Vitamin K: Benefits, Forms, Dosing, and Side Effects

Vitamin K is a group of fat-soluble vitamins sharing a common 2-methyl-1,4-naphthoquinone ring structure, essential for blood clotting, bone metabolism, and cardiovascular health. The designation "K" comes from the German word "Koagulation," reflecting its discovery in the 1920s by Danish biochemist Henrik Dam as an anti-hemorrhagic factor. In 1943, Dam and Edward Doisy shared the Nobel Prize for discovering vitamin K and elucidating its chemical structure [1][2].

The vitamin K family includes two naturally occurring forms: vitamin K1 (phylloquinone), the primary plant-derived form found in green leafy vegetables, and vitamin K2 (menaquinones), a group of bacterial-origin compounds found in fermented foods, cheeses, and animal products. The most clinically relevant K2 subtypes are MK-4 (short half-life, used at pharmacological doses for osteoporosis in Japan) and MK-7 (long half-life of ~72 hours, resulting in 7-8-fold higher serum accumulation during daily intake) [1][3].

Table of Contents

• Overview
• Forms and Bioavailability
• Evidence for Benefits
• Recommended Dosing
• Safety and Side Effects
• Drug Interactions
• Dietary Sources
• References

Overview

Vitamin K functions as a coenzyme for gamma-glutamyl carboxylase (GGCX), an enzyme that converts specific glutamate (Glu) residues to gamma-carboxyglutamate (Gla) residues in vitamin K-dependent proteins, enabling them to bind calcium ions [3][8]. This post-translational modification is required for the activity of coagulation factors (prothrombin/factor II, factors VII, IX, and X), anticoagulant proteins C and S, the bone protein osteocalcin, and the vascular protein matrix Gla protein (MGP) [3][8][10].

The vitamin K cycle maintains a pool of reduced vitamin K through the action of vitamin K epoxide reductase complex subunit 1 (VKORC1), which recycles the vitamin K epoxide produced during carboxylation back to its active hydroquinone form. This recycling mechanism is the target of warfarin and similar anticoagulant drugs [8][9].

Osteocalcin, when carboxylated by vitamin K, binds calcium and hydroxyapatite crystals in bone, contributing to mineralization and matrix stabilization. Undercarboxylated osteocalcin (ucOC) serves as a biomarker of suboptimal vitamin K status in bone tissue [10][11]. Matrix Gla protein (MGP), when carboxylated, inhibits vascular calcification by binding calcium deposits in arterial walls and preventing smooth muscle cell transdifferentiation. Desphospho-uncarboxylated MGP (dp-ucMGP) levels exceeding 500 pmol/L are associated with a 2- to 3-fold increased risk of cardiovascular disease events [12][13][14].

Absorption, Transport, and Metabolism

Ingested vitamin K is incorporated into mixed micelles via bile salts and pancreatic enzymes, then absorbed by enterocytes of the small intestine (primarily jejunum and ileum) through passive diffusion or the NPC1L1 transporter. Absorption requires dietary fat. Following absorption, vitamin K is incorporated into chylomicrons, transported to the liver via the lymphatic system, and repackaged into VLDL and LDL for distribution to tissues including bone, brain, heart, and pancreas [1][3][15][16].

Phylloquinone (K1) has a short plasma half-life of approximately 1-2 hours, with preferential hepatic uptake. MK-7 has an extended half-life of approximately 72 hours, allowing prolonged circulation and preferential distribution to extrahepatic tissues including bones and arterial walls. The body also converts phylloquinone to MK-4 via CYP4F2 and UBIAD1 enzymes — a unidirectional process [18][19][20][21].

Unlike other fat-soluble vitamins, vitamin K is not stored in substantial amounts. The total body pool is estimated at 17-194 mcg (mean ~88 mcg), with rapid turnover of about 1.5 days. The body retains only 30-40% of an oral physiological dose [3][17][22].

Forms and Bioavailability

Vitamin K1 (Phylloquinone)

The primary dietary form, comprising 75-90% of vitamin K intake in Western diets. Found at high concentrations in green leafy vegetables and at lower levels in vegetable oils. Phylloquinone from plant foods is tightly bound to chloroplasts, substantially limiting bioavailability — the body absorbs only 4-17% as much from spinach as from a supplement tablet. The free form achieves approximately 80% absorption [1][3][15]. Boiling vegetables can reduce K1 content by 20-50% through leaching into cooking water, while steaming preserves more of the nutrient [27].

