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Multiple Sclerosis

Multiple Sclerosis

Description

Multiple sclerosis (MS) is a disease of the nervous system that can affect the brain, spinal cord and optic nerves. It involves damage to the myelin sheath which surrounds the nerve and enhances electrical transmission of the nerve impulse. When damaged, the myelin sheath becomes hardened and "sclerotic" plaques form where the myelin used to be, hence the name multiple sclerosis.

The result of this damage is a syndrome of progressive neurological disturbances usually occurring early in life. MS has been recognized since the description by Charcot in 1868. MS is an intriguing condition in that, despite much research, no coherent theory accounts for all the fascinating and provocative evidence about the epidemiology, cause and development of MS. Most current work relates to immune disturbances and autoimmunity.

Epidemiology
In about two-thirds of the cases, onset is between 20 and 40. Rarely is the onset after 50. Women have a slightly higher risk than males (60% female:40% male). One of the very interesting features of MS is the geographic distribution of the disease. Areas with the highest prevalence are all located in the higher latitudes, in both the northern and southern hemispheres. These high risk areas include the northern United States and Canada, Great Britain, Scandinavia, northern Europe, New Zealand, and Tasmania. There are interesting exceptions to this geographic distribution as the disease in uncommon in Japan at any latitude.

It appears the initial event in the development actually occurs in early life. This statement is based on the observation that people who move from a low-risk area to a high risk area before adolescence acquire a high risk of developing MS, whereas those who make the same move after adolescence retain their low risk.

There are many possible reasons for the geographic distribution of MS. Obviously such things as solar exposure, genetics, diet, and other environmental factors quickly come to mind. All of these factors appear to have some rationale as contributing factors in the development of MS and are discussed below in the etiology section.

Causes

The cause of MS remains to be definitively determined. Many causative factors have been proposed, but the data to support theories linking these factors to MS are fragmentary and indirect. The following discussed etiological theories represent only a fraction of the possible explanations as to the cause of MS.

Viruses and MS
Viruses cause several diseases in humans and animals that are quite similar to MS. The virus-associated demyelinating disease seen most commonly is postinfectious encephalomyelitis. This disease starts 10 to 40 days after an acute viral infection or after an immunization. Progressive multifocal leukoencephalopathy and subacute sclerosing panencephalitis are other human demyelinating diseases caused by a virus, respectively: human papovavirus and the measles virus. In animals, many viruses are capable of producing demyelination.

The studies, when looked at collectively, have clearly demonstrated the demyelination can occur as a result of viral infection. The demyelination may be direct viral lysis of the myelin-producing Schwann cell, or viral infection leading to auto-immunity. In addition, a viral infection may lead to alteration in the balance of suppressor to helper T cells which may promote immune-mediated demyelination. All of this information has indicated to many that MS has a viral cause. However, viruses that have been isolated from cultures of material from patients with multiple sclerosis most likely have represented contaminants rather than causal agents.

Viruses isolated include: rabies virus, herpes simplex virus, scrapie virus, subacute myelo-opticoneuropathy virus, parainfluenza virus, measles virus and coronavirus.

Laboratory evidence has also pointed to several viruses and in particular the measles virus. In 1962, Adams and Imagawa reported that the sera of patients with multiple sclerosis had elevated measles antibody titers. Subsequent studies confirmed this association and also demonstrated that patients with MS had central nervous system synthesis of measles antibody. Based on this data, MS was at one time believed to due to an ongoing measles infection. This view has been modified by more recent studies indicating a high percentage of patients with MS have elevated cerebrospinal fluid antibody levels to two or more viruses. More importantly, studies have shown the measles-specific antibody in MS patients accounts for only a small percentage of the total antibodies.

