Overnight Heart Rate Variability During Sleep Disturbance In Peri- And Postmenopausal Women.

OBJECTIVES: Disturbed sleep, common during the climacteric, is associated with increased sympathetic activity, a cardiovascular risk factor. We evaluated sleep disturbance effect on autonomic nervous function in climacteric women. METHODS: Seventeen perimenopausal and 18 postmenopausal women underwent a sleep study protocol: an adaptation night, a reference night, and a sleep disturbance night, with a hand loosely tied to the bed to allow blood sampling. This procedure was repeated after six months of menopausal hormone therapy (MHT) or placebo. Sleep disturbance and MHT effects on overnight heart rate variability (HRV) were analyzed. RESULTS: At baseline, sleep disturbance increased vagal HRV in postmenopausal women, but no changes were seen in perimenopausal women. At six months, sleep disturbance increased total HRV power in the perimenopausal placebo group, and increased nonlinear vagal HRV in the postmenopausal placebo group, but no other changes were seen. MHT did not have any effects on HRV, neither at perimenopause nor at postmenopause. CONCLUSIONS: External sleep disturbance had only minor effects on HRV across menopause. MHT had no detectable HRV effects.

Evolution of sleep-disordered breathing and blood pressure during menopausal transition.

The purpose of this study was to investigate how the blood pressure increase observed during menopausal transition is affected by sleep-disordered breathing and the menopause itself. Further, we aimed to find new sleep-disordered breathing related markers that would predict the development of hypertension. Sixty-four community-dwelling premenopausal women aged 45-47 years were studied. Polysomnography, serum follicle stimulating hormone, forced expiratory volume in 1 s, and a physical examination were performed at baseline and again after 10 years of follow-up. Indices for sleep apnea/hypopnea and inspiratory flow-limitation were determined. Regression models were used to study the relationships between variables. Changes in the apnea-hypopnea index or serum follicle stimulating hormone were not significant for blood pressure change. An increase in morning blood pressure during the follow-up period was associated with a body mass-index increase. An increase in evening blood pressure was associated with an increase in inspiratory flow-limitation during non-rapid eye movement sleep. Incident hypertension during the follow-up was associated with hypopnea (median hypopnea index 7.6/h, p = 0.048) during rapid eye movement sleep at baseline. Users of menopausal hormone therapy had a lower rapid eye movement sleep apnea-hypopnea index (1.6/h vs. 6.9/h, p = 0.026) at baseline whereas at follow-up users and non-users did not differ in any way. The progression of menopause or the use of menopausal hormone therapy had a minimal effect on blood pressure in our population. The effects of inspiratory flow-limitation on blood pressure profile should be studied further.

Effect of menopause and age on vascular impairment.

AIMS: The prevalence of cardiovascular diseases increases in women after menopause. The aim of the study was to determine the impact of conventional cardiovascular risk factors such as age, blood pressure, smoking, cholesterol, obesity, and glucose balance, but also menopausal state and sleep-disordered breathing on vascular impairment during menopausal transition. METHODS: 89 women initiated the study and 74 of them participated in the 10-year follow-up. Cardiovascular disease risk factor assessments, ultrasound measurements of brachial artery function, including nitroglycerin-mediated vasodilatation and flow-mediated endothelium-dependent vasodilation, and sleep studies were repeated at baseline and at 5-year and 10-year follow-ups. RESULTS: Over the study period, all the cardiovascular disease risk estimates increased. Both flow-mediated endothelium-dependent vasodilatation (decline 55 %) and nitroglycerin-mediated vasodilatation (decline 18 %) worsened over the 10 years (p < 0.001). Vascular function was not associated with menopausal state (determined with follicle stimulating hormone). Systolic blood pressure (p = 0.009) and smoking (p = 0.006) at baseline were negatively associated with nitroglycerin-mediated vasodilatation at 5-year follow-up and the use of hormonal therapy at 5-year follow-up was positively associated with concurrent nitroglycerin-mediated vasodilatation (p = 0.041). Intermittent nocturnal hypoxemia at baseline was associated with flow-mediated endothelium-dependent vasodilatation at 10-year follow-up (p = 0.043). High body mass index and impaired glucose balance at 5-year follow-up were associated with nitroglycerin-mediated vasodilatation decline at 10-year follow-up (p = 0.022 and p = 0.037, respectively). CONCLUSIONS: We demonstrate how cardiovascular risk factors and vascular function evolve during menopausal transition. Although menopause was not associated with vascular impairment, short-term improvement in vascular function was observed in those using menopausal hormonal therapy. Intermittent nocturnal hypoxemia, obesity and impaired glucose control are early predictors of vascular decline during postmenopause.

