16-40, 1973).

Experimental Study: 15 pts. received intraspinal B1 and B6 injections combined with mixed tocopherols and vitamin B complex orally. 4 of the 6 pts. with advanced disease improved, and 1 of them relapsed after stopping all vitamin therapy for 1 year. Arrest of the progress of the disease was noted in the other 9 cases with improvement in symptoms, recession of neurologic signs and diminuition of reflex overactivity (Stone S. Pyridoxine and thiamine therapy in disorders of the nervous system. Dis Nerv Sys 11:131-138, 1950).


Rule out food sensitivities.

Review Article: Literature suggesting that MS may be caused by an allergic or other adverse reaction to certain foods, mostly cocoa products, cola and coffee is reviewed. Epidemiology studies have documented a correlation between high cocoa consumption and high MS incidence. When cocoa is introduced to an area, MS incidence rises sharply. Some dogs develop muscle weakness, twitching, loss of sphincter function and myocardial damage when fed chocolate. Cases are reported in which chocolate ingestion by MS pts. was followed by exacerbations (Maas AG, Hogenhuis LAH. Multiple sclerosis and possible relationship to cocoa; A hypothesis. Ann Allergy 59:76-79, 1987).

Observational Study: In a survey of about 2600 pts. in the US, the incidence of MS correlated most strikingly with milk consumption. A similar correlation was found in 21 other countries (Agranoff B, Goldberg D. Diet and the geographical distribution of multiple sclerosis. Lancet 2:1061-66, 1974).

Observational Study: In a survey of 2000 pts. with MS and related diseases, those with the most severe cases were food sensitive, those with moderate symptoms were sensitive to molds or fungi, and the least affected were strongly sensitive to pollens (Jonez HD. Calif Med 79:376-80, November, 1953).

Rule out mercury amalgam toxicity.

There is an epidemiological correlation between multiple sclerosis and dental caries.

Observational Study: Death rates from MS were " linearly related to the numbers of decayed, missing and filled teeth in six Australian and 48 American states and in 45 Asian and European countries," suggesting that dental caries "may be a precursor of one form of MS" (Craelius W. Comparative epidemiology of multiple sclerosis and dental caries. J Epidemiol Comm Health 32:155-65, 1972).

The correlation between multiple sclerosis and rates of dental caries may be due to the placement of mercury amalgams.

Theoretical Discussion: When silver amalgam fillings are exposed to gingival action and oxidation, inorganic mercury in the fillings (especially class V fillings and root canals) may be converted to an organic form which may act as a neurotoxin (Ingalls TH, Epidemiology, etiology and prevention of multiple sclerosis. Am J Forensic Med Pathol 4:55-61, 1983).

Case Report: The author, an MS pt., was found to have lead toxicity (lead line in his gums, positive blood and urine studies) 4 yrs. after symptom-onset. Extraction of a suspicious tooth showed it to be grossly blackened form its amalgam interior, and a biopsy section of the adjacent gingiva stained for heavy metal depositions. Recently he abruptly developed diplopia following the pulverising of 50-year-old amalgam fillings which, he is convinced, was due to released mercuty vapor which reached the oculomotor nerves (probably via the mandibular branch of the trigeminal)(Ingalls TH. Triggers for multiple sclerosis. Letter. Lancet 2:160, 1986).

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