Phosphorus What Type/forms Or What Is The Makeup Of Phosphorus In This Nutrient?

• Consumer
• Datos en español
• Health Professional
• Other Resources

This is a fact sail intended for health professionals. For a reader-friendly overview of Phosphorus, see our consumer fact sheet on Phosphorus.

Introduction

Phosphorus, an essential mineral, is naturally nowadays in many foods and bachelor as a dietary supplement. Phosphorus is a component of basic, teeth, Dna, and RNA [i]. In the form of phospholipids, phosphorus is also a component of prison cell membrane structure and of the torso's key energy source, ATP. Many proteins and sugars in the trunk are phosphorylated. In addition, phosphorus plays central 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 ane to 1.iv% of fat-costless mass. Of this amount, 85% is in bones and teeth, and the other 15% is distributed throughout the blood and soft tissues [i].

Many unlike types of foods contain phosphorus, mainly in the course of phosphates and phosphate esters [1]. Even so, phosphorus in seeds and unleavened breads is in the grade of phytic acid, the storage form of phosphorus [two]. Because human being intestines lack the phytase enzyme, much phosphorus in this course is unavailable for absorption [1]. Phosphorus undergoes passive absorption in the pocket-sized 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 brand upwards hydroxyapatite, the primary structural component in basic and tooth enamel [3]. The combination of high phosphorus intakes with low calcium intakes increases serum PTH levels, only show is mixed on whether the increased hormone levels decrease os mineral density [2,iv-6].

The kidneys, basic, 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 [one,7,viii]. Several hormones, including estrogen and adrenaline, also touch phosphorus homeostasis. When kidney role declines, as in chronic kidney failure, the body cannot excrete phosphate efficiently, and serum levels rise [ix].

Although phosphorus condition is not typically assessed, phosphate tin can be measured in both serum and plasma [10]. In adults, normal phosphate concentration in serum or plasma is 2.five to four.5 mg/dL (0.81 to 1.45 mmol/L) [10]. Hypophosphatemia is defined as serum phosphate concentrations lower than the low stop of the normal range, whereas a concentration higher than the loftier end of the range indicates hyperphosphatemia. Withal, plasma and serum phosphate levels do not necessarily reflect whole-body phosphorus content [ane,eleven].

Recommended Intakes

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

• 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 program nutritionally adequate diets for individuals.
• Adequate Intake (AI): Intake at this level is assumed to ensure nutritional capability; established when show is insufficient to develop an RDA.
• Estimated Average Requirement (EAR): Boilerplate daily level of intake estimated to meet the requirements of 50% of healthy individuals; usually used to appraise the nutrient intakes of groups of people and to plan nutritionally adequate diets for them; can as well be used to assess the nutrient intakes of individuals.
• Tolerable Upper Intake Level (UL): Maximum daily intake unlikely to cause adverse wellness furnishings.

Table ane lists the current RDAs for phosphorus [ii]. 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.

Tabular array one: Recommended Dietary Allowances (RDAs) for Phosphorus [2]

Age	Male	Female	Pregnancy	Lactation
Nascency to six months*	100 mg	100 mg
7–12 months*	275 mg	275 mg
1–3 years	460 mg	460 mg
4–eight years	500 mg	500 mg
nine–13 years	1,250 mg	1,250 mg
14–eighteen years	ane,250 mg	one,250 mg	1,250 mg	i,250 mg
19+ years	700 mg	700 mg	700 mg	700 mg

*Adequate Intake (AI)

Sources of Phosphorus

Food
Many different types of foods incorporate phosphorus, including dairy products, meats and poultry, fish, eggs, basics, legumes, vegetables, and grains [xiii,fourteen]. In the United States, dairy products contribute most 20% of full phosphorus intakes, and bakery products (due east.thou., breads, tortillas, and sweet bakery products) contribute 10% [13]. Vegetables and craven contribute 5% each. The absorption rate for the phosphorus naturally contained in food is 40%–70%; phosphorus from animal sources has a higher absorption charge per unit than that from plants [fifteen,16]. Calcium from foods and supplements can bind to some of the phosphorus in foods and prevent its absorption [1,17]. According to ane analysis, a very high calcium intake of two,500 mg/day binds 0.61–1.05 chiliad phosphorus [17]. In infants, phosphorus bioavailability ranges from 85%–90% for human milk to approximately 59% for soy-based formulas [2].

