Fact Sheet for Health Professionals

This is a fact sheet intended for health professionals. For a general overview, see our consumer fact sheet.


Phosphorus, an essential mineral, is naturally present in many foods and available as a dietary supplement. Phosphorus is a component of bones, teeth, DNA, and RNA [1]. In the form of phospholipids, phosphorus is also a component of cell membrane structure and of the body’s key energy source, adenosine triphosphate (ATP). Many proteins and sugars in the body are phosphorylated. In addition, phosphorus plays key roles in regulation of gene transcription, activation of enzymes, maintenance of normal pH in extracellular fluid, and intracellular energy storage. In humans, phosphorus makes up about 1% to 1.4% of fat-free mass. Of this amount, 85% is in bones and teeth, and the other 15% is distributed throughout the blood and soft tissues [1].

Many different types of foods contain phosphorus, mainly in the form of phosphates and phosphate esters [1]. However, phosphorus in seeds and unleavened breads is in the form of phytic acid, the storage form of phosphorus [2]. Because human intestines lack the phytase enzyme, much phosphorus in this form is unavailable for absorption [1]. Phosphorus undergoes passive absorption in the small intestine, although some is absorbed by active transport [2].

Phosphorus and calcium are interrelated because hormones, such as vitamin D and parathyroid hormone (PTH), regulate the metabolism of both minerals. In addition, phosphorus and calcium make up hydroxyapatite, the main structural component in bones and tooth enamel [3]. The combination of high phosphorus intakes with low calcium intakes increases serum PTH levels, but evidence is mixed on whether the increased hormone levels decrease bone mineral density [2,4-6].

The kidneys, bones, and intestines regulate phosphorus homeostasis, which requires maintenance of urinary losses at equivalent levels to net phosphorus absorption and ensuring that equal amounts of phosphorus are deposited and resorbed from bone [1,7,8]. Several hormones, including estrogen and adrenaline, also affect phosphorus homeostasis. When kidney function declines, as in chronic kidney failure, the body cannot excrete phosphate efficiently, and serum levels rise [9].

Although phosphorus status is not typically assessed, phosphate can be measured in both serum and plasma [10]. In adults, normal phosphate concentration in serum or plasma is 2.5 to 4.5 mg/dL (0.81 to 1.45 mmol/L) [10]. Hypophosphatemia is defined as serum phosphate concentrations lower than the low end of the normal range, whereas a concentration higher than the high end of the range indicates hyperphosphatemia. However, plasma and serum phosphate levels do not necessarily reflect whole-body phosphorus content [1,11].

Recommended Intakes

Intake recommendations for phosphorus and other nutrients are provided in the Dietary Reference Intakes (DRIs) developed by the Food and Nutrition Board (FNB) at the National Academies of Sciences, Engineering, and Medicine [12]. DRI is the general term for a set of reference values used for planning and assessing nutrient intakes of healthy people. These values, which vary by age and sex, include the following:

  • Recommended Dietary Allowance (RDA): Average daily level of intake sufficient to meet the nutrient requirements of nearly all (97%–98%) healthy individuals; often used to plan nutritionally adequate diets for individuals
  • Adequate Intake (AI): Intake at this level is assumed to ensure nutritional adequacy; established when evidence is insufficient to develop an RDA
  • Estimated Average Requirement (EAR): Average daily level of intake estimated to meet the requirements of 50% of healthy individuals; usually used to assess the nutrient intakes of groups of people and to plan nutritionally adequate diets for them; can also be used to assess the nutrient intakes of individuals
  • Tolerable Upper Intake Level (UL): Maximum daily intake unlikely to cause adverse health effects

Table 1 lists the current RDAs for phosphorus [2]. For infants from birth to 12 months, the FNB established an AI for phosphorus that is equivalent to the mean intake of phosphorus in healthy, breastfed infants.

Table 1: Recommended Dietary Allowances (RDAs) for Phosphorus [2]
Age Male Female Pregnancy Lactation
Birth to 6 months* 100 mg 100 mg
7–12 months* 275 mg 275 mg
1–3 years 460 mg 460 mg
4–8 years 500 mg 500 mg
9–13 years 1,250 mg 1,250 mg
14–18 years 1,250 mg 1,250 mg 1,250 mg 1,250 mg
19+ years 700 mg 700 mg 700 mg 700 mg

*Adequate Intake (AI)

Sources of Phosphorus


Many different types of foods contain phosphorus, including dairy products, meats and poultry, fish, eggs, nuts, legumes, vegetables, and grains [13,14]. In the United States, dairy products contribute about 20% of total phosphorus intakes, and bakery products (e.g., breads, tortillas, and sweet bakery products) contribute 10% [13]. Vegetables and chicken contribute 5% each. The absorption rate for the phosphorus naturally contained in food is 40%–70%; phosphorus from animal sources has a higher absorption rate than that from plants [15,16]. Calcium from foods and supplements can bind to some of the phosphorus in foods and prevent its absorption [1,17]. According to one analysis, a very high calcium intake of 2,500 mg/day binds 0.61–1.05 g phosphorus [17]. In infants, phosphorus bioavailability ranges from 85%–90% for human milk to approximately 59% for soy-based formulas [2].

