Alternative names: MS
Multiple Sclerosis (MS) is a disease in which the body's own immune system attacks the protective sheath (myelin) that covers nerve fibers, causing communication problems between the brain and the rest of the body. MS is known as a very unpredictable disease because it causes nerve damage — and nerves reach every part of the body. Symptoms can therefore occur anywhere, depending on which nerves are damaged and how severe the damage is.
The central nervous system (CNS) consists of two types of tissue: grey matter and white matter. Put simply, white matter allows communication between areas of grey matter, which is where 'processing' takes place. In computer terms, areas of grey matter are 'CPUs' and white matter is the 'wires' that connect them.
Myelin is the fatty protective sheath that surrounds axons (nerve fibers) to provide electrical insulation and speed up nerve impulses, just as wires in a computer are protected by an insulating plastic sheath. Myelin is white and gives "white matter" its name.
Multiple Sclerosis is a demyelinating (myelin-removing) disease of the white matter of the central nervous system. Axons form the communication system both within the CNS and between the CNS and the rest of the body.
Multiple Sclerosis is the most common demyelinating disease of the central nervous system, affecting over 2 million people worldwide. In the United States alone, there are at least 250,000 cases. For reasons that remain unclear, it is more common in northern temperate zones and is 20 times more prevalent in those of Northern European descent. MS affects about twice as many women as men; it usually affects those aged between 15 and 50, the average age of onset being 30 years.
How does this damage occur?
The blood-brain barrier is a layer of tightly-packed cells on the walls of blood vessels which only allows certain substances – such as sugars – to enter the brain from the blood. After an infection, the blood-brain barrier may become damaged, allowing immune cells that are circulating in the blood to enter the brain. These immune cells incorrectly recognize myelin as a 'dangerous substance' and produce inflammatory substances that damage it; this is why MS is considered to be an autoimmune disease.
After the demyelinization (destruction of myelin) has taken place and the fragments have been cleared away, multiple scars (or 'sclera') are left behind in the brain and spinal cord at these locations. This damage impedes conduction of nerve signals by blocking or slowing communication, either completely or partially and from time to time. The process can be thought of as being similar to an electrical short circuit. The symptoms of Multiple Sclerosis result from this loss in signal conduction.
The reason why immune cells attack myelin is unknown, which in turn means we don't know the cause of MS itself. Studies indicate that an environmental factor, perhaps exposure to a virus, when combined with a genetic predisposition to the disease, may well dictate occurrence of MS.
Although MS is not a genetically-transmitted disease, having parent(s) with the disease does slightly increase one's risk of developing it. Exposure to certain viruses, such as human herpesvirus 6 (HHV-6) or the Epstein-Barr virus, may trigger MS although no definite connection has been made.
Toxins in tobacco smoke have been linked to a higher risk of developing MS.
Multiple Sclerosis manifests itself primarily through disorders of mobility but is also associated with a variety of other symptoms and complications depending on which parts of the brain have been demyelinated. For example:
The most important fact about MS is its unpredictability and its uncertainty. There are very few certainties to be found anywhere in any aspect of this disease.
Symptoms may appear very rapidly, within minutes or days, or very slowly, over a period of weeks. They may be very transient and come and go rapidly. New symptoms may accumulate; old symptoms may reappear and/or intensify.
Symptoms of MS vary enormously, both from patient to patient and, over time, in one patient. There are three primary courses the disease may take:
Diagnosis of MS is difficult. A medical history and clinical examination must show at least two separate lesions that have occurred at more than one time. Obviously, any other possible causes must be ruled out. Because of the difficulty of diagnosis, the presence of MS is usually deemed to be either definite, probable, or possible. There is no one specific diagnostic test that can either confirm or rule out its presence.
A neurological examination can indicate lesions through the presence or absence of various signs and reflexes. Computerized tomographic (CT) scans will show some lesions. Magnetic resonance imaging (MRI) usually reveals many more lesions than the CT scan, including some that may be subclinical. An autopsy will usually show many more lesions than were suggested by either symptoms or signs. These lesions are probably the result of subclinical attacks of the disease.
