Search Results (43)

Background and Objectives: Pregnancy causes various physiological and hormonal changes that disrupt sleep architecture and modify respiratory patterns, increasing the risk of sleep-related breathing disorders (SBDs) such as obstructive sleep apnea (OSA) and potentially exacerbating pre-existing conditions. These disorders have been linked to adverse maternal and fetal outcomes. However, current screening tools remain inadequate, and data, including from Portugal, remain limited. This study aimed to assess the prevalence of SBD symptoms suggestive of sleep-disordered breathing during pregnancy, characterize the population, and explore associations with demographic and anthropometric parameters. Materials and Methods: A prospective observational study was conducted from July to December 2024 at Hospital da Luz Lisboa, involving pregnant women ≥ 18 years attending routine consultations. Participants completed a structured questionnaire that assessed demographic and anthropometric data, comorbidities, ten SBD symptoms, and the Epworth Sleepiness Scale (ESS). Results: The cohort included 289 participants, with a mean age of 34.4 years and pre-pregnancy body mass index (BMI) of 23.6 kg/m². On average, women reported 3.1 SBD symptoms, with fatigue (65.4%), memory/concentration impairment (52.2%), and non-restorative sleep (50.5%) being the most common. Excessive daytime sleepiness (ESS >10) was present in 22.8% of the population. Snoring was significantly associated with older age and higher BMI (p = 0.0009 and p < 0.0001, respectively). Both the number of symptoms and ESS scores tended to increase with gestational age, particularly in the third trimester. Women with diabetes had higher odds of reporting snoring, nocturnal dyspnea, and witnessed apneas, with odds ratios of 4.65, 8.77, and 11.38, respectively. Conclusions: SBD symptoms and daytime sleepiness are highly prevalent in pregnancy and typically increase with advancing gestation. These findings emphasize the need for improved clinical strategies to enable early identification and management of SBD in pregnant women, thereby reducing maternal-fetal complications. Full article

Background: Surfactant Protein D (SP-D) is a critical immunomodulatory collectin maintaining alveolar homeostasis. Obstructive sleep apnea (OSA)-related intermittent hypoxia (IH) disrupts pulmonary surfactant integrity; however, severity-dependent SP-D dynamics remain incompletely characterized. This study explores SP-D as a potential indicator of IH-induced alveolar stress and evaluates whether Galectin-3 (Gal-3) inhibition modulates surfactant homeostasis. Methods: Forty adult male Sprague-Dawley rats (8 per group) were randomized to Control (normoxia), Moderate IH (MIH; 15–30 events/hour), Severe IH (SIH; 30–60 events/hour), MIH + Gal-3 inhibitor (Modified Citrus Pectin, 800 mg/kg/day), or SIH + Gal-3 inhibitor. IH exposure lasted 8 h/day for 10 days. Outcomes included circulating SP-D, Surfactant Protein B (SP-B), inflammatory markers, physiological parameters, and histopathological lung injury scores assessed via American Thoracic Society guidelines. Results: SP-D levels showed numerical reductions with increasing IH severity (Control: 1969.07 pg/mL [IQR: 262.15]; SIH: 1404.30 pg/mL [IQR: 351.88]), representing a 28.6% decrease. However, between-group variability resulted in non-significant omnibus testing (Kruskal–Wallis p = 0.187). Gal-3 inhibition elevated SP-D levels, particularly in severe IH (2133.95 pg/mL [IQR: 1240.70]), though high inter-individual variability was observed (CV = 58.1%). SP-B showed significant suppression under moderate IH (p = 0.019) with restoration by treatment. Exploratory correlation analysis revealed moderate positive associations between SP-D and heart rate (r = 0.587) and respiratory rate (r = 0.419) in severe IH, though these did not reach statistical significance (p = 0.126 and p = 0.301, respectively). Histologically, severe IH induced diffuse alveolar damage (total lung score: 19.67 ± 0.82). Gal-3 inhibition produced context-dependent effects: protective in severe IH but paradoxically exacerbating inflammation under moderate IH (29.20 ± 4.64 vs. 20.00 ± 4.34; p < 0.05). Gal-3 inhibition significantly attenuated cardiac injury (injury score: 0.00 ± 0.00 vs. 7.17 ± 0.75 in severe IH; p < 0.001, η² = 0.859). Conclusions: SP-D demonstrates severity-associated alterations consistent with alveolar epithelial stress during IH, though high variability limits definitive biomarker validation in this sample. Gal-3 inhibition modulates surfactant homeostasis and attenuates cardiopulmonary injury in a context-dependent manner. These findings support further investigation into SP-D as a component of multimodal severity stratification in OSA and highlight Gal-3 inhibition as a context-dependent anti-inflammatory strategy, pending validation in larger cohorts with tissue-level confirmation. Full article