The cerebrospinal fluid of most MS patients contains an elevated level of antibody in a pattern characteristic of an infectious process. One hypothesis states this pattern is in fact due to an unrecognized infectious agent that causes MS. This hypothesis has been termed the "sense antibody" hypothesis. An alternative hypothesis states MS does not represent an infectious disease and all the antibody in the central nervous system is nonspecific or "nonsense antibody." At present, the data available does not support a common infectious agent as the antigen for the increased antibody. Hyperactivity of circulating lymphocytes during acute attacks is thought to be the responsible factor for the excessive antibody production within the CNS.

Autoimmune factors
The lesions of MS are mimicked by those of experimental allergic encephalomyelitis (EAE), an autoimmune disease induced in animals by immunization with myelin. However, in EAE, T lymphocyte sensitivity is to a single antigen, i.e., myelin basic protein. While in MS, sensitivity to myelin basic protein cannot be demonstrated. This indicates that if MS is an autoimmune condition it is due to some other antigen. Attempts to find an antigen to which only MS patients react have failed.

A variety of immune system abnormalities have been reported in MS patients that would seem to support an autoimmune etiology. During acute episodes, suppressor T-cell levels have been shown to fall just prior to attacks and rise when the attack ends. Loss of suppressor cell activity could permit a latent autoimmune condition to become active. However, if this were the case, evidence of other autoimmune diseases would be expected to manifest themselves at this time as well. An alternative explanation is that the changes in the T-cell suppressor activity during acute attacks may be secondary to viral suppression.

Diet and multiple sclerosis
Many researchers have attempted to correlate various dietary patterns and the geographic distribution of MS. Diets high in gluten and milk are much more common in areas where there is a high prevalence of MS. As intriguing as these associations are, there is little support for them in clinical trials. In contrast, there is support for the role that dietary fat plays as a cause of MS.

Some of the first investigations into diet and MS centered around trying to explain why inland farming communities in Norway had a higher incidence of MS than areas near the coastline. It was discovered the diets of the farmers were had much higher levels of animal and dairy products than the diets of the coastal dwellers. Since animal and dairy products contain much more saturated fatty acids and less polyunsaturated fatty acids than fish, it was only natural for researchers to explore this association in greater detail. Subsequent studies upheld an extremely strong association between a diet rich in animal and dairy products and a higher incidence of MS.

Excessive lipid peroxidation
Many studies have demonstrated reduced glutathione peroxidase (GSH-Px) activity in the erythrocytes and leukocytes of patients affected by multiple sclerosis. As GSH-Px is intricately involved in the protection of cells from free radical damage, a decreased activity level would leave the myelinated sheath particularly sensitive to lipid peroxidation. GSH-Px is found in two forms, a selenium dependent enzyme and a non-selenium dependent enzyme. Since low selenium areas often overlap high prevalence areas for MS, it is only natural to assume there may be a correlation between selenium levels, GSH-Px activity, and MS. Initial studies seemed to support this correlation. However, subsequent studies indicated the reduced GSH-Px activity found in MS patients is independent from the selenium concentration and probably is due to genetic factors.

There appears to be genetic variability in the level of GSH-Px in individuals. In regards to MS, there appears to be an increased occurrence in individuals who inherently possess low GSH-Px activity (GSH-PxL) when compared to those individuals possessing high GSH-Px activity (GSH-PxH).

Treatment
There is no current standard medical treatment of MS, although during acute phases of the illness corticosteroids may offer some benefit. Research is investigating several immunosuppressive compounds that appear promising. Recently there has been renewed interest in the use of hyperbaric oxygen in the treatment of MS. While most studies have been poorly designed or simply anecdotal, a preliminary controlled study indicated hyperbaric oxygen treatment may have a mild therapeutic effect. This was especially true in mild or new cases.

Signs & Symptoms

Symptoms of Multiple Sclerosis may be so mild as to go unnoticed, or extremely severe. Furthermore, symptoms may be difficult to describe by the individual.

