Phosphorus

Phosphorus is an essential mineral required by every cell in the body for normal function (1). Phosphorus in the body is almost always bound to oxygen, forming phosphate (PO₄^3-). Most of the body's phosphorus (~80%-85%) is found in bones and teeth in the form of an insoluble salt called hydroxyapatite [chemical formula: (Ca)₁₀(PO₄)₆(OH)₂] (2,3); the remainder is distributed throughout soft tissues and the extracellular fluid (3).

Function

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 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 regulates oxygen delivery to the tissues of the body (1).

Regulation

Parathyroid hormone-vitamin D and FGF-23-endocrine axis

Dietary phosphorus is readily absorbed in the small intestine via both active transcellular and paracellular pathways with the paracellular route predominating at typical dietary intakes (4). In healthy individuals, excess phosphorus is excreted by the kidneys under the regulatory action of the endocrine hormones: parathyroid hormone (PTH), vitamin D, and fibroblast growth factor-23 (FGF-23). The acute regulation of blood calcium and phosphorus concentrations is controlled through the actions of PTH and the active form of vitamin D. 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, which rapidly decreases urinary excretion of calcium but increases urinary excretion of phosphorus and stimulates bone resorption. This results in the release of bone mineral (calcium and phosphate) — actions that restore serum calcium concentrations. Although the action is not immediate, PTH also stimulates conversion of vitamin D to its active form (1,25-dihydroxyvitamin D; calcitriol) in the kidneys. Increased circulating 1,25-dihydroxyvitamin D in turn stimulates increased intestinal absorption of both calcium and phosphorus. A third hormone, FGF-23, plays a central role in phosphorus homeostasis through binding to the α-Klotho co-receptor and FGF receptors (5). FGF-23 is secreted by bone-forming cells (osteoblasts/osteocytes) in response to increases in phosphorus intake. In a negative feedback loop, FGF-23 inhibits the production and stimulates the degradation of 1,25-dihydroxyvitamin D, as well as promotes an increase in urinary phosphorus excretion independently of PTH and 1,25-dihydroxyvitamin D (6).

Deficiency

Inadequate phosphorus intake rarely results in abnormally low serum phosphorus levels (hypophosphatemia) because renal reabsorption of phosphorus increases to compensate for decreased intake. The effects of moderate to severe 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, difficulty walking, and respiratory failure. Severe hypophosphatemia may occasionally be life threatening.

Since phosphorus is so widespread in food, dietary phosphorus deficiency is usually seen only in cases of near-total starvation. Hypophosphatemia caused by inherited disorders of phosphorus homeostasis (phosphorus-wasting disorders) has been linked to elevated urinary excretion or impaired renal reabsorption of phosphorus in affected subjects (reviewed in 7). Other individuals at risk of hypophosphatemia include persons with alcohol use disorder, individuals with diabetes mellitus recovering from an episode of diabetic ketoacidosis, patients with respiratory alkalosis, and starving or anorexic patients on refeeding regimens that are high in calories but too low in phosphorus (reviewed in 8). A recent review of eight studies (n=26,548) suggested that older adults (≥65 years) — especially those experiencing frailty — may at increased risk for non-severe hypophosphatemia, which has been associated with cognitive decline and increased risk of falls (9).

The RDA

The recommended dietary allowance (RDA) for phosphorus is based on the maintenance of normal serum phosphorus levels in adults (2.5-4.5 milligrams/deciliter [mg/dL]) and is believed to represent adequate phosphorus intakes to meet cellular and bone formation needs (10). Sex- and age-specific RDAs for phosphorus are listed in Table 1.

Sources

Food sources

Phosphorus is found in most food because it is a critical constituent of all living organisms. Dairy foods, cereal products, meat, and fish are particularly rich sources of phosphorus (11). Phosphorus is also a component of many food additives that are used in food processing and is present in cola soft drinks as phosphoric acid (12).

Dietary phosphorus intakes among US adults are well above the RDA of 700 mg/day, with average daily intakes being 1,480 mg in adult males and 1,118 mg in adult females (13). Phosphorus derived from phosphorus-containing additives in food is not always included in food nutrient composition databases, so the total amount of phosphorus consumed by the average person in the US can be underestimated by more than 20% (14). Segments of the US population who consume more highly processed foods and whose phosphorus intakes approach the tolerable upper intake level of 4,000 mg/day are thought by some to be at high risk of developing adverse health outcomes (see Safety) (11, 14).

