#4

I think it might be best to coincide at times, but not always

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#5

fascinated to see the results of this experiment. Over the years I’ve intermittently taken relatively high doses (1mg) but without testing.

#6

Did you find a single night’s sleep disruption or any other anecdotal consequences?

#7

no sleep disruption, only anecdote is that it does seem to effect teeth - they feel smoother
My 1mg dose is equivalent to about 100g of natto. And many Japanese eat 2 x 50g pack daily for breakfast so it felt like a reasonable dose.
Something of interest to me is whether eating natto or other probiotic foods increases endogenous vit k2 production.

4 Likes
#8

I have the same feeling in teeth!

And the sleep disruption even with 200 ug.

I’d love to see studies looking at natto consumption in Japan vs different health outcomes.

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#9

Dietary intake of beans and risk of disabling dementia: The Circulatory Risk in Communities Study (CIRCS) 2022

The group with increased natto intake were inversely associated with risk of disabling dementia (P for trend = 0.003), but tofu intake was not (P for trend = 0.19).

Soy product intake and risk of incident disabling dementia: the JPHC Disabling Dementia Study 2022

By individual soy products, natto intake was marginally inversely associated with disabling dementia in women (trend P = 0.050). When we stratified by age, this inverse association was clearer in women aged under 60 years (multivariate HR for the highest versus lowest quintile was 0.78, 95% CI 0.59–1.04, trend P = 0.020 for those aged under 60 years and 0.90, 95% CI 0.77–1.05, trend P = 0.23 for those aged 60 years and older, respectively).

See also this paper published this month: The role of vitamin K2 in cognitive impairment: linking vascular health to brain health 2025

And looking at MK-4 but not MK-7:

Association of vitamin K with cognitive decline and neuropathology in community‐dwelling older persons 2022

Menaquinone‐4 (MK4) was the main vitamin K form in the brain regions evaluated. Higher brain MK4 concentrations were associated with a 17% to 20% lower odds of dementia or mild cognitive impairment (MCI) (P‐value < .014), with a 14% to 16% lower odds of Braak stage ≥IV (P‐value < 0.045), with lower Alzheimer’s disease global pathology scores and fewer neuronal neurofibrillary tangles (P‐value < 0.012).

#10

I think MK4 is also useful, but has different benefits. I don’t know about the ones that are not available as supplements and am not aware of much research on MK9. The broadest range is in hard cheeses.

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#11

It does this in bacteria not mammals. I have never seen any evidence of vitamin K playing a direct role in electron transport in mammals and would be very surprised if it did.

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#12

I accept its primary function is in bacteria where it is a key part of the ETC. However, I did read this:

https://www.science.org/doi/10.1126/science.1218632

Vitamin K2 Is a Mitochondrial Electron Carrier That Rescues Pink1 Deficiency

Now that is in Drosphila

Abstract: Pink1 is a mitochondrial kinase, and loss of Pink1 function in flies and mice results in the accumulation of inefficient mitochondria. In a screen for modifiers of the Parkinson-associated gene, pink1 , Vos et al. (p. 1306, published online 10 May; see the Perspective by Bhalerao and Clandinin ) identified the fruit fly homolog of UBIAD1, “Heix.” UBIAD1 was localized in mitochondria and was able to convert vitamin K1 into vitamin K2/menaquinone (MK-n, n the number of prenylgroups). In bacteria, vitamin K2/MK-n acts as an electron carrier in the membrane and, similarly, in Drosophila , mitochondrial vitamin K2 appeared to act as an electron carrier to facilitate adenosine triphosphate production. Fruit flies that lack heix showed severe mitochondrial defects that could be rescued by administering vitamin K2.

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#13

There have been negative results in other research in human cells

I think what appears to be clear is that Mk-7 is more capable of getting into mitochondria than Coq10.

I think it is worth experimenting with and it does give some signs of improving cellular processes in some way.

Chat GPT says: " Some research suggests vitamin K2 might act as an alternative electron carrier under certain conditions, such as in mitochondrial dysfunction or CoQ10 deficiency."

