23.3: Absorption and metabolism of calcium (23a.3)
- Page ID
- 117184
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\(\newcommand{\avec}{\mathbf a}\) \(\newcommand{\bvec}{\mathbf b}\) \(\newcommand{\cvec}{\mathbf c}\) \(\newcommand{\dvec}{\mathbf d}\) \(\newcommand{\dtil}{\widetilde{\mathbf d}}\) \(\newcommand{\evec}{\mathbf e}\) \(\newcommand{\fvec}{\mathbf f}\) \(\newcommand{\nvec}{\mathbf n}\) \(\newcommand{\pvec}{\mathbf p}\) \(\newcommand{\qvec}{\mathbf q}\) \(\newcommand{\svec}{\mathbf s}\) \(\newcommand{\tvec}{\mathbf t}\) \(\newcommand{\uvec}{\mathbf u}\) \(\newcommand{\vvec}{\mathbf v}\) \(\newcommand{\wvec}{\mathbf w}\) \(\newcommand{\xvec}{\mathbf x}\) \(\newcommand{\yvec}{\mathbf y}\) \(\newcommand{\zvec}{\mathbf z}\) \(\newcommand{\rvec}{\mathbf r}\) \(\newcommand{\mvec}{\mathbf m}\) \(\newcommand{\zerovec}{\mathbf 0}\) \(\newcommand{\onevec}{\mathbf 1}\) \(\newcommand{\real}{\mathbb R}\) \(\newcommand{\twovec}[2]{\left[\begin{array}{r}#1 \\ #2 \end{array}\right]}\) \(\newcommand{\ctwovec}[2]{\left[\begin{array}{c}#1 \\ #2 \end{array}\right]}\) \(\newcommand{\threevec}[3]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \end{array}\right]}\) \(\newcommand{\cthreevec}[3]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \end{array}\right]}\) \(\newcommand{\fourvec}[4]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \\ #4 \end{array}\right]}\) \(\newcommand{\cfourvec}[4]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \\ #4 \end{array}\right]}\) \(\newcommand{\fivevec}[5]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \\ #4 \\ #5 \\ \end{array}\right]}\) \(\newcommand{\cfivevec}[5]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \\ #4 \\ #5 \\ \end{array}\right]}\) \(\newcommand{\mattwo}[4]{\left[\begin{array}{rr}#1 \amp #2 \\ #3 \amp #4 \\ \end{array}\right]}\) \(\newcommand{\laspan}[1]{\text{Span}\{#1\}}\) \(\newcommand{\bcal}{\cal B}\) \(\newcommand{\ccal}{\cal C}\) \(\newcommand{\scal}{\cal S}\) \(\newcommand{\wcal}{\cal W}\) \(\newcommand{\ecal}{\cal E}\) \(\newcommand{\coords}[2]{\left\{#1\right\}_{#2}}\) \(\newcommand{\gray}[1]{\color{gray}{#1}}\) \(\newcommand{\lgray}[1]{\color{lightgray}{#1}}\) \(\newcommand{\rank}{\operatorname{rank}}\) \(\newcommand{\row}{\text{Row}}\) \(\newcommand{\col}{\text{Col}}\) \(\renewcommand{\row}{\text{Row}}\) \(\newcommand{\nul}{\text{Nul}}\) \(\newcommand{\var}{\text{Var}}\) \(\newcommand{\corr}{\text{corr}}\) \(\newcommand{\len}[1]{\left|#1\right|}\) \(\newcommand{\bbar}{\overline{\bvec}}\) \(\newcommand{\bhat}{\widehat{\bvec}}\) \(\newcommand{\bperp}{\bvec^\perp}\) \(\newcommand{\xhat}{\widehat{\xvec}}\) \(\newcommand{\vhat}{\widehat{\vvec}}\) \(\newcommand{\uhat}{\widehat{\uvec}}\) \(\newcommand{\what}{\widehat{\wvec}}\) \(\newcommand{\Sighat}{\widehat{\Sigma}}\) \(\newcommand{\lt}{<}\) \(\newcommand{\gt}{>}\) \(\newcommand{\amp}{&}\) \(\definecolor{fillinmathshade}{gray}{0.9}\)Calcium balance refers to the state of the calcium body stores (in bone) which are a function of dietary intake, intestinal absorption, renal excretion, and bone remodeling. A major control of calcium balance is the amount of calcium absorbed. Calcium is absorbed across the intestinal mucosa in two ways: active transport and passive para-cellular diffusion. Active absorption of calcium is influenced by calcium and vitamin D status of the individual, age, pregnancy, and lactation. Active absorption occurs when intakes of calcium are low relative to need, and is regulated primarily via 1,25(OH)2D and its intestinal receptors. Passive absorption is more important at high intakes of calcium (Weaver and Peacock, 2019).
Efficiency of calcium absorption is highest when dietary calcium intakes are low or during periods of rapid growth in infancy, early childhood, and adolescence, and during pregnancy and lactation. Indeed, absorption is very high during infancy (about 60%) (Abrams et al., 1997) and about 34% during puberty (Abrams and Stuff, 1994), stabilizing at about 25–30% in young adults. Subsequently, the intestinal absorption of calcium decreases progressively with age (Christakos et al., 2011).
Urinary calcium excretion is also regulated in response to need. Normally calcium re-absorption in the kidney nephrons is not 100%. When there is hypocalcemia to stimulate PTH release, one action of PTH is to increase efficiency of calcium re-absorption thus reducing calcium losses in urine(Peacock, 2010). Several dietary variables affect both calcium absorption and retention and, hence, calcium status. Diets high in protein increase the urinary excretion of calcium (hypercalciuria), which, however, is compensated by increased calcium absorption (Mangano et al., 2014). Dietary sodium also influences urinary calcium losses, with high sodium intakes increasing urinary calcium losses (Bedford and Barr, 2011), and lowering bone density in women (Devine et al., 1995). Caffeine, like protein and sodium, also increases urinary calcium loss but has only a small negative effect on calcium retention, which can be offset by increasing dietary calcium intakes (Barrett-Connor et al., 1994).
High phosphorus intakes reduce urinary calcium losses (i.e., have a hypocalciuric effect), but because they increase losses of endogenous fecal calcium at the same time (Heaney and Recker, 1994), their net effect on calcium balance is still under debate. One might assume that there would be no effect except in conditions in which the coordination between calcium and phosphate homeostasis occurs through the actions of PTH, FGF‑23 and 1,25(OH)2D. The disruption of this coordination, however, can occur with disease states such as chronic kidney disease (CKD) (Peacock, 2010).However, increasing dietary phosphorus through inorganic phosphate additives may have detrimental effects on bone and mineral metabolism in humans and animals (Vorland et al., 2017).
Phytates and oxalates can inhibit the absorption of calcium by forming insoluble calcium complexes in the gastrointestinal tract (Barger‑Lux et al., 1995). Hence, they may have a negative effect on calcium status, although their overall effect may be small unless dietary calcium intakes are low. Some other dietary components, including lactose and inulin, enhance passive calcium absorption by increasing calcium solubility in the ileum (Weaver et al., 2016).
Several clinical conditions are associated with disturbances in calcium absorption. Calcium malabsorption is associated with gastrointestinal diseases such as Crohn's and celiac disease, and intestinal resection or bypass. Intestinal absorption of calcium is also impaired in patients with renal failure, caused by the reduced synthesis of 1,25‑dihydroxyvitamin D (Peacock, 2010). Excessive intestinal absorption of calcium and hypercalcemia occur in sarcoidosis, when excessive calcitriol appears in serum, and also in vitamin D intoxication.