Longitudinal studies show that the menopausal transition (MT) is associated with poorer self-reported sleep. Increases in sleep disturbances across and beyond the MT are strongly associated with vasomotor symptoms (VMS) but occur even without VMS. We analyzed data from baseline through 13 annual or biennial follow-up assessments from SWAN's multi-racial/ethnic cohort of midlife women, specifically focusing on patterns of sleep problems in the years preceding and following the final menstrual period (FMP). The FMP demarcated the MT and the postmenopausal period. We addressed the following questions: (1) are there distinct trajectory patterns of sleep problems across the MT, and (2) do pre-FMP sleep trajectories predict sleep problems around the time of FMP (trans-FMP) and post-FMP? Group-based trajectory modeling using repeated measures log-binomial regression with generalized estimating equation methods was used to describe trajectory patterns of the most prevalent sleep problem, waking several times at least 3 nights weekly during the previous 2 weeks, in 1,285 naturally menopausal women.We found (1) 4 distinct trajectories for waking several times per night across the MT [low prevalence (n=487; 37.9%), moderate prevalence (n=365; 28.4%), increasing prevalence (n=197; 15.3%), and high prevalence (n=236; 18.4%)], (2) the prevalence of sleep problems increased overall, but in one trajectory group (increasing prevalence) more than in the other three, and (3) trouble falling asleep, early morning awakening, and frequent VMS were strongly associated with problems waking several times that persist into postmenopause.Using trajectory analysis, we showed that, in general, awakenings were stable from pre-FMP to post-FMP.

Sleep disturbance is one of the most common and debilitating symptoms experienced by women during the menopause transition. However, there are currently no therapies specifically approved for sleep disturbance associated with the menopause. Here, we consider how to characterize sleep disturbance associated with the menopause and discuss its etiology, including the latest advances in our understanding of the neuronal circuits that regulate reproduction, body temperature, sleep, and mood; and reflect on its impact on women's health and well-being. We also examine the current treatment landscape and look to the future of treatment for this condition.We conducted a review of the literature and combined this with discussion with experts in the fields of sleep and menopause as well as experiences from our own clinical practices.Sleep disturbance associated with the menopause is characterized by frequent night-time awakenings and increased awake time after sleep onset. Its impacts are wide-ranging, negatively affecting health as well as personal and social relationships, productivity, and work performance. There is currently an unmet need for effective, safe, and well-tolerated treatments to address this important symptom, and wider recognition of the association between sleep disturbances and the menopause is needed. Sleep disturbances associated with the menopause can result from hormone changes as well as vasomotor and mood symptoms. Growing research has contributed to our knowledge of the role of hypothalamic estrogen-sensitive kisspeptin/neurokinin B/dynorphin neurons. These neurons are thought to integrate the gonadotropin-releasing hormone pathway and the pathways responsible for the homeostatic control of body temperature and the circadian regulation of sleep-wake cycles. Understanding these neurons offers the potential to create treatments that target a key cause of sleep disturbance associated with the menopause. Further research to understand their etiology and characterize the neuronal circuits responsible could benefit the development of these targeted treatment approaches.Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The Menopause Society.

