Abstract
This study shows that lack of estrogens plays a decisive role in the development of postmenopausal bone loss. It seems that one of the physiological changes after the menopause is that bone, in the absence of estrogens, becomes more sensitive to the action of parathyroid hormone. Thus oophorectomy is accompanied by a rise in plasma and urine calcium and urine hydroxyproline due to increased bone resorption, and this imbalance between parathyroid hormone and bone is restored by the administration of estrogens which return the biochemical abnormalities towards the normal premenopausal state. Retrospective studies on patients who have received estrogen therapy have shown that treated patients maintain their bone status better than controls. As there are no long term studies of bone density on patients taking progestational compounds it is as yet uncertain how important their role may be. However, since their biochemical effects on calcium metabolism are very similar to those of estrogens they may also help to preserve bone status. The data provide a rational basis for the prevention of postmenopausal bone loss. Both estrogen and progesterone appear to block bone resorption, and when given together it may be possible to use smaller doses of both hormones to achieve the same effect that each produces when given separately in larger doses. This type of 'combined preparation' may be more acceptable physiologically than either hormone alone. This paper has not dealt with calcium therapy. The authors have reason to believe that estrogen deficiency has the effect of increasing the calcium requirement in the postmenopausal women. An alternative approach to the prevention of osteoporosis would be to increase the calcium intake, and data published elsewhere show that this too can be effective. The ultimate therapy may be the combination of hormones with calcium supplements, but long term results of such therapy are not yet available.