350 replies to this topic

[stephen_b]

Most epidemiology finds associations with MK-7 not MK-4 or phylloquinone.

But has our diet changed? It would be helpful if we could find out how much K2-MK4 there is in organ meats, marrow, or even roly poly fish heads. I'm not sure anyone has ever bothered to measure.

[VespeneGas]

This table is taken from (you guessed it) a weston A price article. The studies the author cites are here and here, but I can't get access to the full texts.

FOOD

VITAMIN K2 (MCG/100G)

Natto

1103.4 (0% MK-4)

Goose Liver Paste

369.0 (100% MK-4)

Hard Cheeses

76.3 (6% MK-4)

Soft Cheeses

56.5 (6.5% MK-4)

Egg Yolk (Netherlands)

32.1 (98% MK-4)

Goose Leg

31.0 (100% MK-4)

Curd Cheeses

24.8 (1.6% MK-4)

Egg Yolk (United States)

15.5 (100% MK-4)

Butter

15.0 (100% MK-4)

Chicken Liver

14.1 (100% MK-4)

Salami

9.0 (100% MK-4)

Chicken Breast

8.9 (100% MK-4)

Chicken Leg

8.5 (100% MK-4)

Ground Beef (Medium Fat)

8.1 (100% MK-4)

Bacon

5.6 (100% MK-4)

Calf Liver

5.0 (100% MK-4)

Sauerkraut

4.8 (8% MK-4)

Whole Milk

1.0 (100% MK-4)

2% Milk

0.5 (100% MK-4)

Salmon

0.5 (100% MK-4)

Mackerel

0.4 (100% MK-4)

Egg White

0.4 (100% MK-4)

Skim Milk

0.0

Fat-Free Meats

0.0

[Logan]

This table is taken from (you guessed it) a weston A price article. The studies the author cites are here and here, but I can't get access to the full texts.

FOOD

VITAMIN K2 (MCG/100G)

Natto

1103.4 (0% MK-4)

Goose Liver Paste

369.0 (100% MK-4)

Hard Cheeses

76.3 (6% MK-4)

Soft Cheeses

56.5 (6.5% MK-4)

Egg Yolk (Netherlands)

32.1 (98% MK-4)

Goose Leg

31.0 (100% MK-4)

Curd Cheeses

24.8 (1.6% MK-4)

Egg Yolk (United States)

15.5 (100% MK-4)

Butter

15.0 (100% MK-4)

Chicken Liver

14.1 (100% MK-4)

Salami

9.0 (100% MK-4)

Chicken Breast

8.9 (100% MK-4)

Chicken Leg

8.5 (100% MK-4)

Ground Beef (Medium Fat)

8.1 (100% MK-4)

Bacon

5.6 (100% MK-4)

Calf Liver

5.0 (100% MK-4)

Sauerkraut

4.8 (8% MK-4)

Whole Milk

1.0 (100% MK-4)

2% Milk

0.5 (100% MK-4)

Salmon

0.5 (100% MK-4)

Mackerel

0.4 (100% MK-4)

Egg White

0.4 (100% MK-4)

Skim Milk

0.0

Fat-Free Meats

0.0

What about yogurt? Specifically plain yogurt.

[Blue]

Most epidemiology finds associations with MK-7 not MK-4 or phylloquinone.

But has our diet changed? It would be helpful if we could find out how much K2-MK4 there is in organ meats, marrow, or even roly poly fish heads. I'm not sure anyone has ever bothered to measure.

It may well be that whatever the macronutrient intake of prehistoric man he ate more partially rotten foods, lacking refrigerators and regular fresh food, and maybe thus more MK-7.

Edited by Blue, 16 October 2009 - 07:55 AM.

