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Multiple Sclerosis

Pathology of Disease Progression


MS is an immuno-inflammatory disease in which immune cells enter the central nervous system (CNS) and destroy the myelin sheath. Immune cells, which become activated through complex mechanisms migrate into the CNS, and attack the myelin sheath. The resultant demyelination is thought to be carried out by T lymphocytes, B lymphocytes, and macrophages, three primary classes of immune cells, which are routinely found in MS lesions.2

Loss of myelin followed by subsequent lack of neural communication and neuronal death is accepted as the primary cause of disability in MS patients.3 Axonal transection, or the severing of axons, occurs under conditions of both acute and chronic demyelination.4-6


Remyelination is the process by which demyelinated axons are naturally re-wrapped with myelin, restoring nerve conduction and functionality.7 This phenomenon is the result of oligodendrocytes repairing the damage to the myelin sheath that occurs during an episode of increased disease activity. However, as the disease progresses over years (usually decades) the oligodendrocytes begin to lose their ability to repair the damage, and symptoms become progressively worse and episodes more frequent due to remyelination failure. In addition to developing therapies that slow MS disease progression, many laboratories are developing novel therapeutics that aim to promote remyelination and reverse existing CNS damage.


In addition to immune-mediated loss of myelin, another characteristic feature of MS is inflammation caused by a class of white blood cells called T cells.8,9 Some of the damage in the CNS is directly carried out by two subpopulations of T lymphocytes called T helper 1 and T helper 17 which produce pro-inflammatory factors.10 Recent studies have identified that chemical mediators, interleukin-23 (IL-23) and granulocyte macrophage colony-stimulating factor (GM-CSF), contribute to the autoimmune characteristics of these T cells. Data suggest absence of these pro-inflammatory signals was sufficient to prevent inflammation in the brain.11 This suggests that therapeutic strategies directed at blocking the production of inflammatory mediators could be effective for treating MS.

Vitamin D and Multiple Sclerosis: A Panacea?

Mainstream medicine has failed to recognize the pivotal role of vitamin D in regulating the overactive immune system in MS patients.

Greater than 30 years have passed since vitamin D was originally hypothesized to be an important environmental determinant of the prevalence of MS.12,13 During the three decades following the initial linking of vitamin D and MS, evidence has continued to mount. It is now known that MS occurs more frequently in individuals with lower blood levels of vitamin D. A study published in the prestigious Journal of the American Medical Association found that, compared to those with the highest vitamin D blood levels, those with the lowest blood levels were 62% more likely to develop MS.

MS attacks occur less frequently during seasons corresponding with the highest exposure to sunlight; since vitamin D synthesis depends upon exposure of the skin to sunlight, the summer months also bring the highest blood levels of vitamin D.14 A recent study has quantified the impact of vitamin D blood levels on risk for MS relapse—for each 4 ng/ml increase in 25-hydroxy vitamin D in the blood, the risk for MS relapse is reduced by 12%. The investigators who conducted this study concluded that "Clinically, raising 25-hydroxy vitamin D levels by [20 ng/ml] could halve the hazard of a relapse."15

Vitamin D mediates these disease-modifying effects through complex and powerful interactions with the immune system. Hostile immune cells, which attack the myelin sheath, are calmed upon exposure to vitamin D. In fact, when aggressive immune cells taken directly from MS patients are exposed to the active form of vitamin D, the cells divide and reproduce much more slowly, indicating that vitamin D has the ability to impede the aberrant autoimmunity that is a driving force in MS.

However, vitamin D does more than just arrest damaging immune cells; it also supercharges protective immune cells.

T-reg cells are specialized components of the immune system that help keep immunity balanced. If too few T-reg cells are present, the immune system becomes overactive, as in autoimmune diseases like MS. Vitamin D increases the number of protective T-reg cells, restoring equilibrium to an overactive immune system.16

In a randomized controlled trial, supplementation with doses of vitamin D ranging from 10,000 IU to 40,000 IU daily over the course of 52 weeks resulted in a reduction in relapses and a reduction in the number of aggressive immune cells in patients with MS.17

Despite robust findings across a range of studies on the link between vitamin D and MS, mainstream medicine and the federal government have only just recently begun to realize the need to initiate federally funded trials. Results of a large scale, randomized, controlled clinical trial to assess the effects of vitamin D in MS are currently pending.1

Life Extension customers should not be surprised if vitamin D emerges as a frontline treatment for MS in the coming years. However, instead of waiting for mainstream physicians to begin recommending vitamin D to MS patients, Life Extension suggests all individuals monitor their blood levels of 25-hydroxyvitamin D and maintain a blood level of 50–80 ng/mL. This is because low vitamin D levels are also an emerging risk factor for numerous other diseases, such as type 1 diabetes, heart disease, and rheumatoid arthritis.18-22 The amount of supplementation required to achieve this blood level varies from person to person, but it appears many individuals require supplementation of 5,000‒8,000 IU vitamin D daily to reach these levels.

More information about the role of vitamin D in health is available in the compelling Life Extension Magazine article entitled "Startling Findings About Vitamin D Levels in Life Extension Members."