(Ivanhoe Newswire) — Diminished bone density, caused by low levels of estrogen common among menopausal women, raises the risk of osteoporosis, bone fractures and subsequent complications. Traditional therapies have sought to maintain the level of estrogen in the body. New research suggests, however, that another hormone, follicle-stimulating hormone (FSH), also may be involved in decreasing bone density during menopause, and may guide researchers to an alternative avenue for treatment of this debilitating condition.
In the five years leading up to menopause, FSH levels gradually increase as bone density begins to decrease over the same period of time. Data from animal studies has pointed to a link between FSH and bone density.
During menopausal bone loss, the destructive activity of osteoclasts, which break down bone, outweighs rebuilding activity of osteoblasts, which regenerate bone, resulting in an overall weakening of the bone.
Cytokines, which are secreted by white blood cells, are thought to play a role in this imbalance as well. One cytokine in particular is known to activate osteoclasts. “Our hypothesis . . . was that [FSH] was decreasing bone mineral density by influencing the production or action of cytokines,” Dr. Joseph Cannon of the Medical College of Georgia in Augusta, was quoted as saying.
The researchers conducted a study of 36 women aged 20 to 50 years. By measuring each woman’s level of FSH and then using a low-energy x-ray to analyze her bone density, the researchers saw that women who had higher levels of FSH did indeed have lower bone density.
“Our current data suggest that if there was a way to modulate FSH receptors on cells, or some other way to modulate the ability of FSH to influence cells, the result might be a new way of treating or preventing osteoporosis,” said Dr. Cannon. “These data support the possibility that controlling the actions of FSH may be a therapeutic way of dealing with osteoporosis that will work beyond the scope of treatments that have been used in the past.”
SOURCE: Presented at the American Physiological Society’s Experimental Biology conference, Anaheim, CA, April 24-28, 2010.
