Infection, Autoimmunity, and Vitamin D

Microbes capable of persisting inside nucleated cells can significantly alter human metabolism by changing the expression of human genes. An increasing number of studies show that the human microbiome shifts away from homeostasis in patients with chronic inflammatory conditions. Several key pathogens previously tied to inflammatory disease persist by dysregulating expression of the vitamin D nuclear receptor and subsequently the innate immune response. Vitamin D is an immunosuppressive secosteroid. Its use as a supplement may temporarily palliate inflammation but allows pathogens in the microbiome to proliferate more readily. This contributes to relapse and comorbidities over time. Further, low concentrations of 25-hydroxyvitamin D (25-D) in patients with inflammatory disease are likely a result rather than a cause of the inflammatory disease process. It seems that blood-borne 25-D levels must be kept at less than 50–60 nmol/L to optimize microbiome stability.