And you would propose to use -- which -- form of calcium?

(Yes, it's a trick question.)

+--------------- D. C. Sessions <dcs@lumbercartel.com> --------------+

On Jan 16, 2:35 pm, drcee...@insightbb.com wrote:

First, limestone by way of hard water is an ancient calcium
source. Second, since the invention of grain flour and the
use of limestone grindstones, calcium carbonate has
been added directly to a foods stuff even if unintentionally.

On Jan 16, 4:35 pm, drcee...@insightbb.com wrote:

DrCee,

You are correct that calcium carbonate is one of the worst forms of
calcium supplementation.  However, more to the point, this article is
a perfect example of junk science.  I just read the entire article,
not just the abstract, and the authors made no measurements of serum
levels of calcium before or after supplementation.  Since elderly
people have low levels of stomach acid, and calcium carbonate
increases pH, it is possible that some of the participants might have
ended up with lower levels of serum calcium as a result of ingesting
the calcium carbonate.  In any case, there is no excuse for such
sloppy experimental protocols.

Ed Friedman

Are you saying calcium citrate is inorganic?

And you may want to lookup the
disassociation constant for calcium citrate.
And then you need ask yourself why
this is important.

See the following cut and paste on
the topic.

Calcium Supplements May Increase MI Risk in Older Women
BMJ Online First, January 16, 2008, as reported by WebMD

Healthy postmenopausal women randomly assigned to receive 1 g of
elemental calcium citrate supplements daily for 5 years had a more
than 2-fold greater relative risk for myocardial infarction (MI)
compared with women receiving placebo, reports WebMD. Calcium takers
were also at greater risk for a composite cardiovascular event
endpoint of MI, stroke,
or sudden death. The investigators, from the University of Auckland,
New Zealand, concluded that the potential benefits of calcium
supplementation for preservation of skeletal health may not outweigh
the detrimental cardiovascular events in this population.

More likely a matter of making sure there's enough of both and not
too much of either.  Excess Mg is more readily excreted than
excess Ca, so the exact amount of Mg in particular isn't all that
critical.

It's not like natural foods have precise ratios, after all -- animals
have to be pretty flexible about such things and have mechanisms to
manage the variations.

+--------------- D. C. Sessions <dcs@lumbercartel.com> --------------+

And w know this -- how?

Why, by doing exactly what this study did: supplement calcium alone.
Now someone else can do a study with Ca+Mg (or various ratios thereof)
and prove exactly what you're telling us.  That way, when someone like
me asks "how do you know that the correct ratio is 3:1 instead of 2:1?"
you can point him to blinded, controlled studies instead of an opinion
piece disagreeing with another opinion piece.

My, aren't  you charitable today towards someone who actually went to the
trouble of publishing work that supports your beliefs!

+--------------- D. C. Sessions <dcs@lumbercartel.com> --------------+

We really disagree here and this is worthy of
a much longer response. While intestinal flora
do provide enough vitamin K to keep the
blood clotting, it isn't enough to prevent
ectopic calcification in the face of a population
likely getting too little vitamin K, D3, and magnesium.
Had these test subject got enough vitamin
K, D3 and Mg, it likely wouldn't have had
problem due to excessive calcium intake.

I'll add another much longer posting on
this point in just a moment with some
provided abstracts.

Fair enough.

Some of us maybe be seen being the middle ground.
Though as I see it, I am simply holding to the tenets of as you
call it "evil orthodox medicine" more accurately though
does many of it's practitioners.

A longer response to your idea that intestinal
flora provides all one needs in the way of vitamin
K.
=================

Although what you say has been considered to be
biologically plausible but support for your view is
not strong and is no more than a hypothesis i.e. 'that
gut flora provides sufficient vitamin K for optimal health.'
Indeed, the evidence for my view that this isn't true
is supported by more evidence, IMO.
See abstract 1 provided below.
This is not to say the last word has been issued on
the topic or the theory I offer. And some correlation
studies given mixed results which hardly a surprise
given the generally poor level on intake and poor
absorption of K1. See abstract 5 below.
And I suppose probiotics and specific gut flora specific
to an individual may also make a difference.

