This test is most useful if any of these apply to you.
Your body cannot make vitamin K1. Every microgram has to come from food, mainly leafy greens and plant oils. And unlike most nutrients, there is no routine blood test that checks it. That means you could be running low for years without knowing it, quietly underpowering the proteins that keep calcium in your bones and out of your arteries.
Serum vitamin K1, also called phylloquinone, measures the circulating concentration of this vitamin in your blood. It reflects your recent dietary intake and absorption, and it serves as the raw material your liver uses to activate clotting factors and your tissues use to activate proteins that protect your skeleton and blood vessels. A single reading gives you a snapshot of your current supply, though it fluctuates more than most nutrients from day to day.
Vitamin K1 is the fuel for a chemical reaction called gamma carboxylation. In plain terms, it activates a set of specialized proteins that would otherwise sit idle. The best known of these are the clotting factors (II, VII, IX, and X) made in the liver. When vitamin K1 is too low, these factors cannot do their job, and bleeding risk rises. This is the biology behind warfarin: the drug works by blocking vitamin K recycling.
But clotting is only part of the story. The same activation chemistry powers proteins outside the liver, including osteocalcin (which helps lock calcium into bone) and a protein called matrix Gla protein, or MGP, which prevents calcium from depositing in artery walls. When vitamin K1 supply is marginal, your liver gets first priority, so clotting stays normal even as your bones and blood vessels quietly lose protection.
A number of large studies link higher vitamin K1 intake to lower cardiovascular risk. In a Danish cohort of over 53,000 adults followed for a median of 21 years, those with the highest dietary vitamin K1 intake (around 192 micrograms per day) had roughly a 21% lower rate of hospitalization for atherosclerotic vascular disease compared to those eating the least (about 57 micrograms per day). That association held after adjusting for other dietary and lifestyle factors.
In a study of about 1,400 older Australian women followed for 14.5 years, those eating at least 120 micrograms of vitamin K1 per day had about 29% fewer atherosclerotic vascular disease events and 43% fewer deaths from atherosclerotic vascular disease than those eating the least. Women in the highest intake group also had measurably thinner carotid artery walls, a sign of less plaque buildup.
A meta-analysis pooling data from over 220,000 participants across 21 prospective studies found that the highest dietary vitamin K1 intake was associated with about an 8% lower risk of coronary heart disease. When researchers looked at a functional marker of vitamin K deficiency, a protein called dp-ucMGP (dephosphorylated uncarboxylated matrix Gla protein, which rises when vitamin K is too low), the signal was even stronger: the highest levels of this deficiency marker were linked to roughly 84% higher risk of dying from any cause and about double the risk of dying from cardiovascular disease.
If your vitamin K1 is low and you have cardiovascular risk factors, ordering hs-CRP (high sensitivity C-reactive protein, an inflammation marker), a coronary calcium score, and ApoB (apolipoprotein B, a measure of cholesterol-carrying particles) can help you and your physician see the full picture of your vascular risk.
A separate Danish study of over 55,000 people found that higher dietary vitamin K1 was associated with a lower incidence of aortic valve stenosis, a condition where the heart's aortic valve stiffens and narrows due to calcium buildup. Participants with the highest vitamin K1 intake had a 23% lower risk of aortic stenosis compared to those with the lowest intake. This aligns with the biology: MGP, which needs vitamin K to function, is one of the body's main defenses against inappropriate calcification.
In a study of nearly 55,000 Danish adults without diabetes at baseline, followed for about 21 years, those in the highest fifth of vitamin K1 intake had about 31% lower risk of developing type 2 diabetes compared with the lowest fifth. The relationship was linear: more vitamin K1, less diabetes risk. The association was particularly strong in men, current smokers, people with obesity, and those with low physical activity.
A prospective study of over 101,000 American adults found that those in the highest quarter of dietary vitamin K1 intake had about 43% lower risk of developing pancreatic cancer compared to the lowest quarter, after adjusting for other dietary and lifestyle factors. This was specific to phylloquinone (K1); vitamin K2 intake showed no such association.
