scholarly journals Sleeping Disorders as a Symptom of Depression

2021 ◽  
Vol 04 (07) ◽  
Author(s):  
Lalitpat Suthisripok ◽  
Keyword(s):  
Sleep Deprivation ◽  
Seasonal Affective Disorder ◽  
Major Depressive ◽  
Sleeping Disorders ◽  
Effective Care ◽  
Bidirectional Relationship ◽  
Acute Sleep Deprivation ◽  
Almost All ◽  
Sleeping Disorder ◽  
Chronic Sleep

Recently, people pay less attention to their sleep since there are a lot of stimulants to keep them awake more than sleeping. According to many reports, the results have shown that many are facing a serious condition, which is sleeping disorder. This condition is related to sleep and affects the ability to sleep well on a regular basis. It is a serious problem that if left untreated, the condition can lead to many more severe problems. There is a significant correlation between sleeping disorder and depression which is called “bidirectional relationship”. The studies show that sleeping disorders are a “symptom” of almost all types of depression such as Major Depressive Disorder, Bipolar Disorder, Seasonal Affective Disorder and so forth. On the other hand, depression itself can also be a cause of sleeping disorders. In addition, the studies show chronic sleep deprivation can cause the changes in Serotonin, which is the brain’s neurotransmitter, and will have a chance to lead to depression greater than acute sleep deprivation. As a result, people should raise awareness in sleeping and usually examine their sleep. To have less chance of depression, a person requires a healthy sleep period and effective care.

Sleep Disorders and Depression

2014 ◽  
Author(s):  
Colleen E. Carney ◽  
Taryn G. Moss
Keyword(s):  
Sleep Disorders ◽  
Sleep Disorder ◽  
Clinical Management ◽  
Sleep Disturbances ◽  
Sleep Problems ◽  
Clinical Care ◽  
Major Depressive ◽  
Bidirectional Relationship ◽  
Assessment And Treatment ◽  
Almost All

Major depressive disorder (MDD) commonly occurs with several sleep disorders, including hypersomnia, breathing or limb-related sleep disturbances, and most notably chronic insomnia. A bidirectional relationship exists between sleep and mood problems, and both issues often warrant timely clinical management. However, there are several assessment- and treatment-related complexities that complicate the clinical management of such patients. For example, there are several overlapping symptoms for MDD and both insomnia and hypersomnia, and the two sleep conditions are both listed as possible symptoms in the diagnostic criteria for MDD. This has led to a well-documented problem of underrecognizing and undertreating these significant disorders in the context of MDD. Moreover, certain effective depression treatments can actually worsen the coexisting sleep disorder. Understanding and treating both disorders (i.e., MDD and the co-occurring sleep disorder) is imperative for effective clinical care. Almost all (i.e., up to 90%) of those with depression report sleep problems. This chapter provides an overview of the etiologic, assessment, and treatment issues inherent in this very large, highly prevalent group.

scholarly journals 0270 Somnolence Profiles in Mice Submitted to Acute and Chronic Sleep Deprivation

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A103-A103
Author(s):  
G L Fernandes ◽  
P Araujo ◽  
S Tufik ◽  
M Andersen
Keyword(s):  
Sleep Deprivation ◽  
Individual Variation ◽  
Individual Variability ◽  
Interindividual Variation ◽  
Dark Phase ◽  
Sleep Regulation ◽  
Study Objective ◽  
Acute Sleep Deprivation ◽  
Chronic Sleep Deprivation ◽  
Chronic Sleep

