Terms, Tips, Trivia

• We constantly come across information about vitamin K and people, that is interesting and valuable to know!

• We thought this page was a way to offer those nuggets of knowledge in an ongoing, random manner.

• For the sake of reference, we are numbering the items, and providing a scientific reference if you'd like to investigate the information further.

• The research on vitamin K and vitamin K-dependent proteins is rapidly expanding, and offers a wealth of information. We thought you'd enjoy the chance to read about it in a new format.

 

 

1. Vitamin K is a multifunctional nutrient! Various tissues throughout the body function differently in the presence of vitamin K, due to proteins in those tissues that depend on vitamin K.  (Shiraki,Tsugawa et al, 2015).

 

2. One vitamin K dependent protein is osteocalcin (OC). Ostelcalcin is the most abundant non collagenous protein in bone.  Osteocalcin needs vitamin K to carboxylate and active it. 
   Osteocalcin stabilizes bone.
   Osteocalcin is regarded as a bone derived hormone
   Osteocalcin helps regulate glucose or blood sugar
   Osteocalcin research supports that higher intakes of vitamin K is associated with a reduction in insulin resistance and improved glycemic status (Pittas et al 2009; Shea et al 2009).

 

3. The ICIM, International College of Integrative Medicine ( https://icimed.com/ ) is a community of dedicated physicians who seek the latest research in preventative, alternative, and innovative treatments.  The members are physicians who are interested in utilizing more than just drugs or surgical procedures in the holistic care of our patients.  ICIM creates a space where physicians and other health care providers can learn about the latest scientific evidence for integrative medicine from around the world.  They also create a space for people seeking a physician that treats the whole of them, rather than a simple symptom.       If you click here, you can look for the nearest practitioner.  https://icimed.com/icim-member-search/

 

4. Commonly used anticoagulant drugs such as warfarin, that act as vitamin K antagonists (VKA), have been shown to lead to aortic calcification (Basta et al, 2004; Chatrou et al, 2012; Flore et al, 2013).

 

5. Carboxylated MGP forms a mass complex with calcium phosphate and Fetuin (Price, Thomas, Pardini et al 2002). Fetuin is complementary, important circulatory protein that inhibits calcium phosphate crystal precipitation.  Deficiencies in fetuin protein has been linked with soft tissue mineralization (Merx, Schafer, Westenfeld, et al, 2005).

 

6. Measures of Fetuin could provide a complementary adjunct to assess the level of calcification inhibitory action present.

 

7. -Dp-ucMGP stands for dephosphorylated-uncarboxylated matrix Gla protein. It can measured as the circulating levels of inactive MGP.  Dp-ucMGP reflects the burden of vitamin K-dependent proteins that have not been activated by vitamin K and could be regarded as a biomarker of a vitamin K deficit.  Dp-ucMGP levels decreased after vitamin K supplementation, meaning that more of the MGP is carboxylated and active. 

 

8. -Warfarin is an antagonist of vitamin K. Warfarin restrains the turnover of vitamin K and prevents its recycling, which leads to the depletion of functional vitamin K.  It also blocks the carboxylation of matrix Gla protein, a key calcification inhibitor (Jiang et al, 2016). 

 

12. At present there are at 17 types of vitamin K-dependent proteins, though there is discussion of adding two more. They are prothrombin (II) , proconvertin (VII), antihemophilic factor (IX), Stuart Factor (X), Matrix Gla Protein (MGP), Growth arrest-specific protein 6 (Gas6), anticoagulant proteins, C, S, and Z, osteocalcin (OC), Gla-rich protein (GRP), periostin, Periostin-like-factor(PLF), proline-rich Gla protein 1 (PRGP1), PRGP2, Transmembrane Gla protein 3 (TMG), and TMG4.  (there are four isoforms of periostin and each of these subtypes could be considered to be a VKDP)
    1. Vitamin K-dependent protein, MGP, OC, Gas6, and GRP are in tissue outside the liver.
    2. The coagulation factors and the anticoagulation proteins C,S, and Z, all depend on vitamin K in liver synthesis.
    3. The function of the proline-rich Gla proteins, PRGP1, PRGP2, and the Transmembrane Gla proteins, TMG3 and TMG4, remain unclear at this time.

 

13. MK7 is the most hydrophobic form (fails to mix with water) of a K-dependent protein due to its longer isoprenoid chain.  Its properties permit it to be transported by plasma lipoproteins, increases its extrahepatic availability, and lets it exhibit the longest half-life (3 days)  (Price, 1988).

 

14. ALP is a bone metabolism marker. ALP is often used as a maker of vascular calcification, which is the key enzyme for promoting matrix mineralization and is an early indicator of osteogenic differentiation (calcium precursor).

 

15. Calcification of atherosclerotic plaques mainly occurs in the intimal layer of the vasculature. Medial calcification, which is in a different layer is more frequently observed in the arteries of patients with renal disease and diabetes (Lanzer, Boeh  et al, 2014).

 

16. CAC (coronary artery calcification) can be measured clinically by noninvasive electron beam computed tomorgraph (EBCT) and by multidetector computed tomography (MDCT) and by invasive intravascular ultrasound (IVUS). These techniques register and quantify plaque volume and macrocalcification (calcium deposited greater than 200 um).  They do not detect microcalcifications. (Vengrenyuk, Cartier et al, 2006).

 

17. Warfarin a vitamin K antagonist that targets both vitamin K-dependent coagulation factors and vitamin K-dependent extra-hepatic proteins, such as matrix Gla protein.  Warfarin treatment of people with CAD is associated with increased progression of coronary artery calcification.  (Andrews et al, 2018; Chatrou et al, 2012). 

 

18. Animal experiments also demonstrated that warfarin increases both medial calcification and intimal calcification of atherosclerotic plaques. Warfarin treatment also shifts atherosclerotic plaques toward a vulnerable phenotype by producing intimal micro-calcifications, increasing cell death (apoptosis), and promoting outward remodeling (Schurgers, et al, 2012).