Vitamin K1 (Phylloquinone): The Complete Supplement Guide

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Overview

The Basics

Vitamin K1, also known as phylloquinone, is the main form of vitamin K found in food. It is made by plants, and the richest sources are dark green leafy vegetables like kale, spinach, and collard greens. The "K" in its name comes from the Danish word "koagulation," reflecting the vitamin's most important and best-understood role: helping your blood clot properly.

Without enough vitamin K1, your body cannot make several of the proteins needed for blood to clot normally. This is why newborn babies receive a vitamin K injection at birth, as they are born with very low levels and are vulnerable to a rare but potentially fatal condition called Vitamin K Deficiency Bleeding (VKDB). In adults, true deficiency is exceptionally rare, because green vegetables are widely consumed and gut bacteria also produce some vitamin K.

Beyond clotting, vitamin K1 plays a supporting role in bone health. It is required for the activation of osteocalcin, a protein involved in bone mineralization. It also helps activate Matrix Gla Protein (MGP), which is believed to help prevent calcium from depositing in arteries and other soft tissues. These "extrahepatic" functions are an active area of research, though the evidence for K1 specifically (as opposed to K2) in these roles is still emerging [1][2].

Vitamin K1 is the predominant form of vitamin K in the Western diet, accounting for roughly 75-90% of total vitamin K intake. Despite this, your body retains very little of it at any given time. It is rapidly metabolized and excreted, which is unusual for a fat-soluble vitamin. This rapid turnover means your body relies on regular dietary intake rather than long-term storage [1].

The Science

Phylloquinone (2-methyl-3-phytyl-1,4-naphthoquinone) is a fat-soluble vitamin synthesized by plants during photosynthesis, where it functions as an electron carrier in Photosystem I. It derives its name from its phytyl side chain (identical to the side chain of chlorophyll) attached to the 2-methyl-1,4-naphthoquinone ring that defines the vitamin K family [1][2].

Phylloquinone serves as an essential cofactor for the enzyme gamma-glutamyl carboxylase, which catalyzes the post-translational carboxylation of specific glutamic acid (Glu) residues to gamma-carboxyglutamic acid (Gla) residues in a group of proteins collectively designated as vitamin K-dependent proteins (VKDPs). At least 17 VKDPs have been identified in humans. Seven of these are coagulation factors synthesized in the liver (factors II/prothrombin, VII, IX, X, and proteins C, S, and Z), while the remainder include extrahepatic proteins such as osteocalcin (bone Gla protein), Matrix Gla Protein (MGP), Gas6, and Gla-rich protein (GRP) [1][2][3].

The body maintains vitamin K homeostasis through the vitamin K cycle, an oxidation-reduction loop that allows each molecule of vitamin K to be recycled and reused multiple times. In this cycle, vitamin K hydroquinone (the reduced, active form) serves as the electron donor for gamma-carboxylation, yielding vitamin K 2,3-epoxide (the oxidized form). The enzyme vitamin K epoxide reductase (VKOR) then regenerates vitamin K quinone from the epoxide, which can be re-reduced to hydroquinone. The anticoagulant drug warfarin inhibits VKOR, effectively blocking vitamin K recycling and creating a functional vitamin K deficiency in coagulation proteins [1][2].

Despite being classified as fat-soluble, phylloquinone has uniquely rapid metabolic turnover. The body retains only approximately 30-40% of an oral dose, with 20% excreted renally and 40-50% excreted in feces via bile. This results in lower tissue stores relative to other fat-soluble vitamins (A, D, E), making consistent dietary intake important [1].

Chemical & Nutritional Identity

Phylloquinone is a yellow, viscous oil at room temperature that is practically insoluble in water but soluble in organic solvents and dietary fats. It is stable to heat during normal cooking but sensitive to light and strongly alkaline conditions. All naturally occurring phylloquinone is in the trans configuration; the cis isomer has significantly reduced biological activity (approximately 1-10% of the trans form in animal studies) [1][3].

The Food and Nutrition Board at the Institute of Medicine (now NASEM) established Adequate Intakes (AI) rather than Recommended Dietary Allowances (RDA) for vitamin K because insufficient data existed to calculate an Estimated Average Requirement (EAR). The AI values are based on median phylloquinone intakes from NHANES data in healthy populations. Notably, no Tolerable Upper Intake Level (UL) has been set because no adverse effects from high-dose vitamin K1 consumption have been reported in any human or animal study [1][3].

Mechanism of Action

The Basics

Vitamin K1 works behind the scenes as a helper molecule that activates certain proteins in your body. Think of these proteins as tools that need to be "turned on" before they can do their job. Without vitamin K1, they sit idle.

The most critical of these proteins are the clotting factors made in your liver. When you cut yourself, a cascade of these proteins activates in sequence to form a blood clot and stop the bleeding. Four of the essential clotting factors (II, VII, IX, and X) require vitamin K1 to become functional. This is why vitamin K deficiency causes abnormal bleeding and why the blood-thinning drug warfarin works by intentionally blocking vitamin K recycling.

Your body is efficient with its vitamin K1 supply. Rather than using each molecule once and discarding it, the body has a recycling system (the vitamin K cycle) that regenerates each vitamin K1 molecule so it can be used again and again. This is necessary because, unlike other fat-soluble vitamins, your body does not store large amounts of vitamin K1 [1][2].

Beyond blood clotting, vitamin K1 helps activate proteins involved in bone health (osteocalcin) and vascular health (Matrix Gla Protein). Osteocalcin needs to be "carboxylated" (activated by vitamin K) before it can bind calcium and contribute to bone mineralization. Matrix Gla Protein, once activated, helps prevent calcium from accumulating in blood vessel walls, a process that contributes to arterial stiffness and cardiovascular disease [1][2][3].