Background/Objectives: Non-restorative sleep (NRS)—a subjective feeling of unrefreshing/insufficient rest despite adequate sleep duration—an important sleep-quality indicator is associated with depression and mortality. We examined whether insoluble dietary fiber intake is associated with NRS in Japanese adults, after adjusting for socioeconomic, lifestyle, and dietary factors. Methods: Using cross-sectional data from 5034 adult (≥20 years) respondents of the National Health and Nutrition Surveys (2014 and 2018), Japan, self-assessed NRS (coded as 1, absence as 0) was analyzed with insoluble fiber intake (g/1000 kcal) modeled as a continuous variable; logistic regression analyses with progressive adjustments included Model 1, adjusted for sex, age, and body mass index; Model 2, comprising socioeconomic and lifestyle factors; Model 3, adjusted for sleep duration; and Model 4, which included dietary energy, protein, fat, vitamin D, and magnesium. Results: Among 19.3% of participants with NRS, the median (interquartile range) insoluble dietary fiber intake was 5.45 (4.10–6.97) g/1000 kcal, with higher NRS prevalence among younger adults (<60 years), non-drinkers (no habitual alcohol consumption), and individuals with short sleep (<6 h). Higher insoluble dietary fiber intake was consistently associated with a lower NRS likelihood, before and after adjustment for potential confounders. In the fully adjusted model, younger age (<60 years), no habitual alcohol consumption, and short sleep (<6 h) were independently associated with greater odds of NRS. Conclusions: Higher insoluble dietary fiber density correlated with lower odds of NRS, indicating a significant association, rather than causation, that warrants longitudinal clarification of the temporal relationship between dietary fiber intake and perceived sleep restorativeness. Full article

Fibromyalgia is a chronic syndrome characterized by widespread musculoskeletal pain, fatigue, non-restorative sleep, and cognitive impairment. Its pathogenesis reflects a complex interplay between central and peripheral mechanisms, including altered pain modulation, neuroinflammation, mitochondrial dysfunction, autonomic imbalance, and genetic and epigenetic factors. Evidence from neuroimaging, omics studies, and neurophysiology supports this multifactorial model. Epidemiological updates confirm a global prevalence of 2–8%, with a strong female predominance and a significant impact on quality of life and healthcare costs. Diagnostic criteria have evolved from the 1990 American College of Rheumatology tender points to the 2010/2011 revisions and the 2016 update, improving case ascertainment but still lacking objective biomarkers. Recent omics and systems biology approaches have revealed transcriptional, proteomic, and metabolic signatures that may enable molecularly informed stratification. Therapeutic management remains multidisciplinary, combining pharmacological interventions (e.g., duloxetine, pregabalin, milnacipran) with non-pharmacological strategies such as graded aerobic exercise and cognitive behavioral therapy. Emerging approaches include drug repurposing to target neuroinflammation, mitochondrial dysfunction, and nociceptive pathways. Despite promising advances, progress is limited by small sample sizes, heterogeneous cohorts, and lack of standardization across studies. Future priorities include large-scale validation of biomarkers, integration of multi-omics with clinical phenotyping, and the design of precision-guided trials. By synthesizing mechanistic insights with clinical evidence, this review provides an updated framework for the diagnosis and management of fibromyalgia, highlighting pathways toward biomarker-guided, personalized medicine. Full article

