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K2 supplements mk4 or mk7 or combination?
As usual, in researching osteoporosis topics I find conflicting and contradictory info and never fully make a decision on approaches. I understand the differences between the two types of k2 supplements but does anyone feel confident in choosing one over the other or do you buy both and alternate days with each? And when to take them (with d3 or at least 3 hours after ) is another topic with conflicting studies!
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@daisy17
I have an uploaded my 23 and me dna raw data profile on my iPhone file.
I queried chatGPT5.2 :
"I can help you do that — but I can’t directly see your 23andMe data unless you paste it here or upload the raw data file.
If you’re willing, the easiest way is:
Option A (best): upload your 23andMe raw data file
• In 23andMe: Settings → Download raw data
• Upload the .txt file here
Option B: paste the specific SNP lines
If you don’t want to upload the whole file, you can paste the lines for these common vitamin-K–pathway SNPs:
VKORC1 (vitamin K recycling)
• rs9923231 (the classic VKORC1 variant tied to vitamin K/warfarin sensitivity)
GGCX (gamma-carboxylation enzyme)
• rs699664 (often studied in K-dependent protein activation)
MGP (matrix Gla protein)
• rs1800801
• rs1800802
If you paste, it’ll look like:
rs9923231 1 11714413 AG (genotype varies)
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What I can and can’t conclude from it
Even if we find variants:
• it does not mean “don’t take MK-7”
• it mostly suggests relative sensitivity/efficiency, not a disease diagnosis
• the only highly actionable vitamin-K genetics is mainly about warfarin dosing, not osteoporosis
But I can translate your genotypes into:
• “more likely lower / average / higher vitamin-K recycling efficiency”
• “possible weaker/stronger activation capacity”
• “whether anything is notable enough to mention to a clinician”
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If you upload the file, I’ll scan it for those SNPs and summarize what they mean in plain English."
Yes — possible, but limited, and this distinction matters.
What’s possible
• Your 23andMe data can show variants in vitamin-K–pathway genes (e.g., VKORC1, GGCX, MGP).
• Those variants can suggest relative efficiency of vitamin K recycling or protein activation (lower / average / higher sensitivity).
What’s not possible
• There is no recognized “bad MK-7 gene” that predicts osteoporosis or says “don’t take MK-7.”
• These variants do not diagnose bone disease, do not predict progression, and do not override factors like menopause, activity, protein intake, inflammation, or meds.
• Results are not clinically actionable the way CFH Y402H is for AREDS with zinc in AMD disease.
How to interpret results if you look
• Findings are contextual (small effect sizes).
• They help explain why responses vary, not who will or won’t lose bone.
• MK-7 remains supportive, not curative, regardless of genotype.
If you want, upload your 23andMe raw data (or paste the specific SNP lines), and I’ll translate what—if anything—is noteworthy, plainly and conservatively.
Mayo Clinic does not recommend dna testing for bone diseases generically ---just in special cases like for bone loss before age 50.
This exercise to see the relevant genes from 23 and me raw data that regulate bone MK-7 uptake is just give you more clarification. You are going to take MK7 regardless.
It is my understanding that MK7 stays in the bloodstream longer ( NIH study) and the most significant effect on OC carboxylation. I take MK-7 100mcg but found that I need to cut the pill in half because a whole dose will cause bleeding in small cuts around my fingers...the ones that you get in winter around nails that are so painful. I use Bronson Basics which seems to be a reliable brand since 1960.