John J B Anderson. Cambridge World History of Food. Editor: Kenneth F Kiple & Kriemhild Conee Ornelas. Volume 1, Cambridge University Press, 2000.
Phosphorus (abbreviated as P) is a highly toxic element, which, when it occurs in the form of a phosphate salt, becomes a nutrient essential for human health. Phosphates are found in practically every type of food and, consequently, are plentiful in the typical diet. Inorganic phosphates (abbreviated as Pi) are absorbed from food as electrically charged salt anions. The organic phosphates (Po) that exist in cells and extracellular compartments of foods are primarily converted to Pi through digestive processes prior to absorption. A few organic phosphates are apparently absorbed as part of small fat-soluble organic molecules, such as the phosphates of phospholipids. The concentration of Po molecules, however, is not under homeostatic control, in contrast to the concentration of Pi, which is regulated along with calcium (Ca) in blood and extracellular fluids.
The close association between calcium and Pi in the extracellular body fluids and in bone tissue requires joint consideration of dietary calcium and dietary phosphates for an understanding of their physiological linkages and the important relationship between low calcium intakes and high phosphate intakes. This relationship potentially contributes to altered calcium homeostasis and the loss of bone mass.
Several aspects of Pi are reviewed here in an attempt to place these essential chemical anions in the perspective of their utilization in human health and disease. The physiological functions of P are reviewed first, and a number of general references have also been included in the bibliography for the interested reader.
Physiological Functions of Phosphates
The regulation of Pi in the blood is maintained by a complex homeostatic system that also controls the blood concentration of Ca. Pi ions can follow several potential metabolic pathways after entry into cells. One immediate use of Pi ions is to phosphorylate glucose through enzymatic steps via kinases. They are also used in the phosphorylation of several other molecules; for example, creatine phosphate serves as an energy reserve in skeletal muscle tissue, and adeno-sine triphosphate is the primary donor of energy from its high-energy bonds within cells. In addition, several types of phospholipids and nucleic acids incorporate Pi within their molecular structures.
Cellular uses of P in intermediary metabolism are very extensive. Practically all energetic steps utilize high-energy phosphate bonds (adenosine triphosphate, or ATP) for the synthesis of organic molecules: to drive transport systems across cell membranes, to make muscles contract, to allow nerves to conduct impulses and transfer information, to convey genetic information, and to provide skeletal support and protection. In addition, phosphates circulating in blood have buffering activity. Clearly, Pi ions have multiple uses both within and without cells. Mineralized bone serves as an important store of Pi ions that can be retrieved through the action of parathyroid hormone (PTH) on bone cells. Because of the large reservoir of Pi ions, hypophosphatemia and P deficiency are rare events in adults without other major complications.
Phosphates in Foods
In terms of dietary sufficiency, P does not present a problem for human health because of the abundance of molecules containing this element in the food supply. Rather, the potential health problem is dietary Ca insufficiency in relation to excess intake of phosphates over periods of years, or even decades. Phosphorus deficiency, a rare clinical disorder, occurs almost exclusively because of a pathological change in the handling of phosphates, rather than because of a dietary inadequacy. The reason for these encompassing statements is that almost all foods contain phosphate groups in both organic (Po) and inorganic (Pi) forms, and many of the foods—especially animal products—commonly consumed by all populations of the world are rich in P.
The approximate percentage distribution of foods (by food group) that provide dietary P in the United States is as follows: Milk and dairy products—30 percent; meat, poultry, and fish—27 percent; cereal grains and grain products—20 percent; legumes, nuts, and seeds—8 percent; vegetables—7 percent; and other (miscellaneous) foods, including fruits—8 percent (Figure IV.B.5.1). Although accurate data are lacking, it is presumed that these percentages are similar for the nations of the European Union, along with other Western countries. For populations that consume few dairy foods (or none), the percentage of dietary P contributed by grains, legumes, vegetables, and fruits would be greatly increased, depending on the food traditionally available. Vegetarians of all types, but especially “vegans” (strict vegetarians), have lower P intakes than do omnivores who consume several servings a day of dairy foods and meats. But, even though P intakes by vegans could be insufficient, deficiency symptoms are very unlikely.
