Vitamin K2 and D in Patients With Aortic Valve Calcification: A Randomized Double-Blinded Clinical Trial

David PS

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tankasnowgod

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This is bit disappointing.
Or, is it just poorly conducted?

First off, the Vitamin D dose is very low (only 1000 iu), and they used the MK-7 form instead of MK-4.

But did you take a look at the drugs these patients were on?

Meds.png


That second column is the intervention group. 74% on Statins, 69% on Antiplatelet Therapy, 29% on a Beta Blocker, and 54% on an ACE inhibitor.

Just a quick search for statins indicates they can affect calcium scores-



So I don't know what this study really shows. Does it show that Vitamin K2 doesn't decrease calcification? Or that MK-7 doesn't work? Or that common drugs used in elderly and those with suspected heart conditions can completely neutralize any K2 effect?
 
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David PS

David PS

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Or, is it just poorly conducted?

First off, the Vitamin D dose is very low (only 1000 iu), and they used the MK-7 form instead of MK-4.

But did you take a look at the drugs these patients were on?

View attachment 36099

That second column is the intervention group. 74% on Statins, 69% on Antiplatelet Therapy, 29% on a Beta Blocker, and 54% on an ACE inhibitor.

Just a quick search for statins indicates they can affect calcium scores-



So I don't know what this study really shows. Does it show that Vitamin K2 doesn't decrease calcification? Or that MK-7 doesn't work? Or that common drugs used in elderly and those with suspected heart conditions can completely neutralize any K2 effect?

Thank, your comments were truly helpful. I am no longer disappointed in the outcome of their trial. It looks like the trial was designed so that it would fail to show any benefit.
 

yerrag

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A study like this assumes there is no microbial aetiology if not explicitly stated it is implied.

This already misses the mark if it leads people that the pathology is idiopathic, which is just a nice way of saying we really don't know.

But a lot of studies have to be made with assumptions that restrict the search for solutions to where no solutions can really be found.

Many studies are purposely defective in their design on many levels. Such defects give us the impression that solutions are complex and require geniuses using arcane language to explain. And to tide us by we should be glad there are drugs available while we wait for that discovery or breakthrough. One day someone will break that impasse and be awarded a Nobel Prize.

But could it just be that the powers that be want us to operate on the wrong plane of assumptions?

A lot of valve calcifications can't be overcome by focusing merely on chemical interactions. There is the bio component in biochemistry. And when microbes are not well understood, the discoveries are at best half-cooked no matter how long you simmer.

The germ theory needs to give way to pleomorphism and terrain theory to have true discovery and solutions.

Our Age of Science is so gamed that we have to use what we learn from the Age of Reason to expose the falsehoods embedded in this supposedly advanced age. If anything, the only thing advanced is the level by which we are played.
 
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Thank, your comments were truly helpful. I am no longer disappointed in the outcome of their trial. It looks like the trial was designed so that it would fail to show any benefit.
That’s what I’m thinking as well.
 

Tom K

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It showed that K2 had no effect on arterial calcification. It can be legitimately reported that supplemental K-2 had no influence on coronary calcium scores. Now, I present one of my favorite sayings, "Is it alie? No. Is it the truth? No."

If a person reads what took place in this study, it becomes apparent why supplemental K had little effect on anything. The dose of K-2 was 720 mcg: 720mcg is equal to .72 mg. Less than 1 milligram. In studies that demonstrated K-2 effectiveness, doses as high as 45 mg were employed (45 mg = 45000 mcg). If the study was intended to be truthful, the title would be, "Supplementation With Less than 1 mg of Vitamin K-2 Does Not Reduce Coronary Calcium Scores."
 
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David PS

David PS

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It showed that K2 had no effect on arterial calcification. It can be legitimately reported that supplemental K-2 had no influence on coronary calcium scores. Now, I present one of my favorite sayings, "Is it alie? No. Is it the truth? No."

If a person reads what took place in this study, it becomes apparent why supplemental K had little effect on anything. The dose of K-2 was 720 mcg: 720mcg is equal to .72 mg. Less than 1 milligram. In studies that demonstrated K-2 effectiveness, doses as high as 45 mg were employed (45 mg = 45000 mcg). If the study was intended to be truthful, the title would be, "Supplementation With Less than 1 mg of Vitamin K-2 Does Not Reduce Coronary Calcium Scores."

Thank you for your observations.

It seems that this study showed that if you use an ineffective amount of Vitamin D and an ineffective amount of Vitamin K-2, the synergy between the two vitamins (if any) is insufficient to make the combination of the two vitamins effective.
 

Amazoniac

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Or, is it just poorly conducted?

First off, the Vitamin D dose is very low (only 1000 iu), and they used the MK-7 form instead of MK-4.

But did you take a look at the drugs these patients were on?

View attachment 36099

That second column is the intervention group. 74% on Statins, 69% on Antiplatelet Therapy, 29% on a Beta Blocker, and 54% on an ACE inhibitor.

Just a quick search for statins indicates they can affect calcium scores-



So I don't know what this study really shows. Does it show that Vitamin K2 doesn't decrease calcification? Or that MK-7 doesn't work? Or that common drugs used in elderly and those with suspected heart conditions can completely neutralize any K2 effect?
Snow god, it was a mq-7 experiment, the "vitamin" D was there as a bonus.

"To study whether treatment with MK-7 may modulate this disease, delaying the progression of AVC, we conducted a randomized trial in which men with AVC were randomly assigned to receive either supplemental MK-7 and vitamin D or placebo."​

Statins can indeed be a confounder:

- Statins Stimulate Atherosclerosis And Heart Failure: Pharmacological Mechanisms

Abstract said:
In contrast to the current belief that cholesterol reduction with statins decreases atherosclerosis, we present a perspective that statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels through the depletion of coenzyme Q10 and ‘heme A’, and thereby ATP generation. Statins inhibit the synthesis of vitamin K2, the cofactor for matrix Gla-protein activation, which in turn protects arteries from calcification. Statins inhibit the biosynthesis of selenium containing proteins, one of which is glutathione peroxidase serving to suppress peroxidative stress. An impairment of selenoprotein biosynthesis may be a factor in congestive heart failure, reminiscent of the dilated cardiomyopathies seen with selenium deficiency. Thus, the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically reevaluated.

However, I don't think that it was poorly conducted because these confounders are going to be there for patients (title). If they was removed, we may wonder: would the effects be applicable to medicated persons, who represent a major share of their population? Patients won't have the medications discontinued, it has to be something that helps in the given circumstances.

Interestingly, inactive Matrix Gla proteid was reduced in the treated group (and it wasn't a low mq-7 dose):

"The highest dose used so far was in a randomized dose-finding study including hemodialysis patients.[16] After a hemodialysis session, the patients were supplemented with oral MK-7 360 μg, 720 μg, or 1080 μg 3 times per week, corresponding to 1080 μg, 2160 μg, and 3240 μg per week, whereas we supplemented with 5040 μg per week. In addition, in accordance with previous studies,[10,17] we observed a significant reduction in dp-ucMGP in the intervention group, suggesting that our dosage significantly modulated vitamin K deficiency."​
"Compared with patients treated with placebo, a significant reduction in dp-ucMGP seen in patients treated with MK-7 plus vitamin D (–212 pmol/L versus 45 pmol/L; P<0.001; Table 2) [from baseline (~730 pmol/L)]."​

Could the medications have lowered active Matrix Gla proteid too?

It's possible to derive mq-4 from mq-7, but differences in distribution must favor the use of straight mq-4.
 
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