Facts, Articles, Research

What the science says (1990–2026): Phosphorus

These citations support correction of deficiency, specified forms, and elemental amounts — the same logic used in MD's Choice formulas. They are not claims that a supplement treats disease.

Calvo & Uribarri 2013; 2023 mineral-balance reviews. Phosphorus is abundant in processed food. The clinical problem is often ratio with calcium, not a need for extra phosphate pills in healthy people.

These products are not intended to diagnose, treat, cure, or prevent disease. Historic monograph text below is kept for the original library.

Phosphorus

I. Physiological Roles

Phosphorus has more known functions than any other mineral element in the animal body. It is located in every cell of the body and is vitally concerned in many metabolic processes
Phosphorus plays a major role, along with Ca, in formation of bones and teeth
Phosphorus, in combination with other elements, is involved in maintenance of osmotic and acid-base balance
A component of nucleic acids which are important in genetic transmission and control of cellular metabolism
Carbohydrates such as glucose are absorbed from the intestinal mucosa and phosphorylated compounds
Fatty acids are transported throughout the body as phospholipids
Phosphorus is a component of and activator of many enzyme systems
Energy transfer inside living cells. Practically every energy transfer inside living cells involves the forming and breaking of chemical bonds between phosphorus and carbon or carbon-nitrogen compounds
1. Low-energy phosphates
  1. Glucose-6-phosphate and triose phosphate are vital intermediates to the glycolysis scheme of energy metabolism
  2. Low energy phosphates liberate 2-3 Kcal/mole on hydrolysis
2. High energy phosphate bonds
  1. Energy liberated by catabolism is not used directly by cells
  2. It is applied instead to the formation of ester bonds between phosphoric acid residues and certain organic compounds
  3. Energy transfer inside living cells involves the forming or breaking of these ester linkages
    1. Adenosine triphosphate (ATP)
      – The most important high-energy phosphate compound
      – Upon hydrolysis to ADP, it liberates energy directly to such processes as muscle contraction, active transport, and synthesis of many chemical compounds
      – Loss of another phosphate to form AMP liberates more energy
    2. Guanosine triphosphate (GTP)
    3. Cytidine triphosphate (CTP)
    4. Uridine triphosphate (UTP)
    5. Inosine triphosphate (ITP)
    6. Creatine phosphate in muscle
  4. Relatively large amounts of energy (10-12 Kcal/mole) are released when high-energy bonds are hydrolyzed

II. Tissue Distribution of Phosphorus

Phosphorus is located in every cell of the body
The skeleton contains 80% of the total phosphorus in the body
The remaining 20% is distributed throughout the soft tissues

III. Metabolism, Absorption, and Excretion

See Ca section for bone metabolism of Ca and P
Phosphorus in the form orthophosphate is absorbed primarilyy in the upper small intestine
Transit by the small intestine consists of both an active and passive process
1. The active process is separate and distinct from that associated with Ca transport
2. When P intake is low, active transport is stimulated via the vitamin D pathway (see J. Dairy Sci. 69:604.1986)
3. Low plasma P will stimulate 1,25(OH)₂D synthesis independent of Ca influences
4. The resulting increase in 1,25(OH)₂D stimulates the intestine to absorb P more efficiently
5. At higher luminal P concentrations, active transport of P is saturated and passive absorption predominates

IV. Homeostatic Control of Phosphorus

The greater the need, the more efficient the absorption (see above)
When normal to high dietary P is consumed, P absorption is almost directly related to amount in the diet
In nonruminants the kidney is a major route of P excretion
In ruminants, the salivary glands supplant the kidney as the major route of P excretion
1. Flow of saliva in cattle is 25-290 l/d
2. This contributes 30 to 40 g (70 – 80%) of total endogenous P
In ruminants, alteration in salivary P appears also to play a major role in P homeostasis
1. P in saliva is directly correlated with P in plasma
  1. Injection of 1aOHD₃ or IV infusion of P solution will raise both plasma P and salivary P
  2. In contrast, a low-P diet, which results in hypophosphatemia, leads to a decrease in salivary P
  3. PTH increases P concentration in plasma, thereby increasing salivary P secretion
  4. Salivary P mixes with dietary P before a portion of the total P is absorbed in the small intestine
    
    Mechanism of adaptation to alterations in dietary phosphorus
    (J. Dairy Sci. 69:604. 1986) or (J. Anim. Sci 65:1727-1743. 1987.)
2. Changes in salivary P represent an efficient method of P regulation unique to the ruminant
  1. Salivary P is reduced during P deficiency
  2. Salivary P is increased during P excess

