Mega D - How it Works

Background

Structure and physical properties: Vitamin D3 is a three-ringed hydrocarbon, containing a single hydroxyl group and structurally related to cholesterol. For full activity, D3 is further hydroxylated by the enzyme cytochrome P-450 in the liver, biosynthesizing the active vitamin D3, di-hydroxyD3. Human plasma seems to acts as the storehouse for vitamin D3 because no repository organ has been identified. The lifetime of di-hydroxyD3 in the bloodstream is several weeks¹. A small portion of the circulating di-hydroxyD3 is removed by the kidney for yet another hydroxylation, forming the important vitamin D hormone, calcitriol. This final hydroxylation is stimulated by the parathyroid hormone (PTH) when calcium levels are low. An overabundance of calcitriol is prevented, in the presence of plentiful calcium, under the direction of PTH, to “incorrectly” hydroxylate excess D3 into an inactive form. Hence, the levels of vitamin D3 and calcitriol are rigorously controlled in the body and overdoses are very uncommon.

Physiology:

The di-hydroxyD3 (1α,25-(OH)2D3) is the form of vitamin D3 with the highest bloodstream concentration. It has been shown to rapidly signal the release of calcium from intracellular stores in bone-forming osteoblasts and from extra-cellular stores into these cells in a manner of minutes². It also modulates levels of cyclic AMP, protein kinase signaling activities, phosphate transport and skeletal muscle cell calcium content. Though calcitriol and di-hydroxyD3 are known to interact with transcription promoters within the nucleus, much like steroid hormones, many forms of stimulation like cyclic AMP, protein kinase and calcium transport occur much too rapidly to be the result of new protein synthesis. These enhanced activities must occur through direct interaction of D3 with these signaling enzymes. Circulating levels of vitamin D3 and calcitriol are inversely correlated with levels of the PTH, and high PTH damages the body by stimulating bone catabolism and degenerative joint disease.

Intake:

Much Vitamin D is synthesized in the human skin from the organic fatty precursor, 7-dehydrocholesterol and sunlight, converting this form of cholesterol into previtamin D3. Less than an hour per day of sunshine is thought sufficient for this transformation and no overdose of D3 from sunlight exposure has been documented. Synthesis is reduced in darkly pigmented skin or for people with minimal skin exposure. Vitamin D3 is slowly synthesized from this intermediate over a period of days then released from the skin into the bloodstream in a measured fashion³ to be further modified in the liver and kidney. While this unique and “free” biosynthesis is adequate for humans at low latitudes and good weather, increasing latitude, cloud cover and our indoor life style enormously decrease the effectiveness of the photosynthetic biosynthesis. During digestion vitamin D3 is rapidly assimilated by a specific calcium transport protein located in the duodenal and intestinal epithelia. This is the protein responsible for vitamin D assisted calcium transport from lunch into the bloodstream. Again, this stimulation of calcium transport occurs much too quickly to be the result of gene transcription and then protein synthesis and is thought to be another case of vitamin D directly stimulating enzyme activity. Oral vitamin D3 results in a 70% higher level of vitamin D in the bloodstream⁴ when compared to dosing with oral D2. (Vitamin D2 is a product from fungi fermentation.)

Insufficiency and Deficiency:

Vitamin D3 deficiency has become a problem of epidemic proportions for the elderly and blacks of all ages across North America⁵. This deficiency has lead to a rise in reports of rickets in small children with dark skin in the US and Canada. Elderly folks, bedridden or confined to rest homes, also suffer low levels of circulating vitamin D and as many as 40% are now considered insufficient in circulating D3. It seems that people in North America, spending the most time indoors, cannot generate enough vitamin D in the summer to sustain an adequate level through the winter months and many people are deficient in vitamin D for many months. Therapy for clinical osteoporosis now includes liberal amounts of vitamin D3⁶. Clinicians in sunny Australia now consider the deficiency problem so serious as to study routine injection of massive doses of vitamin D3⁷.

Symptoms of Vitamin D Deficiency:

Osteopathy – can lead to loss of spinal minerals in women of any age and hip fractures in the aged. Studies of vitamin D and bone density concluded the low dosage given during these studies, was not enough to be efficacious. Myopathy – insufficient vitamin D impedes calcium transport in muscles creating musculoskeletal pain and is even suspected for causing heart weakness⁸. Immune weakness – vitamin D deficiency is correlated with increased respiratory infections and is strongly correlated to tuberculosis and multiple sclerosis. Inflammation– lack of vitamin D is correlated with rheumatoid arthritis and irritable bowel syndrome⁹.

Food Sources:

Few food sources provide natural vitamin D3; egg yolk and fish oils. Much of our dietary vitamin D3 is provided by fortified milk and margarine. Children on high rice diets low in protein and fats can develop severe vitamin D deficiency manifesting as rickets. Replacing milk with soft drinks in our adolescent diets exacerbates the problem. There is a growing consensus among those immersed in vitamin D research and clinical work that the current US government recommendation is much too low for the general public welfare¹.

References

1. Zittermann A (2003). Vitamin D in preventative medicine: are we ignoring the evidence? Brit. J. Nutri. 89: 552-572. Vieth R.(1999). Vitamin D supplementation, 25-hydroxyvitamin D concentrations and safety. Amer. J. Clin. Nutr. 69: 842-856.
2. Falkenstein E, Tillmann HC, Chris, M, Feuring M and Wehling M (2000). Multiple actions of steroid hormones – a focus on rapid, nongenomic effects. Pharmocol. Rev. 52: 513-555.
3. Holick MF (1981). The cutaneous photosynthesis of previtamin D3: a unique photoendocrine system. J. Invest. Dermatol. 77: 51-58.
4. Trang H, Cole DE, Rubin LA, Pierratos A, Siu S and Vieth R (1998). Evidence that vitamin D3 increases serum 25-hydroxy-vitamin D more efficiently than does vitamin D2. Amer. J. Clin. Nutri. 68: 854-858.
5. Hanley DA and Davison KS (2005). Vitamin D insufficiency in North America J. Nutr. 135: 332-337.
6. Heaney RP (2003). Advances in therapy for osteoporosis. Clin. Med. & Res. 1: 93-99.
7. Diamond TH, Ho KW, Rohl PG and Meerkin M (2005). Annual intramuscular injection of a megadose of cholecalciferol for treatment of vitamin D deficiency. efficacy and safety. Med. J. Aust. 183: 10-12.
8. Zittermann A, Schulze Schleithoff S, Tenderich G, Berthold HK, Körfer R and Stehle P (2003). Low vitamin D status: a contributing
9. Cantorna MT and Mahon BD (2004). Mounting evidence for vitamin D as an environmental factor affecting autoimmune disease prevalence. Exp. Biol. Med. 229: 1136-1142.

Supplement Facts - Mega D

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The Need To Consider Quality:

Of the magnesium supplements tested by ConsumerLab.com, 25% failed to meet quality standards. One magnesium supplement contained only 45.4% of labeled amount, despite boasting a "GMP" (Good Manufacturing Practices) seal on its label, and another supplement provided only 28.8% of the labeled amount.
Reference: ConsumerLab.com, Magnesium Supplement Reviews and Quality Ratings, Posted 5/19/09

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ConsumerLab.com, New Product Review: Multivitamin and Multimineral Supplements, Posted 4/1/09

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Reference: June 22, 2007, FDA @ http://www.cfsan.fda.gov/~dms/dscgmps7.html