As a measure of the adequacy vitamin K intake, we can look
the the evidence that higher level intakes of
the various vitamers of vitamin K in improving
bone strength and health. This line evidence
suggest that most standard diets provide too little
for optimal health. Moreover, since the underlying
biochemistry of osteocalcin for both bone health
and MGP (abstracts 4, 7 & 8) for blood vessel health are related and
vitamin K driven and these indicate the need for
much more vitamin K than derive from gut flora.

I also included an abstract (number 6) favorable to your
view point and notice that it presents your
view with this comment, "Nonetheless, no direct
evidence is available to support this
contention." The study seems to be the first
human study that provides support for 'your' view.
Anyway there is NO REASON to assume the
levels of vitamin K derived from gut flora
are enough to prevent ectopic calcifications or help
keep bone strength in an optimal condition.

----------------------------------------------
1: Clin Invest. 1993 Apr;91(4):1761-8.

Comment in:
   J Clin Invest. 1993 Apr;91(4):1268.

Dietary induced subclinical vitamin K deficiency
in normal human subjects.

Ferland G, Sadowski JA, O'Brien ME.

U.S. Department of Agriculture,
Tufts University, Boston, Massachusetts 02111.

A subclinical vitamin K deficiency was induced in 32
healthy subjects (four groups of eight males and females)
aged 20-40 and 60-80 yr residing in the Metabolic
Research Unit of the Human Nutrition Research
Center on Aging at Tufts University. Volunteers
were initially fed (4 d) a baseline-period diet
containing the recommended daily allowance
for vitamin K which is equivalent to 80
micrograms/d of phylloquinone (vitamin K1).
During the baseline period various parameters
of vitamin K nutritional status were monitored.
The baseline period was followed by a 13-d depletion
period during which the subjects were fed a very
low vitamin K1 diet (approximately 10 micrograms/d).
After depletion, the subjects entered a 16-d repletion
period (four stages lasting 4 d each) during
which time they were repleted with 5, 15, 25, and
45 micrograms of vitamin K1 per day. Vitamin K1
depletion dramatically and significantly decreased
plasma vitamin K1 levels (P < 0.0001) in both elderly
and young groups to values 13-18% of day 1
(elderly 0.22 nM, young 0.14 nM). Repleting the
subjects with up to 45 micrograms
of vitamin K1 per day failed, in the
case of the young subjects, to bring plasma
vitamin K1 levels back into the normal
range. Dietary vitamin K1 restriction
induced different responses in the
urinary excretion of gamma-carboxyglutamic
acid between the young and the elderly
subjects with values decreasing significantly
(P < 0.03) in the young while remaining unchanged
in the elderly. The vitamin K1 depletion period
had no significant effect on either prothrombin
and activated partial thromboplastin times, or
Factor VII and protein C (as determined by
antigenic and functional assays). By using a
monoclonal antibody, decarboxy prothrombin was
found to increase slightly but significantly in both
groups (P < 0.05) as a consequence of the low
vitamin K1 diet. This study clearly shows that
a diet low in vitamin K1 can result in a
functional subclinical deficiency of vitamin K
(decreased urinary gamma-carboxyglutamic acid excretion)
without affecting blood coagulation.

-------------------------------

Obviously if gut flora were a large source of vitamin
such an experiment would not work as the above
depletion study did.
==========================================
3: J Nutr. 2003 Aug;133(8):2565-9.

Dietary phylloquinone depletion and repletion in
older women.

Booth SL, Martini L, Peterson JW, Saltzman E, Dallal GE, Wood RJ.

Jean Mayer U.S. Department of Agriculture Human
Nutrition Research Center on Aging at Tufts University,
Boston, MA 02111, USA.
sarah.booth@tufts.edu