Phosphate additives (e.g., phosphoric acid, sodium phosphate, and sodium polyphosphate) are present in many foods, especially processed food products. These additives are used for such purposes as preserving moisture or color and enhancing and stabilizing frozen foods [18]. Foods containing these additives have an average of 67 mg more phosphorus per serving than similar foods not containing the additives, and these additives contribute to overall phosphorus intakes in the United States [18,19].

Phosphate additives are estimated to contribute 300 to 1,000 mg to total daily phosphorus intakes [11,20], or about 10%–50% of phosphorus intakes in Western countries [21]. The use of phosphate additives is rising, as are the amounts of these additives in foods [22,23]. The absorption rate for the phosphorus in phosphate additives is approximately 70% [24].

Several food sources of phosphorus are listed in Table 2.

Table 2: Phosphorus Content of Selected Foods [25]
Food Milligrams
(mg) per
Yogurt, plain, low fat, 6-ounce container 245 20
Milk, 2% milkfat, 1 cup 226 18
Salmon, Atlantic, farmed, cooked, 3 ounces 214 17
Scallops, breaded and fried, 3 ounces 201 16
Cheese, mozzarella, part skim, 1.5 ounces 197 16
Chicken, breast meat, roasted, 3 ounces 182 15
Lentils, boiled, ½ cup 178 14
Beef patty, ground, 90% lean meat, broiled, 3 ounces 172 14
Cashew nuts, dry roasted, 1 ounce 139 11
Potatoes, russet, flesh and skin, baked, 1 medium 123 10
Kidney beans, canned, ½ cup 115 9
Rice, brown, long grain, cooked, ½ cup 102 8
Peas, green, boiled, ½ cup 94 8
Oatmeal, cooked with water, ½ cup 90 7
Egg, hard boiled, 1 large 86 7
Tortillas, corn, 1 medium 82 7
Bread, whole wheat, 1 slice 60 5
Sesame seeds, 1 tablespoon 57 5
Bread, pita, whole wheat, 4-inch pita 50 4
Asparagus, boiled, ½ cup 49 4
Tomatoes, ripe, chopped, ½ cup 22 2
Apple, 1 medium 20 2
Cauliflower, boiled, 1” pieces, ½ cup 20 2
Beverages, carbonated, cola, 1 cup 18 1
Clementine, 1 medium 16 1
Tea, green, brewed, 1 cup 0 0

*DV = Daily Value. The U.S. Food and Drug Administration (FDA) developed DVs to help consumers compare the nutrient contents of foods and dietary supplements within the context of a total diet. The DV for phosphorus is 1,250 mg for adults and children age 4 years and older [26]. FDA does not require food labels to list phosphorus content unless phosphorus has been added to the food. Foods providing 20% or more of the DV are considered to be high sources of a nutrient, but foods providing lower percentages of the DV also contribute to a healthful diet.

The U.S. Department of Agriculture’s (USDA’s) FoodData Centralexternal link disclaimer [27] lists the nutrient content of many foods and provides a comprehensive list of foods containing phosphorus arranged by nutrient content.external link disclaimer

Dietary supplements

Phosphorus is available in dietary supplements containing only phosphorus, supplements containing phosphorus in combination with other ingredients, and a few multivitamin/mineral products [28]. Phosphorus in supplements is usually in the form of phosphate salts (e.g., dipotassium phosphate or disodium phosphate) or phospholipids (e.g., phosphatidylcholine or phosphatidylserine). Products typically provide 10% or less of the DV for phosphorus, but a small proportion deliver more than 100% [28].

The bioavailability of phosphate salts is approximately 70% [15,24]. The bioavailability of other forms of phosphorus in supplements has not been determined in humans.

Phosphorus Intakes and Status

Most Americans consume more than the recommended amounts of phosphorus. Data from the 2015–2016 National Health and Nutrition Examination Survey (NHANES) show that among children and teens age 2–19 years, the average daily phosphorus intake from foods is 1,237 mg [29]. In adults age 20 and older, the average daily phosphorus intake from foods is 1,189 mg for women and 1,596 mg for men.

