Sleep in women: a narrative review of hormonal influences, sex differences and health implications

Sleep is a fundamental biological behavior that affects various aspects of health and wellbeing. However, there are some differences in respect of sleep between men and women. Notably, there are sex differences in relation to sleep problems and the potential comorbidities, such as diabetes and cardiovascular diseases, that are associated with these problems, with some evidence suggesting that women may have a greater predisposition to sleep disturbances. This narrative review provides a comprehensive analysis of the literature in respect of sex differences in the sleep, with the main focus being on women. Basic research has investigated sex-specific distinctions in sleep architecture, sleep quality, and circadian rhythms, while clinical studies have examined sex differences in sleep disorders, such as insomnia, sleep apnea, and restless leg syndrome. This narrative review also highlights the impact of the periods of hormonal fluctuations that occur across a woman's lifespan - such as during the menstrual cycle, pregnancy, and menopause phase - and examines their effects on sleep. It also explores the influence of social and cultural factors on sleep patterns in women. Taken together, the evidence suggests that women may be more susceptible to sleep disturbance, and that gender-specific factors should be considered when evaluating sleep in clinical practice. Further research is warranted to elucidate the mechanisms that underlie this and help guide the development of sex-specific interventions to improve sleep quality and promote holistic health in women

Post-transcriptional regulation of satellite cell quiescence by TTP-mediated mRNA decay.

Skeletal muscle satellite cells in their niche are quiescent and upon muscle injury, exit quiescence, proliferate to repair muscle tissue, and self-renew to replenish the satellite cell population. To understand the mechanisms involved in maintaining satellite cell quiescence, we identified gene transcripts that were differentially expressed during satellite cell activation following muscle injury. Transcripts encoding RNA binding proteins were among the most significantly changed and included the mRNA decay factor Tristetraprolin. Tristetraprolin promotes the decay of MyoD mRNA, which encodes a transcriptional regulator of myogenic commitment, via binding to the MyoD mRNA 3' untranslated region. Upon satellite cell activation, p38α/β MAPK phosphorylates MAPKAP2 and inactivates Tristetraprolin, stabilizing MyoD mRNA. Satellite cell specific knockdown of Tristetraprolin precociously activates satellite cells in vivo, enabling MyoD accumulation, differentiation and cell fusion into myofibers. Regulation of mRNAs by Tristetraprolin appears to function as one of several critical post-transcriptional regulatory mechanisms controlling satellite cell homeostasis

Activation of C-fiber nociceptors by low-power diode laser

Objective: The evaluation of selective activation of C-fibers to record evoked potentials using the association of low-power diode laser (810 nm), tiny-area stimulation and skin-blackening. Method: Laser-evoked potentials (LEPs) were obtained from 20 healthy young subjects. An aluminum plate with one thin hole was attached to the laser probe to provide tiny-area stimulation of the hand dorsum and the stimulated area was covered with black ink. Results: The mean intensity used for eliciting the ultra-late laser-evoked potential (ULEP) was 70 +/- 32 mW. All subjects showed a clear biphasic potential that comprised a negative peak (806 +/- 61 ms) and a positive deflection (1033 +/- 60 ms), corresponding to the ULEP related to C-fiber activation. Conclusion: C-fiber-evoked responses can be obtained using a very low-power diode laser when stimulation is applied to tiny areas of darkened skin. This strategy offers a non-invasive and easy methodology that minimizes damage to the tissue.Univ Fed Sao Paulo, Dept Psicobiol, Sao Paulo, SP, BrazilUniv Fed Sao Paulo, Setor Neurofisiol Clin, Sao Paulo, SP, BrazilUniv Fed Sao Paulo, Dept Psicobiol, Sao Paulo, SP, BrazilUniv Fed Sao Paulo, Setor Neurofisiol Clin, Sao Paulo, SP, BrazilWeb of Scienc

Association Between Uric Acid Levels and Obstructive Sleep Apnea Syndrome in a Large Epidemiological Sample

