Vitamin K1 (Phylloquinone): The Clotting Vitamin from Leafy Greens — A Research-Backed Guide
⚡ 60-Second Summary
Vitamin K1 (phylloquinone) is the primary dietary form of vitamin K — found in leafy green vegetables and plant oils. Its central function is activating the vitamin K-dependent coagulation factors (II, VII, IX, X) and anticoagulant proteins (C and S) that control blood clotting. Without K1, blood cannot clot normally. K1 is efficiently absorbed from food in the presence of dietary fat and has a half-life of about 1–2 hours.
Key clinical distinction from K2: K1 is the dominant form for hepatic (clotting) functions; K2 (MK-7 in particular) distributes more broadly to bone and arteries. For bone and cardiovascular benefits, K2 has stronger RCT evidence. For clotting factor support, K1 from diet is the standard source.
The warfarin interaction: This is the most important safety consideration for K1 (and K2) in clinical practice. Warfarin users must maintain consistent vitamin K intake — not avoid it.
What is vitamin K1?
Vitamin K is a family of fat-soluble compounds sharing a 2-methyl-1,4-naphthoquinone ring that functions as an essential cofactor for a gamma-glutamyl carboxylase enzyme. This enzyme adds carboxyl groups to glutamate residues in vitamin K-dependent proteins — a process called gamma-carboxylation that is required for these proteins to bind calcium and become biologically active.
Phylloquinone (K1) is the plant-kingdom form of vitamin K. It is found in:
- Leafy greens (by far the richest sources): spinach (~800 µg/cup cooked), kale (~1,000 µg/cup cooked), collard greens, Swiss chard, broccoli (~220 µg/cup cooked)
- Plant oils (especially soybean, canola, cottonseed oils)
- Smaller amounts in avocado, blueberries, and grapes
After absorption (requiring dietary fat — a fat-free meal greatly reduces K1 absorption), phylloquinone is transported in chylomicrons to the liver, where it serves primarily as a cofactor for clotting factor carboxylation. Its short half-life (1–2 hours) means stores are rapidly depleted without regular dietary intake — which is why consistent daily leafy green consumption matters for anticoagulation stability.
Evidence-based benefits of vitamin K1
1. Blood coagulation — the primary established function
Phylloquinone is the indispensable cofactor for activating the vitamin K-dependent clotting proteins:
- Procoagulant factors: II (prothrombin), VII, IX, X — blocking any of these (as warfarin does) produces an anticoagulated state
- Anticoagulant proteins: Protein C, Protein S, Protein Z — these naturally limit clot extension
K1 deficiency impairs all these proteins simultaneously, resulting in a bleeding diathesis. This is the established, essential nutritional function of vitamin K1 with no clinical controversy.
2. Bone health — present but limited compared to K2
Osteocalcin (bone Gla protein) and matrix Gla protein (MGP) are both vitamin K-dependent. K1 can carboxylate these proteins, but because it is rapidly cleared from circulation and has poor uptake into extrahepatic tissues, its contribution to bone and vascular vitamin K-dependent protein activation is substantially less than that of K2 menaquinones at comparable intakes. Some studies show K1 supplementation improves markers of bone turnover in older adults, but the effect sizes are smaller than with MK-7 at equivalent amounts. For bone and cardiovascular benefit, K2 (especially MK-7) is the preferred supplemental form.
3. Newborn hemorrhage prevention
Neonates are born with very low vitamin K stores (K1 does not cross the placenta efficiently, and breast milk is low in K1). Hemorrhagic disease of the newborn (neonatal vitamin K deficiency bleeding) can cause life-threatening brain and gut hemorrhage. A single intramuscular injection of phylloquinone (0.5–1 mg) at birth is standard practice in most countries and effectively prevents this condition.
