FREE REPORT -- Alternative Therapies for Multiple Sclerosis - 11-11-11

8/2/2019 FREE REPORT -- Alternative Therapies for Multiple Sclerosis - 11-11-11

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2011

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2011

Dr. Steenblock’s

Alternative Therapies forMultiple Sclerosis

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© 2011 by David A. Steenblock, D.O., Inc. All rights reserved.

DISCLAIMER: The use of stem cells or stem cell rich tissues as well as the mobilization of stem cells byany means, e.g., pharmaceutical, mechanical or herbal-nutrient is not FDA approved to combat aging orto prevent, treat, cure or mitigate any disease or medical condition mentioned, cited or described in anydocument or article on this website. This report and the information featured, showcased or otherwiseappearing in it is not to be used as a substitute for medical advice, diagnosis or treatment of any healthcondition or problem. Those who read this report should not rely on information provided in it for theirown health problems. Any questions regarding your own health should be addressed to your physicianor other duly licensed healthcare provider. This report and its authors, owners and sponsors make noguarantees, warranties or express or implied representations whatsoever with regard to the accuracy,completeness, timeliness, comparative or controversial nature, or usefulness of any informationcontained or referenced in it. This report and its authors, owners and sponsors do not assume any riskwhatsoever for your use of this document or the information posted herein. Health-related informationand opinions change frequently and therefore information contained in this report may be outdated,incomplete or incorrect. All statements made about products, drugs and such in this report have notbeen evaluated by the Food and Drug Administration (FDA). Use of this Website does not create anexpressed or implied professional relationship.



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Alternative Therapies for Multiple Sclerosis ©By

David Steenblock, M.S., D.O. and Lyn Darnell

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

advice.

Multiple Sclerosis (MS) is an inflammatory, autoimmune, demyelinating disease of the central nervoussystem that destroys myelin, oligodendrocytes, and axons (14). Oligodendrocytes are white matter cellsthat produce myelin for the myelin sheath, a protective covering around nerve fibers that speeds neuraltransmission. Axons are nerve fibers that conduct nerve impulses away from a neuron. Between 250,000- 350,000 people in the United States suffer from Multiple Sclerosis. The name relates to the multiplehardened (sclerotic) lesions and scars in the brain and spinal cord. Initial symptoms may include extremefatigue, vertigo, optic neuritis, and numbness in the extremities. Most patients experience relapsing-remitting episodes that over time can lead to progressive neurological deterioration.

MS lesions are found in various stages in MS, from new, active lesions to old but inactive lesions.Lucchinetti and associates analyzed MS tissues from human biopsies and autopsies and found fourdistinct lesion patterns. Therefore, four distinct causes may be involved in MS.

Pattern I showed autoimmune destruction mediated by T-cells and antibodies. Lesion edges weresharply demarcated and located around veins. Active demyelination was associated with inflammationbut also present was remyelination and the preservation of oligodendrocytes. In the injured myelinsheaths, all myelin proteins were lost at the same rate.

Pattern II lesions were the same as Pattern I but with the addition of IgG deposition and activatedcomplement.

Pattern III lesions were similar to viral or toxin-induced oligodendroycte dystrophy. Lesions were notaround veins and lesion borders were diffuse and irregular. Lymphocytes and activated myeloid cellswere detected but activated complements of IgG were not. The myelin sheaths showed a loss of Myelin

Oligodendrocyte Glycoprotein (MOG). Oligodendrocyte death from apoptosis was prominent.

Pattern IV lesions were similar to those of Pattern III, except oligodendrocyte death appeared necrotic.

In the 83 cases analyzed, pattern II lesions were most common and characteristic of relapsing, remittingdisease. Pattern IV lesions were found in patients with primary progressive disease and pattern IIIlesions were seen as "starter" lesions capable of converting to another pattern. Brain regions unaffectedby inflammation and neurons with intact myelin sheaths also showed axonal damage (13).



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In the central nervous system, microglia are tissue macrophages (immune cells) which have the ability toregulate and be regulated by immune cells (lymphocytes, macrophages, B cells) and stromal cells(neurons and glia). Microglia are found throughout the central nervous system and participate in theonset and progression of CNS inflammatory responses. Microglia, when activated, are highly damagingto CNS function through their production of neurotoxins, inflammatory cells (Inflammatory Protein-10,

Macrophage Inflammatory Protein-1, Macrophage Inflammatory Protein-2, C-C Chemokine Ligand 19,Monocyte Chemoattractant Protein-1, Monocyte Chemoattractant Protein-2) and immune cells thatproduce antibodies. Microglia direct inflammatory responses can result in the brain and spinal cordbeing infiltrated with immune cells against foreign invaders as well as T-cells that destroy myelinproteins. They also limit inflammation by producing neuroprotectants and immunosuppressive factors.

Whether activated microglia produce growth factors or neurotoxins such as nitric oxide and excessglutamate depends on the signals received from neurons, T cells, glia and macrophages (13). Thedestruction may be further enhanced by the presence of heavy metals, viruses and endotoxins. Thesefactors contribute to a downward cycle of local inflammation, demyelination and axonal damage, which

results in further inflammation, demyelination and axonal damage.

Current therapies for MS are designed to delay disease progression by immuno-modulation orimmunosuppression. Until recently, the persisting neurological damage has remained mostlyirreversible. Today, there is increased optimism about slowing and perhaps reversing the disease with acomprehensive program that includes therapies that improve blood circulation, myelin regeneration,cell energy production, gut normalization, and dietary, anti-inflammatory, antimicrobial, immune-modulating and antioxidant factors.

Improved Blood CirculationReduced oxygen levels are found in MS patients and those patients with advanced cerebral atrophyhave significantly reduced cerebral blood circulation and oxygen concentrations (114). Increasedischemia (lack of blood flow) and hypoxia (lack of oxygen) can contribute to a vulnerable blood-brainbarrier, allowing the entry of pathogens and toxins.

