Vitamin D is not technically a true vitamin. By definition, a vitamin is something you can’t make yourself and so has to be acquired from food or supplements. It got lumped in with vitamins early on before it wasn’t well understood.
There are five forms of Vitamin D. The one we’re concerned with, the one important to health, is cholecalciferol. Cholecalciferol is a secosteroid, a steroid molecule with one ring open. (I’m sure you remembered this from biochem.)
Cholecalciferol is synthesized in the skin from 7-dehydrocholesterol when the skin is subject to ultraviolet B (UVB) light. How much cholecalciferol is made depends on several things: the intensity of the UVB as determined by the latitude, season, cloud cover, and altitude, and the age and amount of pigmentation of the skin. Equilibrium can be reached in the skin within a few minutes of exposure. After that, cholecalciferol degrades as fast as it’s made, making it impossible to get vitamin D overdose from UV exposure.
It’s generally accepted that 5–30 minutes of exposure of the face, arms, and legs twice a week provides enough vitamin D for most people. I’m at 4,700 feet elevation. I can burn in the spring at 15-20 minutes if I’m not careful as we regularly have a UV index of 10. The higher the altitude, the less atmosphere to filter out UVB rays. Cholecalciferol can also be produced from UV lamps in tanning beds, though at much lower levels as most tanning beds produce only 4–10% UVB. Blood levels have been found higher in people who tan frequently.
Cholecalciferol is inactive. It travels from the skin to the liver, where it’s converted to calcifediol, also known as 25-(OH)D, by the enzyme 25-hydroxylase. Conversion to 25-(OH)D is loosely regulated, if at all. Calcifediol is what’s measured in the blood to determine a patient’s vitamin D status and is the sum of what was produced in the skin as well as any ingested D2 or D3. After a typical daily intake of vitamin D3, it takes about seven days to convert it to calcifediol.
Although we measure 25-(OH)D in the blood, it’s not the active form of the vitamin. It travels to the kidney where it’s converted into calcitriol (1,25-(OH)2 vitamin D3), the bioactive form, by an enzyme called 1-alpha-hydroxylase and under the influence of parathyroid hormone. Unlike calcifediol, this conversion is tightly regulated. When these metabolites travel through the blood they’re bound to vitamin D-binding protein.
Calcitriol is very important for maintaining calcium levels and promotes bone health and development. It increases the absorption of calcium from the intestines, promotes reabsorption of lost calcium back into bones, and increases the production of brain-derived neurotrophic factor (influences the brain and peripheral nervous system), nitric oxide (an important vasodilator), and glutathione (the body’s main antioxidant). Lastly, calcitriol promotes the formation and differentiation of new cells. Pretty important substance, wouldn’t you say?
Low levels of vitamin D have been associated with multiple sclerosis, asthma, flu, tuberculosis, and certain cancers. And, as we’ll discuss, certain autoimmune conditions.
For vitamin D to act, it needs to bind to a set of receptors called, not surprisingly, vitamin D receptors (VDRs), principally located in the nuclei. VDRs can be found in most organs, including the brain, heart, skin, gonads, prostate, and breast. And, here’s one tie-in to the thyroid: VDRs are a subset of thyroid hormone receptors.
In general, vitamin D deficiencies are caused by decreased exposure of the skin to sunlight. Far fewer people work outdoors now than before and the use of a sunscreen with an SPF of only 8 can block 95% of vitamin D production. The following conditions are considered risk factors for vitamin D deficiency:
I found several studies that establish a relationship between low vitamin D levels and autoimmune disease (both Hashimoto’s thyroiditis and Graves’ disease). Vitamin D deficiency was 3–5 times as common in patients with an autoimmune thyroid disease than in controls.
The results of the studies indicate:
Vitamin D needs to be present in adequate amounts for T3, the active thyroid hormone, to get into and energize the cell. They both work in the cell nucleus. Put another way, thyroid hormones won’t work well when vitamin D levels aren’t optimal.
However, vitamin D’s involvement in autoimmune thyroid disorders goes deeper still.
Autoimmune diseases are thought to be caused by genetic polymorphism: small changes at the genetic level that affect the structure and function of important cells and proteins, including VDRs.
In fact, several studies have shown that VDR polymorphism is common in those with autoimmune thyroid disease. This means the biological activity of vitamin D is reduced, even when it properly binds to receptors. If VDRs in the thyroid gland are polymorphic, even normal levels of vitamin D can’t produce the same effects as it can on normal VDRs.
Therefore, people with polymorphic VDRs need higher than normal serum levels of vitamin D to avoid deficiency. We’ll visit this topic again when discussing vitamin D therapy.
Assessment of and Ideal Vitamin D Levels
The test to order is the 25-hydroxy vitamin D test. Most labs will have a normal range of 30–100. Many, if not most, MDs won’t consider vitamin D therapy if levels are with the normal range, even just inside the normal range. 1,25()H)D is not tested because it’s regulated by other hormones, such as parathyroid hormone. 1,25(OH)D levels can be normal in a vitamin D-deficient individual.
Research is clear that 35 ng/ml is the minimum level for optimum function, for healthy people. But people with an autoimmune thyroid condition aren’t healthy.
They often have stress, excess weight, GI problems, high inflammation, VDR polymorphisms, and other factors that inhibit production, absorption, and utilization of vitamin D. So, the minimal 25-hydroxy vitamin D level for those with Hashimoto’s thyroiditis may be significantly higher. But how high?
Too much vitamin D is toxic. Get too much of it and it can increase odds of heart disease and, oddly, lower bone density.
There appears to be a close relationship of vitamin D to vitamins A and K2. Higher D levels increase the demand for demand for K2 and A so increasing D intake, especially the higher amount commonly recommended, in the presence of inadequate A and K2 intake is probably unwise.
Vitamin D Therapy
How much and what kind of vitamins D, A, and K2 turned out to be a more complicated topic than expected, so I’ll cover this in a future post. We'll also discuss the SET-DB™ approach to improving vitamin D (and A and K2) levels.
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Dr. Teryl Boothe and selected guests.