The international supplier of MenaQ7 (vitamin K2 as menaquinone-7) spotlights a newly published cross-sectional clinical study published in Kaohsiung Journal of Medical Sciences which adds to evidence that statins, a regularly prescribed cholesterol medication, may enhance calcium accumulation in the arterial wall by inhibiting vitamin K-dependent proteins involved in vascular protection.
Statins are first‐line drugs in the prevention and treatment of established atherosclerotic cardiovascular disease. Paradoxically, intensive statin therapy has been shown to increase vascular calcification and accelerate its progression however the clinical significance of statin-induced calcification is a matter of controversy and the underlying mechanisms are still to be elucidated.
The aim of the recently published study, “Statins, vascular calcification, and vitamin K-dependent proteins: Is there a relation?”, was to find a putative relation between statin use, coronary calcification, and the vitamin K-dependent proteins as a possible mechanism mediating statins’ pro-calcification.
“According to the study, statins negatively influence vitamin K status. To that end, supplementation with Vitamin K2, which has been shown to effectively improve vitamin K status and activate extrahepatic K-dependent proteins, might prove beneficial for statin users,” says Dr. Hogne Vik, chief medical officer with NattoPharma.
The study enrolled 98 patients – patients with established cardiovascular disease (CVD) and a control group of healthy patients at moderate risk for CVD – and split the groups into statin users and non‐users. The results revealed that both CVD and statin use are independently and significantly associated with vascular calcification.
Among all the study participants, coronary artery calcification score (CACS) was more pronounced in statin users than non‐users; researchers found the same among the CVD patients and the controls. Moreover, the researchers found that statins influenced vitamin K status represented by the activation of osteocalcin (OC), a vitamin K-dependent protein.
Inactive OC and the ratio of inactive and active form of OC (UCR) were significantly elevated in statin users, indicating vitamin K deficiency. According to researchers, statins also impacted the international normalized ratio and interacted with vitamin K antagonists.
These results are in agreement with the existing evidence about the positive association between statins and vascular calcification. A 2015 paper published in Expert Review Clinical Pharmacology stated that statins may act as “mitochondrial toxins” with adverse effects on the heart and blood vessels not only via the depletion of coenzyme Q10 (CoQ10), but also by inhibiting “the synthesis of vitamin K2, the cofactor for matrix Gla-protein activation, which in turn protects arteries from calcification”.
Dr. Vik adds: “NattoPharma has driven research confirming that Vitamin K2 as MK-7 (as MenaQ7) is the only known inhibitor of vascular calcification through the activation of matrix gla protein (MGP). Yet this new study provides further evidence that statins interrupt the mechanism of action by which vitamin K2 is a cardio-protective nutrient.
"And while CoQ10 and vitamin K2 are both affected by statins, no recommendation exists for prescribing supplemental vitamin K2 to statin patients.
“NattoPharma continues to work with the medical community on trials exploring Vitamin K2 as a potential therapy for patients that express heavy calcification,” Dr. Vik concludes. “We hope to encourage K2 supplementation as a recommendation in the future for statin users; especially considering this new evidence.”