Vitamin K2 as MK-7 (Menaquinone-7)

A long-chain menaquinone with seven isoprenoid units, primarily obtained from natto (fermented soybean, containing ~1,100 mcg per 100 g). The key pharmacokinetic advantage of MK-7 is its extended plasma half-life of approximately 72 hours, compared to 1-2 hours for K1 and MK-4. This results in 7-8-fold higher serum accumulation during prolonged daily intake [1][18]. A study by Schurgers et al. (2007) suggested that 25 mcg of daily MK-7 may be more potent than 100 mcg of K1 due to longer persistence in the body [18].

MK-7 from fermented and animal sources achieves higher absorption rates (~20-30%) than K1 from leafy greens (5-10%) [27][28]. Supplementation with 180-360 mcg/day for 3-12 months increases carboxylated osteocalcin, reduces ucOC by up to 60%, boosts carboxylated MGP by ~70%, and decreases dp-ucMGP by 50-86% [10][12]. Most supplement MK-7 is soy-derived from natto; chickpea-derived MK-7 (certain MenaQ7 formulations) is available for those with soy allergy [1].

Dr Brad Stanfield's MicroVitamin includes 90 mcg of vitamin K2 as MK-7 — the long-acting form with superior bioavailability for bone and cardiovascular support. This dose works synergistically with the included Vitamin D3 (1,000 IU) and Boron (1 mg) to support calcium metabolism and bone density.

Vitamin K2 as MK-4 (Menaquinone-4)

The shortest-chain menaquinone, found in small amounts in meats, egg yolks (15-32 mcg per 100 g), and dairy products. MK-4 is unique in that the body can synthesize it from phylloquinone via CYP4F2 and UBIAD1, without bacterial action [20][21]. MK-4 is absorbed as efficiently as MK-7 but has a much shorter half-life (1-2 hours), similar to K1 [1][18]. Despite this, MK-4 accumulates preferentially in extrahepatic tissues and is the form most extensively studied at pharmacological doses for bone health. In Japan and other parts of Asia, MK-4 at 45 mg (45,000 mcg) daily is approved as a treatment for osteoporosis [3][29].

Other Menaquinone Forms

Longer-chain menaquinones (MK-8 through MK-13) are produced by gut bacteria and found in fermented foods, particularly cheeses (10-50 mcg per 100 g of MK-8 and MK-9). The gut microbiota's output is estimated at 10-50% of human vitamin K requirements, predominantly as long-chain menaquinones, but absorption is limited because synthesis occurs in the distal colon [5][28][30].

Comparative Pharmacokinetics

Property	K1 (Phylloquinone)	K2 as MK-4	K2 as MK-7
Plasma half-life	1-2 hours	1-2 hours	~72 hours
Primary tissue uptake	Liver (hepatic)	Extrahepatic (bone, arteries)	Extrahepatic (bone, arteries)
Serum accumulation (daily use)	Baseline	Moderate	7-8-fold higher than K1
Absorption from food	4-17% (leafy greens)	~20-30% (animal foods)	~20-30% (fermented foods)
Absorption from supplements	~80%	High	High
Typical supplement dose	100-1,000 mcg	100-45,000 mcg	90-375 mcg

Fat-Soluble Vitamin Interactions

A laboratory experiment using mouse intestinal cells found that uptake of vitamin K was reduced by approximately half in the presence of vitamins A, D, and E — likely due to competition for absorption among fat-soluble vitamins. Vitamin K did not significantly reduce uptake of the other fat-soluble vitamins [31]. While unconfirmed in humans, taking vitamin K at least 3 hours apart from high-dose vitamin D may be prudent [1][31]. Large doses of vitamin E may specifically antagonize vitamin K [32].

Evidence for Benefits

Bone Health

Low vitamin K consumption or impaired vitamin K status is associated with lower bone mass and higher risk of hip fracture in older individuals [33][34]. Vitamin K is required for osteocalcin carboxylation, which is essential for calcium binding and bone mineralization. High serum levels of undercarboxylated osteocalcin are associated with lower bone mineral density [3][10][11].

A 2006 systematic review and meta-analysis by Cockayne et al. included 13 randomized controlled trials (predominantly in Japanese postmenopausal women, 6-36 months duration). Twelve of 13 trials found that supplementation with K1 or MK-4 improved bone mineral density. Seven trials provided fracture data — all used MK-4 at 15 mg/day (1 trial) or 45 mg/day (6 trials). MK-4 supplementation significantly reduced rates of hip, vertebral, and all nonvertebral fractures [29].

