Calcium is an essential nutrient that is involved in most metabolic processes and the phosphate salts of which provide mechanical rigidity to the bones and teeth, where 99% of the body’s calcium resides. The calcium in the skeleton has the additional role of acting as a reserve supply of calcium to meet the body’s metabolic needs in states of calcium deficiency. Calcium deficiency is easily induced because of the obligatory losses of calcium via the bowel, kidneys, and skin. In growing animals, it may impair growth, delay consolidation of the skeleton, and in certain circumstances give rise to rickets but the latter is more often due to deficiency of vitamin D. In adult animals, calcium deficiency causes mobilization of bone and leads sooner or later to osteoporosis, i.e., a reduction in the “amount of bone in the bone” or apparent bone density. The effects of calcium deficiency and oophorectomy (ovariectomy) are additive. In humans, osteoporosis is a common feature of aging. Loss of bone starts in women at the time of the menopause and in men at about age 55 and leads to an increase in fracture rates in both sexes. Individual fracture risk is inversely related to bone density, which in turn is determined by the density achieved at maturity (peak bone density) and the subsequent rate of bone loss. At issue is whether either or both of these variables is related to calcium intake. The calcium requirement of adults may be defined as the mean calcium intake needed to preserve calcium balance, i.e., to meet the significant obligatory losses of calcium through the gastrointestinal tract, kidneys, and skin. The calcium allowance is the higher intake recommended for a population to allow for individual variation in the requirement. The mean requirement defined in this way, calculated from balance studies, is about 20 mmol (800 mg) a day on Western diets, implying an allowance of 25 mmol (1000 mg) or more. Corresponding requirements and allowances have been calculated for pregnancy and lactation and for children and adolescents, taking into account the additional needs of the fetus, of milk production, and of growth. There is a rise in obligatory calcium excretion at menopause, which increases the theoretical calcium requirement in postmenopausal women to about 25 mmol (1000 mg) and implies an allowance of perhaps 30 mmol (1200 mg) or even more if calcium absorption declines at the same time. At issue here, however, is whether menopausal changes in calcium metabolism are the cause or the result of postmenopausal bone loss. The first interpretation relies on evidence of a positive action of estrogen on the gastrointestinal absorption and renal tubular reabsorption of calcium; the latter interpretation relies on evidence of a direct inhibitory effect of estrogen on bone resorption. The calcium model for postmenopausal bone loss tends to be supported by the effect of calcium therapy. An analysis of the 20 major calcium trials in postmenopausal women reported in the last 20 years yielded a mean rate of bone loss of 1.00% per annum (p.a.) in the controls and 0.014% p.a. (NS) in the treated subjects (P < 0.001). However, trials in which calcium and estrogen have been directly compared have shown that the latter is generally more effective than calcium in that it produces a small, but often significant bone gain. This superiority of estrogen over calcium could be due to the former's dual action on calcium absorption and excretion or to a direct action of estrogen on bone itself. In older women, the importance of calcium intake is overshadowed by the strong association between vitamin D insufficiency and hip fracture. Whether this insufficiency arises primarily from lack of exposure to sunlight or to a progressive failure to activate the vitamin D precursor in the skin or both is uncertain but it is compounded by a general decline in dietary vitamin D intake with age. The biological effect is probably an impairment of calcium absorption and c

Nordin BE
Nutrition 1997 Jul-Aug;13(7-8):664-86
PMID: 9263260