Primary symptoms
Weakness
Paresthesia
Visual impairment
Incoordination
Vertigo
Sphincter muscle impairment

Ocular disturbances including
Optic neuritis
Diplopia
Blurred vision
Sudden loss of vision in one eye

Muscular dysfunction such as
Weakness
Variable paralysis
Spasticity
Hyperreflexia
Intention tremor
Gait ataxia

Urinary disturbances
Incontinence
Frequent need to urinate
Urgency to urinate
Frequent infections

Emotional disorders:
Mood swings
Euphoria
Irritability
Depression

Speech difficulties
Dizziness
Nausea
Vomiting

Nutritional Supplements

Structure & Function:
        Antioxidants &
        Essential Fatty Acids


---------------------------------
General Supplements
---------------------------------

Adult
B complex*
DHEA*
EPO*
Flax seed oil 10 - 20 grams
Fish oils 2 - 3 grams
Pancreatic enzymes
Selenium 200 mcg
Vitamin E400 - 800 IU.
Wheat germ oil concentrate 1 - 4 perles.



* Please refer to the respective topic for specific nutrient amounts.

Discussion:-

Flax seed oil

Flax seed oil provides both essential fatty acids, linoleic and alpha-linolenic acid, and appears to be the most suitable oil for supplementation. Other oils such as safflower, sunflower, and soy contain primarily linoleic acid with very little alpha-linolenic acid. Linoleic acid supplementation has been investigated in three double-blind trails in the treatment of MS. Combined analysis of these studies indicated patients supplementing with linoleic acid had a smaller increase in disability, and reduced severity and duration of relapses than controls.

In these studies, a sunflower seed oil emulsion was used to provide a total daily dose of 17.2 grams linoleic acid.

Although originally thought to overcome an essential fatty acid deficiency, it appears linoleic acid supplementation lessens the immune response against the myelin. It is interesting to note linoleic acid is quite successful in the treatment of experimental allergic encephalomyelitis (EAE) in animals, a condition that mimics MS quite closely.

Fish oils - Eicosapentaenoic acid (EPA)

Supplementation with marine lipids provides the fatty acids eicosapentaenoic and docosohexaenoic acid which can be incorporated into the myelin sheath and other membranes, thereby increasing the fluidity and improving neural transmission. The presence of these two oils in fish could be responsible for the lower rate of MS observed in northern coastal areas when compared to inland farming areas.

With advances in our knowledge of essential fatty acids since Dr. Swank's original work in the 1940s, a selection of gamma linolenic acid sources may also be beneficial. These include black currant, borage and primrose oils as well as spirulina.

Pancreatic enzymes

The health of the alimentary tract may be crucial in MS. Pancreatic enzymes and probiotics e.g. FOS have produced good results, especially in Europe and Mexico.

Selenium

Selenium is a potent antioxidant that may prevent some of the excessive lipid peroxidation occurring in MS. It functions in the role as the mineral portion in the free radical scavenging enzyme glutathione peroxidase. This enzyme is reduced in many patients with MS. While selenium will not increase activity of this enzyme in the majority of patients with MS, it is a relatively inexpensive supplement that may benefit some individuals with MS.

Selenium may form part of a multi-mineral, as magnesium, manganese and zinc have also been suggested.

Vitamin E

MS is characterized by excessive lipid peroxidation. Vitamin E acting as an antioxidant may prevent some of this damage from occurring. In addition, anytime the intake of polyunsaturated fatty acids occurs, the physiologic need of vitamin E is increased.

Wheat germ oil concentrate

Rich in octacosanol, essential fatty acids and vitamin E, wheat germ oil concentrate is an appropriate supplement for individuals with MS.

Note: All amounts are in addition to those supplements having a Recommended Dietary Allowance (RDA). Due to individual needs, one must always be aware of a possible undetermined effect when taking nutritional supplements. If any disturbances from the use of a particular supplement should occur, stop its use immediately and seek the care of a qualified health care professional.

