Nutrition and osteoporosis

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Abstract
Osteoporosis is best defined in terms of whole bone density (apparent density) and is present when this variable falls below the young normal range. Low bone density may be genetically determined or acquired. If acquired it may in principle be due to low bone formation or high resorption. It is most easily produced in experimental animals by calcium deprivation and/or ovariectomy, both of which induce high bone resorption; their effects are additive. The postmenopausal rise in bone resorption is associated with a fall in calcium absorption and a renal tubular leak of calcium which combine to increase requirement of this element but there is also an increase in the sensitivity of bone to resorbing agents. Calcium supplementation inhibits postmenopausal bone loss but not as effectively as oestrogen. Protein and sodium are nutrients which increase calcium requirement by increasing obligatory urine calcium loss. Vitamin D is a nutrient, the deficiency of which increases the risk of hip fracture and the administration of which (with calcium) has been shown to reduce the risk of this fracture in vulnerable nursing-home residents. The implications of these findings are that postmenopausal women should ingest more calcium than premenopausal women, be moderate in their consumption of protein and salt, and receive vitamin D supplementation if their 25-hydroxyvitamin D level falls below about 50 nmol/L.

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