The impact of hot flashes on sleep is of great clinical interest, but results are inconsistent, especially when both hot flashes and sleep are measured objectively. Using objective and subjective measurements, we examined the impact of hot flashes on sleep by inducing hot flashes with a gonadotropin-releasing hormone agonist.The gonadotropin-releasing hormone agonist leuprolide was administered to 20 healthy premenopausal volunteers without hot flashes or sleep disturbances. Induced hot flashes were assessed objectively (skin conductance monitor) and subjectively (daily diary) during 1-month follow-up. Changes from baseline in objective sleep quality (actigraphy) and subjective sleep quality (Pittsburgh Sleep Quality Index) were compared between women who developed and women who did not develop objective hot flashes and, in parallel analyses, subjective hot flashes.New-onset hot flashes were recorded in 14 (70%) women and reported by 14 (70%) women (80% concordance). Estradiol was universally suppressed. Objective sleep efficiency worsened in women with objective hot flashes and improved in women without objective hot flashes (median decrease, 2.6%; median increase, 4.2%; P = 0.005). Subjective sleep quality worsened more in those with subjective hot flashes than in those without subjective hot flashes (median increase in Pittsburgh Sleep Quality Index, 2.5 vs 1.0; P = 0.03). Objective hot flashes were not associated with subjective sleep quality, nor were subjective symptoms linked to objective sleep measures.This experimental model of induced hot flashes demonstrates a causal relationship between hot flashes and poor sleep quality. Objective hot flashes result in worse objective sleep efficiency, whereas subjective hot flashes worsen perceived sleep quality.

The aim of the study was to assess the association of sleep disturbance with psychological characteristics, somatic symptoms and previously identified risk factors.Data were from 148,938 postmenopausal women enrolled in The Women's Health Initiative who provided cross-sectional information about psychological characteristics, somatic symptoms and the character of their sleep. Overall sleep quality was based on the Women's Health Initiative Insomnia Rating Scale (WHI IRS), a measure that assessed five types of sleep disturbance.Three factors accounted for nearly 20% of the variation in the WHI IRS: a scale for somatic symptoms, daytime restlessness and either depression or emotional well-being. Other independently associated factors were night sweats, pain and worry about expressing anger. Several factors that had been linked to sleep disturbance in other studies were found to have at most a weak independent association in this analysis. These included income, education, marital status, activity level, obesity level, hot flashes, coffee drinking and smoking.Factors strongly associated with sleep disturbance in this study deserve further evaluation to determine the reasons for the association and whether the associations suggest possible treatments for sleep disturbance.Copyright © 2012 Elsevier B.V. All rights reserved.

To determine whether hot flashes produce sleep disturbance in postmenopausal women.This study was performed in a university medical center laboratory with 18 postmenopausal women with hot flashes, six with no hot flashes, and 12 cycling women, all healthy and medication free. Polysomnography, skin and rectal temperatures, and skin conductance to detect hot flashes were recorded for four nights. Nights 2, 3, and 4 were run at 30 degrees C, 23 degrees C, and 18 degrees C in randomized order.During the first half of the night, the women with hot flashes had significantly more arousals and awakenings than the other two groups and the 18 degrees C ambient temperature significantly reduced the number of hot flashes, from 2.2 +/- 0.4 to 1.5 +/- 0.4. These effects did not occur in the second half of the night. In the first half of the night, most hot flashes preceded arousals and awakenings. In the second half, this pattern was reversed.In the second half of the night, rapid eye movement sleep suppresses hot flashes and associated arousals and awakenings. This may explain previous discrepancies between self-reported and laboratory-reported data in postmenopausal women with hot flashes.

Sleep is crucial for optimal well-being, and sex differences in sleep quality have significant implications for women’s health. We review the current literature on sex differences in sleep, such as differences in objective and subjective sleep measures and their relationship with aging. We then discuss the convincing evidence for the role of ovarian hormones in regulating female sleep, and survey how these hormones act on a multitude of brain regions and neurochemicals to impact sleep. Lastly, we identify several important areas in need of future research to narrow the knowledge gap and improve the health of women and other understudied populations.