Brain wave testing of responses to various forms of stimulation of the eyes, ears or other parts of the body may demonstrate delays in these responses and indicate lesions that are clinically silent (producing no symptoms) and can sometimes firm up a questionable diagnosis from probable to definite MS. Testing of the cerebrospinal fluid for protein content, the number and type of white blood cells, and the amount of Ig6, a gamma globulin, can also support a diagnosis. An old diagnostic technique is to see whether a person becomes worse after a hot bath.
There is no cure for Multiple Sclerosis. Many promising modes of treatment are being developed and tested but most remain experimental. Current conventional treatment focuses on regulating or suppressing the immune system with a variety of different drugs. Unfortunately, prolonged usage of these drugs decreases their effectiveness and increases side-effects.
The Swank Diet
Dr. Roy Swank has provided convincing evidence that a diet low in saturated fats over a long period of time can slow down and in some cases stop the degenerative process in Multiple Sclerosis. The Swank diet calls for:
The results of Dr. Swank's 34-year study from 1949-1984 are impressive. Patients diagnosed as minimally disabled showed very little progression of the disease. Only 5% of the diet group failed to survive the 34 years of the study while a remarkable 80% of those not following the diet failed to survive the same time period. Moderately and severely disabled patients progressed much better subjectively and objectively than those that did not follow the diet. The diet has been credited with preventing a worsening of the disease, greatly reducing fatigue, and dramatically reducing the death rate.
Some of those with an exacerbating-remitting course will eventually develop a slow progression involving fewer and less complete remissions with cumulative disabilities. Very rarely, there is a rapidly progressive course leading to death. MS itself is almost never the cause of death; death results from accompanying complications or infections. Generally speaking, the life expectancy of those with MS is at least 75% of normal, often only reducing lifespan by a few months. However, quality of life is decreased significantly due to the various debilitating symptoms.
Exacerbations and remissions are difficult to define. An exacerbation is an acute appearance of new symptoms or worsening of old symptoms which lasts at least 24 hours, while a remission is a total or more often partial clearing of symptoms and signs which lasts more than 24 hours.
Exacerbations (episodes of new disease activity) are not easy to diagnose with certainty. New symptoms may result from old areas of disease that were previously silent. Conversely, recurrence of old symptoms is not a sure indication of lack of exacerbation. Over time, the disease process may result in the formation of new plaques or the enlargement of existing ones. Exacerbations can be caused by heat, physical trauma, extreme fatigue, psychological stress, infections, or any other kind of stress. While all of these factors have been associated with exacerbations, there is little empirical data to support these associations.
There does seem to be a direct correlation between the degree of remission from an exacerbation and its duration. For example, 85% will usually improve spontaneously from an exacerbation that lasts one week, but only 7% will improve after an exacerbation lasting one to two years. Over time, a series of exacerbations and remissions may result in a gradual accumulation of irreversible changes and disability.
There are factors that may be predictive of the course of the disease. An earlier age at onset may mean a more benign course. If, at onset, symptoms are sensory, the course of the disease may be less severe, while motor symptoms (weakness or poor coordination) at onset may be predictive of greater disability. Again, as with everything to do with this disease, variation is extreme and the course and progression of the disease is unpredictable.
An enormous amount of research is currently being done on the causes and processes of Multiple Sclerosis, and understanding of the disease continues to increase.
Very cold temperatures, or changes in temperature, can cause MS symptom flare-ups, in particular spasticity.
Damaged nerve fibers have a strongly diminished tolerance for heat. Increases as little as 0.1 degrees centigrade can decrease conduction or cause blockage, which will result in the appearance of symptoms.
Very cold temperatures, or changes in temperature, can cause MS symptom flare-ups, in particular spasticity.
Demyelinated nerve fibers use more energy to conduct impulses and thus fatigue more easily than normal fibers. MS involves large numbers of nerve fibers in a state of borderline function, which suddenly turn off when the body temperature is elevated only one or two degrees. The signals suddenly cease to be transmitted, and one has to stop. Muscles that have been weakened result in a reliance on stronger muscles, which then tire faster. One recent report indicates that for those with MS the energy cost of walking is two to three times that of a normal person over the same distance. Such an increased use of energy obviously results in increased fatigue. The fatigue of MS is hard to describe.
