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Evidence for alteration of the vitamin D-endocrine system in obese subjects. Bell NH, Epstein S, Greene A, Shary J, Oexmann MJ, Shaw S. J Clin Invest. 1985 Jul;76(1):370-3. PMID: 2991340 The results provide evidence that alteration of the vitamin D-endocrine system in obese subjects is characterized by secondary hyperparathyroidism which is associated with enhanced renal tubular reabsorption of calcium and increased circulating 1,25(OH)2D. The reduction of serum 25-OHD in them is attributed to feedback inhibition of hepatic synthesis of the precursor by the increased serum 1,25(OH)2D.

"UV-related web tools maintained by Ola Engelsen * FastRT - Fast simulations of downward UV doses, indices and irradiances at the Earth's surface: http://nadir.nilu.no/~olaeng/fastrt/fastrt.html. * VitD_quartMED - Calculated Ultraviolet Exposure Levels for a Healthy Vitamin D Status: http://nadir.nilu.no/~olaeng/fastrt/VitD_quartMED.html. * VitD - Duration of Vitamin D Synthesis in Human Skin: http://nadir.nilu.no/~olaeng/fastrt/VitD.html. "

"Last Wednesday night I gave a lecture to my clients on hunter-gatherer diets. The turnout was great and the information was well-received. I had it professionally video-recorded and will probably offer this as a DVD for sale (with the handout included). Watch for it in the future. Part of what I discussed was vitamin D3 supplementation. Since I have been supplementing with 4,000-10,000 Units of D3 per day I have noted enhanced recovery and size response from my training. Apparently, skeletal muscle has both surface receptors and nuclear receptors for D3 that augment calcium flux during contraction (from surface receptors) and have steroid-like effects at the nuclear level WRT protein synthesis. This D3 supplementation is not really "supplementation" but is instead "augmentation" to levels that would be normal if we got normal sun exposure as we did in our evolutionary past. Check out www.vitamindcouncil.org for more information. Also, check out this abstract below for your consideration. Also, check out this article."

Vitamin D-induced up-regulation of tumour necrosis factor alpha (TNF-alpha) in prostate cancer cells. Golovko O, Nazarova N, Tuohimaa P. Life Sci. 2005 Jun 17;77(5):562-77. Epub 2005 Feb 25. PMID: 15904673 doi:10.1016/j.lfs.2004.10.072 Combined addition of human recombinant TNF-alpha with calcitriol or CB1093 cause enhanced effect in induction of apoptosis. We conclude that under physiological conditions vitamin D activates only the transcription of TNF-alpha gene, for TNF-alpha protein synthesis additional cofactors are required. Therefore a cooperation of vitamin D and TNF-alpha may play an important role in the control of cell growth in prostate cancer.

Vitamin D production in human skin occurs only when UV radiation exceeds a threshold. From simulations of UV irradiances, the VitD-ez www page ( http://zardoz.nilu.no/~olaeng/fastrt/VitD-ez.html) computes the daily duration of dermal vitamin D production at midday when UV radiation exceeds the required threshold. The VitD-ez www page is a simplified version of the more complex VitD web page ( http://zardoz.nilu.no/~olaeng/fastrt/VitD.html). The simplified VitD-ez www page is convenient for users unfamiliar to radiative transfer modelling, because the model input is limited and more intuitive.

An acknowledged benefit of exposure to ultraviolet radiation is synthesis of vitamin D in human skin. Here we have defined a standard vitamin D dose based upon recommended requirements for vitamin D, and present a simplified web-based tool that enables the user to calculate associated exposure times for any time and place ( http://nadir.nilu.no/~olaeng/fastrt/VitD-ez_quartMED.html). This www page is a simplified version of the more complex web tool ( http://nadir.nilu.no/~olaeng/fastrt/VitD_quartMED.html). The simplified www page is convenient for users unfamiliar to radiative transfer modelling, because the model input is limited and more intuitive.

An acknowledged benefit of exposure to ultraviolet radiation is synthesis of vitamin D in human skin. Here we have defined a standard vitamin D dose based upon recommended requirements for vitamin D, and present a web-based tool that enables the user to calculate associated exposure times for any time and place ( http://nadir.nilu.no/~olaeng/fastrt/VitD_quartMED.html). The recommended UV exposure times depends on latitude, time, total ozone, clouds, aerosols, surface reflectivity and altitude all of which can be specified by the user. A simpler version for non-experts is available at http://nadir.nilu.no/~olaeng/fastrt/VitD-ez_quartMED.html