Dietary Considerations

The Swank low-fat diet for the treatment of MS. A Portland, Oregon physician, Dr. Roy L. Swank has provided convincing evidence a diet low in saturated fats maintained over a long period of time tends to retard the disease process and reduce the number of attacks. Swank began successfully treating MS patients with a low-fat diet in 1948. Swank's diet recommends a saturated (animal) fat intake of no more than 10 gm. per day and daily intake of 40 to 50 gm. of polyunsaturated (vegetable) oils with at least 1 tsp. of cod liver oil daily. Margarine, vegetable shortening, hydrogenated oils were disallowed (The beneficial effects of essential fatty acid supplementation is discussed in the nutritional supplements section).

Protein is kept at normal levels, however, a diet low in saturated fats significantly restricts such sources of protein as meat. In contrast, fish consumption appears to be particularly indicated due to the high amounts of the beneficial fish oils eicosapentaenoic and docosohexaenoic acid, and its excellent protein content. Swank recommends consuming fish three or more times a week. Mackerel, salmon and other cold water fishes are particularly good sources of these beneficial oils.

For further information regarding Swank's dietary protocol please consult "The Multiple Sclerosis Diet Book".

Homeopathic Remedy

1.* Aurum muriaticum - 30C use long term
2.* Tarantula hispanola - 30C long term
3. Conium maculatum - 30C
4. Plumbum metallicum - 30C

Sclerosis familial tubular

1. Artemesia abrotanum - 30C proving by Dr. Robert Brown, November, 1993 - patient a 32 year old female from Waco, Texas - lesion (bony) on hands and in brain causing seizures.

Treatment Schedule

Doses cited are to be administered on a 3X daily schedule, unless otherwise indicated. Dose usually continued for 2 weeks. Liquid preparations usually use 8-10 drops per dose. Solid preps are usually 3 pellets per dose. Children use 1/2 dose.

Legend

X = 1 to 10 dilution - weak (triturition)
C = 1 to 100 dilution - weak (potency)
M = 1 to 1 million dilution (very strong)
X or C underlined means it is most useful potency
Asterisk (*) = Primary remedy. Means most necessary remedy. There may be more than one remedy - if so, use all of them.

References

Boericke, D.E., 1988. Homeopathic Materia Medica.

Coulter, C.R., 1986. Portraits of Homeopathic Medicines.

Kent, J.T., 1989. Repertory of the Homeopathic Materia Medica.

Koehler, G., 1989. Handbook of Homeopathy.

Shingale, J.N., 1992. Bedside Prescriber.

Smith, Trevor, 1989. Homeopathic Medicine.

Ullman, Dana, 1991. The One Minute (or so) Healer.

Herbal Approaches

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Herbs
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Ginkgo biloba
Ginseng

Note: The misdirected use of an herb can produce severely adverse effects, especially in combination with prescription drugs. This Herbal information is for educational purposes and is not intended as a replacement for medical advice.

Discussion:

Dr. Bernard Jensen offers a recipe to feed the myelin sheath: 1/3 cup of chlorophyll with an egg yolk.

Other common recommendations are herbs that relax the nervous system e.g. Lobelia, Skullcap and Valerian.

It is always worth attempting to detoxify the system with herbs like: Burdock, Dandelion, Pau d'arco and Yarrow.

Contraindications:

Although evidence is slight, it is always better to err on the side of caution.

Progressive conditions (e.g. multiple sclerosis and lupus as well as auto-immune disorders, including AIDS) are considered by some authorities to warrant a warning against the use of echinacea.

More research is needed to ascertain whether the whole extract, or which part, has this effect and if it translates to the clinical situation.

Certainly, echinacea seems to be most effective in short term usage and loses its effectiveness over the longer term. This is incosistent with a chronic condition, like MS.

References:

Blumenthal, M. German Commission E Monograph for Echinacea purpurea herb. HerbalGram, 1994, 30:48.

Bodinet, C. et al: Host resistance increasing activity of root extracts from Echinacea species. Planta Med. 1993, 59(Supp): A672.

