vitamin k (dihydrophylloquinone)

Vitamin K refers to a family of structurally related, fat‑soluble vitamins that play critical roles in blood clotting, bone health, and cellular functions. The principal form in plants is phylloquinone (vitamin K1), which is chemically known as dihydrophylloquinone. In addition to vitamin K1, the vitamin K family includes various forms of menaquinones (vitamin K2), which are mostly derived from bacterial synthesis and found in certain animal products and fermented foods. Dihydrophylloquinone specifically denotes the hydrogenated form of phylloquinone that exists in foods and supplements. Vitamin K1 is abundant in green leafy vegetables and is the predominant dietary form in most Western diets, while K2 forms differ in their side‑chain length (e.g., MK‑4, MK‑7) and have distinct tissue distribution and half‑lives. As a fat‑soluble vitamin, vitamin K is absorbed with dietary fats in the small intestine and transported in chylomicrons via lymphatic circulation to the liver and peripheral tissues. In the liver, it serves as a cofactor for the enzyme gamma‑glutamyl carboxylase, which catalyzes the carboxylation of glutamic acid residues on vitamin K‑dependent proteins. This post‑translational modification is essential for the biological activity of several clotting factors (II, VII, IX, X) and proteins involved in bone matrix formation, such as osteocalcin. Vitamin K was first identified through its role in coagulation; the 'K' stands for 'Koagulation,' the German spelling of 'coagulation.' Without adequate vitamin K, clotting is impaired, which historically manifested in hemorrhagic disease in newborns and adults with dietary insufficiency or malabsorption. In addition to its classical roles, emerging research suggests that vitamin K may support vascular health by activating proteins that inhibit calcification and may influence bone turnover beyond its role in osteocalcin production. While vitamin K status is often assessed indirectly through clotting measures such as prothrombin time, plasma concentrations of phylloquinone provide a biochemical marker of intake, with typical fasting levels in healthy adults varying widely. Because vitamin K is rapidly metabolized and stored in small amounts compared with other fat‑soluble vitamins, regular dietary intake is necessary to maintain adequate status. Overall, vitamin K (dihydrophylloquinone) is an essential micronutrient whose primary functions in hemostasis and skeletal health make it indispensable for life.

Vitamin K’s most well‑established function is enabling the post‑translational carboxylation of specific proteins essential for blood clotting. The gamma‑carboxyglutamate (Gla) residues formed in clotting factors II (prothrombin), VII, IX, and X enable these proteins to bind calcium ions, a step necessary for their cascade activation and effective hemostasis. Without vitamin K, these clotting factors remain inactive, leading to prolonged bleeding times and hemorrhagic complications. Beyond coagulation, vitamin K is integral to bone metabolism: it activates osteocalcin, a protein synthesized by osteoblasts that binds calcium in the bone matrix and supports mineralization. Observational studies have linked higher vitamin K intake with greater bone mineral density and lower fracture risk, although randomized controlled trials on supplementation yield mixed results. Vitamin K also activates matrix Gla‑protein (MGP), a potent inhibitor of vascular calcification, suggesting a possible role in cardiovascular health. Some observational research indicates that diets rich in vitamin K are associated with reduced arterial calcification, although definitive evidence for supplementation is still emerging. Additional research has examined vitamin K’s role in metabolic health and inflammation, with some studies showing modest associations with insulin sensitivity and inflammatory markers. Vitamin K also participates in the regulation of cell growth and apoptosis, further implicating it in potential health effects beyond classic roles. From a mechanistic perspective, vitamin K’s benefits derive from its function as an enzymatic cofactor for gamma‑glutamyl carboxylase. This enzyme requires the reduced form of vitamin K to carboxylate specific glutamate residues, forming Gla residues necessary for calcium binding. These Gla proteins are not only critical in hemostasis but are also expressed in bone, cartilage, and vascular tissues. In bone, insufficient carboxylation may compromise matrix quality, contributing to bone fragility over time. While definitive clinical recommendations for vitamin K supplementation to prevent osteoporosis or cardiovascular disease remain unsettled, current evidence supports an important role for dietary vitamin K in maintaining normal physiological processes. Ensuring adequate intake through diet aligns with observational evidence linking high vitamin K diets to better bone health outcomes and potentially lower cardiovascular risk.

