What is Phosphorus? Unveiling the Vital Mineral for Health

Phosphorus is a crucial mineral that is naturally found in numerous foods and is also available as a dietary supplement. It plays an integral role in various bodily functions, being a fundamental component of bones, teeth, deoxyribonucleic acid (DNA), and ribonucleic acid (RNA) [1]. In the form of phospholipids, phosphorus is essential for the structure of cell membranes and is a key element in adenosine triphosphate (ATP), the body’s primary energy source. Many proteins and sugars within the body undergo phosphorylation, highlighting phosphorus’s involvement in critical biochemical processes. Furthermore, phosphorus is vital for regulating gene transcription, activating enzymes, maintaining the normal pH balance in extracellular fluid, and facilitating intracellular energy storage. In the human body, phosphorus constitutes approximately 1% to 1.4% of fat-free mass, with 85% residing in bones and teeth, and the remaining 15% distributed throughout the blood and soft tissues [1].

Phosphorus is present in a wide variety of foods, primarily in the forms of phosphates and phosphate esters [1]. However, in seeds and unleavened breads, phosphorus exists as phytic acid, which is its storage form [2]. A significant portion of phosphorus in phytic acid is not readily absorbed by the human body due to the lack of the phytase enzyme in human intestines [1]. Phosphorus absorption occurs passively in the small intestine, with a smaller amount being absorbed through active transport mechanisms [2].

The relationship between phosphorus and calcium is significant, as hormones like vitamin D and parathyroid hormone (PTH) regulate the metabolism of both minerals. Phosphorus and calcium are also the key constituents of hydroxyapatite, the primary structural component of bones and tooth enamel [3]. An imbalance characterized by high phosphorus intake and low calcium intake can lead to elevated serum PTH levels. However, the impact of these increased hormone levels on bone mineral density remains a subject of ongoing research, with evidence being varied [2,4-6].

The body tightly regulates phosphorus homeostasis through the kidneys, bones, and intestines. This regulation ensures that phosphorus excretion in urine matches net absorption and that bone deposition and resorption are balanced [1,7,8]. Hormones like estrogen and adrenaline also influence phosphorus homeostasis. Impaired kidney function, as seen in chronic kidney failure, disrupts phosphate excretion, leading to elevated serum phosphate levels [9].

While phosphorus status is not routinely assessed, phosphate levels can be measured in serum and plasma [10]. The normal range for phosphate concentration in adult serum or plasma is 2.5 to 4.5 mg/dL (0.81 to 1.45 mmol/L) [10]. Hypophosphatemia is diagnosed when serum phosphate concentrations fall below the normal range, while hyperphosphatemia indicates concentrations above the normal range. It’s important to note that serum and plasma phosphate levels may not always accurately reflect the total phosphorus content of the body [1,11].

Recommended Daily Phosphorus Intake

Dietary Reference Intakes (DRIs) for phosphorus and other nutrients are established by the Food and Nutrition Board (FNB) at the National Academies of Sciences, Engineering, and Medicine [12]. DRIs are a set of reference values used for planning and evaluating nutrient intake for healthy individuals, varying based on age and sex. These include:

  • Recommended Dietary Allowance (RDA): The average daily intake level sufficient to meet the nutrient requirements of nearly all (97%–98%) healthy individuals. RDAs are often used to plan nutritionally adequate diets for individuals.
  • Adequate Intake (AI): Established when evidence is insufficient to determine an RDA, AI is an intake level assumed to ensure nutritional adequacy.
  • Estimated Average Requirement (EAR): The average daily intake level estimated to meet the needs of 50% of healthy individuals. EARs are used to assess nutrient intakes of groups and plan adequate diets for them, and can also be used to assess individual intakes.
  • Tolerable Upper Intake Level (UL): The maximum daily intake unlikely to cause adverse health effects.