The Science

Phylloquinone functions exclusively as a cofactor for the microsomal enzyme gamma-glutamyl carboxylase (GGCX), which catalyzes the conversion of specific glutamic acid (Glu) residues to gamma-carboxyglutamic acid (Gla) residues in VKDPs. This carboxylation introduces a second carboxyl group that enables the Gla residues to chelate calcium ions (Ca²⁺), a property essential for the biological activity of all VKDPs [1][2].

Coagulation VKDPs (hepatic):

• Procoagulant factors: Factor II (prothrombin), Factor VII, Factor IX, Factor X. These form the core of the coagulation cascade, with prothrombin being the direct precursor to thrombin, the enzyme that converts fibrinogen to fibrin for clot formation [1].
• Anticoagulant factors: Protein C, Protein S, Protein Z. These provide negative feedback regulation of coagulation, preventing excessive clot formation [1][2].

Extrahepatic VKDPs:

• Osteocalcin (bone Gla protein): Synthesized by osteoblasts; once carboxylated, it binds hydroxyapatite in the bone matrix. Undercarboxylated osteocalcin (ucOC) is used as a functional marker of vitamin K status [2][3].
• Matrix Gla Protein (MGP): Expressed in vascular smooth muscle cells, chondrocytes, and other soft tissues. Carboxylated MGP is a potent inhibitor of vascular and soft-tissue calcification. Uncarboxylated (inactive) MGP has been associated with increased vascular calcification risk [2][3].
• Gas6 (Growth arrest-specific 6): Expressed in the nervous system; involved in cell survival, proliferation, migration, and adhesion through TAM receptor signaling [3].

The Vitamin K Cycle:
The gamma-carboxylation reaction requires the reduced form of vitamin K (vitamin K hydroquinone, KH₂). During carboxylation, KH₂ is oxidized to vitamin K 2,3-epoxide (KO). The enzyme vitamin K epoxide reductase complex subunit 1 (VKORC1) reduces KO back to vitamin K quinone (K), which is subsequently reduced to KH₂ by either VKORC1 or NAD(P)H-dependent quinone oxidoreductase 1 (NQO1). Warfarin inhibits VKORC1, blocking both reduction steps and depleting KH₂ [1][2][3].

Phylloquinone to MK-4 Conversion:
The body converts a fraction of dietary phylloquinone to menaquinone-4 (MK-4) via the enzyme UbiA prenyltransferase domain-containing protein 1 (UBIAD1). This conversion occurs in extrahepatic tissues (brain, kidney, pancreas, salivary glands) and is independent of gut bacterial action. The physiological significance of this tissue-specific MK-4 production is not yet fully understood [1][3].

Dietary & Natural Sources

Phylloquinone is synthesized by plants as part of the photosynthetic apparatus. Green leafy vegetables are by far the richest dietary sources, as phylloquinone concentrations correlate with chlorophyll content. Certain vegetable oils, particularly soybean and canola oil, are also significant sources.

Top Food Sources (phylloquinone content per serving):

A single cup of raw kale provides over four times the daily AI. Even moderate consumption of green vegetables easily meets the recommended intake.

The most common sources of vitamin K in the American diet are spinach, broccoli, iceberg lettuce, soybean oil, and canola oil. Meat, dairy, and eggs contain low levels of phylloquinone but provide modest amounts of menaquinones (K2) [1].

Vitamin K is also produced by bacteria in the human large intestine, primarily as long-chain menaquinones (MK-7 through MK-13). The extent to which bacterially produced vitamin K contributes to overall vitamin K status remains uncertain, though it is believed to provide at least a partial contribution [1][3].

Absorption & Bioavailability

The Basics

How well your body absorbs vitamin K1 depends heavily on whether you are getting it from food or from a supplement. In supplement form (free phylloquinone), absorption is quite efficient, around 80%. From foods, particularly green leafy vegetables, absorption is dramatically lower, typically only 4% to 17% of what you eat.

The reason for this difference is that phylloquinone in plants is tightly locked inside structures called chloroplasts. Your digestive system has to break down the plant cell walls and liberate the vitamin before it can be absorbed. Cooking, chopping, and chewing help, but they only partially release the bound phylloquinone. Eating your greens with some dietary fat (olive oil on a salad, butter on steamed broccoli) further improves absorption, because vitamin K1 is fat-soluble and needs to dissolve into dietary fat for efficient uptake [1].

Once absorbed, vitamin K1 is packaged into particles called chylomicrons and transported through the lymphatic system to the liver. From there, it is repackaged into very low-density lipoproteins (VLDL) for distribution to other tissues. Compared to vitamins A, D, and E, your body stores surprisingly little vitamin K1. It is rapidly metabolized and cleared, with about 60-70% of an absorbed dose excreted within hours to days. This means that, unlike vitamin D, you cannot "stock up" on vitamin K1 for weeks at a time. Regular intake is important [1].

The Science

Dietary phylloquinone is absorbed in the small intestine via a process that requires bile salts, pancreatic lipase, and dietary fat for micellar solubilization. Absorption occurs primarily through incorporation into mixed micelles, followed by uptake by enterocytes. The mechanism involves both passive diffusion and carrier-mediated transport, with the scavenger receptor class B type 1 (SR-B1) and Niemann-Pick C1-Like 1 (NPC1L1) transporters implicated [1][3].

