nels known as transient receptor potential cation channel, vanilloid family member 5 or TRPV5 control active calcium transport and this process is regulated by calcitriol and estradiol (Hoenderop et al., 2000). Finally, the collecting duct also can participate in passive calcium transport, although the relative percentage of total calcium reabsorption in the collecting duct is low. Overall, a typical daily calcium loss for a healthy adult man or woman via renal excretion is 5 mmol/day (Weaver and Heaney, 2006a).
Calcium is excreted through the feces as unabsorbed intestinal calcium and is shed in mucosal cells and secretions including saliva, gastric juices, pancreatic juice, and bile. Endogenous fecal calcium losses are approximately 2.1 mg/kg per day in adults and about 1.4 mg/kg per day in children (Abrams et al., 1991). These intestinal losses as well as minor losses in sweat are referred to collectively as endogenous calcium excretion. Endogenous calcium excretion, in contrast to urinary excretion, does not change appreciably with aging (Heaney and Recker, 1994).
PTH can be a major determinant of urinary calcium excretion; during states of low calcium intake, secondary increases in PTH levels result in reduced urinary calcium excretion. Impaired renal function due to aging paradoxically reduces calcium loss due to impaired filtration, but there is also a secondary increase in PTH levels due to reduced phosphate clearance. However, renal 1α-hydroxylase activity declines with impaired renal function, so the net result is calcium loss from the kidney, but also reduced active transport of calcium from the intestine.
Although excess intake of calcium is almost never due to calcium intake from foods, the use of calcium supplements (including the voluntary fortification of a range of foods that are not naturally sources of calcium) has increased (Ricci et al., 1998; Riedt et al., 2005), and excess calcium intake may occur as a result of high intake from calcium supplements. Excess calcium intake can result in adverse effects. Calcium plays a major role in the metabolism of virtually every cell in the body and interacts with a large number of other nutrients, and as a result, disturbances of calcium metabolism may give rise to a variety of adverse effects (IOM, 1997). A review of the considerations related to adverse effects from excess calcium ingestion can be found in Chapter 6, which focuses on the establishment of Tolerable Upper Intake Levels (ULs).
Calcium is an integral component of the skeleton, and the skeleton provides a reservoir of calcium for other essential calcium-dependent functions throughout the body. The skeleton serves at least three main func-