🧬 Aging Wiki

vitamin-k

Properties1
aliasesphylloquinone, menaquinone, vitamin K1, vitamin K2, MK-7, menaquinone-7, MK-4, menaquinone-4, K1, K2, fat-soluble vitamin K, VKDPs cofactor

19 min read

Vitamin K (Family Page)

The fat-soluble vitamin family serving as the obligatory cofactor for gamma-glutamyl carboxylase (GGCX), the enzyme responsible for gamma-carboxylation of glutamate residues (converting Glu to Gla) on vitamin K-dependent proteins (VKDPs). Without sufficient reduced vitamin K, VKDPs remain as uncarboxylated, functionally inert forms — the coagulation consequences (prolonged clotting time) are the well-known clinical marker, but the extrahepatic consequences in vascular and bone tissues are the aging-relevant axis.

Scope note: This page covers the vitamin K family with the K1 (phylloquinone) versus K2 (menaquinones, especially MK-7) distinction as the central aging-relevant axis. The primary canonical form (PubChem CID 5284607) is K1 phylloquinone — the most abundant dietary form and the benchmark for coagulation studies. The primary alt form (PubChem CID 5287554) is MK-7 — the form with the largest anti-aging and vascular evidence base. MK-4 (PubChem CID 5282367) is documented in the identity section but is not a primary focus. Individual sub-form pages may be seeded later if warranted by evidence depth.

Identity

FieldK1 (phylloquinone)MK-7 (menaquinone-7)MK-4 (menaquinone-4)
PubChem CID528460752875545282367
Common nameVitamin K1, phylloquinoneVitamin K2 MK-7Vitamin K2 MK-4
Molecular formulaC₃₁H₄₆O₂C₄₆H₆₄O₂C₃₁H₄₀O₂
Molecular weight450.7 Da649.0 Da580.9 Da
InChIKeyMBWXNTAXLNYFJB-NKFFZRIASA-NRAKQPZMEYJZGPI-LJWNYQGCSA-N—
SourcePlant-derived (leafy greens, vegetable oils)Bacterial fermentation; natto (fermented soybeans); some hard cheesesAnimal products; biosynthetically converted from K1 by tissue-specific enzymes (including brain)
Plasma half-life~1 hour~3 days~1–2 hours
Hepatic preferenceHighLower; superior peripheral tissue distributionModerate

Critical pharmacokinetic difference: MK-7’s ~3-day half-life (compared to ~1 hour for K1) enables sustained tissue distribution, including to extrahepatic sites such as the vascular wall. This is the pharmacokinetic basis for the MK-7 positioning for vascular and bone endpoints — not a distinct mechanism, but superior substrate delivery to peripheral GGCX.

Mechanism of action

The vitamin K cycle (GGCX/VKOR)

Vitamin K functions as a cofactor via a two-step enzymatic cycle 1:

  1. Gamma-carboxylation (GGCX step): Vitamin K hydroquinone (KH2, the reduced active form) is oxidised to vitamin K epoxide during GGCX catalysis. GGCX uses this oxidation energy to carboxylate glutamate residues on VKDPs — adding a second carboxyl group to form gamma-carboxyglutamate (Gla). Each Gla residue gains calcium-chelating capacity.
  2. Epoxide reductase (VKOR step): Vitamin K epoxide is regenerated to the active hydroquinone (KH2) by the vitamin K epoxide reductase complex (vkor, gene VKORC1). This regeneration allows a single molecule of vitamin K to be reused in multiple carboxylation cycles.
  3. Warfarin block: Warfarin (and acenocoumarol, phenprocoumon) inhibit VKOR, depleting KH2 and preventing GGCX from carboxylating VKDPs in all tissues — both hepatic coagulation factors and extrahepatic substrates including MGP 2.

Vitamin K-dependent proteins (VKDPs) relevant to aging

ProteinLocationRequires Gla?Aging relevance
Prothrombin (Factor II), VII, IX, XLiver/plasmaYes — Gla-domain essential for phospholipid bindingCoagulation; warfarin target; not direct aging mechanism
Matrix Gla Protein (MGP)Vascular smooth muscle, cartilageYes — uncarboxylated ucMGP is biologically inertPrimary anti-calcification factor in the arterial wall; the central aging-relevant VKDP — see matrix-gla-protein
Osteocalcin (BGLAP)Bone, osteoblastsYesBone mineralisation marker; some endocrine functions claimed (disputed)
Gas6 (Growth Arrest-Specific 6)Widely expressedYesTAM receptor (Tyro3/Axl/MerTK) ligand; roles in cell survival, inflammation, efferocytosis
Protein SLiver/plasmaYesAnticoagulant cofactor for activated Protein C

MGP is the central VKDP for the aging/vascular calcification axis. For the full mechanistic description see matrix-gla-protein.

