Alternative Therapies for Multiple Sclerosis ©

By David Steenblock, M.S., D.O.

This review is for educational purposes only and is not intended to be a substitute for your physician's advice.

In animals studies, corticosterone significantly reduces the proliferation of oligodendrocyte precursors throughout the white and gray matter regions of the brain (2). Since oligodendrocyte precursors play a major role in remyelination, the use of anti-inflammatory therapies may actually perpetuate depression as well as brain injury. In contract to the use of steroids for treating MS, stem cell therapies promote the proliferation of new oligodendrocytes, with the secondary benefit of alleviating depression. Generally, depression clears within 30 days following CD34+ stem cell transplantation.

Methylation and Multiple Sclerosis

Folate and vitamin B12 deficiencies (methylcobalamin has greater neurological importance than cyanocobalamin) can cause neurologic and psychiatric disturbances, including depression, dementia, and demyelinating myelopathy (9). In most cases, folate and methylcobalamin injections improve MS symptoms and prevent relapses. Treatment with additional methyl donors such as S-adenosylmethionine, betaine, or methionine can also relieve depression and promote remyelination in patients with inborn errors of folate metabolism (8).

A Comprehensive Program for MS

Stem cells seem to have the ability to greatly assist in regenerating the glial cells injured and destroyed in MS. Other wholistic approaches such as anti-virals, growth factors, antioxidants, nutritional therapies, and heavy metal detoxification should be helpful as well. Such a program could include stem cell injections while inflammation is present in the CNS (but not in other organs), followed by anti-virals, growth factors, antioxidants and nutrients to continue protecting the oligodendrocytes and axons from oxidative stress. Care must be taken for several months after stem cell administration to avoid products that inhibit neurogenesis and stem cell proliferation. Such products include cortisone, alcohol, and monosodium glutamate. Physical and emotional stress increases glucocosteroid release, and should also be avoided as much as possible.

Autoimmune Disease and Patterns of Relapsing-Remitting Episodes

The first two patterns of lesions observed in Lucchinetti's research were most common and resembled the autoimmune destruction observed in T-cell mediated and antibody-augmented forms of experimental autoimmune encephalomyelitis (13).

The Myelin Sheath

Myelin sheaths are formed around axons by spiraling plasma membranes of Schwann cells in the peripheral nervous system and oligodendrocytes in the central nervous system. Glycoproteins are prominent components of the plasma membranes and include protein zero and peripheral myelin protein-22 in peripheral nervous system myelin, myelin-associated glycoprotein located on the inside of sheaths in both the PNS and CNS and which functions in glia-axon interactions, and myelin-oligodendrocyte glycoprotein (MOG) located on the outside of CNS myelin sheaths. MOG appear to be an important target antigen in multiple sclerosis (70).

Autoimmune T-cell responses to myelin components are being investigated for their role in initiating and/or maintaining inflammatory responses resulting in myelin destruction. Myelin oligodendrocyte glycoprotein (MOG) is a myelin protein that in one study, elicits greater anti-MOG B-cell responses (38) in MS patient samples, and in another study, elicits similar T cell responses in MS patient samples and controls but with different cytokine activity. The MS samples elicited increased levels of TNF-alpha upon stimulation compared to the control samples (93). Tejada-Simon and associates found that MS patient MOG samples elicited anti-MOG antibodies reacting predominatly to the extracellular 1-60 region while control samples elicited anti-MOG antibody reactions to the transmembrane/cytoplasmic domains (residues 154-218) (89).

Autoimmune reactions have also been shown against cardiolipin (important in heart and brain mitochondrial function) and DNA in MS patients (80).

Patterns resembling Virus and Toxin-induced Immune Responses

Pattern IV was found only in patients with primary progressive disease and patterns III and IV both resembled viral or toxin-induced oligodendrocyte dystrophy.

Mercury Toxicity

Mercuric chloride is toxic at low concentrations to oligodendroglial cells, resulting in cell death through apoptosis. (34). Symptoms of mercury toxicity include chronic fatigue, depression, poor memory and cognitive function, emotional instability, peripheral numbness or tingling, decreased sensations of touch, hearing or vision, hypersensitivity and allergies, persistent infections including chronic yeast overgrowth, compromised immune function and cardiovascular disease (71). Mercury levels are often elevated in MS patients, and may result from a variety of sources.

1. Dental Amalgams . Though research findings are contradictory, Huggins found a change in cerebrospinal fluid proteins following dental intervention, using CSF photolabeling. Changes were seen in ceruloplasmin, transferrin, IgG heavy and light chains, Apo E, transthyretin and other proteins. Additional markers that can be used to monitor MS include CSF, S100B and Glial-Fibrillary Acidic Protein (GFAP) (32b). S100 B was found to be a good marker for relapsing MS and GFAP correlated with Disability Scales and may therefore be a marker for neurological damage (67).

2. Mercury contamination in fish and soil . Mercury is a major environmental concern, traditionally in freshwater fish and more recently because of the toxic effects on soil microorganisms. Those patients living near mercury emission sources are at greater risk of mercury contamination (58). Shark and Swordfish are reported to have the highest methyl mercury levels, and shrimp, scallops and salmon the lowest concentrations in ocean fish (31). Fish farms may not be safer than ocean fish. Fish farms may be producing fish with higher pesticide and mercury concentrations due to the use of contaminated feed sources (21).

3. Elevated insulin levels allow the cellular entry of heavy metals. Insulin is elevated by large meals, high sugar and refined carbohydrate diets, and oxidative stress. Antioxidants can help protect the cells from heavy metal toxicity.

4. Leaky Gut Syndrome can be caused by Candida endotoxins, alcohol, nutritional deficiencies,etc.which allows heavy metals and macromolecules to enter the bloodstream, causing immune and autoimmune responses, free radicals, and cell injury and death. An animal study by Keshavarzian and associates demonstrated that supplementation with oats prevented gut leakiness and endotoxin-induced liver damage (40).

Chelating factors in various foods can prevent mercury absorption, including citric acid, tartaric acid, and cysteine, (22), selenium (29), garlic (46), chlorella (also an anti-inflammatory) (101), and cilantro (64). Methyl mercury can bind with L-cysteine and be transported across the blood brain barrier. L-leucine inhibits this transport. A balanced leucine/cysteine ratio is found in whey protein (71). Calcium and magnesium are also protective against mercury and methyl mercury toxicity (81). EDTA oral and i.v. chelation methods are currently being promoted for the removal of mercury and methylmercury as well as other heavy metals. Since heavy metals can inhibit stem cell growth, chelation is advised before stem cell therapy. Oral DMSA is a proven generally safe and effective method for removing mercury and lead.