Bioavailability

Phosphorus in plant seeds (beans, peas, cereals, and nuts) is primarily present in a storage form of phosphate called phytic acid or phytate. Only about 50% of phosphorus from these plant foods is available to humans because we lack the enzyme phytase, which is required to release phosphorus from phytate (15). Yeasts, however, possess phytase, so phosphorus in whole grains used for leavened breads is more bioavailable than that in breakfast cereals or flatbreads (10).

In general, phosphorus from animal-based foods is more bioavailable or bioaccessible than phosphorus from plant sources, and phosphorus from phosphorus-containing food additives has an even higher bioavailability, with phosphoric acid reported to be 100% bioavailable (12). One analysis identified 28 FDA-approved inorganic phosphate salts are frequently used as additives, particularly in ultra-processed foods (16); another recent analysis found that phosphorus additives were present in more than one-half of US packaged food products (17).

Because reducing dietary phosphorus absorption may benefit individuals with impaired kidney function who are at risk of hyperphosphatemia (serum phosphorus at or above the high-normal range), protein sources of phosphorus in grain-based vegetarian diets may be preferred over meat-based diets (18).

Table 2 lists several phosphorus-rich foods, along with their phosphorus content in milligrams (mg). For more information on the nutrient content of food, search USDA's FoodData Central.

Supplements

Phosphorus content of multivitamin/mineral (MVM) supplements varies, with most MVMs containing 20 to 350 mg of phosphorus (10); a US national survey found that MVM supplements contributed an average of 108 mg to daily phosphorus intake (15).

Sodium phosphate and potassium phosphate salts are used for the treatment of hypophosphatemia that occurs in hereditary disorders of phosphate wasting, and their use requires medical supervision. Calcium phosphate salts are sometimes used as calcium supplements (21). Commonly used over-the-counter and prescription drugs also contribute to phosphorus intakes at levels yet to be defined (15).

Safety

Toxicity

Several disorders characterized by serum phosphorus levels above normal (hyperphosphatemia) have been described, including those resulting from increased intestinal absorption of phosphate salts taken by mouth or by colonic absorption of the phosphate salts in enemas (1). Yet, the disruption of phosphorus homeostasis is most often associated with limited excretion in patients with chronic kidney disease (CKD) or end-stage kidney disease (advanced CKD). When kidney function is only 20% of normal, even phosphorus intakes within the recommended range may lead to hyperphosphatemia. Hyperphosphatemia may also affect individuals with inappropriately low parathyroid hormone (PTH) levels (hypoparathyroidism) as they lack PTH stimulation of renal phosphate excretion and fail to stimulate synthesis of 1,25-dihydroxyvitamin D (the active form of vitamin D). These individuals cannot excrete excess phosphorus in the absence of both hormones (22). Elevated serum phosphorus concentrations have been associated with accelerated disease progression in individuals with impaired kidney function and have been linked to increased risk of adverse health outcomes in the general population (14, 23).

High serum phosphorus concentrations in the general population

High serum phosphorus within the normal range (2.5-4.5 mg/dL) has been associated with increased incidence of cardiovascular disease in individuals with normal kidney function. Two studies conducted in the general population and in individuals with prior cardiovascular disease have linked high-normal serum phosphorus concentrations (≥3.5 mg/dL) to a greater cardiovascular risk (24, 25). In a prospective cohort study, which followed 4,005 healthy young adults for more than 15 years, higher serum phosphorus within the normal range was also associated with left ventricular hypertrophy, a condition often linked to adverse cardiovascular outcomes (26). In another study of 3,088 middle-aged healthy participants followed for over 17 years, serum phosphorus concentrations in the top quartile of the normal range were associated with a two-fold higher risk of heart failure compared to the lowest quartile (≥3.5 mg/dL vs. <2.9 mg/dL) (24). Moreover, meta-analyses of prospective cohort studies have found a 36%-44% increased risk of cardiovascular mortality with higher versus lower serum phosphorus concentrations (27, 28).  

Additionally, observational studies have found serum phosphorus concentrations equal to or above 4 mg/dL to be associated with a doubling of the risk of developing incident CKD and end-stage renal disease in individuals free of renal disease at study inception (29). It is thought that vascular calcification, which may explain the relationship between high phosphorus and cardiovascular disease risk in CKD patients (see Hyperphosphatemia in subjects with kidney disease below), contributes to this association in individuals with normal kidney function, even when their serum phosphorus is within the normal range and their intakes are below the tolerable upper intake level (UL) (30, 31).