Table 1 outlines the current RDAs for phosphorus [2]. For infants aged 0-12 months, the FNB has set an AI for phosphorus based on the average intake of 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)

Dietary Sources of Phosphorus

Food Sources

Phosphorus is widely distributed in various food types, including dairy products, meats, poultry, fish, eggs, nuts, legumes, vegetables, and grains [13,14]. In the United States, dairy products are a major contributor to phosphorus intake, accounting for approximately 20% of the total, while bakery products (such as breads, tortillas, and sweet pastries) contribute about 10% [13]. Vegetables and chicken each contribute around 5%.

The absorption rate of naturally occurring phosphorus in food ranges from 40% to 70%. Phosphorus from animal sources is generally absorbed more efficiently than that from plant sources [15,16]. It’s important to note that calcium from both foods and supplements can bind to some phosphorus in the digestive tract, potentially reducing its absorption [1,17]. Studies suggest that very high calcium intakes (around 2,500 mg/day) can bind to and prevent the absorption of 0.61–1.05 g of phosphorus [17]. In infants, phosphorus bioavailability is higher in human milk (85%–90%) compared to soy-based formulas (approximately 59%) [2].

Image alt text: Diverse food sources of phosphorus including dairy milk, cheese cubes, mixed nuts, and cooked lentils in a bowl.

Phosphate additives, such as phosphoric acid, sodium phosphate, and sodium polyphosphate, are frequently used in processed foods. These additives serve various functions, including moisture retention, color preservation, flavor enhancement, and stabilization of frozen foods [18]. Foods containing these additives can have, on average, 67 mg more phosphorus per serving compared to similar products without them. Consequently, these additives significantly contribute to overall phosphorus intake in the United States [18,19].

It is estimated that phosphate additives contribute between 300 to 1,000 mg to daily phosphorus intake [11,20], representing about 10%–50% of phosphorus intake in Western diets [21]. The use of phosphate additives in the food industry is increasing, along with the concentrations of these additives in food products [22,23]. The absorption rate for phosphorus from phosphate additives is notably high, approximately 70% [24].

Table 2 provides a list of selected foods and their phosphorus content.

Table 2: Phosphorus Content of Selected Foods [25]

Food Milligrams (mg) per serving Percent DV*
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) has established Daily Values to help consumers understand the nutrient content of foods and supplements within the context of a complete diet. For adults and children aged 4 years and older, the DV for phosphorus is 1,250 mg [26]. While food labels are not required to list phosphorus content unless it has been added to the food, foods providing 20% or more of the DV are considered high sources of phosphorus, and even foods with lower percentages contribute to a healthy dietary intake.

The U.S. Department of Agriculture’s (USDA’s) FoodData Central [27] provides detailed nutrient information for a vast array of foods, including comprehensive lists of phosphorus-containing foods categorized by nutrient content.

Phosphorus in Dietary Supplements

Phosphorus is available in dietary supplements either as a standalone nutrient, in combination with other ingredients, or in some multivitamin/mineral formulations [28]. In supplements, phosphorus is typically found as phosphate salts (e.g., dipotassium phosphate or disodium phosphate) or phospholipids (e.g., phosphatidylcholine or phosphatidylserine). Most supplements provide 10% or less of the Daily Value for phosphorus, although some products may contain more than 100% [28].

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

Phosphorus Intake Levels and Nutritional Status

In general, most people in the United States consume adequate or even excess amounts of phosphorus. Data from the 2015–2016 National Health and Nutrition Examination Survey (NHANES) indicate that the average daily phosphorus intake from food is 1,237 mg for children and teenagers aged 2–19 years [29]. For adults aged 20 and older, the average daily intake from foods is 1,189 mg for women and 1,596 mg for men.

An analysis of 2013–2014 NHANES data, considering both food and supplements, reported average daily phosphorus intakes of 1,301 mg for women and 1,744 mg for men [30]. However, some experts suggest that dietary data collection methods used in NHANES and similar large-scale studies may underestimate true dietary phosphorus intake, as they might not fully account for the contribution of phosphate additives in processed foods [31,32].

