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720 mcg Vitamin K2 + D3 Ngerem Kalikasi Arteri nganti 21 % ing RCT

Dr. Synapse · · 4 min read
#clinical trial #vitamin d3 #cardiovascular health #vitamin k2 #coronary calcification #mk 7

Asil utama, nganggo tembung prasaja

Panlitén randomised rong taun sing diterbitaké ing Circulation taun 2026 nuduhaké yèn kombinasi vitamin K2 lan vitamin D3 ing dosis dhuwur bisa ngerem pertumbuhan kalikasi arteri koroner ing wong sing wis nduwèni akumulasi kalsium akeh. DANCODE trial ngrekrut 400 wong diwasa kanthi kalikasi koroner parah, diartèkaké minangka skor calcium arteri koroner (CAC) paling ora 400 unit Agatston (AU). Padha diparingi K2 + D3 utawa plasebo sajrone 24 sasi, kanthi desain double‑blind.

Skor CAC rata‑rata munggah 196 AU ing grup K2 + D3 lan 248 AU ing grup plasebo. Iki artiné beda antarane grup ‑52 AU (95 % CI, ‑79 nganti ‑24). Dibandhingaké karo progresi grup plasebo, iki kira‑kira ngerem pertambahan nganti 21 %.

Iku asil utama. Cathetan watesan uga penting, lan bakal dibahas ing ngisor iki.

Apa sing ditindakake panlitén iki

DANCODE iku panlitén multicenter, double‑blind, kontrol plasebo. Peserta didaftar antara Februari 2023 lan Februari 2024. Poin desain utama:

  • Peserta: 398 dianalisis (30 % wanita), median umur 71 taun, median CAC awal 903 AU. Kira‑kira 44 % nduwèni CAC ≥ 1000 AU.
  • Intervensi: vitamin K2 720 µg saben dina + vitamin D3 25 µg saben dina (1 000 IU), dibandhingaké karo plasebo.
  • Durasi: 24 sasi, nganggo CT kardio non‑kontras ing wiwitan, 12 sasi, lan 24 sasi.
  • End‑point utama: owah‑owahan skor CAC ing 24 sasi, dianalisis kanthi intention‑to‑treat.
  • Registrasi: ClinicalTrials.gov NCT05500443.

Efeké dilaporké konsisten antarane jinis kelamin lan antarane loro subkelompok CAC dhasar (400‑999 AU lan ≥1000 AU).

Ngapa progresi CAC penting

Skor CAC dadi cara umum kanggo ngukur plak kalkifikasi ing arteri koroner. Progresi sing cepet gegandhengan karo risiko luwih dhuwur kanggo kejadian kardiovaskular, mulané dadi surrogate marker umum ing kardiologi. Sadurungé iki, ora ana apa‑apa sing jelas bisa ngerem progresi saliyane ngatur faktor risiko dhasar. Statin, contoné, penting kanggo ngurangi risiko, nanging biasané karo peningkatan kepadatan kalkifikasi amarga plak dadi luwih stabil.

Protein‑protein sing gumantung vitamin K, utamané matrix Gla protein, mbantu nahan deposit kalsium ing tembok pembuluh, lan iki dhasaré alasan biologis kanggo nyoba K2. DANCODE minangka uji coba gedhé, terkontrol sing nyoba hipotesis iki ing populasi kanthi penyakit tahap akhir.

Temuan komposisi plak

Kekhawatiran marang terapi sing nyasar kalsium asring kuwatir yèn bakal mung ngalihaké plak dadi wujud sing kurang stabil. Plak kalkifikasi umumé dianggep luwih stabil tinimbang plak lunak non‑kalkifikasi.

Kanggo mangertèni iki, sub‑kelompok 143 peserta (sing CAC‑ne < 1000 AU) uga nindakake coronary CT angiography ing wiwitan lan 24 sasi. Hasilé:

  • Volume total plak mundhak kanthi cara sing padha ing loro grup.
  • Volume plak non‑kalkifikasi ora béda antarane grup, dadi ora ana tandha yèn kalsium dipindhahake dadi plak lunak.
  • Volume plak kalkifikasi mundhak luwih sithik ing grup K2 + D3, kanthi beda antarane grup ‑8 mm³ (95 % CI, ‑13 nganti ‑2).

Penulis nyimpulaké yèn penurunan progresi kalkifikasi ora disambung karo peningkatan volume plak non‑kalkifikasi. Iki nyenengaké, nanging analisis subkelompok kanthi sampel cilik, lan interval kapercayané cukup amba.

