There are times in life when we can't seem to "come back up to our own level" and we may need the help of friends or even a professional to try to find buoyancy even while dwelling within the flood. We continuously create our body with the nurturance of earth. We create the shelter where our body dwells, and our hands mold and shape our world.
We are all artists of our own lives. The home we live in, the clothing we wear, the food we cook, these are just a few of the most basic, and beautiful, elements of how we create in our world. The earth element calls upon us to manifest energy into form. The center of our being is our own individual balance of the four elements, or four directions. We all have our own center and our own varying levels of different elemental strengths and weaknesses. Our center is like the axis of the compass.
Navigating our path forward necessitates understanding from what point we are beginning. Vintage Style Astronomy Posters available on Amazon Sometimes setting the stage can clarify our place in the systematic movement of time Of the imaginary coordinate lines that astronomers and navigators use in mapping the sky, perhaps the most important one is the ecliptic, the apparent path the sun appears to take through the sky as a result of the Earth's revolution around it. Call to mind the poetic wisdom of a beloved astronomer The surface of the Earth is the shore of the cosmic ocean.
On this shore, we've learned most of what we know. Recently, we've waded a little way out,. Some part of our being knows this is where we came from. We long to return, and we can, because the cosmos is also within us. We're made of star stuff. We are a way for the cosmos to know itself. Recently, we've waded a little way out, maybe ankle-deep, and the water seems inviting. Such broad function of calcium in the body requires precise regulation, and calcium oscillates between 2. This free form is the regulated calcium and accounts for bone mineralization as well as pathological calcification Several formulations of calcium are available on the market, differing in bioavailability, and elemental calcium content.
Calcium carbonate is the most common form available.
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However, many studies showed superiority of calcium citrate over calcium carbonate, due to higher bioavailability and because it does not require acidic stomach conditions before ingestion In a study carried out in post-menopausal women supplemented with di-calcium phosphate over a period of 12 months, serum calcium levels did not vary significantly, and only urinary calcium increased progressively in time when compared to the control group. The increased excretion of calcium may indirectly reflect the rise of the renal threshold for excretion and together with the amount of absorbed calcium it may contribute to complications such as deposition in the vasculature One of the most applied therapeutic intervention for fracture risk is calcium in the form of pills or organic powder.
Commercially available calcium is often marketed in combination with vitamin D3 to increase intestinal absorption of calcium Table 1. It has been proposed that no more than mg of elemental calcium should be taken as single dose to maximize absorption and to avoid side effects, like gastrointestinal complaints When calcium supplements are not exceeding the nutritional daily intake of mg, a low cardiovascular risk was observed Numerous studies and extensive meta-analyses reported on the efficacy and cost effectiveness of calcium supplementation with or without vitamin D , in improving bone mineral density as well as decreasing fracture risk 83 — 85 , , Furthermore, in individuals with inadequate calcium intake, the supplementation plan seems to be beneficial in reducing fragility fractures especially in osteoporotic women 86 , Calcium supplementation was also demonstrated to be effective in preventing reduction in bone loss and turnover in healthy population A recent double-blind controlled trial also proved the effectiveness of medium and high calcium intake in maximizing bone mineral density in adolescent girls In addition, many studies described neutral or protective effects of calcium rich foods on cardiovascular outcomes including atherosclerosis, risk of infarction, stroke, and cardiovascular mortality 89 , 90 , — However, recent data challenge the assumption that calcium supplementation improves bone mineral density.
With such low effects it would be challenging to implement calcium supplementation into standard treatment for reduction of fracture risk in the healthy elderly population A recent review summarizing the use and efficacy of calcium supplementation in treating osteoporosis and fracture risk questions the use of calcium supplements because of the weak beneficiary effect on fracture risk while increasing the risk on gastrointestinal problems, kidney stones, and cardiovascular risk Despite positive outcomes of calcium supplementation, a risk for cardiovascular risk events may exist in specific population.
It was recently shown that women who receive calcium supplementation were at higher risk for increased vascular morbidity and mortality, including myocardial infarction , — In turn, recent systematic reviews and meta analyses do not confirm that supplementing calcium with or without vitamin D increased prevalence of coronary heart disease, cardiovascular mortality or all-cause mortality, data on which the above-mentioned statement by the National Academy of Medicine is based upon , Rapidly elevated transient calcium levels in blood caused by excessive supplementary calcium have been suggested to promote coagulation when compared with placebo in postmenopausal women, likely due to interaction with platelets expressing calcium-sensing receptor CaSR , Hypercoagulability is considered to have a reinforcing effect on atherosclerosis in animal studies, contributing to cardiovascular disease.
