LONGECITY

no it does not. you gonna prove it or not? (jeez be a man dude)

45 mg mk4 does cause serious adverse effects but since you for some reason were unable to follow the link I will post the text here again:

Looking at this review is seems that the 15mg x 3 MK4 used in all the Japanese osteoporosis studies likely is too much. "The OF
study noted a signifcantly higher incidence of skin and skin appendage lesions in patients receiving menatetrenone (0.5 per 100 patient-years compared with 0.1 in the control group, p < 0.001). ". The manufacturer of the Japanese supplement/medication states that 4.3% of users experience various adverse effects, some relatively serious, which are listed in table 11.
http://www.hta.ac.uk...ono/mon1345.pdf
Edited by Blue, 27 March 2010 - 04:00 PM.

ok, i'll just repeat.

here, i even provide you proof that 45mg mk-4 is being successfuly practiced.

http://www.google.co...n...sis&spell=1

what is your excuse now?
Edited by full_circle, 27 March 2010 - 04:00 PM.

ok, i'll just repeat.

here, i even provide you proof that 45mg mk-4 is being successfuly practiced.

http://www.google.co...n...sis&spell=1

what is your excuse now?

A link to Google's homepage?

45 mg mk4 is successful against osteoporosis. But with serious adverse effects in some people as noted in my last post.

.
Edited by full_circle, 27 March 2010 - 04:06 PM.

i have no idea what you are reading and i do not even care what you are reading because my mother is on mk-4 therapy and she is taking 60mg mk-4 a day. in fact, upto 90mg a day mk-4 therapy is officially approved. jeez dude..

i have no idea what you are reading and i do not even care what you are reading because my mother is on mk-4 therapy and she is taking 60mg mk-4 a day. in fact, upto 90mg a day mk-4 therapy is officially approved. jeez dude..

Looking at this review is seems that the 15mg x 3 MK4 used in all the Japanese osteoporosis studies likely is too much. "The OF
study noted a signifcantly higher incidence of skin and skin appendage lesions in patients receiving menatetrenone (0.5 per 100 patient-years compared with 0.1 in the control group, p < 0.001). ". The manufacturer of the Japanese supplement/medication states that 4.3% of users experience various adverse effects, some relatively serious, which are listed in table 11.
http://www.hta.ac.uk...ono/mon1345.pdf

i'll just keep repeat.

i have no idea what you are reading and i do not even care what you are reading because my mother is on mk-4 therapy and she is taking 60mg mk-4 a day. in fact, upto 90mg a day mk-4 therapy is officially approved. jeez dude..

i'll just keep repeat.

i have no idea what you are reading and i do not even care what you are reading because my mother is on mk-4 therapy and she is taking 60mg mk-4 a day. in fact, upto 90mg a day mk-4 therapy is officially approved. jeez dude..

Did you miss the study in my last post?

i have no idea what you are reading and i do not even care what you are reading because my mother is on mk-4 therapy and she is taking 60mg mk-4 a day. in fact, upto 90mg a day mk-4 therapy is officially approved. jeez dude..

i have no idea what you are reading and i do not even care what you are reading because my mother is on mk-4 therapy and she is taking 60mg mk-4 a day. in fact, upto 90mg a day mk-4 therapy is officially approved. jeez dude..

A hint. It looks really stupid to repeat the same statement about your mother in every reply.

what an unmanly dude..

human do not efficiently convert k1 to k2.
in korea and japan, 45mg a day (not mcg, mg) of k2 mk-4 is administered for osteoporosis and atherosclerosis (off label) patients.
in fact officially approved upper limit is 90mg mk-4 a day.

now i'll propose a challenge to you all.
take 45mg of either k1 or k2 mk-7 a day and see if you are still alive. (3x15mg will do)
chances are, you get hospitalised with ischemic stroke on the FIRST day.

Our body can tolerate megadose (45mg) of k2 mk-4 because it is almost immediately absorbed where it is needed, i.e. it is very bio-avaiable, but not k1 and k2 mk-7.
Go ahead try 45mg of k1 or k2 mk-7. if not, plz stop needless argument.

