Vitamin K deficiency: the linking pin between COPD and cardiovascular diseases?
Respir Res. 2017 Nov 13;18(1):189. doi: 10.1186/s12931-017-0673-z.
Piscaer I1, Wouters EFM2,3, Vermeer C4, Janssens W5, Franssen FME2,3, Janssen R6.
1 Department of Respiratory Medicine, Maastricht University Medical Center+, Maastricht, The Netherlands. ianthe.piscaer@mumc.nl.
2 Department of Respiratory Medicine, Maastricht University Medical Center+, Maastricht, The Netherlands.
3 CIRO, Center of Expertise for Chronic Organ Failure, Horn, The Netherlands.
4 R&D Group VitaK, Maastricht University, Maastricht, The Netherlands.
5 Department of Chronic Diseases, Metabolism and Ageing, Laboratory of Respiratory Disease, University of Leuven, Leuven, Belgium.
6 Department of Pulmonary Medicine, Canisius-Wilhelmina Hospital, Nijmegen, The Netherlands.
Note: This paper adds another hypothesis as to WHY increased COPD increases CVD
Seem feasible - I was unable to find out how often anticogulants are used with worsening COPD
- COPD and Osteoporosis are related – vitamin D is one possible connection – 2013
- Vascular calcification greatly reduced by 3 per week 1000 ug of Vitamin K2 MK-7 – Dec 2013
- Low Vitamin K2 is as risky as smoking for heart disease - Oct 2016
- Decreased need for warfarin after Vitamin D levels optimized – RCT May 2016
less warfarin needed and thus less loss of Vitamin K if high level of Vitamin D
See also web
- Anticoagulation therapy in patients with chronic obstructive pulmonary disease in the acute exacerbation stage May 2013 free PDF online
- COPD increases many CVD problems- 1999
Download the PDF from VitaminDWiki
Cardiovascular diseases are prevalent in patients with chronic obstructive pulmonary disease (COPD). Their coexistence implies that many COPD patients require anticoagulation therapy. Although more and more replaced by direct oral anticoagulants, vitamin K antagonists (VKAs) are still widely used. VKAs induce profound deficiency of vitamin K, a key activator in the coagulation pathway. It is recognized however that vitamin K is also an essential cofactor in the activation of other extrahepatic proteins, such as matrix Gla protein (MGP), a potent inhibitor of arterial calcification. No or insufficient MGP activation by the use of VKAs is associated with a rapid progression of vascular calcification, which may enhance the risk for overt cardiovascular disease. Vitamin K consumption, on the other hand, seems to have a protective effect on the mineralization of arteries.
Furthermore, vascular calcification mutually relates to elastin degradation, which is accelerated in patients with COPD associating with impaired survival. In this commentary, we hypothesize that vitamin K is a critical determinant to the rate of elastin degradation. We speculate on the potential link between poor vitamin K status and crucial mechanisms of COPD pathogenesis and raise concerns about the use of VKAs in patients with this disease. Future intervention studies are needed to explore if vitamin K supplementation is able to reduce elastin degradation and vascular calcification in COPD patients.
PMID: 29132356 PMCID: PMC5683584 DOI: 10.1186/s12931-017-0673-z