Bioavailability by source:

• Supplement form (free phylloquinone): Approximately 80% bioavailability [1]
• Oils (soybean, canola, olive): Higher bioavailability than vegetables, as phylloquinone is already dissolved in a lipid matrix [1]
• Green leafy vegetables: 4-17% bioavailability relative to supplement form. Phylloquinone is bound to chloroplast thylakoid membranes, requiring mechanical and enzymatic disruption for release [1]
• Phytonadione (synthetic K1): Bioequivalent to natural phylloquinone in supplement form [1]

Post-absorptive pharmacokinetics:
Following absorption, phylloquinone is incorporated into chylomicrons and enters the circulation via the lymphatic system. Hepatic uptake occurs through chylomicron remnant receptors. The liver is the primary site of vitamin K1 storage, though total body stores are small relative to other fat-soluble vitamins. Phylloquinone is redistributed from the liver in VLDL and LDL particles [1].

The circulating half-life of phylloquinone is relatively short (1.5-3 hours for the initial distribution phase). In healthy adults, fasting plasma phylloquinone concentrations range from 0.29 to 2.64 nmol/L. Approximately 30-40% of an oral dose is retained; the remainder is excreted via urine (20%) and bile/feces (40-50%) [1].

Factors affecting absorption:

• Fat co-ingestion markedly improves absorption from food sources
• Bile acid sequestrants (cholestyramine, colestipol) reduce absorption
• Orlistat (lipase inhibitor) reduces fat-soluble vitamin absorption
• Mineral oil use may impair absorption
• MK-7 (a K2 form) has a substantially longer half-life than K1, maintaining higher steady-state levels with the same dosing frequency [1][3]

Understanding how your body absorbs a supplement is only useful if you can act on it. Doserly lets you log exactly when you take each form, whether it's a capsule with a meal, a sublingual tablet on an empty stomach, or a liquid taken with a cofactor, so you can see how timing and form choices affect your results over time.

The app also tracks cofactor pairings that influence absorption. If a supplement works better alongside vitamin C, fat, or black pepper extract, Doserly reminds you to take them together and logs both. Over weeks, your personal data reveals whether those pairing strategies are translating into measurable differences in the biomarkers you're tracking.

Research & Clinical Evidence

The Basics

The evidence behind vitamin K1 supplementation falls into two main areas: bone health and cardiovascular health. For both, the picture is nuanced.

For bone health, vitamin K1 is clearly involved in activating osteocalcin, the protein that helps bind calcium into bone. When people have low vitamin K status, they have higher levels of "undercarboxylated" (inactive) osteocalcin, which some studies associate with lower bone mineral density and higher fracture risk. Supplementing with vitamin K1 reliably reduces undercarboxylated osteocalcin levels. However, whether this translates into meaningfully stronger bones or fewer fractures is where the evidence becomes less clear. Several randomized controlled trials of K1 supplementation at doses ranging from 200 to 5,000 mcg/day over 12 to 36 months have shown mixed results on bone mineral density, with most finding no significant effect [3].

For cardiovascular health, the story diverges between K1 and K2. Large observational studies, including the Rotterdam Study, found that higher intake of vitamin K2 (menaquinones) was associated with reduced coronary calcification and lower cardiovascular mortality. However, phylloquinone (K1) intake showed no significant association with cardiovascular outcomes in the same studies. One clinical trial did find that phylloquinone supplementation (500 mcg/day for 3 years) slowed coronary artery calcification progression in adherent participants, but the overall intention-to-treat analysis was not significant [1][3].

The Science

Bone health evidence:
The carboxylation of osteocalcin by vitamin K is well-established biochemically. Supplementation with phylloquinone at doses of 200-5,000 mcg/day consistently reduces serum undercarboxylated osteocalcin (ucOC) in clinical trials [3]. However, the clinical translation to BMD and fracture outcomes has been disappointing for K1 specifically:

• A review of five RCTs found that phylloquinone supplementation decreased ucOC in all five studies but improved BMD in only one (Braam et al., 2003: 1,000 mcg/day K1 + minerals + vitamin D reduced femoral neck BMD loss over 3 years in postmenopausal women) [3].
• The 2006 Cockayne meta-analysis of 13 RCTs found improved BMD in 12 and reduced fractures in 7, but nearly all positive fracture data came from MK-4 trials at 45 mg/day, not K1 trials [1].
• Binkley et al. (2009): 381 postmenopausal women received 1 mg K1, 45 mg MK-4, or placebo daily for 12 months (all with calcium and vitamin D). Both K groups reduced ucOC but neither improved BMD versus placebo [1].

The overall evidence suggests that K1 supplementation reliably improves biochemical markers of vitamin K status (reducing ucOC) but has limited evidence for improving clinical bone outcomes (BMD, fracture reduction). The positive fracture prevention data is primarily associated with MK-4 at pharmacological doses (45 mg/day), which is used therapeutically for osteoporosis in Japan and other Asian countries [1][3].

Cardiovascular evidence:

• Rotterdam Study (n=4,807): Dietary menaquinone intake (upper tertile >32.7 mcg/day) was associated with 57% lower coronary heart disease mortality. Phylloquinone intake showed no association [1].
• Beulens et al. (2009): Dietary menaquinone intake was inversely associated with coronary calcification in postmenopausal women. Phylloquinone was not associated [1].
• Shea et al. (2009): 388 older adults, 3-year RCT. Phylloquinone 500 mcg/day with multivitamin, calcium, and vitamin D vs. control. No significant difference in coronary artery calcification overall, but adherent participants in the K1 group had less calcification progression [1].