But I have not managed as yet to find which research this refers to.

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#14

Synergia research group has identified Menaquinone-7’s pivotal role in mitochondrial ATP generation by acting as a mitochondrial electron transport carrier, thus participating in the energy cycle of the cell. In human cell experiments, it has been shown that the cells’ maximum capacity to generate energy, defined as the reserve energy, increases by 30–40% with Menaquinone-7, thus, identifying the role of Menaquinone-7 in redox cycle by transporting electrons in electron transport chain and also mitochondrial generation of ATP (Figure 3). This dual role of Menaquinone-7 is especially important to the aging geriatric population and athletes in their need of a greater oxygen supply for the oxidative phosphorylation.

In another in vitro study, Menaquinone-7 rescued mitochondrial defects in numerous conditions that affect mitochondrial function. Menaquinone-7 was also effective at improving systemic locomotion defects in fully developed adult pink1 and parkin mutant flies. Menaquinone-7 did not affect mitochondrial remodeling directly, but by increasing Electron Transfer Chain efficiency, it contributed to the proton motif force that facilitates ATP production. Menaquinone-7 may thus constitute a promising compound to treat mitochondrial pathology, also in Parkinson’s disease (PD) patients suffering from Pink1 or Parkin deficiency [29]. A clinical study has been proposed to investigate the potential effects of Menaquinone-7 in genetically determined PD with mitochondrial dysfunction [30].

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#15

One of the studies referred to indicates that K2 MK-7 really does result in boosted ATP in humans: 12 % increased maximal output with a huge supplementation. For weeks 1 to 4, participants received 300 mg/d; for weeks 5 to 8, they received 150 mg/d… Is this practically doable…?

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#16

I think the response is dose dependent. The most i have taken is a single dose of 12ml/8mg That has some effects

Later edit:
Warning the paper reported to use 150 and 300 milligrams of mk7 was on fact using micrograms

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#17

150mg a day!? Wow. And here I’ve been debating bewteen 90, 100, 120mcg a day, lol. I guess this is a completely different ball game…

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#18

Yes, but that’s mostly irrelevant if it doesn’t act as an electron carrier once in the mitochondria. The study you linked to does not support your theory. In that study they state that vitamin K2 did not restore electron flow or ATP synthesis even though it entered the mitochondria.

You can’t trust ChatGPT. This statement likely refers to the potential role of vitamin K in bacteria and other lower organisms, not mammals.

That’s an interesting study. Unfortunately it’s nowhere to be found on PubMed so probably not peer reviewed. Also the concentration of MK7 they used was 10 µM which would be hard to reach even with high supplemental doses.

Now we’re talking! Very interesting. Unfortunately it’s hard to tell by the abstract how much vitamin K2 they were given. The abstract mentions 150 and 300 mg but that may be the amount of some formulation containing some percentage of vitamin K2. If it’s the K2 amount that’s a super high dose. Does anyone have access to the full text?

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#19

Sadly I don’t have access to the paper. However, in the round there appears to be some evidence that higher MK7 levels do improve eukaryotic mitochondrial efficiency. I would not say it is 100% or that the dosing or other strategy is clear.

This to me is an ideal situation for biohacking. In the end I have learnt a lot myself by trying out various substances at various stages. This is on my list of interesting molecules that I will continue experimenting with.

It would be helpful if other people could experiment with it as we may find it has a pattern of results that is useful. However, people do need to do testing.

a) It does seem to be safe
b) If it increases the ΔΨM (MMP - Mitochondrial Membrane Potential) then that is a useful tool. Even if only temporarily. This would, however, require a reasonably high concentration in the body to ensure that enough is in the mitochondria to help.

#20

I wonder if they had this wrong. it is possible that a really high dose is needed, but it is hard to find any pills more than 0.6mg. I am using a liquid form and a single bottle has around 32-35mg in it. Hence they would be either taking 500 pills or drinking 10 bottles of K2.

