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alization (formation) to occur normally (Marel et al., 1986) and play a passive role in any mass changes that occur. They help to replace minerals lost by obligatory processes (in urine, feces, and sweat) or those normally distributed to bone and soft tissues (Heaney, 1986).

Maximum bone mass is achieved by about 25 to 30 years of age, is maintained without much change until 35 to 45 years of age, and is lost at a constant rate of 0.2 to 0.5% per year in men and women thereafter (Heaney, 1986; Marcus, 1982; Parfitt, 1983). About 8 to 10 years immediately before and after menopause, women lose bone at a rate of 2 to 5% per year. Subsequently, bone loss returns to the slower rate shared by the sexes. Those few men who also lose sex hormone function usually very late in life (>70 years) also lose bone mass at rates similar to postmenopausal women (Odell and Swerdloff, 1976).

Evidence Associating Dietary Factors with Osteoporosis

Epidemiologic and Clinical Studies
Calcium
Absorption and Balance

Calcium balance generally reflects the degree to which bone formation is coupled with resorption (see Chapter 13). Thus, negative balances are recorded when bone resorption exceeds formation, and positive balances occur when bone formation exceeds bone resorption. Since 99% of the body's calcium is located in bone, it is not possible to build bone without positive calcium balance or to be in negative balance without losing bone. The metabolic technique used to determine calcium balance has important theoretical and practical limitations that can result in inaccuracies in determining the amount of dietary calcium needed to achieve zero balance—data that are key to determining nutritional requirements for calcium.

Calcium balance depends on such factors as the amount of calcium in the diet, the efficiency of calcium absorption by the intestine, and the losses of calcium in the urine, feces, and sweat. Intestinal absorption decreases with age (Gallagher et al., 1979; Ireland and Fordtran, 1973). This may be due to the age-related decrease in serum levels of 1,25-dihydroxy vitamin D [1,25(OH)2D3] (Tsai et al., 1984)—the biologically active metabolite of vitamin D produced by the kidney that regulates intestinal absorption of calcium (DeLuca, 1983; Norman, 1985). The age-related decrease in calcium absorption may lead to secondary hyperparathyroidism. That this endocrine adaptive response occurs is supported by the observation that serum immunoreactive and bioactive parathyroid hormone increases with age (Forero et al., 1987). Whether this response to decreased calcium absorption contributes to the decreased skeletal mass and increased incidence of fractures in the elderly is not known.

Relationship of Dietary Calcium to Bone Mass, Osteoporosis, and Fracture

There are two major methodological problems involved in evaluating the evidence relating dietary calcium to bone mass (see Chapter 13). First are the inaccuracies inherent in determining dietary calcium by historical recall. Second are the different methods used to measure bone mass—some measure predominantly cortical bone and others measure predominantly trabecular bone.

Decreased skeletal mass is the most important risk factor for bone fracture without significant trauma (Heaney, 1986; Heaney et al., 1982; Parfitt, 1983; Riggs and Melton, 1986). It is important to achieve genetically programmed peak bone mass, because the greater the mass attained before age-related loss, the less likely bone loss will reach the level at which fracture will occur (Heaney, 1986; Marcus, 1982; Parfitt, 1983).

The quantity of dietary calcium  required to achieve peak bone mass is greater than that required to replace obligatory losses of this ion in urine, feces, and sweat (approximately 200 to 300 mg/day). Thus, as described in Chapter 13, people under the age of 25 years need to ingest sufficient calcium to ensure that they absorb more calcium from their intestines than they excrete and thus achieve positive balance.

Many published reports have shown either no relationship or only a modest positive relationship between dietary calcium and cortical bone mass (see Chapter 13). The most widely cited of the papers showing a positive effect of calcium is that of Matkovic et al. (1979), who reported a 5 to 10% greater metacarpal cortical volume in the inhabitants of a Yugoslavian district with a high calcium intake as compared with the inhabitants of a Yugoslavian district with a low calcium intake. The population in the high-calcium district also consumed more calories, fats, and protein and fewer carbohydrates than did the population in the low-calcium district. People in the high-calcium district had a 50% lower incidence of hip fractures and a significantly greater metacarpal cortical bone



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