Background/Objective: Sleep is a vital determinant of human health, where both its quantity and quality directly impact physical and mental well-being. Thermoregulation plays a pivotal role in sleep quality, as the body’s ability to regulate temperature varies across different sleep stages. This study examines the effects of a novel real-time temperature adjustment (RTA) mattress, which dynamically modulates temperature to align with sleep stage transitions, compared to constant temperature control (CTC). Through polysomnographic (PSG) assessments, this study evaluates how adaptive thermal regulation influences sleep architecture, aiming to identify its potential for optimizing restorative sleep. Methods: A prospective longitudinal cohort study involving 25 participants (13 males and 12 females; mean age: 39.7 years) evaluated sleep quality across three conditions: natural sleep (Control), CTC (33 °C constant mattress temperature), and RTA (temperature dynamically adjusted: 30 °C during REM sleep; 33 °C during non-REM sleep). Each participant completed three polysomnography (PSG) sessions. Sleep metrics, including total sleep time (TST), sleep efficiency, wake after sleep onset (WASO), and sleep stage percentages, were assessed. Repeated-measures ANOVA and post hoc analyses were performed. Results: RTA significantly improved sleep quality metrics compared to Control and CTC. TST increased from 356.2 min (Control) to 383.2 min (RTA, p = 0.030), with sleep efficiency rising from 82.8% to 87.3% (p = 0.030). WASO decreased from 58.2 min (Control) and 64.6 min (CTC) to 49.0 min (RTA, p = 0.067). REM latency was notably reduced under RTA (110.4 min) compared to Control (141.8 min, p = 0.002). The REM sleep percentage increased under RTA (20.8%, p = 0.006), with significant subgroup-specific enhancements in males (p = 0.010). Females showed significant increases in deep sleep percentage under RTA (12.3%, p = 0.011). Conclusions: Adaptive thermal regulation enhances sleep quality by aligning mattress temperature with physiological needs during different sleep stages. These findings highlight the potential of RTA as a non-invasive intervention to optimize restorative sleep and promote overall well-being. Further research could explore long-term health benefits and broader applications. Full article

Background/Objectives: Sleep is pivotal for recovery, immunity, and energy restoration; however, sleep problems exist in elite athletes. Nutrition and supplementation strategies can play both a positive and negative role in sleep quality and quantity. Elite athletes experience unique psychological and physiological demands above non-elite athletes and may require different nutrition strategies to promote sleep. Nutrient interventions and their effect on sleep in elite athletes is an emerging area, with further research warranted. Methods: Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) extension for Scoping Reviews and Joanna Brigg’s Institute Reviewer’s Manual for Scoping Reviews were utilised to assess the available evidence on nutrition strategies used to promote sleep in elite athlete cohorts, and we tried to identify the interventions that could be best researched in the future. NUtrition QUality Evaluation Strengthening Tools (NUQUEST) was used to enhance rigour and assess risk of bias in studies. The Paper to Podium (P2P) Matrix was used to offer practitioners practical recommendations. Results: 12 studies met the inclusion criteria for nutrition interventions or exposures to promote sleep in elite athletes. The median participant group size was 19 and study designs were considered together to ascertain potential sleep promoting strategies. Kiwifruit, Tart Cherry Juice and high dairy intake, limited to females, have demonstrated the highest potential to promote sleep in elite athletes, despite limited sample sizes. A-lactalbumin, carbohydrate pre-bed, casein, tryptophan, probiotic and meeting energy demands showed varying results on sleep quality in elite athletes. Conclusions: Kiwifruit, Tart Cherry Juice and dairy consumption offer potential nutritional interventions to promote sleep in elite athletic populations, while protein-based interventions may have a ceiling effect on sleep quality when elite athletes are already consuming >2.5 g·kg⁻¹ body mass (BM) or are already meeting their sleep duration needs. Full article

