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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.
Omega-3 fatty acid and menaquinone-7 combination are helpful for aortic calcification prevention, reducing osteoclast area of bone and Fox0 expression of muscle in uremic rats
Published in Renal Failure, 2022
Su Mi Lee, Eu Gene Jeong, Yu In Jeong, Seo Hee Rha, Seong Eun Kim, Won Suk An
In the absence of proven therapies, it is necessary to develop therapeutic agents or preventive medicines for osteopenia, sarcopenia, and VC for advanced CKD. Omega-3 fatty acids (FAs), including eicosapentaenoic acid, are known to have beneficial effects on cardiovascular disease (CVD) and mortality [8,9]. Notably, omega-3 FAs attenuate arterial medial calcification, improve vascular endothelial function, reduce inflammatory response, and inhibit thrombogenesis [10]. Vitamin K is a cofactor for activation of matrix-Gla-protein (MGP), a potent inhibitor of arterial calcification [11]. Therefore, omega-3 FA and vitamin K supplementation could be a viable supplementation option to reduce VC. Because of the close association between osteopenia, sarcopenia, and VC, effective drugs may simultaneously affect on bone, muscle, and vessel. However, the effect of omega-3 FA and vitamin K supplementation on osteopenia and sarcopenia is currently unclear.
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.
Reproductive factors and breast arterial calcification: a systematic review and meta-analysis
Published in Climacteric, 2022
S. C. Lee, S. Pirikahu, M. Phillips, J. Bellinge, J. Stone, E. Wylie, B. G. A. Stuckey, C. Schultz
Similarly, atherosclerosis is positively associated with early menopause and inversely associated with HRT use [36–38]. There is growing evidence that intimal and medial arterial calcification share one feature characteristic in its pathogenesis: the deposition of hydroxyapatite by vascular smooth muscle cells as they acquire an osteoblastic phenotype [39]. This transformation is mediated by several factors such as receptor-activator of κB ligand (RANKL), which increases bone-morphogenic protein 2 (BMP-2), reduces matrix-Gla protein (MGP) and induces other bone-related genes (e.g. osteocalcin, alkaline phosphatase, osteopontin) to promote osteogenic trans-differentiation of vascular smooth muscle cells [9]. Estrogens have been demonstrated both in vitro and in animal models to inhibit RANKL and BMP-2 [9], and therefore could mediate the trans-differentiation of vascular smooth muscle cells in both the tunica intima and the tunica media through this mechanism. However, the relationship between atherosclerosis and estrogen is likely to be more complex. For example, the timing of HRT use plays an important role, as suggested by the Women’s Health Initiative Study [40] and the AGES-Reykjavik Study [41] which found that women who started HRT earlier in relation to menopause had lower coronary artery calcium scores compared to those who started HRT later. Other potential factors that may be important include the HRT formulation and the method of menopause (e.g. natural vs. surgical menopause) which may influence the effects of HRT on vascular calcification. This could not be examined in our current analysis but will need to be explored in future studies involving BAC.