[Blue]

"OBJECTIVE: Vitamin K has a potentially beneficial role in insulin resistance, but evidence is limited in humans. We tested the hypothesis that vitamin K supplementation for 36 months will improve insulin resistance in older men and women. RESEARCH DESIGN AND METHODS: This was an ancillary study of a 36-month, randomized, double-blind, controlled trial designed to assess the impact of supplementation with 500 microg/day phylloquinone on bone loss. Study participants were older nondiabetic men and women (n = 355; aged 60-80 years; 60% women). The primary outcome of this study was insulin resistance as measured by homeostasis model assessment (HOMA-IR) at 36 months. Fasting plasma insulin and glucose were examined as the secondary outcomes. RESULTS: The effect of 36-month vitamin K supplementation on HOMA-IR differed by sex (sex x treatment interaction P = 0.02). HOMA-IR was statistically significantly lower at the 36-month visit among men in the supplement group versus the men in the control group (P = 0.01) after adjustment for baseline HOMA-IR, BMI, and body weight change. There were no statistically significant differences in outcome measures between intervention groups in women. CONCLUSIONS: Vitamin K supplementation for 36 months at doses attainable in the diet may reduce progression of insulin resistance in older men."

http://www.ncbi.nlm....pubmed/18697901


"Background: The skeletal protein osteocalcin is -carboxylated by vitamin K. High serum uncarboxylated osteocalcin reflects low vitamin K status. In vitro and animal studies indicate that high uncarboxylated osteocalcin is associated with reduced insulin resistance. However, associations between osteocalcin and measures of insulin resistance in humans are less clear.

Objective: Our aim was to examine cross-sectional and longitudinal associations between circulating forms of osteocalcin (total, uncarboxylated, and carboxylated) and insulin resistance in older men and women.

Design: Cross-sectional associations between serum measures of total osteocalcin, carboxylated osteocalcin, and uncarboxylated osteocalcin and insulin resistance were examined in 348 nondiabetic men and women (mean age: 68 y; 58% female) by using the homeostasis model assessment of insulin resistance (HOMA-IR). Associations between each form of osteocalcin at baseline and 3-y change in HOMA-IR were examined in 162 adults (mean age: 69 y; 63% female) who did not receive vitamin K supplementation.

Results: Lower circulating uncarboxylated osteocalcin was not associated with higher HOMA-IR at baseline or at 3-y follow-up. Those in the lowest tertiles of total osteocalcin and carboxylated osteocalcin at baseline had higher baseline HOMA-IR (P = 0.006 and P = 0.02, respectively). The concentration of carboxylated osteocalcin at baseline was inversely associated with a 3-y change in HOMA-IR (P = 0.002).

Conclusions: In older adults, circulating uncarboxylated osteocalcin was not associated with insulin resistance. In contrast, elevated carboxylated osteocalcin and total osteocalcin were associated with lower insulin resistance, which supports a potential link between skeletal physiology and insulin resistance in humans. The role of vitamin K status in this association remains unclear and merits further investigation. This trial is registered at clinicaltrials.gov as NCT00183001."
http://www.ajcn.org/...cn.2009.28151v1

[Blue]

Extract from the 5 mg K1 study regarding serious adverse events (SAE):
"SAEs occurred in 9.1% (40/440) of participants: 6.9% (15/217) in the vitamin K group and 11.2% (25/223) in the placebo group. These included hospitalizations for pneumonia, heart failure, gastrointestinal bleeding, elective and nonelective surgeries, cancer, and death. Cancer incidence was lower in the vitamin K group than in the placebo group (three versus 12, p = 0.02; HR = 0.25, 95% CI 0.07 to 0.89) (Figure 4B). Higher mean serum vitamin K levels over the duration of the study correlated with lower cancer incidence (p < 0.05) (Figure 4C). Because half of the cases were breast cancers (one in the vitamin K group and six in the placebo group), we calculated the Gail breast cancer risk score [21] from baseline data and found that there was no difference between the vitamin K and the placebo groups (1.70% versus 1.71% risk of having invasive breast cancer in the next 5 y). There were five deaths during the study and follow-up period: one woman on vitamin K (passenger in a car accident) and four women on placebo (three who died of cancers, and one who died in her sleep from arrhythmogenic right ventricular cardiomyopathy). There was no difference in health-related quality of life between groups."
http://www.plosmedic...al.pmed.0050196

There really should be a larger study of high-dose K1 and all-cause mortality. Also there should be a follow-up study of all these Japanese 45 mg MK4 osteoporosis patients who presumably has continued with MK4 to see what has happened to their mortality and morbidity.