EFSA health claim: The European Food Safety Authority has approved a health claim that vitamin K contributes to "maintenance of normal bone" and "normal blood coagulation." The FDA has not authorized a health claim for vitamin K in the United States [1].

Evidence & Effectiveness Matrix

Evidence Strength scoring basis: Derived from quality, volume, and consistency of clinical evidence from KB sources. Bone health scores moderate due to strong biochemical data (ucOC reduction) but weak clinical outcome data (BMD, fractures) for K1 specifically. Heart health scores low-moderate because observational data favors K2 over K1, and the single K1 RCT was mixed. Side effect burden scores very strong because multiple large studies and the IOM review found zero adverse effects.

Community-Reported Effectiveness scoring basis: Derived from sentiment analysis. Vitamin K1 is rarely discussed as a standalone supplement in community forums; most vitamin K discussion centers on K2 (MK-4, MK-7). Community data for K1 specifically is thin.

Categories Not Scored: Fat Loss, Muscle Growth, Weight Management, Appetite & Satiety, Food Noise, Sleep Quality, Memory & Cognition, Anxiety, Stress Tolerance, Motivation & Drive, Emotional Aliveness, Emotional Regulation, Mood & Wellbeing, Libido, Sexual Function, Joint Health, Inflammation, Pain Management, Recovery & Healing, Physical Performance, Gut Health, Digestive Comfort, Nausea & GI Tolerance, Skin Health, Hair Health, Blood Pressure, Heart Rate & Palpitations, Hormonal Symptoms, Temperature Regulation, Fluid Retention, Body Image, Immune Function, Longevity & Neuroprotection, Cravings & Impulse Control, Social Connection, Treatment Adherence, Withdrawal Symptoms, Daily Functioning

Benefits

The Basics

The primary, well-established benefit of vitamin K1 is supporting normal blood clotting. This is not a theoretical benefit; it is the reason vitamin K was discovered and the basis for its name. Without adequate K1 intake, your blood cannot form clots properly, leading to excessive bleeding from cuts, surgical wounds, or internal injuries.

The second established benefit is the maintenance of normal bone. Vitamin K1 activates osteocalcin, a protein that helps incorporate calcium into the bone matrix. While clinical trials of K1 supplementation for bone mineral density have shown mixed results, the underlying biochemistry is clear, and regulatory bodies like EFSA recognize the relationship between vitamin K intake and normal bone maintenance.

A potential benefit, still under investigation, is vascular health. Vitamin K1 activates Matrix Gla Protein, which inhibits soft tissue calcification. However, the cardiovascular evidence currently favors vitamin K2 (menaquinones) over K1 for this outcome [1][2][3].

The Science

Established benefits (strong evidence):

1. Hemostasis (blood coagulation): Vitamin K1 is an essential cofactor for the hepatic synthesis of coagulation factors II, VII, IX, and X, as well as anticoagulant proteins C, S, and Z. This function is indispensable and is the basis for the clinical use of phytonadione in treating vitamin K deficiency bleeding and reversing warfarin overdose [1][2].
2. Neonatal hemorrhagic disease prevention: Prophylactic intramuscular injection of phytonadione (0.5-1 mg) at birth is the global standard of care for preventing Vitamin K Deficiency Bleeding (VKDB), which can cause life-threatening intracranial hemorrhage [1].

Probable benefits (moderate evidence):
3. Bone metabolism support: Phylloquinone is required for the gamma-carboxylation of osteocalcin. Supplementation reduces undercarboxylated osteocalcin levels, indicating improved functional vitamin K status in bone tissue. Clinical bone density outcomes remain inconclusive for K1 specifically [1][3].

Potential benefits (limited/emerging evidence):
4. Vascular calcification inhibition: Via carboxylation of MGP. Observational associations primarily support K2, not K1, for this outcome [1][3].
5. Insulin sensitivity: Limited preliminary data suggest vitamin K status may influence glucose metabolism via uncarboxylated osteocalcin's endocrine function, but evidence is insufficient for any clinical recommendation [3].

Side Effects & Safety

The Basics

Vitamin K1 has an exceptionally strong safety record. The Institute of Medicine reviewed all available evidence and concluded: "No adverse effects associated with vitamin K consumption from food or supplements have been reported in humans or animals." Because of this, no Tolerable Upper Intake Level (UL) has been established. This is not because the evidence has been insufficient to study, but because no toxicity has been found at any dose tested.

The one major safety concern with vitamin K1 is its interaction with warfarin and other vitamin K antagonist anticoagulants. If you take warfarin, you must maintain a consistent vitamin K intake from day to day. Sudden increases in vitamin K intake can reduce warfarin's blood-thinning effect, while sudden decreases can enhance it. This does not mean you need to avoid vitamin K, but rather that you need to keep your intake stable and discuss any changes with your healthcare provider [1].

Phytonadione injection (the synthetic form used in clinical settings) carries distinct safety considerations that do not apply to oral supplements. Intravenous phytonadione has been associated with rare but serious anaphylactoid reactions, which is why the injectable form carries specific warnings. Oral vitamin K1 supplements do not carry this risk [1].

The Science

Toxicity profile:
No adverse effects have been documented for phylloquinone at any oral dose in humans or animals. The FNB determined that the available data were insufficient to derive a UL not because of uncertainty about safety, but because no ceiling of safe intake has been identified. Studies have used phylloquinone at doses up to 10 mg/day (10,000 mcg/day, approximately 80 times the AI) without reported adverse effects [1][3].

