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The Integrative Coronary Heart Disease (CHD) Prevention Program
Published in Mark C Houston, The Truth About Heart Disease, 2023
The most important vitamin K in relation to CHD is vitamin K2 MK 7. Vitamin K2 MK 4 is also good but is less potent and requires 5–10 times the dose of vitamin K2 MK 7. Vitamin K2 MK 7 also has better absorption and a longer half-life of 3 days vs hours compared to vitamin K2 MK 4. Menaquinones are vitamin K2 (gut bacteria) (75% of K) are more effective than phylloquinone or vitamin K1 (dietary intake) (25% of K) to prevent vascular disease and vascular calcification. Vitamin K2MK7 is important for the production of a protein called gamma carboxyglutamate (Gla matrix protein-MGP) through a process called “carboxylation” that is important in the prevention of calcification of the coronary arteries, calcification of coronary artery plaque, CHD, and MI. (Figure 21.1) The dose is 360 micrograms per day or two caps per day. K2 MK 7 is produced by Ortho Molecular labs. See the Sources section at the end of this book.
Lifestyle and Environment
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Special interest has recently emerged on the effect of vitamin K supplementation on the reversal or attenuation of the vitamin K deficiency–associated (either inherent or treatment mediated, i.e. from warfarin) development of arterial stiffness and calcifications. The effect seems to be mediated by the vitamin K–dependent activation of matrix Gla protein that is a potent inhibitor of vascular calcification. MGP activation in initial studies has shown modest but promising results, but further large-scale studies are warranted for infiltration of vitamin K as a valid de-stiffening therapy in clinical practice (Lees et al., 2018).
The vitamins
Published in Geoffrey P. Webb, Nutrition, 2019
Similar carboxylated Gla proteins are found in other tissues. Three Gla proteins are found in bone: osteocalcin, matrix Gla protein and protein S. The presence of these proteins in bone suggests that vitamin K may play an important role in bone metabolism, and it has been suggested that vitamin K insufficiency may be a contributory cause of osteoporosis. Preliminary support for an association between vitamin K insufficiency and osteoporosis risk is summarised as follows. On a normal diet with normal blood clotting, the osteocalcin that circulates in the blood is not fully carboxylated and substantial supplements are needed to achieve full carboxylation. In very elderly women, there is reduced carboxylation of circulating osteocalcin. High levels of under-carboxylated osteocalcin in elderly women are associated with reduced bone density at the hip and increased risk of fracture. Low intakes of vitamin K have been associated with increased hip fracture risk. Women in the lowest quartile of vitamin K intakes have been reported to have lower bone density than those in the highest quartile.
Emphysema: looking beyond alpha-1 antitrypsin deficiency
Published in Expert Review of Respiratory Medicine, 2019
Rob Janssen, Ianthe Piscaer, Frits M. E. Franssen, Emiel F. M. Wouters
Vitamin K is generally known as an activator of coagulation factors in the liver, however, it is also an essential cofactor for extrahepatic proteins [140]. Matrix Gla protein (MGP) is vitamin K-dependent and an important inhibitor of calcification [141]. Elastin has high tendency to calcify, and protease production increases parallel to calcium levels in elastin fibers [142]. An animal study has suggested that vitamin K-activated MGP is also an inhibitor of elastin degradation [143], and an inverse correlation between vitamin K status and rates of elastin degradation has been found in patients with COPD [144]. Arterial stiffness, lung cancer, and osteoporosis have been related to vitamin K deficiency [145–147], and it has previously been hypothesized that vitamin K deficiency might be the missing link between emphysema and these frequent comorbidities [148]. Effects of vitamin K supplementation on progression of pulmonary and extrapulmonary features of emphysema should be assessed.
Relationship of matrix Gla protein and vitamin K with vascular calcification in hemodialysis patients
Published in Renal Failure, 2019
Sonoo Mizuiri, Yoshiko Nishizawa, Kazuomi Yamashita, Kyoka Ono, Takayuki Naito, Chie Tanji, Koji Usui, Shigehiro Doi, Takao Masaki, Kenichiro Shigemoto
Matrix Gla protein (MGP) is primarily secreted by chondrocytes and smooth vascular muscle cells, and acts as a potent local inhibitor of vascular calcification [1]. However, to be active, MGP must be phosphorylated and carboxylated; such carboxylation is vitamin K-dependent, and phosphorylation is necessary for the secretion of MGP [2]. The vitamin K family includes phylloquinone (vitamin K1) and several menaquinones (vitamin K2) [2–4]. Notably, 72% of patients with chronic kidney disease (CKD) exhibit vitamin K intake lower than recommended levels [5]. Vitamin K status can be quantified by using high-performance liquid chromatography (HPLC) [6,7], a method that requires specific and expensive equipment. It has been suggested that vitamin K-dependent proteins (i.e. plasma abnormal prothrombin, osteocalcin, growth arrest-specific gene-6 protein, and MGP) can be used as indicators of vitamin K status [7]; indeed, previous studies have used these markers to evaluate vitamin K status in hemodialysis (HD) patients [7–10]. A theoretical link exists among MGP, vitamin K, vascular calcification, and cardiovascular disease (CVD); this link is more notable in CKD and HD patients [2,4]. However, atherosclerotic calcification is more prevalent in elderly HD patients; thus, age is a primary risk factor for vascular calcification in such patients [11,12]. Simultaneous assessment of MGP levels, vitamin K levels, and vascular calcification should be performed in age-matched populations. To the best of our knowledge, there are no such studies in the literature. In the present study, we investigated MGP and vitamin K status in age-matched HD patients and healthy controls; in addition, we assessed vascular calcification and CVD in HD patients.
SOPH Syndrome with Growth Hormone Deficiency, Normal Bone Age, and Novel Compound Heterozygous Mutations in NBAS
Published in Fetal and Pediatric Pathology, 2018
Xin Li, Qing Cheng, Niu Li, Guoying Chang, Yu Ding, Juan Li, Yiping Shen, Jian Wang, Xiumin Wang
We speculate that growth hormone deficiency may be one of the reasons for the short stature of this patient. Longman et al. have shown that depletion of NBAS led to a significant upregulation of matrix Gla protein (MGP) that regulates bone formation. Thus, an increased MGP activity would be compatible with a described short stature and associated bone defects present in the SOPH syndrome [7].