A drug that boosts body’s receptivity to Vitamin D

PTI Melbourne | Updated on July 31, 2012

Patients taking a multiple sclerosis drug, interferon-beta, receive almost three times as much vitamin D from exposure to sun than those who do not take the treatment, according to a new study.

Multiple sclerosis (MS) is an autoimmune disease that damages the brain and spinal cord (central nervous system).

There is currently no cure, but treatments are available to ease some of the symptoms.

MS is caused by damage to the myelin sheath that protects nerve cells.

This damage causes the nerve signals to slow down or cease. Inflammation occurs when the body’s own immune cells attack the nervous system. This can affect any area of the brain, optic nerve, and spinal cord, journal Neurology reported.

This observation by the Menzies Research Institute ( Menzies) Tasmania, based on data from 178 MS patients, suggests that one of the main treatments for MS may also increase the amount of vitamin D patients receive from sun exposure.

Around 60 per cent of MS patients are treated with interferon-beta. Derived from a naturally-occurring component of the human immune system, the drug has been found to reduce the frequency of relapse and other specific symptoms of MS, according to a statement of Menzies Institute, according to the Menzies statement.

Steve Simpson Jr, who co-authored the study with Niall Stewart from Menzies, said the findings suggest that part of the therapeutic effects of interferon-beta on MS may be through its effects on vitamin D, since it has the ability to reduce inflammatory pathways in the immune system.

“Not only did we find that persons taking interferon-beta had higher vitamin D levels than those not taking it, we also found that this increase in vitamin D was due to enhancement of the association between sun and vitamin D, with persons on interferon-beta having nearly three-times as much vitamin D from similar amounts of sun exposure to those not taking interferon-beta,” Simpson said.

Published on July 31, 2012

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