350 replies to this topic

[rwac]

Regarding cis/trans: I go that from a comment Stephan made on his blog here -- search for "cis." I emailed thorne too, and also never got a reply. I have no additional information.

I emailed RI about this, and they said that it's from biofermentation, and it is what was used in the osteoporosis studies.

Edited by rwac, 03 February 2010 - 02:20 PM.

[Blue]

Searching for something else I happened upon a study finding only two dietary factors reducing the risk for rheumatoid arthritis. Olive oil and cooked vegetables.With cooked vegetables having a stronger effect than olive oil. But notably no association with fish or uncooked vegetables.
http://www.ajcn.org/...tract/70/6/1077

That seems weird. What is it with cooked vegetables that is better than raw? Well, one possibility would be more available lycopene from cooked tomato products.. But I have not been that impressed with this compound. Looking for something else improved by cooking it turns out that the amount of available K1 increases in vegetables with cooking.
http://www.nal.usda....a18_751-758.pdf

Also, very high vitamin K1 vegetables like spinach and broccoli are usually cooked.

Furthermore,
Vitamin K2 [menaquinone-4 (MK-4)] has been reported to induce apoptosis in hepatocellular carcinoma, leukemia, and MDS cell lines. The effects of MK-4 on the development of arthritis have never been addressed so far. In this study, we investigated the effect of MK-4 upon the proliferation of rheumatoid synovial cells and the development of arthritis in collagen-induced arthritis (CIA). We analyzed the effect of MK-4 on the proliferation of fibroblast-like synoviocytes (FLSs) using the3-(4,5-demethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The proapoptotic effect of MK-4 upon FLS was investigated with annexin V staining and DNA fragmentation and caspase 3/7 assays. Moreover, we analyzed the effect of MK-4 on the development of CIA in female dark agouti rats. Our results indicated that MK-4 inhibited the proliferation of FLS and the development of CIA in a dose-dependent manner. We concluded that MK-4 may represent a new agent for the treatment of RA in the setting of combination therapy with other disease-modifying antirheumatic drugs. © 2008 IUBMB IUBMB Life, 60(6): 355-361, 2008
http://www3.intersci...140700/abstract

Edited by Blue, 25 February 2010 - 08:18 PM.

[DarrenMer]

Quick question.

I got Vitacost's Vitamin K complex (100mcg of MK-7, 1000mcg of K1 and 1300 mcg of MK-4. ) and I'm wondering. When, and with what should I take it ? Does it have to be with a meal ? I was thinking before bed with omega3 pill and water ?

[rwac]

Quick question.

I got Vitacost's Vitamin K complex (100mcg of MK-7, 1000mcg of K1 and 1300 mcg of MK-4. ) and I'm wondering. When, and with what should I take it ? Does it have to be with a meal ? I was thinking before bed with omega3 pill and water ?

Vitamin K is fat soluble, so take it with a fatty meal.

[Jay]

I got a reply from Thorne regarding their mk-4 product. The trans forms of mk-4 is the natural form so I think this is a pretty good answer. I might start using my drops again.

"Thank you for your inquiry! This is the answer I received from the purchasing department –



E-isomer is trans form and Z-isomer is Cis form.

Content in the K2: E-isomer is 99.9% and Z-isomer is 0.1%"

Edited by Jay, 16 March 2010 - 03:57 PM.

[rollo]

How safe is vitamin K to take? I mean, just as some believe anti-oxidant supplementation is dangerous, are there any that believe vitamin K could be too?

[Blue]

How safe is vitamin K to take? I mean, just as some believe anti-oxidant supplementation is dangerous, are there any that believe vitamin K could be too?

http://www.imminst.o...o...st&p=364074

Also, the K vitamins are partially metabolized to menadione which may have undesirable properties like being a prooxidant. But K1 and K2 seem to be antioxidants.

Edited by Blue, 17 March 2010 - 07:38 PM.

[Blue]

"We measured the vitamin K status in postmortem human tissues (brain, heart, kidney, liver, lung, pancreas) to see if there is a tissue-specific distribution pattern. Phylloquinone (K1,) was recovered in all tissues with relatively high levels in liver, heart and pancreas (medians, 10·6 (4·8), 9·3 (4·2), 28·4 (12·8) pmol(ng)/g wet weight tissue); low levels (< 2 pmol/g) were found in brain, kidney and lung. Menaquinone-4 (MK-4) was recovered from most of the tissues; its levels exceeded the K1 levels in brain and kidney (median, 2·8 ng/g) and equalled K1 in pancreas. Liver, heart and lung were low in MK–4. The higher menaquinones, MK-6–11, were recovered in the liver samples (n 6), traces of MK-6–9 were found in some of the heart and pancreas samples. The results show that in man there are tissue-specific, vitamin-K distribution patterns comparable to those in the rat. Furthermore, the accumulation of vitamin K in heart, brain and pancreas suggests a hitherto unrecognized physiological function of this vitamin."
http://journals.camb...l...&aid=877476

* K1 had higher concentrations than mk4 in several issues. Just for storage or something else? Something for those advocating only the mks to consider.
* The highest concentrations of both k1 and mk4 were in the pancreas. Why?