That’s for the 300mg version of the experiment, of course. To be honest I think if anyone is doing experimentation they should probably not go that high without first testing out much lower levels.

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#21

It would be if we had some simple way to measure mitophagy or MMP or ATP production, but we don’t. So if vitamin K2 were to increase or decrease ATP production in some tissues by a modest amount you most likely would have no clue it just did so. The best we could do is probably using some very indirect markers, like in the above study where maximum cardiac output was increased. Of course that’s a problematic marke because various other things could change cardiac output.

#22

You are right that there is a question about how to measure things. I look at issues like how quickly my digestion system is operating (I keep records), what my RHR is, what my HRV is.

Interestingly there is a question as to whether a high MK7 level reduces PSA or ApoB. (which is where this topic started).

To some extent with interventions we need first to try them and measure any changes and then continue taking out the intervention and putting it back in and monitoring whether the same change occurs.

Directly measuring membrane potential, however, is hard.

However, for example, I got an unusually low Sodium serum level last week. My supplementation is consistent. Is that because the kidney cells had more mitochondrial energy. I don’t know. However, I will continue tracking this to see if there is a correlation.

Happily this sort of tracking can be done whilst doing other things.

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#23

I was rummaging around to find a copy of the article about cardiac output. I did find this which references it, but actually clarifies that the dose was in micrograms rather than milligrams.

