Vitamin K2 And Calcium Paradox PdfBy Karel R. In and pdf 19.01.2021 at 18:25 10 min read
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Author: BSc. Narrator: Virginia Wolf. Unabridged: 7 hr 12 min.
- [PDF Download] Vitamin K2 and the Calcium Paradox: How a Little-Known Vitamin Could Save Your
- DOWNLOAD PDF Vitamin K2 and the Calcium Paradox: How a Little-Known Vitamin Could Save Your Life
- Vitamin K2 and the Calcium Paradox: How a Little-Known Vitamin Could Save Your Life
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MP3 Audio Sample play pause Update Required To play the media you will need to either update your browser to a recent version or update your Flash plugin. Synopsis Reviews Awards Media Short Synopsis An essential book for anyone interested in bone health, or maintaining their overall health, Vitamin K2 and the Calcium Paradox is the guide to taking the right combination of supplements—and adding Vitamin K2 to a daily regimen. Full Synopsis Are you taking calcium or vitamin D?
[PDF Download] Vitamin K2 and the Calcium Paradox: How a Little-Known Vitamin Could Save Your
Vascular Calcification View all 12 Articles. Calcium supplements are broadly prescribed to treat osteoporosis either as monotherapy or together with vitamin D to enhance calcium absorption. It is still unclear whether calcium supplementation significantly contributes to the reduction of bone fragility and fracture risk. Data suggest that supplementing post-menopausal women with high doses of calcium has a detrimental impact on cardiovascular morbidity and mortality.
Chronic kidney disease CKD patients are prone to vascular calcification in part due to impaired phosphate excretion. Calcium-based phosphate binders further increase risk of vascular calcification progression. In both bone and vascular tissue, vitamin K-dependent processes play an important role in calcium homeostasis and it is tempting to speculate that vitamin K supplementation might protect from the potentially untoward effects of calcium supplementation.
This review provides an update on current literature on calcium supplementation among post-menopausal women and CKD patients and discusses underlying molecular mechanisms of vascular calcification.
We propose therapeutic strategies with vitamin K2 treatment to prevent or hold progression of vascular calcification as a consequence of excessive calcium intake.
Calcium is also widely abundant in the human body, primarily in bone, and teeth. Calcium salts are occasionally found outside bone in a variety of tissues; this is broadly termed as extra-skeletal calcification. In these extra-skeletal sites, calcium exists in multiple forms, including amorphous calcium phosphate, hydroxyapatite, and magnesium whitlockite. A remarkable observation is that under several pathological conditions, as will be discussed, calcium mineral content of bone declines, while it is increasing on these extra-osseous sites.
The calcium paradox refers to epidemiological data reporting that postmenopausal women experience bone loss, yet simultaneously screen positive for vascular calcification.
This phenomenon is common in osteoporotic women and patients suffering from chronic kidney disease CKD. Prevalence and morbidity of both cardiovascular disease and osteoporosis are increasing in the global population.
Such observations have been noted in several studies, where a correlation of low bone mineral density BMD was associated with increased cardiovascular mortality 2 — 6.
The use of calcium supplements has been widely advised due to their assumed ability to support bone health and BMD 7 , 8. Calcium is an essential element for bone growth during childhood 9 , as well as in preserving bone mineral density during adolescence However, a systematic review and meta-analysis of the effects of calcium supplementation along with vitamin D treatment showed that this treatment was not associated with a lower incidence of fracture risk in adults, questioning whether calcium supplementation contributes to the maintenance of healthy bone In turn, recent data suggest that calcium supplements increase prevalence of myocardial infarction 12 , and may increase risk of coronary artery calcification CAC Moreover, higher doses of calcium from supplements than calcium obtained from dietary intake might promote cardiovascular calcification Thus, despite the relative benefit of calcium supplementation for bone, calcium supplements became controversial because of a possibly increased cardiovascular risk.
Substantially different from calcium from dietary sources, calcium form supplements induce an acute rise in serum calcium levels that highly oscillates in blood for up to 6 h 15 , The plasma calcium concentration is tightly regulated by vitamin D, parathyroid hormone PTH , and calcitonin 17 , Vitamin K-dependent proteins VKDP also play an important role regulating mineralization both in bone and the vasculature. Osteocalcin OC is produced exclusively by osteoblasts and supports the binding of calcium to the bone mineral matrix, whereas matrix Gla-protein MGP is synthesized by vascular smooth muscle cells and chondrocytes to prevent ectopic calcification.
While hepatically produced coagulation factors are the prototypical VKDP, the extra-hepatic VKDP also unequivocally need vitamin K as cofactor to become biologically active. Related to that, vitamin K2 has been shown to prevent bone loss and strength and prevents stiffening of arteries 19 , Also in CKD patients, vitamin K deficiency is prevalent, so K2 supplementation has been suggested as treatment option to attenuate vascular calcification 23 , In this review we provide the latest insights of the calcium paradox and the potential of using vitamin K to support both bone and vascular health.