Abstract Introduction Sleepiness is a behavioral marker of homeostatic sleep regulation and is related to several negative outcomes with interindividual variation, which may amount to central sleep mechanisms. However, there is a lack of evidence linking progressive sleep need and sleepiness with factors of individual variability, which could be tested by acute and chronic sleep deprivation. Thus, the study objective was to investigate the development of sleepiness in sleep deprived mice. Methods C57BL/6J male mice (n=340) were distributed in 5 sleep deprivation groups, 5 sleep rebound groups and 10 control groups. Animals underwent acute total sleep deprivation for 3, 6, 9 or 12 hours or chronic sleep deprivation for 6 hours for 5 consecutive days. Sleep rebound groups had the opportunity to sleep for 1, 2, 3, 4 hours after acute sleep deprivation or 24 hours after chronic sleep deprivation. During the protocol, sleep attempts were counted as a sleepiness index. After euthanasia, blood was collected for corticosterone assessment. Results Using the average group sleep attempts, it was possible to differentiate between sleepy (mean>group average) and resistant to sleepiness animals (mean<group average). Frequency of resistant mice was 65%, 56%, 56% and 53% for 3, 6, 9 and 12 hours of acute sleep deprivation, respectively, and 74% in chronic sleep deprivation. 52% of the sleepiness variance might be explained by individual variation during chronic sleep deprivation and 68% of sleepiness variance during acute sleep deprivation was attributed to extended wakefulness. A normal corticosterone zenith was observed at the start of the dark phase, independent of sleep deprivation. Conclusion Different degrees of sleepiness in sleep deprived mice were verified. Sleep deprivation per se was the main factor explaining sleepiness during acute sleep deprivation whereas in chronic deprivation individual variation was more relevant. Support This work was financially supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) (#2017/18455-5), Coordenação de Aperfeiçoamento de Pessoal Nível Superior (CAPES) - grant code 001, ConselhoNacional de Desenvolvimento Científico e Tecnológico (CNPq) (#169040/2017–8)and Associação Fundo de Incentivo à Pesquisa (AFIP).

scholarly journals Insomnia as a predisposing factor for medical conditions

2021 ◽  
Vol 68 (1) ◽  
pp. 31-33
Author(s):  
Ana Maria Alexandra Stanescu ◽  
◽  
Oana Nicolescu ◽  
Alexandru Mihai Stefanescu ◽  
Gabriela Carmen Obilisteanu ◽  
...  
Keyword(s):  
Public Health ◽  
Sleep Deprivation ◽  
Brain Function ◽  
Public Health Problem ◽  
Disease Development ◽  
Predisposing Factor ◽  
Lack Of Sleep ◽  
Acute Sleep Deprivation ◽  
Chronic Sleep

An essential aspect of human health is sleep. Sleep, among others, interacts with the immune system, plays a role in restoring the body's energy, healing and brain function. Insomnia is often noticed in medical practice, is considered a public health problem. Acute sleep deprivation can alter cognitive performance, and chronic sleep deprivation can lead to disease development. Lack of sleep affects all major systems in the human body, and the major changes that occur in chronic insomnia have been associated with many conditions such as type 2 diabetes, cardiovascular disease, asthma, thyroid disease and gastroesophageal reflux disease.

scholarly journals The effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment

2020 ◽  
Author(s):  
Séverine Lamon ◽  
Aimee Morabito ◽  
Emily Arentson-Lantz ◽  
Olivia Knowles ◽  
Grace Elizabeth Vincent ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Sleep Deprivation ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Metabolic Dysfunction ◽  
Skeletal Muscle Protein ◽  
Skeletal Muscle Protein Synthesis ◽  
Acute Sleep Deprivation ◽  
Chronic Sleep

AbstractChronic sleep loss is a potent catabolic stressor, increasing the risk of metabolic dysfunction and loss of muscle mass and function. To provide mechanistic insight into these clinical outcomes, we sought to determine if acute sleep deprivation blunts skeletal muscle protein synthesis and promotes a catabolic environment. Healthy young adults (N=13; 7 male, 6 female) were subjected to one night of total sleep deprivation (DEP) and normal sleep (CON) in a randomized cross-over design. Anabolic and catabolic hormonal profiles, skeletal muscle fractional synthesis rate and markers of muscle protein degradation were assessed across the following day. Acute sleep deprivation reduced muscle protein synthesis by 18% (CON: 0.072 ± 0.015 vs. DEP: 0.059 ± 0.014 %•h-1, p=0.040). In addition, it increased plasma cortisol by 21% (p=0.030) and decreased plasma testosterone, but not IGF-1, by 22% (p=0.029). A single night of total sleep deprivation is sufficient to induce anabolic resistance and a pro-catabolic environment. These acute changes may represent mechanistic precursors driving the metabolic dysfunction and body composition changes associated with chronic sleep deprivation.

scholarly journals Residual, differential neurobehavioral deficits linger after multiple recovery nights following chronic sleep restriction or acute total sleep deprivation

SLEEP ◽  
2020 ◽  
Author(s):  
Erika M Yamazaki ◽  
Caroline A Antler ◽  
Charlotte R Lasek ◽  
Namni Goel
Keyword(s):  
Sleep Deprivation ◽  
Response Speed ◽  
Sleep Loss ◽  
Sleep Restriction ◽  
Total Sleep Deprivation ◽  
Psychomotor Vigilance Test ◽  
Recovery Sleep ◽  
Time In Bed ◽  
Neurobehavioral Deficits ◽  
Chronic Sleep