Early signs of sleep-disordered breathing in healthy women predict carotid intima-media thickening after 10 years.

BACKGROUND: Cardiovascular disease (CVD) is the leading cause of death in women. The risk of CVD increases in women after menopause. The aim was to study how sleep parameters and cardiovascular risk factors in 46-year-old women predict future carotid intima-media thickness (IMT) 10 years after. METHODS: Prospective study of 92 healthy women, aged 46 years, were studied at baseline and at 10-year follow-up. Polysomnography for sleep and breathing; blood samples for cholesterol, glucose and follicle stimulating hormone; blood pressure (BP), weight and height measurements; questionnaires for background variables and vasomotor symptoms were carried out at both time points. Carotid ultrasound was scanned for IMT at 10-year follow-up. RESULTS: After adjusting for conventional risk factors, apnea-hypopnea index (AHI) during rapid-eye-movement (REM) sleep was the only parameter at baseline that predicted IMT 10 years after (IMT mean: ß 81.4 [95% CI, 14.0-148.8]; IMT max: ß 104.7 [95% CI, 15.4-194.1]). At 10-year follow-up, higher arousal index (IMT mean: ß 55.6 [95% CI, 19.5-91.8]; IMT max ß 59.9 [95% CI, 11.4-108.4]) and lower vasomotor symptoms (IMT max: ß -60.5 [95% CI, -119.0 to -2.0]) were associated with concurrent higher IMT. The conventional risk factors at baseline did not associate with future IMT but 10 years after higher concurrent HbA1c (IMT mean: ß 11.0 [95% CI, 3.4-18.5]; IMT max ß 14.0 [95% CI, 4.1-23.8]) and systolic BP (IMT mean: ß 2.4 [95% CI, 1.1-3.7]; IMT max: ß 2.7 [95% CI, 1.03 to 4.53]) were associated with higher IMT. CONCLUSIONS: In healthy 46-year-old women, AHI during REM sleep predicted IMT 10 years after. The conventional risk factors (HbA1c and BP) only associated with the concurrent IMT at 10-year follow-up.

Nighttime melatonin secretion and sleep architecture: different associations in perimenopausal and postmenopausal women.

BACKGROUND: Sleep quality typically decreases after menopause, but the underlying mechanisms are poorly understood. Concentrations of melatonin are lower and its secretion profiles different before and after menopause. However, whether and how melatonin and sleep architecture are associated in women of different reproductive states have not been examined to date. METHODS: Overnight serum melatonin samples were taken from 17 perimenopausal and 18 postmenopausal healthy women. Sleep quality was measured with all-night polysomnography recordings. RESULTS: Melatonin concentrations tended to be the lowest during NREM sleep, and were associated with higher odds of transitions from wake to NREM sleep. The curves of predicted overnight melatonin values from linear mixed models varied according to sleep phases (NREM, REM, Wake) in perimenopausal, but not in postmenopausal women. In perimenopause higher melatonin area under curve (AUC) correlated with higher slow-wave activity (p = 0.043), and higher minimum concentrations with shorter slow-wave sleep (SWS) latency (p = 0.029). In postmenopause higher mean and maximum melatonin concentrations and AUC correlated with lower SWS percentage (p = 0.044, p = 0.029, p = 0.032), and higher mean (p = 0.032), maximum (p = 0.032) and minimum (p = 0.037) concentrations with more awakenings from REM sleep. In the age- and BMI- adjusted regression models, the association between higher maximum (p = 0.046) melatonin concentration and lower SWS percentage remained. CONCLUSIONS: The relationship between melatonin and sleep architecture differed in perimenopausal and postmenopausal women. After menopause, high melatonin concentrations were associated with worse sleep. Whether these different patterns are related to aging of the reproductive system, and to decrease in menopausal sleep quality, remains to be elucidated.