K1 vs K2 — the hepatic-preferential split

  • Vitamin K1 (phylloquinone): Rapidly cleared by the liver (~1-hour plasma half-life). Efficient for hepatic VKDP carboxylation (coagulation factors, Protein S/C). Limited peripheral tissue accumulation. The majority of dietary vitamin K in Western diets.
  • Vitamin K2 (menaquinones, especially MK-7): The extended half-life (~72 hours for MK-7) enables accumulation in extrahepatic tissues — most critically, the vascular wall. When vascular vitamin K status is assessed via dp-ucMGP (the circulating biomarker of extrahepatic GGCX activity), MK-7 supplementation reduces dp-ucMGP far more effectively than equivalent mass doses of K1 3.

This pharmacokinetic split is the mechanistic justification for using MK-7 — not K1 — for the vascular calcification indication.

Biomarker: dp-ucMGP

Dephosphorylated-uncarboxylated MGP (dp-ucMGP) is the validated clinical biomarker of extrahepatic vitamin K insufficiency. It is inversely proportional to vascular vitamin K status:

  • High dp-ucMGP → insufficient K2 reaching the vascular wall → MGP not carboxylated → calcification risk elevated
  • Low dp-ucMGP → adequate vascular K2 status → MGP activated → anti-calcification function preserved

Reference ranges vary by assay (InaKtif MGP, ELISA-based), but dp-ucMGP > 400–500 pmol/L is commonly used to define “low extrahepatic vitamin K status” in RCT inclusion criteria 4.

MK-7 supplementation at 180 µg/day consistently reduces dp-ucMGP by 25–50% in RCTs regardless of underlying population (healthy postmenopausal women, CKD/hemodialysis patients, diabetic patients) — this is the most reproducible pharmacodynamic effect. Whether this biomarker reduction translates to structural (calcification) or functional (arterial stiffness) benefit is the open question (see Human Evidence section).

Clinical evidence

Coagulation — well-established, not the aging axis

Vitamin K’s role in coagulation (hepatic carboxylation of factors II, VII, IX, X) is foundational biochemistry established over decades. Dietary vitamin K deficiency (rare in adults; occurs in fat malabsorption syndromes, prolonged antibiotic use, or neonates) causes coagulopathy. Warfarin anticoagulation operates entirely through this VKOR/coagulation pathway. This is not in dispute and carries no relevant translation gap. The evidence is strong for coagulation, but this page focuses on extrahepatic aging-relevant effects.

Vascular calcification and arterial stiffness — limited surrogate-endpoint evidence

Knapen 2015 (strongest positive arterial stiffness RCT): Double-blind, placebo-controlled RCT in n=244 healthy postmenopausal women, MK-7 180 µg/day vs placebo, 3 years. Primary endpoints: carotid-femoral PWV (cfPWV) and Stiffness Index β — both decreased significantly in MK-7 vs placebo in the overall group; benefit greatest in women with above-median baseline stiffness. Local carotid PWV improved significantly in the above-median-stiffness subgroup. dp-ucMGP reduced ~50%. No effect on acute-phase markers or endothelial function markers 5. Key limitation: postmenopausal women only; 3-year treatment window.

de Vries 2025 (post-hoc, 1-year, low-K-status cohort): Post-hoc analysis of NCT02404519, n=165 women with elevated dp-ucMGP (>400 pmol/L), MK-7 180 µg/day vs placebo. Vascular stiffness significantly attenuated in post-menopausal women only (Young’s modulus: MK-7 +9.4% ± 67.1 vs placebo +49.1% ± 77.4; adjusted p=0.035). Blood pressure effect (−3.0%, p=0.007) was in a post-hoc high-stiffness-index subgroup (n=26), not the overall analysis. dp-ucMGP significantly reduced 4. Caveat: post-hoc; women only; industry-funded.