Drug interactions (critical):

• Warfarin and vitamin K antagonists (VKAs): Phylloquinone directly counteracts the mechanism of action of warfarin by providing substrate for VKORC1, the enzyme warfarin inhibits. Fluctuations in vitamin K intake can destabilize INR (International Normalized Ratio) and increase the risk of either bleeding (too little K) or thrombosis (too much K). Patients on VKAs require consistent daily vitamin K intake and should not initiate or modify supplementation without medical supervision [1][3].
• Antibiotics (especially cephalosporins): Prolonged antibiotic use may reduce vitamin K status by destroying gut bacteria that produce menaquinones and, in some cases, by directly inhibiting VKORC1 [1].
• Bile acid sequestrants (cholestyramine, colestipol): May reduce absorption of fat-soluble vitamins including K1 [1].
• Orlistat: Reduces dietary fat absorption, potentially impairing K1 absorption [1].

Special populations:

• Individuals with liver disease may have impaired vitamin K metabolism
• Patients with fat malabsorption syndromes (celiac disease, cystic fibrosis, short bowel syndrome, inflammatory bowel disease) may require supplementation
• Bariatric surgery patients may have reduced vitamin K status [1]

Knowing the possible side effects is the first step. Catching them early in your own experience is what keeps a supplement routine safe. Doserly lets you log any symptoms as they arise, tagging them with severity, timing relative to your dose, and whether they resolve on their own or persist.

The app's interaction checker cross-references everything in your stack, supplements and medications alike, flagging known interactions before they become a problem. It also monitors your total intake against established upper limits, alerting you if your combined sources of a nutrient are approaching thresholds where risk increases. Think of it as a safety net that works quietly in the background while you focus on the benefits.

Dosing & Usage

The Basics

The Adequate Intake (AI) for vitamin K1 is 120 mcg per day for adult men and 90 mcg per day for adult women. These values were set based on the median intake of healthy Americans, not on dose-response studies, so they represent "enough to prevent deficiency" rather than "optimal for all health outcomes."

Most people who eat green vegetables regularly already meet or exceed the AI through diet alone. A single cup of raw kale delivers over 500 mcg, and a half cup of cooked broccoli provides about 110 mcg. If you eat salads, cooked greens, or use soybean or canola oil regularly, you are likely getting adequate vitamin K1 without supplementation.

If you do choose to supplement, the doses that have been studied in clinical trials for bone health outcomes range from 200 mcg to 5,000 mcg per day (0.2-5 mg/day) of phylloquinone. The higher end of this range (1,000-5,000 mcg/day) has been used in research examining osteocalcin carboxylation and bone mineral density [2][3].

There is no established maximum safe dose. No UL has been set because no toxicity has ever been reported. However, the absence of a UL does not automatically mean mega-dosing is beneficial. The lack of consistent clinical benefit for K1 at high supplemental doses, particularly for bone outcomes, suggests that more is not necessarily better [1][3].

The Science

Adequate Intake (AI) by age group:

Supplemental dose ranges studied:

• Phylloquinone (K1): 100-10,000 mcg/day (0.1-10 mg/day)
• Doses of 100-5,000 mcg/day have been found to improve markers of carboxylation (reduce ucOC) [2]
• The bone health RCTs used 200-5,000 mcg/day for 12-36 months [3]

Population-level intake data (NHANES 2011-2012):

• Average daily vitamin K intake from foods: 122 mcg for women, 138 mcg for men
• With supplements included: 164 mcg for women, 182 mcg for men
• Approximately one-third of the U.S. population has vitamin K intake below the AI [1]

Clinical notes:

• Multivitamin/mineral supplements typically contain less than 75% of the DV for vitamin K (under 90 mcg) [1]
• Standalone vitamin K supplements range from 100 mcg to over 4,000 mcg per dose [1]
• The FNB based AI values on intakes associated with normal prothrombin time, which may not reflect the intake needed for optimal extrahepatic VKDP carboxylation [3]

Getting the dose right matters more than most people realize. Too little may be ineffective, too much wastes money or introduces risk, and inconsistency undermines both. Doserly tracks every dose you take, across every form, giving you a clear record of what you're actually consuming versus what you planned.

The app helps you compare RDA recommendations against therapeutic ranges discussed in the research, so you can see exactly where your intake falls. If you switch forms, say from a standard capsule to a liposomal liquid, Doserly adjusts your tracking to account for different bioavailabilities. Pair that with smart reminders that keep your timing consistent, and the precision that makes a real difference in outcomes becomes effortless.

What to Expect (Onset & Timeline)

Vitamin K1 is not a supplement where most people notice subjective effects. Unlike magnesium (which can improve sleep within days) or caffeine (which works within minutes), vitamin K1 operates silently in the background, supporting coagulation and protein activation processes that you do not feel.

Biochemical changes: Supplementation with phylloquinone reduces undercarboxylated osteocalcin levels within 2-4 weeks. Coagulation parameters (prothrombin time) respond to vitamin K status changes within days, but these changes are only clinically relevant in deficiency states or in individuals on anticoagulant therapy [1][3].

Bone health outcomes: The clinical trials that showed any positive bone outcomes used supplementation periods of 12-36 months. Bone metabolism is a slow process, and any effects of vitamin K1 on bone density would develop over months to years, not days or weeks [3].

Deficiency correction: In cases of clinical vitamin K deficiency (prolonged prothrombin time due to malabsorption or medication), oral phytonadione can begin normalizing clotting parameters within 6-12 hours, with full correction typically within 24-48 hours [1].