Abstract Study Objectives The amount of recovery sleep needed to fully restore well-established neurobehavioral deficits from sleep loss remains unknown, as does whether the recovery pattern differs across measures after total sleep deprivation (TSD) and chronic sleep restriction (SR). Methods In total, 83 adults received two baseline nights (10–12-hour time in bed [TIB]) followed by five 4-hour TIB SR nights or 36-hour TSD and four recovery nights (R1–R4; 12-hour TIB). Neurobehavioral tests were completed every 2 hours during wakefulness and a Maintenance of Wakefulness Test measured physiological sleepiness. Polysomnography was collected on B2, R1, and R4 nights. Results TSD and SR produced significant deficits in cognitive performance, increases in self-reported sleepiness and fatigue, decreases in vigor, and increases in physiological sleepiness. Neurobehavioral recovery from SR occurred after R1 and was maintained for all measures except Psychomotor Vigilance Test (PVT) lapses and response speed, which failed to completely recover. Neurobehavioral recovery from TSD occurred after R1 and was maintained for all cognitive and self-reported measures, except for vigor. After TSD and SR, R1 recovery sleep was longer and of higher efficiency and better quality than R4 recovery sleep. Conclusions PVT impairments from SR failed to reverse completely; by contrast, vigor did not recover after TSD; all other deficits were reversed after sleep loss. These results suggest that TSD and SR induce sustained, differential biological, physiological, and/or neural changes, which remarkably are not reversed with chronic, long-duration recovery sleep. Our findings have critical implications for the population at large and for military and health professionals.

scholarly journals Sleep Deprivation and Sleep-Onset Insomnia are Associated with Blunted Physiological Reactivity to Stressors

2021 ◽  
Vol 186 (Supplement_1) ◽  
pp. 246-252
Author(s):  
Devon A Hansen ◽  
Brieann C Satterfield ◽  
Matthew E Layton ◽  
Hans P A Van Dongen
Keyword(s):  
Sleep Deprivation ◽  
Laboratory Study ◽  
Salivary Cortisol ◽  
Sleep Onset ◽  
Deprivation Condition ◽  
Increased Risk ◽  
Significant Difference ◽  
Sleep Deficiency ◽  
The Impact ◽  
Chronic Sleep

ABSTRACT Introduction Military operations often involve intense exposure to stressors combined with acute sleep deprivation, while military personnel also experience high prevalence of chronic sleep deficiency from insomnia and other sleep disorders. However, the impact of acute and chronic sleep deficiency on physiologic stressor responses is poorly understood. In a controlled laboratory study with normal sleepers and individuals with chronic sleep-onset insomnia, we measured responses to an acute stressor administered in a sleep deprivation condition or a control condition. Methods Twenty-two adults (aged 22-40 years; 16 females)—11 healthy normal sleepers and 11 individuals with sleep-onset insomnia—completed a 5-day (4-night) in-laboratory study. After an adaptation day and a baseline day, subjects were assigned to a 38-hour total sleep deprivation (TSD) condition or a control condition; the study ended with a recovery day. At 8:00 PM after 36 hours awake in the sleep deprivation condition or 12 hours awake in the control condition, subjects underwent a Maastricht Acute Stress Test (MAST). Salivary cortisol was measured immediately before the MAST at 8:00 PM, every 15 minutes after the MAST from 8:15 PM until 9:15 PM, and 30 minutes later at 9:45 PM. Baseline salivary cortisol was collected in the evening of the baseline day. Additionally, before and immediately upon completion of the MAST, self-report ratings of affect and pain were collected. Results The MAST elicited a stressor response in both normal sleepers and individuals with sleep-onset insomnia, regardless of the condition, as evidenced by increases in negative affect and pain ratings. Relative to baseline, cortisol levels increased immediately following the MAST, peaked 30 minutes later, and then gradually returned to pre-MAST levels. At the cortisol peak, there was a significant difference across groups and conditions, reflecting a pronounced blunting of the cortisol response in the normal sleepers in the TSD condition and the sleep-onset insomnia group in both the TSD and control conditions. Conclusions Blunted stressor reactivity as a result of sleep deficiency, whether acute or chronic, may reflect reduced resiliency attributable to allostatic load and may put warfighters at increased risk in high-stakes, rapid response scenarios.

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