Phosphate additives (eastward.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 take an boilerplate of 67 mg more phosphorus per serving than similar foods not containing the additives, and these additives contribute to overall phosphorus intakes in the U.s. [18,nineteen].

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

Several nutrient sources of phosphorus are listed in Table two.

Tabular array 2: Phosphorus Content of Selected Foods [25]

Food	Milligrams (mg) per serving	Percent DV*
Yogurt, apparently, low fat, 6-ounce container	245	20
Milk, 2% milkfat, one cup	226	xviii
Salmon, Atlantic, farmed, cooked, iii ounces	214	17
Scallops, breaded and fried, three ounces	201	sixteen
Cheese, mozzarella, part skim, 1.5 ounces	197	16
Chicken, breast meat, roasted, 3 ounces	182	15
Lentils, boiled, ½ loving cup	178	14
Beef patty, ground, xc% lean meat, broiled, 3 ounces	172	14
Cashew nuts, dry roasted, 1 ounce	139	eleven
Potatoes, Russet, flesh and skin, broiled, 1 medium	123	x
Kidney beans, canned, ½ cup	115	9
Rice, chocolate-brown, long-grain, cooked, ½ cup	102	viii
Peas, green, boiled, ½ cup	94	8
Oatmeal, cooked with water, ½ cup	90	7
Egg, hard boiled, 1 large	86	vii
Tortillas, corn, one medium	82	7
Staff of life, whole wheat, one piece	60	v
Sesame seeds, 1 tablespoon	57	five
Bread, pita, whole wheat, 4-inch pita	50	4
Asparagus, boiled, ½ cup	49	4
Tomatoes, ripe, chopped, ½ cup	22	2
Apple, i medium	20	2
Cauliflower, boiled, 1" pieces, ½ cup	20	two
Beverages, carbonated, cola, ane loving cup	18	1
Clementine, 1 medium	16	1
Tea, green, brewed, 1 cup	0	0

*DV = Daily Value. The U.Southward. Nutrient and Drug Administration (FDA) developed DVs to aid consumers compare the nutrient contents of foods and dietary supplements inside the context of a total diet. The DV for phosphorus is ane,250 mg for adults and children age four years and older [26]. FDA does not crave nutrient labels to listing phosphorus content unless phosphorus has been added to the food. Foods providing 20% or more than of the DV are considered to exist loftier sources of a nutrient, merely foods providing lower percentages of the DV also contribute to a healthful nutrition.

The U.Southward. Section of Agriculture'due south (USDA's) FoodData Central [27] lists the nutrient content of many foods and provides a comprehensive list of foods containing phosphorus arranged past food content.

Dietary supplements
Phosphorus is available in dietary supplements containing only phosphorus, supplements containing phosphorus in combination with other ingredients, and a few multivitamin/multimineral products [28]. Phosphorus in supplements is unremarkably in the grade of phosphate salts (e.g., dipotassium phosphate or disodium phosphate) or phospholipids (due east.k., 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 Wellness and Diet Examination Survey (NHANES) testify that amid children and teens anile 2–19 years, the average daily phosphorus intake from foods is 1,237 mg [29]. In adults anile 20 and older, the average daily phosphorus intake from foods is 1,189 mg for women and one,596 mg for men.