[full_circle]

mk-4 is the preferred form by our body. mk-4 and mk-7 have been studied in korea and japan for decades (koreans too, consume natto-equivalent traditional food that is also rich in mk-7) and study after study, mk-4 shows superior efficacy. this is why, unlike mk-4, mk-7 has earned no official approval in treating any illness or condition in korea and japan.

note that mk-7 is only recently being pushed by studies paid for by nattokinase manufacturers. why? mk-7 is a byproduct of nattokinase (nattokinase is basically mk-7 removed natto) and as nattokinase gains huge popularity in the US, which btw is a ludicrous thing since nattokinase can be extremely dangerous, nattokinase manufacturers now are trying to catch two rabbits with one stone: clearing their huge surplus of mk-7 and profiting while doing so.

also note that k1, mk-4 and mk-7 all will shorten thrombin time (thicken blood: headaches some ppl get by supplementing these are most likely due to temporarily reduced blood flow) thus longer plasma half-life means higher risk of ischemic stroke i.e. mk-7 is also undesirable in this regard (mk-4's short plasma half life is due to its superior bio-availability, not because of its fast excretion)

human in general, unlike rats, are very inefficient in converting either k1 or mk-7 into mk-4.

Edited by full_circle, 24 March 2010 - 07:44 PM.

[Blue]

mk-4 is the preferred form by our body. mk-4 and mk-7 have been studied in korea and japan for decades (koreans too, consume natto-equivalent traditional food that is also rich in mk-7) and study after study, mk-4 shows superior efficacy. this is why no illness or condition is treated by mk-7 in korea and japan. note that mk-7 is only recently being pushed by studies paid for by nattokinase manufacturers. why? mk-7 is a byproduct of nattokinase (nattokinase is basically mk-7 removed natto) and as nattokinase gains huge popularity in the US, which btw is a ludicrous trend since nattokinase can be very very dangerous, nattokinase manufacturers now are trying to catch two rabbits with one stone: clearing their huge surplus of mk-7 and profiting doing so.

also note that k1, mk-4 and mk-7 all will shorten thrombin time (thicken blood), which means longer plasma half-life will raise possibility of ischemic stroke i.e. mk-7 is undesirable in this regard also (mk-4's short plasma half life is due to its superior availability, not because it is excreted fast)

What studies are you talking about? Sources please.

Look at the studies in this thread. Many were mk7 beats the others epidemiologically (although these are limited to the amounts food in normal diets). K1 has, for example, a very interesting, placebo-controlled, four year long, but rather small, study, were fractures, cancer, and general serious disease were greatly reduced. Mk4 regarding prevention only has several Japanese osteoporosis and fracture studies using very high amounts.

The claims regarding ischemic stroke is false. Unless you have a source. For example the K1 study found no such an effect. All the Ks are necessary for proper functioning of certain clotting proteins but once that is done they have no further effect regarding this.

Also a source please for the claim regarding inefficient conversion.

Edited by Blue, 24 March 2010 - 07:12 PM.

[full_circle]

don't have time and you are free to disregard my sincere 2 cents.

Edited by full_circle, 24 March 2010 - 07:24 PM.

[Blue]

don't have time and you are free to disregard my sincere 2 cents.

I will certainly disregard unsourced opinions for which there is no evidence in the literature I have read.

Edited by Blue, 24 March 2010 - 07:26 PM.

[Jay]

don't have time and you are free to disregard my sincere 2 cents.

I will certainly disregard unsourced opinions for which there is no evidence in the literature I have read.

That's probably a good idea.

To address the question you originally asked, I don't think anybody knows how the pancreas uses vitamin K, at least that's what the introduction to this 2008 study indicates. The authors speculate as follows:

The potential biological mechanisms relating phylloquinone to insulin resistance and glucose homeostasis are not understood. Two forms of vitamin K, phylloquinone and menaquinone-4, are found in the pancreas (21). However, vitamin K–dependent proteins specific to the pancreas have not been identified. A recent study proposed that osteocalcin, one of the vitamin K–dependent proteins in the bone, may improve insulin sensitivity and increase β-cell functions, partially through the enhancement of adiponectin expression (5). Alternatively, it has been suggested that vitamin K has potential physiologic functions in addition to its classic role as a cofactor for -carboxylation (22). In vivo, in vitro, and observational studies showed that vitamin K decreases inflammation-induced cytokines (23-25), so it is plausible that phylloquinone may improve insulin sensitivity and glycemic status by the suppression of inflammation.

