Vitamin K for Cardiovascular Disease

Verdict: No proven cardiovascular benefit from vitamin K

Despite encouraging observational data and a plausible mechanism, vitamin K (including K2/MK-7) has not been shown in rigorous trials to prevent heart disease or slow arterial and valve calcification, so it is not a justified supplement for cardiovascular protection. Anyone on warfarin or another vitamin K antagonist should not change their vitamin K intake without medical supervision.

D 🔴 D Counter-Evidence Insufficient Evidence

🔬Why this grade7-layer evidence engine

The evidence shows a classic split between observation and intervention. The Rotterdam Study (PMID 15514282, n=4,807) linked higher dietary K2 intake to lower coronary heart disease mortality (RR 0.43, 95% CI 0.24-0.77), but observational diet cohorts cannot rule out reverse causation or that K2-rich eaters are simply healthier overall.

Randomized trials, which carry far more weight, do not confirm a benefit. The largest and best-designed trial, AVADEC (PMID 35465686, n=365, MK-7 720 ug plus vitamin D over 24 months), found no slowing of aortic valve calcification (between-group difference 17 AU, P=0.64) and no effect on coronary calcification. Positive signals are confined to surrogate markers and are weak: a 2023 meta-analysis (PMID 37252246, 14 RCTs, n=1,533) found only a marginal reduction in coronary calcium score (MD -17.37 AU, upper CI essentially at null, P=0.04), Knapen 2015 (PMID 25694037) improved arterial stiffness but was industry-funded, and a 2024 meta-analysis (PMID 38282652, 17 RCTs) found everything but HOMA-IR unchanged. The earlier positive Brandenburg trial (PMID 28533322) was small, open-label, and superseded by AVADEC.

Regulators and clinicians reinforce the low grade. The FDA, EFSA, and WHO authorize vitamin K only for blood clotting, bone maintenance, and newborn bleeding prophylaxis, with no cardiovascular claim, and the NHS advises a food-first approach. Mayo Clinic states clinical trials show no evidence it slows arterial calcium, Harvard calls the research very limited, and the American Heart Association highlighted AVADEC's negative result. No trial has demonstrated reduced heart attack, stroke, or cardiovascular death.

⚖️

Scoring transparency

All scores computed by a 7-layer evidence engine — fully auditable
Raw score 0.39
D
C
B
A
S
← counter-evidence / ineffectiveeffective / strong evidence →
Final grade
D · Insufficient Evidence
Confidence
85%
Highly consistent evidence
Evidence level
E2
Multiple high-quality MAs (≥2 independent, consistent)

How strongly each layer supports this effect

lower = less supportive
L11 AI re-checkIndependent read
0.20
L5 Clinical bodiesAuthoritative stance
0.35
L2 PubMedPrimary literature
0.45
L3 MechanismPlausibility
0.45
L1 ExamineGlobal benchmark
0.50
Against Mixed Supports
View the full decision path (audit trail)
  1. compute_raw_score — 加權公式: L2×0.30 + L3×0.25 + L5×0.25 + L11×0.10 + L1×0.10 = 0.385
  2. tier_from_score — 依分數區間映射至 tier letter
  3. apply_hec_rules — 無高階證據可裁決
  4. tier_strict_requirement_check — Tier 條件達標,未降階
  5. detect_disputes — 偵測到 0 個 hard + 1 個 soft dispute
  6. decide_status — 依 tier + dispute 結果決定 status