Human Studies
Vitamin K2 (MK-7), and other menaquinones, have been investigated in multiple human clinical
studies. In an article on the safety of Vitamin K2 (MK-7), the available evidence on the safety of Vitamin
K2 (MK-7) as dietary supplement ingredient was reviewed (Marles et al., 2017). In this review,
published clinical trials that made no mention of whether adverse events occurred or of any other
aspects of safety were excluded. The following section provides an overview of relevant human
studies where safety was considered.
In a double-blind, randomized, placebo-controlled trial with study in 55 healthy pre-pubertal children,
van Summeren et al. (2009) investigated the effects of 45 mcg of Vitamin K2 (MK-7)/day for eight
weeks on different biomarkers and coagulation-related parameters, including serum levels of MK-7
(van Summeren et al., 2009). The details of study participants were as follows: placebo group
consisted of 27 male children- age 6-10 years, average height 133.8 cm, weight 30.4 kg, and BMI 16.8;
the MK-7 receiving group consisted of 28 male children- age 6-10 years, average height 132.2 cm,
weight 29.2 kg, and BMI 16.6. Bone markers and coagulation parameters remained constant over time
in both the placebo and treatment group. The results of this study suggest that oral administration of
45 mcg MK-7/day to healthy, pre-pubertal children for eight weeks increased serum levels of MK-7
and osteocalcin carboxylation without affecting blood coagulation. Periodically the subjects were
checked for the occurrence of adverse events of treatment and none were reported.
In a randomized controlled trial, McFarlin et al. (2017) investigated the effects of dietary
supplementation of Vitamin K2 (MK-7) on cardiovascular responses to a graded cycle ergometer test.
In this study, aerobically trained young (average age 21 years) males and female athletes (n=26) were
randomly assigned either to a control group that received a rice flour placebo or to an intervention
group that received MK-7. For weeks 1 to 4, participants received 320 mcg MK-7/day; for weeks 5 to
8, they received 160 mcg MK-7/day. MK-7 supplementation was associated with a 12% increase in
maximal cardiac output, with a trend toward an increase in heart-rate AUC. No significant changes
occurred in stroke volume. As regards safety, the investigators stated, “At no time during the study
did any participant report an adverse effect to taking either the supplement or the placebo.” (McFarlin
et al., 2017).
Moller et al. (2016) compared the biological effects of placebo, fermentation-derived Vitamin K2 (MK7) (90 mcg) and 3 doses of synthetic MK-7 (45, 90 and 180 mcg) in a randomized double-blinded
parallel study. In this study, healthy adult subjects (n=43; 20-60 years of age) took one of the
supplements daily for 43 days, and the fraction of carboxylated osteocalcin (OC) was compared
between day 1 and day 43 as a marker for Vitamin K activity. The serum concentrations of carboxylated
OC (cOC) and unOC were increased and reduced, respectively, after daily intake of 180 mcg of
synthetic MK-7 for 43 days, indicating increased Vitamin K activity. In this study, 27 subjects reported
a total of 40 adverse events; 32 of these were judged unlikely to be related to the study supplement.
In two cases, the adverse events were judged possibly to be related to the study supplement: dry
mouth from day 4 to the end of the study (180 mcg synthetic MK-7 group) and diarrhea (fermentationderived MK-7 group). Another case of diarrhea in the fermentation-derived MK-7 group was judged
probably to be due to the study supplement. The investigators concluded that the findings provide
evidence that the tested synthetic form of MK-7 is bioequivalent to fermentation-derived MK-7,
exhibits vitamin K activity and is well tolerated in healthy subjects (Moller et al., 2016).
In a double-blind, placebo-controlled trial, Knapen et al. (2015a) investigated effects of 180 mcg MK7/day supplementation on arterial stiffness. In this study, healthy postmenopausal women (n=244)
received either placebo (n=124) or MK-7 (n=120) for three years. At baseline, desphosphouncarboxylated matrix Gla-protein (dp-ucMGP) was associated with intima-media thickness (IMT),
Diameter, carotid-femoral Pulse Wave Velocity (cfPWV) and with the mean z-scores of acute phase