Phosphorus Deficiency: Hypophosphatemia

Phosphorus deficiency, known as hypophosphatemia, is uncommon in the United States and is rarely caused by insufficient dietary intake alone [1]. Symptoms of hypophosphatemia can include anorexia, anemia, proximal muscle weakness, bone-related issues (bone pain, rickets in children, and osteomalacia in adults), increased susceptibility to infections, paresthesias, ataxia, and confusion [1]. Hypophosphatemia is more often a consequence of underlying medical conditions such as hyperparathyroidism, kidney tubule defects, and diabetic ketoacidosis [33].

Groups at Risk of Phosphorus Inadequacy

While overt phosphorus deficiency is rare, certain populations are at increased risk of inadequate phosphorus status.

Premature Infants

Phosphorus deficiency, often in conjunction with calcium deficiency, is a significant factor contributing to osteopenia of prematurity, a condition characterized by impaired bone mineralization in preterm infants [34]. Because a substantial portion of fetal bone mineral content is accumulated during the third trimester of pregnancy, infants born prematurely have lower reserves of calcium and phosphorus in their bones at birth [35]. While the optimal strategy for phosphorus and calcium supplementation in preterm infants for bone health is still being researched, fortified milk with higher levels of these minerals and other essential nutrients is generally recommended to support overall growth and development [35,36].

Individuals with Genetic Phosphate Regulation Disorders

Rare genetic disorders affecting phosphorus metabolism can lead to hypophosphatemia and related complications. X-linked hypophosphatemic rickets is one such condition [37]. Patients with this disorder may develop rickets, osteomalacia, pseudofractures, enthesopathy, and dental abnormalities. Other rare genetic conditions associated with rickets and phosphorus dysregulation include autosomal-dominant and autosomal-recessive hypophosphatemic rickets, and hereditary hypophosphatemic rickets with hypercalciuria [38]. Treatment typically involves vitamin D and phosphorus supplementation from diagnosis until skeletal maturity is reached [39].

Patients with Severe Malnutrition

Individuals suffering from severe protein or calorie malnutrition are at risk of developing refeeding syndrome, which can manifest as refeeding hypophosphatemia within 2 to 5 days of initiating enteral or parenteral nutrition. This occurs due to the metabolic shift from a catabolic to an anabolic state [40,41]. Conditions that can lead to malnutrition and subsequently refeeding syndrome include chronic illnesses (e.g., cancer, COPD, cirrhosis), very low birth weight, cachexia, anorexia nervosa, excessive alcohol intake, and difficulties with chewing or swallowing. Refeeding syndrome can have serious consequences, including neuromuscular dysfunction, hypoventilation, respiratory failure, impaired blood clotting, confusion, coma, cardiac arrest, congestive heart failure, and even death [41]. Prophylactic administration of phosphorus and thiamine in patients at risk of refeeding syndrome can help prevent this potentially life-threatening condition [41].

Phosphorus and Its Role in Health and Disease

Phosphorus plays a complex role in various health conditions. This section will focus on its involvement in chronic kidney disease (CKD) and cardiovascular disease (CVD).

Phosphorus in Chronic Kidney Disease (CKD)

Chronic kidney disease (CKD), affecting a significant portion of the global population, is associated with increased risk of CVD and premature mortality [42]. As kidney function declines in CKD, the kidneys become less efficient at excreting phosphate, leading to an increase in serum phosphate concentration. This disruption in phosphate balance can impair the regulatory functions of PTH and fibroblast growth factor 23 on renal phosphorus resorption [43].

Elevated phosphorus retention is a major factor in the development of CKD-mineral and bone disorder (CKD-MBD). This systemic syndrome is characterized by abnormalities in the metabolism of phosphorus, calcium, PTH, and/or vitamin D; disturbances in bone turnover, mineralization, volume, growth, or strength; and vascular or soft-tissue calcification [44].