Phosphorus is widely found in foods in their natural unprocessed condition, and available food composition tables report the amounts of P measured in natural foods without any phosphate additives. Unfortunately, no food tables exist for the P content of processed foods. This lack is a serious hindrance to the accurate estimation of total phosphorus consumption from all foods, processed and unprocessed.
Although cereal grains and most vegetables yield good amounts of phosphates, these are nonetheless typically smaller amounts than those provided by animal foods. Moreover, except for highly processed wheat flours and polished rice, cereal grains have much of their Po bound in phytates that are not completely digested within the gastrointestinal (GI) tract, and therefore, the total amount of P in grains is not available for absorption. Legumes and foods made from them, including soy flour and peanuts, are good sources of P, but this is not the case for most other plant foods, save for nuts such as almonds. Fruits, fruit juices, and vegetable oils contain negligible amounts of P. Table IV.B.5.1 lists the amounts of P (as a combination of both Pi and Po) and calcium in commonly consumed foods.
Cereal grains contain significant amounts of the polyphosphate phytic acid (inositol hexaphosphate) in the bran and other parts. Each phytate molecule contains 6 Po groups that become Pi groups when phytates are digested within the lumen of the GI tract by phosphatase enzymes. Food composition tables should be consulted for the phosphorus (combined Po and Pi) content of specific foods.
Table IV.B.5.1.Content of phosphorus and calcium in commonly consumed food in mg per serving
|Cheese, Amer.||1 oz||211||174||1:1.2|
|Mozzarella, skim||1 oz||149||207||1:0.7|
|Beef, ground||3 oz||135||8||1:16.9|
|Pork chop, loin||one||184||8||1:23|
|Turkey, white mt||3 oz||186||16||1:11.6|
|Tuna, water pack||3 oz||103||10||1:10.3|
|Bread, whole wheat||slice||74||20||1:3.7|
|Peas, green||0.5 cup||72||19||1:3.8|
|Baked beans||0.5 cup||132||64||1:2.1|
|Corn, kernel||0.5 cup||39||2||1:19.5|
Source: Hands, FOOD Finder: Food Sources of Vitamins and Minerals (1990).
Animal foods are rich in P, with eggs, meats, fish, crustaceans, mollusks, poultry, and dairy products containing large amounts of this element. Liver, cheeses, and eggs (yolks) are highest in phosphorus, followed by meats, fish, and poultry, and then by milks (of any fat content). (See Table IV.B.5.1 for a listing of the P content of commonly consumed foods.) Mixed dishes that feature cheese or milk also have large amounts of P.
Phosphates (both Pi and Po) are increasingly found in the food supplies of economically developed nations because of their widespread use as chemical additives in food applications. The food and beverage industries add a significant amount of phosphates to many foods and to cola-type beverages. Phosphate additives represent a diverse group of molecules, practically all of which are readily solubilized within the stomach or upper small intestine and are thereby highly bioavailable. Processed foods currently consumed by North Americans often have a significantly increased phosphorus content because of the intentional addition of one or more of these phosphate salts (Calvo 1993; Calvo and Park 1996). Phosphate additives have several functions in foods, notably as acids, buffers, anti-caking agents, emulsifiers, and sequestrants (Dziezak 1990), and individuals who consume many processed foods (especially those with cheese in them) are estimated to have an increased daily phosphorus intake of 10 to 15 percent.
Because practically all foods naturally contain phosphorus, and many processed foods have phosphates added to them, no need for supplementation exists in healthy individuals with normal renal function. Except for very rare clinical cases of renal phosphate wasting condition, or phosphate deficiency in newborns or premature babies, it is difficult to conceive of a situation requiring phosphate supplements.