Vitamin K1 activates osteocalcin, a protein that helps bind calcium into the bone matrix. In postmenopausal women with low bone density, a large randomized trial (the ECKO trial) gave 440 women either 5 mg of vitamin K1 daily or a placebo for 2 to 4 years. The supplement did not slow the overall loss of bone density. However, as an exploratory finding, women taking vitamin K1 had fewer clinical fractures. A separate two-year trial of 244 older women found that 200 micrograms per day of K1 combined with vitamin D3 and calcium modestly improved bone density at the wrist, though not at the hip.
Systematic reviews describe the fracture prevention evidence as mixed. Vitamin K1 clearly activates the right bone proteins, but whether supplementation prevents fractures in the general population is still uncertain. What is clear is that very low vitamin K1 is associated with weaker bones: in a study of 374 postmenopausal women with osteoporosis, each 1 microgram per liter increase in serum K1 was associated with about 45% lower odds of having had a fracture.
One Mendelian randomization study (which uses genetic variants to approximate a lifelong exposure) found that genetically higher circulating vitamin K1 was associated with an increased risk of large artery stroke. This stands in apparent tension with the protective cardiovascular findings above. The resolution is that vitamin K1 may have different effects on different vascular beds and disease processes. Protecting against arterial calcification is not the same as protecting against every type of stroke. This single genetic study does not overturn the weight of observational evidence, but it is a reason to avoid assuming that more is always better.
A participant-level meta-analysis of three U.S. cohorts (about 3,891 older adults, median follow-up 13 years) found that those with the lowest circulating phylloquinone (0.5 nmol/L or below) had about 19% higher risk of dying from any cause compared to those above 1.0 nmol/L, after full adjustment. The association with cardiovascular death specifically did not reach statistical significance in this pooled analysis, but the all-cause mortality signal was clear.
No major medical guideline defines clinical decision thresholds for serum vitamin K1. The ranges below come from population studies and should be treated as orientation, not targets. Your lab may use different units or methods, so always compare your results within the same lab over time.
These ranges are drawn from a study of 3,808 healthy Danish adults (ages 26 to 78) measured by a validated mass spectrometry method, and are among the largest population-based reference intervals published. They are specific to Caucasian adults and may not apply directly to other populations. Ethnicity matters: in the Multi-Ethnic Study of Atherosclerosis, Chinese Americans had roughly double the serum K1 of white, African American, and Hispanic participants, even after adjusting for diet.
| Category | Serum K1 Range (nmol/L) | What It Suggests |
|---|---|---|
| Low (possible insufficiency) | Below 0.50 | In a pooled analysis of three U.S. cohorts, levels at or below 0.50 nmol/L were associated with a 19% higher risk of all-cause mortality. Worth retesting and increasing green vegetable intake. |
| Reference range (age 26 to 44) | 0.22 to 3.95 | Represents the 2.5th to 97.5th percentile in healthy younger adults. |
| Reference range (age 45 to 78) | 0.35 to 3.70 | Slightly higher lower bound reflects age-related shifts in the healthy population. |
| Above 1.0 | Greater than 1.0 | Associated with lower risk of death in two independent U.S. cohorts. The reference category in the largest pooled mortality analysis. |
Serum vitamin K1 is one of the most variable nutritional biomarkers. A single reading can be thrown off by several common factors.
Because serum K1 fluctuates so much with diet, fasting status, and triglyceride levels, a single reading carries limited weight. A value that looks low might just reflect what you ate (or did not eat) in the past 48 hours. The real value of this test comes from serial measurements over time, taken under consistent conditions (fasted, at the same time of day, ideally at the same lab).
Results reported in ng/mL (common in some labs) can be roughly converted: 1 ng/mL is approximately 2.2 nmol/L. Compare your results within the same lab over time for the most meaningful trend.
Evidence-backed interventions that affect your Vitamin K1 level
Vitamin K1 is best interpreted alongside these tests.