Problem of Sleep Deprivation Cause and Effect Essay

Introduction.

  • What is Sleep Deprivation?

Causes of Sleep Deprivation

  • Effects of Sleep Deprivation

Managing Sleep Deprivation

Works cited.

The functioning of the human body is influenced by a number of factors, which are mainly determined by the health status of an individual. Oftentimes, people seek medication when the body deviates from its normal and usual functioning mechanisms. Through different activities and processes, the body is able to use energy and replenish itself. Sleeping is one of the activities that has a direct effect on the functioning of the body.

This sleep deprivation essay explores how the functioning of the human body is influenced by various factors, primarily determined by an individual’s health status. While most people do not understand the implications of sleep, human effectiveness solely depends on the amount of time dedicated to sleeping. However, for various reasons, people fail to get enough sleep daily, weekly, or on a regular basis.

What Is Sleep Deprivation?

This cause and effect of sleep deprivation essay defines sleep deprivation as a condition occurring among human beings when they fail to get enough sleep. Sleep deprivation is defined as a condition that occurs when human beings fail to get enough sleep. Many experts argue that sleep deficiency is widespread even though most people do not consider it to be a serious issue, which affects their (Gaine et al.). Sleep deprivation has become a major problem in the United States, with almost 47 million suffering from the condition (Wang and Xiaomin). This lack of sleep can lead to a variety of physical and mental health issues, impacting daily functioning and quality of life.

The present essay about sleep deprivation defines sleep deprivation as a condition that occurs among human beings when they fail to get enough sleep. Many experts argue that sleep deficiency is widespread even though most people do not consider it to be a serious issue that affects their lives. Sleep deprivation has become a major problem in the United States, with almost forty-seven million suffering from the condition (Wang and Xiaomin). Among other reasons, one may get insufficient sleep in a day as a result of various factors. Some people sleep at the wrong time due to busy daily schedules, while others have sleep disorders, which affect their sleeping patterns. The following segment of the paper discusses the causes of deprivation.

Sleep deprivation may occur as a result of factors that are not known to the patients. This is based on the fact that sleep deprivation may go beyond the number of hours one spends in bed. In some cases, the quality of sleep matters in determining the level of deprivation.

In this context, it is possible for one to be in bed for more than eight hours but suffer from the negative effects of sleep deprivation. Whilst this is the case, there are people who wake every morning feeling tired despite having spent a recommended number of hours in bed (Griggs et al.14367).

Sleep deprivation can be caused by medical conditions, which may include but are not limited to asthma, arthritis, muscle cramps, allergies, and muscular pain. These conditions have been classified by researchers as common medical conditions that largely contribute to most of the cases of sleep deprivation being witnessed in the United States.

Similarly, these medical conditions have a direct impact on not only the quality but also the time one takes in bed sleeping. It is worth noting that sometimes people are usually unconscious to realize that their sleep is not deep enough (Wang and Xiaomin). This also explains the reason why it is not easy for a person to recall any moment in life when he or she moved closer to waking up.

Treatment of cases like sleep apnea is important because it affects the quality of sleep without necessarily awakening the victim. This is because medical surveys have revealed fatal effects of sleep apnea, especially on the cardiovascular system. Besides these, one is likely to experience breathing difficulties caused by insufficient oxygen.

Even though the treatment of sleep deprivation is important, it has been found that some drugs used to treat patients may worsen the case or lead to poor quality of sleep. It is, therefore, necessary for the doctor to determine the best drugs to use. Discussions between doctors and victims are imperative in order to understand patients’ responses (Conroy et al. 185).

Sleep deprivation is also caused by sleep cycle disruptions, which interfere with the fourth stage of sleep. Oftentimes, these disruptions are described as night terrors, sleepwalking, and nightmares.

Though these disorders are known not to awaken a person completely, it is vital to note that they may disrupt the order of sleep cycles, forcing a person to move from the fourth stage to the first one. Victims of these disruptions require attention in order to take corrective measures.

In addition, there are known environmental factors which contribute to several cases of sleep deprivation. However, doctors argue that the impact on the environment is sometimes too minimal to be recognized by people who are affected by sleep deficiency (Gaine et al.). In other words, these factors affect the quality of sleep without necessarily arousing a person from sleep.

Common examples include extreme weather conditions, like high temperatures, noise, and poor quality of the mattress. As a result, they may contribute to a person’s awakening, depending on the intensity when one is sleeping.

