Abstract
Although estradiol (E2) has been believed to be the most critical factor in the menopause-associated decrease in bone mineral density (BMD), the role of increasing follicle stimulating hormone (FSH) during menopause is relatively unclear. We determined the extent to which hip and lumbar spine BMD differ among the stages of menopause in healthy women, and whether BMD is associated with FSH and E2 levels. A cross-sectional study of 141 healthy women classified as premenopausal (Pre; 38 ± 6 yrs; mean ± SD, n = 30), early perimenopausal (EPeri; 50 ± 3yrs, n = 31), late perimenopausal (LPeri; 50 ± 4yrs, n = 30), early postmenopausal (EPost; 55 ± 3yrs, n = 24), or late postmenopausal (LPost; 62 ± 4 yrs, n = 26), was conducted. Spine/hip BMD and sex hormones were measured using dual-energy X-ray absorptiometry and enzymatic/colorimetric methods, respectively. Compared to EPeri, spine BMD was lower (p < 0.05) in LPeri, EPost, and LPost and hip BMD was lower (p < 0.05) in EPost and LPost. BMD was inversely associated with FSH (spine: r = −0.341; hip: r = −0.271, p < 0.05) and directly associated with E2 (spine: r = 0.274; hip: r = 0.256, p < 0.05). The menopause-related loss of spine and hip BMD is associated not only with low E2 but also higher FSH. Future studies are essential to delineating the mechanisms by which FSH regulates bone health in aging women.
Highlights
Fractures and the consequent loss of independent living are critical health issues in aging women [1]
There were no significant differences in body weight, height, body mass index (BMI), total body fat mass, testosterone, energy intake, IL6, and leisure time physical activity (LTPA) among the menopausal stages (Table 1)
L1-4 bone mineral density (BMD) and T-score were not significantly different in Pre and early perimenopausal (EPeri), whereas they were significantly lower in late perimenopausal (LPeri), early postmenopausal (EPost), and late postmenopausal (LPost) compared to EPeri (Table 2, all p < 0.05)
Summary
Fractures and the consequent loss of independent living are critical health issues in aging women [1]. BMD loss starts before the final menstrual period [3], and continues throughout the menopausal transition [4,5]. This fast decline in BMD can be associated with irreversible disruption of bone microarchitecture [6,7] and a greater risk of spine and hip fractures [8]. The goal of the present study was to determine how menopausal stages and levels of sex hormones are associated with BMD at the total hip and lumbar spine. For many years, declining estradiol (E2 ) was believed to be the most critical direct hormonal regulator of the menopause-associated decline in BMD [9,10,11,12].
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