decreased absorption of calcium and increased urinary loss of calcium (Nordin et al., 2004). Evidence suggests that remodeling in women becomes imbalanced just prior to, during, and immediately after menopause, when the rate of bone loss becomes more rapid. However, the rate of bone loss as a result of menopause varies greatly depending upon a number of factors, including genetics, body composition, other hormonal changes and endogenous production of estradiol.

The effects of lower estrogen levels on calcium balance continue to be debated. However, the principal effect of estrogen deficiency on the skeleton is increased bone resorption. The range of bone loss in the 7 to 10 years around the onset of menopause can range from 3 to 7 percent annually (Kenny and Prestwood, 2000). In women over age 65, the rate of bone loss slows again to 0.5 to 2 percent per year (Greenspan et al., 1994). Later in menopause—and in men over 70 years of age—if reduced calcium intake occurs, it contributes to a secondary form of hyperparathyroidism, which serves as a compensatory mechanism to maintain extracellular calcium balance. This compensation results in accelerated bone resorption, leading to a net loss of bone mass under these conditions.

For men over 65 years of age, the loss of bone is about 1 to 2 percent per year (Orwoll et al., 1990; Hannan et al., 1992). Additionally, reduced glomerular filtration rate is another factor associated with aging that affects renal conservation of calcium in both men and women (Goldschmied et al., 1975) and also leads to secondary hyperparathyroidism, which can cause significant bone loss. This is underscored by patients with renal disease who have renal osteodystrophy, now referred to as chronic kidney disease–mineral disorder (Demer and Tintut, 2010; Peacock, 2010).

The fetal need for calcium is met by maternal physiological changes, primarily through increased calcium absorption. There is currently debate about whether calcium is also mobilized from maternal skeleton, as discussed in Chapter 4. In any case, calcium is actively transported across the placenta from mother to fetus, an essential activity to mineralizing the fetal skeleton. Calcium accretion in the developing fetus is low until the third trimester of pregnancy when the fetus requires about 200 to 250 mg/day calcium to sustain skeletal growth (Givens and Macy, 1933; Trotter and Hixon, 1974). Intestinal calcium absorption of the mother doubles beginning early in pregnancy—even though there is little calcium transfer to the embryo at this stage (Heaney and Skillman, 1971; Kovacs and Kronenberg, 1997)—and continues through late pregnancy (Kent et al., 1991). Overall,