markers (APMscore) and of markers for endothelial dysfunction (EDFscore). After three years of MK7 supplementation, cfPWV and the Stiffness Index-β significantly decreased in the total group,
whereas distension, compliance, distensibility, Young’s Modulus, and the local carotid PWV (cPWV)
improved in women having a baseline Stiffness Index β above the median of 10.8. MK-7 decreased dpucMGP by 50% compared to placebo, but did not influence the markers for acute phase and
endothelial dysfunction. The investigators concluded that long-term use of MK-7 supplements
improves arterial stiffness in healthy postmenopausal women, especially in women having a high
arterial stiffness. The investigators stated that no side-effects have been reported for the long-term
use of MK-7 (Knapen et al., 2015a).
In another study, Knapen et al. (2015b) investigated the effects of a Vitamin K2 (MK-7)-fortified yogurt
drink (28 mcg MK-7/yogurt drink) on Vitamin K status and markers of vascular health. The yogurt drink
was also fortified with n-3 PUFA, Vitamin D, Vitamin C, Ca and Magnesium to support vascular and/or
general health. In this study, 32 healthy men and 28 postmenopausal women with a mean age of 56
± 5 years received either basic or fortified yogurt drink twice per day for 12 weeks. MK-7 was efficiently
absorbed from the fortified yogurt drink. Levels of circulating MK-7 were significantly increased from
0.28 to 1.94 ng/ml. Accordingly, intake of the fortified yogurt drink improved Vitamin K status, as
measured by significant decreases in uncarboxylated osteocalcin and dp-ucMGP. No effects were seen
on markers of inflammation, endothelial dysfunction and lipid metabolism. No adverse effects were
reported (Knapen et al., 2015b).
In a three year study, Knapen et al. (2013) investigated the effects of low-dose Vitamin K2 (MK-7) on
bone health. In this study, healthy postmenopausal women (n=244) received placebo or MK-7 (180
mcg/day) capsules for three years. In addition to bone mineral density (BMD) and bone mineral
content (BMC), circulating ucOC and cOC were measured (the ucOC/cOC ratio served as marker of
Vitamin K status) at baseline and after 1, 2, and 3 years of treatment. MK-7 intake significantly
improved Vitamin K status and decreased the age-related decline in BMC and BMD at the lumbar spine
and femoral neck, but not at the total hip. Bone strength was also favourably affected by MK-7. MK-7
significantly decreased the loss in vertebral height of the lower thoracic region at the mid-site of the
vertebrae. At the end of the study, twelve women in the placebo group and nine women in the MK-7
group had withdrawn from the study. The overall drop-out rate was 8.6%. Few complaints were
reported during the study. The complaints in the placebo group were: hair loss and/or brittle nails
(n=2), hot flashes (n=1), knee pain (n=1), numb sensation in arms and legs, washed-out (n=1), and
weight gain (n=2); and in the MK-7 group: bone pain (n=1), hot flashes (n=1), rash around eyes and
ears (n=1), smelly capsules (n=1), and weight gain (n=1). Five women withdrew due to these
complaints; four women in the placebo group and one in the MK-7 group. Compliance was measured
by capsule counts at the end of every half-year period; the mean compliance for both treatment
groups was 97%. The results of this study suggest that MK-7 is well tolerated (Knapen et al., 2013).
In a randomized, double-blind, placebo-controlled trial, Dalmeijer et al. (2012) investigated the effects
of Vitamin K2 (MK-7) supplementation on carboxylation of matrix Gla-protein (MGP). In this study, 60
subjects (age 40-65 years) received supplementation of 180, 360 mcg/day of MK-7 or placebo for 12
weeks. At the end of 12 weeks, a significant and dose-dependent decrease in desphosphouncarboxylated MGP (Dp-ucMGP) was noted groups treated with 180 μg and 360 μg MK-7 (31% and
46%, respectively), while dp-ucMGP levels remained unchanged after placebo treatment. The
osteocalcin ratio also decreased significantly after 12-week supplementation with 180 mcg (60%) and
360 mcg (74%) MK-7, while levels remained unchanged after placebo treatment. These results indicate
improved vitamin K levels and good compliance to the study treatment. Changes over time of dp-
