Its complicated because the number of isoprene residues has a material effect.
Using MK4 here.
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MK4 is thought to be too hydrophilic to operate in the ETC.
“Using MK4 here.”
“Using”? How? K2 MK-4 dietary sources in quantity are almost exclusively animal, not vegetable. Were the mice fed mk-4? We know it’s not gut bacteria derived. It can be synthesized in the body - I was assuming that’s what was happening in the mice, they were measuring mk-4 in the brains that was synthesized from dietary K1.
In any case it would make no sense to recommend:
“Researchers stress the importance of a healthy diet rich in leafy greens rather than relying on supplements to support brain health during aging.”
Leafy greens have very little mk-4, so that would be an odd recommendation, if the idea was to get mk-4 from dietary sources. I assumed that they were recommending leafy greens for the K1 content, which then is converted to mk-4.
Also, I don’t understand this recommendation - the part where they urge against supplementing with VK. If it is indeed the VK that’s the active agent, what harm is there in supplementing with it? Is there any research showing K1 or K2, including mk-4 not being absorbed from supplements? Sounds like garbage generic advice - they should stick to the evidence and nothing more.
"Both Booth and Zheng emphasize that their research doesn’t mean that people should rush out and start taking vitamin K supplements.
“People need to eat a healthy diet,” says Booth. “They need to eat their vegetables.”"
What is this sh|t? Vegetables may have all sorts of good effects, but this study is strictly about VK, and not vegetables. If you want to promote vegetables, do a study on those. This is about one component, and no evidence was given why VK supplements are inferior.
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I don’t have access to the whole paper unfortunately: Low Vitamin K Intake Impairs Cognition, Neurogenesis, and Elevates Neuroinflammation in C57BL/6 Mice 2025
Tufts University, Boston, so not too bad an institution.
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I have not measured any benefit in this area. I measure my HRV every morning for 5 years now. About 3 years ago I started both MK-7 and Nattokinase. I have not seen any change in my HRV or RHR that I could attribute to those 2 supplements.
I have seen significant benefit in other areas from the Nattokinase though. The effect is very noticeable and repeatable if I stop and start Nattokinase.
How much MK7 do you take? In which form?
We take 1 of these per day. Maybe our dose is too low??
Naka Platinum K2 (MK-7 form)100 mcg SUPER BONUS Size 330 Veggie Caps (300+30 FREE) Bioactive Form of Vitamin K2
And for Nattokinase - we take 2gm per day = 10,000FU’s
Belle Chemical - Pure Organic Nattokinase Powder – Non-GMO, Gluten Free, Vegan (454 grams)
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I am experimenting with high doses. The highest so far is 50mg (which was a bottle and a half of mk7 in olive oil). I think it has dose dependent effects up to quite high levels. What I am doing, however, is taking a high dose on a single day and then stopping and tracking what happens as it goes back down. The half life is quite long (I think about 75 hours) that means that a single dose of x is equivalent at peak to a continuous dose of over x/5.
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I’m taking 10x more MK7 (so 1,000 µg = 1 mg), in oil form.
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How did you settle on the dose? I ask, because I see recommendations all over the place, depending on what the aim is, bone health, CV, brain whatnot.
I take one of those Life extension Super K pills. It’s a mix of 2mg K1, 1mg K2 MK-4, 180mcg K2 MK-7 in extra virgin olive oil stabilized with 10mg vit C.
My thought was that if there is some persistence or accumulation of vitamin K on account of being fat soluble, then if you supplement long term, it matters less if you take in 200mcg or 500mcg daily in a long perspective. But maybe that’s wrong.
I feel better with 1 mg 
Might be placebo, I don’t know, but the higher the better and whenever I lower it I feel worse.
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I think the key distinction is whether or not there are at least 7 isoprene residues. This enables the molecule to be hydrophobic and sit in the mitochondrial membrane accepting electrons.
AIUI this makes the mitochondria more efficient. Obviously the more MK-7 molecules there are then the more it adds to efficiency.
It has a long half life (75 hours). Hence if you take 200 μg the steady state concentration is equivalent to the peak of a dose of 1mg and 500μg is 2.5mg.
The rat experiments had a NOAEL at about 5% of the diet. However, I am not inclined to go too high not least it starts getting quite expensive.
Would for me be 170g per day.