According to an analysis of 2013–2014 NHANES information, the average daily phosphorus intake from both foods and supplements is 1,301 mg for women and i,744 mg for men [30]. Some experts question whether the dietary data collection instruments used past NHANES and other large population-based studies capture truthful dietary phosphorus intakes because these surveys practise non 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 furnishings of hypophosphatemia can include anorexia, anemia, proximal muscle weakness, skeletal effects (bone hurting, rickets, and osteomalacia), increased infection hazard, paresthesias, ataxia, and confusion [1]. In most cases, hypophosphatemia is caused by medical weather condition, such equally hyperparathyroidism, kidney tubule defects, and diabetic ketoacidosis [33].

Groups at Risk of Phosphorus Inadequacy

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

Preterm newborns
Phosphorus deficiency in preterm infants is one of the chief causes, along with calcium deficiency, of osteopenia of prematurity (impaired os mineralization) [34]. Because 2-thirds of fetal bone mineral content is acquired during the third trimester of pregnancy, preterm infants are born with depression stores of calcium and phosphorus in their bones [35]. The benefits of providing actress phosphorus and calcium for os health in preterm babies is non clear. However, milk fortified with higher amounts of these minerals and other nutritional components is typically recommended to back up overall growth and evolution [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-ascendant 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 consummate [39].

Patients with severe malnutrition
People with severe protein or calorie malnutrition can develop refeeding syndrome, likewise known every bit refeeding hypophosphatemia, within 2 to v days of starting enteral or parenteral nutrition considering of the shift in metabolism from a catabolic to an anabolic state [xl,41]. Causes of malnutrition that can pb to refeeding syndrome include chronic diseases (e.g., cancer, chronic obstructive pulmonary affliction, or cirrhosis), very depression birthweight, cachexia, low body weight, anorexia nervosa, excessive alcohol intake, and chewing or swallowing issues. The furnishings of refeeding syndrome can include impaired neuromuscular office, hypoventilation, respiratory failure, impaired blood clotting, confusion, coma, cardiac abort, congestive heart failure, and expiry [41]. Safe administration of phosphorus and thiamin in patients at hazard of refeeding syndrome can preclude this status [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 affliction
CKD, which affects five%–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 gene 23 lose their ability to suppress phosphorus resorption past the kidneys [43].

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

An assay of 2003–2006 NHANES data illustrates the association between CKD and phosphate levels. In vii,895 adults (mean historic period 47 years, 52% Caucasian), participants with moderately reduced kidney function had significantly higher serum phosphate levels (4.12 ml/dL) than those with normal kidney function (3.74 mg/dL) [45].

Several studies have shown an increased gamble of mortality or disease progression in patients who have CKD and high phosphate levels [46-48]. A meta-analysis of 9 cohort studies in 199,289 patients anile 50–73 years with finish-stage renal illness showed, for example, that patients on dialysis with the highest phosphate levels (greater than 5.2–7.5 mg/dL, depending on the report) had a 39% greater risk of all-cause bloodshed during 12 to 97.vi months of follow-upwards than those with normal phosphate levels (defined in the analysis as 3.0–five.5 mg/dL, depending on the study) [49].

However, high phosphate levels exercise not seem to take 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 historic period 67–71 years, depending on their phosphate intake tertile) with moderate CKD establish 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 three.5 mg/dL in the highest intake tertile (i,478 mg/day)—and that high phosphorus intakes were not associated with increased mortality rates over 6–12 years, mayhap considering 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 (due east.g., by replacing nearly animal proteins in their diets with plant-based poly peptide sources, whose phosphorus is less bioavailable) and consume more than calcium-rich foods [9,52]. Some show shows that replacing foods containing phosphorus additives with foods that lack these additives can reduce serum phosphate levels [53]. All the same, restricting phosphorus intakes tin also reduce protein intakes because many foods (e.g., fish, meats, and legumes) containing big amounts of phosphorus also contain large amounts of poly peptide [54]. Furthermore, a Cochrane review of ix studies in 634 participants with CKD followed for 1–xviii months found simply express, low-quality bear witness indicating that dietary interventions might take 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 iii–5 (more severe) CKD limit dietary phosphorus intake either alone or in combination with other treatments to reduce phosphate levels [55]. Even so, 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.

