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Phosphorus is an essential mineral that is required by every cell in the body for normal function (1). The majority of the phosphorus in the body is found as phosphate (PO4). Approximately 85% of the body's phosphorus is found in bone (2).
Phosphorus is a major structural component of bone in the form of a calcium phosphate salt called hydroxyapatite. Phospholipids (e.g., phosphatidylcholine) are major structural components of cell membranes. All energy production and storage are dependent on phosphorylated compounds, such as adenosine triphosphate (ATP) and creatine phosphate. Nucleic acids (DNA and RNA), which are responsible for the storage and transmission of genetic information, are long chains of phosphate-containing molecules. A number of enzymes, hormones, and cell-signaling molecules depend on phosphorylation for their activation. Phosphorus also helps to maintain normal acid-base balance (pH) by acting as one of the body's most important buffers. Additionally, the phosphorus-containing molecule 2,3-diphosphoglycerate (2,3-DPG) binds to hemoglobin in red blood cells and affects oxygen delivery to the tissues of the body (1).
A study of 11 adult men found that a diet high in fructose (20% of total calories) resulted in increased urinary loss of phosphorus and a negative phosphorus balance (i.e., daily loss of phosphorus was higher than daily intake). This effect was more pronounced when the diet was also low in magnesium (3). A potential mechanism for this effect is the lack of feedback inhibition of the conversion of fructose to fructose-1-phosphate in the liver. In other words, fructose-1-phosphate accumulates in the cell but this compound does not inhibit the enzyme that phosphorylates fructose, which consumes large amounts of phosphate. This phenomenon is known as phosphate trapping (1). This study's finding is relevant because fructose consumption in the U.S. has been increasing rapidly since the introduction of high fructose corn syrup in 1970, while magnesium intake has decreased over the past century (3).
Calcium and vitamin D
Dietary phosphorus is readily absorbed in the small intestine, and any excess phosphorus absorbed is excreted by the kidneys. The regulation of blood calcium and phosphorus levels is interrelated through the actions of parathyroid hormone (PTH) and vitamin D (diagram). 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 conversion of vitamin D to its active form (calcitriol) in the kidneys. Increased calcitriol levels in turn 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 (4).
Is high phosphorus intake detrimental to bone health?
Some investigators are concerned about the increasing amounts of phosphates in the diet which can be attributed to phosphoric acid in soft drinks and phosphate additives in a number of commercially prepared foods (5, 6). Because phosphorus is not as tightly regulated by the body as calcium, serum phosphate levels can rise slightly with a high phosphorus diet, especially after meals. High phosphate levels in the blood reduce the formation of the active form of vitamin D (calcitriol) in the kidneys, reduce blood calcium, and lead to increased PTH release by the parathyroid glands. However, high serum phosphorus levels also lead to decreased urinary calcium excretion (2). If sustained, elevated PTH levels could have an adverse effect on bone mineral content, but this effect has only been observed in humans on diets that were high in phosphorus and low in calcium. Moreover, similarly elevated PTH levels have been reported in diets that were low in calcium without being high in phosphorus (7). Recently, a controlled trial in young women found no adverse effects of a phosphorus-rich diet (3,000 mg/day) on bone-related hormones and biochemical markers of bone resorption when dietary calcium intakes were maintained at almost 2,000 mg/day (8). At present, there is no convincing evidence that the dietary phosphorus levels experienced in the U.S. adversely affect bone mineral density. However, the substitution of phosphate-containing soft drinks and snack foods for milk and other calcium rich foods does represent a serious risk to bone health (see Calcium).
Inadequate phosphorus intake results in abnormally low serum phosphate levels (hypophosphatemia). The effects of hypophosphatemia may include loss of appetite, anemia, muscle weakness, bone pain, rickets (in children), osteomalacia (in adults), increased susceptibility to infection, numbness and tingling of the extremities, and difficulty walking. Severe hypophosphatemia may result in death. Because phosphorus is so widespread in food, dietary phosphorus deficiency is usually seen only in cases of near-total starvation. Other individuals at risk of hypophosphatemia include alcoholics, diabetics recovering from an episode of diabetic ketoacidosis, and starving or anorexic patients on refeeding regimens that are high in calories but too low in phosphorus (1, 2).
The recommended dietary allowance (RDA) for phosphorus was based on the maintenance of normal serum phosphate levels in adults, which was believed to represent adequate phosphorus intake to meet cellular and bone formation needs (2).
|Recommended Dietary Allowance (RDA) for Phosphorus|
|Infants||0-6 months||100 (AI)||100 (AI)|
|Infants||7-12 months||275 (AI)||275 (AI)|
|Adults||19 years and older||700||700|
|Pregnancy||18 years and younger||-||1,250|
|Pregnancy||19 years and older||-||700|
|Breast-feeding||18 years and younger||-||1,250|
|Breast-feeding||19 years and older||-||700|
Phosphorus is found in most foods because it is a critical component of all living organisms. Dairy products, meat, and fish are particularly rich sources of phosphorus. Phosphorus is also a component of many polyphosphate food additives and is present in most soft drinks as phosphoric acid. Dietary phosphorus derived from food additives is not calculated in most food databases, so the total amount of phosphorus consumed by the average person in the U.S. is not entirely clear. A large survey of nutrient consumption in the U.S. found that the average phosphorus intake was 1,495 mg/day in men and 1,024 mg/day in women. The Food and Nutrition Board estimates phosphorus consumption in the U.S. has increased 10% to 15% over the past 20 years (2).