Gonadal steroids and gender are risk factors for sleep disruptions and insomnia in women. However, the relationship between ovarian steroids and sleep is poorly understood. In rodent models, estradiol (E2) suppresses sleep in females suggesting that E2 may reduce homeostatic sleep need. The current study investigates whether E2 decreases sleep need and the potential mechanisms that govern E2 suppression of sleep. Our previous findings suggest that the median preoptic nucleus (MnPO) is a key nexus for E2 action on sleep. Using behavioral, neurochemical, and pharmacological approaches, we tested whether (1) E2 influenced the sleep homeostat and (2) E2 influenced adenosine signaling in the MnPO of adult female rats. In both unrestricted baseline sleep and recovery sleep from 6-h sleep deprivation, E2 significantly reduced nonrapid eye movement (NREM) sleep-delta power, NREM-slow wave activity (NREM-SWA, 0.5–4.0 Hz), and NREM-delta energy suggesting that E2 decreases homeostatic sleep need. However, coordinated with E2-induced changes in physiological markers of homeostatic sleep was a marked increase in MnPO extracellular adenosine (a molecular marker of homeostatic sleep need) during unrestricted and recovery sleep in E2-treated but not oil control animals. While these results seemed contradictory, systemically administered E2 blocked the ability of CGS-21680 (adenosine A2A receptor agonist) microinjected into the MnPO to increase NREM sleep suggesting that E2 may block adenosine signaling. Together, these findings provide evidence that E2 may attenuate the local effects of the A2A receptors in the MnPO, which in turn may underlie estrogenic suppression of sleep behavior as well as changes in homeostatic sleep need.

Nocturnal vasomotor symptoms (nVMS), depressive symptoms (DepSx), and female reproductive hormone changes contribute to perimenopause-associated disruption in sleep continuity. Hormonal changes underlie both nVMS and DepSx. However, their association with sleep continuity parameters resulting in perimenopause-associated sleep disruption remains unclear.To determine the association between female reproductive hormones and perimenopausal sleep discontinuity independent of nVMS and DepSx.Daily sleep and VMS diaries, and weekly serum assays of female reproductive hormones were obtained for 8 consecutive weeks in participants with mild DepSx. Generalized estimating equations were used to examine associations of estradiol, progesterone, and follicle-stimulating hormone (FSH) with mean number of nightly awakenings, wakefulness after sleep-onset (WASO) and sleep-onset latency (SOL) adjusting for nVMS and DepSx.Academic medical center.Forty-five perimenopausal women with mild DepSx but no primary sleep disorder.Diary-measured sleep continuity parameters.Sleep disruption was common (median 1.5 awakenings/night, WASO 24.3 and SOL 20.0 minutes). More awakenings were associated with estradiol levels in the postmenopausal range (β=0.14, 95%CI 0.04 to 0.24, p=0.007), and higher FSH levels (β [one-unit increase]=0.12, 95%CI 0.02 to 0.22, p=0.02), but not with progesterone (β [one-unit increase]=-0.02, 95%CI -0.06 to 0.01, p=0.20) in adjusted models. Female reproductive hormones were not associated with WASO or SOL.Associations of more awakenings with lower estradiol and higher FSH levels provide support for a perimenopause-associated sleep discontinuity condition that is linked with female reproductive hormone changes, independent of nVMS and DepSx.© The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Background/Objectives: Perimenopause, impacting 80–90% of women, encompasses a range of vasomotor, urogenital, cognitive, and psychiatric symptoms associated with the fluctuation and gradual reduction of gonadal hormones. Moreover, the onset or worsening of sleep disturbances is prevalent during the menopausal transition. This narrative review seeks to elucidate the pathogenetic processes behind sleep disturbances during perimenopause and the main therapeutic options. Methods: The electronic databases PubMed, Scopus, Google Scholar, Web of Science, and Embase were queried for publications up to May 2024. Longitudinal, observational, case–control, and cross-sectional studies, as well as reviews and meta-analyses, were included in the review in order to explore the prevalence of sleep disorders during perimenopause, the pathogenetic mechanisms underlying the association between menopausal transition and sleep disorders, and the available non-pharmacological and pharmacological treatment options. Results: Sleep disturbances are common among perimenopausal women and include insomnia, sleep-related breathing disorders, and movement disorders. Fluctuations in estrogen and progesterone affect sleep quality, while vasomotor symptoms can disrupt sleep. Circadian changes, decreased melatonin production, and physiological changes associated with aging and mood disorders further exacerbate sleep disturbances. Conclusions: Managing sleep disorders in perimenopause requires an individualized approach, considering the multifactorial nature of these disturbances and providing background knowledge about the relationship between reproductive hormonal changes and sleep. Non-pharmacological treatments should be considered the first-line therapy; hormone therapy or non-hormonal pharmacological treatments can be considered according to the patients’ specific needs and risk factors. However, there is still a lack of standards on the appropriate management and treatment of sleep disorders in perimenopause.

