What's more, the researchers reported, mice with symptoms of severe estrogen deficiency, lacking either the FSH hormone or its receptor, became resistant to bone loss.
FSH normally triggers egg development and stimulates estrogen production by the ovaries, the researchers explained. As women approach menopause and estrogen levels decline, the pituitary gland responds by releasing more FSH.
Treatments that prevent bone loss by blocking FSH might therefore offer alternative methods to treat or prevent osteoporosis without the risks associated with other hormone replacement therapies, said Mone Zaidi of Mount Sinai School of Medicine. For example, estrogen replacement therapy has been linked to an increased risk of breast cancer, especially when taken in combination with progesterone, he said.
"For the last three decades, the idea has clearly been that estrogen loss is responsible for the changes experienced in postmenopausal women--including flushing, dryness, and bone loss," Zaidi said. "Although FSH levels rise sharply in parallel to estrogen decline, a direct effect of FSH on the skeleton had never before been explored."
"We've now found that, irrespective of the nature or severity of estrogen deficiency, an intact pituitary and, more specifically, high FSH levels are prerequisites for bone loss in animals with reduced or absent ovarian function."
Osteoporosis affects nearly 45 million women worldwide with fracture rates that far exceed the combined incidence of breast cancer, stroke, and heart attacks, the researchers said. The disease results from a disruption of
Contact: Heidi Hardman