Hyperbaric (high pressure) oxygen improves the delivery of oxygen to damaged tissues in the brain andspeeds their repair. Pressurized oxygen offers the following benefits:

1. Increases oxygen delivery to injured cells and tissues.

2. Reduces swelling and inflammation.

3. Increases the formation of new blood vessels to injured tissue.

4. Improves wound healing.

5. Improves the body's resistance to infections.

http://www.strokedoctor.com/library/hyperbaric-oxygen-library/hyperbaric-review/87





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6. Renews damaged neurons and their axons and dendrites.

7. Speeds the elimination of toxins.

Most trials using hyperbaric oxygen for MS are for a month with higher pressures (1.75 - 2.5 ATA) butlonger treatments at low pressures (1.2-1.5 ATA) may be more effective in reducing hypoxia andischemia while reducing the risk of free radical generation caused by higher pressures. Long term HBOTwithin a comprehensive program that includes antioxidants may show more promise in promotingremission (46).

With hyperbaric oxygen therapy, the patient is placed in a chamber and breathes 100% oxygen by maskwhile the pressure in the chamber is increased to 1.5 - 2.0 times the normal atmospheric pressure. Thistherapy provides a significant increase in oxygen delivery to the brain compared with that received bybreathing air at normal pressure. Damaged brain tissue, either from immune attacks, infections, ortoxins, is also hypoxic tissue (lacking oxygen). Hyperbaric oxygen pushes oxygen into the plasma (theliquid portion of the blood) and from the plasma, the oxygen diffuses into the white and grey matter of

the brain, fights infection, reduces inflammation and speeds wound healing. Oxygen may also bebeneficial for myelin production at low pressures of 1.5 ATA or 1.5 times the atmospheric pressure atsea level by supporting neural stem cell differentiation and the production of oligodendrocytes. Wewould like to see more research done in this area, especially in combination with ECP.

External Counterpulsation (ECP) is a fairly new non-invasive alternative to heart surgery for someconditions of heart disease. ECP is FDA approved for the treatment of angina and congestive heartfailure. The device pumps blood from the legs back to the heart. In the process, ECP also increases theblood supply (and therefore increased oxygen and nutrients and the removal of waste products) toother organs such as the brain, liver and kidneys. (112,115) It has been our experience that ECP, in

combination with hyperbaric oxygen, improves brain function in patients with stroke and brain injuriesand may also prove to be beneficial in MS cases as well.

Stem cell therapies show great promise as a treatment for MS. However, the causes of myelindegeneration need to be addressed before the stem cells are given to maximize stem cell growth,migration, differentiation and renewed function.

Stem Cells and Multiple SclerosisCD34+

CD34 refers to an adhesion structure expressed on embryonic fibroblasts and nervous tissue. CD34+stem cells are primitive, undifferentiated cells of the embryo, bone marrow, umbilical cord blood andadult tissue that have the capacity to differentiate into hematopoietic cells as well as a variety of othercells, including neurons and glial cells.

http://en.wikipedia.org/wiki/Enhanced_external_counterpulsation





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The "First Cell" (fertilized egg) at the beginning of life is "totipotent," capable of generating every othercell of the body. When this First Cell divides into three embryonic layers (the ectoderm, mesoderm andendoderm), the daughter cells become "multipotent", able to transform into a variety of cell types, butunable to make an entire individual. CD34 (+) is a purified multipotent stem cell found in bone marrowand umbilical cord blood. These stem cells are capable of "homing" to an injured area where they move

into the tissue and proliferate into the specific cells needed to repair the tissue. CD34(+) cells, andespecially its CD133 subset, are capable of balancing the immune system as well as transforming intoneuroprotective glia and myelin-producing oligodendrocytes and astrocytes. Such potency makes CD34+stem cells a valuable treatment modality in immune disorders of the central nervous system such asMultiple Sclerosis.

Mesenchymal Stromal/Stem CellsMesenchymal stem cells are also multipotent cells, found in the bone marrow and umbilical cord blood.They are able to differentiate into adipocytes (fat cells), chondrocytes (cartilage making cells),

osteocytes (bone producing cells) and neuronal/glial cells when specific growth factors are used.Mesenchymal stem cells help M.S. by releasing growth factors that protect the nerves and stimulate thegrowth of new neurons. Mesenchymal stem cells help support the matrix that supports neurons andthey also reduce inflammation.

Dr. Fernando Ramirez is treating patients with umbilical cord blood derived CD34+ and mesenchymalstem cells in Tijuana, Mexico. To date, these treatments twice a year have been able to slow theprogression of M.S. and help people continue to work and be activ e.

Dr. Steenblock has done over 1,000 whole bone marrow treatments in which a person's ownCD34+ and mesenchymal stem cells are used for brain repair. Bone marrow blood is extracted from theleg and then transfused into the arm and bloodstream. Numerous patients with M.S. have shownimpressive responses following this procedure. It is, however, important that heavy metals, pesticides,viruses, etc. be eliminated before this treatment or any treatment to maximize the benefits of thecirculating stem cells.

Any reader who’d like to discuss whether an autologous (from self) stem cell -rich bonemarrow treatment would help their particular medical issues can do so by calling 1-800-300-1063 and setting up a phone consultation.

Also: Dr. Steenblock has developed an all natural stem cell mobilizer:www.stemgevity.com

http://stemcell.md/newsletters/nov2010.pdf


http://www.stemgevity.com/






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Remyelination StudiesSince 1965, scientists have observed spontaneous myelin repair. However, the many factors involved inpromoting a more profound repair than what occurs naturally and maintaining that repair are still beinginvestigated.

In the relapsing-remitting pattern, some remyelination is observed. Spontaneous remyelination isthought to be caused by previously quiescent oligodendrocyte progenitor cells rather than matureoligodendrocytes. Platelet-derived growth factor has been found to stimulate the multiplication andgrowth of these oligodendrocyte progenitor cells.

In the progressive degeneration pattern, oligodendrocytes are destroyed. Implants of oligodendrocyteprogenitor cells into MS patients have been successful. However, while Schwann cells also promoteremyelination, their implants have a greater risk of fibroblast overgrowth that subsequently can destroyaxonal pathways. Glial cell implants have had good results in creating oligodenrocytes (6).