cMGP and t-ucMGP levels did not differ between treatment arms. Other cardiovascular risk factors
did not differ between treatments arms. No adverse effects were reported (Dalmeijer et al., 2012).
Theuwissen et al. (2013) carried out a dose-escalation study to measure the antidotal potency of lower
doses (10, 20 and 45 mcg/day) of Vitamin K2 (MK-7) supplements in healthy volunteers stabilized on
acenocoumarol, a VKA therapy. In addition to conventional INR measurements, response on thrombin
generation and the γ-carboxylation status of specific Gla-proteins with coagulation and
noncoagulation functions were monitored. In this study, 18 healthy men and women (age 18-45 years)
were anticoagulated for four weeks with acenocoumarol; of these 15 subjects attained a target INR of
2.0. In the six successive weeks, subjects were supplemented with increasing doses of MK-7 (10, 20,
45 mcg/day) while continuing acenocoumarol treatment at established individual doses. Apart from
the INR, acenocoumarol treatment significantly increased under-carboxylated forms of prothrombin
(ucFII), osteocalcin (ucOC) and matrix Gla-protein (dp-ucMGP), and decreased endogenous thrombin
generation (ETP). A daily intake of 45 mcg MK-7 significantly decreased the group mean values of both
the INR and ucFII by about 40%. Daily intakes of 10 and 20 mcg MK-7 were independently judged by
two hematologists to cause a clinically relevant lowering of the INR in at least 40% and 60% of subjects
respectively, and to significantly increase ETP by ~20 and ~30%, respectively. Circulating ucOC and dpucMGP were not affected by MK-7 intake. The investigators concluded that MK-7 supplementation at
doses as low as 10 mcg (lower than commonly recommended dose of 45 mcg) significantly influenced
anticoagulation sensitivity in some individuals. Hence, the investigators recommended avoiding use
of MK-7 supplements in patients on VKA therapy (Theuwissen et al., 2013).
Theuwissen et al. (2012) investigated the dose-response effects of extra intake of Vitamin K2 (MK-7)
on the carboxylation of extra-hepatic vitamin K-dependent proteins in a double-blind, randomized,
controlled trial. In this study, a total of 42 healthy adult men and women (age 18 to 45 years) were
randomized into seven groups to receive: placebo capsules or MK-7 capsules at a dose of 10, 20, 45,
90, 180 or 360 mcg/day for 3 months. Circulating ucOC, OC and desphospho-uncarboxylated MGP
(ucMGP) were measured. As the study was conducted with few participants, in order to increase the
statistical power, the researchers collapsed the treatment groups into three dosage groups: placebo,
low-dose supplementation (doses below RDA), and high-dose supplementation (doses around RDA).
The results of this study showed that MK-7 supplementation at relatively low doses in the order of the
RDA increased the carboxylation of circulating OC and MGP. No adverse effects on thrombin
generation (blood clotting) were observed (Theuwissen et al., 2012).
In a double-blind, randomized, placebo-controlled trial, Emaus et al. (2010) investigated the effects of
Vitamin K2 (MK-7) supplementation on bone mineral density in healthy postmenopausal Norwegian
women. In this study, 344 healthy women (ages- 50 to 60 years, 1-5 years after menopause) were
recruited and randomly assigned into two groups, one receiving 360 mcg MK-7 in the form of Nattoderived MK-7 capsules (treatment group- age: 54.7±2.5; weight: 67.5±9.0) and the other with placebo
(age: 54.2±2.5 weight: 67.5±9.8) capsules containing olive oil. The subjects were treated daily for 12
months. In the treatment and placebo group, 131 and 133 subjects completed the study, respectively.
At baseline and 12 months after supplementation, BMD was measured at total hip, femoral neck,
lumbar spine and total body together with serum levels of bone-specific alkaline phosphatase,
Crosslaps, total osteocalcin, cOC and ucOC. No statistical differences in bone loss rates between the
groups at the total hip or any other measurement site were noted at the end of 12 months. Serum
levels of cOC increased and ucOC decreased in the treatment versus the placebo group. No treatment
related significant adverse effects of MK-7 were noted. The results of this study suggest that daily
ingestion of 360 mcg MK-7/day for one year is safe (Emaus et al., 2012)