What most people experience: For the majority of healthy adults who supplement with vitamin K1, there are no perceptible changes in how they feel. The benefits are preventive and subclinical rather than immediately noticeable. The few community reports of subjective effects (mental clarity, energy) are isolated and not supported by clinical evidence.

Interactions & Compatibility

SYNERGISTIC

CAUTION / AVOID

How to Take / Administration Guide

Timing: Take with any meal that contains dietary fat. There is no strong evidence for morning versus evening preference. Consistency of timing matters more for individuals on warfarin than for the general population.

With food: Yes, always. Vitamin K1 is fat-soluble and requires dietary fat for optimal absorption. Taking it on an empty stomach reduces absorption significantly.

Form selection:

• Phylloquinone (natural K1): The standard supplemental form. Well-absorbed in free form (~80%).
• Phytonadione (synthetic K1): Bioequivalent to natural phylloquinone. Used in clinical/pharmaceutical settings.
• Combination K1+K2 products: Many supplements combine K1 with K2 (MK-4 and/or MK-7) for broad vitamin K coverage.

Stacking guidance:

• Safe and commonly stacked with vitamin D3 and calcium for bone health support
• Often included in multivitamin/mineral supplements at sub-AI doses
• Can be taken at the same time as vitamin D; they are absorbed in different intestinal regions and do not compete at supplemental doses

Cycling/breaks: Not required. Vitamin K1 has no established toxicity, no known tolerance development, and no withdrawal effects. Consistent daily intake is preferred, especially for individuals concerned about extrahepatic VKDP carboxylation.

Special considerations:

• If on warfarin or any vitamin K antagonist: do NOT start, stop, or change vitamin K supplementation without direct consultation with your prescribing physician
• If you have fat malabsorption (celiac, cystic fibrosis, IBD, post-bariatric): discuss vitamin K supplementation with your healthcare provider, as oral absorption may be impaired

Choosing a Quality Product

When selecting a vitamin K1 supplement, consider the following quality markers:

Form matters:

• Look for supplements listing "phylloquinone" or "phytonadione" as the vitamin K1 form
• Some supplements label vitamin K1 without specifying the exact form; this is acceptable as all commercial K1 supplements use either phylloquinone or phytonadione, both of which are well-absorbed
• Be aware that some "vitamin K" supplements contain only K2 (MK-4, MK-7) and no K1; check the label if K1 specifically is what you want

Third-party testing certifications to look for:

• USP Verified Mark (identity, strength, purity, performance)
• NSF International certification (NSF/ANSI 173 standard)
• NSF Certified for Sport (athletes)
• Informed Sport (batch-tested for banned substances)
• ConsumerLab Approved Quality (independent testing)

Red flags:

• Proprietary blends that obscure individual ingredient amounts
• Claims that K1 "reverses" or "cures" any condition
• Extremely high doses (>10,000 mcg) without clear rationale
• Products that do not list the specific form of vitamin K on the label

Excipient and filler considerations:

• Vitamin K1 supplements are generally simple formulations with few excipient concerns
• Softgels typically contain soybean oil or another vegetable oil as a carrier, which enhances absorption
• Individuals with soy allergies should check for soybean oil in softgel carriers

Brand transparency indicators:

• Certificate of Analysis (CoA) available on request or website
• Lot-specific testing results published
• GMP (Good Manufacturing Practices) certified facility
• Clear labeling of vitamin K form, dose per serving, and other ingredients

Population-Specific Considerations

Pregnant and lactating women: The AI for pregnant and lactating women is the same as for non-pregnant females (90 mcg/day for ages 19+, 75 mcg/day for ages 14-18). Vitamin K crosses the placenta poorly, which is why newborns have low vitamin K status at birth regardless of maternal intake. Standard prenatal vitamins may contain some vitamin K but often less than the AI [1].

Newborns: All major pediatric societies recommend a single intramuscular injection of 0.5-1 mg phytonadione at birth to prevent VKDB. This is one of the most well-supported prophylactic interventions in pediatric medicine [1].

Older adults: Vitamin K status may be particularly relevant for older adults due to age-related bone loss and vascular calcification. However, clinical evidence for K1 supplementation improving outcomes in this population is mixed [1][3].

Individuals on anticoagulant therapy: This is the most important population-specific consideration. Patients on warfarin or other VKAs must maintain a consistent daily vitamin K intake and should not supplement without physician approval [1].

Malabsorption conditions: Individuals with celiac disease, cystic fibrosis, ulcerative colitis, short bowel syndrome, or those post-bariatric surgery may have impaired vitamin K absorption and should discuss supplementation with their healthcare provider [1].

Athletes: Vitamin K1 is not a prohibited substance under WADA, USADA, or any major anti-doping framework. It is a naturally occurring vitamin in food and poses no doping risk. Athletes seeking third-party tested products should look for NSF Certified for Sport or Informed Sport certification [1].

Regulatory Status & Standards

United States (FDA):

• Vitamin K1 is regulated as a dietary supplement under DSHEA
• Available over-the-counter in supplement form
• Phytonadione is also available as a prescription drug (Mephyton tablets, injectable forms) for treating vitamin K deficiency and reversing warfarin anticoagulation
• FDA DV for vitamin K is 120 mcg for adults and children age 4+
• No approved health claims for vitamin K in the US

European Union (EFSA):

• EFSA has approved health claims that vitamin K contributes to "normal blood coagulation" and "maintenance of normal bones" under Regulation (EC) No 1924/2006

Japan and Asia:

• MK-4 (a K2 form, not K1) at 45 mg/day is used as a licensed pharmaceutical for osteoporosis treatment in Japan

Canada (Health Canada):

• Vitamin K is regulated as a Natural Health Product. Products require a Natural Product Number (NPN).