Vitamin K1 deficiency
Clinical K1 deficiency — manifesting as coagulopathy (prolonged PT/INR, easy bruising, bleeding) — is unusual in healthy adults eating any leafy greens. It occurs in:
- Fat malabsorption: Celiac disease, Crohn's, primary biliary cholangitis, cystic fibrosis, short bowel syndrome, obstructive jaundice — fat-soluble vitamin absorption is compromised
- Long-term antibiotics: Gut bacteria contribute some menaquinone (K2) production; broad-spectrum antibiotics can reduce this along with eliminating dietary K sources if intake is poor
- Very poor dietary intake: Institutionalized elderly with very limited vegetable intake; eating disorders
- Newborns (addressed by routine K injection)
Vitamin K supplement forms compared
| Form | Source | Primary function | Half-life | Notes |
|---|---|---|---|---|
| Phylloquinone (K1) | Leafy greens, plant oils | Hepatic coagulation factor activation | 1–2 hours | The standard dietary K form; well absorbed with fat; limited extrahepatic distribution. Used in supplements and multivitamins as a general K source. |
| Menaquinone-4 (MK-4) | Animal tissues, synthesized from K1 | Bone and tissue-specific K-dependent protein activation; Japanese osteoporosis Rx (45 mg/day) | 1–4 hours | Short half-life but tissue-specific distribution. At pharmacologic doses (45 mg) shows bone benefits. See MK-4 page. |
| Menaquinone-7 (MK-7) | Natto (fermented soybeans), supplements | Bone (osteocalcin) and vascular (MGP) protein activation; cardiovascular calcification prevention | ~72 hours | Best-evidenced form for bone and cardiovascular outcomes at supplemental doses (90–200 µg/day). See MK-7 page. |
How much vitamin K1 should you take?
- Adequate Intake (AI): 90 µg/day (women); 120 µg/day (men) — applies to all vitamin K forms combined
- No RDA established — AI was set based on observed intakes in people with normal clotting
- No Tolerable Upper Intake Level established for healthy adults without anticoagulation — no toxicity documented from high dietary K1 or supplemental K1 in non-warfarin users
- Warfarin users: Consistent intake is the goal; sudden large changes in dietary or supplemental K1 will shift INR. Some anticoagulation clinics use low-dose supplemental K1 (100–150 µg/day) to stabilize INR variability
- If using K1 for bone/cardiovascular benefit: Consider K2 MK-7 instead — better tissue distribution and stronger clinical evidence at supplemental doses
Safety and side effects
Vitamin K1 from food or supplements has an excellent safety record in non-anticoagulated individuals. No UL has been established because adverse effects have not been identified.
- High dietary K1 intake from leafy greens does not cause thrombosis or other adverse effects in healthy people
- K1 administered intravenously at high doses (used to reverse over-anticoagulation) can cause anaphylactic reactions in rare cases — not relevant to oral supplementation
- No hepatotoxicity, endocrine disruption, or other systematic adverse effects documented
The only meaningful safety concern for K1 supplementation is the anticoagulant drug interaction detailed below.
Drug interactions — the warfarin connection
The vitamin K / warfarin interaction is one of the most important in clinical pharmacology:
- Warfarin mechanism: Warfarin inhibits vitamin K epoxide reductase (VKORC1), blocking the recycling of vitamin K epoxide back to reduced vitamin K needed for carboxylation reactions. The result is reduced activity of all vitamin K-dependent proteins — therapeutic anticoagulation for clotting prevention
- Vitamin K overcomes the block: Providing supplemental K1 (or K2) supplies reduced vitamin K substrate that can activate clotting factors despite warfarin's inhibition, raising INR toward normal (reducing anticoagulant effect)
- What warfarin patients should do:
- Maintain consistent daily vitamin K intake — do not dramatically change leafy green intake week to week
- Inform your anticoagulation prescriber before starting any vitamin K supplement
- Expect warfarin dose adjustment if K supplement is added or removed
- Monitor INR more frequently when changing vitamin K habits
- DOAC (direct oral anticoagulant) users — apixaban, rivaroxaban, dabigatran, edoxaban: these drugs do not work through the vitamin K pathway and do not interact with vitamin K supplements
Check our free interaction checker for additional combinations.