Difficulty speaking may result from a variety of neurological disturbances, including Multiple Sclerosis. Weakness, stiffness, or uncoordinated movement of the muscles controlling the lips, tongue, jaw, soft palate, vocal cords and diaphragm can all cause speech problems.
Gait disorders varying from an inability to walk the usual distance to an inability to walk at all are the principal problems of patients with MS.
Multiple sclerosis that affects auditory nerve pathways in the brain can cause sensorineural hearing loss.
Vertigo is a fairly common symptom of multiple sclerosis, occurring in about 20% of sufferers at some point. It is an acute, uncomfortable sensation, making those who are already a little unsteady feel even more nervous about moving around. It is not a permanent symptom, but may indicate a new lesion or inflammation.
This vertigo can be caused by lesions in the cerebellum, or it can be a result of damage to the nerves that control the vestibular functions of the ear in the brain stem. Vertigo is, however, not always a direct result of the MS disease process.
It has been reported that MS (possibly associated with low uric acid) and gout (associated with high uric acid) are mutually exclusive. A study of 20 million Medicare and Medicaid records found no overlap between MS and gout.
A study at the University of Bergen in Norway, reported October 28th, 2003 in the journal Neurology, found that smoking can more than double a person's chances of developing multiple sclerosis. The risk was higher even if people had given up cigarettes. The authors, Dr. Trond Riise and colleagues, examined 22,312 people aged between 40 and 47. Of those, 87 had MS. The smokers were 1.81 times more likely to get MS than the non-smokers and men had a higher (2.75 times more likely) risk than women (1.61) who had smoked.
A 1987 study showed that the levels of mercury in the spinal fluid of MS patients was 8 times higher than normal. [Silberod, R: A comparison of mental health of multiple sclerosis patients with silver/mercury dental fillings; Psychological Reports 70: pp.1139-51, 1992]. Mercury has long been linked to autoimmune diseases such as MS because of its affinity to attach to collagen tissue, which is the most common protein in the body. Polluted by mercury infiltration, the collagen is seen by the immune system as 'not self.'
The leakage of toxic waste from the gut into the bloodstream is believed to be a primary cause of Multiple Sclerosis.
Progesterone has been shown in animal studies to promote the formation of new myelin sheaths [Human Reproduction 2000 Jun;15 Suppl 1: pp.1-13, J Steroid Biochem Mol Biol 1999 Apr-Jun;69 pp.97-107, Mult Scler 1997 Apr;3 pp.105-12]
Physicians have known for years that pregnancy can suppress some forms of immune response, such as allergies. In the early and mid-1980s, several doctors observed that MS patients had fewer symptoms during pregnancy and post-partum recovery. This may be due to the high progesterone level in the blood of a pregnant woman. Progesterone tends to be anti-inflammatory. Progesterone therapy may therefore be useful for MS especially as a medical report noted the association between enlarged adrenal glands and MS. Progesterone, being a steroid, often helps the adrenals deal with inflammation.
Other studies have indicated that symptoms are worse during periods when the progesterone to estrogen ratio is low.
It has been proposed – and research is supporting the idea – that low uric acid levels are associated with increased frequency and longer bouts of multiple sclerosis. Uric acid works by inactivating peroxynitrite, a toxic compound that may cause damage to the central nervous system in MS patients. Researchers report that they found lower levels of uric acid in the blood of MS patients than of people without the disease. It appears that high serum uric acid levels protect against the development of MS. These results raise the possibility that the natural biologic product, uric acid, or a more soluble peroxynitrite scavenger that penetrates the blood brain-barrier more readily might have clinical utility in the treatment of MS. [Proceedings of the National Academy of Sciences 1998;95: pp.675-680]
It is interesting to note that the incidence of MS is quite low in Japan, where consumption of marine foods, seeds, and fruit oil is quite high. These foods contain abundant polyunsaturated fatty acids, including the omega-3 oils (alpha-linolenic, eicosapentaenoic, and docosahexanoic acids). Deficiencies of the omega-3 oils are thought to interfere with lipid elongation and permanently impair formation of normal myelin.