Phosphorus homeostasis is tightly regulated by the PTH/vitamin D/FGF-23 axis in individuals with normal kidney function (see Regulation). Increased secretion of PTH and FGF-23 helps maintain phosphorus serum concentrations in the normal range (2.5-4.5 mg/dL) even in the setting of high phosphorus intake (14). This contributes to serum phosphorus being only weakly correlated to phosphorus consumption (32). Of note, sustained increases in FGF-23 and PTH are commonly observed during CKD in order to maintain normal serum phosphorus concentrations despite a reduction in urinary phosphorus excretion (33). Elevated FGF-23, rather than serum phosphorus, appears to be an early marker of disordered phosphorus homeostasis and a predictor of adverse health outcomes in patients with early-stage CKD (33, 34). Thus, it is reasonable to assume that measuring serum phosphorus in people with normal renal function cannot adequately reflect early disturbances in phosphorus metabolism due to high phosphorus consumption.

Hyperphosphatemia in subjects with kidney disease

Observational studies have reported high rates of mortality and cardiovascular events in association with high blood phosphorus levels in subjects with CKD, in both dialysis patients and in non-dialysis patients (35, 36). A meta-analysis of 13 prospective cohort studies, conducted in over 90,000 CKD patients, found an 18% increase in all-cause mortality per 1 mg/dL increase in serum phosphorus concentration above 3.5 mg/dL. A 10% increased risk in cardiovascular disease (CVD)-related death was also calculated for each 1 mg/dL higher concentration in the meta-analysis of three studies (35).

Although no causality has been established between vitamin D deficiency and CVD risk, it has been suggested that failure to produce 1,25-dihydroxyvitamin D in individuals with hyperphosphatemia may modify the risk of developing cardiovascular and kidney disease, as well as worsen kidney insufficiency in CKD patients (37). Another plausible mechanism for hyperphosphatemia-induced cardiovascular dysfunction is the deposition of calcium phosphate in non-skeletal tissues, especially the vasculature (38). Indeed, high phosphorus concentrations may stimulate the expression of bone specific markers in blood vessel-forming cells, resulting in a shift in their functions; this process, called osteochondrogenic differentiation, transforms vascular smooth muscle cells (VSMCs) into bone-like cells. The culture of human aortic VSMCs in hyperphosphatemic conditions was found to result in the mineralization of the extracellular media, mimicking in vivo vascular calcification (39). Vascular calcification has been associated with at least a three-fold increase in risk for cardiovascular events and mortality; the risk for cardiovascular events is twice as high (i.e., six-fold increased risk) in individuals with kidney insufficiency (40).

In CKD patients, disorders in bone remodeling may result in excess release of phosphorus and calcium into the blood, which exacerbates hyperphosphatemia and vascular calcification and accelerates the decline of kidney function. Clinical practice guidelines currently recommend adjustment of dietary phosphorus intake to normalize serum concentrations in patients with advanced CKD (i.e., stages 3 to 5D) (41); understanding the bioavailability of different phosphorus-containing foods may be helpful in designing a diet to control serum phosphorus concentrations (see Bioavailability) (42, 43). CKD patients should follow the advice of their medical practitioner.

The tolerable upper intake level (UL)

To avoid the adverse effects of hyperphosphatemia, the US Food and Nutrition Board set a tolerable upper intake level (UL) for oral phosphorus in generally healthy individuals (Table 3; 10). The lower UL for individuals over 70 years of age, compared to younger age groups, reflects the increased likelihood of impaired kidney function in older individuals. The UL does not apply to individuals with significantly impaired kidney function or other health conditions known to increase the risk of hyperphosphatemia.

Adverse health outcomes have been associated with normal serum phosphorus concentrations, suggesting that in individuals with adequate kidney function, the measurement of tightly controlled serum phosphorus levels may misrepresent the detrimental effect of high dietary phosphorus intake (see High serum phosphorus concentrations in the general population). While phosphorus intakes below the UL of 4,000 mg/day should not result in hyperphosphatemia or cardiovascular risk in healthy adults ages 19-70 years, a recent study found that daily phosphorus intakes more than twice the RDA (i.e., >1,400 mg/day) were significantly associated with an increased risk of all-cause mortality (30).

Adverse health outcomes have been associated with normal serum phosphorus concentrations, suggesting that in individuals with adequate kidney function, the measurement of tightly controlled serum phosphorus levels may misrepresent the detrimental effect of high dietary phosphorus intake (see High serum phosphorus concentrations in the general population). While phosphorus intakes below the UL of 4,000 mg/day should not result in hyperphosphatemia or cardiovascular risk in healthy adults ages 19-70 years, a prospective cohort study found that daily phosphorus intakes more than twice the RDA (i.e., >1,400 mg/day) were significantly associated with an increased risk of all-cause mortality (44).

Is high phosphorus intake detrimental to bone health?

