Re: Amy Proal and the Trevor Marshall - blecch!

John,
there are many factors that contribute to what is perceived as a Vitamin D deficiency.

In Nature our bodies are designed to live in the fresh air, with sun exposure on our skin, with the need to exercise and keep warm, with good wholesome food. These are just some of the tenets of Natural Hygiene: a proven system of health recovery and maintenance based on Physiological Laws.

For many, these elements of health are restricted either voluntarily or involuntarily for one reason or another.

Nature has designed our bodies to receive Cholcalciferol, or Vitamin D3, through sunlight exposure: along with other benefits that sunlight produces within the body. Food sources of Vitamin D3 are considered to be minimal and therefore inadequate.

In the absence of sunlight exposure (for whatever reason) the body still needs Cholcalciferol in the amounts determined by the body from sunlight exposure, and where this is the logical amount determined for supplementation.

What I would like to ask you John you is........

Where do humans receive their sunlight (and therefore their Cholcalciferol) in the Winter months, and especially in Northern climes unless supplemented?
No sunlight exposure results in a deficiency of this Vitamin.

You should try to understand that Cholcalciferol is not a drug, but a natural element of nutrition required by the body for optimal health and the prevention of disease.

You still have yet to provide any evidence that L-form Bacteria blocks the VDR'S (Vitamin D Receptors): meaning any intake of Cholcalciferol, from any source, becomes toxic to the body.

For those who are more technically minded, this is the most recent take on the erroneous assumption that VDR's become blocked...........

"VDRs are NUCLEAR receptors, and as such they aren't directly exposed to circulating (plasma) calcidiol (manufactured by the Liver).
In the plasma, calcidiol is bound to DBP (D binding protein) and (to a much lesser extent) albumin. Following transport through the plasma, DBP and calcidiol in turn bind to megalin proteins that are expressed on some cell surfaces, which binding in turn triggers clathrin to induce endocytosis. Following endocytosis, calcidiol is released from DBP into the cytoplasm, where it is immediately bound to hsc70 (a constitutively expressed chaperone protein that binds many things, including other D-metabolites such as calcitriol). From there, different metabolites of D appear to be selectively directed to specific intracellular organelles. Most relevantly, hsc70-bound calcitriol (aka 1,25(OH)2D, aka the "active D metabolite") has a higher binding affinity to a nuclear chaperone called BAG-1 than hsc70-bound calcidiol does.
This is important because since BAG-1 guides D-metabolites to the VDR, it means that high calcidiol levels won't significantly interfere with VDR binding of calcitriol--and thus Marshall's "in silico"-supported hypothesis that exogenous Vitamin D supplementation interferes with VDR activation turns out to be erroneous.
http://jme.endocrinology-journals.o...e2=tf_ipsecsha

http://stuff.mit.edu/people/london/universe.htm


Thank you.

Chrisb1.


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