Higher organisms use organic phosphorus, getting it from plant sources with food..

Phosphate rather than phosphorus is the focus of nutritional biochemistry.

Phosphoric acid (H3PO4) is a strong acid. Monovalent cations (sodium, potassium and ammonium) can form highly soluble phosphate salts, while divalent cations (calcium and magnesium) form relatively insoluble compounds.. Living matter has a huge need for phosphorus. DNA and RNA are polymers based on phosphate ester monomers.; high-energy bond of adenosine triphosphate (ATP) - the main energy of living organisms.

Cell membranes are made up largely of phospholipids. The diversity of enzymatic functions is determined by the alternation of phosphorylation and dephosphorylation of proteins by cellular kinases and phosphatases.. Metabolism depends on the functioning of phosphorus as a cofactor for a variety of enzymes and as the main reservoir for metabolic energy in the form of ATP, creatine phosphate, and phosphoenolpyruvate..

Another important role of phosphorus is that neutral molecules are lipid soluble and pass through membranes.. Since phosphates are ionized at physiological pH, they can transport phosphorylated molecules within cells.. Finally, phosphorus combines with calcium to form hydroxyapatite, the main inorganic compound in bone..

Phosphorus in extracellular fluids is only 1% of the total body phosphorus. Most (70%) of total plasma phosphorus is found as a constituent of organic phospholipids.. However, the clinically useful fraction in plasma is inorganic phosphorus, 10% of which is protein bound, 5% is calcium or magnesium complexes, and most of the plasma inorganic phosphorus is represented by two orthophosphate fractions.. Phosphorus is found in all cells of the body. The main sites containing it are hydroxyapatite in bones and skeletal muscles.. The total phosphorus content is approximately 500 g for men and 400 g for women..

Phosphorus metabolism.

Phosphorus metabolism in the body is a complex interplay between various factors that can affect digestion, absorption, distribution and excretion.. Insoluble mineral phosphate salts are formed at elevated pH. The acidic environment of the stomach (pH \u003d 2) and most of the proximal small intestine (pH \u003d 5) may play an important role in maintaining the solubility and bioavailability of inorganic phosphorus. In this regard, the potential effects of hypochlorhydria (in elderly and antisecretory patients) on the solubility and bioavailability of phosphorus are important..

Approximately 60-70% of phosphorus is absorbed from a typical mixed diet. It has been shown that the absorption of phosphorus is in the range from 4 to 30 mg/kg of body weight per day and is associated with its consumption.. Physiological conditions characterized by an increase in the need for phosphorus (growth, pregnancy and lactation) are accompanied by a corresponding increase in its absorption.. In people of older age groups, there are changes in the excretion of phosphorus and adaptation to dietary phosphorus.. It is shown that, despite the consumption of the recommended norm of phosphorus, its negative balance is observed at the age of over 65 years, due to the loss of phosphorus in the urine..

The cellular and molecular mechanism of intestinal absorption of phosphorus is not fully understood.. Transport of phosphorus through the intestinal cell is an active, sodium-dependent pathway. Intracellular phosphorus levels are relatively high. Parathyroid hormone does not directly regulate intestinal phosphorus absorption.. Administration of an active vitamin D metabolite results in increased phosphorus absorption in both healthy and uraemic patients.. Regulation of the overall level of phosphorus in the body requires a coordinated effort of the kidney and intestines..

Under conditions of low dietary phosphorus intake, the intestine increases absorption and the kidney increases renal transport to minimize urinary loss.. This adaptation is mediated by changes in plasma levels of the active metabolite of vitamin D and parathyroid hormone.. If adaptive measures fail to compensate for low phosphorus intake, bone phosphorus may be redistributed to soft tissues.. However, these compensatory possibilities are not unlimited..

Fecal loss of phosphorus is 0.9-4 mg/kg per day. The main excretion occurs through the kidneys in a wide range (0.1-20%). Therefore, the kidneys have the ability to efficiently regulate plasma phosphorus.. The rate of renal reabsorption is regulated by plasma phosphorus concentration. Hormonal regulator of renal reabsorption of phosphorus - parathyroid hormone and nephrogenic cAMP. Plasma parathyroid hormone concentration positively correlates with urinary phosphorus excretion.