Edited by Blue, 17 October 2009 - 03:32 PM.

[Blue]

"BACKGROUND: Dietary vitamin K is usually inadequate to maximize serum osteocalcin gamma-carboxylation. Phylloquinone supplementation increases osteocalcin gamma-carboxylation; however, the amount required to maximize carboxylation is not known. OBJECTIVE: This study assessed the ability of various doses of phylloquinone (vitamin K(1)) to facilitate osteocalcin gamma-carboxylation. DESIGN: Healthy adults aged 19-36 y participated in 2 substudies. In an initial dose-finding study (substudy A), 6 women and 4 men received a placebo daily for 1 wk and then phylloquinone daily for 3 wk: 500, 1000, and 2000 micro g during weeks 2, 3, and 4, respectively. Osteocalcin and undercarboxylated osteocalcin were measured at baseline and after each week of supplementation. Subsequently, to further delineate the gamma-carboxylation response of osteocalcin to various doses of vitamin K, 58 women and 42 men were randomly assigned to receive placebo or phylloquinone supplementation (250, 375, 500, and 1000 micro g/d) for 2 wk (substudy B). The percentage of undercarboxylated osteocalcin (%ucOC) was measured at baseline and weeks 1 and 2. RESULTS: In substudy A, %ucOC decreased with phylloquinone supplementation (P less than 0.0001); a greater reduction was observed with 1000 and 2000 micro g than with 500 micro g (P less than 0.05). In substudy B, %ucOC decreased in all supplemented groups by week 1 (P for the trend less than 0.0001), which was sustained through week 2. Phylloquinone supplementation decreased %ucOC dose-dependently; %ucOC was significantly different between the 250- micro g and the placebo groups and between the 1000- and 500- micro g groups but not between the 250-, 375-, and 500- micro g groups. CONCLUSION: A daily phylloquinone intake of approximately 1000 micro g is required to maximally gamma-carboxylate circulating osteocalcin."

Actually, 2000 mcg achieved higher carboxylation but the difference was not statistically significant. Higher amounts was not tested.
http://www.ajcn.org/.../full/76/5/1055

Edited by Blue, 17 October 2009 - 04:14 PM.

[Kutta]

OK, reading through this thread made me rather confused.


- Krillin argues that K1 meddles with Phase II detox and says that it's a no-go. But, a bit more exactly, what is the magnitude of this disadvantage?

- Should I supplement K1 anyway, and for what reason (Carboxylation? K2 conversion? Cancer epidemiology?), and how much?

- All Vitamin K may convert to menadione (k3) which is toxic, therefore, as Krillin says, Mk-7 is optimal because of low dosages. However, david ellis says that menadione is generally not a risk. If there is a dosage above which it starts being a risk, what is it?

- Are there biochemical roles that Mk-7 alone cannot fulfill, or: do Mk-4 and K1 have benefits that Mk-7 does not? I'm asking this because currently I'm somewhat leaning towards Mk-7 only supplementation.

[tunt01]

- Are there biochemical roles that Mk-7 alone cannot fulfill, or: do Mk-4 and K1 have benefits that Mk-7 does not? I'm asking this because currently I'm somewhat leaning towards Mk-7 only supplementation.

http://wholehealthso...vitamin-k2.html

i came down in favor of mk-4 after reading that.

[rwac]

http://wholehealthso...vitamin-k2.html

i came down in favor of mk-4 after reading that.

If anybody doesn't want to read through that, here's the relevant paper.

http://jme.endocrino...t/full/39/4/239

Vitamin K₂ induces phosphorylation of protein kinase A and expression of novel target genes in osteoblastic cells
T Ichikawa¹, K Horie-Inoue¹, K Ikeda¹, B Blumberg² and S Inoue^{1,3 1}