Moreover, the impact of these factors may develop with time, thus affecting one’s quality of sleep. In addition, most of the environmental factors that contribute to sleep deprivation can be fixed easily without medical or professional skills. Nevertheless, the challenge is usually how to become aware of their existence.

Lastly, sleep deprivation is caused by stress and depression, which have been linked to other health disorders and complications. Together with some lifestyles in America, these factors are heavily contributing to sleep deficiency in most parts of the world. Even though they might not be acute enough to awaken an individual, their cumulative effects usually become significant.

There are countless stressors in the world that affect youths and adults. While young people could be concerned with passing exams, adults are normally preoccupied with pressure to attain certain goals in life. These conditions create a disturbed mind, which may affect a person’s ability to enjoy quality sleep.

Sleep deprivation has a host of negative effects which affect people of all ages. The commonest effect is stress. Most people who suffer from sleep deficiency are likely to experience depression frequently as compared to their counterparts who enjoy quality sleep (Conroy et al. 188). As a result, stress may lead to poor performance among students at school.

Research has revealed that students who spend very few hours in bed or experience disruptions during sleep are likely to register poor performance in their class assignments and final exams. Additionally, sleep deprivation causes inefficiency among employees.

For instance, drivers who experience this disorder are more likely to cause accidents as compared to those who are free from it (Griggs et al.14367). This is based on the fact that un-refreshed people have poor concentration and low mastery of their skills.

Besides stress and anxiety, sleep deprivation has a wide-range of health-related effects. For instance, medical experts argue that people who spend less than six hours in bed are likely to suffer from high blood pressure. Quality sleep gives the body an opportunity to rest by slowing down the rate at which it pumps blood to the rest of the body (Wang and Xiaomin).

Inadequate sleep implies that the heart has to work without its normal and recommended rest. Additionally, sleep deprivation is known to affect the immune system. People who experience this disorder end up with a weakened immune system, leaving the body prone to most illnesses. This reduced immune response accumulates and may become fatal with time.

Sleep paralysis is also a common effect of inadequate sleep. This is due to disruption of the sleep cycle. It primarily occurs when the body is aroused during the fourth stage of the sleep cycle. In this case, the body is left immobile as the mind regains consciousness. Due to this conflict, one may experience pain and hallucinations.

Based on the negative effects of sleep deprivation, there is a need to manage this disorder among Americans. Firstly, it is necessary for people to seek medical advice concerning certain factors which could be contributing to this condition, like stress and infections (Wang and Xiaomin).

Proper counseling is also vital in stabilizing a person’s mental capacity. Physical exercises are also known to relieve a person from stressful conditions, contributing to sleep deficiency. Lastly, it is essential to ensure that the environment is free from noise and has regulated weather conditions.

Sleep deprivation remains a major problem in America, affecting millions of people. As discussed above, sleep deprivation is caused by a host of factors, ranging from environmental to health-related issues. Moreover, sleep deficiency has countless effects, most of which may become fatal in cases where the disorder is chronic.

Conroy, Deirdre A., et al. “ The Effects of COVID-19 Stay-at-home Order on Sleep, Health, and Working Patterns: A Survey Study of US Health Care Workers. ” Journal of Clinical Sleep Medicine , vol. 17, no. 2, Feb. 2021, pp. 185–91.

Gaine, Marie E., et al. “ Altered Hippocampal Transcriptome Dynamics Following Sleep Deprivation. ” Molecular Brain, vol. 14, no. 1, Aug. 2021.

Griggs, Stephanie, et al. “ Socioeconomic Deprivation, Sleep Duration, and Mental Health During the First Year of the COVID-19 Pandemic. ” International Journal of Environmental Research and Public Health, vol. 19, no. 21, Nov. 2022, p. 14367.

Wang, Jun, and Xiaomin Ren. “ Association Between Sleep Duration and Sleep Disorder Data From the National Health and Nutrition Examination Survey and Stroke Among Adults in the United States .” Medical Science Monitor , vol. 28, June 2022.

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Bibliography

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Kristen stewart embraces androgyny in bold rolling stone cover shoot – explore style essay topics, most written responses on staar exams will be graded by a computer, quizrise review: ace tests with ai, what a lack of sleep does to you essay sample, example.

