Read SLOWLY (entire paper!!) & test PROPERLY before trying again to be smarter than Mother Nature!! “Inflammation and vitamin D: the infection connection, Inflamm Res. 2014

Abstract

INTRODUCTION:
Inflammation is believed to be a contributing factor to many chronic diseases. The influence of vitamin D deficiency on inflammation is being explored but studies have not demonstrated a causative effect.
METHODS:
Low serum 25(OH)D is also found in healthy persons exposed to adequate sunlight. Despite increased vitamin D supplementation inflammatory diseases are increasing. The current method of determining vitamin D status may be at fault. The level of 25(OH)D does not always reflect the level of 1,25(OH)2D. Assessment of both metabolites often reveals elevated 1,25(OH)2D, indicating abnormal vitamin D endocrine function.
FINDINGS:
This article reviews vitamin D's influence on the immune system, examines the myths regarding vitamin D photosynthesis, discusses ways to accurately assess vitamin D status, describes the risks of supplementation, explains the effect of persistent infection on vitamin D metabolism and presents a novel immunotherapy which provides evidence of an infection connection to inflammation.
CONCLUSION:
Some authorities now believe that low 25(OH)D is a consequence of chronic inflammation rather than the cause. Research points to a bacterial etiology pathogenesis for an inflammatory disease process which results in high 1,25(OH)2D and low 25(OH)D. Immunotherapy, directed at eradicating persistent intracellular pathogens, corrects dysregulated vitamin D metabolism and resolves inflammatory symptoms.

“...Autoimmune disease
Numerous examples can be found in which pathogens express antigens that cross-react with host antigens or induce local inflammatory responses that can lead to autoimmune responses through a very complex set of circumstances [127]. The prevailing theory regarding the etiology of autoimmune disease states that an overactive immune system produces auto-antibodies against self, but infection as an environmental factor in autoimmunity has long been recognized. An alternate hypothesis posits a bacterial etiology in which a persistent intracellular infection causes a cytokine release that induces signals to T cells and B cells, and the antibodies they produce (to the intracellular invader) include some that attack human proteins, as well as target the pathogens [128, 129]. Christen et al. [130] explored this hypothesis, “In theory, a structural similarity or identity between the host and an invading pathogen might cause the immune system of the host to react not only to the pathogen but also to self-components.” Infections can act as environmental triggers inducing or promoting autoimmune disease in genetically predisposed individuals [131]; researchers have shown how antinuclear antibodies (ANA) are created in response to infectious agents [132, 133].
Vitamin D appears to have a positive effect on autoimmune disease due to immune system suppression [122, 134, 135] and immune suppression is considered therapeutically beneficial for autoimmune diseases [136, 137]. However, vitamin D proponents have failed to recognize that positive effects are due to the immunosuppressive effect of elevated 25(OH)D or to understand that immunosuppression is contraindicated because of the probable presence of intracellular infection. When the immune system is suppressed clinical disease markers and symptoms are reduced but immunosuppression does not address an underlying cause of persistent bacteria, thus relapse is common [138]. Verway et al. [79] wonder, “Is a specific pathogen responsible for disease or rather is a dysregulated immune response generated against a complex microbial population? Why would immune-suppressive drugs be efficacious if the primary defect is an immune deficiency?” Much of current research focuses on finding drugs to suppress inflammation but, according to Collins [139], 95 % of these studies have failed It seems clear a better direction is needed. Immunotherapy which restores VDR competence corrects dysregulated vitamin D metabolism and eliminates intracellular bacteria could be the answer (as discussed in the section titled Restoring VDR Competence)...”

“...In summary, elevated 1,25(OH)2D, often accompanied by reduced 25(OH)D, is a clinical sign of dysregulated vitamin D metabolism and evidence that the immune system is competing with parasitic microbes for VDR dominance. Failure of the immune system to mount an effective anti-microbial response results in persistent intracellular infection. This induces relentless inflammation (immunopathology) which causes tissue damage and disease symptoms....”

Full paper:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4160567/