Abstract

Vitamin K is known as a critical nutrient required for bone homeostasis and blood coagulation, and it is clinically used as a therapeutic agent for osteoporosis in Japan. Besides its enzymatic action as a cofactor of vitamin K-dependent -glutamyl carboxylase (GGCX), we have previously shown that vitamin K₂ is a transcriptional regulator of bone marker genes and extracellular matrix-related genes, by activating the steroid and xenobiotic receptor (SXR). To explore a novel action of vitamin K in osteoblastic cells, we identified genes up-regulated by a vitamin K₂ isoform menaquinone-4 (MK-4) using oligonucleotide microarray analysis. Among these up-regulated genes by MK-4, growth differentiation factor 15 (GDF15) and stanniocalcin 2 (STC2) were identified as novel MK-4 target genes independent of GGCX and SXR pathways in human and mouse osteoblastic cells. The induction of GDF15 and STC2 is likely specific to MK-4, as it was not exerted by another vitamin K₂ isoform MK-7, vitamin K₁, or the MK-4 side chain structure geranylgeraniol. Investigation of the involved signaling pathways revealed that MK-4 enhanced the phosphorylation of protein kinase A (PKA), and the MK-4-dependent induction of both GDF15 and STC2 genes was reduced by the treatment with a PKA inhibitor H89 or siRNA against PKA. These results suggest that vitamin K₂ modulates its target gene expression in osteoblastic cells through the PKA-dependent mechanism, which may be distinct from the previously known vitamin K signaling pathways.

Edited by rwac, 19 October 2009 - 07:53 PM.

[stephen_b]

I come down on the side of MK-4 too, followed by MK-7. Is it the case though that K2-MK7 is more easily converted to MK4 than is K1?

I don't know if it is worthwhile supplementing K1 if you eat leafy greens.

[stephen_b]

So, one egg yolk from a large egg weighs about 16.5g and provides 1.95 micrograms of K2-MK4. Not a whole lot.

[kismet]

I don't know if it is worthwhile supplementing K1 if you eat leafy greens.

Yes, it is as has been repeatedly pointed out in this thread - or at least somewhere on the forum - and the evidence is the crux of this whole argument: you choose MK-4 based on in vitro evidence over K1 which is supported by randomised controlled trials. MK-7 is also to be considered superior to MK-4 (if you don't suffer from osteo) because it is supported by epidemiology and has been shown to do the same as K1 just at lower doses. The study merely aims to show that MK-4 has (or actually *might* have) special effects on bone, which is irrelevant compared to the effects on the vasculature which are unproven for MK-4. The only evidence-based use of MK-4 is for osteoporosis.

Edited by kismet, 19 October 2009 - 10:27 PM.

[Blue]

Vitamin K₂ induces phosphorylation of protein kinase A and expression of novel target genes in osteoblastic cells
T Ichikawa¹, K Horie-Inoue¹, K Ikeda¹, B Blumberg² and S Inoue^{1,3 1}

Abstract

Vitamin K is known as a critical nutrient required for bone homeostasis and blood coagulation, and it is clinically used as a therapeutic agent for osteoporosis in Japan. Besides its enzymatic action as a cofactor of vitamin K-dependent -glutamyl carboxylase (GGCX), we have previously shown that vitamin K₂ is a transcriptional regulator of bone marker genes and extracellular matrix-related genes, by activating the steroid and xenobiotic receptor (SXR). To explore a novel action of vitamin K in osteoblastic cells, we identified genes up-regulated by a vitamin K₂ isoform menaquinone-4 (MK-4) using oligonucleotide microarray analysis. Among these up-regulated genes by MK-4, growth differentiation factor 15 (GDF15) and stanniocalcin 2 (STC2) were identified as novel MK-4 target genes independent of GGCX and SXR pathways in human and mouse osteoblastic cells. The induction of GDF15 and STC2 is likely specific to MK-4, as it was not exerted by another vitamin K₂ isoform MK-7, vitamin K₁, or the MK-4 side chain structure geranylgeraniol. Investigation of the involved signaling pathways revealed that MK-4 enhanced the phosphorylation of protein kinase A (PKA), and the MK-4-dependent induction of both GDF15 and STC2 genes was reduced by the treatment with a PKA inhibitor H89 or siRNA against PKA. These results suggest that vitamin K₂ modulates its target gene expression in osteoblastic cells through the PKA-dependent mechanism, which may be distinct from the previously known vitamin K signaling pathways.

