calcium supp's cause arterial calcifications?

5.9: web,mis.health/
when do calcium supps cause arterial calcifications?:

. I had erroneously assumed that the
routine finding of arterial calcification in elders
was being made worse by the advice
to take calcium to fight bone resorption .

. calcification is a problem,
but in the calcium deficient test animal,
calcium-supp'ing, reduced calcification by 62%;
because,
when there's a deficit of calcium in the blood,
 the body excessively releases bone calcium
[20. Sanders S, Debuse M. 2003:89-90.]
and saturates soft tissues with calcium .

. so, could there be a bell curve effect,
where a deficit of calcium does
 flood the system with bone calcium,
but likewise, if you're taking megadoses of calcium,
that would have the same effect as low calcium?

. in any case, there is a study showing that
calcium supp's do increase the risk
of heart attacks by 27%;
and, lef.org points out the study's special conditions:
the risk from calcium is eliminated by
combining the calcium with sufficient levels of
calcium controlers (vit'd, vit'k, magnesium).
. not only does vit'k keep calcium in bones,
it has some way of keeping it off arterial walls,
[5.10: likely by making it latch onto more useful things,
that happen to be closer by .]

5.10: depends on form:
. certain forms of vitamin D are provoking bone resorption:
25-hydroxycholecalciferol
vs 1,25-dihydroxycholecalciferol
In 10 patients taking oral 0.25 micrograms of
1,25-dihydroxycholecalciferol twice daily for 7 d,
--[ Rocaltrol Oral Suspension (calcitriol) Rx ]--
calcium absorption increased more than in 10 patients taking
oral 40 micrograms of
25-hydroxycholecalciferol once daily for 7 d (p less than 0.02)
--[ the common D3 found in most supplements ]--
despite both groups having a
similar increase in plasma 1,25-(OH)2D.
These results support the view that the major effects of
oral 1,25-dihydroxycholecalciferol on absorption
is due to a local action on the gut
and that it is possible to increase
calcium absorption in osteoporosis
with oral 1,25-dihydroxycholecalciferol
without increasing its undesirable action on bone resorption.

6.5: may depend on dosing too:
. the form provoking the bone resorption
is also the most common form by far;
so maybe it would still be safer if
the dose was divided and taken with calcium ?
but too much calcium
inhibits conversion to the active form:

The following inhibit the activity of 1-hydroxylase enzyme
needed for making active vitamin D (calcitriol):
    # low parathyroid hormone (PTH)
     - PTH stimulates 1-hydroxylase.
     [see how common low PTH is, and what to do about it]
    # High calcium levels cause lowered PTH .
    # High phosphorus intake/high blood phosphorus.
    (An aside: Fructose we eat gets phosphorylated,
    grabbing phosphorus and holding it in the liver.
    So fructose (fruit) consumption can counter
    high phosphorus intake(dairy, fish, meat, soda) .)
    [don't mix high fructose with high-glycemic diet]
    # High concentrations of calcitriol
    - A negative feedback mechanism is in play, meaning,
    the more active vitamin D you have circulating,
the less active the enzyme.

. the Active vitamin D, also called calcitriol,
is a high-energy, twice-hydroxylated compound
with a very short half-life (about 5 hours)
- such that levels of active vitamin D are tightly controlled .
Serum concentrations of active vitamin D (calcitriol)
are not typically correlated with vitamin D intake,
or vitamin D stored as 25(OH)D3.
It is primarily calcitriol that is responsible for the
benefits we're discovering about this vitamin,
e.g. mineral balance and bone mineralization,
immunity, blood pressure control,
reduction in cancer cell proliferation, and insulin secretion.

list of calcitriol suppliers .
(CAS NO.     32222-06-3; 125338-24-1)