Phosphate Additives—Recent Changes
The use of phosphate additives in food processing has accelerated since 1950, and in fact, for the first time in history, humankind faces an excess of phosphorus in the food supply because of the intentional addition of an estimated 40 to 50 different phosphate salts (Calvo and Park 1996).This, in turn, has introduced the possibility of an adverse effect of total phosphate consumption (from foods, beverages, and additives) on bone health, much as excess sodium intake from sodium-processed foods has contributed to the high prevalence of hypertension in the United States and other nations.
An interesting aspect of this increased intake of P is that it is not included in national survey estimates of total P consumption, meaning that the true intake of phosphorus in the United States is substantially underestimated (Oenning, Vogel, and Calvo 1988; Calvo and Park 1996). A study by M. S. Calvo and Y. K. Park (1996) shows a trend of increasing availability of phosphate additives in the food supply from specific items, such as frozen pizza, frozen processed poultry, and frozen prepared foods. Particularly worrisome is the increased availability of frozen processed poultry products in the marketplace over the last few years. (Frozen-food manufacturers, especially, utilize phosphate additives because of the phosphates’ stability when the foods are thawed or heated.) Fast-food entrees also often contain phosphate additives, but little or none of the phosphate-additive content of these foods is included in estimates of phosphorus consumption (Calvo and Park 1996).
Dietary Intakes of Phosphates
Current dietary patterns in the United States suggest that, on the average, American women are consuming too little Ca in relation to P. In every age category over 11 years, the calcium intakes of females are so low that the median Ca:P ratio falls to 0.6, and approximately 10 percent of the female population has a ratio of 0.4 or less. This low ratio contributes to a persistent elevation (above baseline) of the parathyroid hormone (PTH), the major regulatory hormone affecting Ca and P metabolism.
Figure IV.B.5.2a illustrates the patterns of P and Ca consumption of females in the United States (USDA 1994). These median (50th percentile) intakes are compared to the Recommended Dietary Allowances (RDAs) (National Research Council 1989). Figure IV.B.5.2b shows the Ca:P ratio from the diet of females across the life cycle. The Ca:P ratio of 1:1 is illustrated as a line to demonstrate that this idealized ratio is not met from foods by females (or males) except during the first few months of life when breast milk is consumed.
Requirements and Allowances of Phosphorus
P is an essential nutrient because it is needed for both organic molecules and the mineralized tissues—bones and teeth. Indeed, it has been speculated that calcium-phosphate salts were the substratum for the synthetic steps that resulted in the origin of life in the liquid medium during the early history of the planet Earth.
The amounts of P needed in the diet each day depend on several variables, such as stage of development in the life cycle, gender, body size, and physical exertion. Mean requirements of dietary P are not precisely known for either sex during adulthood, but daily U.S. intakes (roughly between the 10th and 90th percentiles) of P fall in a range of approximately 1,600 to 2,400 milligrams (mg) per day for males and 1,200 to 1,600 mg for females, according to data generated by the U.S. Department of Agriculture’s Continuing Survey of Food Intakes by Individuals (CSFII) (USDA 1994; Calvo and Park 1996).
Requirements of P may be as low as 600 to 800 mg a day for females and 800 to 1,000 mg for males, but these are educated guesses only, which assume adequate consumption patterns of calcium. Excess Pi that is absorbed is excreted by individuals with healthy kidneys in practically a 1:1 ratio to intake. In late life and in individuals who have declining renal function, some phosphate ions may be harbored (not truly stored) in mineralized atheromatous deposits within the arteries and in the skin. P balance-assessment methods have been historically helpful in arriving at estimates of P requirements, but they typically have low precision of measurements in feces; therefore, they are not very reliable.