Diederichsen 2022 Circulation trial (negative hard-endpoint RCT): The most rigorous trial to date for a structural endpoint. Double-blind, multicenter RCT, n=365 elderly men (mean age 71.0 ± 4.4 years), 720 µg MK-7/day + 25 µg vitamin D vs placebo, 24 months, with aortic valve calcification (AVC) progression as the primary endpoint (Agatston CT score). Result: no significant difference in AVC progression (treatment effect −17 AU, 95% CI −86 to +53; p=0.64) — a non-significant trend favouring treatment that did not reach significance. dp-ucMGP decreased significantly in the treatment group (−212 pmol/L vs +45 pmol/L in placebo; p<0.001). Interpretation: 720 µg/day MK-7 reliably reduces the biomarker (dp-ucMGP) but did not translate to reduced structural calcification in the aortic valve in this 2-year trial 6. This is the key null trial; it does not preclude benefit in medial arterial calcification (a different tissue compartment) but sets a cautionary precedent for assuming biomarker → structural endpoint translation. The dose (720 µg/day) was 4× higher than the Knapen/de Vries trials, making under-dosing an unlikely explanation for the null result.

Naiyarakseree 2023 (hemodialysis, multicenter RCT): Open-label, n=96 CKD hemodialysis patients, MK-7 375 µg/day vs standard care, 24 weeks. Primary endpoint cfPWV: no significant overall difference (MK-7 −6.0% vs control −6.7%; p=0.24). Pre-specified diabetic subgroup (n=16/14): significant improvement (MK-7 −10.0% vs control +3.8%; p=0.008). CKD-specific context with extreme baseline K deficiency; limited generalizability to non-CKD aging 7.

Li/Wang 2023 meta-analysis: 14 RCTs (1,842 enrolled; 1,533 in analysis); CAC-specific sub-analysis (4 RCTs, n=424): vitamin K supplementation slowed CAC progression (MD = −17.37 Agatston units; 95% CI −34.18 to −0.56; p=0.04; I²=34%). The positive signal is dominated by the Shea 2009 community-dwelling trial (94.4% weight in fixed-effects). dp-ucMGP analysis (7 trials, n=578): robustly reduced (MD −243.31; 95% CI −366.08 to −120.53; p=0.0001; I²=71%) 8.

Murali 2023 systematic review (contradictory, non-CKD focus): 49 RCTs (n=9,901), explicitly excluding CKD. Vitamin K: 5 RCTs (n=1,074) — classified as “possibly reduces progression” (same tier as other uncertain interventions, not a flat positive). Concludes “the vitamin K pathway may not represent a therapeutic target to mitigate this in a non-CKD cohort.” Only 1 of 5 vitamin K trials (Shea 2009, in adherent/mild-CAC participants) achieved its primary endpoint 9. contradictory-evidence

Framing the discordance: The Li 2023 meta-analysis positive CAC result is dominated by Shea 2009 (a community-dwelling trial). Murali 2023 applied stricter non-CKD inclusion and reached a negative conclusion — the discordance reflects different inclusion criteria and endpoint heterogeneity rather than a clean CKD vs non-CKD split. The Diederichsen 2022 trial (the largest and most rigorous structural endpoint trial) was null for aortic valve calcification. Overall interpretation: the dp-ucMGP biomarker effect of MK-7 is robust and reproducible; the structural (CAC) and functional (PWV) endpoint evidence is mixed and inadequately powered in non-CKD adults. Hard cardiovascular outcome data (MI, CV death, stroke) do not yet exist for MK-7 in any population. needs-human-replication

Bone — limited and conflicting

Osteocalcin (bone Gla protein, BGLAP) is a VKDP expressed by osteoblasts. Like MGP, uncarboxylated osteocalcin (ucOC) is inert. Vitamin K supplementation reduces ucOC, and observational data link higher MK-7 intake to higher bone mineral density. However:

  • The RenaKvit trial (Levy-Schousboe 2023, n=123 dialysis patients, MK-7 vs placebo, 24 weeks) found MK-7 accelerated BMD loss at the distal radius while preventing lumbar spine BMD decline. The authors explicitly conclude findings “do not support MK-7 supplementation to preserve bone” in dialysis patients 10.
  • A pediatric CKD RCT (El Borolossy 2022, n=60, MK-7 100 µg/day + vitamin D) showed significant dp-ucMGP and ucOC reduction with combined K2+D, suggesting the combination may have greater bone effect 11.
  • Non-CKD adult bone-specific RCT evidence is limited; bone endpoint results do not consistently support supplementation independent of adequate vitamin D status.

