There is currently considerable interest in the pathogenesis of
postmenopausal osteoporosis, which is the most common
metabolic bone disease.
Osteoporosis affects approximately 20 million persons in the United States, 90% of whom are postmenopausal women. Although there is evidence that
estrogen deficiency is an important contributory factor, the pathogenesis of
osteoporosis is multifactorial and presently poorly understood. There is evidence that pineal
melatonin is an anti-aging
hormone and that the menopause is associated with a substantial decline in
melatonin secretion and an increased rate of pineal calcification. Animal data indicate that pineal
melatonin is involved in the regulation of
calcium and
phosphorus metabolism by stimulating the activity of the parathyroid glands and by inhibiting
calcitonin release and inhibiting
prostaglandin synthesis. Hence, the pineal gland may function as a "fine tuner" of
calcium homeostasis. In the following communication, we propose that the fall of
melatonin plasma levels during the early stage of menopause may be an important contributory factor in the development of
postmenopausal osteoporosis. Consequently, plasma
melatonin levels taken in the early menopause could be used as an
indicator or perhaps as a marker for susceptibility to
postmenopausal osteoporosis. Moreover,
light therapy, administration of oral
melatonin (2.5 mg at night) or agents which induce a sustained release of
melatonin secretion such as
5-methoxypsoralen, could be useful agents in the prophylaxis and treatment of
postmenopausal osteoporosis. Finally, since application of external artificial magnetic fields has been shown to synchronize
melatonin secretion in experimental animals and humans, we propose that treatment with artificial magnetic fields may be beneficial for
postmenopausal osteoporosis.