Biological markers indicative of poor vitamin K status
have been associated with a greater risk for hip
fracture in older men and women. However, the dietary
phylloquinone intake required to achieve maximal
carboxylation of hepatic and extrahepatic
vitamin K-dependent proteins is not
In an 84-d study in a metabolic unit, 21 older
(60-80 y) women were fed a phylloquinone-restricted diet
(18 micro g/d) for 28 d, followed by stepwise
repletion of 86, 200 and 450 micro
g/d of phylloquinone. Plasma phylloquinone,
urinary gamma-carboxyglutamic acid excretion and
gamma-carboxylation of hepatic (prothrombin) and
extrahepatic proteins (osteocalcin) decreased in
response to phylloquinone restriction (P <
0.001), demonstrating the production of subclinical
vitamin K deficiency. The gamma-carboxylation of
prothrombin was restored to normal levels in
response to phylloquinone supplementation at
200 micro g/d. In contrast, all other
biochemical markers of vitamin K status
remained below normal levels after
short-term supplementation of up to 450 micro g/d of
phylloquinone. These data support previous
observations in rats that hepatic
vitamin K-dependent proteins have preferential
utilization of phylloquinone in response to
phylloquinone dietary restriction.
Moreover, our findings suggest that the
current recommended  Adequate Intake levels
of vitamin K (90 micro g/d) in women do not support
maximal osteocalcin gamma-carboxylation in older women.

PMID: 12888638
--------------------

Note it took up to 450 mcg for repletion not 80 mcg.

============================================

4: Z Kardiol. 2001;90 Suppl 3:57-63.

Role of vitamin K and vitamin K-dependent proteins
in vascular calcification.

Schurgers LJ, Dissel PE, Spronk HM, Soute BA, Dhore CR,
Cleutjens JP, Vermeer C.

Department of Biochemistry,
Maastricht University,
P.O. Box 616, 6200 MD
Maastricht, The Netherlands.

OBJECTIVES:
To provide a rational basis for recommended daily
allowances (RDA) of dietary phylloquinone (vitamin K1)
and menaquinone (vitamin K2) intake that
adequately supply extrahepatic (notably vascular)
tissue requirements.

BACKGROUND:
Vitamin K has a key function in the synthesis of at
least two proteins involved in calcium and bone
metabolism, namely osteocalcin and matrix
Gla-protein (MGP). MGP was shown to be a strong
inhibitor of vascular calcification. Present RDA
values for vitamin K are based on the hepatic
phylloquinone requirement for coagulation factor
synthesis. Accumulating data suggest that extrahepatic
tissues such as bone and vessel wall require higher
dietary intakes and have a preference for menaquinone
rather than for phylloquinone.

METHODS:
Tissue-specific vitamin K consumption under
controlled intake was determined in warfarin-treated
rats using the vitamin K-quinone/epoxide ratio as
a measure for vitamin K consumption.
Immunohistochemical analysis of human vascular
material was performed using a monoclonal
antibody against MGP. The same antibody was used
for quantification of MGP levels in serum.

RESULTS:
At least some extrahepatic tissues including the
arterial vessel wall have a high preference for
accumulating and using menaquinone rather than
phylloquinone. Both intima and media sclerosis are
associated with high tissue concentrations of MGP,
with the most prominent accumulation at the
interface between vascular tissue and calcified
material. This was consistent with increased
concentrations of circulating MGP in subjects
with atherosclerosis and diabetes mellitus.

CONCLUSIONS:
This is the first report
demonstrating the association between MGP and
vascular calcification. The hypothesis is put forward
that undercarboxylation of MGP is a risk factor for
vascular calcification and that the present RDA
values are too low to ensure full
carboxylation of MGP.

PMID: 11374034

------------------------
So we see in the last two piece what
is good for bone is also prevents ectopic
calcification.
=========================================

5: Br J Nutr. 1996 Aug;76(2):223-9.

Effect of food composition on vitamin K absorption
in human volunteers.

Gijsbers BL, Jie KS, Vermeer C.

Department of Biochemistry,
University of Limburg,
Maastrict, The Netherlands.

The human vitamin K requirement is not known precisely,
but the minimal requirement is often assumed to be
between 0.5 and 1 x 10(-6) g/kg body weight.
In the present study we addressed the question to
what extent circulating vitamin K concentrations
are influenced by the form in which the vitamer is
consumed. The experimental group consisted of
five healthy volunteers who received phylloquinone
after an overnight fast. On the first day of three
successive weeks the participants consumed
1 mg (2.2 mumol) phylloquinone, either in the
form of a pharmaceutical preparation (Konakion),
or in the form of spinach + butter, or as spinach
without added fat. Circulating phylloquinone levels
after spinach with and without butter were
substantially lower (7.5- and 24.3-fold respectively)
than those after taking the pharmaceutical concentrate.
Moreover, the absorption of phylloquinone from the
vegetables was 1.5 times slower than from Konakion.
In a second experiment in the same five volunteers
it was shown that relatively high amounts of
menaquinone-4 enter the circulation after
the consumption of butter enriched with this vitamer.
It is concluded that the bioavailability of
membrane-bound phylloquinone is extremely poor and
may depend on other food components, notably fat.
The bioavailability of dietary vitamin K
(phylloquinone + menaquinones) is lower than
generally assumed, and depends on the form in which
the vitamin is ingested. These new insights
may lead to a revision of the
recommended daily intake for vitamin K.