Also many coagulation proteins have been described in human atherosclerotic plaques These findings are in line with the association between high calcium intake and cardiovascular calcification in CKD patients Reconciling these sometimes opposing details difficult. There appears to be some protection from fracture risks by calcium supplements, but its safety is still not sufficiently established.
Therefore, additional research is still needed. Calcium-based phosphate binders have been used extensively as a first-choice option since to alleviate hyperphosphatemia associated with CKD patients due to its low cost, availability, and effectiveness. These calcium-containing phosphate binders are given to CKD patients to complex dietary phosphate, thereby reducing phosphate uptake , As with most supplements, also calcium-containing phosphate binders have side effects, which include abdominal cramps, intestinal bloating, and diarrhea Further, excessive intake of calcium supplements might also result in milk-alkali syndrome and hypercalcemia Vitamin K was discovered in by the Danish biochemist Henrik Dam during his experiments on cholesterol metabolism in chickens.
When fed low-fat diets, chickens experienced prolonged clotting time and hemorrhage, which surprisingly could not be rescued when diet was enriched with cholesterol. Indeed, vitamin K was shown to be a fat-soluble vitamin, consisting a group of structurally related compounds including vitamin K1 phylloquinone and vitamin K2 menaquinones Figure 1. Vitamin K1 contains a phytyl chain, whereas K2 is classified according to the length of isoprenoids and indicated as MK-n, where n represents the number of residues.
Both vitamins share a common 2-methyl-1,4-naphthoquinone ring, also known as menadione.
The main source of vitamin K1 is green vegetables , whereas vitamin K2 can be found in fermented foods such as soy beans, cheese, and sauerkraut. The richest source of vitamin K2 MK-7 is a Japanese dish named Natto , which is produced from fermented soy beans with aid of the Bacillus Subtilis bacteria strain In addition to nutritional consumption, gut bacteria Lactococcus and Escherischia coli are able to synthesize long chain menaquinones Figure 1.
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Figure 1. All vitamins share common menadione ring also known as vitamin K3. The primary biological function of both K-vitamins is being an unequivocal cofactor in the post-translational modification of VKDP via carboxylation of glutamic acid residues Glu to y-carboxylated-glutamic acid residues To fulfill this function, vitamin K needs to be reduced to its active cofactor form KH2 by quinone reductases. Both vitamins K1 and K2 can partake in the activation of VKDP; however, long-chain menaquinones, which are more hydrophobic, have a higher bioavailability and longer half-life and thus bioactivity , VKDP are a group of proteins that require carboxylation of specific protein-bound glutamate-residues, allowing them to bind with high affinity to calcium.
This was first demonstrated in coagulation, showing that VKDP of the coagulation cascade need carboxylation to acquire biological activity.
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This role of vitamin K on coagulation is clinically widely applied by the use of warfarin as anticoagulant treatment. The extra negative charge in VKDP bind via calcium to negatively charged phospholipids to exert their function. The function of non-hepatic VKDP has recently be discovered and include prevention of vascular calcification and importantly also promotion of bone metabolism The current knowledge of vascular calcification inhibitors has gained attention of both scientists and clinicians to research their molecular action, aiming to alleviate disease caused by vascular calcification.
OC is a major non-collagenous protein abundantly present in bone, responsible for management of skeletal mineralization , During skeletal development, bone mass increases due to the dominant function of osteoblasts which secrete OC, amongst other proteins, enabling bone to grow. In addition to bone function, OC is implicated in stimulating testosterone synthesis and insulin release , Other roles of OC are not covered in this review and have been reviewed elsewhere To execute its physiological function, OC needs to be activated by carboxylation, catalyzed by vitamin K.
Carboxylated OC cOC has a high affinity for calcium ions and aids in forming a hydroxyapatite lattice preceding mineralization of bone , Figure 2. Upon bone degradation, OC, incorporated into mineralized bone, is liberated. Serum OC levels were negatively correlated with bone mineral density BMD in post-menopausal woman and healthy subjects — In a study of healthy girls, plasma phylloquinone was inversely correlated with circulating OC concentrations showing that a better vitamin K status was associated with decreased bone turnover in healthy girls Figure 2.