Women frequently experience sleep disturbances, particularly night-time awakenings, as they transition menopause and enter postmenopause. Sleep is essential for optimal functioning and health. Persistent and distressing sleep disturbances across menopause can negatively impact daytime functioning and productivity, and increase risk for mental and physical health conditions. While multiple factors can disturb sleep, two unique factors in the context of menopause are vasomotor symptoms and the changing reproductive hormone environment. Vasomotor symptoms are associated with sleep disturbances and contribute significantly to awakenings and amount of time spent awake during the night. Even after accounting for vasomotor and depressive symptoms, lower estradiol and higher follicle stimulating hormone levels, indicative of menopause, are associated with sleep disturbance, particularly awakenings, suggesting that the hormone environment may directly affect sleep. Management strategies for clinically significant menopausal sleep disturbances include cognitive behavioral therapy for insomnia, which is effective and durable in treating menopausal insomnia. Hormone therapy alleviates sleep disturbances, particularly in the presence of disruptive vasomotor symptoms. Sleep disturbances have a significant impact on women's functioning and health, and there is a need for further research of the underlying mechanisms to advance effective preventative and treatment strategies that ensure optimal health and well-being of midlife women.

This study aims to evaluate subjective sleep quality in premenopausal and postmenopausal women and to study its association with night sweats, hot flashes, and depressive symptoms.A total of 158 healthy women were recruited; 107 were premenopausal (44-48 y) and 51 were postmenopausal (53-58 y). Sleep quality was evaluated with the Basic Nordic Sleep Questionnaire, night sweats and hot flashes were evaluated with a specific symptom questionnaire, and depressive symptoms were evaluated with the Beck Depression Inventory.Postmenopausal women had poorer general sleep quality (P < 0.001), slept more restlessly (P = 0.020), and had more nocturnal awakenings (P = 0.015). However, the frequency of difficulty falling asleep, snoring, witnessed apnea, or use of sleep medication was similar between the groups. Furthermore, sleep latency, morning tiredness, or daytime tiredness did not differ between the groups. Postmenopausal women did not report more unintentional falling asleep at work or during leisure time; however, when not active, they dozed off more easily than premenopausal women (P < 0.001). Postmenopausal women had more night sweats (P < 0.001), hot flashes (P < 0.001), and depressive symptoms (P < 0.001). Even a low frequency of night sweats disturbed sleep in postmenopausal women, whereas only frequent night sweats were disturbing in premenopausal women. Depressive symptoms disturbed sleep regardless of menopause status.Maintenance insomnia, most evidently because of night sweats and hot flashes, seems to be the major type of insomnia in postmenopausal women and has to be considered when choosing insomnia treatment for this group. Initiation of sleep and daytime vitality are not, in general, affected by menopause.