K1 is converted to MK4 so I am not sure that this means that giving MK4 is better. I cited a rodent study previously where K1 actually caused higher tissue leels of MK4 than giving MK4 itself. Especially in the brain where MK4 levels actually decreased by giving MK4. Maybe K1 but not MK4 cross the BBB? K1 may also have effects on its own. It was present in certain tissues in higher levels than MK4.

MK7 may or may not be converted to MK4.

Edited by Blue, 20 October 2009 - 01:17 AM.

[Blue]

Vitamin K also have or may have important interactions with the other fat soluble vitamins:

The dose of vitamin D that some researchers recommend as optimally therapeutic exceeds that officially recognized as safe by a factor of two; it is therefore important to determine the precise mechanism by which excessive doses of vitamin D exert toxicity so that physicians and other health care practitioners may understand how to use optimally therapeutic doses of this vitamin without the risk of adverse effects. Although the toxicity of vitamin D has conventionally been attributed to its induction of hypercalcemia, animal studies show that the toxic endpoints observed in response to hypervitaminosis D such as anorexia, lethargy, growth retardation, bone resorption, soft tissue calcification, and death can be dissociated from the hypercalcemia that usually accompanies them, demanding that an alternative explanation for the mechanism of vitamin D toxicity be developed. The hypothesis presented in this paper proposes the novel understanding that vitamin D exerts toxicity by inducing a deficiency of vitamin K. According to this model, vitamin D increases the expression of proteins whose activation depends on vitamin K-mediated carboxylation; as the demand for carboxylation increases, the pool of vitamin K is depleted. Since vitamin K is essential to the nervous system and plays important roles in protecting against bone loss and calcification of the peripheral soft tissues, its deficiency results in the symptoms associated with hypervitaminosis D. This hypothesis is circumstantially supported by the observation that animals deficient in vitamin K or vitamin K-dependent proteins exhibit remarkable similarities to animals fed toxic doses of vitamin D, and the observation that vitamin D and the vitamin K-inhibitor Warfarin have similar toxicity profiles and exert toxicity synergistically when combined. The hypothesis further proposes that vitamin A protects against the toxicity of vitamin D by decreasing the expression of vitamin K-dependent proteins and thereby exerting a vitamin K-sparing effect. If animal experiments can confirm this hypothesis, the models by which the maximum safe dose is determined would need to be revised. Physicians and other health care practitioners would be able to treat patients with doses of vitamin D that possess greater therapeutic value than those currently being used while avoiding the risk of adverse effects by administering vitamin D together with vitamins A and K.
http://linkinghub.el...306987706007171


BACKGROUND: An adverse hematological interaction between vitamins E and K has been reported, primarily in patients on anticoagulants. However, little is known regarding circulating levels or tissue concentrations of vitamin K in response to vitamin E supplementation. The purpose of this study was to examine the effect of different levels of dietary alpha-tocopherol on phylloquinone and menaquinone-4 concentrations, while maintaining a constant intake of phylloquinone, in rat tissues. METHODS: Male 4-wk old Fischer 344 rats (n = 33) were fed one of 3 diets for 12 wk: control (n = 13) with 30 mg all-rac-alpha-tocopherol acetate/kg diet; vitamin E-supplemented (n = 10) with 100 mg all-rac-alpha-tocopherol acetate/kg diet; and vitamin E-restricted (n = 10) with <10 mg total tocopherols/kg diet. All 3 diets contained 470 +/- 80 microg phylloquinone/kg diet. RESULTS: Phylloquinone concentrations were lower (P < or = 0.05) in the vitamin E-supplemented compared to the vitamin E-restricted group (mean +/- SD spleen: 531 +/- 58 vs. 735 +/- 77; kidney: 20 +/- 17 vs. 94 +/- 31, brain: 53 +/- 19 vs. 136 +/- 97 pmol/g protein respectively); no statistically significant differences between groups were found in plasma, liver or testis. Similar results were noted with menaquinone-4 concentrations in response to vitamin E supplementation. CONCLUSION: There appears to be a tissue-specific interaction between vitamins E and K when vitamin E is supplemented in rat diets. Future research is required to elucidate the mechanism for this nutrient-nutrient interaction.
http://www.ncbi.nlm....les/PMC1544331/

[stephen_b]

Blue, there is a thorough discussion of this study here.