Calcification generally is a physiological process, necessary to build bone and dentin. Bone provides structural support, strength, necessary for locomotion, and protection from the environment. The balance in bone formation and bone resorption is crucial for optimal bone health. A disturbed balance of this process results in bone loss and is termed osteoporosis.
During childhood bone is formed and bone peak mass is achieved during young adulthood, after which bone mass gradually declines. Bone loss is the consequence of bone resorption outbalancing bone formation This is accompanied by bone architectural changes including trabecular bone becoming thinner, less abundant, and osteoclastic perforation of cortical bone The skeleton is systematically renewed in the process of bone remodeling to maintain strength and rigidity.
Bone remodeling can be considered to be part of calcium homeostasis system and enables the skeleton to adapt to changes. Bones adapt their structure depending on their function, mechanical strain and need for stability during development. It is mediated on the surface of cortical and trabecular bone, and at anatomically different sites named basic multicellular subunits Two pathways of bone formation exist, together termed osteogenesis. The first is known as endochondral ossification and involves a differentiation of mesenchymal cells into chondrocytes or osteoblasts 28 , As chondrocytes mature, they expand in size and become hypertrophic and eventually undergo apoptosis, secreting vesicles that initiate mineralization of extracellular matrix As they die, with vascular evasion and matrix remodeling osteoclast mediated , the calcified cartilage is subsequently replaced by bone.
Nestin-positive mesenchymal progenitors associated with the invading vasculature differentiate into bone-forming osteoblasts and deposit a type I collagen-based bone matrix on the degraded cartilage template 31 , The second process of bone formation is intramembranous ossification. First, mesenchymal cells directly differentiate into osteoblasts, which are bone-forming cells. Next, type I collagen matrix is deposited by these cells, that can bind calcium salts, which form hydroxyapatite crystals.
This mineralization of the matrix underlies the strength and compactness of the bone. With time, osteoblasts eventually become trapped in calcified extracellular matrix and transdifferentiate into osteocytes. Osteoblasts are the only bone cell type releasing the vitamin K-dependent protein OC discussed below.
As the newly formed bone is laid, its deposition must be tightly regulated to maintain homeostasis. This balance is achieved by bone-resorbing cells, entering the blood vessels of bone, which are termed osteoclasts and are of macrophage origin. Each osteoclast is able to secrete hydrogen ions, thereby acidifying the bone surface dissolving mineralized matrix, followed by interactions that enhance the action of osteoblasts 33 — Upon resorption, bone-matrix embedded osteocalcin is released contributing to its circulating levels Bone loss is most typical in women after reaching the age of 50 years following menopause.
The pattern of sex hormonal secretion drastically changes after the menopause, resulting in disbalance in bone turnover markers, making postmenopausal women susceptible to osteoporosis and fractures. Remarkably cardiovascular diseases are also more prevalent in postmenopausal women.
Therefore, it is important to understand the molecular mechanisms by which hormonal changes leads to both osteoporosis and cardiovascular disease 37 , The post-menopausal period is accompanied by substantial reduction of estrogen levels leading to bone resorption, yet simultaneously reducing calcium absorption It is not the aim of this review to elaborate on the effect of estrogen on the vasculature [reviewed elsewhere 39 ].
Instead, we will focus on specific pathways involved in calcium metabolism. PTH is released upon hypocalcemia, indirectly stimulating release of calcium from bone. Additionally, PTH promotes reabsorption of ultra-filtered calcium in distal tubules and activates vitamin D thereby increasing circulating calcium levels by raising gastrointestinal uptake of calcium 17 , Calcium-sensing receptors CaR present on the surface of parathyroid glands enable sensing of circulating calcium concentration 40 , contributing to calcium modulation.
Vitamin D is a fat-soluble vitamin that can be obtained from diet, sun exposure, or supplements, and is metabolized by a series of enzymatic reactions in the body producing its active 1,dihydroxyvitamin D form 41 , Vitamin D in inactive form is often prescribed in combination with calcium supplements. Active 1,dihydroxyvitamin D enhances absorption of intestinal calcium and phosphate thus contributing to the regulating of mineral balance 43 , Vitamin D was found to stimulate production of vitamin K-dependent proteins, like osteocalcin Osteocalcin is a protein involved in bone mineralization [reviewed elsewhere 48 ].