According to an analysis of 2013–2014 NHANES data, the average daily phosphorus intake from both foods and supplements is 1,301 mg for women and 1,744 mg for men [30]. Some experts question whether the dietary data collection instruments used by NHANES and other large population-based studies capture true dietary phosphorus intakes because these surveys do not account for the additional contributions of phosphate additives in foods [31,32].

Phosphorus Deficiency

Phosphorus deficiency (hypophosphatemia) is rare in the United States and is almost never the result of low dietary intakes [1]. The effects of hypophosphatemia can include anorexia, anemia, proximal muscle weakness, skeletal effects (bone pain, rickets, and osteomalacia), increased infection risk, paresthesias, ataxia, and confusion [1]. In most cases, hypophosphatemia is caused by medical conditions, such as hyperparathyroidism, kidney tubule defects, and diabetic ketoacidosis [33].

Groups at Risk of Phosphorus Inadequacy

The following groups are most likely to have inadequate phosphorus status.

Preterm newborns

Phosphorus deficiency in preterm infants is one of the main causes, along with calcium deficiency, of osteopenia of prematurity (impaired bone mineralization) [34]. Because two-thirds of fetal bone mineral content is acquired during the third trimester of pregnancy, preterm infants are born with low stores of calcium and phosphorus in their bones [35]. The benefits of providing extra phosphorus and calcium for bone health in preterm babies is not clear. However, milk fortified with higher amounts of these minerals and other nutritional components is typically recommended to support overall growth and development [35,36].

People with genetic phosphate regulation disorders

Rare genetic disorders of phosphorus metabolism include X-linked hypophosphatemic rickets [37]. In addition to rickets, patients with this disease develop osteomalacia, pseudofractures (formation of new bone and thickened connective tissue over injured bone), enthesopathy (mineralization of ligaments and tendons), and dental damage. Other rare genetic disorders of phosphorus regulation associated with rickets include autosomal-dominant and autosomal-recessive hypophosphatemic rickets and hereditary hypophosphatemic rickets with hypercalciuria [38]. Treatment typically consists of vitamin D and phosphorus supplementation from diagnosis until growth is complete [39].

Patients with severe malnutrition

People with severe protein or calorie malnutrition can develop refeeding syndrome, also known as refeeding hypophosphatemia, within 2 to 5 days of starting enteral or parenteral nutrition because of the shift in metabolism from a catabolic to an anabolic state [40,41]. Causes of malnutrition that can lead to refeeding syndrome include chronic diseases (e.g., cancer, chronic obstructive pulmonary disease, or cirrhosis), very low birthweight, cachexia, low body weight, anorexia nervosa, excessive alcohol intake, and chewing or swallowing problems. The effects of refeeding syndrome can include impaired neuromuscular function, hypoventilation, respiratory failure, impaired blood clotting, confusion, coma, cardiac arrest, congestive heart failure, and death [41]. Prophylactic administration of phosphorus and thiamin in patients at risk of refeeding syndrome can prevent this condition [41].

Phosphorus and Health

This section focuses on two diseases in which phosphorus might play a role: chronic kidney disease (CKD) and cardiovascular disease (CVD).

Chronic kidney disease

CKD, which affects 5%–10% of the population worldwide, can lead to CVD and early death [42]. As kidney function declines, phosphate excretion becomes less efficient and serum phosphate concentration rises. As a result, PTH and fibroblast growth factor 23 lose their ability to suppress phosphorus resorption by the kidneys [43].

Increased phosphorus retention often leads to CKD mineral and bone disorder. This systemic condition is characterized by abnormal metabolism of phosphorus, calcium, PTH, and/or vitamin D; abnormal bone turnover, mineralization, volume, growth, or strength; and vascular or other soft-tissue calcification [44].

An analysis of 2003–2006 NHANES data illustrates the association between CKD and phosphate levels. In 7,895 adults (mean age 47 years, 52% Caucasian), participants with reduced kidney function had significantly higher serum phosphate levels (4.12 mg/dL) than those with normal kidney function (3.83 mg/dL) [45].

Several studies have shown an increased risk of mortality or disease progression in patients who have CKD and high phosphate levels [46-48]. A meta-analysis of nine cohort studies in 199,289 patients age 50–73 years with end-stage renal disease showed, for example, that patients on dialysis with the highest phosphate levels (greater than 5.2–7.5 mg/dL, depending on the study) had a 39% greater risk of all-cause mortality during 12 to 97.6 months of follow-up than those with normal phosphate levels (defined in the analysis as 3.0–5.5 mg/dL, depending on the study) [49].

