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Press release – Vitamin D may exacerbate autoimmune disease

April 15, 2009 – Deficiency in vitamin D has been widely regarded as contributing to autoimmune disease, but a review appearing in Autoimmunity Reviews explains that low levels of vitamin D in patients with autoimmune disease may be a result, rather than a cause, of disease and that supplementing with vitamin D may actually exacerbate autoimmune disease.

Authored by a team of researchers at the California-based non-profit Autoimmunity Research FoundationNon-profit foundation dedicated to exploring a pathogenesis and therapy for chronic disease., the paper goes on to point out that molecular biologists have long known that the form of vitamin D derived from food and supplements, 25-hydroxyvitamin D (25-DThe vitamin D metabolite widely (and erroneously) considered best indicator of vitamin D "deficiency." Inactivates the Vitamin D Nuclear Receptor. Produced by hydroxylation of vitamin D3 in the liver.), is a secosteroid rather than a vitamin. Like corticosteroidA first-line treatment for a number of diseases. Corticosteroids work by slowing the innate immune response. This provides some patients with temporary symptom palliation but exacerbates the disease over the long-term by allowing chronic pathogens to proliferate. medications, vitamin D may provide short-term relief by lowering inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue., but may exacerbate disease symptoms over the long-term.

The insights are based on molecular research showing that 25-D inactivates, rather than activates, its native receptor–the Vitamin D nuclear receptorA nuclear receptor located throughout the body that plays a key role in the innate immune response. or VDRThe Vitamin D Receptor. A nuclear receptor located throughout the body that plays a key role in the innate immune response.. Once associated solely with calcium metabolism, the VDR is now known to transcribe at least 913 genes and largely control the innate immune responseThe body's first line of defense against intracellular and other pathogens. According to the Marshall Pathogenesis the innate immune system becomes disabled as patients develop chronic disease. by expressing the bulk of the body's antimicrobial peptidesBody’s naturally produced broad-spectrum antibacterials which target pathogens., natural antimicrobials that target bacteria.

Written under the guidance of Professor Trevor Marshall of Murdoch University, Western Australia, the paper contends that 25-D's actions must be considered in light of recent research on the Human MicrobiomeThe bacterial community in the human body. Many species in the microbiota contribute to the development of chronic disease.. Such research shows that bacteria are far more pervasive than previously thought–90% of cells in the body are estimated to be non-human–increasing the likelihood that autoimmune diseases are caused by persistent pathogens, many of which have yet to be named or have their DNA characterized.

Marshall and team explain that by deactivating the VDR and subsequently the immune response, 25-D lowers the inflammation caused by many of these bacteria, but allows them to spread more easily in the long-run. They outline how long-term harm caused by high levels of 25-D has been missed because the bacteria implicated in autoimmune disease grow very slowly. For example, a higher incidence in brain lesions, allergies, and atopy in response to vitamin D supplementation have been noted only after decades of supplementation with the secosteroid.

Furthermore, low levels of 25-D are frequently noted in patients with autoimmune disease, leading to a current consensus that a deficiency of the secosteroid may contribute to the autoimmune disease process. However, Marshall and team explain that these low levels of 25-D are a result, rather than a cause, of the disease process. Indeed, Marshall's research shows that in autoimmune disease, 25-D levels are naturally down-regulated in response to VDR dysregulation by chronic pathogens. Under such circumstances, supplementation with extra vitamin D is not only counterproductive but harmful, as it slows the ability of the immune system to deal with such bacteria.

The team points out the importance of examining alternate models of vitamin D metabolism. “Vitamin D is currently being recommended at historically unprecedented doses,” states Amy Proal, one of the paper's co-authors. “Yet at the same time, the rate of nearly every autoimmune disease continues to escalate.”

For the past five years, Autoimmunity Research Foundation has been running an observational study in which patients are administered pulsed, low-dose antibiotics and a VDR agonistA substance such as olmesartan (Benicar) or 1,25-D which activates the Vitamin D Receptor and transcribes the genes necessary for a proper innate immune response. in order to kill chronic bacteria implicated in their diseases. Specific data on the cohort was recently presented by Capt. Thomas H. Perez, USPHS (ret), at the International Congress on Autoimmunity in Porto, Portugal:

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