Nephron, a kidney research and clinical journal, and the American Journal of Hypertension 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 recognised 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 individualsi as well as in kidney patients.”
The nephron trial was a cross-sectional study that 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 utilised as an early marker for vascular calcification in CKD patients.
The American Journal of Hypertension trial 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 dpucMGP 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 recognises 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 worldwide 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 3-year interventional study confirmed that adding vitamin K2 to one’s daily diet improves arterial health and flexibility.”