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

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

Several large epidemiologic studies accept besides found associations betwixt higher serum phosphate concentrations and risk of cardiovascular mortality in healthy adults. A meta-assay of data from four prospective cohort studies with thirteen,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 six–29 years showed a 36% higher risk of cardiovascular mortality in those with the highest phosphate concentration (ii.79–four.0 mg/dL) compared with participants with a phosphate concentration of 0.61–three.28 mg/dL [59]. A subsequent study not included in this meta-analysis in thirteen,165 nonpregnant adult participants (mean age 43–45 years, 52% female) in NHANES 3 (1988–1994) followed for a median of fourteen.3 years found that for every one mg/dL increase in phosphate above 3.5 mg/dL, the take a chance of death rose by 35% and the take chances of cardiovascular death increased past 45% [lx].

Non all observational information, however, support a link between serum phosphate concentrations and CVD hazard. A post hoc analysis of information from 7,269 postmenopausal women, mean age 66 years, with osteoporosis found no clan betwixt higher serum phosphate levels and take chances 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 prove on whether restricting phosphorus consumption tin forbid CVD in healthy adults [62]. Additional inquiry is needed to address this issue.

Wellness Risks from Excessive Phosphorus

High phosphorus intakes rarely produce adverse furnishings in good for you people. Although some studies have establish associations between high phosphorus intakes (1,000 mg/twenty-four hour period or higher) and cardiovascular, kidney, and bone adverse furnishings every bit well as an increased risk of decease [23,63,66], others have constitute no link betwixt 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 nether medical supervision.

Table 3: Tolerable Upper Intake Levels (ULs) for Phosphorus [2]

Age	Male	Female	Pregnancy	Lactation
Nascency to half dozen months*	None established*	None established*
7–12 months*	None established*	None established*
1–3 years	3,000 mg	3,000 mg
4–viii years	3,000 mg	3,000 mg
9–thirteen years	4,000 mg	4,000 mg
14–eighteen years	4,000 mg	4,000 mg	3,500 mg	4,000 mg
19–l years	iv,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 but sources of phosphorus for infants.

Co-ordinate to i analysis of information on healthy U.S. adults using NHANES 3 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 beneath 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 case [63].

Very high phosphorus intakes over short periods (east.chiliad., two vi,600 mg doses of sodium phosphate taken in one day) can cause hyperphosphatemia [67,68]. The master 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 tin can take an agin event on phosphate levels. 2 examples are provided below. Individuals taking these and other medications on a regular footing should talk over their phosphorus condition with their healthcare providers.

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

Laxatives
Some laxatives, such as Fleet Prep Kit #1, contain sodium phosphate, and ingesting these products tin increase serum phosphate levels [71]. After 13 reports of deaths associated with taking i dose that was college than recommended on the label of a laxative containing sodium phosphate, the FDA issued a alert 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 authorities'south 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 exist met primarily through foods. ... In some cases, fortified foods and dietary supplements are useful when information technology is non possible otherwise to encounter needs for one or more nutrients (e.yard., during specific life stages such every bit pregnancy)."

For more information nearly building a salubrious dietary pattern, refer to the Dietary Guidelines for Americans and the U.South. Department of Agriculture's MyPlate.

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

• Includes a diverseness of vegetables; fruits; grains (at least half whole grains); fat-costless and low-fatty milk, yogurt, and cheese; and oils.

  Some dairy products are rich in phosphorus, and some vegetables, fruits, and grains contain phosphorus.

• Includes a multifariousness of poly peptide foods such every bit 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 inside your daily calorie needs.

