Vitamin KVitamin

• Blood clottingLikely helps

  This is the part nobody disputes. Vitamin K is the cofactor that activates clotting factors II (prothrombin), VII, IX and X in the liver [1].
  
  It also activates osteocalcin and matrix Gla-protein elsewhere in the body, which is where the bone and artery research starts [1].
  
  Warfarin and its relatives work by blocking exactly this activation — the clearest possible demonstration that the pathway is real [1]. ^[1]

• Bone density and fracture riskPossibly helps

  A 2022 meta-analysis of 16 randomised trials in 6,425 postmenopausal women found vitamin K2 improved lumbar-spine bone mineral density (p=0.006) and lowered undercarboxylated osteocalcin [10].
  
  A separate review of 20 trials found lower odds of vertebral fracture (OR 0.42, 95% CI 0.27–0.66) and clinical fracture (OR 0.44, 95% CI 0.23–0.88) [11]. That same review found no significant effect on femoral-neck bone mineral density, and called the evidence for a real therapeutic effect insufficient.
  
  The sources disagree, and we are not settling it for you. NIH's Office of Dietary Supplements says intervention-trial results are inconsistent overall, and stops short of recommending supplements for osteoporosis [1]. ^[10]

• Coronary calcification and heart disease mortalityPossibly helps

  A Dutch observational cohort found dietary menaquinone (K2), but not phylloquinone (K1), inversely associated with coronary artery calcification [1].
  
  Coronary heart disease mortality was 27% lower in the middle intake tertile (21.6–32.7 mcg/day) and 57% lower in the highest, against the lowest tertile [1].
  
  That is a correlation in a diet-survey cohort, not a trial. NIH ODS calls vitamin K's role in coronary heart disease unclear, an active research area, and draws no clinical recommendation from it [1]. ^[1]

• Newborn bleeding — the injection, not a capsuleLikely helps

  Route is the whole story here. This is a single intramuscular injection given shortly after birth, and nothing on this page suggests an oral supplement does the same job [18].
  
  Newborns start with very low stores, since vitamin K crosses the placenta poorly and neither breast milk nor formula supplies much [18].
  
  The injection is the standard, medically established measure against vitamin K deficiency bleeding, including bleeding inside the skull [1]. Oral schedules used in some European countries have been linked to more breakthrough bleeding and stroke cases than the shot [18]. ^[18]

• OsteoarthritisPossibly helps

  Biologically plausible, barely tested. Vitamin K activates proteins that regulate calcification, and cartilage calcification has a role in osteoarthritis [24].
  
  An academic review found only one small clinical trial, at 500 mcg/day, has actually tested supplementation for it [24].
  
  An NIH-registered pilot trial in knee osteoarthritis is ongoing. Until it reads out, this is a hypothesis [24]. ^[24]

• Blood that takes longer to clot, and bleeding — the main adult signs listed by Australia's government service Healthdirect [8]
• Bone conditions such as osteopenia or osteoporosis [8]
• In adults the cause is usually an existing condition impairing fat absorption or vitamin K metabolism — cholestasis, coeliac disease, cystic fibrosis, small-bowel disease, long-term antibiotics — rather than diet alone [8]
• Newborns are the group at genuine, well-documented risk, because vitamin K crosses the placenta poorly and breast milk contains little [7]
• Uncontrolled bleeding is the main sign of vitamin K deficiency bleeding in infants, and can be a medical emergency [7]
• Subtler infant signs: sleepiness, vomiting, seizures, bruising especially on the head, petechiae, nosebleeds, jaundice, pale skin, and dark, sticky or bloody stool [7]
• Cleveland Clinic estimates early and classical infant bleeding at 1 in 60 to 1 in 250 US newborns, and late bleeding at 1 in 14,000 to 1 in 25,000 [7]^[8]

• Phylloquinone (vitamin K1)Everyday dietary intake, and the form most closely tied to warfarin's dose-consistency problem .

  Elemental content

  The main dietary form. Concentrated in green leafy vegetables and certain vegetable oils [1]

  Absorption

  Clears from blood fast.
  
  Levels fell 86% within 8 hours of a dose in work by Schurgers and colleagues, as reported by industry coverage of the study [16].

  Best for

  Everyday dietary intake, and the form most closely tied to warfarin's dose-consistency problem [1].

• Menaquinone-4 (MK-4)Read MK-4 marketing sceptically.

  Elemental content

  A short-chain K2. Distinctive because the human body converts it from phylloquinone by a non-bacterial route [1]

  Absorption

  Barely shows up in blood.
  
  After a single 420 mcg dose, MK-4 was undetectable in serum in every subject, at every timepoint [6]. Seven days at 60 mcg/day did not raise serum MK-4 at all.

  Best for

  Read MK-4 marketing sceptically. Sato and colleagues concluded that dietary MK-4 does not measurably contribute to vitamin K status as judged by serum levels, while commercial sources still sell it as an effective K2 [6].
  