Edited by stephen_b, 21 October 2009 - 08:02 PM.

[yoyo]

Blue, there is a thorough discussion of this study here.

i don't see the benefit of taking in retinol as opposed to retinol-precursor carotenoids. is there some evidence of conversion problems? carotenoids have benefits beyond just vitaminA activity too.

[Blue]

Blue, there is a thorough discussion of this study here.

Thanks. Very interesting. Maybe the situation with vitamin E is similar? Vitamin E supplementation increases the need for vitamin K?

[Clarity]

I'm new to this board, and was just perusing through the different threads & wanted to add my experience with MK7 because I basically have proof that it works.

Back about a year ago I had a pelvic xray prior to chiropractic treatment. Upon getting the results, my chiro told me I arteriosclerosis in my abdominal aorta. She also told me this is very rare except in people much older (I'm in my early 40s). Having had alot of inflammation in my body over the past 4 years - from what I thought was autoimmune & adrenal problems - but now I think probably from gut inflammation/H Plyori - I was determined to find something that would reverse the plaque, because I've almost always had good success with finding SOMETHING for various health problems.

So I took MK-7 for a year. I took Jarrows MK7 @90 mcg daily. I also at one point started taking Twinlab sublingual K2/D3. However, I don't know how absorbable the twinlab is, because it didn't succeed much in getting my D3 levels up. I also took nattokinase (I think it was 3000FU's) consistently for a period of time (because I have a genetic clotting disorder) and then shifted to only occasionally.

I had 2 CT scans (neck to pelvis) in the past 4 months for other problems. NO arteriosclerosis was found in my aorta. I also had a echo (sono) of my heart valves & carotid arteries very recently, and it showed not a lick of plaque (even though there was some inflammation on the wall of my carotid). I had fully expected to see some plaque, because plaque in the abdominal aorta is usually a very good sign that it is elsewhere.

So I'll continue to take the MK-7, except now I take it about 3-4x wk. With an occasional nattokinase thrown in for good luck (after I heal my stomach).

And continue to stew that the medical establishment & Media is not focusing on this for arteriosclerosis, osteoporosis, and even probably alzheimers & dementia. And instead, they continue to focus on only Vit D/calcium as the way to keep calcium out of the arteries & in your bones. I haven't mentioned this to any of my dr's yet, as I have been getting the sceptical attitude about supplements for so long, and am often told to get off them.

And for anyone who might think that the original xray may have had a shadow in them - the plaque was perfectly aligned with the edge of the aorta. So I know it wasn't a "wayward spot" on the xray.


Wendy

ETA: I wanted to add that I was taking Jarrows at one point, then switched to Twinlab for a period of time, then only recently up until my last vit D testing was taking both. So I really can't say which brand worked....or if the nattokinase helped.

Edited by Clarity, 31 October 2009 - 02:02 AM.

[Blue]

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

[Blue]

Dietary factors may contribute to functional limitations potentially through body composition in older adults. To explore this, dietary intake via 24h recall and physical performance changes in timed up-and-go (UPGO) and 7m walk w/ obstacle (7OB) were assessed over 2 years in women (Black=50, White=137; M±SD age: 68±6 yrs, BMI: 27.7±5.1 kg/m²). Lean (LM) and fat mass (FM) were assessed with DXA. Significant reduction in LM 0.4±1.7 kg (0.8%) occurred. After 2 years, 109 and 106 women (FAST) improved UPGO (9.5±8.1%) and 7OB (12.3±9.3%); 78 and 81 women (SLOW) reduced UPGO (8.6±6.9%) and 7OB (8.8±6.5%) performance. Energy intake was 1666±488 kcal; protein 76±25 g (19±5 % of energy); carbohydrate 205±66 g (50±9 %); fat 63±27 g (33±8 %); vitamin D 3.1±2.5 µg; vitamin A 1378±1334 RE; vitamin K 128±153 µg; calcium 824±410 mg. No absolute nutrient intakes differed between groups. Controlling for race, relative protein (19±5, 17±4 %, FAST and SLOW respectively; p=0.02) and relative vitamin K (92±117, 61±58 µg/1000kcal; p=0.03) differed in UPGO; relative carbohydrate (50±9, 48±9 %; p=0.03) differed in 7OB. Vitamin D intake did not differ between groups in UPGO (p=0.79) or 7OB (p=0.37). Results were not changed when controlling for race and BMI, LM or FM change. Protein, carbohydrate, and vitamin K intake may be related to changes in physical performance in older women, independent of energy intake or changes in body composition.
http://www.fasebj.or...Abstracts/550.4