Sleep during menopausal transition: a 10-year follow-up.

STUDY OBJECTIVES: A 10-year observational follow-up study to evaluate the changes in sleep architecture during the menopausal transition. METHODS: Fifty-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. RESULTS: After 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. CONCLUSIONS: This 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.

The relationship between diurnal cortisol secretion and climacteric-related symptoms.

OBJECTIVES: Chronic stress, also associated with climacteric-related symptoms, may influence cortisol secretion. We studied cortisol metabolism in peri- and postmenopausal women with diverse climacteric-related symptoms. STUDY DESIGN AND MAIN OUTCOME MEASURES: The study population was 35 women, aged 45-70 years. Plasma cortisol levels were measured from blood samples collected every 20 min over 24 h. Urinary cortisol was analysed from 24-hour urine collections. Climacteric-related symptoms (vasomotor, sleep, depressive, anxiety, cognitive, sexual, menstrual, and somatic) were evaluated with the Women's Health Questionnaire (WHQ). Associations between cortisol variables (24-hour, night, day, maximum, minimum, morning baseline, cortisol awakening response (CAR), area under the curve, slope, and 24-hour urinary cortisol) and the symptoms were first examined with a correlation analysis. Then, the women were divided into two groups according to their climacteric symptomatology, and differences in cortisol variables between the groups were investigated. Diurnal cortisol curves by symptomatology were also analyzed visually. RESULTS: In the correlation analysis, more frequent vasomotor symptoms were associated with a higher CAR (rs = 0.37, p = 0.039) and lower 24-hour urinary cortisol excretion (rs= -0.45, p = 0.012), and more frequent depressive symptoms were associated with a higher minimum cortisol level (rs = 0.33, p = 0.0498). When the women were divided into two groups, women with more frequent vasomotor (p = 0.012) or somatic symptoms (p = 0.021) had a lower 24-hour urinary cortisol excretion than less symptomatic women. CONCLUSIONS: Although previous studies have reported associations between climacteric-related symptoms and cortisol secretion, these two factors were not substantially interrelated in our study.

First-Night Effect on Sleep in Different Female Reproductive States.

OBJECTIVES: In sleep laboratory studies, the new environment is generally considered to disturb sleep during the first night. However, older women have rarely been studied. Although menopause and hormone therapy affect sleep, their impact on the first-night effect is virtually unknown. PARTICIPANTS: Four groups of women with no sleep laboratory experience: young on hormonal contraceptives (n = 11, 23.1 [0.5] years), perimenopausal (n = 15, 48.0 [0.4] years), postmenopausal without hormone therapy (HT; off-HT, n = 22, 63.4 [0.8] years) and postmenopausal with HT (n = 16, 63.1 [0.9] years). PROCEDURE: A cross-sectional study. METHODS: Polysomnography was performed over two consecutive nights and the first-night effect and group differences were evaluated. Questionnaire-based insomnia and sleepiness scores were correlated to sleep variables and their between-night changes. RESULTS: Although sleep in young women was deeper and less fragmented than in the other groups, first-night effect was similar in all study groups. Total sleep time, sleep efficiency, and S1 and S2 sleep increased, and wake after sleep onset, awakenings per hour of sleep, S2 and REM latencies, and percentage of SWS decreased from the first to the second night. Perimenopausal women had more insomnia complaints than other women. Insomnia complaints were associated with more disturbed sleep but not with the first-night effect. CONCLUSIONS: A first night in a sleep laboratory elicits a marked interference of sleep architecture in women of all ages, with a carryover effect of lighter sleep on the second study night. Menopausal state, HT use, or insomnia complaints do not modify this effect.

First-night effect on cardiac autonomic function in different female reproductive states.