Coagulation safety of MK-7 supplementation

A relevant concern for oral MK-7 supplementation is potential interference with warfarin anticoagulation. Bladbjerg 2024 (double-blind, n=123 dialysis patients, MK-7 360 µg/day, 1 year) found no detectable effect on biomarkers of coagulation activation in non-anticoagulated patients. PIVKA-II (uncarboxylated prothrombin, an index of hepatic vitamin K sufficiency) decreased in the MK-7 group, confirming pharmacodynamic activity, but coagulation pathway activation was not stimulated 12. This supports a safety profile consistent with the hypothesis that MK-7 at supplemental doses preferentially serves extrahepatic (GGCX) needs without triggering procoagulant overshoot in patients with normal clotting. Caveat: patients on warfarin represent a specific population where MK-7 should not be used without hematology guidance — it would antagonize anticoagulation.

Warfarin and the vascular calcification paradox

Warfarin is among the most prescribed medications globally for atrial fibrillation, venous thromboembolism, and mechanical heart valves. Its anti-K2 pharmacology is directly relevant to aging:

  • Warfarin inhibits VKOR → depletes KH2 in all tissues → MGP in the vascular wall remains uncarboxylated → accelerated vascular calcification
  • Clinical studies show warfarin users have measurably higher dp-ucMGP and higher coronary calcification scores than matched controls 2
  • This is a well-documented iatrogenic calcification mechanism — the very drug preventing thromboembolism accelerates vascular mineral deposition via the anti-K2 side effect
  • The clinical relevance: direct oral anticoagulants (DOACs — apixaban, rivaroxaban, edoxaban, dabigatran) do not inhibit VKOR and do not affect vitamin K cycle — a potential CV advantage in the long-term aging context needs-human-replication — head-to-head DOAC vs warfarin vascular calcification RCT data are limited

Dietary sources and typical intake

SourceVitamin K formApproximate content
Leafy greens (kale, spinach, collards)K1 (phylloquinone)100–800 µg/100 g
Vegetable oils (soybean, canola)K150–200 µg/100 mL
Natto (fermented soybeans)MK-7~900–1100 µg/100 g
Hard cheeses (Gouda, Edam)MK-7 + MK-8, MK-920–75 µg/100 g
Curd/soft cheeses, butterMK-4, low MK-75–15 µg/100 g
Liver, poultry dark meatMK-410–60 µg/100 g

Western diets are generally K1-adequate (from vegetables/oils) but K2-insufficient — natto is not broadly consumed outside Japan. The typical Western diet provides ~5–15 µg/day MK-7 from cheese sources, compared to the 180 µg/day used in the Knapen and de Vries RCTs. This dietary gap underlies the supplementation rationale.

Pharmacokinetics summary

  • Absorption: Fat-soluble; requires dietary fat for micelle incorporation and chylomicron-mediated absorption from the small intestine. All forms require fat co-ingestion for adequate bioavailability.
  • K1 plasma half-life: ~1 hour (rapidly taken up by liver).
  • MK-7 plasma half-life: ~3 days (accumulates in VLDL and subsequently distributes to peripheral tissues, including arterial wall, adipose, and bone).
  • MK-4 conversion: K1 can be converted to MK-4 in certain tissues (brain, testis) by a tissue-specific side chain cleavage and prenylation step; this conversion is not the primary route of MK-4 acquisition and is of limited quantitative importance for the vascular wall.
  • No upper tolerance level established in non-anticoagulated patients at supplement doses (≤1000 µg/day MK-7); no toxicity signals at doses used in RCTs.

Aging hallmark intersections

HallmarkMechanismEvidence tier
altered-intercellular-communicationMGP carboxylation prevents vascular calcification → preserves arterial compliance → maintains systemic vascular-wall-to-systemic-circulation signalling milieu; warfarin-accelerated calcification impairs thisMechanistic in humans (surrogate-endpoint RCTs); hard outcome data absent
chronic-inflammationVascular calcification drives macrophage recruitment and SASP at the arterial wall (secondary effect); also, Gas6 (a VKDP) modulates TAM receptor signalling involved in efferocytosis and inflammation resolutionMechanistic; no direct anti-inflammatory RCT endpoint for MK-7

Hallmark selection rationale: The primary hallmark link is altered-intercellular-communication because the clinically relevant aging effect — vascular calcification → arterial stiffening — operates via degraded systemic vascular communication (pulse pressure transmission, baroreceptor dysfunction, end-organ micro-damage). chronic-inflammation is a downstream consequence of calcification-driven VSMC phenotypic switching but is secondary to the primary mechanism. No direct link to deregulated-nutrient-sensing or other hallmarks has primary-source support for vitamin K specifically.