The purposes of this study were to identify age-related changes in objectively recorded sleep patterns across the human life span in healthy individuals and to clarify whether sleep latency and percentages of stage 1, stage 2, and rapid eye movement (REM) sleep significantly change with age.Review of literature of articles published between 1960 and 2003 in peer-reviewed journals and meta-analysis.65 studies representing 3,577 subjects aged 5 years to 102 years.The research reports included in this meta-analysis met the following criteria: (1) included nonclinical participants aged 5 years or older; (2) included measures of sleep characteristics by "all night" polysomnography or actigraphy on sleep latency, sleep efficiency, total sleep time, stage 1 sleep, stage 2 sleep, slow-wave sleep, REM sleep, REM latency, or minutes awake after sleep onset; (3) included numeric presentation of the data; and (4) were published between 1960 and 2003 in peer-reviewed journals.In children and adolescents, total sleep time decreased with age only in studies performed on school days. Percentage of slow-wave sleep was significantly negatively correlated with age. Percentages of stage 2 and REM sleep significantly changed with age. In adults, total sleep time, sleep efficiency, percentage of slow-wave sleep, percentage of REM sleep, and REM latency all significantly decreased with age, while sleep latency, percentage of stage 1 sleep, percentage of stage 2 sleep, and wake after sleep onset significantly increased with age. However, only sleep efficiency continued to significantly decrease after 60 years of age. The magnitudes of the effect sizes noted changed depending on whether or not studied participants were screened for mental disorders, organic diseases, use of drug or alcohol, obstructive sleep apnea syndrome, or other sleep disorders.In adults, it appeared that sleep latency, percentages of stage 1 and stage 2 significantly increased with age while percentage of REM sleep decreased. However, effect sizes for the different sleep parameters were greatly modified by the quality of subject screening, diminishing or even masking age associations with different sleep parameters. The number of studies that examined the evolution of sleep parameters with age are scant among school-aged children, adolescents, and middle-aged adults. There are also very few studies that examined the effect of race on polysomnographic sleep parameters.

This study aims to estimate the prevalence and predictors of moderate/severe poor sleep in relation to the final menstrual period (FMP) in midlife women.Annual assessments were conducted in a population-based cohort of 255 women. All were premenopausal at cohort enrollment and reached natural menopause during the 16-year follow-up. The outcome measure was severity of poor sleep, as reported by participants in annual interviews for 16 years and as evaluated in relation to the FMP.The annual prevalence of moderate/severe poor sleep largely ranged from about 28% to 35%, with no significant differences in any year relative to the FMP for the sample overall. When sleep status was stratified at premenopausal baseline, premenopausal sleep status strongly predicted poor sleep around the FMP. Women with moderate/severe poor sleep in premenopause were approximately 3.5 times more likely to have moderate/severe poor sleep around menopause than those with no poor sleep at baseline in adjusted analysis (odds ratio, 3.58; 95% CI, 2.50-5.11; P < 0.0001), whereas mild poor sleepers in premenopause were approximately 1.5 times more likely to have moderate/severe poor sleep around menopause (odds ratio, 1.57; 95% CI, 0.99-2.47; P = 0.053). There was no significant association between poor sleep and time relative to the FMP among women who had no poor sleep at premenopausal baseline. Hot flashes were significantly associated with poor sleep (odds ratio, 1.79; 95% CI, 1.44-2.21; P < 0.0001 in adjusted analysis) but had no interaction with baseline sleep severity (interaction P = 0.25), indicating that hot flashes contributed to poor sleep regardless of baseline sleep status.Findings show a high prevalence of moderate/severe poor sleep in midlife women, with only a small "at-risk" subgroup having a significant increase in poor sleep in relation to the FMP. Sleep status at premenopausal baseline and concurrent hot flashes strongly and consistently predict poor sleep in the menopausal transition. Overall, poor sleep does not increase around the FMP and frequently occurs in the absence of hot flashes, indicating that sleep difficulties in the menopausal transition in generally healthy women are not simply associated with ovarian decline.

