Vitamin D, is in fact, not a vitamin. Vitamins are things that cannot be made by humans. Vitamin D is a secosteroid hormone. The active form of Vitamin D, 1,25-D, is the powerful steroid hormone made by the human body.
Chronically ill people are not deficient in Vitamin D
Every day I see new studies claiming that patients with chronic disease are deficient in vitamin D. However, this is generally not the case. This misunderstanding comes from a misplaced focus on the storage form 25(OH)D3. An overwhelming amount of studies have demonstrated that the level of the hormone 1,25-D (the active form) rises in patients with many chronic diseases. Chronically ill patients often have a level of 1,25-D exceeding five or six standard deviations above the standard value.
A vast array of studies also point to the fact that 25(OH)D3 is low in people with numerous chronic inflammatory diseases. What explains these altered levels of 1,25-D and 25-D? As mentioned in part 1, in patients with chronic disease, L-form bacteria create proteins that affect the Vitamin D Receptor (VDR) in a manner similar to 25(OH)D3. These bacteria bind and inactivate the VDR, preventing it from transcribing a wide array of genes and enzymes.
In healthy individuals, the VDR transcribes an enzyme called CYP24. CYP24 breaks down excess 1,25-D, ensuring that the level of 1,25-D in the body stays in the normal range. In chronically ill individuals, the VDR can then no longer transcribe CYP24. This, in turn, leads to the significant elevation of 1,25-D in the body since there is no CYP24 to keep it in check.
1,25-D binds to the PXR receptor, a receptor that is involved in making another enzyme called CYP27A1. CYP27A1 is responsible for converting D3 (cholecalciferol) into 25-D (calcidiol) in the liver. Elevated 1,25-D affects the activity of the PXR receptor in a way that causes less D3 to be converted into 25-D, meaning that the level of 25-D in chronically ill individuals drops.
An enzyme called CYP27B1 normally regulates the amount of 25-D converted into 1,25-D. When more CYP27B1 is produced, conversion occurs at a greater rate. L-form bacteria release cytokines (proteins that cause pain and fatigue) that activate a protein called Protein Kinase A (PKA). PKA then activates CYP27B1, causing more 25-D to be converted to 1,25-D. The level of 25-D in the body then decreases, and the level of 1,25-D increases.
A study conducted by researchers at the University of South Carolina gave healthy subjects high levels of 1,25-D and verified that it can inhibit and down-regulate the conversion of cholecalciferol into calcidiol. The low 25-D levels observed in patients with chronic disease are not a sign of “vitamin D” deficiency, but rather, an indicator of the disease process.
USAW, PICP, MA