Cortisol secretion, bone health, and bone loss: a cross-sectional and prospective study in normal nonosteoporotic women in the early postmenopausal period

Abstract

Objective: The aim of the study was to evaluate the relationship between cortisol secretion, bone health, and bone loss in a cohort of normal women in the early postmenopausal period. Methods: We measured lumbar and hip bone mineral density (BMD) by dual-energy X-ray absorptiometry (DXA) and heel ultrasound parameters in 82 healthy, nonosteoporotic (lumbar Tscore RK2.0) women (median age 52.5 years, range 42-61). These women were examined in two sessions, 1 year apart, in the early postmenopausal period (onset of menopause between 6 and 60 months). Parameters of the hypothalamic-pituitary-adrenal (HPA) axis function were morning serum cortisol, morning and midnight salivary cortisol, 24-h urinary free cortisol (UFC), serum cortisol after 0.5 and 1 mg overnight dexamethasone, and DHEA-S. Results: In multiple regression analyses, the following significant inverse correlations were found: i) lumbar BMD and either 24-h UFC (P!0.005) or morning serum cortisol (P!0.05), ii) total femur and femoral neck BMD with morning serum cortisol (PZ0.05 and P!0.05), and iii) heel ultrasound stiffness index and midnight salivary cortisol (P!0.005). The annual rate of change in lumbar and femoral BMD did not correlate with any of the above-mentioned hormonal variables. No difference was found in the parameters of HPA axis function in slow (loss of BMD !1%) vs fast (loss of BMD R3%) bone losers. Conclusions: HPA axis may contribute to postmenopausal bone health, but differences in cortisol secretion do not influence the differential rate of bone loss between slow and fast bone losers in the early postmenopausal period, at least in healthy women.

Cortisol dysregulation is associated with daily diary‐reported hot flashes among midlife women

“…These findings may also contribute to our understanding of the growing body of research linking hot flashes to chronic health risks among ageing women, including bone health, [29][30][31] inflammation 32,33 and cardiovascular disease. 7,[34][35][36][37] Cortisol secretion contributes to accelerated bone loss, osteoporosis and fracture risk.…”

“…Oestrogen is protective against these cortisol effects on bone, leading to an increased negative impact of cortisol exposure on bone health in the hormonal milieu of the menopause transition. 38 Cortisol dysregulation may contribute to cardiovascular risk by increasing visceral adipose accumulation, promoting chronic inflammation, impairing glucose metabolism, increasing risk for insulin resistance and diabetes mellitus and contributing to hypertension risk through effects on the peripheral vasculature and endothelial function. 39 Links between hot flashes and these health concerns relevant to women in and following the menopause transition may be due in part to underlying associations between hot flashes and HPA axis dysfunction.…”

DIAGNOSIS OF ENDOCRINE DISEASE: Evaluation of bone fragility in endocrine disorders

“…It is possible, however, that even in healthy subjects, the endocrine milieu (in term of degree of secretion, peripheral activation and sensitivity) could play a role in predisposing to fracture risk. Indeed, cortisol levels seems to be associated with BMD in women with postmenopausal osteoporosis (129,130), the activity of the 11β-hydroxysteroid dehydrogenase shuttle, which regulates the glucocorticoid peripheral activity, seems to influence the risk of vertebral fractures (131,132), and the different GC receptor polymorphisms, have been suggested to be associated with the fracture risk in patients with no evidence of cortisol excess (133,134). Furthermore, recent data show that even in primary aldosteronism femur and spine BMD and TBS are reduced (135,136) and that the fracture risk is increased (137,138).…”

Glucocorticoid‐induced osteoporosis: lessons from Cushing's syndrome

“…6 Decrements in BMD were independent of the cause of CS. 6,8,11 Correlations between cortisol concentration and BMD Most studies in healthy people have found negative correlations between various indices of cortisol secretory burden and BMD or loss of BMD at various skeletal sites [48][49][50][51] , although this relationship between serum cortisol and BMD was true only within the upper tertile of physiological cortisol concentrations indicating a threshold in the effect of cortisol on bones. 48 Conversely, the majority of reports have shown no correlation of bone loss with the degree of hypercortisolism in CS.…”