Introduction: Recurrent hypoxia, which is associated with obstructive sleep apnea syndrome (OSAS), leads to an increase in the degradation of adenosine triphosphatase into xanthine, which in turn increases uric acid concentrations.Objective: the current study aimed to determine whether an association exists between OSAS and uric acid levels in the peripheral blood from a representative population of São Paulo (Brazil).Methods: A population-based survey adopting a probabilistic 3-stage cluster sample of São Paulo was used to represent the population according to gender, age, and socioeconomic class. A total of 1,042 volunteers underwent polysomnography recordings for OSAS diagnosis, blood pressure assessment, and biochemical blood analysis, and answered questionnaires.Results: Uric acid levels were correlated with most important risk factors for OSAS, such as AHI, desaturation time and index, minimum oxyhemoglobin saturation (SpO(2)), blood pressure, cholesterol, BMI, triglycerides and arousal, and with OSAS itself. Also, uric acid was increased in OSAS volunteers even after controlling for all confounders. Hyperuricemic volunteers presented lower mean and minimum SpO(2) and increased desaturation index. Importantly, minimum SpO(2) was a significant predictor of uric acid levels, which in turn was considered an independent predictor for OSAS in the binary logistic model. However, a ROC curve analysis for establishing cut-off points for uric acid levels as a biomarker of OSAS revealed moderate sensitivity and specificity.Conclusion: A strong association was found between uric acid levels and OSAS in a representative sample of the population of São Paulo. Although they do not qualify for a biomarker alone, uric acid levels may be involved in OSAS severity and should be considered in sleep apnea management in the future.Associacao Fundo de Incentivo a Pesquisa (AFIP)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Universidade Federal de São Paulo, Dept Psicobiol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Psicobiol, São Paulo, BrazilFAPESP: CEPID 98/14303-3FAPESP: 10/50129-1Web of Scienc

Validation of commonly used reference genes for sleep-related gene expression studies

<p>Abstract</p> <p>Background</p> <p>Sleep is a restorative process and is essential for maintenance of mental and physical health. In an attempt to understand the complexity of sleep, multidisciplinary strategies, including genetic approaches, have been applied to sleep research. Although quantitative real time PCR has been used in previous sleep-related gene expression studies, proper validation of reference genes is currently lacking. Thus, we examined the effect of total or paradoxical sleep deprivation (TSD or PSD) on the expression stability of the following frequently used reference genes in brain and blood: <it>beta-actin (b-actin), beta-2-microglobulin (B2M), glyceraldehyde-3-phosphate dehydrogenase (GAPDH)</it>, and <it>hypoxanthine guanine phosphoribosyl transferase (HPRT)</it>.</p> <p>Results</p> <p>Neither TSD nor PSD affected the expression stability of all tested genes in both tissues indicating that <it>b-actin, B2M, GAPDH </it>and <it>HPRT </it>are appropriate reference genes for the sleep-related gene expression studies. In order to further verify these results, the relative expression of <it>brain derived neurotrophic factor (BDNF) </it>and <it>glycerol-3-phosphate dehydrogenase1 (GPD1) </it>was evaluated in brain and blood, respectively. The normalization with each of four reference genes produced similar pattern of expression in control and sleep deprived rats, but subtle differences in the magnitude of expression fold change were observed which might affect the statistical significance.</p> <p>Conclusion</p> <p>This study demonstrated that sleep deprivation does not alter the expression stability of commonly used reference genes in brain and blood. Nonetheless, the use of multiple reference genes in quantitative RT-PCR is required for the accurate results.</p

Obstructive sleep apnea and objective short sleep duration are independently associated with the risk of serum vitamin D deficiency

BACKGROUND:Studies demonstrate an association between vitamin D (25(OH)D) deficiency and sleep disturbances, such as obstructive sleep apnea (OSA) and short sleep duration. However, to date, no studies have concurrently and objectively evaluated the effect of these factors on 25(OH)D. OBJECTIVES:To evaluate whether OSA and objective short sleep duration are independently associated with reduced 25(OH)D in an adult population sample. METHODS:A cross-sectional study included 657 individuals from the city of Sao Paulo, Brazil, as part of the ERA project. Participants fulfilled questionnaires and underwent clinical evaluation, polysomnography and blood sample collection for 25(OH)D quantification. OSA was classified into three categories (mild, moderate and severe). The risk of 25(OH)D deficiency was considered as levels<30 ng/mL. Short sleep duration was defined as total sleep time<6 hours. RESULTS:The risk of 25(OH)D deficiency was observed in 59.5% of the sample, affecting more individuals of the female gender, obese, with African American ethnicity, and those that were smokers, sedentary and presented hypertension and diabetes. In the final logistic model adjusted for age, gender, ethnicity, obesity, smoking, hypertension, diabetes, sedentary lifestyle, seasonality and creatinine serum levels, both OSA and short sleep duration showed significant independent associations with the risk of 25(OH)D deficiency (moderate OSA: OR for 25(OH)D<30 = 2.21, 95% CI: 1.35-3.64, p<0.01; severe OSA: OR for 25(OH)D<30 = 1.78, 95% CI: 1.06-3.00, p = 0.03; short sleep duration: OR for 25(OH)D<30 = 1.61, 95% CI: 1.15-2.26, p = 0.01). After a subgroup analysis, similar results were observed only in participants ≥50 years. CONCLUSION:OSA and short sleep duration are independently associated with the risk of 25(OH)D deficiency in an adult population. Age-related changes in vitamin D metabolism and the frequency of sleep disorders may be involved in these associations. Future studies exploring whether 25(OH)D levels may modulate OSA and sleep curtailment-related outcomes are needed

The influence of sleep deprivation and obesity on DNA damage in female Zucker rats

