The leafy-green form of vitamin K, specialized for blood clotting.
Mechanisms, studies and evidence grades for each claim above.
Vitamin K has one known job: it's the cofactor for γ-glutamyl carboxylase, an enzyme that adds a second acid group to specific glutamate amino acids in certain proteins, turning them into Gla (γ-carboxyglutamate) residues. A Gla residue has two negative charges side by side, which make a pincer for calcium ions.1
The liver makes four clotting factors with a cluster of 9–12 Gla residues at one end: prothrombin (II), VII, IX and X, plus the anticoagulant proteins C and S. When the Gla residues are fully carboxylated, calcium bridges them to the negatively charged surface of activated platelets and damaged cells (see Calcium). The clotting enzymes gather right at the wound, and the clotting cascade speeds up enormously. Without carboxylation the factors are still made, but they can't bind calcium or reach that surface. They circulate as inactive "PIVKAs" (proteins induced by vitamin K absence), and blood clots slowly.1
The recycling loop and warfarin. Each carboxylation converts vitamin K into an epoxide. The enzyme VKORC1 recycles it back to the active form, so each vitamin K molecule is reused hundreds of times. That's why daily needs are only micrograms. Warfarin works by blocking VKORC1. Mutations in the VKORC1 gene explain both inherited warfarin resistance and much of the variation in warfarin dosing between people.2 It also explains the advice on the card above. A warfarin dose is balanced against your usual vitamin K intake, so big swings in greens shift your INR. Keeping intake steady matters more than keeping it low.
The clearest human evidence is in newborns. Little vitamin K crosses the placenta, breast milk is low in it and a newborn's gut has no bacteria yet, so babies are born with low K stores. A single 1 mg intramuscular dose at birth prevents classic vitamin K deficiency bleeding, a cause of bleeding into the gut and brain in the first week of life.3
↑ back to summaryK1 (phylloquinone) comes from leafy plants, where it is part of photosynthesis. After absorption it is carried in chylomicrons and mostly taken up by the liver, where the clotting factors are made. It leaves the blood within hours. K2 (menaquinones, mainly MK-4 and MK-7) lasts longer in circulation and reaches bone and blood vessel walls better (see Vitamin K2).1
The two aren't completely separate. Many tissues convert some dietary K1 into MK-4 themselves, using the enzyme UBIAD1.4 So leafy greens contribute to tissue K2 too. Getting K1 from greens absorbs better with some fat in the meal.
↑ back to summaryThe adequate intake is 90 mcg/day for women and 120 mcg/day for men. A single serving of cooked greens covers several days. No upper limit is set, because K1 from food isn't toxic. The only caution is the warfarin interaction above. Newer anticoagulants (apixaban, rivaroxaban, dabigatran) don't work through vitamin K and aren't affected by it.
In adults, deficiency is uncommon and usually comes from fat malabsorption, long courses of broad-spectrum antibiotics combined with poor intake, liver disease (where the factors can't be made anyway), or excess vitamin E, which interferes with vitamin K (see Vitamin E). Signs are easy bruising, nosebleeds, bleeding gums, heavy periods, blood in urine or stool, and a prolonged prothrombin time (INR).1 In newborns without prophylaxis it can cause life-threatening bleeding.
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