How to Diagnose Dysregulated Vitamin D Metabolism
Chronic inflammatory diseases develop in reaction to the invasion of nucleated cells by pleomorphic bacteria (L-forms). The intracellular bacterial processes disable a crucial part of the innate immune system, the VDR (Vitamin D Receptor), which results in dysregulated vitamin D metabolism.
Dysregulated vitamin D metabolism is diagnosed by measuring the D-metabolites: 25 hydroxyvitamin-D (25-D) and 1,25 dihydroxyvitamin-D (1,25-D).
It's essential to measure both 25-D and 1,25-D because the level of 25-D doesn't directly reflect the level of 1,25-D. The key vitamin D level is 1,25-D because it is the active metabolite.
Current 25-D lab ranges have been skewed high by dietary supplementation and flawed thinking in response to epidemiological studies showing low levels of 25-D in many chronic diseases. This represents a failure to recognize that low 25-D is caused by the disease process.
The Merck Manual (Oct 2006) states that in healthy persons, the 25-D level is 25 to 40 ng/mL.
Patients with dysregulated vitamin D metabolism (who have not been supplementing with vitamin D) often have a low level of 25-D.
Many labs list inappropriately high ranges for 1,25-D; current ranges are skewed high because a large percentage of patients getting this unusual test are ill with undiagnosed Th1/Th17 inflammation. Therefore, a 1,25-D result that is within current normal lab ranges may still indicate dysregulated vitamin D metabolism.
The Merck Manual (Oct 2006) states that in healthy persons 1,25-D levels are 20 to 45 pg/mL. A large Danish study found that the mean value for 1,25-D in a normal population was 29 pg/ml with a standard deviation of 9.5.
The 1,25-D measurement is a sensitive assay and results can be falsely low if the sample isn't handled correctly. High values of 1,25-D, however, are always reliable and diagnostic of dysregulated vitamin D metabolism.
Elevated 1,25-D (hypervitaminosis-D) can have many negative consequences. For example, at levels above about 42 pg/mL 1,25-D begins to stimulate bone osteoclasts, causing bone to be resorbed (dissolved) back into the bloodstream. Not only does this lead to osteoporosis, but also to calcium being deposited into soft tissues of the body; including lungs, breasts and kidneys (where it may form kidney stones). See this study: Vitamin D Antagonist, TEI-9647, Inhibits Osteoclast Formation Induced by 1alpha,25-dihydroxyvitamin D3 from Pagetic Bone Marrow Cells.
Patients on Inflammation Therapy (IT) take Benicar (olmesartan medoxomil) to up-regulate the VDR so anti-microbial peptides are produced which kill the intracellular bacteria and restore normal vitamin D metabolism. This is evidenced by the eventual reduction in serum 1,25-D to normal levels and resolution of inflammatory symptoms.