The phosphorus in all plant seeds (beans, peas, cereals, and nuts) is present in a storage form of phosphate called phytic acid or phytate. Only about 50% of the phosphorus from phytate is available to humans because we lack enzymes (phytases) that liberate phosphorus from phytate (9). Yeasts possess phytases, so whole grains incorporated into leavened breads have more bioavailable phosphorus than whole grains incorporated into breakfast cereals or flat breads (2). The table below lists a number of phosphorus rich foods along with their phosphorus content in milligrams (mg). For more information on the nutrient content of foods, search the USDA food composition database.
|Milk, skim||8 ounces||247|
|Yogurt, plain nonfat||8 ounces||385|
|Cheese, mozzarella; part skim||1 ounce||131|
|Egg||1 large, cooked||104|
|Beef||3 ounces, cooked*||173|
|Chicken||3 ounces, cooked*||155|
|Turkey||3 ounces, cooked*||173|
|Fish, halibut||3 ounces, cooked*||242|
|Fish, salmon||3 ounces, cooked*||252|
|Bread, whole wheat||1 slice||57|
|Bread, enriched white||1 slice||25|
|Carbonated cola drink||12 ounces||40|
|Almonds#||1 ounce (23 nuts)||134|
|Lentils#||1/2 cup, cooked||178|
*A 3-ounce serving is about the size of a deck of cards.
#Phosphorus from nuts, seeds, and grains is about 50% less bioavailable than phosphorus from other sources (9).
Sodium phosphate and potassium phosphate salts are used for the treatment of hypophosphatemia, and their use requires medical supervision. Calcium phosphate salts are sometimes used as calcium supplements (10).
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 usually only a problem 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 (1). To avoid the adverse effects of hyperphosphatemia, the Food and Nutrition Board set a tolerable upper intake level (UL) for oral phosphorus intake in generally healthy individuals (2). The lower UL for individuals over 70 years of age reflects the increased likelihood of impaired kidney function in elderly individuals. The UL does not apply to individuals with significantly impaired kidney function or other health conditions known to increase the risk of hyperphosphatemia.
|Tolerable Upper Intake Level (UL) for Phosphorus|
|Age Group||UL (mg/day)|
|Infants 0-12 months||Not possible to establish*|
|Children 1-3 years||3,000 (3.0 g)|
|Children 4-8 years||3,000 (3.0 g)|
|Children 9-13 years||4,000 (4.0 g)|
|Adolescents 14-18 years||4,000 (4.0 g)|
|Adults 19-70 years||4,000 (4.0 g)|
|Adults 70 years and older||3,000 (3.0 g)|
|Pregnancy||3,500 (3.5 g)|
|Breast-feeding||4,000 (4.0 g)|
*Source of intake should be from food and formula only.
Aluminum-containing antacids reduce the absorption of dietary phosphorus by forming aluminum phosphate, which is unabsorbable. When consumed in high doses, aluminum-containing antacids can produce abnormally low blood phosphate levels (hypophosphatemia) as well as aggravate phosphate deficiency due to other causes (11). As little as one ounce of aluminum hydroxide gel three times a day for several weeks can diminish serum phosphate levels and lead to increased urinary calcium loss (12). Excessively high doses of calcitriol, the active form of vitamin D, or its analogs may result in hyperphosphatemia (2).
Potassium supplements or potassium-sparing diuretics taken together with a phosphate may result in high blood levels of potassium (hyperkalemia). Hyperkalemia can be a serious problem, resulting in life threatening heart rhythm abnormalities (arrhythmias). People taking such a combination must inform their health care provider and have their serum potassium levels checked regularly (11).
The Linus Pauling Institute supports the RDA for phosphorus (700 mg/day for adults). Although few multivitamin/mineral supplements contain more than 15% of the current RDA for phosphorus, a varied diet should easily provide adequate phosphorus for most people.
Older adults (51 years and older)
At present, there is no evidence that the phosphorus requirements of older adults differ from that of younger adults (700 mg/day). Although few multivitamin/mineral supplements contain more than 15% of the current RDA for phosphorus, a varied diet should easily provide adequate phosphorus for most older people.
Written in April 2003 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University
Updated in August 2007 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University
Reviewed in August 2007 by:
James P. Knochel, M.D.
Clinical Professor, Emeritus
Presbyterian Hospital and
University of Texas Southwestern Medical School
Copyright 2001-2013 Linus Pauling Institute
The Linus Pauling Institute Micronutrient Information Center provides scientific information on the health aspects of dietary factors and supplements, foods, and beverages for the general public. The information is made available with the understanding that the author and publisher are not providing medical, psychological, or nutritional counseling services on this site. The information should not be used in place of a consultation with a competent health care or nutrition professional.
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