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Vitamin K status did not protect bone in a VITAL analysis
Vitamin K is sold as the partner vitamin D needs for bones. In 771 participants of the VITAL trial, higher vitamin K status did not slow two-year bone loss or improve what vitamin D did.
Based on an ancillary study of the VITamin D and OmegA-3 TriaL in 771 US participants with two-year bone imaging
- The theory is real: vitamin D makes a bone protein, and vitamin K switches it on.
- In 771 VITAL participants, higher vitamin K status did not track with better bone density.
- It also did not change what vitamin D supplements did, which was already nothing.
- Three separate measures of vitamin K status all pointed the same way.
- Vitamin K status was measured, not assigned, so this is not a trial of vitamin K itself.
Walk down a supplement aisle and vitamin D and vitamin K are increasingly sold in the same capsule, on a story that is genuinely good biology.
A study in JBMR Plus went and checked whether the biology shows up in anyone’s bones. It did not.
The theory that put the two vitamins together
The story starts with a protein called osteocalcin, made by the cells that build bone.
The synthesis of OC is stimulated by vitamin D, where OC is osteocalcin. But making it is not enough. Osteocalcin needs to be carboxylated, or activated, by vitamin K to deposit calcium into bone.
So vitamin D produces the protein and vitamin K switches it on. Take one without the other, the argument runs, and you are manufacturing a tool nobody turns on.
That chain is real chemistry, and it is why the pairing sells. What had not been tested is whether people with more vitamin K actually keep more bone.
What the VITAL analysis did
The starting point was a trial that had already produced a null result.
VITAL randomized US adults to vitamin D3 or placebo, and its bone arm found no differences in 2-yr changes in areal BMD at the spine, hip, or whole body in 771 U.S. participants, where BMD is bone mineral density. Vitamin D alone did nothing measurable to bone in this group.
This new analysis went back to those same participants and asked a sharper question: was vitamin D failing because vitamin K was the missing ingredient?
Vitamin K status was assessed three separate ways: blood levels of phylloquinone, which is the main dietary form, plus two markers of how much of the relevant proteins were sitting un-activated for want of it.
What higher vitamin K status did to bone
Nothing that the study could detect, across an unusually wide set of measures.
Higher baseline vitamin K status was not associated with favorable 2-yr changes in aBMD at the spine, hip, or whole body, nor in trabecular bone score, volumetric BMD and bone architecture at the wrist and shin, which are finer measures of bone structure than a standard scan produces.
Then the interaction question, which was the point of the exercise. The effects of supplemental vitamin D on aBMD were not modified by baseline measures of vitamin K.
Vitamin D did not work better in people who had plenty of vitamin K. It did not work at all in either group.
The authors’ summary is one sentence and it is the finding: higher vitamin K status, even when accompanied by supplemental vitamin D, did not prevent bone loss.
Why three vitamin K markers matter here
This is the part that makes the null result worth reporting rather than shrugging at.
A single measurement showing nothing is weak evidence, because the measurement itself might be poor. Three different markers, capturing vitamin K from different angles, all showing nothing is a considerably stronger statement.
The same goes for the bone side. The analysis looked at standard density scans, at bone architecture at two skeletal sites, and at a texture score that picks up structural quality density alone misses. Several ways of asking, one answer.
What this vitamin K analysis is not
The important limit is in the design rather than the numbers.
Nobody was given vitamin K. The study measured the vitamin K status people already had and looked at what followed, which makes it an observational analysis sitting inside a randomized trial. Strictly, it tests whether having more vitamin K helps, not whether taking more would.
That leaves a gap a supplement manufacturer could drive through, and it is worth being fair about it. It is also worth being realistic: if the naturally occurring range of vitamin K status shows no relationship with bone across three markers and half a dozen outcomes, a capsule producing one would be an odd result.
For anyone taking a combined vitamin D and K product for their bones, this is the first real test of the premise, and the premise did not survive it. Anyone being treated for osteoporosis should be having that conversation with a doctor rather than a label.
People also ask
Why would vitamin K matter for bone at all?
Because of a protein called osteocalcin. The synthesis of osteocalcin is stimulated by vitamin D, but osteocalcin needs to be carboxylated, or activated, by vitamin K to deposit calcium into bone. So the two vitamins sit on the same assembly line, and the idea that one is useless without the other has a genuine biological basis. This study tested whether that basis translates into bone.
What was VITAL?
A large randomized trial of vitamin D3 (2000 IU/d) and omega-3 supplements in US adults. In its bone sub-study, there were no differences in 2-yr changes in areal bone mineral density at the spine, hip, or whole body in 771 US participants randomized to vitamin D3 versus placebo. This analysis went back to those participants and added vitamin K measurements.
How was vitamin K status measured?
Three ways, which is a strength: blood levels of phylloquinone (the main dietary form of vitamin K), percent undercarboxylated osteocalcin (how much of the bone protein is sitting inactivated), and dephosphorylated undercarboxylated matrix Gla protein (a similar marker for a protein in blood vessels). All three are established markers of whether the body has enough vitamin K to activate these proteins.
What did it find?
Nothing, consistently. Higher baseline vitamin K status was not associated with favorable 2-year changes in bone density at the spine, hip or whole body, nor in trabecular bone score, volumetric bone density, or bone architecture at the radius and tibia. And the effects of supplemental vitamin D on bone density were not modified by baseline measures of vitamin K.
Does this rule out vitamin K supplements for bone?
Not strictly. This measured people's existing vitamin K status rather than assigning them a supplement, so it is a study of whether having more vitamin K helps, not of whether taking more does. That said, if the naturally occurring range showed no signal across three markers and several bone measures, a supplement producing a benefit would be a surprising result.
Who was in the study, and how long did it run?
771 US participants from VITAL, with 687 having follow-up data, over two years of bone imaging. Two years is enough to detect change in bone density, and the sample is reasonable for a bone imaging study, though smaller than the parent trial. Bone decisions belong with a doctor, particularly for anyone already diagnosed with osteoporosis.
References
- Chou, S. H., Booth, S. L., Cook, N. R., et al. Investigating the interrelationship of vitamin K and vitamin D status on bone density: results from the VITamin D and OmegA-3 TriaL. JBMR Plus, 2026.
- National Institutes of Health Office of Dietary Supplements. Vitamin K Fact Sheet for Health Professionals.
- Bone Health and Osteoporosis Foundation. Calcium and Vitamin D.