OBJECTIVE: The aim of this study was to evaluate overall genetic damage induced by total sleep deprivation in obese, female Zucker rats of differing ages. METHOD: Lean and obese Zucker rats at 3, 6, and 15 months old were randomly distributed into two groups for each age group: home-cage control and sleep-deprived (N = 5/group). The sleep-deprived groups were deprived sleep by gentle handling for 6 hours, whereas the home-cage control group was allowed to remain undisturbed in their home-cage. At the end of the sleep deprivation period, or after an equivalent amount of time for the home-cage control groups, the rats were brought to an adjacent room and decapitated. The blood, brain, and liver tissue were collected and stored individually to evaluate DNA damage. RESULTS: Significant genetic damage was observed only in 15-month-old rats. Genetic damage was present in the liver cells from sleep-deprived obese rats compared with lean rats in the same condition. Sleep deprivation was associated with genetic damage in brain cells regardless of obesity status. DNA damage was observed in the peripheral blood cells regardless of sleep condition or obesity status. CONCLUSION: Taken together, these results suggest that obesity was associated with genetic damage in liver cells, whereas sleep deprivation was associated with DNA damage in brain cells. These results also indicate that there is no synergistic effect of these noxious conditions on the overall level of genetic damage. In addition, the level of DNA damage was significantly higher in 15-month-old rats compared to younger rats

Phenotypic contrasts of Duchenne Muscular Dystrophy in women: Two case reports

We discussed two cases of symptomatic female carriers to Duchenne Muscular Dystrophy. The first case is a 20 year-old girl with classical phenotypic manifestation of the disease, similar to the condition in boys. The case 2 is a 62 year-old woman with progressive muscular weakness. The disease is much less common in woman than men so both cases described here are considered rare forms of the disease, with several clinical implications. In both cases, a progressive muscle weakness, impairment in walking and sleeping was observed, in addition to obstructive sleep apnea syndrome and alveolar hypoventilation, that required noninvasive ventilatory support. (C) 2016 Brazilian Association of Sleep. Production and Hosting by Elsevier B.V.AFIPCAPESCNPqFAPESPUniv Fed Sao Paulo, Dept Psychobiol, Sao Paulo, SP, BrazilUniv Fed Sao Paulo, Dept Neurol, Sao Paulo, SP, BrazilUniv Fed Sao Paulo, Dept Psychobiol, Sao Paulo, SP, BrazilUniv Fed Sao Paulo, Dept Neurol, Sao Paulo, SP, BrazilFAPESP: 2014/08067-0Web of Scienc

Progesterone reduces erectile dysfunction in sleep-deprived spontaneously hypertensive rats

BACKGROUND: Paradoxical sleep deprivation (PSD) associated with cocaine has been shown to enhance genital reflexes (penile erection-PE and ejaculation-EJ) in Wistar rats. Since hypertension predisposes males to erectile dysfunction, the aim of the present study was to investigate the effects of PSD on genital reflexes in the spontaneously hypertensive rat (SHR) compared to the Wistar strain. We also extended our study to examine how PSD affect steroid hormone concentrations involved in genital events in both experimental models. METHODS: The first experiment investigated the effects of PSD on genital reflexes of Wistar and SHR rats challenged by saline and cocaine (n = 10/group). To further examine the impact of the PSD on concentrations of sexual hormones, we performed a hormonal analysis of testosterone and progesterone in the Wistar and in SHR strains. Since after PSD progesterone concentrations decreased in the SHR compared to the Wistar PSD group we extended our study by investigating whether progesterone (25 mg/kg or 50 mg/kg) or testosterone (0.5 mg/kg or 1.0 mg/kg) administration during PSD would have a facilitator effect on the occurrence of genital reflexes in this hypertensive strain. RESULTS: A 4-day period of PSD induced PE in 50% of the Wistar rats against 10% for the SHR. These genital reflexes was potentiated by cocaine in Wistar rats whereas this scenario did not promote significant enhancement in PE and EJ in hypertensive rats, and the percentage of SHR displaying genital reflexes still figured significantly lower than that of the Wistar strain. As for hormone concentrations, both sleep-deprived Wistar and SHR showed lower testosterone concentrations than their respective controls. Sleep deprivation promoted an increase in concentrations of progesterone in Wistar rats, whereas no significant alterations were found after PSD in the SHR strain, which did not present enhancement in erectile responses. In order to explore the role of progesterone in the occurrence of genital reflexes, SHR were treated daily during the sleep deprivation period with progesterone; after the administration of this hormone and challenge with cocaine, we observed a significant increase in erectile events compared with the vehicle PSD SHR+cocaine group. CONCLUSION: Our data showed that the low frequency of genital reflexes found in SHR sleep deprived rats may be attributed to the lower concentrations of progesterone in these rats, based on the observation that progesterone replacement increased genital reflexes in this strain