"I discussed in my last post how Dr Vieth has a model of tissue 1,25(OH)2D synthesis and degradation in which the level of active substance is pretty well independent of blood vitamin D level, provided the level is either rising or stable. I think it is also worth pointing out that he is talking, hypothetically, about tissue 1,25(OH)2D, not plasma level... As we know, almost nothing is known about tissue 1,25(OH)2D control. By Vieth's hypothesis tissue 1,25(OH)2D is OK so long as there is at least SOME vitamin D present in plasma and the level dose not vary too much. Obviously there is a level below which you can have as much of the enzyme for converting vitamin D to the active form as you like, if there is no vitamin D in your blood you can't make any 1,25(OH)2D in your tissues, or in your kidneys for export to your blood to control calcium levels. At the lower extremes we have rickets and osteomalacia. These are clear cut, unarguable markers of vitamin D deficiency, in the absence of confounding factors (there are a few)."

Aging decreases the capacity of human skin to produce vitamin D3. MacLaughlin J, Holick MF. J Clin Invest. 1985 Oct;76(4):1536-8. PMID: 2997282

Aging decreases the capacity of human skin to produce vitamin D3. MacLaughlin J, Holick MF. J Clin Invest. 1985 Oct;76(4):1536-8. PMID: 2997282 doi:10.1172/JCI112134 An evaluation of surgically obtained skin (age range, 8-92 yr) revealed that there is an age-dependent decrease in the epidermal concentrations of provitamin D3 (7-dehydrocholesterol). To ascertain that aging indeed decreased the capacity of human skin to produce vitamin D3, some of the skin samples were exposed to ultraviolet radiation and the content of previtamin D3 was determined in the epidermis and dermis. The epidermis in the young and older subjects was the major site for the formation of previtamin D3, accounting for greater than 80% of the total previtamin D3 that was produced in the skin. A comparison of the amount of previtamin D3 produced in the skin from the 8- and 18-yr-old subjects with the amount produced in the skin from the 77- and 82-yr-old subjects revealed that aging can decrease by greater than twofold the capacity of the skin to produce previtamin D3. Recognition of this difference may be extremely important for the elderly, who infrequently expose a small area of skin to sunlight and who depend on this exposure for their vitamin D nutritional needs.

Sunlight regulates the cutaneous production of vitamin D3 by causing its photodegradation. Webb AR, DeCosta BR, Holick MF. J Clin Endocrinol Metab. 1989 May;68(5):882-7. PMID: 2541158 doi:10.1210/jcem-68-5-882 Vitamin D3 proved to be exquisitely sensitive to sunlight, and once formed in the skin, exposure to sunlight resulted in its rapid photodegradation to a variety of photoproducts, including 5,6-transvitamin D3, suprasterol I, and suprasterol II.suprasterol I, and suprasterol II.

White Europeans could have evolved as recently as 5,500 years ago, according to research which suggests that the early humans who populated Britain and Scandinavia had dark skins for millenniums. It was only when early humans gave up hunter-gathering and switched to farming about 5,500 years ago that white skin began to be favoured, say the researchers. This is because farmed food was deficient in vitamin D, a vital nutrient. Humans can make this in their skin when exposed to sunlight, but dark skin is much less efficient at it.

Bioactive vitamin D or calcitriol is a steroid hormone that has long been known for its important role in regulating body levels of calcium and phosphorus, and in mineralization of bone. More recently, it has become clear that receptors for vitamin D are present in a wide variety of cells, and that this hormone has biologic effects which extend far beyond control of mineral metabolism. The active form of vitamin D binds to intracellular receptors that then function as transcription factors to modulate gene expression. Like the receptors for other steroid hormones and thyroid hormones, the vitamin D receptor has hormone-binding and DNA-binding domains. The vitamin D receptor forms a complex with another intracellular receptor, the retinoid-X receptor, and that heterodimer is what binds to DNA. In most cases studied, the effect is to activate transcription, but situations are also known in which vitamin D suppresses transcription. Each of the forms of vitamin D is hydrophobic, and is transported in blood bound to carrier proteins. The major carrier is called, appropriately, vitamin D-binding protein. The halflife of 25-hydroxycholecalciferol is several weeks, while that of 1,25-dihydroxycholecalciferol is only a few hours. The vitamin D receptor binds several forms of cholecalciferol. Its affinity for 1,25-dihydroxycholecalciferol is roughly 1000 times that for 25-hydroxycholecalciferol, which explains their relative biological potencies

Vitamin D effective ultraviolet wavelengths due to scattering in shade. Turnbull DJ, Parisi AV, Kimlin MG. J Steroid Biochem Mol Biol. 2005 Sep;96(5):431-6. Epub 2005 Jul 6. PMID: 16005208