The Food and Nutrition Board at the Institute of Medicine has established Adequate Intake (AI) levels for vitamin K due to insufficient data to derive a Recommended Dietary Allowance (RDA). For infants 0–6 months, AI is 2.0 mcg/day, increasing slightly to 2.5 mcg/day by 7–12 months. Children aged 1–3 years require 30 mcg/day, ages 4–8 years need 55 mcg/day, and ages 9–13 years need 60 mcg/day. Adolescents aged 14–18 years have an AI of 75 mcg/day. Adult males (19+ years) generally have an AI of 120 mcg/day, while adult females have an AI of 90 mcg/day, including during pregnancy and lactation. These values reflect usual intakes associated with normal clotting function in healthy populations. Factors that can influence vitamin K needs include medications such as anticoagulants that impact vitamin K metabolism, conditions affecting fat absorption (e.g., cholestatic liver disease, cystic fibrosis), and genetic variations in enzymes involved in vitamin K recycling. Because vitamin K is fat‑soluble, its absorption improves with dietary fat; therefore, very low‑fat diets may modestly reduce bioavailability. There is no established upper intake limit for vitamin K due to the lack of reported adverse effects at high intakes in healthy individuals, but consistent intake is important for people on vitamin K‑antagonist therapies to maintain stable anticoagulant effects.

Vitamin K deficiency is uncommon in healthy adults because of widespread dietary sources and endogenous production of menaquinones by gut bacteria. However, deficiency can occur in newborns, individuals with fat malabsorption disorders, and those taking medications that interfere with vitamin K metabolism. The hallmark sign of vitamin K deficiency is impaired blood clotting, which can manifest as easy bruising, mucosal bleeding (e.g., nosebleeds, bleeding gums), heavy menstrual bleeding, and prolonged bleeding from wounds. In severe deficiency, bleeding may occur internally, including gastrointestinal bleeding or hematuria, and in newborns, life‑threatening intracranial hemorrhage can occur if prophylactic vitamin K is not administered at birth. Laboratory evidence of deficiency includes prolonged prothrombin time (PT) and elevated international normalized ratio (INR), reflecting impaired synthesis of vitamin K‑dependent clotting factors. Chronic deficiency may also affect bone health over time, potentially reducing bone mineral density and increasing fracture risk. Conditions that increase risk include cystic fibrosis, celiac disease, inflammatory bowel disease, short bowel syndrome, and cholestatic liver disease, where fat absorption is compromised. Certain antibiotics and antiseizure medications may also interfere with vitamin K status by reducing gut flora or altering metabolism. For most adult populations without these risk factors, dietary vitamin K intake from a variety of foods prevents clinically significant deficiency.

Foods richest in vitamin K (particularly phylloquinone/K1) are dark leafy green vegetables such as spinach, collard greens, kale, beet greens, and mustard greens. Cruciferous vegetables such as broccoli and Brussels sprouts also provide substantial vitamin K. Fermented foods like natto are exceptionally high in menaquinones (vitamin K2), while certain animal products like chicken and ground beef contain modest amounts of vitamin K2 (MK‑4). Oils, such as soybean and canola oil, and some nuts and seeds also contribute smaller amounts. Pairing vitamin K‑rich vegetables with dietary fats enhances absorption due to the vitamin’s fat‑soluble nature. Regular consumption of a diversity of these foods ensures adequate intake and supports consistent levels for physiologic processes.

Vitamin K absorption depends on its fat solubility; it is incorporated into micelles with dietary fat and bile salts, then absorbed by enterocytes in the small intestine and transported via chylomicrons. Factors impairing fat absorption (e.g., cholestatic liver disease) reduce bioavailability. Long‑chain menaquinones from fermented foods may have different absorption kinetics and longer half‑lives than phylloquinone.

Individuals with malabsorption disorders or on chronic antibiotics may require supplementation; otherwise most people meet needs via diet.

No UL is established; excess intake has not been shown to cause adverse effects in healthy individuals.

Vitamin K interacts significantly with vitamin K‑antagonist anticoagulants like warfarin; consistent intake is essential to maintain therapeutic INR.

Common Forms: phylloquinone (K1), menaquinone‑7 (K2)

Typical Doses: Supplement doses vary; consult clinician

When to Take: with meals containing fat for absorption

Best Form: menaquinone‑7 for longer half‑life

⚠️ Interactions: warfarin (anticoagulant)