#1

@adssx and I have been experimenting with Menaquinone-7 more recently. I am perhaps more enthused than he is.

Menaquinone-7 is one of the types of Vitamin K2. These range from MK4 to MK13, but MK7 is one of the three types that can be bought as supplements (the other two are MK4 and MK9).

What I find interesting about MK7 is that it can assist the electron transport chain and make mitochondria more efficient (I assume increasing the mitochondrial membrane potential).

In producing more ATP, however, it tends to disrupt sleep when the level of MK7 in the body is going up.

I think that is because the body takes a while to adjust to the greater efficiency of mitochondria. It has a longer half life than Rapamycin being 75 hours. It compares in some ways to Methylene Blue, but MB has a short half life. (5-6.5 hours).

I have myself taken to taking intermittent relatively high doses. Today I got my blood test results following a large dose (2mg) that I took just over a week ago.

What I found interesting was that ApoB was down lower than it has been for a while for me (78) and also PSA went really quite low down (0.78).

I think the PSA is clearly affected by mitochondrial efficiency. I would not be surprised if ApoB was also affected.

I had another blood test today and will get the results during the week. On Friday I took 12ml/8mg of MK7 (which was a quarter of the bottle).

If anyone else is interested in trying higher doses of MK7 and doing blood work whilst it is active (a few days after the dose) this might be an interesting experiment.

It is a prop that supports the mitochondria rather than an intervention that improves the efficiency of the mitochondria, but I think it could be useful in conjunction with mTOR inhibitors as then proteins are properly created to operate mitophagy in an efficient manner.

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I am becoming more bullish on Vitamin D replacement
#2

@John_Hemming Would you separate uses of Mk-7 and MB from doses of rapa? They sound opposing so perhaps MK-7 and MB are good for recovering from a period of autophagy (meaning kick starting a growth cycle)? Thoughts?

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#3
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#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.

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#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 ”M 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 ΔιM (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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