  One review also notes supplemental MK-4, unlike MK-7, can raise PT/INR readings [20].

• Menaquinone-7 (MK-7)Supplement studies where sustained blood levels matter.

  Elemental content

  A long-chain K2 of bacterial origin. Natto is the standout food source [1]

  Absorption

  The long-lived one.
  
  A single 420 mcg dose peaked in serum at 6 hours and was still detectable at 48 hours [6]. Levels were only 50% down after 68 hours, against K1's 86% drop in 8 hours [16].

  Best for

  Supplement studies where sustained blood levels matter. It produced the most pronounced and sustained effect on osteocalcin carboxylation of the three forms [6].

• Generally well tolerated

  The Food and Nutrition Board set no upper limit, citing vitamin K's low toxicity potential [1].
  
  A commercial clinical database summarised by WebMD calls it usually well tolerated, with upset stomach or diarrhoea in some people [22]. ^[22]

• Chronic kidney disease

  Vitamin K status is often poor in CKD, and several causes stack up. Renal diets restrict potassium-rich vegetables that happen to be vitamin K-rich, medications shift gut bacteria, and warfarin depletes the active form [20].
  
  Vascular calcification affects an estimated 47–83% of non-dialysis CKD patients with eGFR under 60, and over 80% of dialysis patients [20].
  
  No dietary reference intake or consensus guideline exists for vitamin K in CKD.
  
  Academic reviews frame better vitamin K status as plausibly useful against calcification, while noting that trials so far have been underpowered [19]. Many of these patients are on warfarin at the same time, which directly opposes vitamin K [19]. ^[20]

• Warfarin — keep intake steady, do not cut it out

  The most consequential item on the page, and the one most commonly misread.
  
  Warfarin (Coumadin) and the European vitamin K antagonists — phenprocoumon, acenocoumarol, tioclomarol — work by blocking vitamin K's activation of clotting factors [1].
  
  NIH's Office of Dietary Supplements is specific about which direction hurts. A sudden increase in vitamin K weakens the anticoagulant effect and raises clot risk; a sudden decrease raises bleeding risk [1].
  
  So the actual guidance is day-to-day consistency of vitamin K from food and supplements — not swearing off greens [1]. ^[1]

• MK-4 supplements can move INR readings

  Supplemental MK-4, unlike MK-7, can raise PT/INR results, per a review of vitamin K in kidney disease [20].
  
  That matters for anyone whose warfarin dose is steered by INR, since the number shifts on the supplement alone. ^[20]

• Long antibiotic courses

  Antibiotics, especially taken beyond a few weeks, reduce the gut bacteria that produce vitamin K [1].
  
  Less bacterial production means less vitamin K available to the body. ^[1]

• Bile acid sequestrants and orlistat

  Cholestyramine and colestipol, both used to lower cholesterol, reduce how much vitamin K the body absorbs from food [1].
  
  The weight-loss drug orlistat does the same. Long-term use is where this matters most [1]. ^[1]

K1 comes from plants; K2 from ferments and animal foods [1].

Natto (fermented soybeans) is the K2 standout at about 850 mcg per 3 ounces, more than seven times the adult Daily Value [12].

Greens carry the K1. Boiled collard greens run about 530 mcg per half cup, boiled turnip greens about 426 mcg, cooked broccoli about 110 mcg [12].

Raw spinach is about 72.5 mcg per half cup and raw kale about 57 mcg [12]. Smaller contributors: dry-roasted cashews about 80 mcg per half cup, soybean oil 25 mcg per tablespoon, canola or olive oil 8–10 mcg per tablespoon [12].

Fruit is modest — blueberries about 14 mcg per half cup, grapes about 11 mcg [12]. Roasted chicken breast, an MK-4 source, gives about 13 mcg per 3 ounces [12].

Separate academic analysis found cheese the richest source of longer-chain menaquinones (MK-5 through MK-9) in a typical Western diet, while meat contains almost exclusively MK-4 [15]. Among vegetables, only fermented ones carry meaningful K2.

⚠ Numbers for the same food vary noticeably by source and serving convention. Raw kale is about 57 mcg per half cup in Cleveland Clinic's USDA-derived figures but roughly 390 mcg per 100 g in a University of Rochester table [23].

No hour of the day wins. Dietitian-reviewed consumer sources agree that consistency of timing matters more than the specific hour [17].

What does matter is fat. Vitamin K is fat-soluble, so it needs dietary fat to trigger bile release and micelle formation before it can cross the intestinal wall [17].

Taking it on an empty stomach may reduce absorption. Olive oil, avocado, nuts and nut butters are the usual pairings suggested [17].

Because it is stored rather than excreted daily, a high-fat meal is not a daily requirement — a consistent routine, taken with food, is the practical advice [17].