Vitamin K2 (MK-7)

Vitamin K2 (MK-7) Common Name

Vitamin K2 | MK-7 | Menaquinone 7

Top Benefits of Vitamin K2 (MK-7)

  • Supports bone health*
  • Supports metabolism*
  • Supports exercise performance*
  • Supports ATP production*
  • Support cardiovascular function*
  • Supports brain function*
  • Supports antioxidant defenses*
  • Supports cellular signaling*

What is Vitamin K2 (MK-7)?

Vitamin K is a collective term for a group of structurally related fat-soluble molecules (vitamers) that act as a cofactor for a carboxylase enzyme. This enzyme transforms glutamate residues in proteins to carboxyglutamate residues, which plays an important role in blood clotting and bone health. Dietary vitamin K1 (phylloquinone) is obtained from vegetables, whereas dietary vitamin K2 (menaquinone) is obtained from products of animal origin or bacterial fermentation (e.g., cheese, natto). Vitamin K2 can also be produced by gut bacteria from vitamin K1. There are nine related vitamin K2 compounds—MK-1, MK-2 ... MK-9. The M stands for menaquinone, the K stands for vitamin K, and the n represents the number of isoprenoid side chain residues. In general, vitamin K2 is the preferred form for supporting bone and vascular health.

Neurohacker’s Vitamin K2 (MK-7) Sourcing

Menaquinone-7 (MK-7) is a bioavailable vitamin K2, needing much lower doses than MK-4.

Produced from natto and manufactured by Japan Bioscience Labs (JBSL), a leading Japanese natto manufacturer for decades.

A clinically studied form of vitamin K2 which has been used in studies lasting up to three years. 

Non-GMO, Vegan, Gluten Free

Vitamin K2 (MK-7) Dosing Principles and Rationale

The dose of vitamin K needed will depend on the use and the form used. Of the available forms of vitamin K2, in general, shorter chain forms (MK-4, -5, and -6) require much higher doses than the longer-chain MK-7. Depending on the purpose the amount of vitamin K2 supplemented can vary (i.e., a higher dose would be used to optimize bone health, while a lower dose would be used if its an ingredient intended to support mitochondrial function).

Vitamin K2 (MK-7) Key Mechanisms 

Mitochondrial structure and function

  • Supports electron transport chain and oxidative phosphorylation (ATP production) (1–12)
  • Mitochondrial electron carrier - alternative electron acceptor/donor (complex I-III bypass) (1–3)
  • Protects from complex I-V inhibition (4–9)
  • Supplies complex III cofactors/substrates (10–12)
  • Protects from mitochondrial dysfunction (3, 4, 13)
  • Supports mitochondrial morphology (14)
  • Upregulates AMP-activated protein kinase (AMPK) signaling 24

Metabolism

  • Supports healthy insulin sensitivity (15–19)
  • Upregulates adiponectin levels 18,24 (18)
  • Upregulates uncoupling protein 1 (UCP-1) (18)

Exercise performance (ergogenic effect)

  • Supports endurance performance (20)
  • Protects from muscle cramps (21)
  • Supports post-exercise recovery (1, 2)

Skeletal system

  • Promotes the formation of bone (22, 23)

Cardiovascular function

  • Regulates blood coagulation (22, 23)
  • Protects from vascular calcification and arterial stiffening (22, 23)
  • Supports cardiac output (during exercise) (20)
  • Protects cardiac cells from hypoxia (4)

Cellular signaling

  • Downregulates the expression of proinflammatory mediators – nuclear factor (NF-κB), glycogen synthase kinase 3 beta (GSK-3β), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α) (13, 24, 25)

Antioxidant defenses

  • Downregulates the generation of reactive oxygen species (8, 13, 26)

Brain function

  • Protects neurons from neurotoxic agents and oxidative damage (8, 26)

Gut microbiota

  • Supports the production of short-chain fatty acids (SCFAs) by the gut microbiota (24)

REFERENCES

1. S. Eleff et al., Proc. Natl. Acad. Sci. U. S. A. 81, 3529–3533 (1984).
2. Z. Argov et al., Ann. Neurol. 19, 598–602 (1986).
3. M. Vos et al., Science. 336, 1306–1310 (2012).
4. V. Shneyvays, D. Leshem, Y. Shmist, T. Zinman, A. Shainberg, J. Mol. Cell. Cardiol. 39, 149–158 (2005).
5. F. A. Wijburg, C. J. de Groot, N. Feller, R. J. Wanders, J. Inherit. Metab. Dis. 14, 293–296 (1991).
6. J. M. Cooper, D. J. Hayes, R. A. Challiss, J. A. Morgan-Hughes, J. B. Clark, Brain. 115 ( Pt 4), 991–1000 (1992).
7. F. A. Wijburg, N. Feller, C. J. de Groot, R. J. Wanders, Biochem. Int. 22, 303–309 (1990).
8. N. K. Isaev, E. V. Stelmashook, K. Ruscher, N. A. Andreeva, D. B. Zorov, Neuroreport. 15, 2227–2231 (2004).
9. T. S. Chan et al., Free Radic. Res. 36, 421–427 (2002).
10. W. W. Anderson, R. D. Dallam, J. Biol. Chem. 234, 409–411 (1959).
11. R. E. Beyer, J. Biol. Chem. 234, 688–692 (1959).
12. C. E. Horth et al., Biochem. J. 100, 424–429 (1966).
13. Y.-X. Yu et al., Acta Pharmacol. Sin. 37, 1178–1189 (2016).
14. L. M. Baldoceda-Baldeon, D. Gagné, C. Vigneault, P. Blondin, C. Robert, Reproduction. 148, 489–497 (2014).
15. H. J. Choi et al., Diabetes Care. 34, e147 (2011).
16. M. Yoshida et al., Diabetes Care. 31, 2092–2096 (2008).
17. N. Sakamoto, T. Nishiike, H. Iguchi, K. Sakamoto, Clin. Nutr. 19, 259–263 (2000).
18. A. G. Hussein, R. H. Mohamed, S. M. Shalaby, D. M. Abd El Motteleb, Nutrition. 47, 33–38 (2018).
19. Y. Li, J. P. Chen, L. Duan, S. Li, Diabetes Res. Clin. Pract. 136, 39–51 (2018).
20. B. K. McFarlin, A. L. Henning, A. S. Venable, Altern. Ther. Health Med. 23, 26–32 (2017).
21. D. S. Mehta et al., The Indian Practitioner. 63, 287–291 (2010).
22. T. Krueger, R. Westenfeld, L. Schurgers, V. Brandenburg, Int. J. Artif. Organs. 32, 67–74 (2009).
23. J. W. J. Beulens et al., Br. J. Nutr. 110, 1357–1368 (2013).
24. Y. Zhang et al., Oncotarget. 8, 24719–24727 (2017).
25. H. Zhang et al., Oncol. Rep. 25, 159–166 (2011).
26. J. Li et al., J. Neurosci. 23, 5816–5826 (2003).

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.