Multiple Sclerosis

Multiple Sclerosis (MS) is a devastating disease that results from lymphocytes attacking the cells in the brain that provide myelin insulation in nerve circuits (oligodendrocytes). Environmental causes of MS are likely but identification of specific causes has been difficult. Associations have been observed between increased MS prevalence and diets high in meat and dairy products and low in fish.

Repeated searches for genetic risk factors do not provide strong clues. Reviewing genomic analyses to 2007, Peltonen concluded: ”One can predict from the accumulated genetic information, including data from twin and family studies, that the susceptibility profile for multiple sclerosis consists of many, probably interacting, risk alleles, each contributing a relatively small effect to the overall risk. “ 

MS is perhaps the most obvious “allergic” brain disease. In animals, a similar brain disease can be induced by injecting myelin-basic protein, a component of nerve cell insulation. The injected protein sensitizes the animals to their own myelin. The blood brain barrier is a property of the blood vessel linings in the brain that control the molecular and cellular input to the brain. If frequent immune skirmishes occurred in the brain as they do, for example in the skin, no-one would remain neurologically intact.

MS usually develops as recurrent attacks of neurologic symptoms associated with multifocal lesions in the central nervous system. These are inflammatory lesions with myelin degradation.  Studies show that axonal injury occurs early in the course of disease. Berger et al    investigated  the presence of serum antibodies against myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP) in patients with a clinically isolated MS like event  and found the antibody tests to be: “a rapid, inexpensive, and precise method for the prediction of early conversion to clinically definite multiple sclerosis. This finding may be important for the counseling and care of patients with a first demyelinating event suggestive of multiple sclerosis. “

Experimental autoimmune encephalomyelitis (EAE) is a multiple sclerosis-like disease induced by injection of myelin oligodendrocyte glycoprotein peptide. Experiments have shown that blocking addressin, a cell adhesion molecule, will prevent the entry of immune cells and prevent immune damage to oligodendrocytes if given early enough in the disease process ( i.e. before damage is apparent). 

Since MS is characterized by attacks and remissions in many patients, a reactive allergy model is one way to approach management of the disease. Attacks may start in an anaphylactic manner with the sudden onset of dramatic and severe symptoms such as vertigo, loss of vision, paralysis, or loss of feeling in a limb. In others, slow, progressive deterioration occurs without conspicuous dynamics. The slow disease will often present as weakness and incoordination with loss of feeling in feet or hands. Usually muscle tone is increased and reflexes are hyperactive. Slow progressive MS suggest the work of an unknown injuring agent X that acts continuously and progressively. Several mechanisms could relate the food supply to MS. Cocoa has be implicated as a culprit. MS tends to occur in northern, industrialized countries where the consumption of chocolate is the highest, along with other staple foods such as coffee, milk, wheat and eggs.

A southern band of the disease passes through New Zealand, southern Australia and S. Africa. New Zealand and Australia have diets similar to the northern countries, including high wheat, milk, egg and cocoa consumption.  A single popular food may cause the disease (as the cycad example described later suggests), but I am inclined to think that the mechanism involves more chaotic immune responses to food proteins and possibly airborne antigens and/or toxins.

You could argue that food protein antigens can cause MS if the necessary conditions are aligned. One mechanism is via lymphocytes, sensitized to food antigens and activated in the digestive tract, travel in the blood and gain access to the brain through a permeable blood brain barrier. Food-activated lymphocytes would recognize a component of myelin-containing oligodendrocytes as their target antigen and attack and/or trigger other cells in the brain that can cause damage. Another mechanism would involve antigens appearing as immune complexes in the blood, which then activate blood vessel wall mechanisms in the brain or spinal cord, gaining access to brain tissues and myelin sheaths. Whenever neurons are damaged, information flow is interrupted; numbness, paralysis, and loss of vision are typical consequences.