Vitamin K1 bone trials:

• Braam et al. (2003): 162 healthy postmenopausal women in the Netherlands — very high-dose K1 (1,000 mcg/day) plus calcium, vitamin D (320 IU), and magnesium for 3 years resulted in significantly less bone loss compared to supplements without K1 or placebo [35].
• Booth et al. (2008): A larger 3-year study — K1 at 500 mcg/day plus calcium (600 mg) and vitamin D (400 IU) failed to show bone loss benefit compared to calcium and vitamin D alone [36].
• Binkley et al. (2009): 381 postmenopausal women received either 1 mg K1, 45 mg MK-4, or placebo for 12 months (all with 630 mg calcium and 400 IU vitamin D3). Both K1 and MK-4 groups had significantly lower ucOC, but no BMD differences at lumbar spine or proximal femur [37].
• Cheung et al. (2008): 440 postmenopausal women in Canada (average age 59) — extremely high-dose K1 (5,000 mcg/day) for 2-4 years did not prevent bone loss but reduced vertebral fracture incidence (9 fractures vs 20 with placebo). No adverse events [38].

Vitamin K2 (MK-4) bone trials:

• Several small clinical trials in Japan, Indonesia, and China found that very high-dose MK-4 (45,000 mcg/day = 45 mg/day) for 1-3 years improved BMD and reduced fracture risk in postmenopausal women with osteoporosis, without toxic effects [40]. A dose-response study showed 45,000 mcg was the minimum effective dose — 15,000 mcg did not show benefit [41].
• In Japan and other parts of Asia, MK-4 at 45 mg is approved as a pharmacological treatment for osteoporosis. The European Food Safety Authority approved a health claim for vitamin K and bone maintenance [42]. The U.S. FDA has not authorized a similar claim.

Vitamin K2 (MK-7) bone trials:

• Knapen et al. (2013): 244 healthy postmenopausal women in the Netherlands — MK-7 at 180 mcg/day for 3 years decreased age-related decline in bone mineral content and density at the lumbar spine and femoral neck (not total hip). Bone strength also improved. Benefits statistically significant after 3 years, not earlier. Calcium and vitamin D were not given [43]. A 2025 meta-analysis confirmed that vitamin K supplementation enhances BMD in middle-aged and older adults, with more pronounced effects in women [44].
• Ronn et al. (2020): 142 postmenopausal women with osteopenia in Denmark — MK-7 at 375 mcg/day plus vitamin D3 (1,520 IU) and calcium (800 mg) for 3 years did not slow BMD decrease at hip, femoral neck, or lumbar spine compared to vitamin D3 and calcium alone [45].
• Zhang et al. (2020): 311 older men and women in China — MK-7 at 90 mcg/day found no bone density benefit for men or combined groups. Among women, slight benefit at femoral neck only. No additional benefit from adding vitamin D (400 IU) and calcium (500 mg), or from lower dose (50 mcg). Single-blind study design [46].

The overall bone evidence suggests MK-4 at pharmacological doses (45 mg/day) has the strongest evidence, primarily in Asian postmenopausal women. MK-7 at 180 mcg/day showed benefit in one well-designed 3-year trial without co-administration of calcium and vitamin D, but results are less promising when added on top of adequate calcium and vitamin D supplementation.

Cardiovascular Health

Observational evidence: In the Rotterdam Study (4,807 men and women aged 55+), higher dietary menaquinone (K2) intake was inversely associated with coronary heart disease mortality — participants in the upper tertile (>32.7 mcg/day) had a 57% lower risk compared to the lower tertile (<21.6 mcg/day). Phylloquinone (K1) intake had no effect [47]. Dietary menaquinone intake was also inversely associated with coronary calcification in 564 postmenopausal women [48].

MK-7 cardiovascular trials — largely negative results:

