What Vitamin Is Needed For Calcium Absorption – Calcium is the most abundant mineral in the human body. About 99% of the calcium in the body is found in the bones and teeth, while the other 1% is found in the blood and soft tissues. The calcium concentration in the blood and in the fluid surrounding the cells (extracellular fluid) must be kept within a narrow concentration range for normal physiological functioning. The physiological functions of calcium are so vital to survival that the body stimulates bone resorption (demineralization) to maintain normal blood calcium concentrations when calcium intake is inadequate. Thus, adequate calcium intake is a critical factor in maintaining a healthy skeleton (1).

Calcium is an important structural element of bones and teeth. The mineral component of bone consists mainly of hydroxyapatite [Ca

What Vitamin Is Needed For Calcium Absorption

] crystals that contain large amounts of calcium, phosphorus and oxygen. Bone is a dynamic tissue that changes throughout life. Bone cells called osteoclasts begin the remodeling process by dissolving or resorbing bone. Bone-forming cells called osteoblasts then synthesize new bone to replace the resorbed bone. During normal growth, bone formation exceeds bone resorption. Osteoporosis can develop when bone resorption chronically exceeds formation (1).

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The calcium concentration in the blood and in the fluid surrounding the cells is tightly regulated to maintain normal physiological function. A slight decrease in blood calcium concentration (e.g. in case of inadequate calcium intake) is detected by the parathyroid glands, which results in increased secretion of parathyroid hormone (PTH). In the kidneys, PTH stimulates the conversion of vitamin D to its active form (1,25-dihydroxyvitamin D; calcitriol), which rapidly decreases urinary calcium excretion but increases urinary phosphorus excretion. An increase in PTH also stimulates bone resorption, resulting in the release of bone minerals (calcium and phosphate)—effects that also contribute to the restoration of serum calcium concentrations. Increased circulating 1,25-dihydroxyvitamin D also initiates the absorption of calcium and phosphorus from the intestine. Like PTH, 1,25-dihydroxyvitamin D stimulates the release of calcium from bone by activating osteoclasts (bone-resorbing cells). When blood calcium levels return to normal, the parathyroid glands stop secreting PTH. A slight increase in blood calcium concentration stimulates the production and secretion of the peptide hormone calcitonin in the thyroid gland. Calcitonin inhibits PTH secretion, reduces both bone resorption and intestinal absorption of calcium, and increases urinary calcium excretion (Figure 1). Finally, acute changes in blood calcium concentration do not appear to induce secretion of the phosphaturic hormone fibroblast growth factor 23 (FGF-23), which is produced by bone-forming cells (osteoblasts/osteocytes) in response to increased phosphorus intake. see article on phosphorus) (2). Although this complex system allows rapid and tight regulation of blood calcium concentration, it does so at the expense of the skeleton (1).

Calcium plays a role in the contraction and relaxation of blood vessels (vasoconstriction and vasodilation), nerve impulse transmission, muscle contraction, and the secretion of hormones such as insulin (1). Excitable cells, such as skeletal muscle and neurons, contain voltage-gated calcium channels in their cell membranes that allow rapid changes in calcium concentration. For example, when a nerve impulse stimulates a muscle fiber to contract, calcium channels in the cell membrane open to allow calcium ions to enter the muscle cell. Inside the cell, these calcium ions bind to activating proteins that promote the release of a flood of calcium ions from storage vesicles in the endoplasmic reticulum (ER) inside the cell. The binding of calcium to the protein troponin-c initiates a series of steps that lead to muscle contraction. The binding of calcium to the calmodulin protein activates enzymes that break down muscle glycogen to provide energy for muscle contraction. Once this action is completed, calcium is pumped out of the cell or into the ER until the next activation (see point 3).

Calcium is necessary for the stabilization of many proteins, including enzymes, to optimize their activity. Binding of calcium ions is required to activate the seven “vitamin K-dependent” coagulation factors in the coagulation cascade. The term “coagulation cascade” refers to a series of events, all interdependent, that stop bleeding through the formation of a blood clot (see the article on vitamin K).

Vitamin D is required for optimal absorption of calcium (see function or article on vitamin D). Many other nutrients (and non-nutrients) affect calcium retention in the body and can affect calcium nutritional status.

