Abstract
Calcium seems to be an intuitively integral part of the treatment of osteoporosis. This is for several reasons. First, osteoporosis, in its original definition, is effectively a disease characterized by a reduced calcium nutrient reserve (i.e., bone mass). Second, animals reared on reduced calcium intakes fail to develop the full bone mass programmed into their genomes. Third, adult animals placed on calcium-deficient diets, lose bone, that is, they draw upon their calcium reserve to support their extraskeletal needs for calcium. Consistent with this intuitive involvement of calcium in the genesis and treatment of osteoporosis is a substantial body of human evidence showing that, so long as intakes of other nutrients are adequate, increased calcium intake produces a substantial antiosteoporosis effect. However, certain features of the action of calcium remain unclear and even puzzling. This chapter will review this use and the questions attending it, while Chapter 32 (Heaney) covers what is known of the metabolism of calcium, and the basis for the calcium intake requirement.