Australia (TGA):

• Vitamin K is regulated as a complementary medicine under the Listed Medicines pathway

Athlete & Sports Regulatory Status

Vitamin K1 is a naturally occurring dietary vitamin with no performance-enhancing classification. No anti-doping organization restricts its use. Athletes should select products with third-party certification (NSF Certified for Sport, Informed Sport, or Cologne List) to minimize contamination risk from manufacturing processes, not because the ingredient itself is restricted.

FAQ

What is the difference between vitamin K1 and vitamin K2?
Vitamin K1 (phylloquinone) is made by plants and is the main dietary form of vitamin K. Vitamin K2 (menaquinones) is a family of related compounds produced by bacteria and found in fermented foods and animal products. Both share the same core mechanism (gamma-carboxylation of proteins), but they differ in tissue distribution. K1 is preferentially taken up by the liver for coagulation, while some K2 forms (MK-4, MK-7) may be more active in extrahepatic tissues like bone and vasculature. Most clinical evidence for bone and cardiovascular benefits comes from K2 studies, not K1.

Do I need to supplement vitamin K1 if I eat green vegetables?
For most people, no. A varied diet that includes green leafy vegetables, broccoli, and vegetable oils easily provides the AI of 90-120 mcg/day. A single cup of raw kale contains over 500 mcg, more than four times the AI. Supplementation may be warranted for individuals with fat malabsorption disorders, those on long-term antibiotics, or those with severely restricted diets lacking green vegetables.

Can I take too much vitamin K1?
No adverse effects have been reported from vitamin K1 at any dose studied in humans. The IOM reviewed all available evidence and found no basis for setting a Tolerable Upper Intake Level (UL). However, this does not mean unlimited mega-dosing is beneficial; clinical trials have not demonstrated clear advantages of very high K1 doses for bone or cardiovascular health.

Does vitamin K1 interfere with blood thinners?
Yes. Vitamin K1 directly counteracts the mechanism of warfarin and other vitamin K antagonist (VKA) anticoagulants. If you take these medications, you must keep your daily vitamin K intake consistent (not eliminate it, but keep it stable) and never start or stop supplementation without consulting your prescribing physician. Importantly, this interaction applies specifically to VKA-type anticoagulants, not to all blood thinners; direct oral anticoagulants (DOACs) like apixaban, rivarelbatan, and dabigatran work through a different mechanism and are not affected by vitamin K intake.

Should I take vitamin K1 with vitamin D?
Taking vitamin K alongside vitamin D is commonly recommended because they work synergistically in calcium metabolism. Vitamin D increases calcium absorption from the gut; vitamin K activates the proteins that direct calcium to bones and away from arteries. However, most practitioners recommend K2 (MK-7) rather than K1 for this pairing, as the extrahepatic tissue evidence is stronger for K2.

Why do newborns need a vitamin K injection?
Newborns have very low vitamin K levels because the vitamin crosses the placenta poorly, breast milk is low in vitamin K, and the infant gut microbiome has not yet established vitamin K-producing bacteria. Without prophylactic vitamin K, newborns are at risk for Vitamin K Deficiency Bleeding (VKDB), which can include life-threatening intracranial hemorrhage. The single intramuscular injection of phytonadione at birth is one of the most well-supported preventive interventions in pediatrics.

Is vitamin K1 better from food or supplements?
Both sources are effective, but their absorption profiles differ. Supplemental K1 is approximately 80% bioavailable, while K1 from green vegetables is only 4-17% bioavailable because it is bound within plant cell structures. However, food sources provide K1 in the context of a meal with other beneficial nutrients and dietary fat, which supports absorption. For most people, dietary sources are sufficient.

How do I know if I am vitamin K deficient?
Clinical vitamin K deficiency is diagnosed by an elevated prothrombin time (PT/INR), which indicates impaired blood clotting. This is very rare in healthy adults eating a varied diet. Subclinical deficiency (suboptimal carboxylation of extrahepatic proteins like osteocalcin) may be more common but is harder to assess clinically. Elevated undercarboxylated osteocalcin (ucOC) is a research marker of suboptimal vitamin K status but is not routinely tested.

Can I take vitamin K1 and K2 together?
Yes. K1 and K2 have complementary tissue distributions. K1 is preferentially used by the liver for coagulation, while K2 (particularly MK-4 and MK-7) may be more active in bone and vascular tissues. Many supplements combine both forms. There are no known adverse interactions between K1 and K2.

Myth vs. Fact

Myth: Vitamin K1 and K2 are interchangeable.
Fact: While both K1 and K2 serve as cofactors for the same enzyme (gamma-glutamyl carboxylase), they have different dietary sources, tissue distributions, and metabolic fates. K1 is preferentially taken up by the liver and used for coagulation proteins. K2 forms (especially MK-7) have longer half-lives and greater distribution to extrahepatic tissues. Clinical evidence for bone and cardiovascular benefits is stronger for K2 than for K1. They complement each other but are not identical in function [1][3].

Myth: If you eat enough salad, you can never have low vitamin K status.
Fact: While green vegetables are rich in phylloquinone, the bioavailability from food is quite low (4-17% compared to supplements). Additionally, K1 from plant foods requires dietary fat for absorption, and K1 is rapidly metabolized with limited body storage. Approximately one-third of the U.S. population has vitamin K intake below the AI, though true clinical deficiency remains rare [1].