The differences in protein and carbohydrate intake seem quite small. Only vitamin K intake really differentiate the groups. There really should be some large, long-term vitamin K placebo controlled studies looking at cancer, physical performance, total mortality etc. See also:
http://www.imminst.o...o...st&p=354898

Edited by Blue, 02 February 2010 - 07:39 AM.

[e Volution]

OK so over a year after this thread was originally created, the picture is still far from crystal. So while we're waiting for 'consensus'; what levels are you extremely well [Vitamin K2] informed individuals supplementing at (if at all)? And obviously what form(s)?

I'll start: Right now I am 'hedging my bets' and going with LEF Super K2
Vitamin K2 (as menaquinone-7) 100 mcg
Vitamin K2 (as menaquinone-4) 1000 mcg
Vitamin K1 1000 mcg

I take this around 5 times a week, trying to ensure I take it along with Vitamin D (sunshine or 5000IU D3), A, and E (both from food). However I certainly feel theres room for improvement dosage wise.

Edited by icantgoforthat, 02 February 2010 - 08:37 AM.

[mikeinnaples]

OK so over a year after this thread was originally created, the picture is still far from crystal. So while we're waiting for 'consensus'; what levels are you extremely well [Vitamin K2] informed individuals supplementing at (if at all)? And obviously what form(s)?

I'll start: Right now I am 'hedging my bets' and going with LEF Super K2
Vitamin K2 (as menaquinone-7) 100 mcg
Vitamin K2 (as menaquinone-4) 1000 mcg
Vitamin K1 1000 mcg

I take this around 5 times a week, trying to ensure I take it along with Vitamin D (sunshine or 5000IU D3), A, and E (both from food). However I certainly feel theres room for improvement dosage wise.

I am taking the same caps as well at about the same rate as you. I tend to take the bulk of my supplements M-F and leave S/S supplement free save for a few staples though, so take that at face value.

[Jay]

OK so over a year after this thread was originally created, the picture is still far from crystal. So while we're waiting for 'consensus'; what levels are you extremely well [Vitamin K2] informed individuals supplementing at (if at all)? And obviously what form(s)?

I'll start: Right now I am 'hedging my bets' and going with LEF Super K2
Vitamin K2 (as menaquinone-7) 100 mcg
Vitamin K2 (as menaquinone-4) 1000 mcg
Vitamin K1 1000 mcg

I take this around 5 times a week, trying to ensure I take it along with Vitamin D (sunshine or 5000IU D3), A, and E (both from food). However I certainly feel theres room for improvement dosage wise.

I'm not sure that's hedging your bets. What about Krillan's point re K1 and phase I detox? Also, I believe that commercially available mk-4 may be in the cis form, at least in part, whereas natural mk-4 is in the trans form. I don't know what difference that makes (it could even be better!), but I don't want to gamble on myself. I take 100 mcg of mk-7 every third day. That's in a form that is natural in a dosage that doesn't blow natural amounts out of the water. I think my approach is a little safer. That said, if you have some arterial calcification or bone loss already, a higher dose may be warranted.

Edited by Jay, 02 February 2010 - 06:38 PM.

[Blue]

OK so over a year after this thread was originally created, the picture is still far from crystal. So while we're waiting for 'consensus'; what levels are you extremely well [Vitamin K2] informed individuals supplementing at (if at all)? And obviously what form(s)?

I'll start: Right now I am 'hedging my bets' and going with LEF Super K2
Vitamin K2 (as menaquinone-7) 100 mcg
Vitamin K2 (as menaquinone-4) 1000 mcg
Vitamin K1 1000 mcg

I take this around 5 times a week, trying to ensure I take it along with Vitamin D (sunshine or 5000IU D3), A, and E (both from food). However I certainly feel theres room for improvement dosage wise.