Recommended Dietary Allowances have long been established for phosphorus as well as for calcium, and age- and gender-specific recommendations have been kept identical for both of these minerals across the life cycle since the first edition of the RDAs in the early 1940s.These identical values presume a 1:1 ratio of dietary intake of calcium and total phosphorus (Piand Po combined), but actual dietary intakes almost never achieve such a ratio except in the early months or years of life.When the typical intake ratio declines to approximately 0.5:1, the homeostatic regulation of serum calcium becomes so significantly challenged that skeletal mass may be lost in order to maintain the blood calcium concentration at a set level.
The Calcium: Phosphorus Ratio and Relationship
The problem with excessive dietary P intakes (or even just adequate intakes) is the imbalance between calcium and phosphorus that can result from typically low dietary calcium consumption patterns. Because practically all foods contain phosphates, but only a few have much calcium, eating behaviors that exclude calcium-rich foods (mainly milk and related dairy foods) may contribute to a condition known as nutritional secondary hyperparathyroidism—and one that can be exacerbated in individuals who consume diets rich in phosphate additives and cola drinks with phosphoric acid (Calvo 1993). The high intake of total P is not in itself so much of a problem as are the behaviors that lead to the avoidance of calcium-rich foods. This is because the latter lowers the Ca:P ratio and causes the development of a persistent elevation of PTH (Calvo, Kumar, and Heath 1990). A diet containing adequate amounts of Ca can overcome these adverse effects of P (BargerLux and Heaney 1993).
Because long-term prospective human studies of high-P diets have not been published, data from short-term and cross-sectional investigations must be used to assess the adverse effects of persistent low-Ca, high-P intakes on bone status. Unfortunately, only a few researchers have examined this issue of the dietary Ca:P ratio. One four-week investigation of young women consuming a Ca:P ratio of 0.25:1 revealed the undesirable persistent rise in PTH (Calvo et al. 1990). Another study of cross-sectional data from healthy, young-adult females indicated that too much P relative to calcium in the usual diet has a negative effect on the mineral content and density of bone (Metz, Anderson, and Gallagher 1993).
The mean Ca:P ratio of U.S. adults approximates 0.5:1 (Calvo 1993), and in fact, healthy ratios of intakes of the two elements range from 0.70 to 0.75 when the recommended number of servings from all food groups (based on the Basic Food Guide or Food Pyramid) are consumed each day. In other words, it is very difficult in the United States to achieve a ratio of 1:1, the ratio recommended in the RDAs (National Research Council 1989), without taking Ca supplements. Nonetheless, a healthy eating pattern should include a ratio within the range of 0.7:1 to 1:1. Intake ratios at or below 0.5:1 are of concern because of the likelihood of persistently elevated PTH concentrations and the potential loss of bone mass, which could lead to fragility fractures.
Digestion of Phosphates from Foods
Phosphates in foods exist mainly as organic molecules that must be digested in order to release inorganic phosphate into fluids of the intestinal lumen. Pianions freed up by digestive enzymes are then ready for absorption; little likelihood exists for their resyn-thesis or precipitation because of the lower pH level (–6.0 to 7.0) of the upper half of the small intestine.
The common types of enzymes of the gut that break the bonds of phosphate-containing molecules are secreted almost entirely by the exocrine pancreas. These enzymes include phospholipases, phosphatase, and nucleotidase—as these names imply, the enzymes have specific target molecules that contain phosphates. Once these Pi molecules are solubilized in the lumen, all are equal in the sense that the absorbing mechanisms of the small intestine do not discriminate based on the molecule of origin.
Phytates, which occur in large amounts in cereal grains, are rather poorly digested by humans.The reason is that phytase enzymes are not made in the human body, and only the phytase enzymes present in the bran and other parts of the grain can accomplish this chemical digestion.