In an animal study, neural stem cells were transplanted into rats with experimental autoimmuneencephalomyelitis (an animal model for MS). The cells migrated into the brain or spinal cord, exclusivelyinto the inflamed white matter but not into adjacent gray matter regions. After two weeks, manytransplanted cells had migrated into distant white matter tracts and acquired astroglial andoligodendroglial lineages. The authors conclude that the inflammatory process may attract themigration of transplanted precursor cells into the brain parenchyma (connective tissue network) (5).

The effectiveness of stem cells in treating autoimmune disease was observed in patients who receivedhematopoietic stem cell transplants for leukemia and aplasia who also suffered from severeautoimmune disorders (lupus and rheumatoid arthritis).

In 1998, Burt and coworkers treated 10 patients having autoimmune disease (6 patients with MS, 2 withLupus, and 2 with rheumatoid arthritis) with autologous hematopoietic stem cells from bone marrow ormobilized from peripheral blood. CD 34+ stem cells were reinfused after either myelosuppressiveconditioning with cyclophosphamide, methylprednisolone and antithymocyte globulin or myeloablativeconditioning with total body irradiation, methylprednisolone and cyclophosphamide. Regimen-relatednonhema-topoietic toxicity was minimal. All patients improved or had stabilization of disease for 5-17months. The author concluded that T cell-depleted hematopoietic stem cell transplantation can beperformed safely in patients with severe and debilitating autoimmune disease (10).

Dr. Ouyang and associates of Nanjing University School of Medicine, China demonstrated positive resultsin a patient with progressive multiple sclerosis who received an autologous peripheral blood stem celltransplantation. The patient showed clinical remission and there was no relapse at the 6 month follow-up. The authors conclude that auto-Peripheral Blood Stem Cell Transplantation is effective and safe forprogressive multiple sclerosis (73).

An MRI study of MS patients who received hematopoietic stem cell transplantations showeddisappearance of brain lesions 18 months after the transplant. These findings correlated with clinicalstabilization in the patients (83).



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In a multicenter Phase II study by Fassas and coworkers investigating autologous hematopoietic stemcell transplantation for multiple sclerosis, 85 patients with progressive MS (with a median ExtendedDisability Status Scale score of 6.5) were treated in 20 European centers. Neurological improvement wasseen in 18 patients (21%). Confirmed progression-free survival was seen in 74% of the patients at 3years. Disease progression was seen in 20%. The authors conclude that autologous HSCT early results

are positive and feasible for the management of progressive MS (25).

In a Phase II report by Fassas and associates, the authors used CD34+ cell transplantation in 15 MultipleSclerosis patients. Patients were selected who had advanced secondary progressive or relapsing-remitting MS or who showed worsening of the extended disability status scale despite interferon andother immunotherapies. They were treated with Cyclophosphamide, granulocyte colony stimulatingfactor, BCNU, Antithymocyte Globules, Methyl Prednisolone, MESNA, Cipor, Fluconoyol, and Acyclovir,Pentomidine, and Trimethoprim Sulfamethoxzaole Immunoglobins. There were a number of complications from this combination of powerful drugs. At 12 months, the Extended Disability StatusScale had improved in three patients, worsened in two and remained stable in nine. Despite withdrawal

of all immunosuppressive therapy, only two patients had relapses. The authors conclude that CD34+autologous stem cell transplantation using BCNU, Cylophosphamide and Antithymocyte Globules asconditioning regimen can be viewed as having an acceptable toxicity and effectiveness in reducing theprogression of Multiple Sclerosis (12).

Umbilical Cord Derived Stem CellsThese results using peripheral blood stem cell mobilization techniques with powerful immunesuppressants, antibiotics, antifungals and steroids had a number of side effects with only marginaleffectiveness. One factor is that some of these medications actually inhibit stem cell growth and

proliferation. When compared with the case studies to date of umbilical cord CD34+ stem celltransplantation given without additional medications, the umbilical cord stem cells show much greatersuccess with virtually no side effects. Immune defenses in the blood of a fetus have to be compatiblewith the mother, so immune defenses are suppressed. Stem cells from umbilical cord blood have theadvantage of having little or no antigens to cause immune reactions in the recipients and are thereforethe safest stem cell for transplantation (if tested by American Association of Blood Banks standards).

Steenblock Research Institute has followed several MS patients who were given umbilical cord stem celltreatments by Dr. Fernando Ramirez in Mexico. No side effects were reported. At first, the patients weregiven 1.5 million CD34+/CD133+ stem/progenitor cells. Improvements were seen in several patients butonly for about four months and then another treatment was needed. Since then Dr. Ramirez has beenusing larger doses of cord stem cells and with additional combinations. New combinations have includedmesenchymal cells from umbilical cord blood and cord stem cells with a fyn gene. The fyn geneincreases the production of myelin base protein for the remyelination of axons. Better results have alsobeen seen with catheter delivery of the cells more directly into the brain.



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Jim Haverlock has been struggling with multiple sclerosis for over twenty years. In 2003, his quest formore effective treatments led to cord stem cells. His story is available now in the book "Challenging theDragon," available at Amazon.com.

A Comprehensive Stem Cell Program for MSStem cells seem to have the ability to greatly assist in regenerating the glial cells injured and destroyedin MS. Care must be taken for several months after stem cell administration to avoid products thatinhibit stem cell growth and differentiation to neural progenitors. Such products include cortisone,alcohol, cigarettes, cocaine, air pollution, pesticides, and monosodium glutamate. Physical andemotional stress increase glutamate, which is toxic to neural stem cells and can damage neurons in thehippocampus, the area of learning and memory.

Depression and Stem Cell TherapyOne of the symptoms of Multiple Sclerosis is depression. A new model of depression is emerging thatrelates the consequences of stress to the inhibition of neural stem cell growth in the hippocampaldentate gyrus, an area of learning and memory as well as stem cell production in the brain (43). Factorssuch as stress-related adrenal hormones (glucocorticoids) that inhibit stem cell growth also seem toinduce depression. The glucocorticoids stimulate corticosterone, an immune suppressant, thatstimulates the production of glutamate which is toxic to neural progenitor cells.

In animals studies corticosterone significantly reduces the proliferation of oligodendrocyte precursors

throughout the white and gray matter regions of the brain (2). Since oligodendrocytes play a major rolein remyelination, the use of immune-suppressive therapies may actually perpetuate depression as wellas brain lesions. In contrast to the use of steroids for treating MS, stem cell therapies promote theproliferation of new oligodendrocytes, with the secondary benefit of alleviating depression. Generally,depression clears within 30 days after umbilical cord stem cell treatments.