Decreases in heart rate variability, a marker of autonomic nervous system function, are associated with increased cardiovascular mortality. Heart rate variability increases in non-rapid eye movement sleep, peaking in slow-wave sleep. Therefore, decreasing the amount of deep sleep, for example, by introducing patients to a sleep laboratory environment, could decrease heart rate variability, increasing cardiovascular risk. We studied four groups of women with no previous sleep laboratory experience: young [n = 11, 23.1 (0.5) years]; perimenopausal [n = 15, 48.0 (0.4) years]; postmenopausal without hormone therapy [n = 22, 63.4 (0.8) years]; and postmenopausal on hormone therapy [n = 16, 63.1 (0.9) years], using a cross-sectional design. Polysomnography including electrocardiogram was performed over two consecutive nights. Heart rate variability was assessed overnight, and the first-night effect on heart rate variability was analysed. Furthermore, correlations between heart rate variability and sleep variables were analysed. Using combined groups, only minor changes were observed in non-linear heart rate variability, indicating increased parasympathetic tone from the first to the second night. No group differences in first-night effect were seen. Heart rate variability and sleep variables were not significantly correlated. Heart rate variability decreased with increasing age, and it was lowest in the postmenopausal women on hormone therapy. We conclude that a first night in a sleep laboratory elicits only minimal changes in overnight vagally mediated non-linear heart rate variability in women irrespective of reproductive state. This finding warrants further analyses in different sleep stages, but suggests that changes in sleep architecture per se do not predict the autonomic strain of a poor night.

Cardiac autonomic changes after 40 hours of total sleep deprivation in women.

OBJECTIVES: The effect of total sleep deprivation on heart rate variability (HRV) in groups of postmenopausal women on oral hormone therapy (HT) (on-HT, n = 10, 64.2 (1.4) years), postmenopausal women without HT (off-HT, n = 10, 64.6 (1.4) years) and young women (n = 11, 23.1 (0.5) years) was studied using a prospective case-control setup. METHODS: Polysomnography was performed over an adaptation night, a baseline night, and a recovery night after 40 h of total sleep deprivation. Time and frequency domain and nonlinear HRV from overnight electrocardiogram recordings were compared between groups during baseline and recovery nights. Further, the changes in HRV from baseline to recovery were analysed and compared between groups. Finally, correlations of HRV to percentages of sleep stages and measures of sleep fragmentation were analysed during baseline and recovery. RESULTS: Young women had higher HRV than older women; the most marked difference was between young and on-HT postmenopausal women. Sleep deprivation induced a decrease in frequency domain HRV in young and in off-HT women, an increase in α2 in off-HT women, and an increase in mean heart rate in on-HT women. The sleep deprivation effect was mainly uncorrelated to changes in sleep parameters. CONCLUSIONS: Acute total sleep deprivation has a deleterious effect on the autonomic nervous system in young women, but an even more pronounced effect in postmenopausal women. Hormone therapy use in late postmenopause does not give protection against these changes. These harmful effects may partly explain the increased cardiovascular morbidity and overall mortality associated with sleep loss.

The relationship between mood and sleep in different female reproductive states.

BACKGROUND: Sleep is disrupted in depressed subjects, but it also deteriorates with age and possibly with the transition to menopause. The nature of interaction between mood, sleep, age and reproductive state is not well-defined. The aim of this study was to evaluate the relationship between mood and sleep among healthy women in different reproductive states. METHODS: We analyzed data from 11 younger (20-26 years), 21 perimenopausal (43-51 years) and 29 postmenopausal (58-71 years) healthy women who participated in a study on menopause, sleep and cognition. The 21-item Beck Depression Inventory (BDI) was administered to assess mood. Subjective sleep quality was assessed with the Basic Nordic Sleep Questionnaire (BNSQ). Objective sleep was measured with all-night polysomnography (PSG) recordings. Perimenopausal and younger women were examined during the first days of their menstrual cycle at the follicular phase. RESULTS: Among younger women, less arousals associated with higher BDI total scores (p = 0.026), and higher SWS percentages with more dissatisfaction (p = 0.001) and depressive-somatic symptoms (p = 0.025), but with less depressive-emotional symptoms (p = 0.001). In specific, less awakenings either from REM sleep or SWS, respectively, associated with more punishment (p = 0.005; p = 0.036), more dissatisfaction (p < 0.001; p = 0.001) and more depressive-somatic symptoms (p = 0.001; p = 0.009), but with less depressive-emotional symptoms (p = 0.002; p = 0.003). In perimenopausal women, higher BNSQ insomnia scores (p = 0.005), lower sleep efficiencies (p = 0.022) and shorter total sleep times (p = 0.024) associated with higher BDI scores, longer sleep latencies with more depressive-somatic symptoms (p = 0.032) and longer REM latencies with more dissatisfaction (p = 0.017). In postmenopausal women, higher REM percentages associated with higher BDI total scores (p = 0.019) and more depressive-somatic symptoms (p = 0.005), and longer SWS latencies with more depressive-somatic symptoms (p = 0.030). CONCLUSIONS: Depressive symptoms measured with the total BDI scores associated with sleep impairment in both perimenopausal and postmenopausal women. In younger women, specific BDI factors revealed minor associations, suggesting that the type of sleep impairment can vary in relation to different depressive features. Our data indicate that associations between sleep and depressed mood may change in conjunction with hormonal milestones.

