Sleep During Menopausal Transition: A 10-year Follow-Up

Study ObjectivesA 10-year observational follow-up study to evaluate the changes in sleep architecture during the menopausal transition.MethodsFifty-seven premenopausal women (mean age 46 years, SD 0.9) were studied at baseline and after a 10-year follow-up. At both time points, polysomnography (PSG) was performed, and the serum follicle-stimulating hormone (S-FSH) concentration was measured. Linear regression models were used to study the effects of aging and menopause (assessed as change in S-FSH) on sleep.ResultsAfter controlling for body mass index, vasomotor, and depressive symptoms, higher S-FSH level was associated with longer sleep latency (B 0.45, 95% confidence interval [CI]: 0.07 to 0.83). Aging of 10 years was associated with shorter sleep latency (B −46.8, 95% CI: −77.2 to −16.4), shorter latency to stage 2 sleep (B −50.6, 95% CI: −85.3 to −15.9), decreased stage 2 sleep (B −12.4, 95% CI: −21.4 to −3.4), and increased slow-wave sleep (B 12.8, 95% CI: 2.32 to 23.3) after controlling for confounding factors.ConclusionsThis study suggests that PSG measured sleep of middle-aged women does not worsen over a 10-year time span due to the menopausal transition. The observed changes seem to be rather age- than menopause-dependent

Tissue-Specific Increases in 11β-Hydroxysteroid Dehydrogenase Type 1 in Normal Weight Postmenopausal Women

With age and menopause there is a shift in adipose distribution from gluteo-femoral to abdominal depots in women. Associated with this redistribution of fat are increased risks of type 2 diabetes and cardiovascular disease. Glucocorticoids influence body composition, and 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) which converts inert cortisone to active cortisol is a putative key mediator of metabolic complications in obesity. Increased 11βHSD1 in adipose tissue may contribute to postmenopausal central obesity. We hypothesized that tissue-specific 11βHSD1 gene expression and activity are up-regulated in the older, postmenopausal women compared to young, premenopausal women. Twenty-three pre- and 23 postmenopausal, healthy, normal weight women were recruited. The participants underwent a urine collection, a subcutaneous adipose tissue biopsy and the hepatic 11βHSD1 activity was estimated by the serum cortisol response after an oral dose of cortisone. Urinary (5α-tetrahydrocortisol+5β-tetrahydrocortisol)/tetrahydrocortisone ratios were higher in postmenopausal women versus premenopausal women in luteal phase (P<0.05), indicating an increased whole-body 11βHSD1 activity. Postmenopausal women had higher 11βHSD1 gene expression in subcutaneous fat (P<0.05). Hepatic first pass conversion of oral cortisone to cortisol was also increased in postmenopausal women versus premenopausal women in follicular phase of the menstrual cycle (P<0.01, at 30 min post cortisone ingestion), suggesting higher hepatic 11βHSD1 activity. In conclusion, our results indicate that postmenopausal normal weight women have increased 11βHSD1 activity in adipose tissue and liver. This may contribute to metabolic dysfunctions with menopause and ageing in women

The relationship between mood and sleep in different female reproductive states

Peer reviewe

Effect of external sleep disturbance on sleep architecture in perimenopausal and postmenopausal women

ObjectiveThis study aimed to use external sleep disturbance as a model to evaluate sleep architecture in climacteric women before and after menopausal hormone therapy (MHT).MethodsSeventeen perimenopausal and 18 postmenopausal women underwent a polysomnography protocol: an adaptation night, a reference night and a sleep disturbance night with one hand loosely tied to the bed for blood sampling. The sleep architecture of the reference and disturbance nights were compared. The 24-h urinary free cortisol concentration (UFC) was measured. The procedure was repeated after 6 months on MHT or placebo.ResultsFifteen perimenopausal and 17 postmenopausal women completed the study. The perimenopausal and postmenopausal groups were combined. During external sleep disturbance, sleep was shorter and more fragmented; with less stage 2, slow-wave and rapid eye movement (REM) sleep and more wake time and awakenings, both at baseline and after the treatment period. Compared to the placebo group, sleep disturbance was minor for women on MHT: sleep was not shortened and the amount of slow-wave sleep did not decrease. Increased 24-h UFC was observed only during MHT.ConclusionsSleep in climacteric women is easily disturbed, leading to shorter and more fragmented sleep with less deep sleep and REM sleep. Six months of MHT attenuates the observed sleep disturbance.Peer reviewe