High Absorption Calcium Citrate

Dietary sodium is a major determinant of urinary calcium loss (1). High sodium intake results in increased urinary calcium loss, possibly due to competition between sodium and calcium for reabsorption in the kidneys, or due to sodium’s effect on parathyroid hormone (PTH) secretion. For every 1-gram increase in sodium (2.5 g of sodium chloride; NaCl salt) excreted by the kidneys, approximately 26.3 milligrams (mg) of calcium is added to the urine (1). A study of adolescent girls reported that a high-salt diet had a greater effect on urinary sodium and calcium excretion in white than in black girls, suggesting differences between ethnic groups (4). In adult women, an extra gram of sodium consumed per day is predicted to cause an additional 1% annual bone loss if the calcium loss is entirely from the skeleton.

Several cross-sectional and interventional studies have suggested that high sodium intake is detrimental to bone health, especially in older women (5). A two-year longitudinal study in postmenopausal women found increased urinary sodium excretion (an indicator of increased sodium intake) to be associated with decreased hip bone mineral density (BMD) (6). Another study of 40 postmenopausal women found that adherence to a low-sodium diet (2 g/day) for six months was associated with significant reductions in sodium, calcium excretion, and the amino-terminal propeptide of collagen type I, which is a biomarker of bone. absorption. However, these associations were observed only in women with elevated baseline urinary sodium excretion (7). Finally, in a randomized, placebo-controlled trial of 60 postmenopausal women, potassium citrate supplementation was found to prevent the increase in calcium excretion induced by consumption of a high-sodium diet (≥5,000 mg/day of elemental sodium). for four weeks (8).

Increasing dietary protein intake increases intestinal calcium absorption and urinary calcium excretion (9). The RDA for protein is 46 grams (g)/day for adult women and 56 g/day for adult men; however, average protein intake in the United States is generally higher (about 70 g/day for adult women and more than 100 g/day for adult men) (10). It was initially thought that a high-protein diet could result in negative calcium balance (when the sum of calcium excretion in urine and feces is greater than calcium intake) and thereby increase bone loss (11). However, most observational studies reported either no association or a positive association between protein intake and bone mineral density in children, adults, and the elderly (reviewed in 12). Overall calcium balance does not appear to be altered by high dietary protein intake in healthy individuals (13), and current evidence suggests that increased protein intake in those with adequate protein, calcium, and vitamin D intake does not adversely affect BMD or fracture risk. 14).

Phosphorus, typically found in protein-rich foods, tends to increase urinary excretion of calcium. A diet with a low calcium-to-phosphorus ratio (Ca:P ≤0.5) has been found to increase parathyroid hormone (PTH) secretion and urinary calcium excretion (15, 16). The absorption of calcium and phosphorus in the intestinal system and its excretion with feces is also influenced by the calcium-phosphorus ratio of the food consumed. In fact, in the lumen of the intestine, calcium salts can bind to phosphorus to form complexes that are excreted in the feces. This forms the basis for the use of calcium salts as phosphorus binders to reduce phosphorus absorption in patients with renal failure (17). Increased phosphorus intake from cola soft drinks (high in phosphoric acid) and food additives (high in phosphate) may have adverse effects on bone health (18). Currently, there is no conclusive evidence that dietary phosphorus levels in the United States have adverse effects on bone health. However, substituting milk or other dietary sources of calcium for high-phosphorous soft drinks may pose serious risks to the bones of adolescents and adults (see article on Phosphorus).

Human Digestive System

Exposure to caffeine concentrations ≤400 mg/day led to an increase in urinary calcium in two randomized controlled trials (19, 20). However, 400 mg of caffeine per day did not significantly alter 24-hour urinary calcium excretion in premenopausal women compared with placebo (21). A recent systematic review of 14 studies concluded that caffeine intake ≤400 mg per day is unlikely to affect calcium homeostasis, negatively affect bone mineral density, or increase the risk of osteoporosis and fractures in individuals with adequate calcium intake (22) .

Low blood calcium levels (hypocalcemia) usually indicate abnormal functioning of the parathyroid gland, as the skeleton provides large calcium reserves to maintain normal blood levels, especially when calcium intake is low. Other causes of abnormally low blood calcium include chronic kidney failure, vitamin D deficiency, and low blood magnesium, often seen in severe alcoholism. Magnesium deficiency

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