• Knapen et al. (2015): 180 mcg/day MK-7 for 3 years reduced arterial stiffness in healthy postmenopausal women (especially with high baseline stiffness), but no improvement in endothelial dysfunction [49].
• de Vries et al. (2025): Same dose (180 mcg/day) showed no meaningful benefit in 87 postmenopausal women (avg age 64) over 1 year — no improvements in vascular stiffness index, pulse wave velocity, blood pressure, carotid artery measures. No benefit in 78 pre/perimenopausal women either [50].
• Bartstra et al. (2021): 360 mcg/day MK-7 for 6 months did not slow arterial calcification in type 2 diabetes patients with cardiovascular history [51].
• Witham et al. (2020): 400 mcg/day MK-7 for 12 months did not reduce vascular stiffness, calcification, or blood pressure in 159 people with stage 3-4 CKD [52].
• Kurnatowska et al. (2015): 90 mcg/day MK-7 plus 400 IU vitamin D for ~9 months lessened carotid intima-media thickness increase by 7.9% in 40 CKD patients, but no significant effect on coronary artery calcification [53].
• Diederichsen et al. (2022): 750 mcg/day MK-7 plus 1,000 IU vitamin D for 2 years did not slow aortic valve calcification or stenosis in 333 older adults (avg age 71), nor reduce cardiovascular events or mortality [54]. Further analysis showed no reduction in epicardial or pericoronary adipose tissue inflammation [55].

Potential benefit in high-risk subgroups: A post-hoc analysis of the Diederichsen cohort found that among those with the highest baseline coronary artery calcification, MK-7 plus vitamin D reduced calcification progression compared to placebo, and fewer experienced adverse cardiovascular events (1.9% vs 6.7%) [56].

Vitamin K1 cardiovascular trials:

• Shea et al. (2009): People with pre-existing coronary artery calcification who took K1 (500 mcg) in a multivitamin plus calcium and vitamin D for 3 years had 6% less calcification progression than those without K1. No benefit in those without pre-existing calcification [57].
• Bellinge et al. (2021): 10 mg K1 daily for 3 months reduced risk of new calcified lesions by 65% (coronary) and 73% (aorta) in diabetic patients with moderate coronary artery calcification [58].

Overall, most interventional trials of MK-7 have failed to demonstrate cardiovascular benefit in general populations. The strongest signal is among people with pre-existing, extensive coronary artery calcification, where both K1 and K2 may slow progression.

Nocturnal Leg Cramps

Tan et al. (2024) conducted a randomized, placebo-controlled trial of 199 older adults in China who took 180 mcg MK-7 nightly for 8 weeks. Results were striking [59]:

• Frequency: Reduced from 2.6 per week to approximately 1 per week
• Severity: Significant reduction in cramp intensity
• Duration: Reduced from over 1 minute to under 10 seconds

Improvements appeared within 1 week, with further gains over 4 weeks that continued for the study duration. No adverse events were identified. The proposed mechanism involves vitamin K's effects on calcium channels in cells, reducing excessive muscular contractions [59][60].

Cancer

Observational evidence is mixed and does not establish causation. A German population study found men with higher dietary K2 intake had lower risk of prostate and lung cancer [61]. However, a U.S. study of 51,662 women found higher dietary K2 intake (from butter and cheeses) associated with 26% higher breast cancer risk and 71% increased risk of breast cancer death [62]. No associations were found for K1 in either study. These observations may reflect confounding from high-fat dairy consumption rather than vitamin K itself.

Emerging preclinical research suggests potential anti-cancer mechanisms — a vitamin K precursor induces oxidative stress in prostate cancer cells via PI3K/AKT signaling disruption [63], and VKORC1L1 downregulation activates ferroptosis in pancreatic and prostate cancer models [64]. These are early-stage findings not yet translated to clinical data.

COVID-19

Dofferhoff et al. (2020) found that COVID-19 patients had significantly higher dp-ucMGP levels (indicating low vitamin K) compared to controls. Dp-ucMGP was significantly higher in patients with unfavorable outcomes (ventilation/death), even after adjusting for age, gender, and medication. Reduced vitamin K was also associated with accelerated elastin breakdown [65]. Linneberg et al. (2020, preprint) reported similar findings — every doubling of dp-ucMGP increased death risk by 50% in hospitalized COVID-19 patients [66]. However, there is currently no direct evidence that vitamin K supplementation can prevent or treat COVID-19.

Blood Clotting

Vitamin K1 is well-established for preventing and treating hypoprothrombinemia caused by vitamin K deficiency or certain medications. K2 may be more potent for clotting support [18]. Symptomatic deficiency is rare in adults. Among warfarin users with unstable INR, low-dose K1 (100-200 mcg/day) was previously recommended, but experts now advise against this after analyses showed no reduction in major bleeding events [67][68][69].

