So, you know how some women of a certain age get kind of… well, thick around the middle? This “enhanced visceral adiposity” is just one of the many joys that accompany the end of fertility. Along with the constant reminder of our impending mortality, menopausal women also have to deal with bone loss, a reduced energy balance, and reduced physical activity. All of these effects stem from the drop in estrogen levels as the ovaries fail.

Follicle stimulating hormone (FSH), like other hormones produced in the pituitary, is ancient; it is evolutionarily conserved and found even in organisms like jellyfishes, corals, and sea anemones. In mammals, it helps fertility by promoting the synthesis and release of estrogen from the ovarian follicles. Levels of FSH rise during perimenopause as the ovaries fail, presumably as the body tries (and fails) to stimulate more estrogen production.

Scientists wondered if blocking FSH might therefore prevent some of the physiological effects associated with menopause. To do so, they generated an antibody that binds to mouse FSH, preventing it from interacting with its receptor and effecting any cellular changes.