Cell Energy ProductionThe mitochondria are the energy factories of the cell. Providing sufficient amounts of the precursors forATP (adenosine 5'-triphosphate) will help the cell defend itself against toxic injury. Nutritional support

for the mitochondria include acetyl-L-carnitine, lipoic acid, creatine, magnesium, coenzyme Q10, vitaminC, vitamin E succinate, biotin, thiamin (vitamin B1), riboflavin (B2), niacinamide (amide of B3) andpantothenic acid (B5). Spices that can reduce Complex I activity include cloves and cinnamon.Biochemical defects in Complex I may be a factor in multiple sclerosis.

There are several pathways that can trigger programmed cell death. The first is the mitochondria beingdepleted of ATP and being overrun with free radicals. Free radical damage leads to increased glutamatewhich stimulates its NMDA receptors to open its channels to calcium influx. The calcium influx then



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initiates programmed cell death, where proteases destroy the cell protein bonds, breaking up the cell insmall enough pieces to be engulfed by immune cells called phagocytes. Antioxidants can help preventfree radical damage in the mitochondria.

The second is injury to the extracellular matrix that supports the neurons. Elevated levels of MMP-2 and

MMP-9 can reflect increases in matrix degradation and subsequent apoptosis or programmed cell deathof the neurons. Nutrients that support the extracellular matrix include vitamin C, zinc metallothionine,alpha-ketoglutarate, glycine, proline and hydroxyproline.

NMDA receptors on the myelin sheath can promote cell injury to axons and reducing free radicaldamage and glutamate toxicity can help reduce myelin damage. Garlic, magnesium, boron, DHAsulphate, lipoic acid, and n-acetyl-cysteine can help modulate glutamate-NMDA activity.

Methylation and Multiple SclerosisFolate 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 MSsymptoms and prevent relapses. Treatment with additional methyl donors such as S-adenosylmethionine, betaine, or methionine can also relieve depression and promote remyelination inpatients with inborn errors of folate metabolism (8).

Autoimmune Disease and Patterns of Relapsing-Remitting EpisodesThe first two patterns of lesions observed in Lucchinetti's research were most common and resembledthe autoimmune destruction observed in T-cell mediated and antibody-augmented forms of

experimental autoimmune encephalomyelitis (13).

The Myelin SheathMyelin sheaths are formed around axons by spiraling plasma membranes of Schwann cells in theperipheral nervous system and oligodendrocytes in the central nervous system. Glycoproteins areprominent components of the plasma membranes and include protein zero and peripheral myelinprotein-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 appears to bean important target antigen in multiple sclerosis (78).

Autoimmune T-cell responses to myelin components are being investigated for their role in initiatingand/or maintaining inflammatory responses resulting in myelin destruction. Myelin oligodendrocyteglycoprotein (MOG) is a myelin protein that can elicit greater anti-MOG B-cell responses in MS patients(42). In another study, MOG elicits similar T cell responses in MS patients and controls but with differentcytokine activity. The MS samples elicited increased levels of Tumor Necrosis Factor-alpha (TNF-alpha)compared to the control samples (105). Tejada-Simon and associates found that MS patient MOG



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samples elicited anti-MOG antibodies reacting predominantly to the extracellular 1-60 region whilecontrol samples elicited anti-MOG antibody reactions to the transmembrane/cytoplasmic domains(residues 154-218) (100).

Autoimmune reactions have also been shown against cardiolipin (important in heart mitochondrial

function) and DNA in MS patients (91).

Patterns resembling Virus and Toxin-induced Immune ResponsesPattern IV was found only in patients with primary progressive disease and patterns III and IV bothresembled viral or toxin-induced oligodendrocyte dystrophy.

Mercury ToxicityMercuric chloride is toxic at low concentrations to oligodendroglial cells, resulting in cell death through

apoptosis. (37). Symptoms of mercury toxicity include chronic fatigue, depression, poor memory andcognitive function, emotional instability, peripheral numbness or tingling, decreased sensations of touch, hearing or vision, hypersensitivity and allergies, persistent infections including chronic yeastovergrowth, compromised immune function and cardiovascular disease (79). Mercury levels are oftenelevated in MS patients, and may result from a variety of sources.

1. Dental Amalgams . Though research findings are contradictory, Huggins found a change incerebrospinal fluid proteins following dental intervention, using CSF photolabeling. Changes were seenin 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) (35). S100 B was found to be a good marker for relapsing MS and GFAP correlated with DisabilityScales and may therefore be a marker for neurological damage (75).

2. Mercury contamination in fish and soil . Mercury is a major environmental concern, traditionally infreshwater fish and more recently because of the toxic effects on soil microorganisms. Those patientsliving near mercury emission sources are at greater risk of mercury contamination (66). Shark andSwordfish are reported to have the highest methyl mercury levels, and shrimp, scallops and salmon thelowest concentrations in ocean fish (33). Fish farms may not be safer than ocean fish. Fish farms may beproducing fish with higher pesticide and mercury concentrations due to the use of contaminated feedsources (22).

3. Elevated insulin levels allow the cellular entry of heavy metals. Insulin is elevated by large meals, highsugar and refined carbohydrate diets, and oxidative stress. Antioxidants can help protect the cells fromheavy 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 andautoimmune responses, free radicals, and cell injury and death. An animal study by Keshavarzian and



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associates demonstrated that supplementation with oats prevented gut leakiness and endotoxin-induced liver damage (44).

Chelating factors in various foods can prevent mercury absorption, including citric acid, tartaric acid, andcysteine, (24), selenium (31), garlic (52), chlorella (also an anti-inflammatory) (117), and cilantro (72).

Methyl mercury can bind with L-cysteine and be transported across the blood brain barrier. L-leucineinhibits this transport. A balanced leucine/cysteine ratio is found in whey protein (79). Calcium andmagnesium are also protective against mercury and methyl mercury toxicity (92). EDTA oral and i.v.chelation methods are currently being promoted for the removal of mercury and methylmercury as wellas other heavy metals. Since heavy metals can inhibit stem cell growth, chelation is advised before stemcell therapy. Oral DMSA is a proven generally safe and effective method for removing mercury and lead.