Intestinal Absorption of Phosphates
Inorganic phosphate anions are efficiently absorbed across the small intestine, primarily in cotransport with cations, in order to maintain the electrical neutrality of cells. The efficiency of absorption (net) of Pi ranges between 60 and 70 percent in adults, almost twice the efficiency (net) of calcium from the diet (that is, 28 to 30 percent) (Anderson 1991). For example, for every 1,000 moles of Pi, approximately 700 are absorbed (net), compared to only 300 (net) from 1,000 of Ca in the diet. Therefore, the excretory mechanisms have to work more efficiently to eliminate the extra Pi absorbed following meals. In children, the net absorption efficiencies may be as high as 90 percent for Pi and 50 percent for Ca. Several factors have adverse effects on Pi absorption, but these typically have little overall influence on Pi utilization, home-ostasis, or metabolism. A few factors may enhance Pi absorption, but these, too, have little significance for the overall economy of Pi in the body (Allen and Wood 1994). A high P intake has been reported to have little effect on calcium absorption (Spencer et al. 1978).
The absorption efficiency of Pi declines later in life so that the net absorption of phosphorus from foods is somewhat reduced; probably this occurs in a similar fashion as calcium absorptive efficiency is lowered with age, especially after age 65 in females.
Pi ions are absorbed across all three segments of the small intestine, but the rapid entry into the bloodstream of radioactively labeled phosphates suggests that duodenal absorption occurs both very efficiently and at a high transfer rate. Therefore, the bulk of the absorbed Pi ions are transported across this segment, lesser amounts across the jejunum, and still lesser amounts across the ileum. If the hormonal form of vitamin D—calcitriol or 1,25-dihydroxyvitamin D—is elevated, Pi absorption can be even further enhanced in all segments of the small intestine.
Regulation of Blood Phosphate (Pi) Concentration
The homeostatic regulation of Pi in blood is primarily controlled by PTH, but several other hormones also exert influences on it. The major sites of regulation are the kidneys and the gut. PTH acts on the renal tubules to inhibit Pi reabsorption, while at the same time enhancing Ca reabsorption. The response of the kidneys to the action of PTH is the primary route of loss of Pi from the body. A secondary route is the small intestine, through which intestinal secretions from glands within the serosa of the intestinal lining remove Pi from the bloodstream to the gut lumen. This route of loss of Pi ions is called endogenous fecal excretion, and the quantity of Pi lost by this route may be almost as great as renal losses over a 24-hour period.
Absorption of an excess of Pi tends to lower the blood Ca ion concentration, which then triggers the secretion of PTH from the parathyroid glands. The role of circulating Pi in the secretion of PTH has been investigated in animal models and in human subjects to establish the connection with high dietary phosphorus intake. As mentioned, the absorption of Pi ions is rapid following a meal, much more so than for calcium ions. When an excess of Pi ions exists in the blood, the Pi concentration increases; this change, in turn, drives down the Ca ion concentration through a mechanism involving ionic binding between the two ions.
The net reduction in the concentration of Ca ions then stimulates the secretion of PTH. In turn, PTH enables the transfer of residual circulating Ca and Pii ons into the bone fluid compartment and into other extravascular compartments of the body. (Some investigators suggest that calcitonin, another calcium-regulating hormone, is involved in the movement of these ions into bone and, hence, in the conservation of calcium after a meal.) The persistently elevated PTH, however, tends to undo calcium conservation in the skeleton because this hormone continuously stimulates the reverse transfer of Ca and Pi ions from bone to blood (Calvo et al. 1990).The net result is that the skeleton loses bone mineral when PTH is elevated, even within the normal range of blood concentration, over extended periods of time. (The actual site of loss of this Ca is the gut, which has a poorly regulated secretion of Ca ions through intestinal glands.) PTH also has other roles in the kidney that, in effect, contribute to Ca retention by the body and to the elimination of Pi via urinary excretion.