Human evidence summary

ContextEndpointVerdict
Coagulation factor carboxylationPT/INR, clottingWell-established; foundational biochemistry
dp-ucMGP reductionMK-7 supplementationRobust and reproducible across populations
Arterial stiffness (cfPWV, SI)MK-7 RCTsKnapen 2015: positive (3-yr, postmenopausal women); de Vries 2025: positive (post-hoc, low-K-status women); Naiyarakseree 2023: null overall, diabetic subgroup positive (HD patients)
Aortic valve calcification (AVC)MK-7 (720 µg/day) + vitamin D RCTDiederichsen 2022: null (treatment effect −17 AU, 95% CI −86 to +53; n=365, 2 yr, Circulation)
Coronary artery calcification (CAC)Meta-analysis + systematic reviewLi 2023: marginally positive (dominated by Shea 2009); Murali 2023: “possibly reduces progression” (non-CKD, no definitive positive)
Bone mineral densityMK-7 RCTsMixed; RenaKvit 2023: divergent effects by anatomic site; insufficient to recommend
Hard CV outcomes (MI, stroke, CV death)None identifiedneeds-human-replication — no hard-outcome RCT exists for MK-7

Human-evidence-level assignment (limited): dp-ucMGP effects are established. Arterial stiffness data show positive signals (Knapen 2015) but the largest structural-endpoint trial is null (Diederichsen 2022). No hard CV endpoint data. Bone evidence is inconsistent. This constitutes a surrogate-level evidentiary basis — limited, not preclinical-only (substantial human trial activity exists) and not strong (no hard outcomes, key structural-endpoint null).

Limitations and knowledge gaps

  • needs-human-replication — No RCT has evaluated MK-7 with hard cardiovascular outcomes (MI, CV death, stroke) as primary endpoints in any population.
  • needs-human-replication — The only rigorous structural-calcification endpoint trial (Diederichsen 2022 Circulation, aortic valve calcification) was null. A powered non-CKD CAC-endpoint RCT for MK-7 has not been completed.
  • contradictory-evidence — Li 2023 meta-analysis and Murali 2023 systematic review reach different conclusions about CAC benefit in non-CKD adults; discordance reflects inclusion criteria and endpoint heterogeneity, not resolution.
  • needs-human-replication — Whether DOAC-vs-warfarin anticoagulation divergence in vascular calcification outcomes has clinical magnitude in prospective RCTs remains open.
  • dose-response-unclear — Optimal dose and form (MK-7 dose ≥180 µg/day? MK-4? combination?) for extrahepatic GGCX saturation in non-CKD older adults is not established.
  • clinical-trials-active count note (verified 2026-06-02): The count of 7 reflects active (RECRUITING + ACTIVE_NOT_RECRUITING) trials on ClinicalTrials.gov where vitamin K2/MK-7 is the study agent and the indication is aging-relevant (cardiovascular calcification, arterial stiffness, bone/osteoporosis, CKD-related calcification). A broad query for “menaquinone” returns 60 active trials, the majority of which are NOAC-vs-warfarin anticoagulation management studies where menaquinone-7 appears as the comparator or reference, not the study agent. Highlighted trials: DANCODE (NCT05500443, Danish coronary decalcification), InterVitaminK (NCT05259046, cardiovascular/metabolic/bone), and Role of Vitamin K2 in CKD (NCT05942053).
  • The vascular calcification mechanism page (vascular-calcification) and the MGP protein page (matrix-gla-protein) carry the detailed mechanistic arguments; this page summarises and cross-links.

Classification

  • SENS strategy: indirect — MK-7 supports MGP carboxylation, which inhibits extracellular hydroxyapatite accumulation; this maps most closely to a GlycoSENS/extracellular-junk prevention strategy, though SENS has not formally categorized vascular calcification.
  • Intervention category: dietary supplement; no prescription indication for vascular calcification.
  • Risk profile for supplementation: Low in non-anticoagulated patients (no established toxicity at ≤1000 µg/day MK-7). Contraindicated with warfarin — MK-7 supplementation will antagonize warfarin anticoagulation.

