Why the study?
Does an anti-FSH agent prevent osteoporosis and obesity in women across the menopausal transition?
Does an anti-FSH agent prevent osteoporosis and obesity in women across the menopausal transition?
Rising FSH levels during perimenopause may independently drive bone loss and visceral adiposity, suggesting anti-FSH agents as a potential therapeutic target.
Rising FSH may drive perimenopausal bone loss and visceral adiposity beyond estrogen; leaves open FSH blockade as a therapeutic target.
The Study of Women's Health Across the Nation has taught us that impending ovarian failure during late perimenopause is associated with a sharp rise in serum FSH, which coincides with the most rapid rate of bone loss and the onset of visceral adiposity. At this time in a woman's life, serum estrogen levels are largely unaltered, so the hypothesis that hypoestrogenemia is the sole cause of bone loss and visceral obesity does not offer a full explanation. An alternative explanation, arising from animal models and human data, is that both physiologic aberrations, obesity and osteoporosis, arise at least in part from rising FSH levels. Here, we discuss recent findings on the mechanism through which FSH exerts biological actions on bone and fat and review clinical data that support a role for FSH in causing osteoporosis and obesity. We will also provide a conceptual framework for using a single anti-FSH agent to prevent and treat both osteoporosis and obesity in women across the menopausal transition.
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Zaidi et al. (2018) studied this question.
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