📄PubMed studies (6)L2 · primary research & systematic reviews

Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study
PMID: 15514282 2004 Cohort n = 4,807
Finding: Highest tertile of dietary menaquinone (K2) intake associated with lower CHD mortality (RR 0.43, 95% CI 0.24-0.77) and reduced severe aortic calcification vs lowest tertile; no association seen for phylloquinone (K1).
Government Effect size: [object Object]
View on PubMed
Menaquinone-7 supplementation improves arterial stiffness in healthy postmenopausal women. A double-blind randomised clinical trial
PMID: 25694037 2015 RCT (double-blind) n = 244
Finding: MK-7 significantly reduced cfPWV and Stiffness Index β vs placebo over 3 years (most pronounced in women with baseline Stiffness Index β > median 10.8); dp-ucMGP fell ~50% confirming biochemical activity. Surrogate endpoints only — no hard CV outcomes.
⚠️ Industry-funded Effect size: [object Object]
View on PubMed
Slower Progress of Aortic Valve Calcification With Vitamin K Supplementation: Results From a Prospective Interventional Proof-of-Concept Study
PMID: 28533322 2017 隨機對照試驗 n = 99
Finding: Vitamin K1 arm showed slower AVC progression than placebo in this small open-label proof-of-concept trial (n=99 enrolled, 72 completed); 27% dropout, no ITT analysis presented. Hypothesis-generating only — not confirmed by larger AVADEC trial.
🟠 Limited quality Academic
View on PubMed
Vitamin K2 and D in Patients With Aortic Valve Calcification: A Randomized Double-Blinded Clinical Trial
PMID: 35465686 2022 RCT (double-blind) n = 365
Finding: AVADEC trial: no significant difference in AVC progression (intervention +275 AU vs placebo +292 AU, between-group diff 17 AU, P=0.64) despite confirmed biochemical effect. Coronary calcification progression also not significantly slowed. Negative for primary endpoint.
🟢 High quality Mixed funding Effect size: [object Object]
View on PubMed
Vitamin K supplementation and vascular calcification: a systematic review and meta-analysis of randomized controlled trials
PMID: 37252246 2023 統合分析 n = 1,533
Finding: Pooled across 14 RCTs (n=1533) vitamin K modestly slowed CAC progression (MD -17.37 AU, 95% CI -34.18 to -0.56, P=0.04) and lowered dp-ucMGP (MD -243.31, P=0.0001). Effect on CAC is small, marginal, surrogate-only; no hard CV event outcome pooled.
Academic Effect size: [object Object]
View on PubMed
The effect of vitamin K supplementation on cardiovascular risk factors: a systematic review and meta-analysis
PMID: 38282652 2024 統合分析
Finding: Across 17 RCTs only HOMA-IR improved with vitamin K (WMD -0.24, 95% CI -0.49 to -0.02, P=0.047); no significant effect on anthropometrics, CRP, glucose, or lipid panel. K2 subgroup slightly stronger on insulin resistance than K1. No hard CV outcomes assessed.
Academic Effect size: [object Object]
View on PubMed

🏛️Regulatory & authoritative positionsL4/L5 · FDA / EMA / NIH ODS / Cochrane / Mayo …

L4a US FDA
Supportive
Vitamin K1 Injection is indicated for prophylaxis and treatment of vitamin K-deficiency bleeding in neonates source↗
L4b EU EFSA
Supportive
a cause and effect relationship has been established between the dietary intake of vitamin K and normal blood coagulation ... and the maintenance of normal bone source↗
L4c UK NHS
Cautious
You should be able to get all the vitamin K you need by eating a varied and balanced diet. Any vitamin K your body does not need immediately is stored in the liver for future use, so you do not need it in your diet every day. source↗
L4d TW TFDA / 衛福部
Supportive
成年男性 120 微克/日,女性 90 微克/日(足夠攝取量 AI) source↗
L4e WHO
Supportive
vitamin K1 should be given to all newborns as a single, intramuscular dose of 0.5–1 mg source↗
L5a NIH Office of Dietary Supplements
Supportive
Vitamin K, the generic name for a family of compounds with a common chemical structure of 2-methyl-1,4-naphthoquinone, is a fat-soluble vitamin source↗
L5b Mayo Clinic
Cautious
Clinical trials have not shown any evidence that vitamin K supplements can slow calcium deposits in artery walls. source↗
L5c Cleveland Clinic
Cautious
Vitamin K may even reduce your risk of cardiovascular disease and death. source↗
L5d Harvard Health
Neutral
Vitamin K is involved with the production of matrix Gla proteins (MGP), which help to prevent calcification or hardening of heart arteries source↗
L5e Specialty Society (condition-mapped)
Against
Vitamin K2 and vitamin D supplements did not slow the progression of calcium deposits on the aortic valves. source↗
PMID 100% verifiedevery citation checked via NCBI Entrez
🔬6 PubMed studiesindependently re-checked by multiple sub-agents
engine_version: v1.0 claim_id: CLM-COND-cardiovascular-disease-INT-vitamin-k-001 繁體中文版 →