The main signs of loss of phosphorus in the urine are an increase in the absorption of phosphorus and an increase in its level in plasma.. Conditions that lead to hyperphosphaturia - hyperparathyroidism, acute respiratory or metabolic acidosis, diuretics, and increased extracellular mass of phosphorus. Decreased urinary phosphorus excretion is associated with dietary phosphorus restriction, increases in plasma insulin, thyroid hormone, growth, or glucagon, alkalosis, hypokalemia, and extracellular phosphorus depletion..

Phosphorus deficiency and hyperphosphatemia.

Signs of chronic phosphorus deficiency in laboratory animals are loss of appetite, development of joint stiffness, brittle bones, and susceptibility to infection. Healthy individuals are unlikely to develop phosphorus deficiency due to its high dietary intake.. However, preterm infants are often prone to developing rickets due to an inadequate supply of phosphorus and calcium.. Vitamin D-independent hypophosphatemic rickets was first described in 1937..

The classic study of phosphorus deficiency in humans was carried out by Lotz in 1968.. At the same time, deficiency was induced by feeding healthy individuals with a diet low in phosphorus.. Overt symptoms of phosphorus deficiency (anorexia, weakness, bone pain) have not been shown to develop until serum phosphorus falls below 1.0 mg/dL. To achieve this level of phosphorus in the serum, the appointment of phosphate-binding antacids is necessary.. Phosphorus deficiency is accompanied by a decrease in its excretion in the urine and an increase in calcium, magnesium and potassium in the urine.. All of the calcium and most of the magnesium comes from the bone..

The causes of hypophosphatemia, depending on the pathogenesis, can be grouped into three categories:.

• rapid movement of extracellular phosphorus into the intracellular space;

• reduced intestinal absorption;

•increased intestinal and urinary losses.

Hypophosphatemia has been clinically associated with overweight without adequate phosphorus intake, gastrointestinal malabsorption, starvation, diabetes mellitus, alcoholism, and renal tubular dysfunction.. It can also be seen with chronic abuse of phosphate-binding antacids.. Excess body weight increases the need for intracellular phosphorus and can cause rapid movement of extracellular phosphorus into the intracellular zone, especially when it is deficient..

Phosphorus malabsorption can develop in diseases that involve large areas of the small intestine (Crohn's disease, celiac disease, short bowel syndrome, and radiation enteritis). Other GI-related hypophosphatemias are due to vitamin D malabsorption and hyperparathyroidism secondary to calcium deficiency.. These conditions increase the risk of developing a negative phosphorus balance.. Increased muscle catabolism during fasting may maintain normal plasma phosphorus levels by removing phosphorus from intracellular stores..

Phosphate depletion in alcoholism can occur for several reasons: low phosphorus intake, malabsorption, increased urinary losses, secondary hyperparathyroidism, hypomagnesemia, and hypokalemia.

Excessive amounts of phosphorus can be lost in the urine in uncontrolled diabetes due to polyuria. Plasma phosphorus, however, may be normal or slightly elevated in ketotic patients due to the release of large amounts of phosphorus from intracellular stores.. Conversely, the administration of insulin and fluids to patients in ketosis with an intense movement of phosphorus from the extracellular to the intracellular space as a result can quickly cause clinically significant hypophosphatemia..

Excessive urinary phosphorus loss has also been seen in patients with proximal tubular dysfunction in Fanconi syndrome..

Hyperphosphatemia and excess phosphorus intake.

Hypocalcemia and secondary hyperparathyroidism with excessive resorption and bone loss have been observed in animals fed long-term diets containing more than a 2:1 ratio of phosphorus to calcium.. Infants formula-fed high phosphorus milk may experience hypocalcemia and tetany.. The ratio of phosphorus to calcium in typical European diets often exceeds the 2:1 ratio.; but there is no firm belief that it is harmful.

Hyperphosphatemia is commonly seen in chronic renal failure.. It can also develop with severe hemolysis, tumor decay, rhabdomyolysis syndrome and various endocrine dysfunctions (hypoparathyroidism, acromegaly, severe thyrotoxicosis).