Bukovsky M et al., [Immunomodulating activity of ethanol-water extracts of the roots of Echinacea gloriosa L., Echinacea angustifolia DC. and Rudbeckia speciosa Wenderoth tested on the immune system in C57BL6 inbred mice] Cesk Farm, 1993 Aug, 42:4, 184-7.

DeSmet, P. et al. (Eds.), Adverse Effects of herbal Drugs 2. Springer Verlag, Berlin, 1994.

Lersch C et al., Nonspecific immunostimulation with low doses of cyclophosphamide (LDCY), thymostimulin, and Echinacea purpurea extracts (echinacin) in patients with far advanced colorectal cancers: preliminary results. Cancer Invest, 1992, 10:5, 343-8.

Luettig B et al., Macrophage activation by the polysaccharide arabinogalactan isolated from plant cell cultures of Echinacea purpurea. J Natl Cancer Inst, 1989 May 3, 81:9, 669-75.

Mengs U et al., Toxicity of Echinacea purpurea. Acute, subacute and genotoxicity studies. Arzneimittelforschung, 1991 Oct, 41:10, 1076-81.

See DM et al., In vitro effects of echinacea and ginseng on natural killer and antibody-dependent cell cytotoxicity in healthy subjects and chronic fatigue syndrome or acquired immunodeficiency syndrome patients.

Wichtl, M. Herbal Drugs & Phytopharmaceuticals. CRC, Boca Raton, 1994.

Aromatherapy - Essential Oils

Juniper Essence,Pine Essence,
Spruce Essence.



Related Health Conditions

Allergy
Amyotrophic Lateral Sclerosis (ALS)
Auto-Immune Disorders
Depression
Diplopia
Dizziness
Fatigue
Infection
Myopathy
Neuromuscular Degeneration
Pregnancy
Stress
Vomiting

Abstracts

References

Aberg, J. A. et al: Prostaglandin Production in Chronic Progressive Multiple Sclerosis. The Journal of Clinical Laboratory Analysis, 1990;4:246-250.

Agranoff, B.W. & D. Goldberg D. Diet and the geographical distribution of multiple sclerosis. Lancet ii:1061-6, 1974.

Alter, M., M. Yamoor & M. Harshe. Multiple sclerosis and nutrition. Archives of Neurology 31:267-72, 1974.

Arria, A.M. et al: Vitamin E and neurologic function in adults with chronic cholestatic liver disease. J. Am. Coll. Nutr. 1987, 6(5): 442. (Abstract)

Baker, A.B. : Treatment of paralysis agitans with vitamin B6 (pyridoxine hydrochloride). JAMA. 1941, 116: 2,484-2,487.

Bates, D., P. Fawcet, D. Shaw & D. Weightman. Polyunsaturated fatty acids in the treatment of acute remitting multiple sclerosis. British Medical Journal II:1390-1, 1978.

Botez, M.I. et al: Polyneuropathy and folate deficiency. Arch. Neurol. 1978, 35: 581-584.

Brin, M.F. et al: Blind loop syndrome, vitamin Emalabsoprtion and spinocerebeller degeneration. Neurology, 1985, 35(3): 338-342.

Butcher, P.J. Milk consumption and multiple sclerosis - an etiological hypothesis. Medical Hypothesis 19:169-178, 1986.

Carroll, J.E. et al : Carnitine intake and excretion in neuromuscular diseases. Am. J. Clin. Nutr. 1981, 34: 2,693-2,698.

Dennis, S. & Clark, J.B. : The synthesis of glutamate by rat brain mitochondria. J. Neurochem. 1986, 46: 1,811-1,819.

Dworkin, R.H., D. Bates, J. Millar & D. Paty. Linoleic acid and multiple sclerosis: a reanalysis of three double-blind trials. Neurology 34: 1441-5, 1984.