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Hi! How do you take the natto. Do you put it in capsules? I am thinking about that risk that the acidic environment in the stomach degrades it.
this is what AI told me:
"the acidic environment in the stomach can degrade nattokinase to some extent. Nattokinase is a serine protease enzyme, and like many proteins, it is susceptible to denaturation and breakdown in highly acidic conditions, such as those found in the stomach (pH 1.5–3.5). The low pH can disrupt the enzyme’s structure, potentially reducing its activity by the time it reaches the intestines, where it is typically absorbed and exerts its fibrinolytic (clot-dissolving) effects.
However, the degree of degradation depends on factors like the formulation of the nattokinase supplement. For example, enteric-coated capsules or other protective delivery methods can shield nattokinase from stomach acid, allowing it to pass into the small intestine relatively intact. Studies suggest that unprotected nattokinase may lose significant activity in the stomach, but precise data on its stability varies. Research on similar enzymes indicates that while some activity may survive gastric conditions, protective measures improve its bioavailability."
I cam across this podcast with Patrick Theut, note he does sell his own vitamin K, yet he also links to a lot of studies and information on MK7. I learned a lot from this interview.
There’s a fair bit of Vitamin K information here, also what are people thoughts on this product?
I asked some questions of chatGPT about MK7 and mTOR and Serum Glucose, I am not of the view that the answers are that much good, but if someone wants to read up on mk7 the answer is worth reading.
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VK2 was administered to HFD-fed C57BL/6 mice for 16 weeks.
For the randomized controlled trial (RCT), a total of 102 T2DM patients aged 50–80 years were recruited and randomly assigned to receive yogurt (one cup per day) with or without VK2 fortification (90 μg/day) for 6 months.
VK2 significantly improved grip strength (p < 0.01) and exercise capacity (all p < 0.05) in HFD-fed mice. At the tissue level, VK2 increased skeletal muscle mass (p < 0.05) and cross-sectional area of muscle fibres (p < 0.05), while reducing the proportion of fast-twitch fibres (p < 0.01). VK2 treatment decreased body fat rate (p < 0.01) accompanied by enhanced whole-body energy metabolism. VK2 also diminished the glucolipid metabolism parameters, including glucose (p < 0.01), HOMA-IR (p < 0.01) and serum lipid levels. Regarding the mechanism, VK2 promoted the phosphorylation of proteins in the FAK-AKT–mTOR-P70S6K pathway by targeting Ccn2, thereby enhancing protein synthesis of C2C12 myotubes. In the RCT study, VK2 supplementation significantly increased grip strength (ptreatment × time = 0.017), SM (ptreatment × time = 0.001), SMI (ptreatment × time < 0.001) and decreased HbA1c (ptreatment × time < 0.001), FBG (ptreatment × time = 0.056), FINS (ptreatment × time < 0.001), and HOMA-IR (ptreatment × time < 0.001) in T2DM subjects.
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In mice, but interesting:
Vitamin K2 (VK2) shows promise as a nutritional intervention for obesity-related disorders, but its mechanisms of action in obesity and associated phenotypes are not yet fully understood. This study aims to elucidate the rescue effects of VK2 on multiple tissues during obesity. Twenty-eight 8-week-old male C57BL6/N mice are divided into four groups and fed a high-fat diet or normal diet for 16 weeks, receiving either menaquinone-7 (MK-7) or soybean oil solvent via gavage. RNA sequencing of brain, colon, muscle, heart, kidney, and liver tissues constructed a multi-organ transcriptional profile. The “rescue differentially expressed genes (DEGs)” are identified and tissue–tissue communication is analyzed. VK2 improves the biochemical profile in high-fat diet-induced obesity. Following VK2 intervention, the brain and kidneys exhibit more changes in autophagy, neurodegenerative diseases, energy metabolism, and immune response pathways. VK2 rescues over 10% of abnormally expressed genes, with most being fully restored. These rescue genes exhibit tissue-specific biological effects, including neuropeptide signaling and neuron ensheathment in the brain; triglyceride metabolism and carboxylic acid catabolism in the colon; microvillus organization and vascular permeability regulation in the heart; regulation of immune processes and collagen biosynthesis in the kidney; transforming growth factor-beta receptor signaling, iron transport and homeostasis in the liver; and muscle contraction, ATP transport, and filament sliding in the muscle. VK2 eliminates elevated ligand–receptor signals in immune response pathways and promotes the tissue–tissue signaling network to approach healthy control levels. VK2 significantly rescues the multi-organ transcriptome and restores tissue-specific pathways in high-fat diet-induced obese mice, providing the molecular mechanisms countering metabolic disorders.
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Without reading the paper I cannot say, but this could be related to splicing changes. It is quite likely to be linked in some way to acetylation.