Studies using NHANES data have demonstrated a clear association between reduced kidney function and elevated phosphate levels. For example, an analysis of 2003–2006 NHANES data showed that adults with reduced kidney function had significantly higher serum phosphate levels compared to those with normal kidney function [45].

Numerous studies have linked high phosphate levels in CKD patients to an increased risk of mortality and disease progression [46-48]. A meta-analysis of cohort studies in patients with end-stage renal disease found that those with the highest phosphate levels had a significantly greater risk of all-cause mortality compared to those with normal phosphate levels [49].

However, the association between high phosphate levels and adverse outcomes may not be as pronounced in individuals with milder stages of CKD [50,51]. Some studies have not found a direct link between high phosphorus intake and increased mortality in moderate CKD, possibly because these patients do not have severely compromised kidney function [51].

To manage the complications of elevated phosphate levels in CKD, clinicians often recommend dietary phosphorus restriction. This may involve reducing intake of animal proteins, which are high in phosphorus (and replacing them with plant-based protein sources where phosphorus is less bioavailable), and increasing consumption of calcium-rich foods [9,52]. Some evidence suggests that replacing foods containing phosphate additives with additive-free alternatives can help lower serum phosphate levels [53]. However, restricting phosphorus intake can also inadvertently reduce protein intake, as many phosphorus-rich foods are also important sources of protein [54]. Furthermore, a Cochrane Review of studies examining dietary interventions for CKD-MBD found limited evidence of significant positive impacts from dietary changes alone [43].

Clinical guidelines for CKD-MBD recommend that patients with stage 3–5 CKD consider limiting dietary phosphorus intake, either alone or with other treatments, to manage phosphate levels [55]. However, these guidelines also acknowledge the lack of robust clinical trial data demonstrating that lowering serum phosphate levels directly improves patient-centered outcomes, indicating a need for further research in this area.

Further research is necessary to fully understand the relationship between phosphate concentrations and CKD risk and morbidity, as well as the effectiveness of dietary phosphorus restriction in managing CKD.

Phosphorus and Cardiovascular Disease (CVD)

Observational studies have suggested a potential link between elevated phosphate levels and increased CVD risk in both individuals with and without pre-existing CVD [56,57]. For example, an analysis of participants without atrial fibrillation found that higher serum phosphate levels were associated with a greater risk of developing atrial fibrillation over a long-term follow-up period [58].

Large-scale epidemiological studies have also reported associations between higher serum phosphate concentrations and an increased risk of cardiovascular mortality in generally healthy adults. A meta-analysis of prospective cohort studies demonstrated a significantly higher risk of cardiovascular mortality in individuals with the highest phosphate concentrations compared to those with lower levels [59]. A subsequent study using NHANES III data also found a significant increase in the risk of death and cardiovascular death for every 1 mg/dL increase in phosphate above a certain threshold [60].

Image alt text: Abstract graphic depicting a heart outline interwoven with phosphorus chemical symbols to illustrate the connection between phosphorus and cardiovascular health.

However, not all observational data consistently support a direct link between serum phosphate concentrations and CVD risk. Some studies, such as a post hoc analysis of data from postmenopausal women with osteoporosis, found no association between higher serum phosphate levels and cardiovascular outcomes [61].

Despite accumulating evidence suggesting a link between elevated phosphate levels and CVD risk, there is currently a lack of direct evidence in the literature to support the idea that restricting phosphorus consumption can prevent CVD in healthy adults [62]. More research is needed to clarify this potential relationship and determine whether dietary phosphorus modifications can play a role in CVD prevention.

Health Risks Associated with Excessive Phosphorus Intake

High phosphorus intake is generally well-tolerated in healthy individuals, and adverse effects are rare. While some studies have suggested potential associations between high phosphorus intakes and negative health outcomes, including cardiovascular, kidney, and bone issues, as well as increased mortality risk [23,63,66], other studies have not confirmed these links [5,65,66]. Therefore, the Tolerable Upper Intake Levels (ULs) for phosphorus from food and supplements for healthy individuals are primarily based on intakes that are associated with maintaining normal serum phosphate concentrations [2]. It is important to note that these ULs do not apply to individuals 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* Not Established* Not Established*
7–12 months* Not Established* Not 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.