However, high phosphate levels do not seem to have the same associations in people with milder CKD [50,51]. For example, an analysis of NHANES III (1988–1994) data on 1,105 adults (mean age 67–71 years, depending on their phosphate intake tertile) with moderate CKD found that serum phosphate levels were very similar, regardless of phosphate intake—3.6 mg/dL in the lowest tertile of phosphorus intake (532 mg/day) and 3.5 mg/dL in the highest intake tertile (1,478 mg/day)—and that high phosphorus intakes were not associated with increased mortality rates over 6–12 years, possibly because these patients did not have severe CKD [51].

To prevent the complications of high phosphate levels in patients with CKD, clinicians sometimes encourage patients to limit their phosphorus intakes (e.g., by replacing most animal proteins in their diets with plant-based protein sources, whose phosphorus is less bioavailable) and eat more calcium-rich foods [9,52]. Some evidence shows that replacing foods containing phosphorus additives with foods that lack these additives can reduce serum phosphate levels [53]. However, restricting phosphorus intakes can also reduce protein intakes because many foods (e.g., fish, meats, and legumes) containing large amounts of phosphorus also contain large amounts of protein [54]. Furthermore, a Cochrane Review of nine studies in 634 participants with CKD followed for 1–18 months found only limited, low-quality evidence indicating that dietary interventions might have a positive impact on CKD mineral and bone disorder [43].

In its clinical practice guideline for CKD mineral and bone disorder, the Kidney Disease: Improving Global Outcomes guidelines development group recommends that patients with stage 3–5 (more severe) CKD limit dietary phosphorus intake either alone or in combination with other treatments to reduce phosphate levels [55]. However, the group notes that clinical trial data showing that treatments that lower serum phosphate levels improve patient-centered outcomes are lacking, and it acknowledges that this recommendation is weak.

Additional studies are needed on the link between phosphate concentrations and both CKD risk and morbidity in patients with CKD as well as the impact of dietary phosphorus restriction in patients with this disease.

Cardiovascular disease

Several observational studies support a link between high phosphate levels and CVD risk in people with and without a history of CVD [56,57]. For example, an analysis of 14,675 participants (55% women) without atrial fibrillation found, based on almost 20 years of follow-up, that each 1 mg/dL increase in serum phosphate was associated with a 13% higher risk of atrial fibrillation [58].

Several large epidemiologic studies have also found associations between higher serum phosphate concentrations and risk of cardiovascular mortality in healthy adults. A meta-analysis of data from four prospective cohort studies with 13,515 participants (with percentages of male participants ranging, depending on the study, from 44 to 100% and mean ages from 43 to 74 years) followed for 6–29 years showed a 36% higher risk of cardiovascular mortality in those with the highest phosphate concentration (2.79–4.0 mg/dL) compared with participants with a phosphate concentration of 0.61–3.28 mg/dL [59]. A subsequent study not included in this meta-analysis in 13,165 nonpregnant adult participants (mean age 43–45 years, 52% female) in NHANES III (1988–1994) followed for a median of 14.3 years found that for every 1 mg/dL increase in phosphate above 3.5 mg/dL, the risk of death rose by 35% and the risk of cardiovascular death increased by 45% [60].

Not all observational data, however, support a link between serum phosphate concentrations and CVD risk. A post hoc analysis of data from 7,269 postmenopausal women, mean age 66 years, with osteoporosis found no association between higher serum phosphate levels and risk of cardiovascular outcomes during 4 years of follow-up [61].

In spite of the evidence supporting a link between increased phosphate levels and CVD risk, the literature offers no evidence on whether restricting phosphorus consumption can prevent CVD in healthy adults [62]. Additional research is needed to address this issue.

Health Risks from Excessive Phosphorus

High phosphorus intakes rarely produce adverse effects in healthy people. Although some studies have found associations between high phosphorus intakes (1,000 mg/day or higher) and cardiovascular, kidney, and bone adverse effects as well as an increased risk of death [23,63,66], others have found no link between high intakes and increased disease risk [5,65,66]. The ULs for phosphorus from food and supplements for healthy individuals are therefore based on intakes associated with normal serum phosphate concentrations [2]. The ULs do not apply to individuals who are receiving supplemental phosphorus under medical supervision.

Table 3: Tolerable Upper Intake Levels (ULs) for Phosphorus [2]
Age Male Female Pregnancy Lactation
Birth to 6 months* None established* None established*
7–12 months* None established* None established*
1–3 years 3,000 mg 3,000 mg
4–8 years 3,000 mg 3,000 mg
9–13 years 4,000 mg 4,000 mg
14–18 years 4,000 mg 4,000 mg 3,500 mg 4,000 mg
19–50 years 4,000 mg 4,000 mg 3,500 mg 4,000 mg
51–70 years 4,000 mg 4,000 mg
71+ years 3,000 mg 3,000 mg

* Breast milk, formula, and food should be the only sources of phosphorus for infants.