*
Blue is too afraid to try it. anyone else..?
Edited by full_circle, 27 March 2010 - 04:21 PM.

No sources as usual?

Hint. Here we are impressed by studies, not by unsourced rants or someone saying "chicken".

Your argument regarding stroke is nonsense. If K1 is not bioavailable and poorly converted to k2 then it cannot cause stroke well either. Furthermore, giving 5 mg K1 for 4 years in humans did not cause such problems. In fact, serious adverse events and cancer were reduced.
http://www.plosmedic...al.pmed.0050196

Looking at this review is seems that the 15mg x 3 MK4 used in all the Japanese osteoporosis studies (the only thing mk4 is shown to prevent) likely is too much. "The OF study noted a signifcantly higher incidence of skin and skin appendage lesions in patients receiving menatetrenone (0.5 per 100 patient-years compared with 0.1 in the control group, p < 0.001). ". The manufacturer of the Japanese supplement/medication states that 4.3% of users experience various adverse effects, some relatively serious, which are listed in table 11.
http://www.hta.ac.uk...ono/mon1345.pdf
Edited by Blue, 27 March 2010 - 04:29 PM.

yeah those adverse effects look real serious.

human do not efficiently convert k1 to k2.
in korea and japan, 45mg a day (not mcg, mg) of k2 mk-4 is administered for osteoporosis and atherosclerosis (off label) patients.
in fact officially approved upper limit is 90mg mk-4 a day.

now i'll propose a challenge to you all.
take 45mg of either k1 or k2 mk-7 a day and see if you are still alive. (3x15mg will do)
chances are, you get hospitalised with ischemic stroke on the FIRST day.

Our body can tolerate megadose (45mg) of k2 mk-4 because it is almost immediately absorbed where it is needed, i.e. it is very bio-avaiable, but not k1 and k2 mk-7.
Go ahead try 45mg of k1 or k2 mk-7. if not, plz stop needless argument.

*
Blue is too afraid to try it. anyone else..?
Edited by full_circle, 27 March 2010 - 04:30 PM.

human do not efficiently convert k1 to k2.
in korea and japan, 45mg a day (not mcg, mg) of k2 mk-4 is administered for osteoporosis and atherosclerosis (off label) patients.
in fact officially approved upper limit is 90mg mk-4 a day.

now i'll propose a challenge to you all.
take 45mg of either k1 or k2 mk-7 a day and see if you are still alive. (3x15mg will do)
chances are, you get hospitalised with ischemic stroke on the FIRST day.

Our body can tolerate megadose (45mg) of k2 mk-4 because it is almost immediately absorbed where it is needed, i.e. it is very bio-avaiable, but not k1 and k2 mk-7.
Go ahead try 45mg of k1 or k2 mk-7. if not, plz stop needless argument.

*
Blue is too afraid to try it. anyone else..?

You know it looks really stupid repeating the same unsourced arguments? Like a small child screaming "I want that..." "I want that... " "I want that..."

human do not efficiently convert k1 to k2.
in korea and japan, 45mg a day (not mcg, mg) of k2 mk-4 is administered for osteoporosis and atherosclerosis (off label) patients.
in fact officially approved upper limit is 90mg mk-4 a day.

now i'll propose a challenge to you all.
take 45mg of either k1 or k2 mk-7 a day and see if you are still alive. (3x15mg will do)
chances are, you get hospitalised with ischemic stroke on the FIRST day.

Our body can tolerate megadose (45mg) of k2 mk-4 because it is almost immediately absorbed where it is needed, i.e. it is very bio-avaiable, but not k1 and k2 mk-7.
Go ahead try 45mg of k1 or k2 mk-7. if not, plz stop needless argument.

*
Blue is too afraid to try it. anyone else..?

I seem to be talking to a parrot.