References

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. Found of Medicine, Food and Diet Lath. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington, DC: National Academies Printing; 1997.
3. Trautvetter U, Ditscheid B, Jahreis G, Glei M. Habitual intakes, food sources and excretions of phosphorus and calcium in three High german written report 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 os mass in the Korean population. Nutr J 2014;13:114.
6. Trautvetter U, Jahreis G, Kiehntopf M, Glei Thousand. 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 report. Nutr J 2016;15:7. [PubMed abstruse]
7. Calvo MS, Lamberg-Allardt CJ. Phosphorus. Adv Nutr 2015;six: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 disquisitional 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. Laboratory Medicine 2014;45:e44-e50.
11. EFSA Console on Dietetic Products Northward, Allergies. Scientific Opinion on Dietary Reference Values for phosphorus. EFSA Journal 2015;13:4185.
12. Institute of Medicine, Food and Diet Board. Dietary Reference Intakes for Vitamin A, Vitamin Thousand, Arsenic, Boron, Chromium, Copper, Iodine, Atomic number 26, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academies Printing; 2001. [PubMed abstruse]
13. Moshfegh AJ, Kovalchik AF, Clemens JC. Phosphorus Intake of Americans: What We Eat in American, NHANES 2011-2012. 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 bear on 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 Printing; 2018:249-66.
17. Heaney RP, Nordin Exist. Calcium effects on phosphorus assimilation: 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 acme-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 Punch 2013;26:54-61. [PubMed abstruse]
20. Calvo MS, Park YK. Changing phosphorus content of the U.South. diet: potential for adverse furnishings 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 Grand, 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. Touch on of phosphorus-based nutrient additives on os and mineral metabolism. J Clin Endocrinol Metab 2015;100:4264-71. [PubMed abstruse]
24. Scanni R, vonRotz Thou, Jehle S, et al. The human response to acute enteral and parenteral phosphate loads. JJ Am Soc Nephrol 2014;25:2730-ix. [PubMed abstruse]
25. U.S. Section of Agriculture, Agricultural Research Service. USDA National Nutrient Database for Standard Reference, Legacy Release. Nutrient Data Laboratory Domicile Page, 2019.
26. U.S. Food and Drug Administration. Food Labeling: Revision of the Nutrition and Supplement Facts Labels. 2016.
27. U.S. Department of Agriculture. FoodData Central. 2019.
28. National Institutes of Wellness. Dietary Supplement Label Database. 2019.
29. U.Due south. Department of Agronomics, Agricultural Enquiry Service. What We Eat in America, 2015-2016. 2019.
30. U.Due south. Section of Agriculture, Agricultural Research Service. What We Eat in America, 2013-2014. 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;four:723-9. [PubMed abstract]
32. Calvo MS, Uribarri J. Public wellness impact of dietary phosphorus excess on bone and cardiovascular health in the general population. Am J Clin Nutr 2013;98:six-15. [PubMed abstract]
33. Hruska One thousand. 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:eleven-28.
34. Karpen HE. Mineral homeostasis and effects on os mineralization in the preterm neonate. Clin Perinatol 2018;45:129-41. [PubMed abstract]
35. Harding JE, Wilson J, Chocolate-brown J. Calcium and phosphorus supplementation of human milk for preterm infants. Cochrane Database Syst Rev 2017;ii:Cd003310. [PubMed abstruse]
36. Abrams SA. In utero physiology: part in food commitment 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 Chiliad. Genetic disorders of phosphate regulation. Pediatr Nephrol 2012;27:1477-87. [PubMed abstract]
39. Pavone V, Testa Chiliad, Gioitta Iachino S, et al. Hypophosphatemic rickets: etiology, clinical features and treatment. Eur J Orthop Surg Traumatol 2015;25:221-half dozen. [PubMed abstract]
40. Parli SE, Ruf KM, Magnuson B. Pathophysiology, handling, and prevention of fluid and electrolyte abnormalities during refeeding syndrome. J Infus Nurs 2014;37:197-202. [PubMed abstruse]
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 abstruse]
42. Moe SM, Drüeke T, Lameire N, Eknoyan Thousand. Chronic kidney illness--mineral-os disorder: a new paradigm. Advances in Chronic Kidney Affliction 2007;fourteen:three-12. [PubMed abstruse]
