BONE LOSS, CONTRACEPTION AND LACTATION

Loss of bone mass with age, is a universal phenomenon and is more pronounced in women than in men. The condition where the bone loss has proceeded to the extent that fractures occur is termed osteoporosis. As the number of elderly persons in the population increases, its magnitude is likely to increase, both in the developing and the developed countries. Bone mass increases rapidly in childhood and the adolescent years, reaching a peak in the third decade of life, and begins to decline soon thereafter. Several factors are thought to influence bone loss: these include race, diet, smoking, and physical exercise. Although the rate of bone loss accelerates in the immediate postmenopausal period, the process actually begins in the premenopausal years. By the time osteoporosis is clinically apparent and manifested by fracture, it probably cannot be reversed. The peak adult bone mass achieved, and the subsequent rate of bone loss are the major factors that determine a woman's susceptibility to postmenopausal osteoporosis. A primary cause of bone loss after menopause is the associated decline in ovarian function. Scanty information is available on the factors that affect bone mineral density or initiate bone loss before menopause, although both estrogens and progestins have been shown to prevent bone loss in postmenopausal women. Available data on the relationship between steroid hormone contraceptive use and bone mass/density is limited to combined oral contraceptives and one report related to the use of depot medroxy progesterone acetate. While there are several studies which show that oral contraceptive preparations have a beneficial effect on bone mass, there are many other studies which fail to demonstrate such an effect. The divergent findings from the research to date reflect the difficulties in controlling not only for the many variables in studies based on small numbers, but also drawing inferences from studies which were undertaken during periods when changes in pill dosages/formulations occurred and diagnostic techniques improved, plus the complex nature of the disease itself. It is not yet clearly understood if the possible protection conferred by steroidal contraception persists throughout the postmenopausal years - a period when there is acceleration of bone loss and whether or not this beneficial effect is specific to the trabecular bone which is more sensitive to metabolic influences. The effect of lactation on bone mass is not well understood. (Cross-sectional and longitudinal studies report conflicting effects, both beneficial and adverse.) The association may be mediated not only through intake of calcium during lactation, the duration of lactation, and age at lactation, but the anatomic site and the technique employed to measure bone mass are important considerations. No single study has addressed all these factors together. Most of them have dealt with small numbers of subjects with low statistical power to detect small or even medium changes in bone mass/density.