Progress in the field of insomnia since 2017 necessitated this update of the European Insomnia Guideline. Recommendations for the diagnostic procedure for insomnia and its comorbidities are: clinical interview (encompassing sleep and medical history); the use of sleep questionnaires and diaries (and physical examination and additional measures where indicated) (A). Actigraphy is not recommended for the routine evaluation of insomnia (C), but may be useful for differential‐diagnostic purposes (A). Polysomnography should be used to evaluate other sleep disorders if suspected (i.e. periodic limb movement disorder, sleep‐related breathing disorders, etc.), treatment‐resistant insomnia (A) and for other indications (B). Cognitive‐behavioural therapy for insomnia is recommended as the first‐line treatment for chronic insomnia in adults of any age (including patients with comorbidities), either applied in‐person or digitally (A). When cognitive‐behavioural therapy for insomnia is not sufficiently effective, a pharmacological intervention can be offered (A). Benzodiazepines (A), benzodiazepine receptor agonists (A), daridorexant (A) and low‐dose sedating antidepressants (B) can be used for the short‐term treatment of insomnia (≤ 4 weeks). Longer‐term treatment with these substances may be initiated in some cases, considering advantages and disadvantages (B). Orexin receptor antagonists can be used for periods of up to 3 months or longer in some cases (A). Prolonged‐release melatonin can be used for up to 3 months in patients ≥ 55 years (B). Antihistaminergic drugs, antipsychotics, fast‐release melatonin, ramelteon and phytotherapeutics are not recommended for insomnia treatment (A). Light therapy and exercise interventions may be useful as adjunct therapies to cognitive‐behavioural therapy for insomnia (B).

Insomnia, vasomotor symptoms (VMS) and depression often co-occur after the menopause, with consequent health problems and reductions in quality of life. The aim of this position statement is to provide evidence-based advice on the management of postmenopausal sleep disorders derived from a systematic review of the literature. The latter yielded results on VMS, insomnia, circadian rhythm disorders, obstructive sleep apnea (OSA) and restless leg syndrome (RLS). Overall, the studies show that menopausal hormone therapy (MHT) improves VMS, insomnia, and mood. Several antidepressants can improve insomnia, either on their own or in association with MHT; these include selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), and mirtazapine. Long-term benefits for postmenopausal insomnia may also be achieved with non-drug strategies such as cognitive behavioral therapy (CBT) and aerobic exercise. Continuous positive airway pressure (CPAP) and mandibular advancement devices (MADs) both reduce blood pressure and cortisol levels in postmenopausal women suffering from OSA. However, the data regarding MHT on postmenopausal restless legs syndrome are conflicting.Copyright © 2019 Elsevier B.V. All rights reserved.

Sleep restriction therapy (SRT) effectively treats insomnia but mechanisms are poorly understood. Theoretical models suggest that potentiation of sleep pressure and reduction of arousal are key mechanisms of action. To our knowledge, this has never been directly tested. We designed a randomized controlled trial with embedded mechanistic measurement to investigate if SRT causally modifies multidimensional assessments of sleep pressure and arousal.

Long-term sleep disturbances in menopausal women are closely related to cardiovascular disorders, metabolic disorders, and cognitive impairment. At present, hormone therapy (HT) is a standard treatment for menopausal symptoms. However, it remains unclear whether HT can improve sleep quality.We did a systematic review and meta-analysis to assess the effects of different HT regimens on menopausal sleep quality.We systematically searched MEDLINE, Embase, the Cochrane Central Register of Controlled Trials, PsycINFO, CINAHL, and Web of Science for randomized controlled trials of menopausal HT on sleep disturbances up to June 14,2021. Information about ongoing and unpublished trials was collected by searching WHOICTRP and ClinicalTrials.gov. Our primary outcome was sleep quality with objective measurements. We estimated the standardized mean difference (SMD) using random-effects models.We identified a total of 3,059 studies and finally included 15 studies in the meta-analysis. Compared with placebo, HT improved self-reported sleep outcomes (SMD = -0.13; 95% CI, -0.18 to -0.08, P  < 0.00001 and I2 = 41%), but not sleep parameters measured by polysomnography. Subgroup analyses according to the regimen of HT showed that 17β-estradiol (17β-E2) (SMD = -0.34; 95% CI, -0.51 to -0.17, P  < 0.0001, and I2 = 0%) and conjugated equine estrogens (SMD = -0.10; 95% CI, -0.12 to -0.07, P  < 0.00001, and I2 = 0%) improved sleep quality. Moreover, transdermal administration (SMD = -0.35; 95% CI, -0.64 to -0.06, and P  = 0.02) was more beneficial than oral (SMD = -0.10; 95% CI, -0.14 to -0.07, and P  < 0.00001). In addition, the combination of estrogen and progesterone had a positive effect on sleep disturbance (SMD = -0.10; 95% CI, -0.13 to -0.07, P  < 0.00001, and I2 = 0%), while estrogen monotherapy did not. The results showed that estrogen/micronized progesterone (SMD = -0.22; 95% CI, -0.37 to -0.06, P = 0.007, and I2 = 0%) and estrogen/medroxyprogesterone acetate (SMD = -0.10; 95% CI, -0.13 to -0.07, P  < 0.00001, and I2 = 0%) could alleviate sleep disturbance.HT has a beneficial effect on sleep disturbance to some extent, and the formulations and routes of administration of hormonal agents influence the effect size.Copyright © 2022 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The North American Menopause Society.

