24: Phosphorus (Chapter 23b)
- Page ID
- 117202
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\(\newcommand{\avec}{\mathbf a}\) \(\newcommand{\bvec}{\mathbf b}\) \(\newcommand{\cvec}{\mathbf c}\) \(\newcommand{\dvec}{\mathbf d}\) \(\newcommand{\dtil}{\widetilde{\mathbf d}}\) \(\newcommand{\evec}{\mathbf e}\) \(\newcommand{\fvec}{\mathbf f}\) \(\newcommand{\nvec}{\mathbf n}\) \(\newcommand{\pvec}{\mathbf p}\) \(\newcommand{\qvec}{\mathbf q}\) \(\newcommand{\svec}{\mathbf s}\) \(\newcommand{\tvec}{\mathbf t}\) \(\newcommand{\uvec}{\mathbf u}\) \(\newcommand{\vvec}{\mathbf v}\) \(\newcommand{\wvec}{\mathbf w}\) \(\newcommand{\xvec}{\mathbf x}\) \(\newcommand{\yvec}{\mathbf y}\) \(\newcommand{\zvec}{\mathbf z}\) \(\newcommand{\rvec}{\mathbf r}\) \(\newcommand{\mvec}{\mathbf m}\) \(\newcommand{\zerovec}{\mathbf 0}\) \(\newcommand{\onevec}{\mathbf 1}\) \(\newcommand{\real}{\mathbb R}\) \(\newcommand{\twovec}[2]{\left[\begin{array}{r}#1 \\ #2 \end{array}\right]}\) \(\newcommand{\ctwovec}[2]{\left[\begin{array}{c}#1 \\ #2 \end{array}\right]}\) \(\newcommand{\threevec}[3]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \end{array}\right]}\) \(\newcommand{\cthreevec}[3]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \end{array}\right]}\) \(\newcommand{\fourvec}[4]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \\ #4 \end{array}\right]}\) \(\newcommand{\cfourvec}[4]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \\ #4 \end{array}\right]}\) \(\newcommand{\fivevec}[5]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \\ #4 \\ #5 \\ \end{array}\right]}\) \(\newcommand{\cfivevec}[5]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \\ #4 \\ #5 \\ \end{array}\right]}\) \(\newcommand{\mattwo}[4]{\left[\begin{array}{rr}#1 \amp #2 \\ #3 \amp #4 \\ \end{array}\right]}\) \(\newcommand{\laspan}[1]{\text{Span}\{#1\}}\) \(\newcommand{\bcal}{\cal B}\) \(\newcommand{\ccal}{\cal C}\) \(\newcommand{\scal}{\cal S}\) \(\newcommand{\wcal}{\cal W}\) \(\newcommand{\ecal}{\cal E}\) \(\newcommand{\coords}[2]{\left\{#1\right\}_{#2}}\) \(\newcommand{\gray}[1]{\color{gray}{#1}}\) \(\newcommand{\lgray}[1]{\color{lightgray}{#1}}\) \(\newcommand{\rank}{\operatorname{rank}}\) \(\newcommand{\row}{\text{Row}}\) \(\newcommand{\col}{\text{Col}}\) \(\renewcommand{\row}{\text{Row}}\) \(\newcommand{\nul}{\text{Nul}}\) \(\newcommand{\var}{\text{Var}}\) \(\newcommand{\corr}{\text{corr}}\) \(\newcommand{\len}[1]{\left|#1\right|}\) \(\newcommand{\bbar}{\overline{\bvec}}\) \(\newcommand{\bhat}{\widehat{\bvec}}\) \(\newcommand{\bperp}{\bvec^\perp}\) \(\newcommand{\xhat}{\widehat{\xvec}}\) \(\newcommand{\vhat}{\widehat{\vvec}}\) \(\newcommand{\uhat}{\widehat{\uvec}}\) \(\newcommand{\what}{\widehat{\wvec}}\) \(\newcommand{\Sighat}{\widehat{\Sigma}}\) \(\newcommand{\lt}{<}\) \(\newcommand{\gt}{>}\) \(\newcommand{\amp}{&}\) \(\definecolor{fillinmathshade}{gray}{0.9}\)The essential nutrient phosphorus (in nature occurring as phosphate) is ubiquitous in all the foods we eat, the human body and, in effect, all living organisms. phosphate is critical to structural and biochemical functions needed to secure energy, reproduce and grow. Most of the body's phosphate is contained within bones, teeth, membranes and intracellular spaces; however, it is the 1% present in the extracellular space, serum that is clinically measured to inform about physiologic and nutritional phosphate status.