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Everyone has at least once in their lives stayed awake throughout an entire night. Usually, being up all night is a choice of high school or college students—commonly for partying; excessively responsible workers and workaholics also tend to spend sleepless nights working on their tasks. It is widely believed that, unlike insomnia (which means a regular lack of sleep), a couple of sleepless nights now and then cannot do much harm. Unfortunately, this is not true— being awake for 24 hours even once for a long period of time has unpleasant effects on health.

Everyone knows a night spent without sleep (or having little sleep) can result in fatigue and a bad mood in the morning; many would consider this a small price for a night of fun or productive labor. However, several sleepless nights can cause more serious mental effects. In particular, your ability to focus and to make decisions will decrease significantly; having a foggy brain and unclear thinking, as well as falling asleep mid-day are also among the possible negative effects. However, in a long-term perspective, the health effects are much worse: proneness to obesity, high blood pressure, heart diseases, diabetes, and so on (NHS).

Fatigue and sleepiness are just the tip of the iceberg. Specifically, experts from Sweden compared the effects of one-night sleep deprivation to a mild concussion. They conducted a study in which a group of healthy young men slept 8 hours one night, and then abstained from sleep another night. The blood samples taken from the men after the sleepless night revealed a 20% increase of neurochemical markers associated with brain cells damage (compared to the samples taken after the full rest night). “Dysfunctional sleep has been linked with a range of health problems, and it looks like that’s because we’re injuring our brain by not getting enough sleep,” says W. Chris Winter, M.D., medical director of the Martha Jefferson Sleep Medicine Center in Charlottesville, Virginia (Men’s Health).

At the same time, some results of the studies were surprising. According to new research, one night without sleep can increase the levels of dopamine in the brain—a substance responsible, in particular, for wakefulness. Scientists believe that by producing more dopamine, the brain tries to compensate for the negative effects of a sleepless night; still, according to the study, cognitive deficits caused by sleep deprivation remain significant. “[…] Dopamine may increase after sleep deprivation as a compensatory response to the effects of increased sleep drive in the brain,” says David Dinges, PhD, at the University of Pennsylvania School of Medicine (ScienceDaily).

Abstaining from sleep has no positive effects on the human body. One-night deprivation of sleep results in fatigue and irritability; several sleepless nights affect one’s ability to concentrate and make decisions. Swedish experts compared the negative effects of the lack of sleep to a mild concussion, and although studies show that the brain tries to compensate the lack of sleep by producing more dopamine, it is still not enough to compensate the harm dealt. So, no matter what your reasons are to stay awake for a prolonged time, make sure to have a normal 8 hours sleep.

Girdwain, Jessica. “The Scary Side Effect of One Sleepless Night.” Men’s Health. N.p., 12 Jan. 2014. Web. 11 Jan. 2016.

“Why Lack of Sleep is Bad for Your Health.” NHS. N.p., n.d. Web. 11 Jan. 2016.

“One Sleepless Night Increases Dopamine in the Human Brain.”ScienceDaily. ScienceDaily, 21 Aug. 2008. Web. 11 Jan. 2016.

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Sleep Deprivation and Deficiency How Sleep Affects Your Health

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Getting enough quality sleep at the right times can help protect your mental health, physical health, quality of life, and safety.

How do I know if I’m not getting enough sleep?

Sleep deficiency can cause you to feel very tired during the day. You may not feel refreshed and alert when you wake up. Sleep deficiency also can interfere with work, school, driving, and social functioning.

How sleepy you feel during the day can help you figure out whether you're having symptoms of problem sleepiness.

You might be sleep deficient if you often feel like you could doze off while:

  • Sitting and reading or watching TV
  • Sitting still in a public place, such as a movie theater, meeting, or classroom
  • Riding in a car for an hour without stopping
  • Sitting and talking to someone
  • Sitting quietly after lunch
  • Sitting in traffic for a few minutes

Sleep deficiency can cause problems with learning, focusing, and reacting. You may have trouble making decisions, solving problems, remembering things, managing your emotions and behavior, and coping with change. You may take longer to finish tasks, have a slower reaction time, and make more mistakes.

Symptoms in children

The symptoms of sleep deficiency may differ between children and adults. Children who are sleep deficient might be overly active and have problems paying attention. They also might misbehave, and their school performance can suffer.

Sleep-deficient children may feel angry and impulsive, have mood swings, feel sad or depressed, or lack motivation.

Sleep and your health

The way you feel while you're awake depends in part on what happens while you're sleeping. During sleep, your body is working to support healthy brain function and support your physical health. In children and teens, sleep also helps support growth and development.