Ellison, G.W., B. Visscher, M. Graves & J. Fahey. Multiple sclerosis. Annals of Internal Medicine 101:514-526, 1984.

Esparza ML et al., Nutrition, latitude, and multiple sclerosis mortality: an ecologic study. Am J Epidemiol, 1995 Oct 1, 142:7, 733-7.

Fawcett J et al., Use of alternative health therapies by people with multiple sclerosis: an exploratory study. Holist Nurs Pract, 1994 Jan, 8:2, 36-42.

Fischer, B.H., M. Marks & T. Reich. Hyperbaric-oxygen treatment of multiple sclerosis. New England Journal of Medicine 308:181-6, 1983.

Folkers, K. et al: Biochemical rationale and the cardiac response of patients with muscle disease to therapy with coenzyme Q10. Proc. Ntnl. Acad. Sci. 1985, 82(13): 4,513-4,516.

Garruto, R.M. et al: Low-calcium, high-aluminum diet-induced motor neuron pathology in cynomolgus monkeys. Acta Neurop. (Berlin). 1989, 78(2): 210-219.

Guggenheim, M.A. et al: Progressive neuromuscular disease in children with chronic cholestasis and vitamin E deficiency: diagnosis and treatment with alpha tocopherol. J. Pediatrics, 1982, 100(1): 51-58.

Harding, A.E. et al : Spinocerebeller degeneration associated with a selective defect of vitamin E absorption. NEJM. 1985, 313(1): 32-35.

Hewson, D.C. Is there a role for gluten-free diets in multiple sclerosis. Human Nutrition: Applied Nutrition 38A:417-20, 1984.

Jonez, H. D: Management of Multiple Sclerosis. Postgraduate Medicine, May 1952;2:415-422.

Kasarskis, E. et al: Malnutrition in amyotropic lateral sclerosis patients. J. Am. Coll. Nutr. 1991, 105(5): 548. (Abstract)

Kirschmann, J.D. 1990. Nutrition Almanac: Nutrition Search. McGrew-Hill: New York.

Krause, Marie V. & Martha A. Hunscher. Food, Nutrition And Diet Therapy. Philadelphia: W.B. Saunders Co., 1972.

Lane, R.J.M. et al: An abnormality of glycine metabolism in ALS patients. J. Neurol. Neurosurg. Psychiat. 1990, 52: 180.

Lauer K: The risk of multiple sclerosis in the U.S.A. in relation to sociogeographic features: a factor-analytic study. J Clin Epidemiol, 1994 Jan, 47:1, 43-8.

Lindegard, B. Aluminum and Alzheimer's disease. Lancet, 1989, 1: 267-268. (Letter)

Lindenbaum, J. et al: Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. NEJM. 1988, 318: 1720-1728.

Mai, J. et al: High Dose Antioxidant Supplementation to MS Patients: Effects on Glutathione Peroxidase, Clinical Safety, and Absorption of Selenium, , Biological Trace Element Research, 1990;24:109-117.

Mazzella, G.L., E. Sinforiani, F. Savoldi, et al: Blood cells glutathione peroxidase activity and selenium in multiple sclerosis. European Neurology 22:442-6, 1983.

Meydani, M. et al: Efficacy of dietary vitamin E and selenium on suceptibility of brain regions to lipid peroxidation. Lipids, 1988, 23: 405-409.

Murray, M.T., & J.E. Pizzorno. 1991. Encyclopedia of Natural Medicine. Rocklin, Ca; Prima Publishing.

Millar, J.H.D., K.J. Zilkha, M.J.S. Langaman, et al: Double-blind trial of linoleate supplementation of the diet in multiple sclerosis. British Medical Journal i:765-8, 1973.

Paty, D.W., H.K. Cousin, S. Read & K. Adlakkha. Linoleic acid in multiple sclerosis: failure to show any therapeutic benefit. Acta Neurologica Scandinavia 58:53-8, 1978.