Through his clinical experiences with thymic supplementation, Dr. Burgstiner said he observed 10 cases of multiple sclerosis go into remission.
Three months of treatment with a Ginkgo biloba product (240mg per day) maintained attention, memory and functioning – without adverse effects – in a double-blind, placebo-controlled study of 23 patients with mild multiple sclerosis. Deterioration of function was observed in patients who had received a placebo. [American Academy of Neurology 54th Annual Meeting, April 13-20, 2002, Denver, Colorado, USA; P06.081]
A minimum of 20gm (4 teaspoons) and a maximum of 50gm (10 teaspoons) per day is recommended as part of the Swank Diet for Multiple Sclerosis sufferers. Persons with MS should use mainly olive oil (monosaturated fat) in conjunction with fish oils to provide most of their fat intake.
The Swank diet includes strict avoidance of fried food and trans-fatty acids.
Avoid dairy products containing 1% butterfat or more. This is part of the Swank Diet for Multiple Sclerosis sufferers.
The Swank diet includes strict avoidance of fried food and trans-fatty acids.
The Swank diet includes eating fish at least 3 times per week. Alternately, fish oils could be substituted at 1500mg three or more times per week.
Epidemiology studies have documented a correlation between high cocoa consumption and high MS incidence. When cocoa is introduced to an area, MS incidence rises sharply. Cases are reported in which chocolate ingestion by MS patients was followed by exacerbations [Maas AG, Hogenhuis LAH. Multiple sclerosis and possible relationship to cocoa: A hypothesis. Ann Allergy 59: pp.76- 9, 1987]
The nurse responsible for the revival of the use of histamine, Elaine DeLack, MS, RN, has collected verbal reports from over 200 individuals diagnosed with multiple sclerosis who have used histamine: 72% report at least one significant improvement in symptoms, and some many more.
One hormone which has been shown to shorten the duration and intensity of acute exacerbations is adrenocorticotropic hormone (ACTH), a pituitary gland substance that stimulates the adrenal glands to produce additional cortisone, which acts to reduce the inflammation in the brain or spinal cord. ACTH does not affect the underlying disease processes but may diminish the frequency and severity of exacerbations and even slow the progression of the disease.
Animal studies indicate that pregnenolone may aid in repairing the degeneration of the myelin sheath, the cause of Multiple Sclerosis. Further studies are required to determine if there is any benefit for humans with MS.
The first step when you receive a diagnosis of multiple sclerosis is to determine if you really have it. A vitamin B12 deficiency has very similar symptoms and is frequently misdiagnosed as MS; the type of anemia resulting from B12 deficiency is called pernicious anemia. [Hosp Pract (Off Ed) 1995 Jul 15;30(7): pp.47-52; discussion 52, 54]
Additionally, researchers found in 45 MS patients that vitamin B12 levels were significantly lower in those who experienced the onset of first neurological symptoms prior to age 18 years (10 patients) compared to patients in whom the disease first manifested after age 18 (35 patients). In contrast, serum folate levels were unrelated to age of onset of the disease. As vitamin B12 levels were statistically unrelated to chronicity of illness, these findings suggest a specific association between the timing of onset of first neurological symptoms of MS and vitamin B12 metabolism. In addition, since vitamin B12 is required for the formation of myelin and for immune mechanisms, a deficiency in MS is of critical pathogenetic significance. [PMID: 8407160, UI: 94011702]
Reports from researchers suggest that low uric acid levels are associated with increased frequency and longer bouts of multiple sclerosis. Uric acid levels should be monitored and, if low, raised by supplemental molybdenum and reducing any copper toxicity.
Calcium EAP protects the myelin sheath from damage by an autoimmune response. Dr. Nieper has found an EAP deficiency state in people with immune dysfunctional diseases, and says that all cell membranes in such people are defective. He claims this defect can be blocked with supplemental EAP.
Dr. Nieper believes that MS is initiated by a viral attack on the nervous system, followed by an error in programming the immune system to defend it. The immune system ends up attacking the nerves, especially the myelin sheath. Normally, certain steroids eliminate this bad programming but certain pollutants such as Chlorine, Fluoride, some heavy metals and especially Aluminum, interfere with the process.
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