PTH is considered the major hormone regulating Pi homeostasis because of its powerful roles in enhancing renal and, possibly, intestinal Pi losses while, at the same time, conserving calcium ions. When PTH is elevated, renal Pi reabsorption is largely inhibited, and similarly, the secretion of Pi ions by intestinal mechanisms is enhanced (although an understanding of this route of Pi loss is less established). PTH also acts on bone tissue to increase the transfer of calcium ions from the bone fluid compartment (BFC) and from the resorption of mineralized bone tissue to the blood plasma to restore the calcium ion concentration. By these same actions of PTH, Pi ions are also indirectly transferred from the BFC and bone to the blood.
P balance means that intake of P from foods equals losses in urine and feces (and other sources, such as sweat and skin, which are seldom measured). In effect, Pi ions that are absorbed are accounted for by losses from the body. Under balance conditions, no net gain or loss of Pi ions occurs. This zero-balance state probably only exists during the adult years from roughly 20 to 60. During growth, and during pregnancy and lactation, positive balance states tend to predominate, whereas in late life, phosphate retention may increase and become a major health problem for individuals with declining renal function. Phosphate retention (positive P balance) results from the declining effectiveness of PTH in enhancing renal excretion of Pi ions with decreasing renal function.
A schematic diagram of the P balance of an adult male is shown in Figure IV.B.5.3.An adult male would typically consume 1,200 to 1,400 mg of P a day, whereas an adult female would consume 900 to 1,000 mg per day (USDA 1994; Calvo and Park 1996). These estimated intakes of P by gender, however, do not include phosphate additives in foods.
Positive P balance (both Po and Pi), or the net gain of this element by the body, is difficult to measure, but numerous balance studies suggest that P home-ostasis (that is, zero balance) is typically maintained even when Ca balance may be significantly negative. Radioisotopic and stable nuclide studies have greatly advanced our knowledge about the fluxes of Pi and Ca ions across the gut and renal tubules in animal models and, to a lesser extent, in human subjects. Balance studies without the use of stable or radioactive nuclides are notoriously fraught with potential errors of collection and measurement, and these difficulties make such studies generally unreliable in the precise quantitative sense.
The uptake of Pi ions by cells requires carrier mechanisms or cotransport systems because of the electrical charge and water-solubility properties of these anions. Pi ions typically cotransport with glucose in postprandial periods, but their charge must be neutralized by cations, typically not calcium ions. Also, after meals, Pi ions enter the bone fluid compartment, but in this case, typically with calcium ions. Calcitonin has been considered primarily responsible for the uptake by bone tissue of these two ionic species following food ingestion and the intestinal absorption of the ions (Talmage, Cooper, and Toverud 1983).After entry into cells, the Pi ions in the cytosol are almost immediately used to phosphorylate glucose or other molecules, and a small fraction of the ions are stored as organic molecules or inorganic salts within cellular organelles.
Some Piions that enter bone may enter bone cells, especially osteoblasts or lining cells, whereas other ions bypass the cells and go directly to the BFC, an extension of the blood/extracellular-fluid continuum. In the BFC, Pi ions in solution increase the Pi concentration (activity) that permits these ions to combine with Ca ions in excess of their solubility product constant (Ksp) and form mineral salts (precipitate) in bone extracellular tissue.The formation of hydroxyapatite crystals (mineralization) is essential for structural support and protection of internal organs from environmental trauma. Pi ions are, therefore, essential for the formation of the endoskeletons typical of most vertebrates except cartilaginous fish.
Approximately 60 to 70 percent of Pi ions are cleared by the kidneys in healthy individuals. If PTH is elevated, Pi excretion is enhanced even more, so that Pi losses are further increased. Under the same conditions of elevated PTH, the secretion of Pi by the gut is also increased. The endogenous fecal secretion of phosphates is the second major route of loss that the body uses to maintain Pi ion homeostasis.