Parkinson’s disease (PD) is a progressive, irreversible neurodegenerative disorder characterized by motor impairments and a wide spectrum of non-motor symptoms, including gastrointestinal dysfunction, sleep disturbances, depression, and cognitive decline. These manifestations arise from disturbances across multiple systems—gastrointestinal, neuroendocrine, immune, enteric, and central nervous systems. Alterations in the gut microbiota may play a causal role in PD onset and frequently accompany disease progression. The gut–brain axis, particularly the vagus nerve, is increasingly recognized as a key communication pathway whose dysregulation contributes to systemic dysfunction and the breakdown of homeostasis, ultimately driving PD pathology. Currently, there is no cure for PD, and existing treatments primarily target symptom relief. Effective management of PD requires a comprehensive approach that integrates multiple pharmacologically active agents aimed at restoring impaired organ functions and, when possible, neutralizing toxic factors that accelerate disease progression. One promising therapeutic avenue lies in functional gut bacteria, which form the basis for developing live biotherapeutic products, postbiotics, and bacterial vesicles. In this review, we summarize current data on the effects of probiotics in PD, drawing on both animal models and clinical studies. We highlight the role of probiotics in modulating PD pathophysiology and discuss their potential as adjunctive therapeutic agents. To provide a broader perspective, we also include sections describing the clinical manifestations of PD, gut microbiota alterations associated with the disease, and the role of artificial intelligence, particularly machine learning, in constructing functional models of PD. Full article

The relationship between sleep and epilepsy involves complex interactions between thalamocortical circuits, circadian mechanisms, and sleep architecture that fundamentally influence seizure susceptibility and cognitive outcomes. Epileptic activity disrupts essential sleep oscillations, particularly sleep spindles generated by thalamic circuits. Thalamic epileptic spikes actively compete with physiological sleep spindles, impairing memory consolidation and contributing to cognitive dysfunction in epileptic encephalopathy. This disruption explains why patients with epilepsy often experience learning difficulties despite adequate seizure control. Sleep stages show differential seizure susceptibility. REM sleep provides robust protection through enhanced GABAergic inhibition and motor neuron suppression, while non-REM sleep, particularly slow-wave sleep, increases seizure risk. These observations reveal fundamental mechanisms of seizure control within normal brain physiology. Circadian clock genes (BMAL1, CLOCK, PER, CRY) play crucial roles in seizure modulation. Dysregulation of these molecular timekeepers creates permissive conditions for seizure generation while being simultaneously disrupted by epileptic activity, establishing a bidirectional relationship. These mechanistic insights are driving chronobiological therapeutic approaches, including precisely timed antiseizure medications, sleep optimization strategies, and orexin/hypocretin system interventions. This understanding enables a paradigm shift from simple seizure suppression toward targeted restoration of physiological brain rhythms, promising transformative epilepsy management through sleep-informed precision medicine. Full article

This narrative review examines the complex relationship between sleep changes during the menopausal transition and cardiometabolic risks. The most common complaint about sleep is increased awakenings during sleep. Other complaints include having trouble falling asleep, waking up too early, insufficient and non-restorative sleep, and overall poor quality. Sleep determined using objective methods also indicates that greater awakenings after sleep onset are associated with the period of menopausal transition. Polysomnography recordings suggest physiological hyperarousal during sleep. Changes in other sleep metrics, such as sleep latency and sleep duration, are less consistent, and some studies suggest they may not worsen during the menopausal transition. These sleep issues are influenced by multiple factors, such as hormonal fluctuations, vasomotor symptoms, and psychosocial factors, and evidence suggests that hypothalamic kisspeptin/neurokinin B/dynorphin (KNDy) neurons are key underlying mechanisms for these associations. The menopausal transition is also associated with increases in cardiometabolic risk factors, such as body fat, altered lipid profiles, blood pressure, and vascular health. Emerging evidence suggests that poor sleep health during this period is associated with increased cardiometabolic risks and adverse cardiovascular outcomes. Thus, addressing sleep disturbances is crucial for comprehensive healthcare during the menopausal transition to safeguard long-term cardiometabolic health. Future research is needed to investigate interventions that can improve sleep and their impact on cardiometabolic health in this population experiencing increases in cardiometabolic risk. Full article

