The Role of Vitamin D in Multiple Sclerosis
Multiple sclerosis (MS) is an autoimmune disease that attacks a person’s own nervous system. Vitamin D deficiency may play a role in the onset and progression of multiple sclerosis. In MS, the myelin sheaths that surround the nerves in the brain and spinal cord are damaged.
Just like the wires in your house can’t transmit properly if they’ve lost their surrounding insulation, so too the nerves can’t conduct an electrical signal without their myelin sheaths, and the function of that nerve is lost. The body tries to restore the myelin but can’t completely do it. The resultant signs and symptoms depend on which areas are most damaged.
When the nerve tissue of a person affected by MS is examined, damage by T cells, a major player in the adaptive immune system, is evident. Ordinarily, T cells don’t get through the blood-brain barrier to enter the brain, but they do in MS. T cells treat the myelin like a foreign protein, leading to signals that bring other cells into the brain and also cause the production of cytokines that kill cells and cause inflammation.
The disease usually begins in young adults and occurs more in females than males. MS comes and goes in multiple cycles called relapses and remissions. Sometimes after a relapse there aren’t any signs of the disease. After some relapses, abnormalities remain. These abnormalities accumulate with additional relapse/remission cycles so that the severity of MS gets worse over time.
Signs and symptoms of multiple sclerosis
Signs and symptoms of multiple sclerosis vary widely and include any or all of the following, all of which may be intermittent:
Acute or chronic pain
Difficulty with speech and vision
Loss of balance
Loss of bladder and/or bowel control
Loss of sensation
Multiple sclerosis is diagnosed in the following way:
MRI scan of the brain and spine show areas consistent with lost myelin covering the nerves.
Cerebrospinal fluid obtained by inserting a needle into the lumbar spine shows chronic inflammation with white blood cells and certain types of proteins.
When certain nerves are stimulated, they respond more slowly than normal.
Relapses are unpredictable but usually happen no more than once or twice a year. They may be brought on by viral infections or stress. The lifespan of a person with MS is five to ten years less than someone who isn’t affected. Doctors use a variety of drugs to treat MS, but none have been completely successful.
Vitamin D and multiple sclerosis
There are a number of different lines of indirect evidence that suggest higher intakes of vitamin D or circulating 25-hydroxyvitamin D levels may delay the onset of MS or improve the disease course. Consider some of the evidence:
Many MS patients have low circulating levels of 25-hydroxyvitamin D, especially during relapses. The problem with this observation is that many people develop lower vitamin D levels during times of illness because they are indoors and not eating well.
Low serum 25-hydroxyvitamin D levels are associated with the relapse rate of MS. Consistent with this, one clinical study found that increasing vitamin D intake might reduce the relapse rate, but there weren’t enough people studied to be certain.
Higher serum 25-hydroxyvitamin D levels have been associated with improved T cell function in MS patients.
There is a widely held belief that as latitude moves away from the equator, the population experiences a progressive increase in the incidence of MS. In fact, people who have lived in the tropics up to age 15 rarely develop the disease, even if they later move to temperate areas. However, a careful review of the evidence found that there is an effect of latitude only in Australia and New Zealand, but not in North America or Europe.
In Sweden, more people affected with MS were born during the months when the mother was low in vitamin D than during the months when the mother had adequate vitamin D. This is interesting because it suggests low vitamin D status during pregnancy might program a person to have a higher risk of MS as an adult.
Calcitriol and drugs designed to look like it inhibit experimental autoimmune encephalitis, an animal model of MS.
These facts suggest that lack of vitamin D may play a role in the onset and progression of MS; however, no one has yet shown that vitamin D supplements prevent the development of MS, slow the rate of relapse of the MS, or reduce the symptoms associated with an outbreak of the disease.
Ongoing clinical trials should give the final answer about this relationship and also determine the level of vitamin D intake or serum 25-hydroxyvitamin D needed to prevent or lessen the impact of MS.