The damage from sleep deficiency can happen in an instant (such as a car crash), or it can harm you over time. For example, ongoing sleep deficiency can raise your risk of some chronic health problems. It also can affect how well you think, react, work, learn, and get along with others.

Mental health benefits

Sleep helps your brain work properly. While you're sleeping, your brain is getting ready for the next day. It's forming new pathways to help you learn and remember information.

Studies show that a good night's sleep improves learning and problem-solving skills. Sleep also helps you pay attention, make decisions, and be creative.

Studies also show that sleep deficiency changes activity in some parts of the brain. If you're sleep deficient, you may have trouble making decisions, solving problems, controlling your emotions and behavior, and coping with change. Sleep deficiency has also been linked to depression, suicide, and risk-taking behavior.

Children and teens who are sleep deficient may have problems getting along with others. They may feel angry and impulsive, have mood swings, feel sad or depressed, or lack motivation. They also may have problems paying attention, and they may get lower grades and feel stressed.

Physical health benefits

Sleep plays an important role in your physical health.

Good-quality sleep:

  • Heals and repairs your heart and blood vessels.
  • Helps support a healthy balance of the hormones that make you feel hungry (ghrelin) or full (leptin): When you don't get enough sleep, your level of ghrelin goes up and your level of leptin goes down. This makes you feel hungrier than when you're well-rested.
  • Affects how your body reacts to insulin: Insulin is the hormone that controls your blood glucose (sugar) level. Sleep deficiency results in a higher-than-normal blood sugar level, which may raise your risk of diabetes.
  • Supports healthy growth and development: Deep sleep triggers the body to release the hormone that promotes normal growth in children and teens. This hormone also boosts muscle mass and helps repair cells and tissues in children, teens, and adults. Sleep also plays a role in puberty and fertility.
  • Affects your body’s ability to fight germs and sickness: Ongoing sleep deficiency can change the way your body’s natural defense against germs and sickness responds. For example, if you're sleep deficient, you may have trouble fighting common infections.
  • Decreases   your risk of health problems, including heart disease, high blood pressure, obesity, and stroke.

Research for Your Health

NHLBI-funded research found that adults who regularly get 7-8 hours of sleep a night have a lower risk of obesity and high blood pressure. Other NHLBI-funded research found that untreated sleep disorders rase the risk for heart problems and problems during pregnancy, including high blood pressure and diabetes.

Daytime performance and safety

Getting enough quality sleep at the right times helps you function well throughout the day. People who are sleep deficient are less productive at work and school. They take longer to finish tasks, have a slower reaction time, and make more mistakes.

After several nights of losing sleep — even a loss of just 1 to 2 hours per night — your ability to function suffers as if you haven't slept at all for a day or two.

Lack of sleep also may lead to microsleep. Microsleep refers to brief moments of sleep that happen when you're normally awake.

You can't control microsleep, and you might not be aware of it. For example, have you ever driven somewhere and then not remembered part of the trip? If so, you may have experienced microsleep.

Even if you're not driving, microsleep can affect how you function. If you're listening to a lecture, for example, you might miss some of the information or feel like you don't understand the point. You may have slept through part of the lecture and not realized it.

Some people aren't aware of the risks of sleep deficiency. In fact, they may not even realize that they're sleep deficient. Even with limited or poor-quality sleep, they may still think they can function well.

For example, sleepy drivers may feel able to drive. Yet studies show that sleep deficiency harms your driving ability as much or more than being drunk. It's estimated that driver sleepiness is a factor in about 100,000 car accidents each year, resulting in about 1,500 deaths.

Drivers aren't the only ones affected by sleep deficiency. It can affect people in all lines of work, including healthcare workers, pilots, students, lawyers, mechanics, and assembly line workers.

Lung Health Basics: Sleep Fact Sheet

Lung Health Basics: Sleep

People with lung disease often have  trouble sleeping. Sleep is critical to overall health, so take the first step to sleeping better: learn these sleep terms, and find out about treatments that can help with sleep apnea.