V. Interaction with Other Elements

Excess dietary Ca can reduce P absorption

As Ca content with the diet increases, availability of phytate phosphorus as well as availability of Ca decreases

Availability of Zn is reduced by the Ca-phytate complex

As Ca content of diet increases, availability of phylate phosphorus decreases
For maximum performance, inorganic P and Ca must be added to most practical diets
As Ca and P must be added to the diet, the phytate molecule becomes complexed with Ca
The net effect is that phytate Ca and P are utilized very little by nonruminants
Much of the phytin phosphorus in wheat is converted to orthophosphate by phytase during leavening and baking of bread
When unleavened bread is used in the Near East, high phytic acid content could contribute to occurrence of osteomalacia as well as reduce utilization of Zn

Excess dietary P can result in nutritional secondary hyperparathyroidism
1. Lowering of serum Ca stimulates secretion of PTH
2. Increased resorption of Ca from bone results in skeletal demineralization
Aluminum can inhibit P absorption
1. Aluminum hydroxide as an antacid
2. Aluminum in baking powder
3. Aluminum soft drink cans

VI. Phosphorus Requirements

P is required for formation of bone mineral in the ratio of 1g of P per 2g of Ca retained
If Ca and P ratio is balanced, wider ranges of P can be tolerated

Recommended allowances of P	% of Dietary DM
Poultry Starting Chicks (0-8 wks) Growing Chicks (8-18 wks) Laying Hens	0.7 0.4 0.5
Swine Growing and finishing animals 1 to 5 kg 5 to 10 kg 10 to 20 kg 20 to 35 kg 35 to 60 kg 60 to 100 kg Breeding animals Boars, bred gilts, sows Lactating sows, gilts	0.7 0.6 0.55 0.5 0.45 0.4 0.6 0.5
Dairy Cattle Baby calves Growing heifers and bulls Dry pregnant cows Lactating cows Mature bulls	0.42-0.5 0.26 0.24 0.31-0.38 0.18

Phosphorus %
Feedstuffs	Total	Phytate	Nonphytate
Alfalfa meal, 17% protein Barley Corn Corn Meal, degermed Oats Wheat Wheat bran Cottonseed meal Soybean meal	0.28 0.34 0.26 0.10 0.34 0.30 1.37 1.07 0.61	0 0.19 0.17 0.07 0.19 0.20 0.96 0.75 0.38	0.28 0.15 0.09 0.03 0.15 0.10 0.41 0.32 0.27

Comparative ratings of phosphate sources
Compound	Biological Value
Beta tricalcium phosphate (reference standard) Phosphoric acid Mono, diammonium phosphates Mono, dicalcium phosphates Mono, disodium phosphates Deflourinated rock phosphate Bone Meal Low fluorine rock phosphate Soft rock phosphate	100 115-125 115-125 105-115 115-125 95-100 90-100 55-75 23-35
Feedstuffs
Fishmeal Meat and bone scraps Dehydrated alfalfa meal Corn gluten meal Yellow corn Soybean oil meal	100 100 80 35 30 25

VII. Deficiency of P

P deficiency in rats (J. Nutr. 115:753-758.1985)
1. Estrous cycle normal
2. Breeding efficiency and numbers of pups per litter were not altered
3. Dams fed 0.04% P weaned fewer pups
4. Pup survival to 45 days of age was lower
5. Reduced average daily gain (pups were continued on their dams' diet after weaning)
Rickets in the young
Osteomalacia in the adult
Hypophosphatemia in humans
1. Causes
  1. Nutritional vitamin D deficiency
  2. Blocks in metabolism of vitamin D due to genetic abnormalities
  3. Liver disease
  4. Pharmacological agents (anticonvulsant, addiction to antacids)
  5. Abnormalities of renal tubular reabsorption of phosphate
2. Effects
  1. Failure of bone mineralization
    1. Rickets in growing bone
    2. Osteomalacia in adult bone
  2. Severe hypophophatemia
    1. Pronounced muscle weakness, possibly due to reduction to organic phosphates in muscle cells
Phosphorus deficiency in ruminants
1. Cause
  1. Most forages contain little more than adequate P
  2. Weathered, leached forage is nearly always borderline or deficient in P
  3. Phosphorus is usually one of the most limiting of the mineral nutrients for ruminants in many situations
2. Effects
  1. A drop in plasma inorganic P below the normal levels (4 to 6 mg/dl in adults; 6 to 8 mg/dl for young animals)
  2. Increased plasma phosphatase
  3. Depletion of mineral content of bones
  4. Stiff joints, lameness, fractures may occur
  5. Anorexia is the first clinical symptom
  6. Depraved appetite (may eat rocks, dirt, wood, bones, or hair)
  7. Reduced gain or milk production
  8. Impaired reproductive performance
    1. Lower conception rates and smaller calf crops
    2. More calving difficulty
    3. Lowered milk yield and consequently lowered weaning weight of calf
Phosphorus deficiency in chickens
1. High mortality
2. Cage layer fatigue syndrome
  1. Affected birds appear paralyzed and cannot rise or stand
  2. They eventually die of starvation

