Multiple Sclerosis and the Baseline of Health

Date: 02/12/2007  Posted By: Jon Barron

MS is a chronic inflammatory disorder of the central nervous system. It is a young person's disease. The mean age at onset is 33.2 years, and the mean age at diagnosis is 39.2 years. It is the most common neurological cause of debilitation in younger populations and affects about 500,000 people in the United States and about 6,500,000 worldwide. The disease involves repeated episodes of inflammation of nervous tissue in any area of the central nervous system. The inflammation, which is caused when the body's own immune cells attack the nervous system, destroys the covering of the nerve cells in that area (the myelin sheath) leaving multiple areas of scar tissue (sclerosis) along the covering of the nerve cells. (Myelin is composed of about 80% fat and about 20% protein). The loss of normal myelin is called demyelination. Demyelination produces a situation not unlike that resulting from cracks in the insulation surrounding an electrical lamp cord. When the insulating surface is disrupted, the lamp will short-circuit and the light bulb will flicker or no longer illuminate.

In contrast to a single wire pathway in a lamp cord, there are thousands of nerve pathways of the Central Nervous System (CNS). The symptoms of multiple sclerosis depend largely on which particular nerve fiber pathway is involved in the CNS. Tingling, numbness, sensations of tightness, or weakness may result when loss of myelin occurs in the spinal cord. If the nerve fibers to the bladder are affected, urinary incontinence may follow. If the cerebellum of the brain is affected, imbalance or lack of coordination may result. Since the damage can occur in any location of the CNS, it is easy to understand why no two MS patients have exactly the same symptoms.

Cause of Multiple Sclerosis Unknown

As with many other illnesses, the actual causes of MS are unknown, but we do know that it is not contagious, and it is not directly inherited. All indications are that the disease probably results from an environmental agent that triggers the illness in genetically susceptible individuals.

The genetic component of multiple sclerosis:

While genetics does not play a defining role in most catastrophic illness, it is often a contributing factor. MS is no exception. Certain genes occur more frequently in persons with MS than those without. The risk of developing MS in the general population is approximately 0.15%. However, the risk to members of families who have a father, mother, sister, or brother with MS is between 1.0 and 4.0%. However, it is important to note that although this data supports the role of genetics in MS, it relegates it to a minority role. Keep in mind that the risk in identical twins, where one twin has MS, is only 25-30% in the other twin. That means at least 70% of the cause lies elsewhere.

Another interesting fact is that women suffer from MS almost twice as much as men. This indicates that hormones may play a role, but it may also indicate a more direct genetic link. Researchers have identified a variation in a gene that controls an immune messenger chemical called interferon (IFN) gamma. Unlike interferon betas, which are used to treat MS, IFN gamma has been linked to immune attacks in MS. Interferon gamma appears to be a new key variable in understanding who gets MS, and recent evidence suggests that it is more active in women than in men.

The environmental component of multiple sclerosis:

A map of the United States shows that the prevalence of MS increases with northern latitude. For example, the prevalence of MS in North Dakota is approximately twice that observed in Florida.

The Role of the Immune System in MS

Whatever the cause of MS, there is considerable evidence that a mis-programmed immune system is involved. The theory is that a virus, bacteria, or environmental toxin excites an immune response, which destroys the invader and builds a memory of it so that the immune system can respond more quickly the next time it sees the invader. There is reason to believe that in MS, the immune system gets confused and identifies peptides in the myelin as identical to the peptides found in the original invader. This "mistaken identity" causes the immune system to attack the perceived invader (the myelin) -- thereby inflaming and damaging the myelin surrounding the CNS nerve cells.

Once again we find commonality with so many other catastrophic illnesses. Look at increasing incidence of thyroid diseases such as Grave's. What triggers the immune system to attack the thyroid? Why does medicine only deal with the final effect and not the possible causes if the disease is triggered by out of balance hormones and environmental factors? Why does the same program, the Baseline of Health program, work so well when dealing with such different diseases as MS and Grave's?

The Hormonal Component of MS

It's no secret that hormones significantly impact autoimmune disorders and any disorder related to systemic inflammation. For example, as I've already mentioned, MS is more common in women than men, as are most thyroid disorders such as Graves disease, and the progress of these diseases follows the rise and fall of hormones during the monthly cycle. It has also been known for years that pregnant woman with MS get better in the last trimester of their pregnancy. In the third trimester, the hormone estriol (the gentle estrogen) is at high levels. It appears that a key role of estriol is to inhibit the "escape" of white blood cells from blood vessels into the Central Nervous System, where they can then attack myelin. In testing with MS patients, after the first three months of estriol treatment, brain scans showed the number of lesions in a group with relapsing-remitting MS decreased by 82 percent, and the volume of those lesions decreased by 79 percent (both compared with pre-treatment scans). The decrease persisted for the rest of the first treatment period. When the women stopped taking the estriol over the next six months, the number of lesions gradually increased again--all the way back up to pre-treatment levels. In another study, administering estriol until treatment levels reached levels consistent with those in late pregnancy completely ameliorated the disease.

And in studies done earlier this year, researchers found that testosterone therapy with those who have MS may help improve cognitive function and slow brain atrophy. It's believed that testosterone helps protect nerve cells from damage caused by the kind of autoimmune system attack that occurs in people with MS.

Recapping MS

So what do we know? From a medical standpoint, mostly hunches and guesswork, but it does appear that MS (as with most idiopathic autoimmune disorders), is the result of an overall system imbalance triggered by things within our ability to alter, and the final causative factor in the chain of events is inflammation.

The primary medical treatment offered is the immunomodulator interferon beta-1a. For many people it can reduce symptoms for 1-4 years, but over time, as the body forms neutralizing antibodies, its effectiveness will diminish. It also comes with a whole host of side effects including: fatigue, chills, fever, muscle aches, and sweating. Symptoms of depression including ongoing sadness, anxiety, loss of interest in daily activities, irritability, low self-esteem, guilt, poor concentration, indecisiveness, confusion, and eating and sleep disturbances, are also possible.

But a quick recap of the possible causative factors in MS makes clear the interferon beta-1a intervenes at only the very last steps and does nothing to eliminate the underlying causes -- a common problem with the medical approach to virtually all of the autoimmune disorders.

Factors we need to account for if we truly want to reverse MS:

For the full story see: http://todayshealthbuzz.com/multiple-sclerosis-baseline.pdf

See Also: http://www.jonbarron.org/baseline-health-program/baseline_program.php

http://todayshealthbuzz.com/It's-All-About-Energy_v1.1.pdf

 

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