The extent to which vitamin D deficiency may increase susceptibility to a wide range of diseases is dramatically highlighted in newly published research. Scientists have mapped the points at which vitamin D interacts with our DNA -- and identified over two hundred genes that it directly influences.
It is estimated that one billion people worldwide do not have sufficient vitamin D. This deficiency is thought to be largely due to insufficient exposure to the sun and in some cases to poor diet. As well as being a well-known risk factor for rickets, there is a growing body of evidence that vitamin D deficiency also increases an individual's susceptibility to autoimmune conditions such as multiple sclerosis (MS), rheumatoid arthritis and type 1 diabetes, as well as certain cancers and even dementia.
Now, in a study whose founders include the Medical Research Council (MRC), the MS Society, the Welcome Trust and the MS Society of Canada, researchers at the University of Oxford have shown the extent to which vitamin D interacts with our DNA. They used new DNA sequencing technology to create a map of vitamin D receptor binding across the genome. The vitamin D receptor is a protein activated by vitamin D, which attaches itself to DNA and thus influences what proteins are made from our genetic code.
The researchers found 2,776 binding sites for the vitamin D receptor along the length of the genome. These were unusually concentrated near a number of genes associated with susceptibility to autoimmune conditions such as MS, Crohn's disease, systemic lupus erythematosus (or 'lupus') and rheumatoid arthritis, and to cancers such as chronic lymphocytic leukaemia and colorectal cancer.
They also showed that vitamin D had a significant effect on the activity of 229 genes including IRF8, previously associated with MS, and PTPN2, associated with Crohn's disease and type 1 diabetes.
"Our study shows quite dramatically the wide-ranging influence that vitamin D exerts over our health," says Dr Andreas Heger from the MRC Functional Genomics Unit at Oxford, one of the lead authors of the study.
The first author of the paper, Dr Sreeram Ramagopalan from the Wellcome Trust Centre for Human Genetics, adds]
The main source of vitamin D in the body comes from exposing the skin to sunlight, although a diet of oily fish can provide some of the vitamin. Research has previously suggested that lighter skin color and hair color evolved in populations moving to parts of the globe with less sun to optimize production of vitamin D in the body. A lack of vitamin D can affect bone development, leading to rickets; in pregnant mothers, poor bone health can be fatal to both mother and child at birth, hence there are selective pressures in favor of people who are able to produce adequate vitamin D.
This new study supports this hypothesis, having found a significant number of vitamin D receptor binding sites in regions of the genome with genetic changes more commonly found in people of European and Asian descent. It is probable that skin lightening as we migrated out of Africa resulted from the necessity to be able to make more vitamin D and prevent rickets]
"Vitamin D status is potentially one of the most powerful selective pressures on the genome in relatively recent times," says Professor George Ebers, Action Medical Research Professor of Clinical Neurology and one of the senior authors of the paper. "Our study appears to support this interpretation and it may be we have not had enough time to make all the adaptations we have needed to cope with our northern circumstances."
Can vitamin D help prevent certain cancers and other diseases such as type 1 diabetes, cardiovascular disease, and certain autoimmune and chronic diseases? To answer these questions and more, UCSD School of Medicine and GrassrootsHealth bring you this innovative series on vitamin D deficiency. Join nationally recognized experts as they discuss the latest research and its implications. In this program, Frank Garland, PhD, discusses vitamin D and the opportunity for prevention of diabetes.
Reply With Quote