PMID: 8813897
---------------------------

Uncooked lettuce is in theory often the largest
source of vitamin K in some diets; yet, much of
it is likely unavailable. This suggests
just adding up list of foods ingested is an ineffective
manner of accessing this vitamins level of
sufficiency in the diet.

===========================

6: Am J Gastroenterol. 1994 Jun;89(6):915-23.

The contribution of vitamin K2 (menaquinones)
produced by the intestinal microflora to
human nutritional requirements for vitamin K.

Conly JM, Stein K, Worobetz L, Rutledge-Harding S.

Department of Medicine,
University of Saskatchewan,
Saskatoon.

BACKGROUND:
Coagulopathy manifest by elevation of the prothrombin
time (PT) in patients receiving broad spectrum
antimicrobials indirectly suggests a role for
intestinal microflora synthesized menaquinone
(MK) in the maintenance of normal coagulation.
Nonetheless, no direct evidence is available to support this
contention.

OBJECTIVE:
Our objective was therefore to provide evidence that
bacterially produced MK may be absorbed by the
distal small bowel of humans.

METHODS:
Using a cell harvester, Staphylococcus aureus
(ATCC 29213) was grown in 12-L batches, harvested,
and extracted by high performance liquid chromatography
(HPLC) to obtain 8 mg of pure MK. Four normal
volunteers were placed on a diet severely restricted
in vitamin K1 (median 32-40 U/day), and were
given warfarin to maintain an International
Normalized Ratio of approximately 2.0. On the
10th day of warfarin administration,
naso-ileal intubation was performed and 1.5 mg of
MK was delivered into the ileum. PT,
factor VII, II and serum vitamin K1 levels
were monitored throughout the study.

RESULTS:
Mean serum vitamin K1 levels were reduced to
30% of the pre-diet value at the time of MK
administration. Within 24  h of ileal MK
administration, there was a significant (p < 0.05)
increase in the factor VII level of
0.28 +/- 0.10 U/ml (mean +/- SEM) and a
significant decrease of 2.5 (+/- 0.1) s in the PT,
whereas in the control phase (during which no MK
was administered), there were no significant
changes in the PT or factor VII at
corresponding time intervals.

CONCLUSION:
These data provide direct evidence for
the absorption of vitamin K2 from the
distal small bowel, supporting a definite
role for bacterially synthesized
vitamin K2 in contributing to the human
nutritional requirements of this vitamin.

PMID: 8198105
-------------------------------------
Note this is the first direct evidence of
your point to the extent it is true.

====================================

Am. J. Clin. Nutr. 2006 Feb;83(2):380-6.

Vitamin K status of healthy Japanese women:
age-related vitamin K requirement for
gamma-carboxylation of osteocalcin.

Tsugawa N, Shiraki M, Suhara Y, Kamao M, Tanaka K, Okano T.

Department of Hygienic Sciences,
Kobe Pharmaceutical University, Kobe, Japan.

BACKGROUND:
Vitamin K deficiency is associated with low bone mineral
density and increased risk of bone fracture.
Phylloquinone (K1) and menaquinone 4 (MK-4) and
7 (MK-7) are generally observed in human plasma;
however, data are limited on their circulating
concentrations and their associations with bone
metabolism or with gamma-carboxylation of the
osteocalcin molecule.

OBJECTIVES:
The objectives
were to measure the circulating concentrations of K1,
MK-4, and MK-7 in women and to ascertain whether each
form of vitamin K is significantly associated with bone
metabolism.

DESIGN:
Plasma concentrations of K1,
MK-4, MK-7, undercarboxylated osteocalcin
(ucOC; measured by using the new electrochemiluminescence
immunoassay), intact osteocalcin (iOC), calcium,
and phosphorus; bone-derived alkaline phosphatase
activity; and concentrations of urinary creatinine,
N-terminal telopeptide, and deoxypyridinoline were
measured in healthy women (n =
396).

