Thanks! :-)

In article
<43a31bc4-1bfd-44cd-a74d-fae8572f8ba8@i12g2000prf.googlegroups.com>,

Cool. Thanks Ron. So...

Vital Prime Labs sells 100grams of 2500ppm K2 powder for $125
2500ppm = 0.25%
100gm x 0.0025 = 0.25gm = 250mg = 250,000mcg
= $0.50/mg

At 100mcg per serving, that's 2500 servings.
That's a 6.8 year supply for $125

The Twinlab K2+D3 dots (if we ignore the D3) cost $8 for 5.4mg K2
= $1.48/mg
A 6.8 year supply costs $370. (costs about 3 times more)

For the price of a 2.3 year supply of Twinlab dots, you can get a 6.8
years supply from Vital Prime Labs.

Hi Mike,

I have not made as far reaching conclusions about saturated fat, yet. I
think that it depends on the person. If one has problems with blood sugar,
insulin resistance and visceral fat controlling carbs is more important than
for lean people, such as me. Personally I try to avoid refined grains. I
also do not drink soft drinks nor do I use any products containing fructose
syrup. But I do eat some whole grains and potatoes, and I am quite convinced
that fruits are healthy for most people and should not be discarded from the
diet.

There is some evidence that all dairy products are not equal in their health
effects. While whole milk has been associated with cardiovascular disease
cheese has not.

Ron: Here are several pieces of evidence (but not yet clinical proof) that
K2 is preventive of arterial calcification. I hope this reformats in a
legible fashion
MikeV

Am J Health Syst Pharm. 2005 Aug 1;62(15):1574-81. Links
Vitamin K in the treatment and prevention of osteoporosis and arterial
calcification.
Adams J, Pepping J.
Castle Medical Center, Kailua, HI 96814, USA.
PURPOSE: The role of vitamin K in the prevention and treatment of
osteoporosis and arterial calcification is examined. SUMMARY: Vitamin K is
essential for the activation of vitamin K-dependent proteins, which are
involved not only in blood coagulation but in bone metabolism and the
inhibition of arterial calcification. In humans, vitamin K is primarily a
cofactor in the enzymatic reaction that converts glutamate residues into
gamma-carboxyglutamate residues in vitamin K-dependent proteins. Numerous
studies have demonstrated the importance of vitamin K in bone health. The
results of recent studies have suggested that concurrent use of menaquinone
and vitamin D may substantially reduce bone loss. Menaquinone was also found
to have a synergistic effect when administered with hormone therapy. Several
epidemiologic and intervention studies have found that vitamin K deficiency
causes reductions in bone mineral density and increases the risk of
fractures. Arterial calcification is an active, cell-controlled process that
shares many similarities with bone metabolism. Concurrent arterial
calcification and osteoporosis have been called the "calcification paradox"
and occur frequently in postmenopausal women. The results of two
dose-response studies have indicated that the amount of vitamin K needed for
optimal gamma-carboxylation of osteocalcin is significantly higher than what
is provided through diet alone and that current dosage recommendations
should be increased to optimize bone mineralization. Few adverse effects
have been reported from oral vitamin K.
CONCLUSION: Phytonadione and menaquinone may be effective for the prevention
and treatment of osteoporosis and arterial calcification.
PMID: 16030366 [PubMed - indexed for MEDLINE]
*****************
Dietary Intake of Menaquinone Is Associated with a Reduced Risk of
Coronary Heart Disease: The Rotterdam Study
Vascular tissue and calcified plaques contain MGP, a vitamin K-dependent
protein known to prevent excessive calcium deposition in bone (1- 4,7,8).
Lack of vascular MGP resulted in excessive aortic and coronary calcification
in knockout mice (9). The inverse association of menaquinone with aortic
calcification and CHD in our study may be explained by undercarboxylation of
vascular MGP and consequently enhanced calcification of atherosclerotic
lesions. Calcified plaques are more prone to rupture, which will elicit a
thrombotic response, thereby increasing the risk of a coronary event (29).
Another vitamin K-dependent protein found in the vessel wall is protein S
(30). Together with activated protein C, this anticoagulant plays an
important role in preventing clot formation at the inner surface of the
vessel wall. However, the quantitative contribution of extrahepatic protein
S synthesis to hemostasis is probably small. There is evidence for a
differential effect of vitamin K subtypes in the cardiovascular system. Rats
at our laboratory were fed diets containing ylloquinone, menaquinone, or
both after treatment with high doses of warfarin. Despite similar in vitro
cofactor activity for
-carboxylase, menaquinone but not phylloquinone
supplementation revented warfarin-induced arterial calcification (31). The
tissue-specific use of phylloquinone and menaquinone in rats was assessed by
measuring the ratios of quinone over epoxide (K:KO ratios) during warfarin
treatment. In the arterial vessel wall, K:KO ratios were substantially lower
for phylloquinone than for menaquinone whereas the reverse was observed for
the liver, suggesting a tissue-specific utilization of vitamin K subtypes
(31). In a recent trial in humans, phylloquinone was almost exclusively
incorporated into the triacylglycerol-rich lipoprotein (TGRLP) fraction
after intestinal absorption, whereas a substantial part of the menaquinones
was recovered from the LDL fraction (32). The TGRLP fraction is mainly
cleared by the liver, whereas LDL forms a transport system to extrahepatic
tissues. Menaquinone supplementation lowered serum cholesterol levels in a
study of 17 dialysis patients (33). In our population of healthy older
subjects, we confirmed the favorable effect of menaquinone on blood lipids
but effects were small and could not explain the inverse relation that we
observed between dietary menaquinone and CHD.
In conclusion, our findings suggest a protective effect of menaquinone
intake against CHD, which could be mediated by inhibition of arterial
calcification. Adequate intake of foods rich in menaquinones, such as curds
and (low-fat) cheese, may contribute to CHD prevention.
extracted from:
http://jn.nutrition.org/cgi/reprint/134/11/3100