VIII. Phosphorus Excess

Nutritional secondary hyperparathyroidism
1. Increased concentration of serum P
2. Secondary lowering of serum Ca
3. Stimulation of PTH secretion
  1. Increased urinary excretion of phosphate
  2. Increased resorption of Ca from bone
  3. Pronounced skeletal demineralization
4. Metastic calcification in soft tissues (especially kidney, stomach and aorta)
Hyperphosphatemia in humans
1. Renal insufficiency can result in failure of urinary excretion of absorbed phosphate
  1. Secondary hyperparathyroidism
  2. Demineralization of bone
  3. Resorption of matrix
2. In some patients, hyperparathyroidism results in elevated serum P because of increased tubular reabsorption of phosphate
3. Treatment of hyperphosphatemia
  1. Reduction of phosphate intake is difficult since even the minimum protein diet compatible with good nutrition supplies too much phosphate
  2. Absorption of phosphate can be reduced by aluminum hydroxide
Hyperphosphatemia in ruminants
1. Relative excess P in relation to Ca can cause urinary calculi (urolithiosis)(J. Anim. Sci. 21:995, 1962: 22:510, 1963; 23:1079, 1964)
  1. Formation of stones in the kidney or bladder with resultant obstruction of urine excretion
  2. Bladder rupture results in temporary relief, but this is followed by abdominal distention, depression, and death due to uremia
  3. Maximum dietary level of P tolerated by sheep without development of calculi lies between 0.37% and 0.69%
  4. Increased dietary Ca provides partial protection against occurrence of calculi in sheep receiving higher levels of P (J. Anim. Sci. 24:671)
2. In contrast to d. above, see Schrier, C. J., and R. J. Emerick. 1986. Diet calcium carbonate, phosphorus and acidifying and alkalizing salts as factors influencing silica urolithiasis in rats fed tetraethylorthosilicate. J. Nutri. 116:823-830, 1986
  1. Rats fed diets containing 2% tetraethylorthosilicate were used as a model to investigate uroliths primarilyy of silica in range cattle and sheep
  2. Supplementary dietary phosphorus offers partial protection against silica uroliths
    1. Not associated with increases in urine volume
    2. Only partial dependent on urine acidification
  3. Increase in urolith incidence of rats fed CaCO₃ appear to result from an alkalization of urine and a reduction in urine
P excess in chickens
1. Reduced egg production and egg shell quality in hens
2. Decreased weight gain and efficiency of feed utilization in broiler
3. Increased mortality when dietary P is raised to 2% (approximately four times requirement)
Maximum tolerable phosphorus levels (assuming dietary Ca is adequate)
1. Cattle 1%
2. Sheep 0.6%
3. Swine 1.5%
4. Poultry 1% (laying hens, 0.8%)
5. Horse 1%

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Phosphorus formula P as phosphate (PO₄³⁻)

Phosphorus — P as phosphate (PO₄³⁻)

Almost always eaten as phosphate, not as the element. It is half of bone mineral and part of DNA, ATP, and cell membranes. Soft drinks and processed food already supply a lot. Balance with calcium matters.

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Vitamin A	Vitamin B1 (Thiamin)	Vitamin B2 (Riboflavin)	Vitamin B3 (Niacin)
Vitamin B5 (Pantothenic Acid)	Vitamin B6	Vitamin B12	Vitamin C
Vitamin D	Vitamin E	Vitamin K	Biotin
Folic Acid

Calcium	Magnesium	Phosphorus	Sodium, Potassium, Chloride
Sulfur (Sulfer)

Boron	Chromium	Cobalt	Copper
Fluorine	Iodine	Iron	Manganese
Molybdenum	Nickel (Nickle)	Selenium	Silicon
Tin	Vanadium	Zinc	Ultra Trace

Aluminum	Arsenic	Cadmium	Lead
Mercury

What the science says (1990–2026): Phosphorus

Phosphorus

Vitamins, Major Elements, Trace Elements, Toxic Elements

Vitamins

Major Elements

Trace Elements

Toxic Elements

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