Over the past decade, vitamin D has distinguished itself as a miracle supplement. Hundreds of research studies suggest that vitamin D can help prevent a multitude of conditions, from osteoporosis to autoimmune disorders, immune function, cardiovascular disease, cancer and more.
Statistics suggest that a large number of adults and children do not have enough vitamin D in the body.
Many doctors and nutritionists routinely prescribe supplements with high doses of vitamin D, ranging from 2,000-10,000 IU (international units) per day to 50,000 IU per week.
Vitamin D obviously supports human health. But why not address the reasons behind the decline in vitamin D?
There is already solid evidence that testing and correcting vitamin D deficiency is much more complex than monitoring hydroxyvitamin D levels and vitamin D3 supplementation. This approach loses sight of the fact that many factors will mediate how 25-hydroxyvitamin D is converted to the active secosteroid hormone calcitriol (1,25-dihydroxyvitamin D) and the most potent metabolite of vitamin D. In addition, many pathogenic influences will alter the course of intracellular transport of calcitriol and nuclear binding to the vitamin D receptor (VDR).
Without investigating these influences, clinicians lose sight of the causes of aberrant fluctuations in vitamin D levels and cannot apply a proper balancing and healing protocol.
The Importance of the Active Form of Vitamin D in Assessing Deficiency.
Recent research suggests that almost every cell in our body has receptors for vitamin D, which indicates a much stronger role for this vitamin than previously thought. This new information has helped us discover that vitamin D also influences the immune system and helps differentiate cells, regulate blood pressure, insulin secretion and more.
Vitamin D in its active form – calcitriol is of great importance for many physiological functions. It is a micronutrient that helps absorb calcium from food in the digestive tract and regulate other minerals in the body.
These functions are activated when calcitriol binds to the site of the VDR nuclear receptor. Among other things, vitamin D receptor (VDR) activation is essential for:
- modulating the immune behavior of T cells and B cells
- reducing the proliferation of pro-inflammatory cytokines (interferon gamma and IL-17).
- interaction with PTH (parathyroid hormone) to absorb calcium from the intestine and reabsorption of calcium into the kidneys, as well as to regulate the excretion of inorganic phosphate.
- neuronal integrity and growth – NGF (nerve growth factor) which is enhanced by activating the VDR receptor.
- activation of the dopamine pathway
- interaction with sexual reproduction processes, including androgen receptor function, testosterone synthesis and gonadal sufficiency
Vitamin D and the Connection with Inflammation and Infections in the Body.
Some medical research has determined that low levels of 25 (OH) D are a consequence of chronic inflammation, rather than its cause.
Research indicates that the proliferation of pathogenic bacteria can lead to a high level of 1.25 (OH) 2D and 25 (OH) D low. Eradicating pathogens and improving immunity can correct the dysfunctional metabolism of vitamin D and can resolve inflammatory symptoms.
Pathogen infections negatively influence Vitamin D receptor function, especially when these are present:
EBV (Epstein Barr virus)
Borrelia burgdorferi (spirochetes that cause Lyme disease)
Gliotoxin, produced by many fungi.
Vitamin D Deficiency and Biochemical Balance.
Random supplementation with high doses of vitamin D without knowing and understanding the person’s entire health profile or the condition of other minerals and vitamins involved in biochemical balance can be even dangerous. For example, high doses of vitamin D can lower the levels of zinc, magnesium, potassium, phosphorus, calcium and vitamin A!
Vitamin D and calcium exist in a delicate balance. If the body cannot regulate calcium levels, it can be deposited on the body’s soft tissues, including the arteries. Some studies suggest that this is a real possibility when vitamin D levels become too high.
In addition to its role in coagulation, vitamin K also helps build and maintain healthy bones and teeth. It does this by activating a specific protein called osteocalcin that helps the body use calcium and deposit it where it belongs. So there is a very strong connection between calcium and vitamin K, and if we are deficient in vitamin K, calcium can accumulate and deposit in the soft tissues of the body. People with a low vitamin K content are more likely to suffer from atherosclerosis or arterial calcification. So, if supplemented with high doses of vitamin D in the presence of vitamin K deficiency, the long-term results could be disastrous.
Magnesium is an important mineral involved in over 300 different processes in the body, including the ability to produce and use ATP, the body’s main form of energy. Magnesium also helps with a number of activities related to the production and use of vitamin D. In particular, it appears to alter the sensitivity of tissues to vitamin D and helps maintain calcium balance.
Because magnesium is used in vitamin D metabolism, supplementation with high levels of vitamin D could cause an even greater magnesium deficiency in an already deficient population and can also cause calcium deposits in the arteries.
Vitamin A can prevent vitamin D toxicity and vice versa. The lower the level of vitamin A, the more vitamin D accumulates.
Other implications that must be considered when evaluating the condition of vitamin D, in addition to the possibility of high inflammation and unresolved infections is the involvement of the parathyroid glands. When they feel a drop in their blood calcium levels, they secrete parathyroid hormone (PTH). PTH stimulates the formation of active vitamin D, which increases calcium absorption in the small intestine and the release of calcium from the bone, in an attempt to restore normal levels of calcium in the blood. High PTH levels can therefore lead to a high level of 1.25 (OH) 2D, low bone mineral density, increased risk of fractures and osteoporosis.
We can thus use PTH, calcium and active vitamin D3 as markers to give us a more complete picture of the state of vitamin D. In his presentation at IHH-UCSF, Dr. Masterjohn suggested that serum PTH levels above 30 pg / ml may be an indication for vitamin D deficiency when 25 (OH) D levels are limited. But if 25 (OH) D levels are low or even slightly below the laboratory reference limit (eg, 25 to 30 ng / ml), but PTH is less than 30 pg / ml, it is unlikely that the patient is deficient in vitamin D, and supplementation is not justified.
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