Persistently Elevated Parathyroid Hormone
Of the many diseases that have significant alterations in P homeostasis, only two are reviewed in any depth here. The first is persistently elevated PTH in response to a low Ca:P dietary intake pattern, whereas the second is renal secondary hyperparathyroidism resulting from chronic renal failure. Previously, the former was often referred to—perhaps erroneously in the case of humans (in contrast to animals)—as nutritional secondary hyperparathyroidism. In the context of human disease, the term “hyperparathyroidism” is inappropriate because the PTH levels that result from a low Ca:P ratio typically remain within the normal range of blood concentration, although usually at the high end of the range. As mentioned, a persistently elevated PTH, even if it remains within the normal range, contributes to increased bone turnover that can result in a reduction of bone mass and density (Calvo et al. 1990). If this condition continues for a year or longer, it could contribute to fragility fractures because of the thinning of trabecular plates at bone sites, such as the vertebrae, wrist, and proximal femur. On the basis of obtaining a benefit from a PTH value at the lower end of the range, individuals with a low Ca:P ratio would be advised to increase their calcium intake from foods first and from supplements second. An adequate calcium intake is known to reduce serum PTH concentration (Krall and Dawson-Hughes 1994).
Figure IV.B.5.4 diagrams the mechanism through which a low dietary Ca:P ratio contributes to the development of a persistently elevated PTH concentration. Figure IV.B.5.5 illustrates the potential changes in bone mass and mineralization of the skeleton in individuals who typically consume diets with low Ca:P ratios compared to those who have normal intake ratios.The persistently elevated PTH is responsible for the limited bone mineralization and the loss of bone mass (Anderson 1996).
Renal Secondary Hyperparathyroidism
Renal secondary hyperparathyroidism results from a severe increase in PTH that occurs because the kidneys can no longer filter and secrete sufficient amounts of Pi ions each day. As the blood concentration of Pi increases, the serum PTH also rises in an attempt to correct the error (increase of serum Pi). The action of PTH on bone tissue then predominates, and the rate of bone turnover continues to increase, unless corrected by renal dialysis or kidney transplantation. Without correction, the net result is a continuing increase in the serum Pi concentration and a rapid thinning of bone tissue at practically every site in the body. If severe enough, this condition can result in fractures at almost any skeletal location. Oral phosphate binders, such as aluminum or magnesium hydroxides, are usually administered to patients to reduce the amount of Pi absorbed by the small intestine and to enhance calcium absorption, but this strategy typically is not sufficient to stem the gradual increase in serum PTH as the disease progresses.
Potential Adverse Effects
“Over-the-counter” antacids contain mineral salts, which bind phosphate ions that are released from foods or secreted into the gut lumen by glands of the GI tract. If excessive amounts of these antacid drugs (also taken as nutrient supplements when containing calcium and/or magnesium) are ingested, individuals may be at increased risk of lowering their serum phosphate concentration to the point of serious deficiency. It is fortunate that the use of mineral antacids containing calcium, magnesium, aluminum, or some combination has declined greatly of late in the United States because of the availability of more effective antacid drugs that previously could only be obtained by prescription.
Phosphorus has important roles in human health. Phosphates participate in diverse functions in the body, both intracellularly and extracellularly as Pi and Po groups. These anions are especially important in energetic reactions within cells, in nucleic acids, and in other structural molecules and the extracellular tissues of bones and teeth. Dietary deficiency of this element is highly unlikely during practically the entire life cycle.
High intakes of P are common because of the natural widespread availability of phosphates in foods. Moreover, processed foods are likely to contain phosphate additives that contribute to a potentially excessive consumption of phosphorus by individuals in the United States and, most likely, in all economically developed nations throughout the world. When a chronic pattern of low Ca consumption is coupled with high dietary intakes of P (both Po and Pi), PTH becomes persistently elevated. The potential outcome is low bone mass and an increased risk of skeletal fractures, especially late in life. This adverse relationship between a high dietary P intake and bone loss strongly suggests that the consumption of adequate amounts of Ca are essential for the development and maintenance of bone mass throughout life.