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Effect of sleep and mood on academic performance—at interface of physiology, psychology, and education

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Academic achievement and cognitive functions are influenced by sleep and mood/emotion. In addition, several other factors affect learning. A coherent overview of the resultant interrelationships is essential but has not been presented till date. This unique and interdisciplinary review sits at the interface of physiology, psychology, and education. It compiles and critically examines the effects of sleep and mood on cognition and academic performance while including relevant conflicting observations. Moreover, it discusses the impact of several regulatory factors on learning, namely, age, gender, diet, hydration level, obesity, sex hormones, daytime nap, circadian rhythm, and genetics. Core physiological mechanisms that mediate the effects of these factors are described briefly and simplistically. The bidirectional relationship between sleep and mood is addressed. Contextual pictorial models that hypothesise learning on an emotion scale and emotion on a learning scale have been proposed. Essentially, convoluted associations between physiological and psychological factors, including sleep and mood that determine academic performance are recognised and affirmed. The emerged picture reveals far more complexity than perceived. It questions the currently adopted ‘one-size fits all’ approach in education and urges to envisage formulating bespoke strategies to optimise teaching-learning approaches while retaining uniformity in education. The information presented here can help improvise education strategies and provide better academic and pastoral support to students during their academic journey.

Introduction

Academic performance and cognitive activities like learning are influenced by sleep and mood or emotion. This review discusses the roles of sleep and mood/emotion in learning and academic performance.

Sleep, mood, and emotion: definitions and descriptions

Sleep duration refers to “total amount of sleep obtained, either during the nocturnal sleep episode or across the 24-hour period” (Kline, 2013a ). Sleep quality is defined as “one’s satisfaction of the sleep experience, integrating aspects of sleep initiation, sleep maintenance, sleep quantity, and refreshment upon awakening” (Kline, 2013b ). Along similar lines, it is thought to be “one’s perception that they fall asleep easily, get sufficient duration so as to wake up feeling rested, and can make it through their day without experiencing excessive daytime sleepiness” (Štefan et al., 2018 ). Sleep disturbance includes disorders of initiating and maintaining sleep (insomnias) and sleep–wake schedule, as well as dysfunctions associated with either sleep or stages of sleep or partial arousals (Cormier, 1990 ). Sleep deprivation is a term used loosely to describe a lack of appropriate/sufficient amount of sleep (Levesque, 2018 ). It is “abnormal sleep that can be described in measures of deficient sleep quantity, structure and/or sleep quality” (Banfi et al., 2019 ). In a study, sleep deprivation was defined as a sleep duration of 6 h or less (Roberts and Duong, 2014 ). Sleep disorder overarches disorders related to sleep. It has many classifications (B. Zhu et al., 2018 ). Sleep disorders or sleep-related problems include insomnia, hypersomnia, obstructive sleep apnoea, restless legs and periodic limb movement disorders, and circadian rhythm sleep disorders (Hershner and Chervin, 2014 ).

Mood is a pervasive and sustained feeling that is felt internally and affects all aspects of an individual’s behaviour (Sekhon and Gupta, 2021 ). However, by another definition, it is believed to be transient. It is low-intensity, nonspecific, and an affective state. Affective state is an overarching term that includes both emotions and moods. In addition to transient affective states of daily life, mood includes low-energy/activation states like fatigue or serenity (Kleinstäuber, 2013 ). Yet another definition of mood refers to mood as feelings that vary in intensity and duration, and that usually involves more than one emotion (Quartiroli et al., 2017 ). According to the American Psychological Association, mood is “any short-lived emotional state, usually of low intensity” and which lacks stimuli, whereas emotion is a “complex reaction pattern, involving experiential, behavioural and physiological elements”. Emotion is a certain level of pleasure or displeasure (X. Liu et al., 2018 ). It is “a response to external stimuli and internal mental representations” (L. Zhang et al., 2021 ). It is “a conscious mental reaction (such as anger or fear) which is subjectively experienced as a strong feeling usually deriving from one’s circumstances, mood, or relationships with others”. “This feeling is typically accompanied by physiological and behavioural changes in the body”. “This mental state is an instinctive or intuitive feeling which arises spontaneously as distinguished from reasoning or knowledge” (Thibaut, 2015 ).

Since there is some overlap between the descriptions of mood and emotion, in the context of the core content of this review, here, mood and emotion have not been differentiated based on their theoretical/psychological definitions. This is because the aim of the review is not to distinguish between the effects of mood and emotion on learning. Thus, these have been referred to as general affective states; essentially specific states of mind that affect learning. Also, these have been addressed in the context of the study being discussed and cited in that specific place in the review.