Cross-references

  • matrix-gla-protein — the primary extrahepatic VKDP; the mechanistic linchpin of vitamin K’s vascular anti-calcification effect
  • vascular-calcification — the process page; carries the detailed mechanistic description, RCT evidence framing, and conflict discussion
  • ggcx — gamma-glutamyl carboxylase; the enzyme for which vitamin K is the cofactor
  • VKOR — vitamin K epoxide reductase; warfarin’s target; regenerates active vitamin K hydroquinone
  • altered-intercellular-communication — the primary hallmark linked via vascular calcification → arterial stiffening
  • chronic-inflammation — secondary via calcification-driven VSMC phenotypic switching
  • arterial-stiffening — downstream phenotype; cfPWV is the primary functional RCT endpoint
  • atherosclerosis — partially overlapping phenotype; intimal vs medial calcification distinction
  • klotho — parallel anti-calcification system; both Klotho and MGP fail in CKD
  • fgf23 — FGF23/Klotho/phosphate axis; distinct but intersecting vascular calcification driver
  • bmp-2 — BMP-2 is sequestered by carboxylated MGP; uncarboxylated MGP allows BMP-2 to drive VSMC osteogenic transdifferentiation

Footnotes

Footnotes

  1. doi:10.1146/annurev.bi.64.070195.003401 · Stafford DW · Annu Rev Biochem 1995;64:551–577 · review · comprehensive description of the vitamin K cycle (GGCX, VKOR), Gla protein biochemistry, and warfarin mechanism; foundational reference for the cofactor mechanism ↩

  2. doi:10.1038/ki.2013.26 · Schurgers LJ et al. · Kidney Int 2013 · review · warfarin inhibition of VKOR → MGP non-carboxylation → vascular calcification; MK-7 vs K1 tissue distribution; dp-ucMGP as biomarker; CKD context with mechanism generalisable · archive: not_oa no-fulltext-access ↩ ↩2

  3. doi:10.1182/blood-2006-04-018697 · Schurgers LJ, Teunissen KJF, Hamulyak K, Knapen MHJ, Vik H, Vermeer C · Blood 2007;109(8):3279–3283 · rct (crossover) · n=32 healthy volunteers · comparative bioavailability K1 vs MK-7 in VKDPs carboxylation; MK-7 significantly more effective at reducing dp-ucMGP than K1 at equivalent molar doses · model: homo-sapiens · archive: not_oa ↩

  4. doi:10.3390/nu17050815 · PMID:40077685 · de Vries F et al. · Nutrients 2025;17(5):815 · post-hoc analysis of double-blind RCT (NCT02404519; full trial n=243 men+women 40–70 yr) · post-hoc cohort: n=165 women with dp-ucMGP >400 pmol/L (78 pre/peri-menopausal, 87 post-menopausal; MK-7 n=82, placebo n=83) · MK-7 180 µg/day × 1 year · vascular stiffness attenuated in post-menopausal women (Young’s modulus: placebo +49.1% ± 77.4 vs MK-7 +9.4% ± 67.1; adjusted p=0.035); BP reduction (brachialis −3.0% ± 9.0; p=0.007) in post-menopausal high-stiffness-index subgroup only (n=26 MK-7); dp-ucMGP significantly reduced in both menopausal groups · industry-funded (Gnosis by Lesaffre) · model: homo-sapiens · archive: local PDF verified ↩ ↩2

  5. doi:10.1160/th14-08-0675 · PMID:25694037 · Knapen MHJ, Braam LA, Drummen NE, Bekers O, Hoeks AP, Vermeer C · Thrombosis and Haemostasis 2015;113(5):1135–1144 · rct (double-blind, placebo-controlled) · n=244 (MK-7 n=120, placebo n=124) · healthy postmenopausal women · MK-7 180 µg MenaQ7/day vs placebo × 3 years · cfPWV and Stiffness Index β significantly decreased in MK-7 group overall; local carotid stiffness parameters improved in women with above-median baseline Stiffness Index β (median 10.8); dp-ucMGP reduced ~50% vs placebo · no effect on acute-phase markers (IL-6, hsCRP, TNF-α) or endothelial dysfunction markers · model: homo-sapiens · archive: not_oa no-fulltext-access — quantitative claims verified against PubMed abstract only ↩