Some investigators are concerned about the increasing amounts of phosphates in the diet, which they largely attribute to phosphoric acid in some soft drinks and the increasing use of phosphate additives in processed foods (45, 46). A controlled feeding study in 10 healthy adults found adherence to a diet enhanced with phosphorus from additives (mean phosphorus intake, 1,677 mg/day) for only one week altered biomarkers of bone metabolism (i.e., FGF-23, osteopontin, and osteocalcin) compared to a diet low in phosphorus additives but with adequate phosphorus (mean phosphorus intake, 1,070 mg/day; 47). Yet, intake of sodium, which may negatively affect bone health, was higher in the phosphorus-enhanced diet (see the article on Sodium) (47). A subsequent controlled feeding study by the same investigators reported that adherence to a diet low in phosphorus additives for six weeks (following a two-week high-additive diet) significantly reduced urinary phosphorus excretion and circulating FGF-23 in adults with (n=11) and without (n=39) CKD (48). The six-week intervention also decreased circulating PTH concentrations in individuals with CKD (48).

High serum phosphorus has been shown to impair synthesis of the active form of vitamin D (1,25-dihydroxyvitamin D) in the kidneys, reduce blood calcium concentrations, and lead to increased PTH release by the parathyroid glands (12). PTH stimulation then results in decreased urinary calcium excretion and increased bone resorption; both contribute to serum calcium concentrations returning to normal (12). If sustained, elevated PTH levels could have an adverse effect on bone mineral content, but this effect appears to be observed with diets that are high in phosphorus and low in calcium, underscoring the importance of a balanced dietary calcium-to-phosphorus ratio.

In a small cross-sectional study, which enrolled 147 premenopausal women with adequate calcium intakes, participants with lower calcium-to-phosphorus (Ca:P) intakes (ratios ≤0.5) had significantly higher serum PTH levels and urinary calcium excretion than those with higher Ca:P ratios (ratios >0.5) (49). A controlled trial in 10 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 (Ca:P = 0.66), again demonstrating the importance of the balance between dietary calcium and phosphorus (50). Moreover, a cross-sectional analysis of the US population (NHANES 2005-2010) found no adverse association of high phosphorus intakes and bone mineral content/density and suggested adequate intakes of both calcium and phosphorus may be associated with a lower risk of osteoporosis (51).

A cross-sectional study conducted in 2,344 Brazilian men and women (median age, 58 years) showed an association between higher phosphorus intakes and increased risk of fracture. Yet, intakes of other minerals and vitamins relevant to bone health, such as calcium, magnesium, and vitamin D, were below the RDA in this population, whereas phosphorus intakes were close to the RDA (52). While hormonal and calcium disorders might be prevented by an adequate calcium-to-phosphorus intake ratio, there is no convincing evidence that the dietary phosphorus levels experienced in the US adversely affect bone mineral density. Nevertheless, the substitution of phosphate-containing soft drinks and snack foods for milk and other calcium-rich food may represent a serious risk to bone health (see the article on Calcium) (53).

Drug interactions

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 phosphorus levels (hypophosphatemia), as well as aggravate phosphorus deficiency due to other causes (54). The reduction of stomach acidity by proton-pump inhibitors may also limit the efficacy of phosphate-binder therapy in patients with kidney failure (55); a retrospective study in 71 hemodialysis patients found use of proton-pump inhibitors reduced the effect of lanthanum carbonate, but not ferric citrate hydrate or secroferric oxyhydroxide, on serum phosphorus concentrations (56). Excessively high doses of 1,25-dihydroxyvitamin D, the active form of vitamin D, or its analogs, may result in hyperphosphatemia (10).

Potassium supplements or potassium-sparing diuretics taken together with phosphorus supplements 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 (54).

Additionally, prevention of bone demineralization by hormone replacement therapy in postmenopausal women is associated with higher urinary phosphorus excretion and lower serum phosphorus levels in treated compared to untreated women (57, 58).
 

LPI Recommendation

The Linus Pauling Institute supports the RDA for phosphorus (700 mg/day for adults). Although some multivitamin/mineral supplements contain little phosphorus, a varied diet should provide adequate phosphorus for most people.

Older adults (>50 years)

At present, there is no evidence that phosphorus requirements of older adults differ from that of younger adults. A varied diet should easily provide the RDA (700 mg/day) of phosphorus for those over 50 years of age.

Authors and Reviewers

Originally written in 2001 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University

Updated 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

Updated in June 2014 by:
Barbara Delage, Ph.D.
Linus Pauling Institute
Oregon State University

Updated in September 2025 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University

Reviewed in February 2026 by:
Brandon Kistler, Ph.D., R.D.
Assistant Professor
Purdue University

Copyright 2001-2026  Linus Pauling Institute

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