Clinical manifestation of chronic hyperphosphatemia - ectopic calcifications. In chronic hyperphosphatemia, when possible, restriction of dietary phosphorus intake is recommended and oral phosphate binders, substances containing salts of aluminum, calcium or magnesium are prescribed.. However, long-term intake of aluminum and magnesium is contraindicated in patients with chronic renal failure..

Phosphorus Status Assessment.

Serum levels are often used to assess phosphorus status.. However, it is inadequate. Only 1% of the body's total phosphorus is in the extracellular fluid. In addition, plasma phosphorus is tightly regulated, primarily by renal excretion.. It can also be elevated due to muscle and bone catabolism or reduced by rapid changes in phosphorus in the intracellular space..

Phosphorus Requirements and Dietary Sources.

The need for phosphorus.

The established norm for adults over 24 years old is 800 mg.

Food sources of phosphorus. Phosphorus is widely distributed in foods. Average daily phosphorus intake is approximately 1500 mg for men and 1000 mg for women..

Food sources that are high in protein (meat, milk, eggs, and grains) are also high in phosphorus.. The relative contribution of major food groups to total phosphorus intake is approximately: 60% from milk, meat, poultry, fish and eggs; 20% - from cereals and legumes; 10% - from fruits and juices. Alcoholic beverages on average supply 4% of phosphorus intake, while other beverages (coffee, tea, soft drinks) provide 3%. Various dietary components may inhibit or increase phosphorus bioavailability.. Its bioavailability is higher if it is contained in products of animal origin than vegetable.

Animal Products. Phosphorus is well absorbed from meat - more than 70%, where it is present mainly in the form of intracellular organic compounds, which are hydrolyzed in the gastrointestinal tract to release inorganic phosphorus, which is well absorbed.. Inorganic phosphates make up 1/3 of the phosphorus in milk; 20% are compounds of esters with casein amino acids; 40% - for casein.

Inorganic phosphates in milk are calcium, magnesium and potassium salts.. The relative bioavailability of phosphorus in milk is 65-90% in infants. However, all the phosphorus in milk casein (20% of the total) is reduced by a phosphopeptide that is resistant to enzymatic breakdown by trypsin and less bioavailable.. The lower casein content in human milk compared to cow's milk may be responsible for the higher bioavailability of phosphorus from human milk..

Herbal products. In wheat, rice and corn, more than 80% of total phosphorus is found in the form of phytic (inositol hexaphosphoric) acid and 35% is found in mature potato tubers..

Humans do not have the enzyme phytase needed to break down phytates and release phosphorus. But prokaryotes (yeast and bacteria) contain phytase. This curious property of nature is important for dietary phosphorus for two reasons.. Initially, the traditional use of yeast in bread production results in the degradation of phytate due to the hydrolytic action of the yeast prior to baking.. Further, gut bacteria are able to degrade some of the dietary phytate..

Phytate is poorly digested in the human gastrointestinal tract. But water absorption can effectively remove phytate from some foods.. For example, 99.6% of the phytate in beans can be extracted by soaking them in water.. Grinding the grain removes the outer husks, which contain significant amounts of phytate in some cereals.. But such processing reduces the content of both phosphorus and other minerals..

Interactions between nutrients. High levels of phosphorus in infant formula may reduce magnesium absorption.. Phosphorus has been shown to reduce lead absorption in humans..

It is known that a diet containing 2 g of calcium daily does not affect the absorption of phosphorus.. However, high dietary calcium and dietary absorption suppression may be useful therapeutically to improve hyperphosphatemia in patients with chronic renal failure.. Dietary intake of 1,000 mg of calcium at 372 mg of phosphorus reduces phosphorus absorption, i.e. excess calcium supplementation may have an adverse effect on phosphorus balance.

OTC aluminum- or magnesium-containing antacids bind phosphorus in the gastrointestinal tract and reduce its absorption. Three grams of aluminum hydroxide (25 mmol of aluminum) reduces the absorption of phosphorus by 70-35%.

The current challenge is adapting to diets high in phytates.. The inhibitory effects of phytates on iron absorption are known to be observed in people who have been consuming a diet high in phytates for many years (for example, in vegetarians).

Baranovsky.

medbe. en.