Feel 2 much: VITAMIN D THE ROOT OF INFECTIONS AND OF AUTOIMMUNE DISORDERS

INFECTIONS AND VITAMIN D AS THE CAUSE OFAUTOIMMUNE DISORDERS

Nov 7, 2011
Elaine Moore

: Yersinia in blood smear - CDC

Research suggests that treating underlying infections and vitamin D receptor dysfunction may benefit and even reverse a number of autoimmune disorders.

For several decades researchers have known that mutations and other causes of dysfunction to the vitamin D receptor are routinely seen in a number of autoimmune disorders, particularly Graves’ disease and multiple sclerosis. Because low vitamin D levels are seen in many of the autoimmune disorders that are more common in women, including Hashimoto’s thyroiditis, researchers have studied the vitamin D receptor, particularly the receptor expressed in the human cycling endometrium.
In a related line of study, researchers at the Autoimmunity Research Foundation report that scientists have identified a common intracellular bacterial infection as the cause of many chronic diseases, including those considered autoimmune as well as other idiopathic conditions, including chronic fatigue syndrome, myalgic encephalomyelitis, (CFS/ME), fibromyalgia, sarcoidosis and post-treatment Lyme disease syndrome (PTLDS). The role of vitamin D regulator dysfunction in perpetuating chronic bacterial infection has led to further research showing that correcting the infection and receptor dysregulation is key to treating autoimmune diseases.

The Vitamin D Receptor

To cause their intended effects, hormones and drugs attach to and activate protein receptors that reside on cells. For vitamin D to perform its intended functions, it must activate the vitamin D receptors found in the nucleus of cells located throughout the body. Besides its role in maintaining adequate blood levels of vitamin D, the vitamin D receptor controls expression of various antimicrobial peptides that offer natural protection against infection.

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When the vitamin D receptor is dysregulated and no longer functioning properly, these peptides aren't produced and the innate immune response is compromised. This invariably leads to a chronic infection that contributes furhter to the vitamin D receptor dysregulation, which, in turn, causes the infection to persist. In addition, this dysregulation can prevent the normal breakdown of 1,25-OH vitamin D by metabolic enzymes. When present in high levels, 1,25-OH vitamin D binds the alpha and beta thyroid receptors, the glucocorticoid receptor and the androgen receptor, thereby displacing the hormones that normally react with these receptors and causing hormonal imbalances and endocrine disorders.
Amy Proal and her team at Georgetown University have found that if triiodothyronine (T3) is displaced, patients may develop thyroiditis. Because these receptors also express multiple types of antimicrobial peptides, production of these naturally occurring antibiotics declines even further, which allows infections to take hold. When levels of 1,25-OH remain elevated, conversion to the biologically active 25-OH vitamin D3 is impaired, and, consequently, 25-OH vitamin D3 levels decline. Because women have an extra vitamin D receptor in the endometrium, they’re more likely to have low production of antimicrobial peptides, higher bacterial loads (notably in pregnancy when levels of 1,25-OH vitamin D typically rise by 40 percent), and increased susceptibility to autoimmune disorders. This also explains why some autoimmune disorders such as systemic lupus tend to worsen or emerge during pregnancy and the postpartum period.

Linking Infection, Vitamin D, and Autoimmune Disease

The initial dysfunction in the vitamin D receptor leads to low levels of antimicrobial peptides and chronic infection. In addition, patients with vitamin D receptor dysfunction are susceptible to additional infections. The infections contribute to further vitamin D receptor dysregulation, causing low levels of vitamin D, reduced innate immune system function, and susceptibility to autoimmune disease.
Evidence from several studies indicates that a number of autoimmune diseases can be reversed by gradually restoring function of the vitamin D receptor. Studies show that vitamin D receptor function can be restored with the vitamin D receptor agonist drug olmesartan and long-term low doses of certain antibiotics. To date, diseases showing favorable responses to this treatment include systemic lupus erythematosis, rheumatoid arthritis, scleroderma, sarcoidosis, Sjogren’s syndrome, autoimmune thyroid disease, psoriasis, ankylosing spondylitis, Reiter’s syndrome, type 1 and II diabetes mellitus, and uveitis. When using this type of treatment vitamin D supplementation needs to be limited in an effort to avoid vitamin D's contribution to dysfunction of nuclear receptors, which could lead to further imbalances in endocrine and immune function.

Sources

Proal, A; Albert, P; and TG Marshall. “Dysregulation of the vitamin D nuclear receptor may contribute to the higher prevalence of some autoimmune diseases in women.” Annals of the New York Academy of Science, 2009 Sep; 1173: 252-259.
Waterhouse, J; Perez T; and PJ Albert. “Reversing bacteria-induced vitamin D receptor dysfunction is key to autoimmune disease,” Annals of the New York Academy of Science, 2009 Sep; 1173:757-765.

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