Hint. If you want to win a factual argument, try sourced facts. I will respond if you do.

human do not efficiently convert k1 to k2.
in korea and japan, 45mg a day (not mcg, mg) of k2 mk-4 is administered for osteoporosis and atherosclerosis (off label) patients.
in fact officially approved upper limit is 90mg mk-4 a day.

now i'll propose a challenge to you all.
take 45mg of either k1 or k2 mk-7 a day and see if you are still alive. (3x15mg will do)
chances are, you get hospitalised with ischemic stroke on the FIRST day.

Our body can tolerate megadose (45mg) of k2 mk-4 because it is almost immediately absorbed where it is needed, i.e. it is very bio-avaiable, but not k1 and k2 mk-7.
Go ahead try 45mg of k1 or k2 mk-7. if not, plz stop needless argument.

*
Blue is too afraid to try it. anyone else..?

15 mg x 3 caused adverse reactions in 4.3% of patients:

* Stomach discomfort, abdominal pain, nauseas, diarrhoea, dyspepsia, thirst, anorexia, glossitis, constipation, vomiting, stomatitis.
* Rash, pruritus, redness
* Headache, light-headedness, numbness, dizziness
* Increase in blood pressure, palpitations
* Elevation of liver enzymes
* Elevation of blood urea nitrogen, urinary frequency
* Oedema, eye abnormalities, malaise, arthralgia
* Also, "The OF study noted a signifcantly higher incidence of skin and skin appendage lesions in patients receiving menatetrenone (0.5 per 100 patient-years compared with 0.1 in the control group, p < 0.001). "

http://www.hta.ac.uk...ono/mon1345.pdf

Note that these are relatively short-term effects after one or a few years. Who knows what the long-term adverse bad effects of taking a k vitamin dose 1000 higher than normal dietary intake will be.
Edited by Blue, 27 March 2010 - 05:01 PM.

I seem to be talking to a parrot.

Hint. If you want to win a factual argument, try sourced facts. I will respond if you do.

just read this thread... LOL !

yeah those adverse effects look real serious.

human do not efficiently convert k1 to k2.
in korea and japan, 45mg a day (not mcg, mg) of k2 mk-4 is administered for osteoporosis and atherosclerosis (off label) patients.
in fact officially approved upper limit is 90mg mk-4 a day.

now i'll propose a challenge to you all.
take 45mg of either k1 or k2 mk-7 a day and see if you are still alive. (3x15mg will do)
chances are, you get hospitalised with ischemic stroke on the FIRST day.

Our body can tolerate megadose (45mg) of k2 mk-4 because it is almost immediately absorbed where it is needed, i.e. it is very bio-avaiable, but not k1 and k2 mk-7.
Go ahead try 45mg of k1 or k2 mk-7. if not, plz stop needless argument.

*
Blue is too afraid to try it. anyone else..?

come to

http://www.imminst.o...o...c=39856&hl=

"Vitamin K is essential for blood coagulation and bone metabolism in mammals. This vitamin functions as a cofactor in the posttranslational synthesis of γ-carboxyglutamic acid (Gla) from glutamic acid residues. However, other functions of vitamin K have been reported recently. We previously found that vitamin K suppresses the inflammatory reaction induced by lipopolysaccharide (LPS) in rats and human macrophage-like THP-1 cells. In this study, we further investigated the mechanism underlying the anti-inflammatory effect of vitamin K by using cultures of LPS-treated human- and mouse-derived cells. All the vitamin K analogues analyzed in our study exhibited varied levels of anti-inflammatory activity. The isoprenyl side chain structures, except geranylgeraniol, of these analogues did not show such activity; warfarin did not interfere with this activity. The results of our study suggest that the 2-methyl-1,4-naphtoquinone ring structure contributes to express the anti-inflammatory activity, which is independent of the Gla formation activity of vitamin K. Furthermore, menaquinone-4, a form of vitamin K2, reduced the activation of nuclear factor κB (NFκB) and inhibited the phosphorylation of IKKα/β after treatment of cel with LPS. These results clearly show that the anti-inflammatory activity of vitamin K is mediated via the inactivation of the NFκB signaling pathway."
http://dx.doi.org/10...bio.2009.09.011

Another example of the Ks doing more than their traditional role.
Edited by Blue, 27 March 2010 - 05:49 PM.

