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Food-Info.net > Minerals Phosphorus (P) |
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The European Union RDA for the general population is set at 800 mg/day.
Calcium and Vitamin D Dietary phosphorus is readily absorbed in the small intestine, and the kidneys excrete any excess phosphorus absorbed. The regulation of blood calcium and phosphorus levels is interrelated through the actions of parathyroid hormone (PTH) and vitamin D. A slight drop in blood calcium levels (e.g., in the case of inadequate calcium intake) is sensed by the parathyroid glands resulting in their increased secretion of PTH. PTH stimulates increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol, calcitriol) in the kidneys. Increased calcitriol levels result in increased intestinal absorption of both calcium and phosphorus.
Both PTH and vitamin D stimulate bone resorption, resulting in the release of bone mineral (calcium and phosphate) into the blood. Although PTH stimulation results in decreased urinary excretion of calcium, it results in increased urinary excretion of phosphorus. The increased urinary excretion of phosphorus is advantageous in bringing blood calcium levels up to normal because high blood levels of phosphate suppress the conversion of vitamin D to its active form in the kidneys.
Fructose some studies have shown that a diet high in fructose (20% of total calories) resulted in increased urinary loss of phosphorus and a negative phosphorus balance.
Structure
Phosphorus is a major structural component of bone and teeth in the form of a calcium phosphate salt called hydroxyapatite.
Energy needs
All energy production and storage are dependent on phosphorylated compounds, such as adenosine triphosphate (ATP) and creatine phosphate. When phosphate links to an adenosine diphosphate (ADP) molecule adenosine triphosphate (ATP) is formed, processing a high energy phosphate bond. When broken, this bond releases energy and the phosphate, reforming and ADP molecule. The ATP "energy" molecule is formed during glycolysis and other processes involving the release of chemical energy from food. ATP is used as the primary source of energy for many metabolic and enzymatic activities, especially muscle contraction, active transport, and the formation of DNA.
DNA
Phosphate is an important constituent of RNA and DNA. Nucleic acids (DNA and RNA) responsible for the storage and transmission of genetic information are long chains of phosphate-containing molecule Phosphate links the individual bases with one another.
Cell wall
Phosphate, from ATP, reacts with choline to initiate synthesis of phospholipids. Phospholipids (e.g., phosphatidylcholine) are major structural components of cell membranes. Phospholipids are instrumental in regulating cellular permeability and are found in the exterior membrane of nerve cells. They are also helpful in solubilising relatively nonsoluble triglycerides and cholesterols.
Hormone and enzyme regulation
A number of enzymes, hormones, and cell signalling molecules depend on phosphorylation for their activation. Phosphorus also helps to maintain normal acid-base balance (pH) in its role as one of the body's most important buffers. The phosphorus-containing molecule 2,3-diphosphoglycerate (2,3-DPG) binds to haemoglobin in red blood cells and affects oxygen delivery to the tissues of the body.
Sodium/potassium pump
The energy released from the high energy phosphate bond of ATP is essential for the operation of the sodium/potassium pump, which exchanges three sodium ions for two potassium ions across a biological membrane. This pump is used to regulate relative amounts of sodium and potassium excreted and retained in the body.
Blood clotting
Adenosine diphosphate, which contains two phosphate molecules, is a constituent of blood platelets and is secreted from platelet granules to stimulate platelet aggregation for blood clotting.
Inadequate phosphorus intake results in abnormally low serum phosphate levels (hypophosphatemia). Because phosphorus is so widespread in food, dietary phosphorus deficiency is usually seen only in cases of near total starvation.
Phosphate deficiencies can be the result defective renal phosphate absorption, as seen in familial vitamin D-resistant rickets, a genetically linked disorder which affects vitamin D utilization. Symptoms are characteristic of other forms of rickets.
The most serious adverse effect of abnormally elevated blood levels of phosphate (hyperphosphatemia) is the calcification of non-skeletal tissues, most commonly the kidneys. Such calcium phosphate deposition can lead to organ damage, especially kidney damage. Because the kidneys are very efficient at eliminating excess phosphate from the circulation, hyperphosphatemia from dietary causes is a problem mainly in people with kidney failure (end-stage renal disease) or hypoparathyroidism. When kidney function is only 20% of normal, even typical levels of dietary phosphorus may lead to hyperphosphatemia. Pronounced hyperphosphatemia has also occurred due to increased intestinal absorption of phosphate salts taken by mouth, as well as due to colonic absorption of the phosphate salts in enemas.
Excretion through the urine regulated the body's level of phosphorus.
Ursel, A. : Natural care Vitamins & Minerals Handbook. Dorling Kindersley, London, 2001. ISBN 80-89179-01-0
Dutch Nutrition Centre : www.voedingscentrum.nl/
Images adapted from here.
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