***Geleijnse JM, Vermeer C, Grobbee DE, et al. Dietary intake of menaquinone
is associated with a reduced risk of
coronary heart disease: the Rotterdam Study. J Nutr. Nov
2004;134(11):3100-3105

*********************************************************************************************

Vermeer C, Braam L. Role of K vitamins in the regulation of tissue
calcification. J Bone Miner Metab. 2001;19(4):201-6.
Shearer MJ, Bach A, Kohlmeier M. Chemistry, nutritional sources, tissue
distribution and metabolism of vitamin K with special reference to bone
health. J Nutr. 1996 Apr;126(4 Suppl):1181S-1186S.
Shearer MJ. Vitamin K. Lancet. 1995 Jan 28;345(8944):229-34.
Vermeer C, Jie KS, Knapen MH. Role of vitamin K in bone metabolism. Annu Rev
Nutr. 1995;15:1-22.

It seems that you did not notice that higher vitamin K2 (mainly from cheese)
was also associated with lower cardiovascular and all-cause mortality in the
same study, no matter what.

According to renowned professor Serge Renaud cheese is "a 9000 year old
invention not linked to coronary disease".

http://www.thelancet.com/journals/lancet/article/PIIS0140673605719905/fulltext

I am aware of that. Ideally one should try to prevent both processes.

The data from a Finnish database does not support those assumptions.

*Vitamin K content in cheese*                               µg/ 100 g

1  Hard cheese, edam type, 24-27 g fat                  49.41
2  Cheese fondue                                                  32.61
3  Mould-ripened soft cheese, 40 g fat                   10.32
4  Cheese average                                                10.00
5  Cheese emmental , 27-30 g fat, blue-label           7.78
6  Cream cheese, 30 g fat                                       7.05
7  Cheese, tilsit type, 25-35 g fat                            6.48
8  Cheese, cheddar type                                         4.70
9  Semi-hard cheese, edam, 15-18 g fat                  3.40
10 Blue cheese, 17 g fat                                         2.54
11 Blue cheese, 27-30 g fat                                     2.54
12 Goat cheese, 20-25 g fat, hard cheese                2.54
13 Camembert, 26-30 g fat                                     2.38
14 Semi-hard cheese, edam, 9-11 g fat, low-fat       2.35
15 Cheese, gouda type, 28-30 g fat                         2.06
16 Fetacheese, fat 10-13 g                                      1.80
17 Fetacheese in oil                                                1.50
18 Feta cheese in brine, cow milk, 18 g fat              1.49
19 Beestings in oven                                               0.73
20 Semi-hard cheese, 5 g fat, low-fat                      0.50
21 Camembert, 16 g fat                                               0
22 Feta cheese in brine, goat milk, 25 g fat                  0

http://www.tinyurl.dk/2583

Thanks, I just found the same source again.

An excerpt from a study:

"MK-7 has probably a comparable effect as MK-4 [35], but it has a halflife
in the circulation of 3 days, resulting in more constant plasma levels and
accumulation in the blood and various tissues. Therefore, MK-7 is the most
logical choice for use as a low-dose food supplement, because even at low
intake relatively high blood and tissue levels can be obtained. Clinical
trials in which the efficacy of MK-7 is tested are, however, lacking at this
time."

Stated in Knapen et al. Vitamin K2 supplementation improves hip bone
geometry and bone strength indices in postmenopausal women. Osteoporos Int.
2007 July; 18(7): 963-972.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1915640