RESULTS: On average, MK-7 and MK-4 were the highest
and lowest, respectively, of the 3 vitamers in all
age groups. K1 and MK-7 correlated inversely
with ucOC, but associations between nutritional
basal concentration of MK-4 and ucOC were not observed.
Multiple regression analysis indicated that not
only K1 and MK-7 concentrations but also age were
independently correlated with ucOC concentration
and the ratio of ucOC to iOC. The plasma K1 or MK-7
concentration required to minimize the ucOC
concentration was highest in the group aged >
or =70 y, and it decreased progressively for
each of the younger age
groups.

CONCLUSIONS: The definite role of ucOC remains
unclear. However, if submaximal gamma-carboxylation
is related to the prevention of fracture or bone
mineral loss, circulating vitamin K concentrations
in elderly people should be kept higher than those
in young people.

Publication Types:
   Research Support, Non-U.S. Gov't

PMID: 16469998
=================================

7: Biochem Biophys Res Commun.
2001 Nov 30;289(2):485-90.

Matrix Gla protein accumulates at the border
of regions of calcification and normal
tissue in the media of the arterial vessel wall.

Spronk HM, Soute BA, Schurgers LJ, Cleutjens JP,
Thijssen HH, De Mey JG, Vermeer
C.

Department of Biochemistry,
Maastricht University,
Maastricht, The Netherlands.

Vitamin K-dependent matrix Gla protein (MGP) has been
suggested to play a role in the inhibition of
soft-tissue calcification. Here we report the
expression of recombinant prokaryotic MGP as
part of a fusion protein and the preparation of
two antibodies that specifically recognize MGP.
Monoclonal antibodies were raised against
synthetic peptides homologous to the sequences
3-15 and 63-75 of human MGP. Both antibodies
recognize recombinant and synthetic human MGP.
Immunohistochemical analysis showed that MGP
was associated with the extracellular
matrix of noncalcified bone and with chondrocytes
in cartilage. In the healthy human arterial
vessel wall, MGP antigen was demonstrated in
association with smooth muscle cells and
elastic laminae of the tunica media and
with the extracellular matrix of the
adventitia. Colocalization with the elastic
laminae was lost at sites of medial calcification;
in both human and rat arteries, high amounts
of MGP were found in the extracellular matrix
at borders of intimal and medial calcification.
Our data demonstrate the close association
between MGP and calcification. It is
suggested that undercarboxylated MGP is
biologically inactive and that poor
vascular vitamin K status may form a risk
factor for vascular calcification.

PMID: 11716499
-----------------------------------
Looks like the calcium takers needed
vitamin K.

=============================

8: Blood. 2004 Nov 15;104(10):3231-2.
Epub 2004 Jul 20.

Oral anticoagulant treatment:
friend or foe in cardiovascular disease?

Schurgers LJ, Aebert H, Vermeer C,
Bultmann B, Janzen J.

Department of Biochemistry,
Cardiovascular Research Institute,
University Maastricht,
PO Box 616,
6200 MD Maastricht, The Netherlands.
l.schurgers@bioch.unimaas.nl.

Calcification is a common complication in cardiovascular
disease and may affect both arteries and heart valves.
Matrix gamma-carboxyglutamic acid (Gla) protein
(MGP) is a potent inhibitor of vascular
calcification, the activity of which is regulated
by vitamin K. In animal models, vitamin K
antagonists (oral anticoagulants [OACs]) were
shown to induce arterial calcification. To
investigate whether long-term OAC treatment
may induce calcification in humans also, we have
measured the grade of aortic valve calcification
in patients with and without preoperative OAC
treatment. OAC-treated subjects were matched with
nontreated ones for age, sex, and disease.
Calcifications in patients receiving preoperative
OAC treatment were significantly (2-fold) larger
than in nontreated patients. These observations
suggest that OACs, which are widely used for
antithrombotic therapy, may induce cardiovascular
calcifications as an adverse side effect.

PMID: 15265793

-----------------------------------
This suggests low vitamin K causes
the same problem as too much calcium....
ectopic calcification