It is common for patients with delayed pattern food allergy to have symptoms suggestive of MS. They have absorbed food proteins which become attached to antibodies and circulate as immune complexes. Symptoms tend to be chaotic; episodes of weakness, numbness, and blurring of vision suggest the possibility of MS. Changes in the brain scans (MRI) of patients with chronic fatigue syndrome suggest patchy swelling which often occurs in MS patients. The majority of patients with immune responses to food proteins, fortunately, will not develop MS, but may go through periods of uncertainty, wondering if their disease will become progressively disabling.

A defect in the blood brain barrier and/ or in suppressor side of the immune system is required before the immune activity in the brain is severe enough to damage axons and myelin-containing oligodendrocytes. Brain scanning with magnetic resonance imaging (MRI) has shown that disease activity is more active in MS patients than was previously thought. MRI scans show areas of transient inflammatory activity in the brain which may resolve on their own or develop into damaging lesions. This evidence matches my experience with MS patients; periods of transient dysfunction are more common than episodes that create permanent damage.

The first meeting I attended forty years ago that addressed the cause of MS focused on the rubella virus. Antibody levels to Rubella were higher in MS patients than controls. The connection was never confirmed, but idea of an occult brain infection remains viable there is a long list of known chronic brain infections that are difficult diagnose and a longer list of infections that could be involved such as herpes viruses and toxoplasmosis.

The addition of doxycycline, an antibiotic, to standard therapy with interferon beta-1a improved patients with relapsing remitting multiple sclerosis (RRMS). It is possible that the investigators were treating an infection; however, they preferred a non-infection explanation. The tetracycline family of antibiotics, specifically minocycline and doxycycline, have anti-inflammatory effects. They inhibit matrix metalloproteinases (MMPs), enzymes that play a role in the pathogenesis of MS. It has also been shown that MMPs can degrade interferon beta making it ineffective. 15 patients with RRMS on 30 µg of interferon beta-1a weekly for a minimum of 6 months had breakthrough disease activity and were switched to intramuscular interferon beta-1a 30 µg monthly plus oral doxycycline 100 mg/day for 4 months:  60% of patients had more than a 25% reduction in the number of brain lesions compared with baseline; also observed was a median decrease in Expanded Disability Status Scale (EDSS) score of 2.3, compared with an average pretreatment score of 3.8. Only 1 patient experienced a relapse. All 15 subjects tolerated the combination therapy well, with only mild adverse effects that resolved spontaneously. Commonly associated effects of doxycycline include gastrointestinal symptoms, such as nausea, vomiting, and diarrhea. Those commonly associated with interferon beta-1a therapy include influenza-like syndromes, fatigue, headache, and muscle pain.

Lymphocytic attacks on myelin occur sporadically and major events tend to be infrequent; this is an avalanche effect. A number of conditions must be aligned before the damage occurs. In tracking the progress of immune events, it is important to pay attention to minor symptoms which are occurring more often than major events. If minor symptoms increase (like warnings of an earthquake), precautions can increase, including careful food control and immune-suppression treatment.  As soon as an acute attack begins, I suggest a food holiday on Alpha ENF . You can take a large dose of prednisone or other immune suppressant in an effort to get the immune attack to stop. If you wait too many hours, the damage is done and it will take months to repair.

In slow, progressive MS, there may be few clues about the disease activity and the victim must pursue a protective policy for a long period of time without symptom feedback. Patients who have a lot of dynamic symptoms have an easier time identifying attacks and usually will become aware of food and/or environmental reactivity. Others seem to have little awareness of what is going on and will usually not recognize any food reactivity. The latter group should still pursue diet revision, but on the basis of a policy decision to stick with "safe foods". They probably should eat Phase 1 and 2 foods primarily.

