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Sleep Science
Published in Gia Merlo, Kathy Berra, Lifestyle Nursing, 2023
Glenn S. Brassington, Glenn T. Brassington
It is now believed that our sleep–wake circadian rhythm is 10–15 minutes longer than 24 hours, requiring us to reset our internal clock each day. The daily pattern of action of the circadian alerting rhythm is to begin to alert the organism at about 9 a.m. and to increase alertness slowly until 9 p.m. with the greatest alerting effect occurring between 6 a.m. and 9 p.m. The circadian alerting rhythm decreases its action slowly and almost completely withdrawn between 3 a.m. and 6 a.m. Figure 4.2 depicts this process, known as the Opponent Process Model (Edgar, 1993). The “afternoon dip” (i.e., between 1 and 3 p.m.) in energy is associated with the withdrawal of circadian alerting and increasing sleep drive.
Medications
Published in Henry J. Woodford, Essential Geriatrics, 2022
Melatonin is an endogenous hormone produced at night by the pineal gland and plays a role in maintaining normal circadian rhythm. Its production may be reduced in older people. There has been hope that this could be a safer, yet effective, alternative. Unfortunately, some data suggest that the risk of falls and fractures may be as high with melatonin as that seen with benzodiazepines or Z-drugs.41 In addition, melatonin only has a small effect on sleep. A meta-analysis found that, on average, users fell asleep just seven minutes quicker and slept for just eight minutes longer than people given a placebo.42
Sleep–Wake Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Margaret Kay-Stacey, Eunice Torres-Rivera, Phyllis C. Zee
Sleep and circadian rhythm disorders are common, and can increase the risk, as well as contribute to the expression and severity of common medical, neurologic, and psychiatric disorders. Given the frequent overlap of sleep disturbance with many neurologic conditions, neurologists are well positioned to identify and provide treatment of sleep–wake disorders. A basic sleep history, including questions about snoring, sleep habits, sleep initiation and continuity, daytime fatigue or sleepiness, leg symptoms, and bed partner complaints, should become a part of every neurologic evaluation. Addressing sleep disorders will not only help improve sleep quality, but also optimize treatment of comorbid disorders.
A National Survey of U.S. Adolescent Sleep Duration, Timing, and Social Jetlag During the COVID-19 Pandemic
Published in Behavioral Sleep Medicine, 2023
Katherine L. Wesley, Emily H. Cooper, John T. Brinton, Maxene Meier, Sarah Honaker, Stacey L. Simon
School closures and the implementation of virtual learning during the early months of the pandemic caused changes to school start times and academic demands for many adolescents. Many high schools in the U.S. have start times prior to 8:30AM, which, in combination with a physiological delay in circadian rhythms that results in later sleep onset, limits sleep opportunity for adolescents (Adolescent Sleep Working Group, Committee on Adolescence & Council on School Health, 2014; Crowley et al., 2018). Additionally, this can create an increase in social jetlag, defined as a > 2-hour difference in sleep timing from weekdays to weekends, which may result in daytime tiredness or fatigue (Mindell & Owens, 2015). In adolescence, this often looks like going to bed later and waking up later on weekends compared to weekdays. A shift to a more flexible or delayed school schedule may provide the opportunity for adolescents, particularly those with an evening chronotype, or later sleep timing preference, to obtain significantly more sleep and reduce social jetlag (Becker & Gregory, 2020). Indeed, in a Canadian study of qualitative phone interviews during COVID-19, adolescents reported increased sleep duration (primarily due to later wake times), improved sleep quality, and less daytime sleepiness (Gruber et al., 2020). Adolescents attributed these changes to not having to wake at a set time to attend school and reduced school stress (Gruber et al., 2020).
Heart rate variability and chronotype – a systematic review
Published in Chronobiology International, 2021
Kirsi Honkalampi, Susanna Järvelin-Pasanen, Mika P. Tarvainen, Terhi Saaranen, Anneli Vauhkonen, Saana Kupari, Merja Perkiö-Mäkelä, Kimmo Räsänen, Tuula Oksanen
The results suggest that circadian rhythm is based mainly on biological differences between individuals and is highly hereditary (Fischer et al. 2017). While heart rate (HR) defines the number of heart beats per minute, heart rate variability (HRV) measures the beat-to-beat changes in time intervals between successive heart beats at millisecond resolution (Van Ravenswaaij-Arts et al. 1993). HRV is commonly monitored to assess the function of the parasympathetic and sympathetic branches of the autonomic nervous system (ANS) (Malik et al. 1996; Van Ravenswaaij-Arts et al. 1993). In general, the activity of the parasympathetic nervous system tends to decrease HR and increase HRV, whereas sympathetic nervous activity typically has the opposite effect. However, sympathetic activation is known to affect the low frequency (LF) component of HRV and an increase in sympathetic activation may sometimes increase LF power (Malik et al. 1996).
Association between hair cortisol, hair cortisone, and fatigue in people living with HIV
Published in Stress, 2021
Quan Zhang, Xiaoming Li, Shan Qiao, Shuaifeng Liu, Zhiyong Shen, Yuejiao Zhou
Of the putative mechanisms contributing to fatigue, glucocorticoids (GCs) abnormalities, indicators of dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, has been proposed as one of the crucial causes of fatigue in PLHIV (Barroso, 1999; Jong et al., 2010). Cortisol is the principal GC hormone in humans, plays an essential role in the energy balance, the 24 h circadian rhythm, and stress responses. Cortisol abnormalities are well documented in PLHIV (Zapanti et al., 2008), with some studies find elevated cortisol levels in PLHIV (Christeff et al., 1999; Collazos et al., 2003), whereas others contradict these findings with lower or normal cortisol levels in PLHIV (Langerak et al., 2015; Merenich et al., 1990; Odeniyi et al., 2013). In addition, cumulative evidence has shown an association between GCs abnormalities and fatigue in patients with chronic fatigue syndrome (CFS) (Papadopoulos & Cleare, 2011; Powell et al., 2013). However, data are limited on the relationship between GCs levels and fatigue in PLHIV (Jong et al., 2010). To the best of our knowledge, only one study reported data on the relationship between salivary cortisol and fatigue in PLHIV without empirically tested (n = 40) (Barroso et al., 2006).