Reply #36: "..what you are saying.." No, that's what YOU are saying, despite quoting Dr. Veith to the contrary! [View All]

[tiptoe]

Sun-to-skin, supplement and diet:

Cholecalciferol -- biologically inactive substrate, pre-hormonal == the one-and-only natural "vitamin D" (vitamin D3)

Liver metabolises cholecalciferol:

Calcidiol -- biologically inactive metabolite of vitamin D, stored in blood, pre-hormonal == "25-hydroxycholecalciferol", 25(OH)D

Kidney metabolises calcidiol (& in situ as needed):

Calcitriol -- biologically active metabolite of vitamin D, a secosteroid hormone == "1,25-dihydroxycholecalciferol", 1,25(OH)₂D₃

The measure of "true" vitamin D status is the concentration of the pre-hormone metabolite, Calcidiol, i.e. 25(OH)D3, "on reserve", "on call" in the bloodstream, convertible by the kidney or in situ -- immediately as needed -- to the powerful, oldest-known mammalian hormone, Calcitriol:

If you get an infection, how much vitamin D does your body use up fighting the infection?
If you have cancer, how much vitamin D does your body use up fighting the cancer?
If you have heart disease, how much vitamin D does your body use up fighting the heart disease?
If you are a child with autism, how much vitamin D does your brain need to turn on the genes that autism has turned off?
If you are an athlete, how much vitamin D does your body use to make you stronger and quicker?

("Is Vitamin D an antibiotic?" Technically, no; vitamin D, per se, is inactive. But its active metabolite, calcitriol, demonstrates antibiotic-like actions == another example, like the above, of a professional taking liberty with the term 'vitamin D'.)

Cholecalciferol is a prehormone

Although vitamin D is said to be a vitamin, significant amounts of vitamin D are not found in the foods humans naturally consume. A hundred years ago, after we were steadily migrating out of the sun and into buildings, cars, and layers of sun block, Northern Europeans realized that adding a teaspoon of fish oil to infants' diets helped them thrive. How did we decide how much to add? We guessed based on animal models of rickets. Correctly, it turned out, to prevent rickets in children. But the same dose was applied to adults, and therefore the adult dose was off by a factor of 10. This mistake continues to this day.

Cholecalciferol, the naturally occurring form of vitamin D, is a prehormone made in the skin by the action of sunlight on 7-dehydrocholesterol (also known as provitamin D3). As this is meant to be a clinical paper, we will not detail the physiology and biochemistry of vitamin D. For excellent clinical reviews that give more details of vitamin D physiology, see Holick , Zittermann , and Vieth.

For our purposes, suffice it to say that nature designed a system in which humans go in the sun, make thousands of units of cholecalciferol which the liver then hydroxylates into 25-hydroxyvitamin D, or 25(OH)D. Our organs then make a steroid hormone, 1,25-dihydroxyvitamin D, which has both endocrine and paracrine functions. Although the endocrine function of 1,25(OH)2D3 made in the kidney is well known, the paracrine function is a relatively new discovery and appears to occur in every organ in the body.
hello
1,25(OH)2D3 helps regulate gene expression in more than 30 tissues and the list keeps growing. More succinctly, humans have a vitamin D system which makes thousands of units of the prehormone 25(OH)D within hours of sun exposure so various organs can then make the steroid hormone 1,25(OH)2D3 to help regulate genes in apparently every organ in the body. We assume nature created this system for a good reason.
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Vitamin D and Brain Function

In 2002 Garcion, et al, reviewed clues about vitamin D function in the brain. They concluded 1,25(OH)2D3 is involved in brain function with nuclear receptors for vitamin D localized in neurons and glial cells. Genes encoding the enzymes involved in the metabolism of this hormone (1,25(OH)2D3) are also expressed in brain cells. The reported biological effects of 1,25(OH)2D3 in the nervous system include the biosynthesis of neurotrophic factors and at least one enzyme involved in neurotransmitter synthesis. 1,25(OH)2D3 can also inhibit the synthesis of inducible nitric oxide synthase and increase glutathione levels, suggesting a role for the hormone in brain detoxification pathways. Neuroprotective and immunomodulatory effects of this hormone have been described in several experimental models, indicating the potential value of pharmacological analogs in neurodegenerative and neuroimmune diseases. In addition, 1,25(OH)2D3 induces glioma cell death, making the hormone of potential interest in the management of brain tumors.