OSLO, NORWAY and METUCHEN, NJ (5 January 2017) – Nephron¸ a kidney research and clinical journal, and the American Journal ofHypertension have each just published new papers linking the vitamin K-dependent protein MGP (matrix GLA-protein) to vascular calcification, vascular and arterial stiffness. The two studies, “Correlations of Plasma Desphosphorylated Uncarboxylated Matrix Gla Protein with Vascular Calcification and Vascular Stiffness in Chronic Kidney Disease,” and “Inactive Matrix Gla-Protein and Arterial Stiffness in Type 2 Diabetes Mellitus,” respectively, have linked increased risk of arterial calcification and stiffness to a lack of the active protein. One set of authors even recommended supplementation of vitamin K as a potential treatment.
“The mechanism of MGP inhibiting arterial calcification has been clearly established in cellular, animal and now human studies,” says Hogne Vik, chief medical officer with NattoPharma, world pioneer in vitamin K2 product development. “In fact, adequate vitamin K is required to activate MGP. It is widely recognized that vitamin K2 as Menaquinone-7 is the most bioavailable and bioactive form of vitamin K available as a supplement today.”
Vik continued, “These new clinical investigations have documented correlations between arterial calcification and high amounts of inactive MGP – both in diabetic patients and in patients with CKD. The good news is that Vitamin K2 – our MenaQ7® brand MK-7 ingredient – is demonstrated to reduce the levels of ‘inactive’ dp-uc-MGP, and that MenaQ7 is documented to reduce arterial stiffness in healthy individuals[i] as well as in kidney patients.[ii]”
The nephron trial was a cross-sectional study which enrolled 83 CKD stages 3–5 patients. Vascular calcification scores were determined by measuring calcific lesions in the abdominal aorta, vascular stiffness was assessed using a cardio-ankle vascular index (CAVI) and pulse wave velocity, while plasma dpucMGP, or inactive MGP, levels were measured using an ELISA method. The study selected factors that were independently associated with vascular calcification and vascular stiffness.
The authors concluded the inactive MGP levels in blood plasma increase according to the severity of chronic kidney disease. Also, inactive MGP levels were positively associated with increased vascular calcification and might be utilized as an early marker for vascular calcification in CKD patients.
The American Journal of Hypertension trail sought to identify pathways related to arterial stiffness to provide novel therapeutic targets to help reduce arterial stiffness in diabetes patients as large artery stiffness is increased in diabetes which increases the burden to the heart and microvasculature. Looking at a group of 66 diabetes type 2 patients, pulse wave velocity (PWV) was used as a measure of stiffness, and inactive or dp-ucMGP was measured by the vitamin K experts at VitaK, the Netherlands.
The authors concluded that inactive MGP was independently associated with pulse wave velocity in these diabetes patients. The authors noted: “This suggests that deficient vitamin K-dependent activation of MGP may lead to large artery stiffening and could be targeted with vitamin K supplementation in the patients with diabetes.”
“NattoPharma recognizes and is appreciative of the growing body of evidence definitively linking vitamin K status and active vitamin K-dependent proteins to health outcomes,” notes Dr. Vik. “NattoPharma is the world-wide pioneer in developing and providing MenaQ7 products as dietary supplements, and the recent publications are increasing the recognition of intake of vitamin K2 as a pathway to better health outcomes. Our three-year interventional studyi confirmed that adding vitamin K2 to one’s daily diet improves arterial health and flexibility.”
1 Mayank Sardana, Izzah Vasim, Swapna Varakantam, Uzma Kewan, Ali Tariq, Maheshwara R. Koppula, Amer Ahmed Syed, Melissa Beraun, Nadja E.A. Drummen, Cees Vermeer, Scott R. Akers, and Julio A. Chirinos
Inactive Matrix Gla-Protein and Arterial Stiffness in Type 2 Diabetes Mellitus. Am J Hypertens 2016 : hpw146v1-hpw146 http://ajh.oxfordjournals.org/content/early/2016/12/06/ajh.hpw146.abstract
2 Thamratnopkoon S.a · Susantitaphong P.a · Tumkosit M.b · Katavetin P.a · Tiranathanagul K.a · Praditpornsilpa K.a · Eiam-Ong S.a. Correlations of Plasma Desphosphorylated Uncarboxylated Matrix Gla Protein with Vascular Calcification and Vascular Stiffness in Chronic Kidney Disease. Nephron. 2016 Dec 13. [Epub ahead of print] DOI: 10.1159/000453368 https://www.karger.com/Article/Abstract/453368
MenaQ7® is the best documented, commercially available vitamin K2 as MK-7 with guaranteed actives and stability, clinical substantiation, and international patents granted and pending. MenaQ7® is available in two varieties: natural vitamin K2 as MK-7 Crystals and nature-identical synthetic vitamin K2 as MK-7 PURE. For more information on the health benefits of MenaQ7, visit menaq7.com.
NattoPharma ASA, based in Norway, is the world’s leader in vitamin K2 research and development. NattoPharma is the exclusive international supplier of MenaQ7® Vitamin K2 as MK-7, and has a multi-year research and development program to substantiate and discover the health benefits of vitamin K2 for applications in the marketplace for functional food and dietary supplements. With a global presence, the company established its North American subsidiary, NattoPharma USA, Inc., in Metuchen, NJ. For more information, visit nattopharma.com.
For more information, please contact:
Eric Anderson, Marketing Director, NattoPharma USA, Inc.
Phone: 609-454-2992; E-mail: email@example.com
[i] Knapen MH et al, Braam LAJL, Drummen NE, Bekers O, Hoeks APG, Vermeer C. Menaquinone-7 supplementation improves arterial stiffness in healthy postmenopausal women: double-blind randomised clinical trial. Thrombosis and Haemostasis. 2015 113 5: 1135-1144. doi: 10.1160/TH14-08-0675.
[ii] Bahous SA, Hariri E, Mansour A, Daaboul Y, Korjian S, Alam A, Protogerou AD, Kilany H, Karam A, Stephan A. Vitamin K2 Supplementation and Arterial Stiffness in the Renal Transplant Population – A Single-Arm, Single-Center Clinical Trial. Presented at XXX November 24, 2016.