Anti-virals

Multiple Sclerosis is associated with viral infections, including Herpesvirus 6, Epstein-Barr virus, herpessimplex, infectious mononucleosis, measles and mumps (especially after 15 years of age), Chlamydia,Mycoplasma pneumoniae, Varicella zoster, retroviruses, and nidoviruses (46).

Medicinal PlantsEcinacea purpurea and Panax ginseng significantly enhanced Natural Killer activity and antibody-dependent cellular immunity against human herpesvirus 6 infected cells (87).

ReticulosaReticulosa is a peptide-nucleic acid immunomodulator that boosts immune system activity in virally-infected patients (51). It has broad-spectrum antiviral activity that includes the stimulation of gammainterferon, interleukin-1, interleukin-6 and Tissue Necrosis Factor-alpha (34). In general, it appears freeof side effects, is reasonably priced and often effective.

AcyclovirThe antiviral drug acyclovir inhibits herpesvirus-6 infection and markedly reduces the frequency of disease exacerbations in patients with MS (46).

Sea CucumberSea cucumber (Cucumaria japonica) (102) and coumarins from lemon peels (67) have been shown tohave an inhibitory effect on Epstein-Barr virus.



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Palm OilGamma- and delta-tocotrienols derived from palm oil exhibit a strong activity against Epstein-Barr virusexpression (29) and may be of benefit to MS patients.

Factors that Promote Remyelination

The Ciliary Neurotrophic Family

CNTF, leukemia inhibitory factor, cardiotrophin-1, and oncostatin M have been shown to induce a strongpromyelinating effect by promoting oligodendrocyte maturation, mediated through the 130 kDaglycoprotein receptor to the CNTF family (97).

ThyroidT4 administration to experimental allergic encephalomyelitis animals resulted in an up-regulation of oligodendrocyte progenitors and mature oligodendrocytes in the spinal cord, ofactory bulb, andsubventricular zone (11).

ThymusIkehara reports that the success rate of bone marrow transplants in patients over 45 years of age is low,due to the aging of the thymus. BMT plus embryonal thymus grafts can be used to treat late-onset

autoimmune disease in mice and can be a valuable strategy for treating older patients with variousintractable diseases, including autoimmune diseases. (36). NatCell Thymus, a thymus extract providing abroad spectrum of thymic peptides (www.atrium-bio.com) is being used successfully to restore immunebalance in patients with autoimmune disease who are not on immune suppressants.

Adrenal Support

Krenn presents a case of Adrenoleukodystrophy that mimicks the symptoms of multiple sclerosis. Bothconditions include lesions of the white matter which may be alleviated with adrenal support.(49).Adrenal insufficiency is present in 85% of the childhood cerebral forms and in about 70% of the adultforms of adrenoleukodystrophy (28) and may contribute to white matter lesions in multiple sclerosis aswell. Since adrenal extracts may also promote corticosteroid-induced stem cell injury, products such theAtrium adrenal extracts should be used several weeks before stem cell therapy to strengthen theadrenal glands.



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Interleukin-1

Mason writes that interleukin-1 beta promotes remyelination and CNS repair through inducing astrocyteand microglia-macrophage-derived insulin-like growth factor-1 (63).

Interleukin-10

Interleukin-10 was found to protect against oligodendroglial death evoked by lipopolysaccharide andinterferon-gamma. IL-10 downregulates the function of inflammatory cells and promotes survival of progenitors and differentiated oligodendrocytes. (68).

Interleukin-17Interleukin-17 (Il-17) increases interferon-gamma that promotes nitric oxide synthesis that is toxic toneurons, especially in the presence of free radicals. Il-17 also stimulates the production of interleukin 1Band interleukin-6 and may play a role in inflammatory neurological diseases such as multiple sclerosis.

Interleukin-19Interleukin-19 (Il-19) assists in the modulation of cytokines to preserve a balance in the system andprevent autoimmune disorders. Il-19 was shown to suppress inflammation in the development of experimental autoimmune encephalomyelitis in mice.

Immunoglobulin TherapyHigh-dose intravenous immunoglobulin (IVIg) treatment is being used for inflammatory demyelinatingdisease. The treatment protects oligodendrocyte precursor cells and oligodendrocytes by inhibitinginflammatory mechanisms (96). Unfortunately, it has a high cost, needs to be given every three weeksand does not result in remissions.

Growth FactorsThe more we learn about brain regeneration, the more complex it becomes. Certain growth factors canhelp stimulate oligodendrocyte cells and the production of myelin. However, oligodendrocytes andmyelin also inhibit the growth of axons. It would seem that the system has a time for myelin productionand a time for axonal growth. Therefore the alternate use of certain growth factors is suggested.

Glial Growth FactorGlial growth factor 2 (GGF2) is a neuronal signal that promotes the proliferation and survival of oligodendrocytes. Mice with experimental autoimmune encephalomyelitis were treated withrecombinant human GGF2 during both acute and relapsing phases leading to increased remyelination,decreased symptom severity and statistically significant reductions in relapse rate (59).



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Platelet-Derived Growth FactorPlatelet-Derived Growth Factor (PDGF) promotes oligodendrocyte progenitor cell proliferation andmaturity (113).

Neurotrophin-3Neurotrophin-3 (NT-3) promotes oligodendrocyte progenitor cell proliferation and maturity (113).Incorporating the gene of NT-3 in umbilical cord derived stem cells may help promote oligodendrocytematuration in multiple sclerosis patients.

Leukemia Inhibitory FactorLeukemia Inhibitory Factor (LIF) can be produced by myelin-reactive T cells in MS patients and is able toprotect oligodendrocytes from tumor necrosis factor alpha-induced programmed cell death.

Insulin-like Growth FactorInsulin-like Growth Factor promotes maturation in oligodendrocyte precursor cells (113).

Fibroblast Growth Factor 2Fibroblast Growth Factor 2 (FGF2) inhibits oligodendrocytes and myelin production but stimulatesaxonal growth.