Transcranial direct current stimulation (tDCS) can modulate cortical excitability in a polarity-specific manner, yet identical protocols often produce inconsistent outcomes across sessions or individuals. This narrative review proposes that much of this variability arises from the brain’s intrinsic temporal landscape. Integrating evidence from chronobiology, sleep research, and non-invasive brain stimulation, we argue that tDCS produces reliable, polarity-specific after-effects only within a circadian–homeostatic “window of efficacy”. On the circadian (Process C) axis, intrinsic alertness, membrane depolarisation, and glutamatergic gain rise in the late biological morning and early evening, whereas pre-dawn phases are marked by reduced excitability and heightened inhibition. On the homeostatic (Process S) axis, consolidated sleep renormalises synaptic weights, widening the capacity for further potentiation, whereas prolonged wakefulness saturates plasticity and can even reverse the usual anodal/cathodal polarity rules. Human stimulation studies mirror this two-process fingerprint: sleep deprivation abolishes anodal long-term-potentiation-like effects and converts cathodal inhibition into facilitation, while stimulating at each participant’s chronotype-aligned (phase-aligned) peak time amplifies and prolongs after-effects even under equal sleep pressure. From these observations we derive practical recommendations: (i) schedule excitatory tDCS after restorative sleep and near the individual wake-maintenance zone; (ii) avoid sessions at high sleep pressure or circadian troughs; (iii) log melatonin phase, chronotype, recent sleep and, where feasible, core temperature; and (iv) consider mild pre-heating or time-restricted feeding as physiological primers. By viewing Borbély’s two-process model and allied metabolic clocks as adjustable knobs for plasticity engineering, this review provides a conceptual scaffold for personalised, time-sensitive tDCS protocols that could improve reproducibility in research and therapeutic gain in the clinic. Full article

Suk-SaiYasna (SSY) is a well-documented traditional Thai herbal formula in the Royal Scripture of King Narai’s Traditional Medicine. SSY contains Cannabis sativa leaves as a key ingredient and has traditionally been used to promote sleep, alleviate stress-related symptoms, and stimulate appetite. This study aimed to investigate the neuroprotective effects of SSY in a mouse model of unpredictable chronic mild stress (UCMS)-induced cognitive impairment and explore the underlying mechanisms, particularly antioxidant enzyme pathways. Behavioral tests, including the Y-maze test, novel object recognition test, and Morris water maze test, demonstrated that UCMS-exposed mice exhibited cognitive impairment compared to non-stress mice. However, SSY treatment significantly improved learning and memory performance in UCMS-exposed mice. Mechanistic studies revealed that SSY reduced lipid peroxidation in the hippocampus and frontal cortex, key brain regions affected by chronic stress. Furthermore, UCMS significantly reduced the activity of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT), whereas SSY treatment restored their activity, indicating antioxidative and neuroprotective effects in vivo. Gene expression analysis further revealed that SSY regulates oxidative stress via the Nrf2/Keap1 signaling pathway. In vitro studies using 2,2′-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid (ABTS) and 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay confirmed the radical scavenging activities of SSY and its herbal components, demonstrating significant antioxidant potential. Phytochemical analysis identified delta-9-tetrahydrocannabinol, delta-9-tetrahydrocannabinolic acid A, and cannabinoids as bioactive compounds in SSY, along with potent antioxidants such as gallic acid, myricetin, myristicin, piperine, costunolide, and gingerol. These findings suggest that the SSY formula mitigates UCMS-induced cognitive function through its antioxidant properties via multiple pathways, including radical scavenging activities, modulating the Nrf2-Keap1 pathway, inducing the expression of HO-1, NQO1 mRNAs, and other antioxidant enzymes. This work bridges traditional Thai medicine with modern neuropharmacology. Full article

Sleep behaviors, particularly midday rest periods, represent an often overlooked yet potentially significant factor in workplace attitudes and experiences. Despite their common practice in many cultures, the relationship between these restorative breaks and employees’ evaluations of their work environment remains underexplored in organizational research. This study investigates this relationship using longitudinal data from the China Family Panel Studies (CFPS), applying the work, non-work, and sleep framework (WNSF) as our theoretical foundation. Through a quasi-natural experimental approach, we discovered that midday rest periods positively influence workplace evaluations, but in a nuanced manner. Our findings reveal a pronounced inverted U-shaped relationship, suggesting that both insufficient and excessive duration of these breaks might diminish their benefits, while optimal duration maximizes positive outcomes. We strengthened these conclusions through rigorous methodological approaches including instrumental variable techniques, sensitivity analysis, treatment effect models, and matching models. The consistency of results across multiple analytical approaches corroborates our findings. This research both validates and extends the WNSF, highlighting the importance of strategic rest periods in organizational settings and offering practical insights for workplace policy development that can benefit both individuals and organizations in contemporary work environments. Full article