Petersdorf, R.G. & R.D. Adams. 1983. Harrison's Principles Of Internal Medicine. 10th ed. McGraw Hill Pub Co., New York. 2212 pp.

Pincus, J.H. : Folic acid deficiency: a cause of subacute combined system degeneration. In: Botez, M.I. & Reynolds, E.H. (Eds): Folic Acid in Neurology, Psychiatry and Internal Medicine, Raven Press, NY, 1979.

Plaitakis, A. & Caroscio, J.T.: Abnormal glutamate metabolism in amyotrophic lateral sclerosis. Ann. Neurol. 1987, 22: 575-579.

Robbins, S.L. & R.S. Cotran. 1979. Pathologic Basis of Disease. 2nd ed. Saunders Pub Co., Philadelphia. 1598 pp.

Shamberger, R. J Selenium and the Antioxidant Defense System. Journal of Advancement in Medicine, Spring 1992;5(1):7-19.

Shukla, V.K.S., G.E. Jensen & J. Clausen. Erythrocyte glutathione peroxidase deficiency in multiple sclerosis. Acta Neuro Scand. 56:542-50, 1977.

Sokol, R.J. et al: Frequency and clinical progression of the vitamin E deficiency neurologic disorder in children with prolonged neonatal cholestasis. Am. J. Dis. Children, 1985, 139(12): 1,211-1,215.

Sokol, R.J. et al: Improved neurologic function after long-term correction of vitamin E deficiency in children with chronic cholestasis. NEJM. 1985, 313(25): 1,580-1,586.

Spies, T.D. et al: Some recent advances in vitamin therapy. JAMA. 1940, 115(4): 292-297.

Spies, T.D. & Vilter, R.W. : A note on the effect of alpha-tocopherol (vitamin E) in human nutrition. South. Med. J. 1940, 33: 663.

Swank, R.L. Multiple sclerosis: twenty years on low fat diet. Archives of Neurology 23:460-74, 1970.

Swank, R.L. & M.H. Pullen. The Multiple Sclerosis Diet Book. Doubleday, Garden City, NY 1977.

Swank, R.L. Multiple sclerosis: a correleation of its incidence with dietary fat. American Journal of Medical Sciences 220:421-30, 1950.

Swank, R.L. & Bourdillon: Multiple Sclerosis: assessment of treatment with a modified low-fat diet. J. Nerv Ment. Dis. 1960, 131:468-488.

Swank, R.L. Multiple Sclerosis: twenty years on a low fat diet. Arch. Neurol. 1970, 23:460-474.

Swank, R. L. & Dugan, B.B.: Effect of Low Saturated Fat Diet in Early and Late Cases of Multiple Sclerosis. The Lancet, July 7, 1990;336:37-39.

Swank, R. L. Multiple Sclerosis: the lipid relaitonship. Am. J. Clin. Nutr. 1988, 48:1,387-1,393.

Swank, R.L. MS: Fat-oil relationship. Nutrition, 1991, 7:368-376.

Walji, H. 1992. Vitamin Guide: Essential Nutrients for Healthy Living. Rockport, MA: Element, Inc.

Wechsler, I.S.: The treatment of amyotrophic lateral sclerosis with vitamin E (tocopherols). Am. J. Med. Sci. 1940, 200: 765-778.

Weinreb, H.: Preliminary Trial of Colchicine in Progressive Multiple Sclerosis, Annals of Neurology, July 1986;20(1):165-166.

Weinreb, H.: Intravenous Colchicine in Chronic Progressive Multiple Sclerosis. Neurology, March 1989;39(Suppl. 1):318/PP462.

Weinreb, H.: Clinical Protocol For The Use of Intravenous Colchicine in Multiple Sclerosis. Correspondence, September 25, 1990.

Yasui, M. et al: Magnesium Concentration in Brains From Multiple Sclerosis Patients. ACTA Neurol. Scand., 1990;81:197-200.