CALCIUM AND OSTEOPOROSIS

Authors
Citation
Bec. Nordin, CALCIUM AND OSTEOPOROSIS, Nutrition, 13(7-8), 1997, pp. 664-686
Citations number
262
Categorie Soggetti
Nutrition & Dietetics
Journal title
Nutrition
ISSN journal
08999007 → ACNP
Volume
13
Issue
7-8
Year of publication
1997
Pages
664 - 686
Database
ISI
SICI code
0899-9007(1997)13:7-8<664:CAO>2.0.ZU;2-T
Abstract
Calcium is an essential nutrient that is involved in most metabolic pr ocesses and the phosphate salts of which provide mechanical rigidity t o the bones and teeth, where 99% of the body's calcium resides. The ca lcium in the skeleton has the additional role of acting as a reserve s upply of calcium to meet the body's metabolic needs in states of calci um deficiency. Calcium deficiency is easily induced because of the obl igatory losses of calcium via the bowel, kidneys, and skin. In growing animals, it may impair growth, delay consolidation of the skeleton, a nd in certain circumstances ve rise to rickets but the latter is more often due to deficiency of vitamin D. In adult animals? calcium defici ency causes mobilization of bone and leads sooner or later to osteopor osis, i.e., a reduction in the ''amount of bone in the bone'' or appar ent 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 a nd in men at about age 55 and leads to an increase in fracture rates i n both sexes. Individual fracture risk is inversely related to bone de nsity, 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 intak e. The calcium requirement of adults may be defined as the mean calciu m intake needed to preserve calcium balance, i.e., to meet the signifi cant obligatory losses of calcium through the gastrointestinal tract, kidneys, and skin. The calcium allowance is the higher Intake recommen ded for a population to allow for individual variation in the requirem ent. The mean requirement defined in this way, calculated from balance studies, is about 20 mmol (800 mg) a day on Western diets,;implying a n allowance of 25 mmol (1000 mg) or more. Corresponding requirements a nd 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 obli gatory 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 i f 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 reli es on evidence of a positive action of estrogen on the gastrointestina l absorption and renal tubular reabsorption of calcium; the latter int erpretation relies on evidence of a direct inhibitory effect of estrog en on bone resorption. The calcium model for postmenopausal bone loss lends to be supported by the effect of calcium therapy. An analysis of the 20 major calcium trials in postmenopausal women reported in the l ast 20 years yielded a mean rate of bone toss 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 in sufficiency and hip fracture. Whether this insufficiency arises primar ily from lack of exposure to sunlight pr to a progressive failure to a ctivate the vitamin D precursor in the skin or both is uncertain but i t is compounded by a general decline in dietary vitamin D intake with age. The biological effect is probably an impairment of calcium absorp tion and consequent acceleration of bone loss. This is not to imply th at all forms of osteoporosis are due to negative calcium balance. In c orticosteroid osteoporosis and In age-related osteoporosis in men, dep ression of bone formation is probably a critical factor. Nonetheless, established osteoporosis of all kinds is so commonly associated with m alabsorption of calcium and/or high obligatory calcium excretion as to suggest that negative calcium balance has at least a contributory, if not a causal role in most forms of osteoporosis. (C)Elsevier Science inc. 1997.