According to one analysis of data on healthy U.S. adults using NHANES III data collected in 1988–1994, high phosphorus intakes (1,000 mg/day or more) were associated with increased rates of all-cause and cardiovascular mortality in adults through 2006 [63]. These intakes are twice the RDA for adults—less than daily intakes in many men (especially those who are white or Hispanic) and well below the UL. The implications of this analysis for the potential adverse effects of high phosphorus intakes are unclear. High phosphorus intakes might be signs of diets that are unhealthy in other ways, for example [63].

Very high phosphorus intakes over short periods (e.g., two 6,600 mg doses of sodium phosphate taken in 1 day) can cause hyperphosphatemia [67,68]. The main effects of hyperphosphatemia include changes in the hormones that regulate calcium metabolism and calcification of nonskeletal tissues, especially in the kidney [2].

Interactions with Medications

Phosphorus can interact with certain medications, and some medications can have an adverse effect on phosphate levels. Two examples are provided below. Individuals taking these and other medications on a regular basis should discuss their phosphorus status with their health care providers.


Antacids that contain aluminum hydroxide, such as Maalox HRF and Rulox, bind phosphorus in the intestines, and their chronic use for 3 months or longer can therefore lead to hypophosphatemia [1,69]. These drugs can also aggravate existing phosphate deficiency. Antacids containing calcium carbonate (Rolaids, Tums, Maalox) also decrease instestinal absorption of dietary phosphorus [70].


Some laxatives, such as Fleet Prep Kit #1, contain sodium phosphate, and ingesting these products can increase serum phosphate levels [71]. After 13 reports of deaths associated with taking one dose that was higher than recommended on the label of a laxative containing sodium phosphate, FDA issued a warning that these products are potentially dangerous if more than recommended doses are taken, especially in people with kidney disease, heart disease, or dehydration [72].

Phosphorus and Healthful Diets

The federal government's 2020–2025 Dietary Guidelines for Americans notes that "Because foods provide an array of nutrients and other components that have benefits for health, nutritional needs should be met primarily through foods. ... In some cases, fortified foods and dietary supplements are useful when it is not possible otherwise to meet needs for one or more nutrients (e.g., during specific life stages such as pregnancy)."

For more information about building a healthy dietary pattern, refer to the Dietary Guidelines for Americansexternal link disclaimer and the USDA's MyPlate.external link disclaimer

The Dietary Guidelines for Americans describes a healthy dietary pattern as one that

  • Includes a variety of vegetables; fruits; grains (at least half whole grains); fat-free and low-fat milk, yogurt, and cheese; and oils.
    • Some dairy products are rich in phosphorus, and some vegetables, fruits, and grains contain phosphorus.
  • Includes a variety of protein foods such as lean meats; poultry; eggs; seafood; beans, peas, and lentils; nuts and seeds; and soy products.
    • Some meats, seafoods, fish, and nuts and seeds are rich in phosphorus or are good sources of the mineral, and other types of meats, fish, and beans contain phosphorus.
  • Limits foods and beverages higher in added sugars, saturated fat, and sodium.
  • Limits alcoholic beverages.
  • Stays within your daily calorie needs.