Who might benefit from vitamin K1 supplementation
| Clear indication for K1 supplementation | Better served by K2 MK-7 (see separate page) |
|---|---|
| People with fat malabsorption conditions (celiac, Crohn's, bariatric surgery) | Adults seeking bone mineral density support |
| As part of a general multivitamin at nutritional AI doses (90–120 µg) | Adults concerned about arterial calcification |
| Newborns (K1 injection at birth — medical procedure) | People supplementing vitamin D3 at >1,000 IU/day (K2 MK-7 is the preferred companion) |
| Those on long-term antibiotics with very poor diet (rare clinical scenario) | People with osteoporosis (K2 MK-4 at 45 mg or K2 MK-7 at 90–200 µg) |
Frequently asked questions
Does vitamin K1 help with osteoporosis?
K1 can carboxylate osteocalcin and thereby participate in bone mineralization, but because K1 is cleared from circulation rapidly and distributed primarily to the liver, its contribution to bone K-dependent protein activation is limited compared to K2. The RCT evidence for bone outcomes is substantially stronger for K2 MK-7 (90–200 µg/day) and MK-4 (45 mg/day) than for K1. If bone health is the goal, K2 MK-7 is the preferred supplement form.
Can too many leafy greens cause blood clots?
In healthy, non-anticoagulated adults: no. The body's clotting system has multiple regulation mechanisms, and high dietary K1 from leafy greens does not push healthy people into a pro-thrombotic state. In warfarin patients, high K1 intake will reduce the drug's anticoagulant effect and could increase clotting risk in the context of the condition being treated. This is a pharmacological interaction, not a toxicity of vitamin K itself.
Does vitamin K1 prevent calcification?
K1 does carboxylate MGP (matrix Gla protein, the vascular calcification inhibitor) in the liver, but because it distributes poorly to vascular smooth muscle cells, its calcification-prevention effect in arteries is less than that of K2 (MK-7 in particular, which reaches extrahepatic tissues). The Rotterdam Study and subsequent cardiovascular studies have found associations between dietary K2 (not K1) and reduced aortic calcification and cardiovascular events. For vascular calcification prevention, K2 MK-7 is recommended over K1.
Is vitamin K1 in multivitamins enough?
Most multivitamins contain 75–120 µg of K1, which meets or approaches the AI. This is adequate for meeting the basic nutritional requirement for clotting factor support. It is not equivalent to the 90–200 µg MK-7 studied for bone and cardiovascular outcomes — because K1 in a multi does not achieve the tissue distribution that K2 provides.
What foods are highest in vitamin K1?
Per 100 g cooked: kale ~817 µg, spinach ~888 µg, collard greens ~623 µg, Swiss chard ~327 µg, broccoli ~141 µg. Per tablespoon of oil: soybean oil ~25 µg, canola oil ~17 µg. A single serving of kale or spinach provides 7–10 times the daily AI. People who regularly eat leafy greens do not need supplemental K1 for nutritional purposes.
Related ingredients and articles
Vitamin K2 MK-7
The long-chain menaquinone with superior bone and cardiovascular evidence at supplemental doses.
Vitamin K2 MK-4
The short-chain menaquinone used as 45 mg/day Rx for osteoporosis in Japan.
Vitamin D3 + K2
Why D3 and K2 are the most scientifically coherent vitamin pair for calcium management.
Retinyl Palmitate (Vitamin A)
Another fat-soluble vitamin with overlapping absorption considerations and drug interactions.
Disclaimer: This information is for educational purposes only and should not replace medical advice. Always consult a qualified healthcare provider before starting any supplement, especially if you have a medical condition, are pregnant, or take prescription medications. These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.