The effect of hormone therapy on serum melatonin concentrations in premenopausal and postmenopausal women: a randomized, double-blind, placebo-controlled study.

OBJECTIVES: Melatonin levels decrease physiologically with age, and possibly with the transition to menopause. The plausible influence of hormone therapy (HT) on melatonin is poorly understood. The aim of this randomized, placebo-controlled, double-blind trial was to investigate the effect of HT administration on serum melatonin concentrations in late premenopausal and postmenopausal women. STUDY DESIGN: Analyses were carried out among 17 late premenopausal and 18 postmenopausal healthy women who participated in a prospective HT study in Finland. Serum melatonin was sampled at 20-min (21:00-24:00 h; 06:00-09:00 h) and 1-h (24:00-06:00 h) intervals at baseline and after 6 months with HT or placebo. MAIN OUTCOME MEASURES: Melatonin levels and secretion profile after 6 months of HT compared to placebo. RESULTS: Mean melatonin levels, mean melatonin exposure level (area under curve, AUC) and mean duration of melatonin secretion did not differ after 6 months with HT vs. placebo, irrespectively of the reproductive state. However, in postmenopausal women the melatonin peak time (acrophase) was delayed by 2.4h (2 h 21 min) on average after 6 months with HT vs. placebo (p<0.05). No interaction between time and group was detected when melatonin level was modelled before or after treatment. CONCLUSIONS: Administration of HT to postmenopausal women alters melatonin peak time, but not melatonin levels. Further research on larger clinical samples is needed to better understand the effects of HT on melatonin profile.

Melatonin in perimenopausal and postmenopausal women: associations with mood, sleep, climacteric symptoms, and quality of life.

OBJECTIVE: Melatonin synthesis and secretion are partly modulated by estrogen and progesterone. Changes in melatonin concentrations, possibly related to the menopausal transition, may be associated with climacteric mood, sleep, and vasomotor symptoms. The aims of this study were to compare the serum concentrations of melatonin in perimenopausal and postmenopausal women and to evaluate melatonin's influence on mood, sleep, vasomotor symptoms, and quality of life. METHODS: We analyzed the data of 17 healthy perimenopausal women (aged 43-51 y) and 18 healthy postmenopausal women (aged 58-71 y) who participated in a prospective study. On study night (9:00 pm-9:00 am), serum melatonin was sampled at 20-minute (9:00 pm-12:00 midnight; 6:00-9:00 am) and 1-hour (12:00 midnight-6:00 am) intervals. Questionnaires were used to assess depression (Beck Depression Inventory), anxiety (State-Trait Anxiety Inventory), insomnia and sleepiness (Basic Nordic Sleep Questionnaire [BNSQ]), subjective sleep quality, vasomotor symptoms, and quality of life (EuroQoL). RESULTS: Postmenopausal women had lower nighttime serum melatonin concentrations than perimenopausal women. The duration of melatonin secretion tended to be shorter in postmenopause, whereas melatonin peak time did not differ. Mean melatonin concentrations and exposure levels did not correlate with follicle-stimulating hormone level, estradiol level, body mass index, Beck Depression Inventory score, State-Trait Anxiety Inventory score, BNSQ insomnia score, BNSQ sleepiness score, subjective sleep score, climacteric vasomotor score, or quality of life. In perimenopause, the later is the melatonin peak, the higher is the level of anxiety (P = 0.022), and the longer is the melatonin secretion, the better is the quality of life (P < 0.001). CONCLUSIONS: Longitudinal research is needed to better understand the possible contributory role of menopause in lower melatonin levels.

