Vitamin K production

This stool result estimates your gut bacteria's genetic capacity to make vitamin K2. Carrying the genes, producing the vitamin, and supplying it to your tissues are separate steps. A gene-based estimate cannot establish how much vitamin K your body receives from bacteria.

It's a research-stage marker. Studies have linked these microbial functions to several health conditions, but testing has not been shown to improve diagnosis, guide warfarin dosing, or identify a production level that improves health.

What Your Gut Bacteria Are Making

Vitamin K comes in two main forms. Plants supply vitamin K1, including the vitamin found in leafy greens. Vitamin K2 is a family of compounds called menaquinones. Bacteria make several of these compounds and use them in reactions that help generate energy. Much of the bacterial vitamin remains associated with bacterial cell membranes.

The names MK-5 through MK-13 distinguish forms with different molecular side-chain lengths. Different bacterial species tend to make different forms:

• Bacteroides species: commonly make MK-10 and MK-11.
• Prevotella species: can make longer forms, including MK-11 through MK-13.
• Escherichia coli: makes MK-8.
• Veillonella species: commonly make MK-7.
• Eubacterium lentum: is a reported producer of MK-6.

Production capacity depends on the genes present across the microbial community. Counting one bacterial species cannot capture that capacity, and the presence of production genes does not establish how actively those genes are being used.

Production Capacity and Vitamin Concentration

A controlled feeding study of 80 healthy adults measured vitamin K2 compounds directly in stool, a different measurement from this gene-based estimate. Daily stool excretion varied widely from person to person and was associated with bacterial composition. That variation describes vitamin leaving the body, which also depends on stool output and absorption.

No K2 forms were detectable in the participants' serum samples with the study's method. The study therefore could not establish whether stool K2 tracked circulating K2. Undetectable blood concentrations also do not mean that none had been absorbed.

How Much Reaches Your Body

Dietary vitamin K is absorbed in the small intestine with help from bile and the processes that digest fat. Much of the bacterial K2 in the gut is found farther down, in the colon. Its release from bacterial membranes and absorption into your body remain poorly quantified.

Separate research chemically measured vitamin K in intestinal contents. In samples from the distal colon, the combined concentration of MK-9 and MK-10 was many times that of K1. This shows that the colon can contain a substantial reservoir, but it does not measure how much of that reservoir becomes available to you.

There is evidence that bacterial menaquinones can be absorbed. The proportion of your daily requirement supplied by your gut bacteria has not been reliably established, and this stool result cannot calculate it.

Warfarin and Clotting

Warfarin reduces clotting by interfering with vitamin K recycling. Changes in vitamin K intake or absorption can affect its action, and bacterial vitamin production is one possible contributor.

A study of 246 cardiac surgery patients found associations between gut bacterial composition, blood vitamin K measurements, and variation in warfarin response. The vitamin measurements were K1 and MK-4. Human tissues can make MK-4 from other vitamin K forms, so blood MK-4 does not specifically measure bacterial production. The study did not establish that a stool production score improves warfarin management.

A separate hospital study found that acute diarrhea was associated with excessive anticoagulation among people taking vitamin K antagonists. It measured clotting and illness, without measuring microbial production capacity. Reduced vitamin absorption is one possible explanation.

Kidney Disease and Inflammation

Vitamin K helps activate matrix Gla protein, which inhibits calcium deposits in blood vessels. An inactive form is called dp-ucMGP. Its blood concentration is used in research on vitamin K status, but kidney function also influences the result.

A study of 107 people on hemodialysis found higher inflammatory signals among those classified as having poorer vitamin K status using dp-ucMGP. Stool bacteria were assessed in a subgroup, where poorer status was associated with fewer Bacteroides. The study measured bacterial composition and a blood protein, rather than this stool production estimate.

Because these measurements were taken at one point in time, they cannot establish that reduced bacterial production caused vitamin K deficiency or inflammation. They also do not establish that this test can guide treatment in kidney disease.

Colon Polyps, Diabetes, and Arthritis

Research on microbial vitamin-making genes has found differences between people with and without several conditions. The direction is not consistent across diseases:

• Colon polyps: a study enrolling 136 adults undergoing colonoscopy found lower abundance of certain K2-production pathways in stool from people with adenomas. These are polyps that can develop into cancer. The pathway findings were exploratory and have not been validated as a screening test.
• Type 2 diabetes: a study of 18 people found greater abundance of a K2-production pathway in those with diabetes.
• Early rheumatoid arthritis: a study predicted lower abundance of a function shared by vitamin K2 and coenzyme Q10 production from bacterial profiles. Coenzyme Q10 is a different molecule involved in energy production. This was a broader, indirect estimate rather than direct sequencing of all K2-production genes.

These findings do not establish that higher production capacity is healthier. They describe microbial differences associated with disease, and none shows that changing this stool result changes your risk.

Cognition in Older Adults

An exploratory study of 74 older adults examined both microbial production genes and chemically measured K2 in stool. Gene profiles differed across groups with different cognitive scores. Stool MK-6, MK-12, and MK-13 were positively associated with performance on a memory and thinking assessment, while total stool K2 was not.

The study could not establish whether these microbial differences influenced cognition or reflected differences in health, diet, or living circumstances. It did not validate this result as a test of brain aging.

Where the Heart Health Evidence Comes From

Studies linking vitamin K to cardiovascular outcomes mostly measure dietary intake or blood markers. They provide context about the vitamin, but their findings cannot be assigned to a stool estimate of bacterial production.

In a 2019 meta-analysis, the estimate for dietary K2 and coronary heart disease came from two prospective studies. People with the highest intake had about 30% lower risk than those with the lowest intake. Across five studies of blood dp-ucMGP, higher concentrations were associated with about 84% higher risk of death from any cause. These were observational associations.

In a Danish cohort of 53,372 adults followed for a median of 21 years, the highest fifth of K2 intake had a 14% lower risk of hospitalization for atherosclerotic cardiovascular disease than the lowest fifth. This concerned a first qualifying hospitalization, not the total number of hospital stays. Diet and other health differences can influence such associations.

Neither dietary associations nor associations with blood proteins establish that increasing microbial production prevents heart disease.

When Results Can Be Misleading

This result describes genetic potential in a stool sample. It does not measure the rate of vitamin synthesis, the amount released from bacterial cells, or the amount absorbed by your body.

• Changing microbial proportions: a gene's share of the sample can increase because other microbial genes become less abundant. That does not necessarily mean more vitamin is being produced.
• Stool consistency and transit: water content and the time stool spends in your gut are associated with bacterial composition. Diarrhea or constipation can therefore change the context of a result.
• Recent illness or antibiotics: these can alter microbial communities. The direction and duration of changes depend on the drug, illness, and starting community.
• Laboratory methods: DNA extraction, sequencing depth, reference databases, and analysis methods affect which genes are detected and how their abundance is reported.
• Sample handling: contamination, storage conditions, and delays outside the collection kit's instructions can affect the microbial profile.

Daily sampling of 20 women over six weeks found that most bacterial genera varied more within a person than between people, with some changing by up to 100-fold over the study period. That study measured bacterial abundance, so it does not establish the day-to-day variability of this production estimate.