Recommended Dosing

No RDA has been established for vitamin K. The Food and Nutrition Board established Adequate Intakes (AIs) based on intake levels in healthy populations [3]:

Age/Sex Group	AI (mcg/day)
Birth to 6 months	2.0
7-12 months	2.5
Children 1-3 years	30
Children 4-8 years	55
Children 9-13 years	60
Adolescents 14-18 years	75
Males 19+ years	120
Females 19+ years	90
Pregnancy (all ages)	75-90
Lactation (all ages)	75-90

The EFSA sets a different AI of 1 mcg/kg/day, equating to ~70 mcg/day for average adults [71]. No Tolerable Upper Intake Level (UL) has been established due to low toxicity — the FNB stated "no adverse effects associated with vitamin K consumption from food or supplements have been reported in humans or animals" [3].

Population Intake Data

NHANES 2011-2012: Average daily vitamin K from foods is 122 mcg for U.S. women and 138 mcg for men. With supplements, intake rises to 164 mcg for women and 182 mcg for men. Approximately two-thirds of the U.S. population has vitamin K intake below the AI, though overt deficiency is extremely rare [3][73].

Clinical Research Doses

Doses used in trials far exceed the AI:

• K1: 500-5,000 mcg/day for bone; up to 10,000 mcg/day for cardiovascular calcification
• MK-4: 45,000 mcg/day (45 mg) for osteoporosis — the dose approved in Japan; lower doses (15,000 mcg) not effective [40][41]
• MK-7: 90-375 mcg/day for bone (1-3 years); 90-750 mcg/day for cardiovascular (6 months to 3 years); 180 mcg/day for leg cramps (8 weeks) [43][45][49][54][59]

Dietary intake of ~250 mcg/day from food is associated with decreased hip fracture risk. For MK-7 bone benefits, 180 mcg/day required 3 years of continuous use [33][34][43]. Over-the-counter MK-7 supplements typically provide 100-200 mcg per capsule [1].

Safety and Side Effects

Vitamins K1 and K2 are generally considered safe with low toxicity potential [1][3][74]. No UL has been established. Supplemental doses of K1 up to 10 mg and MK-4 up to 45 mg/day have not been associated with toxicity in clinical studies. Vitamin K3 (menadione) is hepatotoxic and has been banned for human supplement use [1][7][75].

Specific Safety Considerations

• Soy allergy: MK-7 from natto is soy-derived. Chickpea-derived MK-7 (certain MenaQ7 formulations) is available as a soy-free alternative. Note: "MenaQ7 Natto MK-7" is soy-derived while "MenaQ7" from chickpeas is not — read labels carefully [1].
• Sleep concerns: Despite anecdotal reports, a clinical study of 115 Japanese adults taking 100 mcg MK-7 daily for 12 weeks showed no worsening of sleep parameters [76]. Some research links short sleep (<7 hours) with inadequate vitamin K intake in women aged 19-50, though no association in men [77].
• Breast cancer: A U.S. observational study associated higher dietary K2 intake (from dairy) with increased breast cancer risk [62], but this may reflect confounding from high-fat dairy rather than vitamin K. No convincing evidence that supplemental MK-7 increases breast cancer risk or recurrence [1].
• Thyroid function: No evidence of soy-based vitamin K supplements affecting thyroid function, despite theoretical soy concerns [1][78].
• IV administration: Intravenous K1 is associated with rare anaphylactoid reactions (~3 per 10,000 doses), attributed to the Cremophor EL solubilizing agent rather than vitamin K itself. Oral administration does not carry this risk [79][80].

Newborn Vitamin K Prophylaxis

Newborns are vulnerable to vitamin K deficiency due to limited placental transfer, sterile gut, and low breast milk K content. Without prophylaxis, classical VKDB incidence reaches ~1.7% (1 in 60 births); late VKDB occurs in 4-7 per 100,000 births and can cause intracranial hemorrhage with ~20% mortality [81][82][84][85]. The AAP recommends a single IM dose of 0.5-1 mg K1 at birth, reducing late VKDB risk by 81-fold [84][86][87]. Oral prophylaxis (three 2 mg doses) achieves 70-90% efficacy but with higher residual risk [88].

Drug Interactions

Warfarin and Vitamin K Antagonists

The most significant interaction. Warfarin inhibits VKORC1, reducing active vitamin K availability by ~90%. Vitamin K supplementation can counteract warfarin by restoring clotting factor synthesis. MK-7 may interfere at doses as low as 10 mcg/day due to its long half-life [18][90]. Some experts suggest people on warfarin should avoid MK-7 supplements entirely [90]. Experts now recommend against routine low-dose K supplementation for warfarin users due to limited benefit evidence [68][69]. People on warfarin should maintain consistent dietary vitamin K intake without large fluctuations [3].

