Menstrual glitches may spur bone loss.

Menstrual glitches mayspur bone loss

For the first time, research findings hint that "silent" abnormalities affecting the sex hormone progesterone can cause bone loss in young, healthy women. The new results suggest that subtle problems with the menstrual cycle can cause ongoing bone loss, a process that can lead to osteoporosis later in life.

The study's implications run counter to conventional thinking about osteoporosis. Scientists have blamed this crippling bone disorder primarily on a deficiency of the hormone estrogen, which slows the ongoing destruction of adult bone. The estrogen theory fits with the observation that many older women, who lose this hormone during menopause, experience rapid bone loss. In addition, scientists have held estrogen deficiency accountable for the bone loss plaguing some young female athletes who fail to menstruate.

Endocrinologist Jerilynn C. Prior started with a hunch that estrogen was only part of the osteoporosis story. She and her colleagues at the University of British Columbia in Vancouver set out to determine whether progesterone and/or exercise played any role in bone loss among a group of young women with no obvious mentstrual difficulties.

The team focused on 66 women aged 21 to 42 who had normal menstrual cycles in the first two months of the study. The group consisted of 21 marathon runners, 22 recreational joggers and 23 women with normal activity levels. The researchers charted each volunteer's menstrual cycle, used an X-ray technique to estimate changes in spinal bone mass and developed a statistical method to reveal any correlations between bone density, exercise and menstrual cycle.

During the year-long study, they identified 28 women who had more than one menstrual cycle with a short luteal phase -- the interval between ovulation and the beginning of menstruation -- and andther 13 women who failed to ovulate during at least one cycle. These 41 women (62 percent of the total) lost an average of 4.3 milligrams of spinal bone per cubic centimeter annually. In contrast, the 25 women who cycled normally showed no bone loss or gained a small amount of spinal bone during the year.

Prior notes that short luteal phases or anovulatory cycles frequently go undetected because they do not change the amount of blood flow or the total length of a woman's cycle.

When the researchers completed their statistical analyses, they saw no correlation between exercise and bone loss. Instead, they found that a short luteal phase or a cycle without ovulation strongly predicted bone loss, both for runners and for their less athletic peers.

"It was one of those exciting moments in science," Prior says.

A short luteal phase or a cycle without ovulation results in decreased blood levels of progesterone, she told SCIENCE NEWS. Evidence from many sources suggests that progesterone spurs the growth of new bone, she says. Prior's team observed that the women with the lowest blood levels of progesterone showed the greatest degree of bone destruction. Such findings suggest that bones need the proper balance between estrogen and progesterone to remain healthy, Prior asserts. She speculates that scientists might one day prevent bone loss in young women with luteal phase or ovulatory abnormalities by giving synthetic progesterone.

Prior has yet to prove the connection between bone loss and progestrone, cautions C. Conrad Johnston Jr. of the Indiana University School of Medicine in Indianapolis. Johnston, who coauthored an editorial accompanying the research report in the Nov. 1 NEW ENGLAND JOURNAL OF MEDICINE, says he "can't imagine" 60 percent of young women losing bone each year due to progesterone deficiency alone.