Jujur babagan apa sing ora dituduhaké

Asilé ndadékaké harapan, nanging gampang kanggo nggedhekaké. Watesan‑watesan sing kudu dielingi:

  • Ngerem progresi, ora mbalèkaké kalsium. Loro grup tetep nambah kalsium. Skor grup K2 + D3 munggah rata‑rata 196 AU, tegesé intervensi mung ngurangi laju pertambahan, ora ngilangi deposit sing wis ana.
  • Ora ana data kejadian klinis. End‑point utama iku marker imaging. Panlitén ora dirancang utawa dilaporaké kanggo nuduhaké suda serangan jantung, stroke, revaskularisasi, utawa mortalitas. Apa beda 52 AU ing rong taun bakal nyebabaké suda kejadian isih ora jelas.
  • Populasi khusus, tuwa, risiko tinggi. Median umur 71 taun lan kabeh peserta nduwèni CAC parah. Asil ora mesti bisa digeneralisasi kanggo wong enom, sing CAC‑ne rendah utawa nol, utawa sing nduwèni penyakit luwih enteng.
  • Tindak lanjut loro taun. Panlitén luwih suwe dibutuhaké kanggo ndelok apa efek iki lestari utawa tambah.
  • Desain kombinasi. K2 lan D3 diparingi bareng, dadi panlitén ora bisa misahake kontribusi K2 dhéwé.

Produk apa sing digunakaké?

Abstrak ora nyebut jeneng produk komersial. Laporan saka NutraIngredients nyebut yèn K2 sing dipigunakaké iku Balchem's K2VITAL, wujud menaquinone‑7 (MK‑7). Iki mung informasi saka pers, dudu konfirmasi resmi saka abstrak, mula priksa metodologi lengkapé kanggo rincian formulasi. Asil saka siji bentuk lan dosis ora otomatis bisa dipindhahaké marang produk K2 liyané, utamané sing dosisé luwih endhek lan dijual bebas.

Ringkesan praktis

  • Dosis sing diuji: 720 µg K2 + 25 µg (1 000 IU) D3 saben dina. Iki jauh luwih dhuwur tinimbang jumlah K2 ing akèh multivitamin standar.
  • Sapa sing bisa relevan: wong tuwa kanthi kalikasi koroner parah, paling apik yèn ing rangka rencana kardiologi. Bukti ora ndhukung yèn wong kanthi skor kalsium rendah kudu ngonsumsi iki.
  • Ora nggentosi perawatan standar. Pengendalian tekanan darah, LDL, gula darah, mandheg rokok, lan terapi resep tetep dadi dhasar pencegahan kardiovaskular.
  • Rembugan dhokter dhisik yen ngombe warfarin utawa antagonis vitamin K liyané. Vitamin K langsung mengaruhi cara kerja obat iki, lan owah‑owahan asupan bisa ngowahi anticoagulation. Aja miwiti suplemen K2 dosis dhuwur tanpa pengawasan klinis lan monitoring INR.
  • Uga konsultasi dhokter yen sampeyan duwe penyakit ginjal, njupuk antikoagulan liya, utawa kondisi kompleks liyané.

Kesimpulan

DANCODE dadi salah siji bukti randomised paling kuat nganti saiki yèn vitamin K2 + D3 bisa ngowahi marker imaging saka penyakit koroner, kanthi efek konsisten antar subkelompok lan tanpa sinyal peningkatan plak lunak. Nanging panlitén mung nuduhaké perlambatan akumulasi kalsium ing kohort tuwa, risiko tinggi, ora mbalèkaké kalsium sing wis ana, lan durung ana bukti manfaat klinis. Pitakon sabanjuré yaiku apa efek iki lestari, apa nyuda kejadian kardiovaskular nyata, lan pira kontribusi K2 dhéwé. Samentara iku, iki dadi adjunct sing menjanjikan kanggo dibahas karo kardiolog, ora dadi pengganti terapi sing wis kabukten.

Source: Hasific et al., Circulation (2026), PMID 42661461, DOI 10.1161/CIRCULATIONAHA.126.082363.

Original study

Read the original research on pubmed.ncbi.nlm.nih.gov →

This article summarizes published research for general information. It is not medical advice.

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DS

Written by

Dr. Synapse

Dr. Synapse writes for Biocracked: biohacking science, longevity & human performance.

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