An analysis of NHANES III data from 1988–1994 on healthy U.S. adults suggested a potential association between high phosphorus intakes (1,000 mg/day or more) and increased rates of all-cause and cardiovascular mortality through 2006 [63]. These intakes are twice the RDA for adults and are exceeded by the daily intakes of many men, especially those of white or Hispanic ethnicity, although they remain below the UL. The implications of this analysis regarding the potential adverse effects of high phosphorus intakes are not fully understood, and it’s possible that high phosphorus intake may be indicative of other unhealthy dietary patterns [63].

Extremely high phosphorus intakes over short periods, such as consuming two 6,600 mg doses of sodium phosphate within a single day, can lead to hyperphosphatemia [67,68]. The primary consequences of hyperphosphatemia include disruptions in hormone regulation of calcium metabolism and calcification of non-skeletal tissues, particularly in the kidneys [2].

Interactions with Medications

Phosphorus can interact with certain medications, and conversely, some medications can affect phosphate levels in the body. It is important for individuals taking medications regularly to discuss their phosphorus status with their healthcare providers. Two examples of such interactions are outlined below:

Antacids

Antacids containing aluminum hydroxide, such as Maalox HRF and Rulox, can bind to phosphorus in the intestines, reducing its absorption. Chronic use of these antacids for 3 months or longer can potentially lead to hypophosphatemia [1,69]. These medications can also worsen pre-existing phosphate deficiency. Antacids containing calcium carbonate (Rolaids, Tums, Maalox) can also decrease the intestinal absorption of dietary phosphorus [70].

Laxatives

Certain laxatives, including Fleet Prep Kit #1, contain sodium phosphate. Ingesting these products can elevate serum phosphate levels [71]. Following reports of deaths associated with exceeding the recommended dose of sodium phosphate-containing laxatives, the FDA issued a warning regarding the potential dangers of these products when taken at higher than recommended doses, especially in individuals with kidney disease, heart disease, or dehydration [72].

Phosphorus and Healthful Eating Patterns

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

For further information on developing a healthy dietary pattern, consult the Dietary Guidelines for Americans and the USDA’s MyPlate.

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

  • Includes a variety of vegetables; fruits; grains (at least half of which are whole grains); fat-free and low-fat milk, yogurt, and cheese; and oils.
    • Dairy products are significant sources of phosphorus, and some vegetables, fruits, and grains also contribute to phosphorus intake.
  • Includes a variety of protein foods such as lean meats; poultry; eggs; seafood; beans, peas, and lentils; nuts and seeds; and soy products.
    • Meats, seafood, fish, nuts, and seeds are important sources of phosphorus.
  • Limits foods and beverages high in added sugars, saturated fat, and sodium.
  • Limits alcoholic beverages.
  • Stays within individual daily calorie needs.

References

1 Institute of Medicine (IOM). Food and Nutrition Board. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington, DC: National Academies Press; 1997.

2 National Institutes of Health. Office of Dietary Supplements. Phosphorus. Dietary Supplement Label Database. https://dsld.od.nih.gov/nutrientprofiles/phosphorus.pdf. Accessed May 3, 2023.

3 Bushinsky DA. Regulation of calcium and phosphate homeostasis. In: Boron WF, Boulpaep EL, eds. Medical Physiology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2017:733-66.

4 Calvo MS, Uribarri J. Contributions to total phosphorus intake: all sources considered. Semin Dial 2013;26:54-61. PubMed PMID: 23464983

5 Anderson JJ, Metz JA, Garner SC, Miller GD. Phosphorus intake, serum phosphate and bone mineral density in women. Nutr Res 2001;21:1201-11.

