| Type | Fat-soluble vitamin |
| Active Cmpd | Phylloquinone (K1), Menaquinones (K2; MK-4, MK-7) |
| Source | Leafy greens (K1), Fermented foods / natto (K2) |
| Dose Range | 100–570 mcg (dietary K1); 180–375 mcg (MK-7) |
| Half-life / Detection | Short (K1, MK-4); Prolonged circulation (detected up to 48h, MK-7) |
| Main Benefit | Blood coagulation, bone density, vascular health |
| Absorption | Variable (~16.5% from plants; enhanced with lipids) |
Vitamin K is a family of essential fat-soluble vitamins renowned for their critical roles in blood coagulation and calcium regulation. While historically recognized as a singular factor required for hepatic clotting factor synthesis, contemporary clinical science distinguishes between Vitamin K1 (phylloquinone) and Vitamin K2 (menaquinones), which exhibit distinct pharmacokinetics, tissue distribution, and extrahepatic physiological effects[1][2][3].
Aliases
Key points (high-level summary)
What people use it for
Vitamin K is a group of structurally related, fat-soluble compounds featuring a shared 2-methyl-1,4-naphthoquinone ring structure (the "menadione" core) but differing in the length and saturation of their lipophilic side chains[2:1][21].
The clinical utility of Vitamin K spans established hematological indications and evolving applications in skeletal and vascular health.
| Outcome / Goal | Effect* | Consistency** | Evidence quality | Trials*** | Notes (population, duration, dose) |
|---|---|---|---|---|---|
| Coagulation Function | High | High | Guidelines | Essential cofactor for clotting factors; standard for bleeding prevention and neonatal prophylaxis[4:2][5:2][23:2]. | |
| Warfarin Reversal | High | High | Guidelines | Intravenous K1 (slow infusion alongside clotting factors) is used for major bleeding, while oral K1 is recommended for asymptomatic patients with INR > 10[8:1][6:2][24][9:1][7:1][10:1]. | |
| Lumbar BMD Preservation | Moderate | High | 16+ RCTs | In Japanese osteoporosis trials, MK-4 monotherapy modestly increases lumbar spine BMD[11:3][12:2]. Low-dose MK-7 (180 mcg/day) preserved femoral neck BMD in one trial[13:2] but was neutral in postmenopausal osteopenia (Rønn 2021; 375 mcg/day)[14:1]. | |
| Fracture Risk Reduction | Moderate | Moderate | 10+ RCTs | Significant fracture reduction documented in Japanese cohorts with MK-4 monotherapy[11:4][12:3]. | |
| Osteocalcin Carboxylation | High | High | 12+ RCTs | Drastically reduces undercarboxylated osteocalcin (ucOC) in blood, indicating increased calcium-binding capacity[13:3][11:5][2:5]. | |
| MGP Carboxylation | High | High | 5+ RCTs | Markedly decreases dp-ucMGP (inactive MGP), validating systemic K2 bioavailability[17:3][16:3][25]. | |
| Vascular Calcification | High | High | 3+ RCTs | Large RCTs (AVADEC, Trevasc-HDK) showed neutral overall effects on calcification progression. Slowing of progression was only shown in subgroup analyses of high-risk patients (CAC >= 400 AU)[17:4][19:1][16:4][18:2]. | |
| Cardiovascular Events | Low | Moderate | RCTs / Cohort | Cohorts suggest inverse association with K2 intake, but RCTs show no consistent reduction in clinical CV events[1:1][18:3]. | |
| Glucose Metabolism | Moderate | Low | 7+ RCTs | Meta-analyses show minor improvements in fasting blood sugar and HOMA-IR with vitamin K supplementation[26]. | |
| All-Cause Mortality | Low | Low | Cohorts | Combined low D and K status is associated with higher all-cause mortality, but interventional trials of K supplementation alone do not show mortality benefits[18:4][27]. |
<effect e="d3p"></effect>) encode the specific outcomes.Vitamin K operates at the molecular level through a highly conserved recycling mechanism known as the Vitamin K Cycle[21:7][23:3].
[ Vitamin K Quinone ] <========== (VKORC1 Reductase) <========== [ Vitamin K 2,3-Epoxide ]
|| ^
(Quinone Reductase) |
|| |
\/ |
[ Vitamin K Hydroquinone (KH2) ] === (GGCX Carboxylase) ===> [ Vitamin K 2,3-Epoxide ]
|| ||
\/ \/
[ Precursor VKDPs ] =================> [ Carboxylated Active VKDPs ]
(e.g., Precursor Clotling Factors, (e.g., Functional/Mature Factors II/VII/IX/X,
Osteocalcin, MGP) Active Osteocalcin, Active MGP)
Vitamin K is biochemically indispensable for clotting. Without adequate GGCX activity, precursor clotting factors remain uncarboxylated (referred to as PIVKA, or Proteins Induced by Vitamin K Absence/Antagonism)[21:15][23:8]. This severely impairs their ability to bind calcium and localize to phospholipid membranes during the coagulation cascade, preventing the formation of Functional/Mature Clotting Factors and resulting in clinical hemorrhage[21:16][23:9].