  1. Heaney RP. Phosphorus. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition. 10th ed. Washington, DC: Wiley-Blackwell; 2012:447-58.
  2. Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington, DC: National Academies Press; 1997.
  3. Trautvetter U, Ditscheid B, Jahreis G, Glei M. Habitual intakes, food sources and excretions of phosphorus and calcium in three German study collectives. Nutrients 2018;10. [PubMed abstract]
  4. Anderson JJB, Adatorwovor R, Roggenkamp K, Suchindran CM. Lack of influence of calcium/phosphorus ratio on hip and lumbar bone mineral density in older Americans: NHANES 2005-2006 cross-sectional data. J Endocr Soc 2017;1:407-14. [PubMed abstract]
  5. Lee KJ, Kim KS, Kim HN, et al. Association between dietary calcium and phosphorus intakes, dietary calcium/phosphorus ratio and bone mass in the Korean population. Nutr J 2014;13:114.
  6. Trautvetter U, Jahreis G, Kiehntopf M, Glei M. Consequences of a high phosphorus intake on mineral metabolism and bone remodeling in dependence of calcium intake in healthy subjects - a randomized placebo-controlled human intervention study. Nutr J 2016;15:7. [PubMed abstract]
  7. Calvo MS, Lamberg-Allardt CJ. Phosphorus. Adv Nutr 2015;6:860-2. [PubMed abstract]
  8. Lederer E. Regulation of serum phosphate. J Physiol 2014;592:3985-95. [PubMed abstract]
  9. Calvo MS, Sherman RA, Uribarri J. Dietary phosphate and the forgotten kidney patient: a critical need for FDA regulatory action. Am J Kidney Dis 2019;73:542-51. [PubMed abstract]
  10. Bazydlo LAL, Needham M, Harris NS. Calcium, Magnesium, and Phosphate.external link disclaimer Laboratory Medicine 2014;45:e44-e50.
  11. EFSA Panel on Dietetic Products N, Allergies. Scientific Opinion on Dietary Reference Values for phosphorus.external link disclaimer EFSA Journal 2015;13:4185.
  12. Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academies Press; 2001. [PubMed abstract]
  13. Moshfegh AJ, Kovalchik AF, Clemens JC. Phosphorus Intake of Americans: What We Eat in American, NHANES 2011-2012.external link disclaimer Food Surveys Research Group Dietary Data Brief No. 15. 2016.
  14. McClure ST, Chang AR, Selvin E, et al. Dietary Sources of Phosphorus among Adults in the United States: Results from NHANES 2001-2014. Nutrients 2017;9. [PubMed abstract]
  15. Calvo MS, Moshfegh AJ, Tucker KL. Assessing the health impact of phosphorus in the food supply: issues and considerations. Adv Nutr 2014;5:104-13. [PubMed abstract]
  16. Calvo MS, Uribarri J. The Regulatory Aspects of Phosphorus Intake: Dietary Guidelines and Labeling. In: Uribarri J, Calvo MS, eds. Dietary Phosphorus: Health, Nutrition, and Regulatory Aspects. Boca Raton, Florida: CRC Press; 2018:249-66.
  17. Heaney RP, Nordin BE. Calcium effects on phosphorus absorption: implications for the prevention and co-therapy of osteoporosis. J Am Coll Nutr 2002;21:239-44. [PubMed abstract]
  18. Leon JB, Sullivan CM, Sehgal AR. The prevalence of phosphorus-containing food additives in top-selling foods in grocery stores. J Ren Nutr 2013;23:265-70.e2. [PubMed abstract]
  19. Calvo MS, Uribarri J. Contributions to total phosphorus intake: all sources considered. Semin Dial 2013;26:54-61. [PubMed abstract]
  20. Calvo MS, Park YK. Changing phosphorus content of the U.S. diet: potential for adverse effects on bone. J Nutr 1996;126:1168S-80S. [PubMed abstract]
  21. Itkonen ST, Karp HJ, Lamberg-Allardt CJ. Bioavailability of phosphorus. In: Uribarri J, Calvo MS, eds. Dietary Phosphorus: Health, Nutrition, and Regulatory Aspects. Boca Raton, Florida: CRC Press; 2018:221-33.
  22. Calvo MS, Uribarri J. Phosphorus in the modern food supply: Underestimation of exposure. In: Gutierrez OM, Kalantar-Zadeh K, Mehrotra R, eds. Clinical Aspects of Natural and Added Phosphorus in Foods. New York, New York: Springer-Verlag; 2017:47-76.
  23. Gutierrez OM, Luzuriaga-McPherson A, Lin Y, et al. Impact of phosphorus-based food additives on bone and mineral metabolism. J Clin Endocrinol Metab 2015;100:4264-71. [PubMed abstract]
  24. Scanni R, vonRotz M, Jehle S, et al. The human response to acute enteral and parenteral phosphate loads. JJ Am Soc Nephrol 2014;25:2730-9. [PubMed abstract]
  25. U.S. Department of Agriculture, Agricultural Research Service. USDA National Nutrient Database for Standard Reference, Legacy Release.external link disclaimer Nutrient Data Laboratory Home Page, 2019.
  26. U.S. Food and Drug Administration. Food Labeling: Revision of the Nutrition and Supplement Facts Labels.external link disclaimer 2016.