Serum phosphate in healthy individuals usually reflects phosphate balance that is maintained within a narrow range by hormonal control of renal reabsorption and excretion, and intestinal absorption when dietary phosphate intakes are low or excessive. Regulation of serum phosphate involves the interplay of four organs (kidneys, intestine, bone and parathyroid glands), phosphate in these organs, and the actions of three endocrine hormones (parathyroid hormone, calcitriol (the active form of vitamin D), and bone-secreted fibroblast growth factor‑23 (FGF‑23), all of which influence the activity of the phosphate transporters to increase or decrease absorption, reabsorption or excretion of phosphate.
Hyperphosphatemia (i.e., serum phosphate > 1.45mmol/L) is often related to excess dietary phosphate intake by the consumption of phosphate additive-rich processed foods, or the typical Western diets when kidney function is impaired. Higher serum phosphate has been associated with disruption of endocrine pathways that may link high phosphate intake with pathology associated with chronic disease risk, including cardiovascular disease. In contrast, hypophosphatemia (i.e., serum phosphate < 0.87mmol/L) is rarely related to dietary deficiency of phosphate except in cases of severe malnutrition, and more likely due to inborn errors of metabolism or tumor production of excess FGF‑23 that causes renal phosphate wasting and bone disease (rickets and osteomalacia).
- 24.1: Phosphorus (23b.1)
- This page discusses the importance of phosphorus, the 11th most abundant element, which exists mainly as phosphate and is vital for living organisms' growth. It highlights how limited phosphate-rich rock deposits contribute to soil fertility through microbial activity. Phosphorus is crucial for energy production, growth, and cellular functions but requires careful regulation, as both deficiency and excess can adversely affect health and development.
- 24.2: Biological forms of phosphate and their measurement (23b.2)
- This page details the various forms of phosphorus in nature, such as ionic anions, inorganic salts, and organic compounds like phytate. It underscores the role of inorganic phosphates in the human body, particularly in bones and teeth as calcium phosphate hydroxyapatite. The text discusses the detection of inorganic phosphate in biological samples and measurement methods, noting the common interchangeable use of phosphate and phosphorus in clinical contexts.
- 24.3: Interpretive criterion- serum phosphate (23b.3)
- This page discusses serum phosphate as the main biomarker for phosphorus status, noting that a single measurement can misrepresent total body phosphorus due to variations influenced by factors like age, sex, and seasonal shifts. Normal phosphate levels vary among populations, with children generally having higher levels than adults. Imbalances in serum phosphate can lead to health conditions such as hypophosphatemia and hyperphosphatemia, both associated with serious health risks.
- 24.4: Phosphate balance (23b.4)
- This page discusses the phosphate balance in the body, highlighting the roles of intestinal absorption, renal excretion, and phosphate exchange among different pools. Serum phosphate concentration is a key clinical indicator, but it reflects only a fraction of total body phosphate. The kidneys reabsorb approximately 89% of filtered phosphate, while gastrointestinal absorption averages 60-65%.
- 24.5: Hormonal regulation of serum phosphate (23b.5)
- This page discusses the regulation of serum phosphate levels by the kidneys, bones, intestines, and parathyroid glands, highlighting the roles of hormones such as PTH, calcitriol, and FGF-23. These elements work together to maintain phosphate balance, and any disruption can lead to health issues like hyperphosphatemia, soft tissue calcification, and cardiovascular disease, requiring hormonal adjustments to restore normal phosphate levels.
- 24.6: Nutrient reference values (23b.6)
- This page discusses the 1997 establishment of phosphorus intake guidelines by the Institute of Medicine, setting the Estimated Average Requirement for adults at 580 mg/d and the upper limit at 4000 mg/d. It notes rising concerns about high phosphorus intake from ultra-processed foods in the American diet, prompting a reevaluation of safety levels. Additionally, the European Food Safety Authority has recently reduced the acceptable daily intake for phosphate.
- 24.7: Dietary sources
- This page discusses dietary phosphate sources, highlighting that animal proteins are more bioavailable than plant-based ones, which often contain less absorbable phytate. It notes the prevalence of ultra-processed foods in the US, linked to chronic diseases, and the underreporting of phosphorus intake due to inadequate data on additives.
- 24.8: Abnormalities in serum phosphate (23b.8)
- This page discusses phosphate balance assessment primarily through fasting serum phosphate levels, noting that acute changes may distort actual body stores. It contrasts hypophosphatemia and hyperphosphatemia, highlighting their causes and symptoms. Factors affecting phosphate levels encompass diet, absorption, and renal excretion, with notable variations based on time and demographics.
- 24.9: Inherited and tumor-induced disorders of phosphate metabolism
- This page discusses rare genetic disorders related to phosphate metabolism, especially chronic hypophosphatemia, which are not caused by diet. It highlights key disorders like X-Linked Hypophosphatemic Rickets and others, resulting from FGF-23 metabolism mutations, leading to phosphate wasting and conditions like rickets. Treatment includes oral phosphate and biologics.