Brain Derived Neurotrophic FactorBrain Derived Neurotrophic Factor (BDNF) stimulates neural stem cell growth and providesneuroprotection in the growth and differentiation of neural precursors.

Growth HormoneGrowth Hormone (GH) has been found to be deficient in the cerebrospinal fluid of multiple sclerosispatients. Growth hormone is neuroprotective, supports myelination, and regulates insulin growthfactor-1, which helps the development of oligodendrocyte precursors.

Granulocyte Colony-Stimulating Factor

Granulocyte Colony-Stimulating Factor (G-CSF) has the ability to mobilize bone marrow stem cells.However, with multiple sclerosis, G-CSF can either promote inflammation and exacerbate the symptomsof MS, or it can act as an anti-inflammatory.

PhospholipidsLipids, along with myelin protein assist in maintaining a normal myelin structure. Lipids includesphingomyelin, phosphatidylcholine and phosphatidylserine promote myelin stability. With



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demyelination, there is an increase in lipid polyunsaturation and negatively charged phosphatidylserineand a decrease in sphigomyelin, phosphatidylcholine and sulfaides. This composition allows greatermyelin fluidity, reductions in myelin adhesion, increases in membrane curvature and greater risk of demyelination.

Additional Factors

Uric AcidUric acid suppresses the MS animal model experimental autoimmune encephalomyelitis. In a studyinvolving humans, the MS patients were found to have lower average serum uric acid levels than thecontrols. (18). Scott and associates showed that uric acid selectively inhibits a highly neurotoxiccombination of nitric oxide and hydrogen peroxide called peroxynitrite in multiple sclerosis andimproves experimental autoimmune encephalomyelitis in mice (86).

Inosine is a precursor of uric acid. High levels of inosine given to 11 MS patients stopped the progressionof disease in all of the patients and improved clinical symptoms in 3 of the patients (94). Inosine shouldnot be used in patients prone to gout and arthritis.

Chen and associates found that the administration of inosine to rat models for experimental strokeresulted in significant axonal rewiring and improved motor function (16) and may therefore alsoimprove axonal growth in MS patients. Further work concluded that the mode of inosine inexperimental allergic encephalomyelitis was via its metabolism to uric acid (87).

High copper levels induce low levels of uric acid while also having a pro-inflammatory effect. Thus a low

copper diet may be indicated. Vitamin B2 is a cofactor for xanthine oxidase, and xanthine oxidasedeficiency can also contribute to low uric acid levels (40).

ChlorellaThis single cell fresh water detoxifying algae raises uric acid levels safely and consistently and should beconsidered by any person with MS.

CreatinePhosphocreatine increases ATP regeneration which is important in supporting remyelination byoligodendrocytes (89).

Vitamin B12 Injections (Methylcobalamin rather than cyanocobalamin)

Cyanocobalamin activates glutamate receptors and promotes inflammation. Methylation is important inremyelination. Methyl donors include folate, betaine, methionne and S-adenosylmethionine. Vitamin



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B12 deficiencies are associated with demyelination and axonal degeneration (15). Methylcobalaminimproves evoked potentials and nerve regeneration (48,50).

Ginseng

Ginseng increases Nerve Growth Factor which stimulates the growth of new oligodendrocytes (38).

Gingko bilobaGingko biloba contains factors that stimulate Glial Cell Line-derived Neurotropic Factor in astrocytes.However, Gingko may also inhibit cytochrome P450 metabolism of other medications.

Vitamin ARetinol levels for untreated relapsing-remitting (RR) MS patients was found to be lower than for patientswith noninflammatory neurological disease (82). All-trans-retinoic acid (in cod liver oil) increases Ciliary

Neurotrophic Factor, important in oligodendrocyte maturation and myelin production (111, 57).Retinoic acid also promotes myelin immune defense (57).

TaurineTaurine is an amino acid that plays a role in cell membrane stability, bile salt formation, calciumhomeostasis, growth modulation, cell osmosis, and modulating inflammation and immune response.

Moderate sunshine/vitamin DVitamin D is associated with alleviating autoimmune disorders. Vitamin D stimulates Brain DerivedNeurotropic Factor which protects thymocyte precursors and regulatory feedback mechanisms involvedin thymocyte differentation and immune function (60).

Spasticity

ThreonineHauser and associates used the amino acid L-threonine with 26 ambulatory MS patients with spasticity.Threonine at a daily dose of 7.5 g reduced signs of spasticity without the side effects of sedation andincreased motor weakness found in anti-spasticity drugs used for MS. Threonine is a precursor forglycine biosynthesis and may enhance glycinergic postsynaptic inhibition of the motor reflex (32). Alsosee the section on magnesium below.



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AntioxidantsFree radicals, including peroxynitrite are induced in Multiple Sclerosis. Antioxidants can help protect theneural tissue from damage, induced by inflammatory cascades that result in free radical pathology andoxidative stress. Nordik investigated the clinical effects of providing dietary advice, vitaminsupplementation and fish oil supplementation to newly diagnosed multiple sclerosis patients. At the endof a two year period, there was a significant reduction in the mean annual exacerbation rate and themean Expanded Disability Status Scale (EDSS) as compared to pre-study values. Plasma totalphospholipid n-3 fatty acids increased and n-6 fatty acids decreased significantly (70). The cod liver oiland fish oils used should be free of heavy metals.

Antioxidants and Tissue Necrosis Factor-alphaTNFalpha, a pro-inflammatory cytokine, has been associated with demyelinating disorders, includingMultiple Sclerosis. It reduces the gene expression (PPARdelta), responsible for oligodendrocyte survivaland differentiation in oligodendrocyte progenitor cells. The reduction in PPARdelta gene expression

results in reductions in myelin synthesis, maturation and turnover (17). TNFalpha is inhibited by greentea, curcumin, (85), quercetin (39) and resveratrol (109).

