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A hormone produced by the pituitary gland may play a role in bone loss in postmenopausal women, challenging the notion that declining estrogen levels are solely responsible for the problem.
High levels of the hormone, pituitary-derived follicle-stimulating hormone, caused an increase in bone loss in mice. And mice who lacked either the pituitary-derived follicle-stimulating hormone or its receptor became resistant to bone loss, even if they showed evidence of estrogen deficiency.
The findings open up the possibility that therapies other than estrogen to treat or prevent bone loss may one day be possible.
Estrogen replacement therapy is not an ideal solution because it has been linked to a heightened risk of breast cancer, especially when administered in combination with the hormone progestin.
"In essence, we're revisiting the pathophysiology of bone loss, attributing it not simply to loss of estrogen but to the accompanying elevation of pituitary-derived follicle-stimulating hormone which occurs during menopause," says study author Dr. Mone Zaidi, a professor of medicine and physiology and director of the Mount Sinai Bone Program at Mount Sinai School of Medicine in New York City. "The importance is that you could actually prevent bone loss without using a load of estrogen."
For now, however, the report, which appears in the April 21 issue of Cell, poses more questions than it answers.
"I personally think this is beautiful work and asks a lot of questions," says Dr. J. Christopher Gallagher, a professor of medicine and endocrinology at Creighton University School of Medicine in Omaha, Neb., and a board member of the North American Menopause Society. "But its true clinical importance is not yet clear."
Osteoporosis, a condition in which bones became more fragile and likely to break, affects nearly 45 million women globally, including 8 million in the United States. Healthy bones maintain a fine balance between formation and resorption or breakdown. But after menopause, the bone breakdown outpaces bone formation, resulting in bone loss.
So far, the broken balance has been attributed exclusively to loss of estrogen after menopause. "It has really become virtually gospel that estrogen loss in women after menopause leads to bone loss," Zaidi says.
However, there were some holes in that theory. In some animal studies, taking away estrogen did not always result in bone loss, Zaidi says.
About two years ago, Zaidi's group discovered that thyroid-stimulating hormone, a sister hormone to pituitary-derived follicle-stimulating hormone, affected bone remodeling.
Prior to menopause, pituitary-derived follicle-stimulating hormone's role is to trigger egg development in women and to stimulate production of estrogen by the ovaries. As women get older, however, their estrogen levels decline. At that point, the pituitary gland attempts to restore estrogen levels by releasing more pituitary-derived follicle-stimulating hormone.
"There's a feedback control between estrogen and pituitary-derived follicle-stimulating hormone," Zaidi explains.
"As estrogen falls, pituitary-derived follicle-stimulating hormone rises."
In the new study, Zaidi and his colleagues showed that mice lacking pituitary-derived follicle-stimulating hormone or its receptor did not experience bone loss, even if the ovaries were not producing estrogen. Because this was an animal study, however, more research on humans is necessary.
"The next step would be to have a small molecule or antibody mop up pituitary-derived follicle-stimulating hormone in circulation and see if bone loss can be prevented," Zaidi says.
"If that is the case, we have a new target" for prevention and treatment strategies.
Gallagher adds: "It is an interesting clinical question, because we've always ignored the height of pituitary-derived follicle-stimulating hormone in postmenopausal women. We're going to need some prospective data, and I don't know of any studies currently looking at that. These are important questions."
(The HealthDay Web site is at http://www.HealthDay.com.)
c.2006 HealthDay News