By the way, I'm starting to think of K1 (and not mk-7 k2) as a delayed-release form of mk-4, convertible on an as-and-where-needed basis. I might add a few hundred mcgs k1 per day to my 30mcg/day mk-7 regimen.

Edited by Jay, 24 March 2010 - 08:05 PM.

[ajnast4r]

kale smoothies! i throw 1 cup of kale in my smoothie every morning... 500ug of K1

[stephen_b]

Interesting post on the whole health source blog's comment section by 'Daniel':

Studies showing K2 provides protections that K1 doesn't provide should be interpreted in the context of widespread vitamin D deficiency.

Vitamin D is instrumental in the conversion of K1 to K2. See http://www.ncbi.nlm....pubmed/19022954?.

Vitamin K1 prevented 90% of cancers in a (small) randomized placebo controlled trial when both groups (K1 group and placebo group) were "vitamin D replete" (defined as about 30ng/ml). See http://www.plosmedic...al.pmed.0050196.

Moreover, K1 is widely distributed throughout the organs. See http://journals.camb...l...&aid=877476.

We know that mk-4 activates gene transcription (but not mk-7 or K1). See http://jme.endocrino...t/full/39/4/239.

However, mk-4 has a very short half life in the human body, so, when taken in doses normally found in food, it likely disappears too quickly to do much.

But, in vitamin D sufficient people, I suspect that K1 is basically delayed-release mk-4, converting to mk-4 on a where-and-as-needed basis. I think this theory makes a lot of sense because (i) one of the roles of vitamin K is to protect against soft tissue calcification that can occur at very high vitamin D levels (so only useful when there is sun) and (ii) K1 is in green plants (so only available when there is sun).

Chasing mk-4 is a mistake in my opinion. Vitamin K1 plus D may provide the answer we are all looking for. Until confirmed by experiments, low dose mk-7 + K1 + D is a decent hedge in my opinion.

Edited by stephen_b, 27 March 2010 - 01:29 PM.

[full_circle]

http://wholehealthso...e-arterial.html

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.

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.
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.

Edited by full_circle, 27 March 2010 - 01:28 PM.

[stephen_b]

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.

full_circle, my advice to you is to either add something useful to the discussion or move along.

Edited by stephen_b, 27 March 2010 - 01:36 PM.

[full_circle]

afraid to try?
try it or leave it. it's that simple.

Edited by full_circle, 27 March 2010 - 01:41 PM.

[Blue]

http://wholehealthso...e-arterial.html

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.

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.
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.

That blog does not give a proper source for its claim regarding low conversion of K1 in humans.

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 were reduced.
http://www.plosmedic...al.pmed.0050196

Edited by Blue, 27 March 2010 - 03:12 PM.

[full_circle]

so take 45mg k1 or k2 mk-7 now. 3x15mg a day will do. (trust me, you don't wanna hear chicken from me)

*
the blog does show it somewhere in another page. look 4 it.

Edited by full_circle, 27 March 2010 - 03:26 PM.

[Blue]

so try it (trust me, you don't wanna hear chicken from me)

I care about the scientific literature. Post studies. Not unsourced personal opinions.

Do not ask others to do the work for you. If you have no good sources, then your claims are uninteresting.

Edited by Blue, 27 March 2010 - 03:30 PM.

[full_circle]

u r a chicken that can't be reasoned with (and you know it)

Edited by full_circle, 27 March 2010 - 03:31 PM.

[Blue]

u r a chicken that can't be reasoned with.

Personal attacks is a pathetic response by those who have lost the factual argument.

[full_circle]

you know it. next

Edited by full_circle, 27 March 2010 - 03:34 PM.

[Blue]

you know it. next

Yes, you have lost the factual argumentation.

[full_circle]

stop crying and prove you are right (but you can't and you know it)

[Blue]

stop crying and prove you are right (but you can't and you know it)

I have already proven my case with a study giving 5 mg k1 for four years with no increase in strokes and many benefits.

In contrast, you have only blurted out your unsourced personal opinion.

[full_circle]

45mg, get it? now stop crying and be a man common.

[Blue]

45mg, get it? now stop crying and be a man common.

Why should I try 45 mg when such a high dose produces many serious adverse effects when using mk4?
http://www.imminst.o...o...st&p=364074

[full_circle]

no it does not. you gonna prove it or not? (jeez be a man dude)
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 - 03:58 PM.