Vitamin K2 improves bone mineral density in postmenopausal women on the basis of multiple RCTs, especially in combination with vitamin D. The evidence for reduced arterial calcification and fewer fractures is promising but still insufficient to draw firm conclusions. Users of blood thinners should always consult a doctor.
Vitamin K2 is a fat-soluble vitamin that plays a role in two processes: building strong bone and preventing calcium deposits in blood vessels. The vitamin activates proteins that direct calcium to bone and keep it out of vessel walls. The best-known of these proteins are osteocalcin (for bone) and matrix Gla-protein (for blood vessels). This mechanism of action is well established in the scientific literature.
The evidence for bones is strongest in postmenopausal women. A meta-analysis of 16 randomised controlled trials (RCTs) with a total of 6,425 participants showed that vitamin K2 supplementation significantly improves bone mineral density of the lumbar spine (PMID 36033779). The combination of vitamin K2 with vitamin D also significantly improves total bone mineral density more than a control group, based on 8 RCTs with 971 participants, with the effect being greater at vitamin K doses below 500 micrograms per day (PMID 32219282). Vitamin K2 also reliably lowers the amount of inactive osteocalcin in the blood, which is a clear sign that the supplement is genuinely active in bone.
There are, however, conflicting findings as well. An older review article concluded that vitamin K supplementation in white (Western) populations showed no demonstrable increase in bone mineral density at the most important skeletal sites (PMID 24090644). The effect therefore appears to depend on the population studied, the dose used, and other study characteristics. Several reviews still rate the overall body of evidence for bone health as 'non-conclusive' (PMID 32972636, 24090644).
The effect on fracture risk is uncertain. Without an adjustment for one outlying study, there is no significant difference in fracture incidence. After excluding that single outlier, the risk falls by approximately 57 percent (relative risk 0.43). Because one study influences the result so strongly, the conclusion is fragile and that halving of fracture risk must be interpreted with great caution (PMID 36033779, 24090644).
For blood vessels, the evidence remains limited for now. Vitamin K2 can inhibit arterial calcification via matrix Gla-protein, but this has been demonstrated mainly in mechanistic and observational studies. Large RCTs demonstrating an actual reduction in arterial calcification in humans are still lacking (PMID 38063255, 29749440).
Regarding safety: pooled data from multiple RCTs show that vitamin K2 does not cause more side effects than a placebo (PMID 36033779). There is, however, one important point to bear in mind. People who use blood thinners such as warfarin or acenocoumarol must NOT take vitamin K2 without consulting a doctor or pharmacist. Vitamin K acts directly on the mechanism that these medications influence, which can disrupt the dosing of the anticoagulant.
Based on 2 meta-analyses/reviews of RCTs (PMID 36033779 with 6,425 participants; PMID 32219282 with 971 participants), supplemented by an older review article (PMID 24090644), mechanistic review studies (PMID 38063255, 29749440), and a narrative review (PMID 32972636). Total number of participants in the quantitative RCT analyses: approximately 7,400. Study heterogeneity and population differences limit generalisability.