The Oxford team have shown for the first time that vitamin D interacts directly with a gene, DRB1, which increases the risk of MS threefold. Proof of this has been obtained by infecting human cells with a short piece of DNA bearing the DRB1 gene and treating the cells with vitamin D. In this way the Oxford team were able to show that vitamin D stimulated the gene to work and express itself on the surface of the cell.
Other investigations by the Oxford team in collaboration with Canadian scientists have shown that MS is inherited preferentially through the female line as an “imprinted” gene. This explains why MS affects three or four women to every man.
It now seems likely that insufficient vitamin D is the crucial environmental factor that modifies the DRB1 gene into the imprinted form that causes MS and transmits it from one generation to the next. DRB1 is one of a family of HLA genes that code for structures on the surface of human white blood cells. And it is white blood cells that are involved in the “autoimmune” reaction that destroys the nervous system of MS sufferers.
The Oxford team believe that people with MS have white cells that are incorrectly programmed early in life. There are millions of different T-cells, a particular type of white cell produced in the thymus gland, each programmed to recognise and attack different types of invading bacteria and viruses. Ordinarily the T cells that might attack the body itself are deleted early in life in a stock-taking process. But this process can go wrong when certain genes that are normally masked by the imprinting process are mistakenly unmasked.
It appears that lack of vitamin D early in life impairs the ability of the thymus to delete these T cells and so they go on to mistakenly attack the body with what the Oxford team call “friendly fire”.
George Ebers, of Oxford University, told The Times that for the first time there was hard evidence directly relating both genes and the environment to the origins of MS. His work suggests that vitamin D deficiency during pregnancy and childhood may increase the risk of a child developing the disease.
He has also established the possiblity that genetic vulnerability to MS, apparently initiated by lack of vitamin D, may be passed on to subsequent generations.
These risks might plausibly be reduced to giving vitamin D supplements to pregnant woman and young children. “I think it offers the potential for treatment which might prevent MS in the future,” Professor Ebers said.
“Our research has married two key pieces of the puzzle. The interaction of vitamin D with the gene is very specific and it seems most unlikely to be a coincidence of any kind. Serious questions now arise over the wisdom of current advice to limit sun exposure and avoid sunbathing. We also need to give better advice and help to the public on vitamin D supplements, particularly pregnant and nursing mothers."
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