Myth: Vitamin K1 supplements are dangerous because they promote blood clots.
Fact: Vitamin K1 supports normal, physiological blood clotting. It does not cause pathological clot formation (thrombosis) in healthy individuals. The body's coagulation system includes both procoagulant and anticoagulant vitamin K-dependent proteins (Protein C, Protein S), maintaining a balanced system. The concern about vitamin K and clotting is specific to individuals taking warfarin-type anticoagulants, where changes in K intake can disrupt the drug's calibrated effect [1].

Myth: You should avoid all vitamin K if you take blood thinners.
Fact: The recommendation for patients on warfarin is not to eliminate vitamin K, but to maintain a consistent daily intake. Sudden changes (either increases or decreases) in vitamin K consumption are what destabilize anticoagulation control. A stable, moderate intake of vitamin K-containing foods is both safe and desirable for patients on VKAs [1].

Myth: Vitamin K1 prevents heart disease.
Fact: While vitamin K activates Matrix Gla Protein (MGP), a vascular calcification inhibitor, the observational evidence for cardiovascular benefit is primarily associated with vitamin K2 (menaquinones), not K1 (phylloquinone). The Rotterdam Study and other cohorts found that menaquinone intake was inversely associated with coronary heart disease mortality, while phylloquinone intake showed no significant association. One clinical trial of K1 supplementation showed modest calcification slowing in adherent participants, but the overall analysis was not significant [1][3].

Myth: Cooking destroys vitamin K1 in vegetables.
Fact: Phylloquinone is relatively heat-stable. Normal cooking methods (boiling, steaming, sauteing) do not significantly reduce vitamin K1 content. In fact, cooking can actually increase the bioavailability of phylloquinone by breaking down plant cell walls and releasing it from chloroplast structures, making it more accessible for absorption [1].

Sources & References

Government / Institutional Sources

1. National Institutes of Health, Office of Dietary Supplements. "Vitamin K: Fact Sheet for Health Professionals." Updated March 29, 2021. https://ods.od.nih.gov/factsheets/vitaminK-HealthProfessional/
2. Institute of Medicine (now NASEM). Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press; 2001.
3. Linus Pauling Institute, Oregon State University. "Vitamin K." Micronutrient Information Center. https://lpi.oregonstate.edu/mic/vitamins/vitamin-K

Systematic Reviews & Meta-Analyses

1. Cockayne S, Adamson J, Lanham-New S, et al. "Vitamin K and the prevention of fractures: systematic review and meta-analysis of randomized controlled trials." Arch Intern Med. 2006;166(12):1256-61.

Randomized Controlled Trials

1. Braam LA, Knapen MH, Geusens P, et al. "Vitamin K1 supplementation retards bone loss in postmenopausal women between 50 and 60 years of age." Calcif Tissue Int. 2003;73(1):21-6.
2. Binkley N, Harke J, Krueger D, et al. "Vitamin K treatment reduces undercarboxylated osteocalcin but does not alter bone turnover, density, or geometry in healthy postmenopausal North American women." J Bone Miner Res. 2009;24(6):983-91.
3. Knapen MH, Drummen NE, Smit E, et al. "Three-year low-dose menaquinone-7 supplementation helps decrease bone loss in healthy postmenopausal women." Osteoporos Int. 2013;24(9):2499-507.
4. Shea MK, O'Donnell CJ, Hoffmann U, et al. "Vitamin K supplementation and progression of coronary artery calcium in older men and women." Am J Clin Nutr. 2009;89(6):1799-807.
5. Booth SL, Dallal G, Shea MK, et al. "Effect of vitamin K supplementation on bone loss in elderly men and women." J Clin Endocrinol Metab. 2008;93(4):1217-23.

Observational Studies

1. Geleijnse JM, Vermeer C, Grobbee DE, et al. "Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study." J Nutr. 2004;134(11):3100-5.
2. Beulens JW, Bots ML, Atsma F, et al. "High dietary menaquinone intake is associated with reduced coronary calcification." Atherosclerosis. 2009;203(2):489-93.
3. Feskanich D, Weber P, Willett WC, et al. "Vitamin K intake and hip fractures in women: a prospective study." Am J Clin Nutr. 1999;69(1):74-9.

Review Articles

1. Booth SL. "Vitamin K: food composition and dietary intakes." Food Nutr Res. 2012;56.
2. Shearer MJ, Fu X, Booth SL. "Vitamin K nutrition, metabolism, and requirements: current concepts and future research." Adv Nutr. 2012;3(2):182-95.
3. Suttie JW. "Vitamin K." In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease. 11th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2014:305-16.

Regulatory Sources

1. European Food Safety Authority. "Scientific opinion on the substantiation of health claims related to vitamin K and maintenance of bone pursuant to Article 13(1) of Regulation (EC) No 1924/2006." EFSA Journal. 2009;7:1228.
2. American Academy of Pediatrics Committee on Fetus and Newborn. "Controversies concerning vitamin K and the newborn." Pediatrics. 2003;112(1):191-2.

Related Supplement Guides

Same Category (Fat-Soluble Vitamins)

• Vitamin A
• Vitamin D2 (Ergocalciferol)
• Vitamin D3 (Cholecalciferol)
• Vitamin E
• Vitamin K2 (MK-4, MK-7)

Common Stacks / Pairings

• Calcium
• Magnesium
• Vitamin D3 (Cholecalciferol)
• Vitamin K2 (MK-4, MK-7)

Related Health Goal

• Calcium (bone health)
• Boron (bone health)
• Phosphorus (bone health)
• Vitamin D3 (bone health, calcium metabolism)
• Iron (blood health)