Munger et al suggested that there is a protective effect of dietary vitamin D supplementation on the risk of multiple sclerosis (MS). They examined vitamin D intake in two cohorts of women in the Nurses' Health Study (NHS; 92,253 women followed from 1980 to 2000) and Nurses' Health Study II (NHS II; 95,310 women followed from 1991 to 2001). 173 cases of MS were confirmed. Intake of vitamin D from supplements was inversely associated with risk of MS; the relative risk comparing women with intake of >or=400 IU/day with women with no supplemental vitamin D intake was 0.59.  

Zittermann suggests that there many opportunities for Vitamin D supplementation that are relatively ignored. Calcitriol receptors are present in more than thirty different tissues. There is agreement that a low vitamin D status is involved in the pathogenesis of osteoporosis.  Vitamin D insufficiency can also lead to a disturbed muscle function. Zimmerman states that: “epidemiological data also indicate a low vitamin D status in tuberculosis, rheumatoid arthritis, multiple sclerosis, inflammatory bowel diseases, hypertension, and specific types of cancer. Some intervention trials have demonstrated that supplementation with vitamin D or its metabolites is able: (i) to reduce blood pressure in hypertensive patients; (ii) to improve blood glucose levels in diabetics; (iii) to improve symptoms of rheumatoid arthritis and multiple sclerosis. The oral dose necessary to achieve adequate serum 25(OH)D levels is probably much higher than the current recommendations of 5-15 microg/d.”  

Holick suggested that: “Vitamin D deficiency is a major unrecognized health problem. Not only does it cause rickets in children, osteomalacia and osteoporosis in adults, but may have long lasting effects. Chronic vitamin D deficiency may have serious adverse consequences, including increased risk of hypertension, multiple sclerosis, cancers of the colon, prostate, breast, and ovary, and type 1 diabetes. There needs to be a better appreciation of the importance of vitamin D for overall health and well being.” 

Hayes et al reviewed evidence that the vitamin D endocrine system influences immune system functions and in particular, that the vitamin D endocrine system functions in the establishment and/or maintenance of immunological self tolerance. They stated: “. Studies done in animal models of multiple sclerosis (MS), insulin-dependent diabetes mellitus (IDDM), inflammatory bowel disease (IBD), and transplantation support a model wherein the 1alpha,25-(OH)2D3 may augment the function of suppressor T cells that maintain self tolerance to organ-specific self antigens” In other words, Vitamin D deficiency may predispose susceptible individuals to these autoimmune diseases. 

According to Hoag, MS patients are advised to eat heartily. This is very bad advice. She quotes Stephen Reingold of the National Multiple Sclerosis Society in New York. "The general rule of thumb is that eating a healthy, well-balanced diet is the best thing that you can do for treating MS."   However, in one study mice with the disease improved when they were deprived of food for 48 hours. They had fewer brain lesions and performed better on tests of walking, balance, and muscle strength.  In rats, calorie restriction prevented the development of experimental allergic encephalomyelitis. 

Sanna et al explored the influence of leptin in mice susceptible to autoimmune encephalomyelitis (EAE). They found that serum leptin increased before the onset of EAE and correlated with disease susceptibility. Starvation, which prevents the increase in serum leptin, delayed disease onset and attenuated clinical symptoms by inducing a T helper cytokine switch. Leptin is secreted by activated T cells and sustains their proliferation in an autocrine loop. Antileptin receptor antibodies inhibit the proliferative response of autoreactive T cells. The authors suggest that since leptin regulates EAE susceptibility, inflammatory anorexia, and pathogenic T-cell immune function, it may offer a potential target in the treatment of multiple sclerosis.  

If I had early symptoms of MS, I would be very interested in nutritionally supported fasting using Alpha ENF, followed by food reintroduction using the Alpha Nutrition Program as a guide. I would eat mostly phase 1 foods on the program.

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The Human Brain in Health and Disease, 2011, is a Persona Digital Book. We encourage readers to quote and paraphrase topics from the book published online and expect  citations to accompany all derivative writings. The author is Stephen Gislason and the publisher is Persona Digital Books. The current date of publication is 2011. The URL to the book description is Human Brain