In studying the preventive effects of vitamin D, researchers at the Moores Cancer Center at the University of California, San Diego, have proposed a new model of cancer development that hinges on a loss of cancer cells’ ability to stick together.
The model, dubbed DINOMIT, differs substantially from the current model of cancer development, which suggests genetic mutations as the earliest driving forces behind cancer.
“The first event in cancer is loss of communication among cells due to, among other things, low vitamin D and calcium levels,” said epidemiologist Cedric Garland, DrPH, professor of family and preventive medicine at the UC San Diego School of Medicine, who led the work. “In this new model, we propose that this loss may play a key role in cancer by disrupting the communication between cells that is essential to healthy cell turnover, allowing more aggressive cancer cells to take over.” He suggests that such cellular disruption could account for the earliest stages of many cancers. He said that previous theories linking vitamin D to certain cancers have been tested and confirmed in more than 200 epidemiological studies, and understanding of its physiological basis stems from more than 2,500 laboratory studies.
Vitamin D may halt the first stage of the cancer process by re-establishing intercellular junctions in malignancies having an intact vitamin D receptor. Other scientists have found that the cells adhere to one another in tissue with adequate vitamin D, acting as mature epithelial cells. Without enough vitamin D, they may lose this stickiness along with their identity as differentiated cells, and revert to a stem cell-like state.
Diet and supplements can restore appropriate vitamin D levels, and perhaps help in preventing cancer development. Vitamin D levels can be increased by modest supplementation with vitamin D3 in the range of 2000 IU/day.
[Source]
Chapter: Cancer :: 12 November 2009
