Washington, Apr 26 (ANI): Other than estrogen, another hormone-follicle-stimulating hormone (FSH) may also be involved in decreasing bone mineral density during menopause, according to new research at the Medical College of Georgia in Augusta, GA.
Diminished bone density is common among menopausal women and raises their risk of osteoporosis, bone fractures and subsequent complications.
Traditionally, studies have focused on therapies that seek to maintain the level of estrogen in the body. This hormone seems to sustain bone health, but it drops to an extremely low level during and after menopause.
Dr. Joseph Cannon said that the level of FSH gradually increases in the five years leading up to menopause, when it reaches its peak and estradiol bottoms out.
Research has indicated that bone density begins to decrease over the same period of time.
In addition, data from animal studies indicated a link between FSH and bone density, which made the researchers to probe whether the increase of FSH has an effect on bone density in humans.
Bone mineral density is a balancing act between bone loss and bone growth involving two types of cells in the body- osteoclasts that break down bone, and osteoblasts that regenerate it.
During menopausal bone loss, the osteoclasts' destructive activity outweighs the osteoblasts' rebuilding activity, resulting in an overall weakening of the bone.
Cytokines, which are secreted by white blood cells such as monocytes, are thought to play a role in this imbalance. One cytokine in particular, interleukin-1 beta (IL-1), is known to activate osteoclasts.
"Our hypothesis was that [FSH] was decreasing bone mineral density by influencing the production or action of cytokines," said Dr. Cannon.
To test their hypothesis, the researchers conducted a study of 36 women from 20 to 50 years old.
By measuring each woman's level of FSH and then using a low-energy x-ray to analyse her bone density, the researchers saw that higher levels of FSH among the women were indeed associated with lower bone density.
With the results in hand, the researchers wanted to determine the effects of FSH on a cellular level.
They collected blood samples from the study participants and isolated the monocytes to investigate the effect of FSH on cells outside of the body.
They discovered that the monocytes that make IL-1 have receptors for FSH.
Receptors act like a lock for a key- when the key (FSH) enters the lock (receptor), the cell performs the activity coded by that key.
The researchers determined that FSH stimulates the production of IL-1 if the monocytes have a sufficient number of FSH receptors.
After further analysis, they confirmed that blood FSH levels corresponded to blood levels of IL-1, which indicated that both inside and outside the body, FSH stimulation of monocytes results in the production of IL-1.
On comparing the amount of IL-1 in the participants' blood to their bone density, the researchers found that the higher the level of IL-1, the lower the bone density, when other factors that control IL-1 activity were taken into account.
The study will be presented at the American Physiological Society's Experimental Biology 2010 conference in Anaheim. (ANI)