  27. U.S. Department of Agriculture. FoodData Central.external link disclaimer 2019.
  28. National Institutes of Health. Dietary Supplement Label Database. 2019.
  29. U.S. Department of Agriculture, Agricultural Research Service. What We Eat in America, 2015-2016.external link disclaimer 2019.
  30. U.S. Department of Agriculture, Agricultural Research Service. What We Eat in America, 2013-2014.external link disclaimer 2017.
  31. Gutierrez OM. The connection between dietary phosphorus, cardiovascular disease, and mortality: where we stand and what we need to know. Adv Nutr 2013;4:723-9. [PubMed abstract]
  32. Calvo MS, Uribarri J. Public health impact of dietary phosphorus excess on bone and cardiovascular health in the general population. Am J Clin Nutr 2013;98:6-15. [PubMed abstract]
  33. Hruska K. Overview of phosphorus homeostasis. In: Gutierrez OM, Kalantar-Zadeh K, Mehrotra R, eds. Clinical Aspects of Natural and Added Phosphorus in Foods. New York, New York: Springer-Verlag; 2017:11-28.
  34. Karpen HE. Mineral homeostasis and effects on bone mineralization in the preterm neonate. Clin Perinatol 2018;45:129-41. [PubMed abstract]
  35. Harding JE, Wilson J, Brown J. Calcium and phosphorus supplementation of human milk for preterm infants. Cochrane Database Syst Rev 2017;2:Cd003310. [PubMed abstract]
  36. Abrams SA. In utero physiology: role in nutrient delivery and fetal development for calcium, phosphorus, and vitamin D. Am J Clin Nutr 2007;85:604S-7S. [PubMed abstract]
  37. de Menezes Filho H, de Castro LC, Damiani D. Hypophosphatemic rickets and osteomalacia. Arq Bras Endocrinol Metabol 2006;50:802-13. [PubMed abstract]
  38. Gattineni J, Baum M. Genetic disorders of phosphate regulation. Pediatr Nephrol 2012;27:1477-87. [PubMed abstract]
  39. Pavone V, Testa G, Gioitta Iachino S, et al. Hypophosphatemic rickets: etiology, clinical features and treatment. Eur J Orthop Surg Traumatol 2015;25:221-6. [PubMed abstract]
  40. Parli SE, Ruf KM, Magnuson B. Pathophysiology, treatment, and prevention of fluid and electrolyte abnormalities during refeeding syndrome. J Infus Nurs 2014;37:197-202. [PubMed abstract]
  41. Friedli N, Stanga Z, Culkin A, et al. Management and prevention of refeeding syndrome in medical inpatients: An evidence-based and consensus-supported algorithm. Nutrition 2018;47:13-20. [PubMed abstract]
  42. Moe SM, Drüeke T, Lameire N, Eknoyan G. Chronic kidney disease--mineral-bone disorder: a new paradigm. Advances in Chronic Kidney Disease 2007;14:3-12. [PubMed abstract]
  43. Liu Z, Su G, Guo X, et al. Dietary interventions for mineral and bone disorder in people with chronic kidney disease. Cochrane Database Syst Rev 2015:Cd010350. [PubMed abstract]
  44. Moe S, Drueke T, Cunningham J, et al. Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int 2006;69:1945-53. [PubMed abstract]
  45. Moore LW, Nolte JV, Gaber AO, Suki WN. Association of dietary phosphate and serum phosphorus concentration by levels of kidney function. Am J Clin Nutr 2015;102:444-53. [PubMed abstract]
  46. Da J, Xie X, Wolf M, et al. Serum phosphorus and progression of CKD and mortality: a meta-analysis of cohort studies. Am J Kidney Dis 2015;66:258-65. [PubMed abstract]
  47. Palmer SC, Hayen A, Macaskill P, et al. Serum levels of phosphorus, parathyroid hormone, and calcium and risks of death and cardiovascular disease in individuals with chronic kidney disease: a systematic review and meta-analysis. Jama 2011;305:1119-27. [PubMed abstract]
  48. Cheungpasitporn W, Thongprayoon C, Mao MA, et al. Admission serum phosphate levels predict hospital mortality. Hospital Practice 2018;46:121-7. [PubMed abstract]
  49. Hou Y, Li X, Sun L, Qu Z, Jiang L, Du Y. Phosphorus and mortality risk in end-stage renal disease: A meta-analysis. Clin Chim Acta 2017;474:108-13. [PubMed abstract]
  50. Selamet U, Tighiouart H, Sarnak MJ, Beck G, Levey AS, Block G, et al. Relationship of dietary phosphate intake with risk of end-stage renal disease and mortality in chronic kidney disease stages 3-5: The Modification of Diet in Renal Disease Study. Kidney Int 2016;89:176-84. [PubMed abstract]
  51. Murtaugh MA, Filipowicz R, Baird BC, Wei G, Greene T, Beddhu S. Dietary phosphorus intake and mortality in moderate chronic kidney disease: NHANES III. Nephrol Dial Transplant 2012;27:990-6. [PubMed abstract]
  52. Moorthi RN, Moe SM. Special nutritional needs of chronic kidney disease and end-stage renal disease patients: rationale for the use of plant-based diets. In: Uribarri J, Calvo MS, eds. Dietary Phosphorus: Health, Nutrition, and Regulatory Aspects. Boca Raton, Florida: CRC Press; 2018:235-46.