This study determined whether two different formulations of hormone therapy (HT): oral conjugated equine estrogens (o-CEE; 0.45 mg/d, n = 209), transdermal 17β-estradiol (t-E2; 50 μg/d, n = 201) plus cyclic progesterone (Prometrium, 200 mg) or placebo (PBO, n = 243) affected sleep domains in participants of the Kronos Early Estrogen Prevention Study.Participants completed the Pittsburgh Sleep Quality Index at baseline and during the intervention at 6, 18, 36, and 48 months. Global sleep quality and individual sleep domain scores were compared between treatments using analysis of covariance, and correlated with vasomotor symptom (VMS) scores using Spearman correlation coefficients.Global Pittsburgh Sleep Quality Index scores (mean 6.3; 24% with score >8) were similar across groups at baseline and were reduced (improved sleep quality) by both HT (average change -1.27 [o-CEE] and -1.32 [t-E2]) when compared with PBO (-0.60; P = 0.001 [o-CEE vs PBO] and P = 0.002 [t-E2 vs PBO]). Domain scores for sleep satisfaction and latency improved with both HT. The domain score for sleep disturbances improved more with t-E2 than o-CEE or PBO. Global sleep scores significantly correlated with VMS severity (rs = 0.170, P < 0.001 for hot flashes; rs = 0.177, P < 0.001 for night sweats). Change in scores for all domains except sleep latency and sleep efficiency correlated with change in severity of VMS.Poor sleep quality is common in recently menopausal women. Sleep quality improved with both HT formulations. The relationship of VMS with domains of sleep suggests that assessing severity of symptoms and domains of sleep may help direct therapy to improve sleep for postmenopausal women.

This study aimed to investigate the safety and efficacy of Xiangshao granules for treating emotional disorders in perimenopausal and postmenopausal women.The current investigation was a double-blind, randomized, placebo-controlled, multicenter trial that included 300 perimenopausal and postmenopausal Chinese women aged 40-60 years. Participants received either a placebo ( = 150) or Xiangshao granules ( = 150) for 8 weeks. Outcome measures included Hamilton Depression Rating Scale (HAMD) and Hamilton Anxiety Rating Scale (HAMA) scores, which were assessed at baseline, 4 weeks, and 8 weeks. The primary efficacy variables were changes in HAMD and HAMA scores after 8 weeks.After 8 weeks, the mean HAMD scores decreased from 15.0 to 7.9 in the Xiangshao group and from 16.3 to 10.0 in the placebo group, and the respective mean reductions in HAMA scores were from 16.0 to 8.5 and from 17.1 to 10.9. Clinical improvements in symptoms of both depression and anxiety after 8 weeks differed significantly in the two groups (< 0.05). The cure rate was significantly higher in the Xiangshao group. There were no significant differences in the rates of adverse events in the two groups.Xiangshao granules can relieve symptoms of depression and anxiety significantly and safely.