Vitamin D Deficit May Trigger MS Risk Gene
THURSDAY Feb. 5, 2009 -- A direct interaction between vitamin D and a common genetic variant may affect a person's risk of multiple sclerosis, according to British and Canadian researchers who also said that vitamin D deficiency while in the womb and early in life may increase the risk of MS later in life.
Both genetic and environmental factors play a role in MS, a neurological condition that affects 2.5 million people worldwide. Vitamin D is a major environmental factor, and the largest genetic effect comes from the region on chromosome six containing a gene variant called DRB1*1501 and from adjacent DNA sequences.
In the general population, about one in 1,000 people will develop MS. But that increases to about one in 300 among people who have a single copy of the DRB1*1501 and about one in 100 among people with two copies of the variant.
The study found that proteins activated by vitamin D in the body bind to a particular DNA sequence lying next to the DRB1*1501 variant, which causes the gene to switch on.
The study was published in the Feb. 6 edition of PLoS Genetics.
"In people with the DRB1 variant associated with MS, it seems that vitamin D may play a critical role. If too little of the vitamin is available, the gene may not function properly," study co-author Julian Knight said in a journal news release.
The researchers believe that vitamin D deficiency in mothers or even in a previous generation may lead to altered expression of DRB1*1501 in offspring.
"Our study implies that taking vitamin D supplements during pregnancy and the early years may reduce the risk of child developing MS in later life," lead author Dr. Sreeram Ramagopalan said in the news release. "Vitamin D is a safe and relatively cheap supplement with substantial potential health benefits. There is accumulating evidence that it can reduce the risk of developing cancer and offer protection from other autoimmune diseases."
The Multiple Sclerosis Society has more about genetics and MS.
Posted: February 2009
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