Antioxidants and Lipopolysaccharides

The "leaky gut" syndrome allows bacterial lipopolysaccarides to enter the blood stream.Lipopolysaccharides (LPS) are associated with extensive oligodendrocyte death (53). Several natural

products have the ability to protect the microglia from lipopolysaccharide-induced neurotoxicity. LPS is acomponent of the bacterial wall of gram-negative bacteria and is one of the most potent activators of host inflammatory response and tissue injury. LPS treatment of microglial cells activates both p38mitogen-activated protein kinase and nuclear factor-kappaB (NFkappaB), with consequent increases ininterluekin-1 alpha, tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO) production (55). LPSalso increases stress indicators, including plasma corticosterone and glucose concentrations; alterationsin brain oxidative status, including elevated malondialdehyde levels (a lipid peroxidation index) anddecreases in reduced glutathione; and brain metabolism disturbances including reductions in ATP/ADPratios and increases in mitochondrial/cytosolic hexokinase ratios (45).

1) Silymarin from milk thistle can reduce LPS-induced superoxide generation and nuclear factor kappaBactivation (110).

2) In in vitro studies, Vitamin E (alpha-tocopherol) activated microglial activity and silences an LPS-activated NF kappa B signaling cascade. The results suggest that alpha-tocopherol can induce quiescenceto pathways associated with acute or chronic inflammatory conditions in the central nervous system(23).



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3) Melatonin functions as an antioxidant and has the ability to protect neurons from lipopolysaccharide-induced oxidative stress (80). Blue light (420-480 nm) has been found to increase serotonin, a precursorfor melatonin. (see Dr. Payne's MS article at http://14ushop.com/wizard/)

4) N-acetylcysteine , a thiol antioxidant significantly reduces LPS-induced ROS production (superoxideanion), TNF alpha levels and NF-kappa B activity in macrophages from mice with lethal endotoxic shock.The levels approached those of macrophages from the control animals (105).

5) Estrogen and progesterone , at concentrations consistent with late pregnancy, inhibit LPS-inducednitric oxide and TNF-alpha production by activated microglia, and may contribute to the decreasedseverity of MS symptoms associated with pregnancy (21). Dr. Bansil and associates found a relationshipbetween relapsing-remitting MS in 30 women and hormone fluctuations in the menstrual cycle. Thosepatients with a high estrogen to progesterone ratio had a significantly greater number of active MRIlesions than those with a low ratio (4). Progesterone is a known immune quieting agent.

Foods as Medicine

6) Green Tea , containing catechin and (-)-epigallocatechin-3-gallate (EGCG), has the ability to inhibitlipoplysaccharide and gamma-interferon-induced oxidative stress (3). Black tea has similar effects frominhibiting LPS-induced IkappaB kinase and NFkappaB activity (74).

7) Artichoke (118) has protective properties against inflammatory mediators, TNF alpha and LPS, in

vitro.

8) Carnosol is a naturally occurring phytopolyphenol found in rosemary. Carnosol functions as anantioxidant and anticarcinogen. Carnosol significantly reduced LPS-induced nitric oxide and NF-kappa Bproduction in a dose-dependent manner (56).

9) Quercetin (in onions and garlic) significantly inhibited LPS-induced nitric oxide production andsuppressed the release of NF-kappaB (69).

10) The combination of Ginkgo biloba and quercetin were effective in inhibiting LPS-induced NF-kappaB as well as TNF-alpha activation (107).

11) Avocado contains antioxidants (persenone A and B) that can inhibit superoxide and nitric oxidegeneration induced by lipopolysaccharide and interferon-gamma in mouse macrophage cells (47).

12) Resveratrol in grape juice (red wine's alcoholic content can increase homocysteine levels-(7) hasantioxidant and anti-inflammatory effects. Resversatrol strongly inhibits LPS-induced superoxide radicaland hydrogen peroxide, arachidonic acid release, and cyclooxygenase-2 induction (62).



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13) Curcumin is the active ingredient in Indian curry. It has antitumor, antioxidant, and anti-inflammatory properties. Curcumin inhibits two enzymes involved in inflammation, cyclooxygenase-2(COX-2) and lipoxygenase (LOX).

Alpha-Lipoic AcidAlpha lipoic acid was administered to mice with experimental autoimmune encephalomyelitis resultingin minimal inflammation and reductions in demyelination and axonal loss in the spinal cord. Alpha lipoicacid inhibited the activity of metalloproteinase-9 in a dose-dependent manner. The authors concludethat alpha lipoic acid is highly effective at suppressing and treating experimental autoimmuneencephalomyelitis and does so by inhibiting T cell trafficking into the spinal cord, perhaps by acting as ametalloproteinase inhibitor (59).

Vitamin E Succinate and all-trans-retinoic acid

Vitamin E Succinate suppressed Epstein-Barr growth by 87% in vitro and all-trans-retinoic acid blocked

Epstein-Barr activity by 58% in vitro, via transforming growth factor beta (103). Transforming GrowthFactor Beta plays a role in neuronal survival and regeneration in Schwann Cell lesions (64). Vitamin E hasdirect neuroprotective antioxidant effects as well as anti-inflammatory indirect effects. Vitamin Einhibits microglial activation by suppressing the LPS-induced p38 MAPK and Nfkappa B signaling effectsnecessary for microglial activation (55).

Multiple Antioxidant TherapyOdinak treated 14 patients with relapsing-remitting MS with a combination of antioxidants andneuroprotectors with various mechanisms of action (lipoic acid, nicotinamide, Acetyl cysteine, Beta-

carotine, alpha-tocopheryl acetate, ascorbic acid, selenium, pentoxifylline, cerebrolysin, andAmantadine hydrochloride for a duration of one month, twice a year. The treatment resulted in asignificant reduction (2-3 times) of relapse frequencies in multiple sclerosis patients and a decrease of required corticosteroid medication. After antioxidant therapy the content of lipid peroxide products wassignificantly reduced and the author recommends antioxidant and neuroprotective program inrelapsing-remitting multiple sclerosis (71).

Autoimmune Suppression

Moderate Sunlight/Vitamin DDihydroxyvitamin D3 can prevent or markedly suppress experimental autoimmune encephalomyelitis,rheumatoid arthritis, systemic lupus erythematosus, type I diabetes, and inflammatory bowel disease.The animals also needed to be on moderate to high calcium diets. Vitamin D hormone stimulatestransforming growth factor and interleukin-4 production, which may suppress inflammatory T cellactivity (20). In an animal study using the multiple sclerosis model of autoimmune encephalomyelitis,



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the administration of 1,25-dihydroxyvitamin D3 demonstrated rapid clinical improvement in the rats,accompanied by an inhibition of CD4, MHC class II and type II nitric oxide synthase expression (27). 1,25-dihydroxyvitamin D3 has also been reported to increase intracellular levels of glutathione, important inprotecting neurons from oxidative stress-induced injury (90).