Despite the growing emphasis on cognitive health, evidence regarding individual and environmental factors influencing cognitive functioning remains limited. We aimed to examine the association of personal and environmental factors, specifically perceived acoustic environment exposure and nonrestorative sleep, with cognitive functioning among Chinese adults. Between July and August 2022, we recruited 970 Chinese adults from all districts in Hong Kong for our cross-sectional study. Univariable and structured multiphase linear regression analyses were conducted to identify the contributory factors. Among 970 Chinese adults, the structured multiphase linear regression model revealed that being in their 30s (β = 0.160; 95% CI: 0.004, 0.315) and 40s (β = 0.186; 95% CI: 0.029, 0.343), being female (β = 0.095; 95% CI: 0.018, 0.173), being former smokers, and having medical consultations, medical histories (eczema, hearing problems, and insomnia), perceived acoustic environment exposure (traffic and mechanical sounds (β = 0.011; 95% CI: 0.008, 0.013), nature and music sounds (β = 0.004; 95% CI: 0.001, 0.007), and human sounds (β = 0.002; 95% CI: 0.0004, 0.005)), and psychological symptoms (perceived stress, depressive, and anxiety symptoms) were associated with worse cognitive functioning. Moreover, more nonrestorative sleep (β = −0.015; 95% CI: −0.022, −0.007) was also associated with worse cognitive functioning. This study revealed that increased perceived acoustic environment exposure and a higher degree of nonrestorative sleep were associated with poorer cognitive functioning among Chinese adults. This underscores the need for public health strategies and policies aimed at fostering a healthy acoustic environment and promoting sleep hygiene education in the community. Full article

Stress and sleep share a reciprocal relationship, where chronic stress often leads to sleep disturbances that worsen neurodegenerative and psychiatric conditions. Non-neuronal cells, particularly astrocytes and microglia, play critical roles in the brain’s response to stress and the regulation of sleep. Astrocytes influence sleep architecture by regulating adenosine signaling and glymphatic clearance, both of which can be disrupted by chronic stress, leading to reduced restorative sleep. Microglia, activated under stress conditions, drive neuroinflammatory processes that further impair sleep and exacerbate brain dysfunction. Additionally, the gut–brain axis mediates interactions between stress, sleep, and inflammation, with microbial metabolites influencing neural pathways. Many of these effects converge on the disruption of synaptic processes, such as neurotransmitter balance, synaptic plasticity, and pruning, which in turn contribute to the pathophysiology of neurodegenerative and psychiatric disorders. This review explores how these cellular and systemic mechanisms contribute to stress-induced sleep disturbances and their implications for neurodegenerative and psychiatric disorders, offering insights into potential therapeutic strategies targeting non-neuronal cells and the gut–brain axis. Full article

KNDy (kisspeptine, neurokinin B, dynorphin) neurons, located in the hypothalamus, play a crucial role in the development of vasomotor symptoms (VSM) in menopausal women. Estrogen withdrawal during menopause leads to the hyperactivation of kisspeptin and neurokinin B (NKB) secretion, contributing to the onset of these symptoms. The identification of NKB/neurokinin B receptor (NK3R) signaling as a key mechanism in menopausal hot flashes has driven the development of NK3R antagonists. These antagonists restore the disrupted balance in KNDy neuron activity caused by estrogen deficiency, thereby reducing the frequency and severity of VMS. In 2023, the FDA approved fezolinetant, the first selective NK3R antagonist, for the treatment of moderate to severe VMS associated with menopause. Additionally, elinzanetant, a dual neurokinin-1 and neurokinin-3 receptor antagonist, has demonstrated promising results. The approval application for elinzanetant was supported by positive findings from the OASIS 1, 2, and 3 Phase III clinical studies. The dual antagonism of NK-1 and NK-3 receptors enhances its efficacy by alleviating menopause-related sleep disturbances and modulating peripheral vasodilatation. In this regard, elinzanetant represents a promising non-hormonal treatment that targets the underlying causes of VMS through NK-1 and NK-3 receptor pathways. The development of neurokinin B antagonist for VMS treatment exemplifies the impact of advanced pharmacological research on gynecological endocrinology. Full article