Phosphorus is an essential element in the human body.
It is part of the phospholipid bilayer of cell membranes, is a structural component of bones and teeth and is important for growth and repair. Phosphorus functions also include production of cellular energy (adenosine triphosphate – ATP), buffering the pH of blood, regulation of gene transcription, activation of catalytic activity of enzymes and is involved in signal transduction of several key regulatory pathways. Date of preparation: February 2019.
Importance of phosphorus for health
Phosphorus is an essential part of all known protoplasm with a uniform content across most plant and animal tissues, with the exceptions of cells with a high ribonucleic acid or myelin content. It is most commonly present in nature as phosphate ions (PO43-).
Phosphorus is an essential element in the human body, being part of the phospholipid bilayer of cell membranes, and acting as a structural component of bones and teeth (1). Further, phosphorus functions in critical metabolic pathways to produce and store energy in the adenosine triphosphate (ATP) molecule (1, 2), it buffers the pH of the blood, regulates gene transcription, activates the catalytic activity of enzymes and permits signal transduction for regulatory pathways affecting several organ functions from renal excretion to the immune response (1, 3). Since these reactions do not consume phosphorus indefinitely, the function of dietary phosphorus intake is to support tissue growth, and to replace losses due to growth and excretion (3).
Tissue phosphorus concentration ranges from about 7.8 to 20.1 mg (0.25-0.65 mmol) per g protein (3), and phosphorus makes up about 1% of total body weight (1). About 80% of the phosphorus component of an adult body is held in bone as hydroxyapatite, with the rest distributed through the soft tissues (4). Phosphorus is the main component of phospholipids, which make up most biological membranes, in addition to nucleotides and nucleic acids. In whole blood, most of the phosphorus is in this form, phospholipids of red blood cells, though about 3.1 mg/dl is present as inorganic phosphate (3). Though this is <1% of total body phosphorus, this fraction is critical: for example, osteoblasts require a critical level of inorganic phosphate in the extracellular fluid surrounding these cells for proper functioning, and a depletion impairs osteoblast function and limits mineral deposition in bone (3).
Dietary phosphorus exists as a mixture of inorganic and organic forms, the organic form being hydrolysed by intestinal phosphatases so that most phosphorus is absorbed as inorganic phosphate. This mainly occurs by a passive, concentration-dependent process, however a portion of dietary phosphorus is absorbed via an active transport system facilitated by 1,25-dihydroxyvitamin D. Phosphorus homeostasis is maintained in adults by keeping urinary excretion equivalent to net absorption, with equal amounts deposited and resorbed from bone (1). Regulation is achieved via a complex relationship between bone, kidney and the intestine (1). Phosphorus concentrations are regulated alongside those of calcium by vitamin D, PTH and FGF23.
Phosphorus is widely available in many foods, and bioavailability is generally good, though from plant sources, it may be limited by being present as a complex with phytic acid. Some colonic bacteria can hydrolyse phytic acid, thereby liberating the phosphorus, as can yeasts, thus leavened bread products have a higher phosphorus bioavailability than unleavened bread (3). Phytic acid can also complex with other mineral ions in the intestine e.g. calcium and zinc, which not only blocks the absorption of these minerals, but blocks the hydrolysis of phytate, thereby interfering with the liberation and subsequent absorption of phosphorus(5). This may explain why calcium can inhibit phosphorus uptake. Otherwise, despite much past literature on the ratio of calcium and phosphorus in the diet, a review concluded that there is little evidence that this ratio is important during most of life (3).
Dietary phosphorus deficiency is rare due to the wide availability of phosphorus in the diet and mechanisms in the body to conserve phosphorus. Risk of deficiency is greater with anorexia or alcoholism, and other physiological disorders including genetic disorders and those related to tumours (1). Dietary phosphorus absorption is reduced by aluminium-containing antacids and pharmacologic doses of calcium carbonate (though ingestion within normal recommendations does not interfere with phosphorus absorption) (3).
Depletion of phosphorus leads to low circulating phosphorus (hypophosphatemia) and low urinary phosphorus excretion. Because of the close relationship between calcium and phosphorus excretion, chronically low phosphorus can lead to rickets in children and osteomalacia in adults, however such phosphopenic rickets is usually due to genetic or renal disorders affecting phosphate reabsorption (6).
The risk of excessive phosphorus intake in the modern diet is greater than the risk of inadequacy. The extent and usage of phosphate salts as additives has increased substantially. Phosphates are used for moisture retention, smoothness and binding (3), rather than for a nutritive function. Phosphate intakes may be substantial in those consuming a diet reliant on processed foods, and with a high consumption of cola beverages.
Analysis of the US NHANES III dietary data revealed an association between high dietary phosphorous consumption and increased risk of all-cause mortality in healthy US adults with a normal kidney function (7). The elevated phosphorus intake corresponding to adverse effects occurred at a threshold of 1400 mg P/day. Though this equates to twice the US recommended daily allowance, over one-third of Americans reported consuming >1400 mg P/day, indicating a potentially important public health problem (7).
Elsewhere in the literature, elevated serum phosphorus levels have been associated with indicators for cardiovascular disease (8), though much of the literature to date is mainly focused on subjects with concomitant kidney disease, and epidemiologic data linking dietary phosphorus intake in healthy adults and morbidity or mortality due to cardiovascular disease are too weak to form conclusions (9).