Vitamin K2 and geranylgeraniol, its side chain component, inhibited osteoclast formation in a different manner.

Hiruma Y, Nakahama K, Fujita H, Morita I.

We comparatively examined the mechanism by which vitamin K(2) (Menatetrenone, MK4) and its side chain component, geranylgeraniol (GGO), inhibited osteoclast formation in the co-culture system of stromal cells with spleen cells. Both MK4 and GGO inhibited osteoclast formation induced by 1alpha,25-dihydroxyvitamin D3 (1,25(OH)(2)D(3)). MK4, but not GGO, inhibited cyclooxygenase-2 (COX-2) expression and prostaglandin E(2) (PGE(2)) production in the co-culture system. To elucidate the precise mechanism of the inhibitory effect of GGO on osteoclast formation, the co-cultured cells were stimulated with PGE(2). GGO, but not MK4, inhibited osteoclast formation via suppression of the receptor activator of NF-kappaB ligand (RANKL) expression. Moreover, GGO abolished the disruption of osteoclastic actin rings induced by nitrogen-containing bisphosphonate (N-BP), whereas MK4 did not affect it at all. These data suggest that MK4 inhibited osteoclast formation independently of GGO, and that MK4, but not GGO, has no competitive action on the anti-osteoporotic effect of N-BP.

http://www.ncbi.nlm....pubmed/14715241

Vitamin K(2) inhibits adipogenesis, osteoclastogenesis, and ODF/RANK ligand expression in murine bone marrow cell cultures.

Takeuchi Y, Suzawa M, Fukumoto S, Fujita T.

Division of Endocrinology, Department of Medicine, University of Tokyo School of Medicine, Tokyo, Japan. taeuchi-tky@umin.ac.jp

Several lines of evidence suggest that vitamin K has nutritional and pharmacological effects against bone loss. To clarify effects of vitamin K on bone marrow cells, which contains progenitors of both osteoblasts and osteoclasts, we examined mouse bone marrow cell cultures in the presence of vitamin K(1) (K1) and menatetrenone (MK4), a vitamin K(2) with four isoprene units. Treatment with MK4 but not K1 inhibited the formation of adipocytes and stimulated alkaline phosphatase activity, an early differentiation marker of osteoblast. Although nuclear receptor PPARgamma2 plays a pivotal role in adipogenesis, MK4 had no effects on the expression of PPARgamma2 mRNA and PPARgamma2-dependent transcriptional activity. MK4 inhibited the expression of osteoclast differentiation factor (ODF)/RANK ligand and the formation of osteoclast-like cells induced by 1,25-dihydroxyvitamin D(3). These results suggest that MK4 specifically influences differentiation and functions of bone marrow cells to inhibit adipogenesis and osteoclastogenesis. At the expense of adipogenesis, MK4 might stimulate osteoblastogenesis in bone marrow cells. Therefore, MK4 may favor bone metabolism to spare bone mass as a compound that modulates cellular differentiation and functions in bone marrow in addition to as a nutrient factor.

http://www.ncbi.nlm....pubmed/11113387

It's fascinating that MK4 is also a Cox2 inhibitor.
Would it actually be an effective NSAID ?

"To reveal an essential biological role of menaquinone-4, we have clarified that dietary PK was converted to menaquinone-4 (MK-4) in animal tissues using deuterated vitamin K analogues. However, the kinds of analogue converted into MK-4 have not been elucidated. In this study, we examined structure-activity relationships in the conversion of several vitamin K analogues, with a substituted side-chain, into MK-4 using cultured human cell lines. The results differed with the side chain of the analogues, that is, 1) the length of the isoprene unit and 2) the number of double bonds in the side chain. These findings would be useful for clarifying the mechanism of conversion of other vitamin K homologues into MK-4 as well as related enzymes."
http://dx.doi.org/10...bmc.2010.03.035

Does anyone have the whole study? Sounds like this could be evidence for mk7 to 9 being converted to mk4 or not.

