{Tyler-This was a post by Michael John. I am still very much working towards finding a way to grow taller. Now I am focus on in inducing endochondral ossification of the articular cartilage. I am growing through old studies. It’s just a lot of studies are more of the same}
Note: The efficacy of this compound has been very controversial
I have been spending a ridiculous amount of time recently doing a LOT of research on the chemical compound known as Menaquinone-7, aka MK7, aka Vitamin K2. There has been a lot of research that I have found which confirms this idea that MK7 Supplements will lower the risk of hip femoral neck fractures in post menopausal women.
A recent PubMed Study “Three-year low-dose menaquinone-7 supplementation helps decrease bone loss in healthy postmenopausal women.” finally has admitted to the idea that it may not just be the Bone Mineral Density that can be dramatically reduced in its decreasing rate, but maybe the overall height of a person, at least slightly.
Let me quote the following…”MK-7 significantly decreased the loss in vertebral height of the lower thoracic region at the mid-site of the vertebrae.”
Something that has been worrying me for so long, from looking at so many claims of professional MDs is that since the most well known type of food source which has high concentrations of Vitamin K2 is Natto, was this “Why is it that if the Japanese are eating so much Natto (Since Natto is such a critical part of the Japanese diet, unlike any other country in the world) and soy based products relative to other ethnic groups, do Japanese women (or even Eastern Asian women in general) seem to have the highest rates of osteoporosis?”
Wouldn’t eating Natto have the opposite effect?
Is it just a racial thing, where different races actually have different levels of BMD on average?
The Science behind Menaquinone-7
It seems that with MK7 at least, it can stimulate the level of osteocalcin and GLA in the body. the osteocalcin and GLA have a certain area of their molecular structure which allows them to chelate the Calcium atoms out of the soft tissue areas of the body, like the blood vessels. Remember that one of the things that happen as we get older is that there is a sort of plaque buildup in our blood vessels. 20% of the buildup in our vessels is calcium in nature. Somehow the K2 can cause the calcium buildup in the soft tissue area/blood vessels to reverse in ossification.{Tyler-obviously this would be very powerful if it happened in the bones}
What I am sure about
When the dentist Weston Price did his analysis on all those kids who didn’t seem to develop cavities back in the 30s or 50s (not sure what decade it was), he claimed that the compound was something he called Activator X. Recently people are saying that the activator X compound is just Vitamin K2, specifically the MK-7 version.
The K2 he managed to give to kids to reverse their cavities was some type of grass feed butter, combined with Cod Liver Oil. Remember what Dave Asprey has been asking the people who take his Bulletproof coffee to do? Put some grass-fed butter in it. It turns out that the Grass Feed Butter Oil has a higher than average concentration of K2 in it. Not only that, the entire idea of the possibility of reversing cavities was because I used to lurk in the Bulletproof Executive Forum , and heard other people who claim to have it happen to them. Dr. Pamela Smith has claimed in one Youtube video though that you would need a recommended 100 mcg of Menaquinone-7 to get a reasonable effect.
However, when Price did the X-rays to show that the teeth seemed to fill out, he didn’t consider the factor of Strontium, as well as the fact that to get the caries to reverse, you still need to at least put some filling on the cap of the teeth first. The hole in the center is supposed to be filled up over time from K2 supplementation.
{tyler}-
Here’s more about the effects of Vitamin K2 on GLA
“Matrix GLA protein (MGP), a γ-carboxyglutamic acid (GLA)–rich, vitamin K–dependent and apatite-binding protein, is a regulator of hypertrophic cartilage mineralization during development. However, MGP is produced by both hypertrophic and immature chondrocytes, suggesting that MGP’s role in mineralization is cell stage–dependent, and that MGP may have other roles in immature cells. It is also unclear whether MGP regulates the quantity of mineral or mineral nature and quality as well. To address these issues, we determined the effects of manipulations of MGP synthesis and expression in (a) immature and hypertrophic chondrocyte cultures and (b) the chick limb bud in vivo. The two chondrocyte cultures displayed comparable levels of MGP gene expression. Yet, treatment with warfarin, a γ-carboxylase inhibitor and vitamin K antagonist, triggered mineralization in hypertrophic but not immature cultures. Warfarin effects on mineralization were highly selective, were accompanied by no appreciable changes in MGP expression, alkaline phosphatase activity, or cell number, and were counteracted by vitamin K cotreatment. Scanning electron microscopy, x-ray microanalysis, and Fourier-transform infrared spectroscopy revealed that mineral forming in control and warfarin-treated hypertrophic cell cultures was similar and represented stoichiometric apatite. Virally driven MGP overexpression in cultured chondrocytes greatly decreased mineralization. Surprisingly, MGP overexpression in the developing limb not only inhibited cartilage mineralization, but also delayed chondrocyte maturation and blocked endochondral ossification and formation of a diaphyseal intramembranous bone collar. The results show that MGP is a powerful but developmentally regulated inhibitor of cartilage mineralization, controls mineral quantity but not type, and appears to have a previously unsuspected role in regulating chondrocyte maturation and ossification processes.”