Microsoft word - mega d vitamin d 1000 iu.doc

MEGA D Vit. D3 1,000 I.U.
DESCRIPTION: One softgel provides 1000 IU of vitamin D3
100 count bottle of easily swallowed light beige softgels.
FORMULA: One softgel provides Vitamin D3 of 1000 IU (250% daily value).
Other ingredients: rice bran oil, gelatin, glycerin and purified water.

DIRECTIONS: One capsule per day; recent investigations into the safety and efficacy of
vitamin D3 indicate more vitamin D3 is required during the winter months and periods of
cloud cover. It is advisable to raise the daily dose to 1000 IU, year round.
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
factor in the pathogenesis of congestive heart failure. J. Amer. Coll. Cardiol. 41: 105-112.
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.

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