The temporal relationship between growth hormone and slow wave sleep is weaker after menopause.

OBJECTIVE: To study the temporal association between growth hormone (GH) and slow wave sleep (SWS) in middle-aged women. METHODS: Seventeen premenopausal and 18 postmenopausal women were studied using all-night polygraphic sleep recordings and blood sampling at 20-min intervals. The postmenopausal women were re-studied after six months on hormone therapy (HT) according to a randomized, double-blind, placebo-controlled protocol. RESULTS: The total sleep time (premenopausal 361.9±81.5 min, postmenopausal 358±67.7 min) and the percentages of the sleep stages did not differ between pre- and postmenopausal women. In postmenopausal women the first GH peak after sleep onset occurred later and with a more variable time interval compared to premenopausal women. The percentage of SWS was highest 40-20 min prior to the first GH peak after sleep onset in both groups with a higher SWS proportion in premenopausal women (p=0.048), although the total SWS percent for night did not differ. HT did not affect the distribution of SWS in postmenopausal women. CONCLUSIONS: The temporal relationship between GH and SWS in premenopausal women is less robust after menopause and is not improved with HT.

The association of serum oestradiol level, age, and education with cognitive performance in peri- and late postmenopausal women.

OBJECTIVES: To evaluate whether healthy women show cognitive changes after menopause and whether the possible changes are oestrogen-, age- or education-dependent. METHODS: Forty-eight women, 21 perimenopausal (aged 43-51 years) and 27 late postmenopausal (aged 59-71 years), participated in the study. Verbal and visuomotor functions, visuoconstructive skills, visual and verbal episodic memory as well as attention were evaluated. RESULTS: Perimenopausal women performed better than postmenopausal women. Serum oestradiol (E(2)) level was included in the model in perimenopausal women only given the lack of endogenous oestrogen in postmenopausal women who were also not using hormone therapy (HT). In perimenopausal women, lower E(2) was associated with better visual episodic memory (p<.05), and older age was related to poorer verbal episodic memory (p<.05). In postmenopausal women, more education was associated with better performance in verbal and visuomotor functions, attention as well as verbal episodic memory (p<.05), older age was related to poorer performance in the visuoconstructive test and visual episodic memory (p<.05). CONCLUSIONS: Perimenopausal women had better cognitive performance compared to late postmenopausal women. In perimenopausal women the effect of E(2) was minor. In both groups, age modified cognitive performance, but more so in postmenopausal women. Education did not have any effect on cognitive performance in perimenopausal women, whereas in postmenopausal women education exceeded age as a source of variation. Thus the relevance of education for better cognition was accentuated after menopause.

Estrogen + progestin therapy and cognition: a randomized placebo-controlled double-blind study.

AIMS: The use of hormone therapy (HT) is a relevant and topical issue in the treatment of menopausal symptoms in women. Information regarding the effects of combination treatment with estrogen and progesterone as well as treatment timing on cognitive function is lacking and was evaluated in healthy pre- and postmenopausal women. METHODS: Sixteen premenopausal (45-51 years) and 16 postmenopausal (58-70 years) women were randomly assigned to receive either estrogen + progestin therapy (HT) or placebo (PL) for six months. The study was double-blind. Cognitive performance was measured at baseline and follow up with tests of verbal and visuomotor functions, verbal and visual memory, and attention. RESULTS: In premenopausal women, cognitive attention, when compared to baseline, improved with HT but declined slightly with PL in the two-choice reaction time task (P = 0.049), while PL was associated with better performance in tests of shared attention (P = 0.024) and auditory attention (P < 0.05). In postmenopausal women, HT was associated with improved performance in verbal episodic memory (P = 0.024) and a minor decline in auditory attention (P = 0.025). CONCLUSIONS: HT, with estradiol valerate and norethisterone, in healthy women showed only minor effects on attention around the menopausal transition and on memory in postmenopause.

Sleep and the menopause - do postmenopausal women experience worse sleep than premenopausal women?