43. Liu Z, Su G, Guo X, et al. Dietary interventions for mineral and bone disorder in people with chronic kidney illness. Cochrane Database Syst Rev 2015:Cd010350. [PubMed abstruse]
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 past levels of kidney office. 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 bloodshed: a meta-assay of cohort studies. Am J Kidney Dis 2015;66:258-65. [PubMed abstruse]
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 abstruse]
48. Cheungpasitporn W, Thongprayoon C, Mao MA, et al. Admission serum phosphate levels predict hospital bloodshed. Hospital Practice 2018;46:121-seven. [PubMed abstract]
49. Hou Y, Li Ten, Sun L, Qu Z, Jiang L, Du Y. Phosphorus and mortality risk in end-phase renal disease: A meta-analysis. Clin Chim Acta 2017;474:108-13. [PubMed abstruse]
50. Selamet U, Tighiouart H, Sarnak MJ, Beck Chiliad, Levey AS, Block 1000, et al. Relationship of dietary phosphate intake with risk of end-stage renal disease and mortality in chronic kidney affliction stages three-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 K, Greene T, Beddhu S. Dietary phosphorus intake and mortality in moderate chronic kidney illness: NHANES III. Nephrol Dial Transplant 2012;27:990-half-dozen. [PubMed abstract]
52. Moorthi RN, Moe SM. Special nutritional needs of chronic kidney affliction and end-stage renal disease patients: rationale for the use of establish-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 finish-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 decision-making phosphorus by decreasing dietary protein intake benign or harmful in persons with chronic kidney illness? Am J Clin Nutr 2008;88:1511-8. [PubMed abstruse]
55. Group KDIGOC-MUW. KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Affliction-Mineral and Bone Disorder (CKD-MBD),. Kidney Int Suppl (2011) 2017;7:ane-59. [PubMed abstract]
56. Dhingra R, Sullivan LM, Play a trick on CS, et al. Relations of serum phosphorus and calcium levels to the incidence of cardiovascular disease in the community. Curvation Intern Med 2007;167:879-85. [PubMed abstract]
57. Tonelli G, Sacks F, Pfeffer Thousand, 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] written report). 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-assay. Clin Chim Acta 2016;461:76-82. [PubMed abstract]
60. Chang AR, Grams ME. Serum phosphorus and mortality in the Third National Health and Diet 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 mail service-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-crusade 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 on stages of CKD: a randomized controlled trial. Am J Kidney Dis 2017;69:200-ix. [PubMed abstract]
66. Ito S, Ishida H, Uenishi K, et al. The relationship between habitual dietary phosphorus and calcium intake, and os mineral density in young Japanese women: a cantankerous-sectional report. Asia Pac J Clin Nutr 2011;twenty: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 study and review of the literature. Calcif Tissue Int 1990;47:291-five. [PubMed abstruse]
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;viii:CD006023. [PubMed abstract]
71. Casais MN, Rosa-Diez G, Perez Southward, 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 Assistants. FDA Drug Safety Communication: FDA warns of possible harm from exceeding recommended dose of over-the-counter sodium phosphate products to treat constipation. 2014.
73. U.S. Department of Agronomics, Agricultural Enquiry Service. What We Eat in America, 2013-2014. 2017.

Disclaimer

This fact sheet by the National Institutes of Health (NIH) Function of Dietary Supplements provides information that should not take the place of medical advice. We encourage you lot to talk to your healthcare providers (doctor, registered dietitian, pharmacist, etc.) nigh your interest in, questions nearly, or utilize of dietary supplements and what may exist best for your overall health. Whatever mention in this publication of a specific product or service, or recommendation from an arrangement or professional gild, does not represent an endorsement past ODS of that product, service, or practiced communication.

Source: https://ods.od.nih.gov/factsheets/Phosphorus-HealthProfessional/#:~:text=Phosphorus%2C%20an%20essential%20mineral%2C%20is,body's%20key%20energy%20source%2C%20ATP.

Posted by: mooretandsold.blogspot.com

Share this post