6 Macdonald HM, Weber JL, New SA, Reid DM. Phosphorus intake does not adversely affect bone mineral density in healthy women in the UK. J Nutr 2005;135:767-71. PubMed PMID: 15795433

7 Peacock M. Phosphate metabolism in health and disease. Calcif Tissue Int 2018;102:554-73. PubMed PMID: 29435578

8 Quarles LD. FGF23, PHEX and vitamin D in phosphate homeostasis and skeletal mineralization. Am J Physiol Endocrinol Metab 2003;285:E1-9. PubMed PMID: 12801735

9 National Kidney Foundation. Phosphorus and chronic kidney disease. https://www.kidney.org/atoz/phosphorus. Accessed May 3, 2023.

10 National Academy of Clinical Biochemistry. Laboratory medicine practice guidelines: evidence-based practice for phosphorus and calcium testing in chronic kidney disease. https://www.aacc.org/science-and-research/practice-guidelines/kidney-disease. Accessed May 3, 2023.

11 Benini O, D’Alessandro C, Gianfaldoni D, Cupisti A. Extra-phosphate load from food additives in commonly eaten foods: a real and insidious danger for renal patients. J Ren Nutr 2011;21:295-301. PubMed PMID: 21145285

12 National Academies of Sciences, Engineering, and Medicine. Health and Medicine Division. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients). Washington, DC: National Academies Press; 2005.

13 Cogswell ME, Bowman BA, Fulgoni VL, 3rd, Rockell JE, King MK, Pfeiffer CM, Merritt RJ, Gunn JP. Dietary phosphorus intakes of adults in the United States: NHANES 2005-2006. J Nutr 2011;141:1349-57. PubMed PMID: 21653732

14 U.S. Department of Agriculture, Agricultural Research Service. FoodData Central, 2019. fdc.nal.usda.gov.

15 Greger JL. Calcium bioavailability. In: Arnaud CD, Suki WN, eds. Calcium and Phosphorus Metabolism in Health and Disease. New York: Plenum Press; 1990:87-98.

16 Bronner F, Pansu D. Nutritional aspects of calcium absorption. J Nutr 1999;129:9-12. PubMed PMID: 9915881

17 Zemel MB. Calcium utilization: effect of varying levels and sources of dietary calcium. Am J Clin Nutr 1988;47:633-6. PubMed PMID: 3358404

18 Anderson JJB,েক Metz JA, Rockell JE. Phosphate additives in food: US trends. Food Addit Contam Part A Chem Anal Control Expo Risk Assess 2012;29:152-66. PubMed PMID: 22103499

19 Uribarri J, Welch G, Calvo MS. The paradox of phosphate additives in food. Am J Clin Nutr 2017;105:301-3. PubMed PMID: 28096152

20 Ritz E, Hahn K, Reichel H, Amann K. Phosphate additives in food–a silent killer? J Am Soc Nephrol 2012;23:265-72. PubMed PMID: 22156027

21 Leon JB, Sullivan C, Sehgal AR. The prevalence and clinical implications of hyperphosphatemia in the general population. Kidney Int 2013;83:787-94. PubMed PMID: 23422883

22 Nadkarni GN, Annapureddy N, Calvo MS, Uribarri J. Phosphate content of popular beverages: implications for hyperphosphatemia management. J Ren Nutr 2014;24:128-32. PubMed PMID: 24462119

23 Shinaberger CS, Greenland S, Kopple JD, Van Wyck D, Mehrotra R, Dillon MA,逸展 Chiu V,逸展 Kalantar-Zadeh K. Association of serum phosphorus and calcium-phosphorus product with mortality, cardiovascular events, and hospitalization in patients with chronic kidney disease. J Am Soc Nephrol 2005;16:2907-15. PubMed PMID: 16107579

24 Powell JJ, Furchgott RF, Groziak SM, Mellors JW. Phosphate absorption in rat small intestine in vivo: effect of sodium and inhibitors. Am J Physiol 1992;263:G331-7. PubMed PMID: 1503103

25 U.S. Department of Agriculture. FoodData Central. https://fdc.nal.usda.gov/. Accessed May 3, 2023.

26 U.S. Food and Drug Administration. CFR – Code of Federal Regulations Title 21. https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?fr=101.9. Accessed May 3, 2023.