Vitamin K—dependent carboxylation mechanism keeps extracellular matrix of VSMC free of calcification and simultaneously promotes mineralization of osteoblast matrix. Similarly, in post-menopausal women, calcium homeostasis is further impaired contributing to impairment of calcium utilization by osteoblasts.
In the event of vitamin K deficiency, both MGP and Osteocalcin are not carboxylated and cannot perform their molecular function. The discovery of MGP dates back to where it was first purified from bovine bone matrix and named after the presence of gamma-carboxyglutamate residues on MGP Shortly thereafter MGP was confirmed to be present in cartilage, lung heart, kidney, and vasculature, with highest protein expression in SMCs and chondrocytes — Knocking out MGP in mice induced advanced medial calcification and subsequent vessel rupture followed by death in the majority of mice within 6 weeks after birth.
This animal model resembles the human Keutel syndrome which is caused by a mutation in the MGP gene , , which impairs carboxylation of MGP thereby inducing intimal and medial calcification MGP is also dependent on carboxylation of gla-residues, catalyzed by vitamin K, to execute its function as an inhibitor of vascular calcification Figure 2 , Uncarboxylated MGP ucMGP is associated with increased risk of vascular calcification, and therefore some researchers advocate that vitamin K status in CKD patients should be carefully monitored BMP2 was found to be present in human atherosclerotic lesions , acting as downstream signal for osteogenic phenotype switching of SMC by increasing the influx of phosphate into cells GRP, also known as Ucma, is a vitamin K-dependent protein secreted by chondrocytes , and present in cartilage, bone , and vasculature , Despite the creation of GRP knockout mice its precise molecular action remains to be elucidated, because these animals had no manifest deficits in cartilage or bone development So far, the role of GRP has been implicated in calcium regulation in extracellular matrix , , and thus being an inhibitor of ectopic calcification , Moreover, GRP was found to be directly associated with calcium-phosphate crystals suggesting that this protein-crystal interaction modulates calcification In addition, GRP was found to promote osteoblast and chondrocyte differentiation , Table 2 summarizes vitamin-K dependent proteins involved in calcification.
Table 2. Occurrence of selected vitamin K dependent proteins in different tissue compartments. Despite many years of research there is no definite proof that phosphate binders improve outcome, despite their capacity to control phosphate. Although direct studies suggest superiority of non-calcium containing binders over calcium containing binders, it is still unclear if this is due to an advantage of non-calcium containing binders or added risks from calcium containing binders , — Even more striking is that the use of any phosphate binders in earlier CKD, despite lowering phosphate, did not reduce progression of coronary calcification This conundrum may be explained by the recently demonstrated ability of phosphate binders to also bind vitamin K Table 3.
The advantage of lowering phosphate concentrations if thus offset by aggravation vitamin K deficiency. The lack of difference in this CKD patient subgroup could be explained by effective inherent protection in these patients or by simultaneous undesired binding of vitamin K by some phosphate binders resulting in vitamin K deficiency which serves as co-factor for enzymes that activate calcification inhibitors , Figure 3. More recently, it was shown that CKD patients on dialysis treated with the phosphate binder sevelamer revealed higher circulating levels of dp-ucMGP, the inactive form of MGP These findings support the in vitro notion and hypothesis that phosphate binders induce a vitamin K-deficiency.
Besides the above-mentioned phosphate binders, new forms have recently been developed such as iron-based phosphate binders. Iron oxyhydroxide have been proven to be as potent as sevelamer in decreasing phosphatemia , while apparently not interfering with vitamin K-metabolism Table 3. Summary of selected features and effects of available phosphate binders.
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Figure 3. Representation of systemic action of vitamin K on bone and vasculature in the calcium presence. Calcium based phosphate binders are known to reduce the levels of adsorbed phosphate by directly coupling reaction in the gastro-intestinal tract. Phosphate binders were also shown to bind Vitamin K suggesting it might affect its free circulating form. When coupled with phosphate binders, vitamin K is unable to perform its biological function of positively utilizing calcium into the bone and simultaneously acting as calcification inhibitor.