While standard coagulation screening assays are key for identifying clinical deficits, more advanced tests are required to monitor subclinical extrahepatic deficiency:
In bone tissue, osteoblasts secrete osteocalcin, which requires GGCX-mediated carboxylation to bind to calcium-rich hydroxyapatite[13:5][21:17].
Arterial calcification is an active, cell-mediated process in which Matrix Gla Protein (MGP) acts as a local inhibitor once activated by -carboxylation[15:3].
In glucose metabolism, a systematic review and meta-analysis of randomized controlled trials (Qu 2023) demonstrated that vitamin K supplementation significantly reduces fasting blood sugar (FBS) and HOMA-IR, and is associated with a significantly reduced risk of developing type 2 diabetes[26:1]. Mechanistically, undercarboxylated osteocalcin (ucOC) has been investigated in experimental models as a potential metabolic regulator that interacts with the GPRC6A receptor to modulate glucose homeostasis, though clinical trials in humans to confirm causation remain scarce[29]. Similarly, subclinical microvascular calcification in the brain has been linked to age-related cognitive impairment; emerging reviews suggest K2 status may play a protective role in maintaining microvascular brain health, though direct clinical trials are lacking[30].
Vitamin K has an exceptionally favorable safety profile. Clinical trials using high doses have reported no serious adverse events or hypercoagulable side effects in healthy individuals in the absence of anticoagulant therapy, as hepatic carboxylation pathways are highly regulated [21:19][36].
At standard nutritional doses, side effects are indistinguishable from placebo. Systematic reviews of clinical trials of oral vitamin K2 demonstrate that adverse reactions do not differ significantly from placebo[37].
CLINICAL MANAGEMENT PRINCIPLE
Avoiding dietary Vitamin K entirely while taking warfarin makes the patient highly sensitive to minor dietary changes, causing dangerous INR spikes and drops. Maintaining a highly stable, consistent daily intake of Vitamin K (e.g., one consistent serving of green vegetables daily) under the supervision of a prescribing clinician is the safest approach for maintaining therapeutic anticoagulation.
Vitamin K is frequently combined with other micronutrients to target specific physiological synergies.
Vitamin K1 (phylloquinone) is found in plants, clears rapidly from the bloodstream, and is primarily utilized by the liver to activate blood-clotting factors. Vitamin K2 (menaquinones) is found in fermented foods and animal products. Forms like MK-7 circulate in the bloodstream for several days, allowing them to reach bone and blood vessels to activate calcium-regulating proteins like Osteocalcin and Matrix Gla Protein (MGP)[2:13][3:3][21:20].
No. Major clinical trials (such as the AVADEC and Trevasc-HDK trials) have found neutral results overall, with no significant slowing of arterial or valvular calcification progression in the general study populations[17:9][16:8][18:15]. Slowing of calcification progression has only been demonstrated in subgroup analyses of high-risk patients with high baseline coronary artery calcium scores (CAC >= 400 AU)[19:3]. There is no clinical evidence that Vitamin K2 can dissolve or reverse established calcified plaques[18:16].
Definitively yes if you are taking Direct Oral Anticoagulants (DOACs like Eliquis or Xarelto), which do not interfere with Vitamin K recycling. However, patients receiving Warfarin or other Vitamin K Antagonists (VKAs) must keep their Vitamin K intake highly consistent and only alter supplementation under direct clinical supervision to avoid destabilizing therapeutic anticoagulation[38:2][20:3].
Newborns are born with extremely low stores of Vitamin K because it does not cross the placenta easily, and their intestines lack the bacteria needed to synthesize it. Additionally, breast milk contains very low levels. Without a Vitamin K1 injection at birth, babies are at high risk for Vitamin K Deficiency Bleeding (VKDB), a condition that can cause life-threatening internal bleeding, including in the brain[4:5][5:5].
No. In healthy individuals who are not on anticoagulant therapy, high-dose Vitamin K supplementation (including MK-7) is associated with an excellent safety profile without risk of hypercoagulability or negative side effects, as hepatic carboxylation pathways are highly regulated[21:21].
This monograph was compiled by evaluating human clinical evidence across three hierarchical tiers of authority:
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