None of the above have over 0.5mg per day. There is a table I cannot copy which included 2mg once.

Additional Human Studies
Novozymes A/S have conducted additional human clinical trials with Vitamin K2 (MK-7) in subjects at
nutritional risk and/or specific medical conditions.
Study 1
A preliminary open labeled observational study conducted showed that daily oral dose of 100 mcg of
Vitamin K2 (MK-7) for 3 months was associated with a reduction in the frequency, intensity, and
duration of idiopathic muscle cramps (Mehta et al, 2010). This study was conducted on 21 patients
aged 18 to 81 of both sexes. Administration of Vitamin K2 (MK-7) was found to be well tolerated and
there were no reports of adverse events.
Study 2
A study was conducted on 30 patients to evaluate the effects and tolerability of administration of
Vitamin K2 (MK-7) for two months in patients with Peripheral Neuropathy (PN) due to vitamin B12
deficiency and/or diabetes mellitus (Kulkarni et al., 2013). Vitamin K2 capsules of 100 mcg each were
given to these 30 patients twice a day for two months. Administration of Vitamin K2 (MK-7) was found
to be well tolerated and there were no adverse events were reported during the period of therapy.
Study 3
An open labeled study of Vitamin K2 (MK-7) was conducted in 100 patients with Peripheral
Neuropathy (PN) suffering from either Vitamin B12 deficiency and/or diabetes mellitus (Mehta et al.,
2018). Subjects were administered 200 mcg of Vitamin K2 orally for 8 weeks and the patients were
followed for an additional 4 weeks. Administration of Vitamin K2 (MK-7) was found to be well
tolerated and there were no adverse events were reported during the period of therapy.
Study 4
A double-blind, placebo-controlled trial was conducted in 60 patients presenting with Peripheral
Neuropathy (PN) suffering from either vitamin B12 deficiency and/or diabetes mellitus (Vladimir et al,
2021). The subjects were administered either 200 mcg of Vitamin K2 (MK-7) or placebo control for 8
weeks, and then followed for an additional 4 weeks. Administration of Vitamin K2 (MK-7) was found
to be well tolerated and there were no adverse events were reported during the period of therapy.
Study 6
A double-blind, placebo-controlled was conducted in patients with Peripheral Neuropathy (PN)
suffering from either Vitamin B12 deficiency and/or diabetes mellitus with diabetes mellitus (Mehta
et al., 2021). In this study, 20 patients were administered either 200 mcg of Vitamin K2 (MK-7) capsules
or a placebo control orally for 8 weeks and the patients were followed up to 12 weeks. Circulating
levels of Vitamin K2 were also measured in this study, and results showed that administration of
Vitamin K2 resulted in increased circulating levels of Vitamin K2 by the 4th and 8th week.
Study 7
In an Observational study (case series) in 17 Multiple Myeloma patients (age; 18-65 years) having
drug-induced (caused by chemotherapy) Peripheral Neuropathy, showed significant relief in the
symptoms of peripheral neuropathy after daily administration of Vitamin K2-7 capsules (Bhave et al,
2019).
Recently published Human Studies
In a Randomized Controlled Trial by Nahid (Karamzad et al 2020), it was shown that Vitamin K2-7
supplementation seems to be effective in the improvement of glycemic indices, but not the lipid
profile of patients with type 2 diabetes mellitus. In another study by Nahid Karamzad et al (2022), it
was observed that Vitamin K2-7 supplementation can be effective in improving PIVKAII levels, of
patients with type 2 diabetes mellitus. Habitual natto (particularly rich in Vitamin K2-7) intake is
associated with a reduced risk of osteoporotic fractures independent of confounding factors, including
bone mineral density, in Japanese postmenopausal women (Kojima A et al 2020). In a one year
followup randomized trial, oral administration of vitamin K2-7 in patients on haemodialysis patients
reduced serum uc-MGP levels (Oikonomaki T et al 2019). MGP (Matrix Gla Proteins) are one of the
most potent inhibitors of vascular calcification. In a randomized controlled trial on pediatric patients
on regular hemodialysis, it was observed that Vitamin K2-7 and native vitamin D showed a beneficial
effect on calcification regulators (Radwa B, 2022). In a randomized controlled trial (Rahimi Sakak F et
al 2020) in individuals with type 2 diabetes, daily intake of Vitamin K2-7 360 mcg for 12-weeks reduces
fasting plasma glucose (p-adjusted = 0.031) and glycated hemoglobin (p-adjusted = 0.004). in a 3-year
randomized, placebo-controlled clinical trial in postmenopausal women with osteopenia, treatment
of Vitamin K2-7 375 mcg daily as an add-on to calcium and vitamin D increased carboxylation of
osteocalcin. Vitamin K2-7 acts as a cofactor in the carboxylation of osteocalcin (OC) and carboxylated
OC promotes mineralization of bone (Rønn SH et al, 2020). In another randomized placebo-controlled
trial by Rønn SH et al (2021), in postmenopausal women who received Vitamin K2-7 375 mcg daily or
placebo, as an add-on to calcium and vitamin D for 12 months decreased uncarboxylated osteocalcin
and increased p-adiponectin but there was no change in insulin sensitivity. In a prospective cohort
study in children with acute lymphoblastic leukemia, an early beneficial effect of the combination of
Vitamin K2-7 and vitamin D3 on BMD in all patients especially during the period of intensive steroid

In summary, Vitamin K2 (MK-7) has been extensively investigated in over 25 clinical trials, with over
2000 participants. Several of these trials were double-blind, placebo-controlled that are the most
likely to capture any adverse effects in order to support the safety of MK-7 in a diverse population.
Human clinical studies in which MK-7 was administered up to 180 mcg/day for 3 years, or up to 360
mcg/day for 12 weeks, or up to 1080 mcg thrice weekly for 8 weeks did not reveal any significant
adverse effects compared with placebo. Adverse effects specifically attributed to MK-7 were limited
to gastrointestinal upset associated with the product’s smell. The available information from multiple
clinical trials suggest that MK-7 is unlikely to cause any adverse effects in human subjects.

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