The European Journal of Preventive Cardiology has published a new review paper examining the link between micro-calcification and atherosclerosis, focusing on cardiovascular imaging techniques and evaluating the concept of vitamin K supplementation to preserve cardiovascular health.
The review paper, the result of the INTRICARE grant awarded to NattoPharma's International Research Network by the European Union within the Horizon 2020 Marie Skłodowska-Curie research and innovation programme, is another strong piece of evidence identifying vitamin K2 as an essential cardiovascular nutrient.
The authors of "Locking and loading the bullet against micro-calcification", identified the most suitable technique for detecting micro-calcification and assessed state-of-the-art meta-analysis and clinical studies to identify possible treatment options and evaluate the concept of vitamin K supplementation to preserve vascular health. "Despite recent medical advances, cardiovascular disease remains the leading cause of death worldwide," said Prof Schurgers, Professor of Biochemistry of Vascular Calcification and Vice Chair of Biochemistry at the Cardiovascular Research Institute Maastricht (CARIM), Maastricht University.
"Our exhaustive, structured PubMed search showed that 18 F-socium fluoride ( 18 F-NaF) PET is the most suitable technique for detecting active micro-calcification, a hallmark of atherosclerosis," Schurgers added.
Presenting the pros and cons of available treatments, "vitamin K supplementation should be considered as a possible safe and cost-effective option to inhibit vascular (micro)-calcification," the paper concludes. The paper is significant because it adds to the growing body of evidence substantiating vitamin K2 as an essential cardiovascular support nutrient, according to NattoPharma Chief Medical Officer Dr Hogne Vik.
"There are some who view atherosclerosis as an age-related condition - that calcification simply builds up over time. NattoPharma contends that this condition is not simply age-related; rather, that atherosclerosis is the product of a vitamin deficiency: vitamin K2," said Dr Vik. "Matrix Gla Protein (MGP) is the most potent known inhibitor of vascular calcification to date. MGP is a K dependent protein already present in the body, but it needs adequate Vitamin K2 in order to be activated to perform its function. Our three-year clinical study 2 of healthy postmenopausal women showed that 180mcg of MenaQ7 Vitamin K2 as MK-7 daily resulted in not only cessation, but remarkably regression in arterial stiffness (i.e., their arteries became more flexible) in the MenaQ7 group through activation of MGP."
It is important to note that no other compound to date has been able to produce the results experienced with a daily nutritional dose of Vitamin K2 as MK-7 (as MenaQ7)," Dr. Vik added. "This study has served as a platform for other clinical trials investigating K2 in patient populations with existing coronary artery calcification, aortic valve calcification, and peripheral artery calcification, and these studies are being driven by the medical community."
"The work conducted in collaboration with NattoPharma under the INTRICARE grant has not only helped us shine a light on the most reliable technique for detecting active micro-calcification, providing some hope in getting ahead of compromised cardiovascular health, but also the science supporting various therapy options, including supplementation," said Prof Schurgers.
"Essentially, this work will help drive awareness how we can 'lock in' on the effects of vascular calcification ( 18 F-NaF PET) and 'load' a suitable, cost-effective bullet (vitamin K)"
The review paper is the result of the INTRICARE (grant agreement No 722609) grant funded by the European Union within the Horizon 2020 Marie Skłodowska-Curie research and innovation program, awarded to NattoPharma's International Research Network to train a total of 26 Early Stage Researchers (ESRs) focusing on harnessing endogenous mechanisms for health and the effect of vitamin K to hold or regress microcalcification and subsequent cardiovascular disease.