Rationale for the topic

Sleep is essential for normal physiological functionality. The panel of National Sleep Foundation suggests sleep durations for various age groups and agrees that the appropriate sleep duration for young adults and adults would be 7–9 hours, and for older adults would be 7–8 hours (Hirshkowitz et al., 2015 ). Today, people sleep for 1–2 hours less than that around 50–100 years ago (Roenneberg, 2013 ). Millions of adults frequently get insufficient sleep (Vecsey et al., 2009 ), including college and university students who often report poor and/or insufficient sleep (Bahammam et al., 2012 ; Curcio et al., 2006 ; Hershner and Chervin, 2014 ). During the COVID-19 pandemic, sleep problems have been highly prevalent in the general population (Gualano et al., 2020 ; Jahrami et al., 2021 ; Janati Idrissi et al., 2020 ) and the student community (Marelli et al., 2020 ). Poor and insufficient sleep is a public health issue because it increases the risk of developing chronic pathologies, and imparts negative social and economic outcomes (Hafner et al., 2017 ).

Like sleep, mood and emotions determine our physical and mental health. Depressive disorders have prevailed as one of the leading causes of health loss for nearly 30 years (James et al., 2018 ). Increased incidence of mood disorders amongst the general population has been observed (Walker et al., 2020 ), and there is an increase in such disorders amongst students (Auerbach et al., 2018 ). These have further risen during the COVID-19 pandemic (Son et al., 2020 ; Wang et al., 2020 ).

The relationship between sleep, mood and cognition/learning is far more complex than perceived. Therefore, this review aims to recognise the interrelationships between the aforementioned trio. It critically examines the effects of sleep and mood on cognition, learning and academic performance (Fig. 1 ). Furthermore, it discusses how various regulatory factors can directly or indirectly influence cognition and learning. Factors discussed here are age, gender, diet, hydration level, obesity, sex hormones, daytime nap, circadian rhythm, and genetics (Fig. 1 ). The effect of sleep and mood on each other is also addressed. Pictorial models that hypothesise learning on an emotion scale and vice-versa have been proposed.

figure 1

Sleep and mood/emotion affect cognition and academic achievement. Their effects can be additionally influenced by other factors like diet, metabolic disorders (e.g., obesity), circadian rhythm, daytime nap, hydration level, age, gender, and genetics. The figure presents the interrelationships and highlights the complexity emerging from the interdependence between factors, action of multiple factors on a single factor or vice-versa and the bidirectional nature of some associations. These associations collectively determine learning and thereby, academic achievement. Direction of the arrow represents effect of a factor on another.

Effect of sleep on cognition and academic performance

Adequate sleep positively affects memory, learning, acquisition of skills and knowledge extraction (Fenn et al., 2003 ; Friedrich et al., 2020 ; Huber et al., 2004 ; Schönauer et al., 2017 ; Wagner et al., 2004 ). It allows the recall of previously gained knowledge despite the acquisition of new information and memories (Norman, 2006 ). Sleeping after learning acquisition regardless of the time of the day is thought to be beneficial for memory consolidation and performance (Hagewoud et al., 2010 ). Therefore, unperturbed sleep is essential for maintaining learning efficiency (Fattinger et al., 2017 ).

Sleep quality and quantity are strongly associated with academic achievement in college students (Curcio et al., 2006 ; Okano et al., 2019 ). Sufficient sleep positively affects grade point average, which is an indicator of academic performance (Abdulghani et al., 2012 ; Hershner and Chervin, 2014 ) and supports cognitive functionality in school-aged children (Gruber et al., 2010 ). As expected, insufficient sleep is associated with poor performance in school, college and university students (Bahammam et al., 2012 ; Hayley et al., 2017 ; Hedin et al., 2020 ; Kayaba et al., 2020 ; Perez-Chada et al., 2007 ; Shochat et al., 2014 ; Suardiaz-Muro et al., 2020 ; Taras and Potts-Datema, 2005 ). In adolescents aged 14–18 years, not only did sleep quality affect academic performance (Adelantado-Renau, Jiménez-Pavón, et al., 2019 ) but one night of total sleep deprivation negatively affected neurobehavioral performance-attention, reaction time and speed of cognitive processing, thereby putting them at risk of poor academic performance (Louca and Short, 2014 ). In university students aged 18–25 years, poor sleep quality has been strongly associated with daytime dysfunctionality (Assaad et al., 2014 ). Medical students tend to show poor sleep quality and quantity. In these students, not sleep duration but sleep quality has been shown to correlate with academic scores (Seoane et al., 2020 ; Toscano-Hermoso et al., 2020 ). Students may go through repeated cycles wherein the poor quality of sleep could lead to poor performance, which in turn may again lead to poor quality of sleep (Ahrberg et al., 2012 ). Sleep deprivation in surgical residents tends to decrease procedural skills, while in non-surgical residents it diminishes interpretational ability and performance (Veasey et al., 2002 ).