OBJECTIVE: To examine the sleep characteristics in three cross-sectional populations: young, premenopausal and postmenopausal women, and the associations between sleep, menopause, mood and cognitive performance. STUDY DESIGN: Twenty-one premenopausal (45-51 years), 29 postmenopausal (59-71 years) and 11 young (20-26 years, using oral contraceptives) women were recruited. Polysomnography was used to measure objective sleep quality. Subjective sleep quality, sleepiness and mood were assessed using questionnaires. Cognitive performance was investigated by means of three attentional tests. RESULTS: Total sleep time in pre- and postmenopausal women was similar (404.9 and 384.7 minutes), but shorter than in young women (448.2 minutes, P = 0.030 and <0.003, respectively). Sleep efficiency followed the same pattern, being 84.3% in premenopausal (P = 0.027), 80.2% in postmenopausal (P < 0.003) and 93.4% in young women. Pre- and postmenopausal women had less slow wave sleep (duration or activity) and more wake time after sleep onset (duration or frequency). Insomnia complaints were more frequent after the menopause (P = 0.023). Sleepiness and mood scores were similar in all groups. Reaction speeds slowed with increasing age. After the menopause, better cognitive performance was associated with more rapid eye movement sleep. CONCLUSION: Objective sleep measures differed significantly between the young and postmenopausal groups. These differences may be more because of the physiology of ageing than the rapid changes across the menopause, since similar sleep characteristics were already present in the premenopausal women. The increase in sleep complaints after menopause was not associated with sleepiness or disturbances in objective sleep quality, mood or cognitive performance.

24-hour serum levels of growth hormone, prolactin, and cortisol in pre- and postmenopausal women: the effect of combined estrogen and progestin treatment.

OBJECTIVE: Our objective was to study the 24-h profiles of GH, prolactin (PRL), and cortisol concentrations in older postmenopausal and middle-aged premenopausal women, before and after estrogen-progestin treatment (EPT). DESIGN: The study was a randomized, placebo-controlled, double-blind trial. GH, PRL, and cortisol were sampled every 20 min for 24 h in 18 postmenopausal (aged 58-70 yr) and 17 premenopausal (aged 45-51 yr) women before and after 6 months of EPT. RESULTS: The mean 24-h GH (1.0 vs. 1.8 mU/liter, P = 0.033) and PRL (6.8 vs. 10.0 ng/ml, P = 0.009) concentrations were lower in postmenopausal than in premenopausal women. After EPT, the postmenopausal GH and PRL did not differ from premenopausal baseline levels. Postmenopausal mean 24-h GH (P < 0.001) and PRL (P = 0.002), daytime GH (P < 0.001) and nighttime PRL (P = 0.004) were higher during EPT compared with placebo. Cortisol levels did not differ. Premenopausal mean nighttime PRL (P = 0.026) and cortisol (P = 0.018) were higher during EPT compared with placebo. Postmenopausal PRL and premenopausal GH and PRL concentrations were higher at night than during the day. EPT did not alter this pattern. CONCLUSIONS: Menopause was associated with decreased 24-h levels of GH and PRL, which were reversible with EPT. In contrast, cortisol levels were not affected by menopause or EPT. In middle-aged premenopausal women, the studied effects of EPT were limited to nighttime increases of PRL and cortisol.

Gender differences in age and BMI distributions in partial upper airway obstruction during sleep.

The obstructive sleep apnea-hypopnea syndrome occurs more frequently and with higher apnea-hypopnea indices in men than in women. To investigate the gender differences we extended our respiratory analyses during sleep to cover not only periodic obstruction (apnea and hypopnea) but also nonperiodic partial upper airway obstruction during sleep and their associations with increasing age or body mass index (BMI). The clinical sleep recordings with the static-charge-sensitive bed (SCSB) and oximeter were reviewed in 233 age and BMI-matched men-women pairs. Periodic obstruction increased with increasing BMI only in men. Nonperiodic partial obstruction increased with moderate to morbid obesity in women and men after the age of 65 years. Our findings suggest that while partial upper airway obstruction increases with increasing age and BMI in both genders, men have a gender specific BMI dependent predisposition for periodic obstruction (obstructive sleep apnea). The apnea-hypopnea index is likely to underestimate the impact of sleep-disordered breathing, particularly in elderly patients.