I'm not sure that's hedging your bets. What about Krillan's point re K1 and phase I detox? Also, I believe that commercially available mk-4 may be in the cis form, at least in part, whereas natural mk-4 is in the trans form. I don't know what difference that makes (it could even be better!), but I don't want to gamble on myself. I take 100 mcg of mk-7 every third day. That's in a form that is natural in a dosage that doesn't blow natural amounts out of the water. I think my approach is a little safer. That said, if you have some arterial calcification or bone loss already, a higher dose may be warranted.

Is there a source regarding the cis and trans form statement?

The K1 and phase I studies were cell or animal studies. As noted there is a human, small, placebo controlled study which found an extraordinary decrease in cancer and other forms of severe disease using a very high dose of K1.

No one knows which is the best form or what the optimal dose is. Very little comparative research. There are various good points that can be made for all 3 forms as stated earlier in this thread. Personally I think the LEF combination (or the Vitacost clone) is acceptable until we know more.

Edited by Blue, 02 February 2010 - 07:25 PM.

[rwac]

Also, I believe that commercially available mk-4 may be in the cis form, at least in part, whereas natural mk-4 is in the trans form.

Well, the commercial mk4 is obtained from biofermentation.
So it's probably the same trans form.

I remember the same potential cis/trans issue when resveratrol came out...

[Jay]

Also, I believe that commercially available mk-4 may be in the cis form, at least in part, whereas natural mk-4 is in the trans form.

Well, the commercial mk4 is obtained from biofermentation.
So it's probably the same trans form.

I remember the same potential cis/trans issue when resveratrol came out...

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.

As noted there is a human, small, placebo controlled study which found an extraordinary decrease in cancer and other forms of severe disease using a very high dose of K1.

Blue, any chance you have that reference somewhere convenient?

Edited by Jay, 02 February 2010 - 09:56 PM.

[Blue]

Blue, any chance you have that reference somewhere convenient?

http://www.imminst.o...o...st&p=354898

See also look at the last pages for some comments on the different forms by various people. Regarding the phase I-II relation to K1 in rodents it is unclear if that is important regarding actual diseases even if you a rodent.

Edited by Blue, 02 February 2010 - 10:08 PM.

[Jay]

Blue, any chance you have that reference somewhere convenient?

http://www.imminst.o...o...st&p=354898

See also look at the last pages for some comments on the different forms by various people. Regarding the phase I-II relation to K1 in rodents it is unclear if that is important regarding actual diseases even if you a rodent.

Thanks. That's pretty interesting about K1 and cancer, though (as you alluded) the small sample size and short follow up period made the study underpowered to detect cancers.

As an aside, I noticed that the cohort in your K1 study was similar to Lappe's (see table 1) vit D cohort - vit D replete postmenausal women taking calcium. But, there were many more cancers in this group (note that the placebo group in this K1 study took vit D and calcium) than in Lappe's (vit D) group. Makes you wonder which cohort was off...I guess you could hedge yourself by taking both vit K and vit D (as most of us so).

Edited by Jay, 02 February 2010 - 11:07 PM.

[Blue]

Thanks. That's pretty interesting about K1 and cancer, though (as you alluded) the small sample size and short follow up period made the study underpowered to detect cancers.

As an aside, I noticed that the cohort in your K1 study was similar to Lappe's (see table 1) vit D cohort - vit D replete postmenausal women taking calcium. But, there were many more cancers in this group (note that the placebo group in this K1 study took vit D and calcium) than in Lappe's (vit D) group. Makes you wonder which cohort was off...I guess you could hedge yourself by taking both vit K and vit D (as most of us so).

That the cancer incidence was not identical for the vitamin D + calcium groups does not mean either study was flawed since participants from two different studies may vary in many ways.

That the large decrease in cancer and other severe diseases occurred in a group already given vitamin D and calcium is interesting. It is not impossible there could some synergism here between D and K so it is not sure that same effect would be seen in a K vitamin study not giving vitamin D to both the placebo and K vitamin group. See also:
http://www.imminst.o...o...st&p=355502