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With aging and after menopause, fractional calcium absorption has been reported to decline on average by 0.21 percent per year after 40 years of age (Heaney et al., 1989). Nordin et al. (2004) and Aloia et al. (2010) also reported decreased absorption with age. There are early reports of an inverse correlation between age and calcium absorption in women (Avioli et al., 1965), and several studies have indicated that despite an increase in circulating levels of calcitriol in older women, which would be anticipated to increase calcium uptake, fractional calcium absorption was unaffected (Bullamore et al., 1970; Alevizaki et al., 1973; Gallagher et al., 1979; Tsai et al., 1984; Eastell et al., 1991; Ebeling et al., 1992). Thus, although calcium absorption (active calcium transport) has been reported to decrease with age, it is challenging to take this factor into consideration given that calcium intake must be very high to have a significant effect on calcium uptake via the passive absorption.

Homeostatic Regulation of Calcium

Maintaining the level of circulating ionized calcium within a narrow physiological range is critical for the body to function normally, and control of serum calcium levels is maintained through an endocrine system—a system of glands that secrete hormones and is characterized by controlling factors and feedback mechanisms—that includes a major role for vitamin D metabolites, principally calcitriol, and PTH. Calcium balance within the body is closely linked to the hormonal actions of calcitriol. The vitamin D-related endocrine system that maintains serum calcium levels is discussed in Chapter 3 but is also summarized below and illustrated in Figure 2-1.

The vitamin D metabolic system forms the basis of the calcium homeostatic mechanism in mammals. Total calcium concentration in serum is tightly regulated to remain between 8.5 and 10.5 mg/dL (2.12 and 2.62 mmol/L). If this level deviates slightly, the calcium sensing receptor of the parathyroid gland signals the secretion of PTH, which functions as a calcium sensor. PTH then stimulates the kidney to produce calcitriol, the hormonal form of vitamin D, as well as to activate bone resorption, which will increase extracellular calcium levels. Calcitriol acts in an endocrine manner on the intestine, bone, and kidney to raise serum calcium levels; it also acts on the intestine and, to some extent, the kidneys to raise serum phosphorus levels. As the serum calcium level rises, the feedback mechanism causes the calcium sensing receptor to be turned off and PTH secretion to drop. If there is an overshoot in serum calcium levels, the “C” cells (parafollicular) cells of the thyroid gland secrete calcitonin, which can block bone calcium resorption, helping to keep serum calcium levels in the normal range. Calcitriol, through its receptor, also provides feedback relative to suppressing the production and release of PTH, commonly referred



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