Vitamin D3
Discussion
Ergocalciferol (D2) and cholecalciferol (D3) are very similar biochemically; however, vitamin D(2) is one-third the potency and has shorter duration of action relative to vitamin D(3).[1] Both forms of the vitamin have to undergo two sequential hydroxylation reactions in vivo to make them biologically active. The kidneys convert D3 into the hormone calcitriol which affects bone, intestine, muscle, brain, skin and immune system cells. Calcitriol is important for healthy cell differentiation.
The active metabolites of cholecalciferol increase plasma levels of calcium and phosphorous by increasing the amount of calbindin, the protein responsible for binding calcium in the intestine, and by stimulating transfer of calcium and phosphorus from the bone to the plasma. In addition to the association of vitamin D blood levels to bone metabolism, researchers have also demonstrated associations with healthy blood pressure, and blood sugar levels, as well as healthy pulmonary function. The prevalence of vitamin D insuffi ciency has been shown among patients with chronic musculoskeletal pain and dramatic reduction by supplementation with the vitamin has been demonstrated.
Research demonstrates 1, 25-dihydroxyvitamin D3 is an immune modulator and the majority of 63 observational studies in a PubMed database search demonstrated a chemo protective role of vitamin D. Data also suggests that vitamin D therapy may prolong survival in patients with chronic kidney disease. A study reported in Stroke concluded Vitamin D deficiency is present in most cases of acute stroke and may even precede a stroke event and that post-stroke repletion enhances musculoskeletal health.
The standards for recommended dietary intakes of vitamin D are being scrutinized for being too low. The consensus of scientifi c understanding at this time appears to be that vitamin D defi ciency is reached for serum 25-hydroxyvitamin D (25OHD) levels less than 20 ng/mL (50 nmol/L), insuffi ciency in the range from 20-32 ng/mL, and sufficiency in the range from 33-80 ng/mL, with normal in sunny countries being considered 54-90 ng/mL, and excess greater than 100 ng/ mL.

Dosing
Take as directed by your healthcare practitioner.
References
1. Walaszek Z, et al. Dietary glucarate as anti-promoter of 7,12-dimethyl-benz [1] anthracene-induced mammary
tumorigenesis. Carcinogenesis.1986; 7(9):1463-6. [PMID: 3091283]
2. Dwivedi C, et al. Effect of calcium glucarate on beta-glucuronidase activity and glucarate content of certain vegetables and
fruits. Biochem Med Metab Biol. 1990 Apr;43(2):83-92 [PMID: 2346674]
3. Z. Walaszek, PhD, Metabolism, Uptake, and Excretion of a D-Glucaric Acid Salt and its Potential Use in Cancer
Prevention. Cancer Detection and Prevention 1997; 21(2):178-190. http://www.cancerprev.org/Journal/Issues/21/2/186
{accessed 13 November 2007}
4. Olas B, Protective effects of D-glucaro 1,4-lactone against oxidative/nitrative modifi cations of plasma proteins. Nutrition.
2007 Feb;23(2):164-71 [PMID: 17234507]
5. Calcium D-Glucarate monograph. Natural Medicines Comprehensive Database. http://www.naturaldatabase.com {Accessed
19 November 2007}
Cautions
Keep out of reach of children. Take only under supervision of a healthcare practitioner.
This product is not intended to diagnose, treat, cure, or prevent any disease.