  6. doi:10.1161/CIRCULATIONAHA.121.057008 · PMID:35465686 · Diederichsen ACP et al. · Circulation 2022;145(18):1387–1397 · rct (double-blind multicenter, 4 Danish centres) · n=365 elderly men (mean age 71.0 ± 4.4 yr; n=182 treatment, n=183 placebo) · 720 µg MK-7/day + 25 µg vitamin D vs placebo × 24 months · primary: AVC Agatston progression: null (treatment effect −17 AU; 95% CI −86 to +53; p=0.64) · dp-ucMGP: −212 pmol/L (treatment) vs +45 pmol/L (placebo); p<0.001 · model: homo-sapiens · archive: local PDF verified ↩

  7. doi:10.3390/nu15112422 · PMID:37299386 · Naiyarakseree N et al. · Nutrients 2023 · rct (multicenter open-label) · n=96 hemodialysis patients (MK-7 n=50, control n=46) · MK-7 375 µg/day × 24 weeks · cfPWV overall: null (MK-7 −6.0% vs control −6.7%; p=0.24); diabetic subgroup (n=16/14): MK-7 −10.0% vs control +3.8% (p=0.008) · CKD/ESRD context · model: homo-sapiens · archive: local PDF available (not re-read during this verification pass — claims verified against seeder extraction) ↩

  8. doi:10.3389/fnut.2023.1115069 · PMID:37252246 · Li T, Wang Y, Tu WP · Frontiers in Nutrition 2023 · systematic-review + meta-analysis · 14 RCTs, 1,533 participants in analysis (1,842 enrolled); CAC sub-analysis: 4 RCTs, n=424 (Shea 2009 = 94.4% fixed-effects weight) · CAC: MD −17.37 Agatston (95% CI −34.18 to −0.56; p=0.04; I²=34%); dp-ucMGP: MD −243.31 (95% CI −366.08 to −120.53; p=0.0001; I²=71%) · mixed CKD/non-CKD populations · model: homo-sapiens · archive: local PDF verified ↩

  9. doi:10.1161/jaha.123.031676 · PMID:38014685 · Murali S, Smith ER, Tiong MK, Tan SJ, Toussaint ND · J Am Heart Assoc 2023;12:e031676 · systematic-review · 49 RCTs (n=9,901); CKD patients explicitly excluded · vitamin K: 5 RCTs (n=1,074; median participants 154, range 68–388; median duration 12 months): “possibly reduces progression” — only 1 RCT (Shea 2009, in adherent participants) achieved primary CAC endpoint; conclusion: “insufficient or conflicting data” for vitamin K in non-CKD cohort · model: homo-sapiens · archive: local PDF verified ↩

  10. doi:10.1093/ndt/gfac315 · PMID:36460034 · Levy-Schousboe K et al. (RenaKvit trial) · Nephrol Dial Transplant 2023 · rct (double-blind, placebo-controlled, multicentre) · n=123 dialysis patients · MK-7 vs placebo × 24 weeks · BMD 1/3 distal radius: accelerated loss in MK-7 group; lumbar spine BMD: preserved in MK-7 group · conclusion: “do not support MK-7 supplementation to preserve bone” in dialysis · model: homo-sapiens · archive: pending download — claims from seeder extraction; full-text not verified no-fulltext-access ↩

  11. doi:10.1038/s41430-021-01050-w · PMID:34845313 · El Borolossy R, El-Farsy MS · Eur J Clin Nutr 2022 · rct · n=60 pediatric CKD hemodialysis patients (four groups: K2-only, vitamin D-only, K2+D, control) · combined MK-7 100 µg + native vitamin D showed greatest dp-ucMGP and ucOC reduction over 4 months · pediatric CKD-specific; limited generalizability to non-CKD aging · model: homo-sapiens · archive: local PDF available (not re-read during this verification pass — claims verified against seeder extraction) ↩

  12. doi:10.1053/j.jrn.2023.11.007 · PMID:38128853 · Bladbjerg EM, Levy-Schousboe K, Frimodt-Møller M et al. · J Renal Nutr 2024 · rct (double-blind, placebo-controlled) · n=123 dialysis patients (MK-7 n=61, placebo n=62) · MK-7 360 µg/day × 1 year · coagulation activation markers: no significant differences vs placebo; PIVKA-II decreased in MK-7 group; no adverse event difference · supports coagulation safety of MK-7 at supplemental doses in non-anticoagulated patients · model: homo-sapiens · archive: not_oa no-fulltext-access — claims from seeder extraction; full-text not verified ↩

Graph View

Backlinks