  53. de Fornasari ML, Dos Santos Sens YA. Replacing phosphorus-containing food additives with foods without additives reduces phosphatemia in end-stage renal disease patients: a randomized clinical trial. J Ren Nutr 2017;27:97-105. [PubMed abstract]
  54. Shinaberger CS, Greenland S, Kopple JD, et al. Is controlling phosphorus by decreasing dietary protein intake beneficial or harmful in persons with chronic kidney disease? Am J Clin Nutr 2008;88:1511-8. [PubMed abstract]
  55. Group KDIGOC-MUW. KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD),. Kidney Int Suppl (2011) 2017;7:1-59. [PubMed abstract]
  56. Dhingra R, Sullivan LM, Fox CS, et al. Relations of serum phosphorus and calcium levels to the incidence of cardiovascular disease in the community. Arch Intern Med 2007;167:879-85. [PubMed abstract]
  57. Tonelli M, Sacks F, Pfeffer M, et al. Relation between serum phosphate level and cardiovascular event rate in people with coronary disease. Circulation 2005;112:2627-33. [PubMed abstract]
  58. Lopez FL, Agarwal SK, Grams ME, et al. Relation of serum phosphorus levels to the incidence of atrial fibrillation (from the Atherosclerosis Risk In Communities [ARIC] study). Am J Cardiol 2013;111:857-62. [PubMed abstract]
  59. Bai W, Li J, Liu J. Serum phosphorus, cardiovascular and all-cause mortality in the general population: A meta-analysis. Clin Chim Acta 2016;461:76-82. [PubMed abstract]
  60. Chang AR, Grams ME. Serum phosphorus and mortality in the Third National Health and Nutrition Examination Survey (NHANES III): effect modification by fasting. Am J Kidney Dis 2014;64:567-73. [PubMed abstract]
  61. Slinin Y, Blackwell T, Ishani A, Cummings SR, Ensrud KE. Serum calcium, phosphorus and cardiovascular events in post-menopausal women. Int J Cardiol 2011;149:335-40. [PubMed abstract]
  62. Menon MC, Ix JH. Dietary phosphorus, serum phosphorus, and cardiovascular disease. Ann N Y Acad Sci 2013;1301:21-6. [PubMed abstract]
  63. Chang AR, Lazo M, Appel LJ,et al. High dietary phosphorus intake is associated with all-cause mortality: results from NHANES III. Am J Clin Nutr 2014;99:320-7. [PubMed abstract]
  64. Yamamoto KT, Robinson-Cohen C, de Oliveira MC, et al. Dietary phosphorus is associated with greater left ventricular mass. Kidney Int 2013;83:707-14. [PubMed abstract]
  65. Chang AR, Miller ER, Anderson CA, et al. Phosphorus additives and albuminuria in early stages of CKD: a randomized controlled trial. Am J Kidney Dis 2017;69:200-9. [PubMed abstract]
  66. Ito S, Ishida H, Uenishi K, et al. The relationship between habitual dietary phosphorus and calcium intake, and bone mineral density in young Japanese women: a cross-sectional study. Asia Pac J Clin Nutr 2011;20:411-7. [PubMed abstract]
  67. Beloosesky Y, Grinblat J, Weiss A, et al. Electrolyte disorders following oral sodium phosphate administration for bowel cleansing in elderly patients. JAMA Internal Medicine 2003;163:803-8. [PubMed abstract]
  68. Malberti F. Hyperphosphataemia: treatment options. Drugs 2013;73:673-88. [PubMed abstract]
  69. Chines A, Pacifici R. Antacid and sucralfate-induced hypophosphatemic osteomalacia: a case report and review of the literature. Calcif Tissue Int 1990;47:291-5. [PubMed abstract]
  70. Ruospo M, Palmer SC, Natale P, et al. Phosphate binders for preventing and treating chronic kidney disease-mineral and bone disorder (CKD-MBD). Cochrane Database Syst Rev 2018;8:CD006023. [PubMed abstract]
  71. Casais MN, Rosa-Diez G, Perez S, et al. Hyperphosphatemia after sodium phosphate laxatives in low risk patients: prospective study. World J Gastroenterol 2009;15:5960-5. [PubMed abstract]
  72. U.S. Food and Drug Administration. FDA Drug Safety Communication: FDA warns of possible harm from exceeding recommended dose of over-the-counter sodium phosphate products to treat constipation.external link disclaimer 2014.
  73. U.S. Department of Agriculture, Agricultural Research Service. What We Eat in America, 2013-2014.external link disclaimer 2017.


This fact sheet by the Office of Dietary Supplements provides information that should not take the place of medical advice. We encourage you to talk to your health care providers (doctor, registered dietitian, pharmacist, etc.) about your interest in, questions about, or use of dietary supplements and what may be best for your overall health. Any mention in this publication of a specific product or service, or recommendation from an organization or professional society, does not represent an endorsement by ODS of that product, service, or expert advice.