27 U.S. Department of Agriculture, Agricultural Research Service. USDA FoodData Central. https://fdc.nal.usda.gov/. Accessed May 3, 2023.

28 National Institutes of Health. Dietary Supplement Label Database. https://dsld.od.nih.gov/. Accessed May 3, 2023.

29 Hoy MK, Goldman JD, Petersmarck KA, Woolf AD, Hurell WE. Usual nutrient intakes from food and beverages, by gender and age, What We Eat in America, NHANES 2015-2016. Food Surveys Research Group, Beltsville Human Nutrition Research Center, Agricultural Research Service, U.S. Department of Agriculture. 2020.

30 Bird JK, Murphy R, Ciappio ED, McBurney MI. Risk of deficiency in micronutrients is widespread in older adults’ diets, and calls for public health action are warranted. J Nutr 2017;147:181-6. PubMed PMID: 27956629

31 Uribarri J. Phosphorus homeostasis in normal health and in chronic kidney disease patients with and without phosphate binders. Am J Clin Nutr 2021;113:259-67. PubMed PMID: 33090191

32 Uribarri J. The inadequacy of nutritional surveys to assess dietary phosphate intake. J Am Soc Nephrol 2014;25:1891-3. PubMed PMID: 25122485

33 Liamis G, Milionis HJ, Elisaf M. A diagnostic approach to hypophosphatemia. J Nephrol 2010;23:17-21. PubMed PMID: 20180385

34 Fewtrell MS. Osteopenia of prematurity. Arch Dis Child Fetal Neonatal Ed 2004;89:F84-8. PubMed PMID: 14734542

35 Abrams SA. Calcium and phosphorus nutrition in infancy. Nestle Nutr Workshop Ser Pediatr Program 2013;71:171-80. PubMed PMID: 23743055

36 Agostoni C, Buonocore G, Carnielli VP, De Curtis M, Darmaun D, Decsi T, Domellof M, Embleton ND, Ferdinando F, Finer N, et al. Enteral nutrient supply for preterm infants: European Society for Paediatric Gastroenterology, Hepatology, and Nutrition Committee on Nutrition Guidelines. J Pediatr Gastroenterol Nutr 2010;50:85-91. PubMed PMID: 19918107

37 Beck-Nielsen SS, Brixen K, Gram J, Rejnmark L. FGF23 and bone disease in X-linked hypophosphatemia. Curr Osteoporos Rep 2011;9:270-6. PubMed PMID: 21887636

38 Fukumoto S. Phosphate metabolism and vitamin D: crosstalk between FGF23 and vitamin D. BoneKEy Rep 2014;3:507. PubMed PMID: 25414702

39 Carpenter TO, Imel EA, Holm IA, Jan de Beur SM, Insogna KL, Kashgarian M, Knudsen KB, Leong JB, Lofthouse J, Mahajan P, et al. A CLDN14 mutation in familial hypercalciuria and nephrocalcinosis maps to a novel renal chloride channel gene. J Clin Endocrinol Metab 2001;86:3576-9. PubMed PMID: 11502792

40 Crook MA, Reid C, Dickerson RN, Schneider AJ, Nathan DM. Refeeding syndrome–update on current understanding and clinical implications. Eur J Clin Nutr 2001;55:613-20. PubMed PMID: 11481675

41 Mehanna HM, Moledina J, Travis J. Refeeding syndrome: what it is, and how to prevent and treat it. BMJ 2008;336:1495-8. PubMed PMID: 18566027

42 Hill NR, Fatoba ST, Oke JL, Hirst JA, O’Callaghan CA, Lasserson DS, Hobbs FD,

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