Such effects of sleep deprivation are obvious because it can impair procedural and declarative learning (Curcio et al., 2006 ; Kurniawan et al., 2016 ), decrease alertness (Alexandre et al., 2017 ), and impair memory consolidation (Hagewoud et al., 2010 ), attention and decision making (Alhola and Polo-Kantola, 2007 ). It can increase low-grade systemic inflammation and hinder cognitive functionality (Choshen-Hillel et al., 2020 ). Hippocampus is the region in the brain that plays the main role in learning, memory, social cognition, and emotion regulation (Y. Zhu et al., 2019 ). cAMP signalling plays an important role in several neural processes such as learning and memory, cellular excitability, motor function and pain (Lee, 2015 ). A brief 5-hour period of sleep deprivation interferes with cAMP signalling in the hippocampus and impairs its function (Vecsey et al., 2009 ). Thus, optimal academic performance is hindered, if there is a sleep disorder (Hershner and Chervin, 2014 ).

Caveats to affirming the impact of sleep on cognition and academic performance

Despite the clear significance of appropriate sleep quality and quantity in cognitive processes, there are some caveats to drawing definitive conclusions in certain areas. First, there are uncertainties around how much sleep is optimal and how to measure sleep quality. This is further confounded by the dependence of sleep quality and quantity on various genetic and environmental factors (Roenneberg, 2013 ). Moreover, although sleep enhances emotional memory, during laboratory investigations, this effect has been observed only under specific experimental conditions. Also, the experiments conducted have differed in the methods used and in considering parameters like timing and duration of sleep, age, gender and outcome measure (Lipinska et al., 2019 ). This orientates conclusions to be specific to those experimental conditions and prevents the formation of generic opinions that would be applicable to all circumstances.

Furthermore, some studies on the effects of sleep on learning and cognitive functions have shown either inconclusive or apparently unexpected results. For example, in a study, although college students at risk for sleeping disorders were thought to be at risk for academic failure, this association remained unclear (Gaultney, 2010 ). Other studies showed that the effect of sleep quality and duration on academic performance was trivial (Dewald et al., 2010 ) and did not significantly correlate with academic performance (Johnston et al., 2010 ; Sweileh et al., 2011 ). In yet another example, despite the reduction in sleep hours during stressful periods, pharmacy students did not show adversely affected academic performance (Mnatzaganian et al., 2020 ). Also, the premise underlining the significance of sleep hours in enhancing the performance of clinical duties was challenged when the average daily sleep did not affect burnout in clinical residents, where the optimal sleep hours that would maximise learning and improve performance remained unknown (Mendelsohn et al., 2019 ). In some other examples, poor sleep quality was associated with stress but not with academic performance that was measured as grade point average (Alotaibi et al., 2020 ), showed no significant impact on academic scores (Javaid et al., 2020 ) and there was no significant difference between high-grade and low-grade achievers based on sleep quality (Jalali et al., 2020 ). Insomnia reflects regularly experienced sleeping problems. Strangely, in adults aged 40–69 years, those with frequent insomnia showed slightly better cognitive performance than others (Kyle et al., 2017 ).

The reason for such inconclusive and unanticipated results could be that sleep is not the sole determinant of learning. Learning is affected by various other factors that may alter, exacerbate, or surpass the influence of sleep on learning (Fig. 1 ). These factors have been discussed in the subsequent sections.

Effect of mood/emotion on cognition and learning

Emotions reflect a certain level of pleasure or displeasure (X. Liu et al., 2018 ). Panksepp described seven basic types of emotions, whereby lust, seeking, play and care are positive emotions whereas anger, fear and sadness are negative emotions (Davis and Montag, 2019 ). Emotions influence all cognitive functions including memory, focus, problem-solving and reasoning (Tyng et al., 2017 ). Positive emotions such as hope, joy and pride positively correlate with students’ academic interest, effort and achievement (Valiente et al., 2012 ) and portend a flexible brain network that facilitates cognitive flexibility and learning (Betzel et al., 2017 ).