CKD patients often experience deficiency of 1,dihydroxyvitamin D as a consequence of lost kidney mass and the effects of fibroblast growth factor 23 50 , resulting in declined activity of 1-alpha hydroxylase 51 — Reduced serum levels of 1,dihydroxyvitamin D lead to hypocalcemia on top of positive phosphate balance, both stimulating PTH release and eventually leading to secondary hyperparathyroidism.
Vascular calcification is a pathological process, and has been firmly established as a risk factor for cardiovascular events and mortality 54 , Vascular calcification is a process of extraosseous mineral deposition in blood vessels, including large arteries such as aorta, carotid arteries, iliac arteries, and cardiac valves.
Bone mineralization and vascular calcification share many similarities, including expression of bone-related proteins in the vasculature and secretion of extracellular vesicles EVs both preceding the phase of calcification 56 , Vascular calcification can occur either in the tunica media or tunica intima of the vessel wall. Medial calcification is related to CKD, diabetes mellitus, and aging, and results in increased arterial stiffness and risk of cardiovascular events 58 , In contrast, intimal calcification is associated with atherosclerotic plaque formation and the amount of calcification is considered to be a measure of atherosclerotic burden 1.
For many years vascular calcification was considered as a clinically irrelevant process reliant of passive deposition of calcium crystals, merely reflecting a passive feature of disease and aging.
Recent evidence however suggests otherwise, and vascular calcification appears to be a highly regulated process. SMCs release calcification inhibitors, thus efficiently preventing spontaneous calcification in spite of supersaturation of extracellular calcium and phosphate levels SMCs are the main cellular component of the tunica media in arterial vessels providing structural support and regulating vascular tone and elasticity to alterations in pressure conditions. In physiology SMCs possess a contractile phenotype and express contractile-specific markers, including alpha-smooth muscle actin, calponin, and SM22alpha, enabling them to perform contraction of the vessel wall [reviewed elsewhere 61 , 62 ].
SMC function is associated with a high level of phenotypic plasticity in order to perform a variety of functions including production of extracellular matrix and repair 61 , Several factors have been implicated in regulating SMC phenotype, including mineral imbalance calcium, magnesium, and phosphate-induced loss of calcification inhibitors and presence of calcification promotors Downregulation of contractile markers is a hallmark for SMC phenotypic switching It has been shown that phosphate can induce an osteochondrogenic phenotypic switching of SMC, as will be outlined in more detail below 61 , 66 — 69 , whereas elevated calcium levels shift the contractile phenotype toward a synthetic SMC phenotype Both calcium- and phosphate- induced phenotypic switching are associated with an increase in the secretion of calcifying extracellular vesicles 56 , CKD patients often develop medial calcification In CKD, a strong correlation between serum phosphate levels and vascular calcification is present 71 , In an animal model of CKD, arterial calcification developed after feeding animals a phosphorous-rich diet only Moreover, high circulating phosphate levels have been linked to increased cardiovascular morbidity even among young people receiving dialysis 75 and in CKD patients In vitro , elevated phosphate levels result in upregulation of bone-like markers in SMC including osterix, alkaline phosphatase ALP , and Runx2, and downregulation of SMC contractility markers SMC cultured in osteogenic cell culture media differentiate into calcifying-SMC resembling osteoblasts In aortic valves of patients with aortic stenosis, valvular interstitial cells demonstrate similarities with osteoblasts 78 , which also exhibit lamellar bone formation The paradoxical co-existence of declined calcium-mineral content in bone, and parallel increased arterial calcification, as a consequence of impaired calcium metabolism, is termed the calcium paradox.
This is most pronounced in post-menopausal women and CKD patients.
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It is also involved in the production of another protein called matrix gla protein (MGP), which directs calcium away from blood vessels and soft tissues. Vitamin K2 is.
Vitamin K2 and the Calcium Paradox: How a Little-Known Vitamin Could Save Your Life
Vascular Calcification View all 12 Articles. Calcium supplements are broadly prescribed to treat osteoporosis either as monotherapy or together with vitamin D to enhance calcium absorption. It is still unclear whether calcium supplementation significantly contributes to the reduction of bone fragility and fracture risk. Data suggest that supplementing post-menopausal women with high doses of calcium has a detrimental impact on cardiovascular morbidity and mortality. Chronic kidney disease CKD patients are prone to vascular calcification in part due to impaired phosphate excretion.
We have been eating less meat which had eaten greens, therefore we have been getting less vitamin K2 We have been eating less organ meat, which has concentration of Vitamin K2 and Vitamin D. Any other reason? Thorne's Vitamin K2 Liquid supplies 1 mg of vitamin K2 per drop. Research shows doses up to 15 mg three times daily may be used. Calrson K2 5 MK-7 only 45 mcg.
Но уже через минуту парень скривился в гримасе. Он с силой стукнул бутылкой по столу и вцепился в рубашку Беккера.