Genetic variations in VKORC1 influence warfarin sensitivity — the -1639G>A polymorphism (allele frequency 22-38% in Asian populations) can necessitate 20-50% lower warfarin doses [91].

Other Drug Interactions

• Direct oral anticoagulants (dabigatran/Pradaxa, rivaroxaban/Xarelto): Work through different mechanisms and are not thought to be affected by vitamin K intake [92][93].
• Antiplatelet drugs (aspirin, clopidogrel/Plavix): Prevent platelet aggregation — a mechanism distinct from vitamin K's role. No evidence of interaction [94].
• Antibiotics: Prolonged broad-spectrum therapy (especially cephalosporins) can reduce vitamin K status by destroying gut bacteria and potentially inhibiting VKORC1 directly. Supplements usually unnecessary unless antibiotic use exceeds several weeks with poor dietary intake [6][95][96].
• Bile acid sequestrants (cholestyramine, colestipol): Can reduce vitamin K absorption by binding bile acids. Monitor vitamin K status with long-term use [95][97].
• Orlistat (Alli, Xenical): Reduces dietary fat absorption by ~30%, which can reduce vitamin K absorption. May increase prothrombin time when combined with warfarin. A multivitamin with vitamin K is usually recommended for patients on orlistat [98][99][100].
• Statins: May decrease vitamin K levels, but vitamin K supplementation does not appear to improve cardiovascular outcomes in most statin users [54][101].

Dietary Sources

Vitamin K1 (Phylloquinone) — Plant Sources

Food	Serving	Vitamin K (mcg)	% DV*
Natto (fermented soybean)	3 oz	850 (as MK-7)	708%
Collards, frozen, boiled	1/2 cup	530	442%
Turnip greens, frozen, boiled	1/2 cup	426	355%
Kale, raw	1 cup	113-817	94-681%
Spinach, raw	1 cup	145	121%
Broccoli, chopped, boiled	1/2 cup	110	92%
Prunes	100 g (~10 prunes)	59.5	50%
Soybeans, roasted	1/2 cup	43	36%
Carrot juice	3/4 cup	28	23%
Soybean oil	1 tablespoon	25	21%
Edamame, frozen	1/2 cup	21	18%
Pomegranate juice	3/4 cup	19	16%
Blueberries, raw	1/2 cup	14	12%
Iceberg lettuce, raw	1 cup	14	12%
Canola oil	1 tablespoon	10	8%
Olive oil	1 tablespoon	8	7%

*Daily Value = 120 mcg for adults and children age 4+. A half cup of broccoli or a large mixed green salad provides approximately 250 mcg of vitamin K [1].

Vitamin K2 (Menaquinones) — Animal and Fermented Sources

Food	Serving	Vitamin K2 (mcg)	Form
Natto	3.5 oz (100 g)	~1,100	MK-7
Soft cheeses (Brie, Camembert, mascarpone)	3.5 oz	~506	Mixed MKs
Blue cheese	3.5 oz	~440	Mixed MKs
Semi-soft cheeses (Gouda, Havarti, Swiss)	3.5 oz	~289	Mixed MKs
Hard cheeses (cheddar, parmesan)	3.5 oz	~282	Mixed MKs
Processed American cheese	3.5 oz	~98	Mixed MKs
Full-fat milk	3.5 oz	~38	Mixed MKs
Full-fat yogurt	3.5 oz	~27	Mixed MKs
2% milk	3.5 oz	~19	Mixed MKs
Egg yolk	100 g	15-32	MK-4
Chicken breast, rotisserie	3 oz	13	MK-4
Low-fat kefir	3.5 oz	~10.2	Mixed MKs
Ground beef, broiled	3 oz	6	MK-4
Chicken liver, braised	3 oz	6	MK-4
Fat-free milk	3.5 oz	~5	Mixed MKs

Vitamin K is fat-soluble — full-fat dairy contains significantly more than reduced-fat versions. Full-fat cheddar has ~281 mcg total vitamin K per 100 g while reduced-fat has just 49 mcg. Reduced-fat or non-fat dairy products contain only 5-22% of the vitamin K in full-fat counterparts [1][28][103].

Gut Microbiota Contribution

Gut bacteria (Firmicutes and Bacteroidetes phyla) synthesize menaquinones — Lactobacillus produces MK-7 and MK-8, Bacteroides produces MK-10 and MK-11. Estimated to supply 10-50% of vitamin K requirements, but absorption is limited due to distal colon synthesis [5][30][104]. Antibiotic use reduces microbial vitamin K production; high-fiber diets promote it [95][105].

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