Does anyone have the whole study? Sounds like this could be evidence for mk7 to 9 being converted to mk4 or not.

this would be extremely interesting, if true. i remember looking at AOR's brochure on their Peak K2 (MK-4) product, and it briefly mentioned the possibility of MK-7 converting to MK-4 (by hanging around in the blood for an extended period of time, until the body can slowly convert it over). I'm not sure what the basis is for that possibility, but it must be out there.

Thanks to Sillewater for making it possible for me to read the above Article in Press!

The researchers in vitro for 24 h incubated two different human cancer cells with several vitamin k analgoues. Similar results were seen for both osteosarcoma and hepatocarcinoma cells. The vitamin k analogues in order to be distinguished from native ones already present were deuterated by replacing one common hydrogen with deuterium.

1. All tested deuterated k analgoues except one were converted to some degree to deuterated mk4. In addition, a mk4 metabolite was detected indicating that this deuterated mk4 was utilized in the cells.

2. Longer side chains decreased the 24 h conversion. Eyeballing the graph mk2-d7 was converted around x20 better than mk7-d7. Higher form than mk7 were not tested.

3. K3-d6 was converted around x40 better than mk7-d7.

4. k1-d7 was converted around x1-2 better than mk7-d7.

5. Removing double bonds by hydrogenation reduced conversion.

6. In particular, 2,3-DH-PK, a hydrogenated form of k1 produced by hydrogenation of k1 rich plants oils was not converted at all.

So does this prove that k1 and mk7 are the worst forms for getting mk4? Likely not since this is a 24 h in vitro test. Mk7 has a very long half-life in blood. K1 is present in some tissues in much higher concentrations than mk4. They may both be storage forms that are only slowly converted. What form would have the best conversion if not limiting the time period to 24 h is still unknown.
http://journals.camb...l...&aid=877476
http://bloodjournal....ract/109/8/3279

Is it better to get mk4 directly? We do not know any function that k1 and mk7 does that mk4 cannot do. There seem to be some functions that mk4 does that k1 and mk7 do not. But mk7 has a much longer half-life in the blood and k1 has a much higher concentration in certain tissues. Maybe these forms provide a steady concentration of mk4 while giving mk4 itself causes relatively quickly elimination at least from blood which may be disadvantageous. Furthermore, we have no or little idea what the ks are doing in many tissues so difficult to state that mk4 can do everything as well as mk7 or k1.

So ultimately I do not think this study resolves the question regarding which form is best. The most important finding is likely that the other forms except the one from hydrogenated plant oils are converted to mk4 to some degree.
Edited by Blue, 05 April 2010 - 01:43 PM.

thx for the post blue. i guess we are probably better off with mk-4 anyways, but maybe some Edam cheese is a good insurance policy.

Thanks for the analysis. One thing that stands out is that the body converts all of these forms to MK4, and to me the simplest solution is to use that form. I'm inclined to get a bottle of the Thorne drops at 1mg/drop and dose from there.

thx for the post blue. i guess we are probably better off with mk-4 anyways, but maybe some Edam cheese is a good insurance policy.

Erm, IIRC MK-ns directly act in gamma-carboxylation without any need for conversion (and unsurprisingly long chain Mk-ns are superior in those vitro assays). This study is only relevant to the putative, unique benefits of MK-4, I guess. But one thing is for sure and will not change anytime soon: in vitro evidence tells us nothing about in vivo results. Why are people still swayed by in vitro speculation? And why again this false dichotomy? "Take Mk-4 OR long chain menaquinones" Let's get all the vitamers that are naturally found in our diet, how about that?
Edited by kismet, 05 April 2010 - 05:27 PM.