Ten Reasons Everything We Thought We Knew About Vitamin D Is Wrong: Part 1
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.
There are several forms of vitamin D, including over a dozen forms of D3 formation. We also get this “vitamin” from food, diet, supplements, and sun exposure. D3 is converted by the liver into 25-D, which functions as a steroid. 1,25-D, the activated form of vitamin D, functions as both a steroid and a hormone. It is produced inside various types of cells, including those of the immune system and the kidneys, as well as in the skin and blood in response to sunlight. In healthy individuals, the kidneys continually convert 25-D into its active form, 1,25-D. However, recent research has elucidated facts that show we aren’t even completely correct about the synthesis of 1,25-D.
A paper published by the Institute of Biomedical Research in Birmingham, England, states that the active form of vitamin D, [1,25-D] is a very potent immunomodulatory secosteroid. This means that it is a steroid-like molecule that can control the activity of the immune system. Hormone D synthesized from the sunlight controls both arms of the immune system: the innate and the adaptive systems.
Biophysics research and molecular modeling have shown us that the hormone 1,25-D binds to and activates the Vitamin D Receptor (VDR). The VDR plays a fundamental role in the body. It transcribes over 27,000 genes, according to researchers at McGill University in Canada. The Vitamin D Receptor also serves as a switch that regulates the activity of the innate immune system. The 25-D form also binds to the Vitamin D Receptor and, like the active 1,25-D form, affects the activity of the immune system as well. However, quite the opposite to the 1,25-D form, when 25-D binds to the Vitamin D Receptor, it decreases the activity of the receptor, causing the innate immune system to slow down and shut off. This effect begins around 20 ng/ml (of 25(OH)D3) and gradually increases with higher levels of 25-D in the blood until the VDR becomes completely blocked.
Current molecular research is providing us with a new understanding of the causes of chronic disease. When a person becomes ill with chronic disease, a type of bacteria known as L-form bacteria begin to live inside the cells of the immune system and in various tissues. These bacteria create proteins that can bind and block the Vitamin D Receptor, like the 25-D form. Together with an elevated 25-D, these bacterial proteins can block the ability of the Vitamin D Receptor to turn on the immune system more than either can when alone.
The Vitamin D Receptor also directly controls the expression of many antimicrobial peptides (AMPs). AMPs are proteins that kill bacteria, viruses, and fungi. they do so by a variety of mechanisms such as disrupting membranes, interfering with metabolism, and targeting components inside of the cell. When 25-D reaches such a level that it inactivates the receptor, these AMPs are no longer produced, and bacteria can spread more easily throughout the body.
The innate immune system is responsible for killing bacteria like these L-form bacteria. It is controlled by the Vitamin D Receptor (VDR). Elevated levels of the 25-D form and bacterial proteins will bind to and inactivate the VDR, causing the immune system to work less effectively. As the immune system becomes increasingly inhibited, fewer of these L-form bacteria are taken out by our innate immune system. Additionally, the Vitamin D Receptor is no longer able to transcribe antimicrobial peptides, and because of this, fewer bacteria are killed by DNA fragmentation. As fewer and fewer bacteria die, fewer inflammatory cytokines are released, and fewer toxins enter the bloodstream. This results in a temporary decrease in the levels of systemic inflammation, which is why most of us start to feel much better when we supplement Vitamin D3 in pill form. However, without the innate immune system and the antimicrobial peptides to keep L-form bacteria in check, pathogens easily spread to new cells and other new organs. People who spend long periods of time in the sun typically only have a small or moderate amount of L-form bacteria in their bodies, as this is generally a practice of healthy individuals. However, if 25-D rises to the level at which it inhibits their immune systems minor symptoms may be temporarily relieved. This is very similar to icing an injury. Ice dulls the sensation of pain, which is caused by the inflammatory process. However, it is this inflammatory process that is responsible for healing the actual injury.
This may all sound a bit odd and counterintuitive but we’ve all taken some sort of anti-inflammatory steroid in some form before. Take Prednisone, for example. Prednisone is given to patients with diseases such as multiple sclerosis, rheumatoid arthritis, sarcoidosis, and lupus. These diseases are thought to be auto-immune in nature, so steroids are given to slow down the hyperactive immune system.
Researchers at Duke University found that elderly men and women who consumed higher levels of calcium and, in particular, “vitamin D” are significantly more likely to have greater volumes of brain lesions, which is indicative of regions of damage that can increase the risk of cognitive impairment, dementia, and depression. The team found that “vitamin D” intake, (mean 341 IU and maximum intake 1014 IU), was the only variable that retained a significant correlation with the brain lesions when analyzed by multivariate analysis. The lesions likely result when L-form bacteria in the brain cause the release of cytokines that damage tissues. The resulting inflammation can damages blood vessels and promote calcification.
Next time, reason #2.
Robert C Jacobs
USAW, PICP, MA