In addition, photoimmunology studies have shown that ultraviolet B can specifically attenuateautoimmune disease processes, perhaps by increasing vitamin D levels (76).

Cyclosporin A is widely used as an immunosuppressant by suppressing cytokine gene expression andinhibiting T lymphocytes. It may also protect against white matter lesions in stroke during hypoperfusion(108). However, the use of cyclophosphamide, either alone or in combination with Cyclosporin showed asignificant reduction in oligodendrocyte-mediated remyelination in rat spinal cord demyelinated lesions(93).

Anti-inflammatory Diet

Vegan DietsQuasi-vegan diets are beneficial in the management of rheumatoid arthritis, MS, and SLE (65) In hisIntegrative Management approach to Multiple Sclerosis, Dr. Kidd suggests a diet low in saturated fats,three fish meals per week, and the elimination of allergenic foods and products. Small frequent mealsare preferable to large three meals a day. Also avoid animal fats, fried foods, sugars and sweets, andprocessed and refined foods.

Fresh, whole fruits, vegetables, grains, legumes, nuts and seeds include a synergy of bioavailable

nutrients, enzymes, antioxidants and fiber that can retard and reverse age-related declines in cognitiveand motor performance in rats (26) and can be an important component in a total lifestyle program formaximizing neuronal and cognitive function and reversing disease in humans.

Nicotinamide is a potent inhibitor of inflammation. Nicotinamide is the amid form of niacin, (vitamin B3)and plays an important role in ATP synthesis (adenosine 5'-triphosphate) in the energy producingmitochondria of the cell. ATP is called molecular currency - a form of energy that can maintain theintegrity of DNA and cell membranes against insults and inflammation. Foods containing niacin includebrewer's yeast, chicken, fish, eggs, legumes, leafy vegetables, broccoli, tomatoes, carrots, carrots, dates,asparagus, and avocados.

Reduce Allergenic FoodsThe avoidance of milk may benefit patients with MS. Peptides in milk can mimic antigens in myelin. CNSdegeneration that resembles MS can be induced in mice with milk peptide injections (46).



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Fatty AcidsDietary omega-3 fatty acids can be of great benefit to MS patients. Omega-3 fatty acids have beenshown to alleviate pain in autoimmune disorders by inhibiting inflammatory mediators (eicosanoids andcytokines) in peripheral tissues as well as in glial cells Omega-3 fatty acids modulate voltage-gatedcalcium channels in heart and brain cells, preventing electrical hyperexcitability and a cascade of eventsleading to cell depolarization, oxidative stress, inflammation, cell injury and pain. Omega-3 fatty acidsare safe as long as they supply less than 10% of the total energy intake and are given with sufficientamounts of vitamin E (88). Cod liver oil with its vitamin A and D content (1 tablespoon 2-3 times a day) isoften of great benefit to MS patients.

LecithinAbnormal lipid metabolism in the brain is often seen in subjects with multiple sclerosis. Lecithincholesterol acyltransferase from the cerebrospinal fluid was investigated in 16 subjects, half controlsubjects and half with active demyelinating disease. The levels of lecithin cholesterol acyltransferase in

patients with active demyelinating disease or multiple sclerosis was only about half of that found in thecontrol subjects (1).

MagnesiumMagnesium, zinc and calcium have been found to be deficient in central nervous system tissue in MSpatients, especially in white matter tissue (116). Magnesium is important for the metabolism of thiamine, calcium, potassium, phosphorus, iron, sodium, hydrogen chloride, acetylcholine, nitric oxide,and for many enzymes, and for the elimination of lead and cadmium. Calcium and magnesium are alsoimportant in the development, structure and stability of myelin (30). A magnesium deficiency is

associated with increased inflammation. The pathologies associated with magnesium deficiency rangefrom cardiovascular disease to cancer and include peroxynitrite damage in multiple sclerosis (41). Theeffects of magnesium glycerophosphate oral therapy were studied in a woman with severe spasticparaplegia resulting from MS. There was significant improvement in the spasticity after only one week of treatment. No side effects were reported(81). Natural sources of magnesium include fresh greenvegetables (chlorophyll), raw wheat germ, soybeans, low fat milk, whole grains, fish, figs, corn, apples,and almonds.

Octacosanol contained in wheat germ and wheat germ oil increased endurance, total body reactiontimes, ECG, brachial pulse waves, pulse rate test, basal metabolism and oxygen intake tests in a physicaltraining program with 894 subjects (19). Octacosanol is a constituent of Policosanol, now being used forcardiovascular health.

Dr. Payne has created a diet with supplements suggested before and after meals athttp://www.14ushop.com/wizard/DrPaynesMSsupportregimen32506.html .

http://www.14ushop.com/wizard/DrPaynesMSsupportregimen32506.html





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Digestion, Assimilation and Gut FloraPatients with Inflammatory Bowel Disease have shown MS type lesions on the MRI, suggesting a linkbetween gut dysbiosis and brain disorders (46).

Pancreatic enzymesPancreatic enzymes have been used to help reduce malabsorption and help disperse circulating immunecomplexes.

Anti-Candida ProgramsCandida antibodies are often present in MS patients, suggesting an on-going chronic gastrointestinalyeast infection. This irritates the gut causing increased gut permeability and the subsequent absorptionof glial toxic lipopolysaccharides. Transfer Factor, in conjunction with an aggressive anti-Candidaprogram and probiotic recolonization should improve this condition.

In conclusion, there are a number of factors that can help restore myelin, axonal regrowth, cellularenergy production, reduce viral infections and inflammation, promote antioxidant defenses againstoxidative stress and balance the gut flora, if needed. Test results of specific nutritional deficienciesshould be used to devise rotating diets for each MS patient.



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FREE REPORT -- Alternative Therapies for Multiple Sclerosis - 11-11-11

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