Mood deficit often precedes learning impairment (LeGates et al., 2012 ). In a study by Miller et al. ( 2018 ), the negative mood is referred to as negative emotional induction, as was achieved by watching six horror films by the subjects in that study. Other examples of negative emotions given by the authors were anxiety and shame. Negative mood can unfavourably affect the learning of an unfamiliar language by suppressing the processing of native language that would otherwise help make connections, thereby reiterating the link between emotions and cognitive processing (Miller et al., 2018 ). Likewise, worry and anxiety affect decision-making. High level of worry is associated with poor task performance and decreased foresight during decision-making (Worthy et al., 2014 ). State anxiety reflects a current mood state and trait anxiety reflects a stable personality trait. Both are associated with an increased tendency of “more negative or more threatening interpretation of ambiguous information”, as can be the case in clinically depressed individuals (Bisson and Sears, 2007 ). This could explain why some people who show the symptoms of depression and anxiety may complain of confusion and show an inability to focus and use cognition skills to appraise contextual clues. Patients with major depressive disorder have scored lower on working and verbal memory, motor speed and attention than healthy participants (Hidese et al., 2018 ). Similarly, apathy, anxiety, depression, and mood disorders in stroke patients can adversely affect the functional recovery of patients’ cognitive functions (Hama et al., 2020 ). These examples collectively present a positive correlation between good mood and cognitive processes.

Caveats to affirming the impact of mood/emotion on cognition and academic performance

Based on the examples and discussion so far, a direct relationship between emotions and learning could be hypothesised, whereby positive emotions would promote creative learning strategies and academic success, whereas negative emotions would lead to cognitive impairment (Fig. 2a ). However, this relationship is far more complex and different than perceived.

figure 2

Emotions have been shown on a hypothetical learning scale. a Usually, positive and negative emotions are perceived to match with optimal and poor learning, respectively. b Emotions that lead to sub-optimal/poor and optimal/better learning have been shown on the hypothetical learning scale. Here, distinct from ( a ), both negative emotions and high arousal positive emotions have been implicated in poorer learning compared with low-intensity positive emotion like pleasantness; the latter is believed to lead to optimal learning. The question mark reflects that some negative emotions like shame might stimulate learning, but the exact intensity of such emotions and whether these would facilitate better or worse learning than high arousal positive emotions or pleasantness need to be investigated.

Although positive mood favours the recall of learnt words, it correlates with increased distraction and poor planning (Martin and Kerns, 2011 ). High levels of positive emotions like excitedness and elatedness may decrease achievement (Fig. 2b ) (Valiente et al., 2012 ). It may be surprising to know that negative emotions such as shame and anxiety can arouse cognitive activity (Miller et al., 2018 ). Along similar lines, it has been observed that participants exposed to sad and neutral moods performed similarly in visual statistical (learning) tasks but those who experienced sad stimuli showed high conscious access to the acquired statistical knowledge (Bertels et al., 2013 ). Dysphoria is a state of dissatisfaction that may be accompanied by anxiety and depression. Participants with dysphoria have shown more sensitivity to temporal shifts in outcome contingencies than those without dysphoria (Msetfi et al., 2012 ), and these participants reiterated the depressive realism effect and were quicker in endorsing the connection between negative words and ambiguous statements, demonstrating a negative bias (Hindash and Amir, 2012 ). Likewise, not the positive emotion but negative emotion has been shown to influence the learning outcomes, and it increased the efficiency and precision of learning morphosyntactic instructions involving morphology and syntax of a foreign language (X. Liu et al., 2018 ). Thus, negative emotions can allow, and at times, stimulate or facilitate learning (Figs. 2 and 3 ). Further investigation is needed on the intensity of these emotions, whether these would facilitate better or worse learning than high-intensity positive emotions and whether the results would be task specific.

figure 3

The figure depicts that low-to-medium intensity positive emotion like pleasantness leads to optimal learning, whereas high-intensity emotions, either positive or negative, may lead to suboptimal or comparatively poorer learning. The model considers the apparently unexpected data that negative emotions may stimulate learning. However, which negative emotions these would be, their intensities and their corresponding level of learning are not known, and so these are not shown in the figure. Also, the figure shows bias towards positive emotions in mediating optimal learning. This information is based on the literature so far. Note that the figure represents concepts only and is not prescriptive. It shows inequality and differences between the impacts of high arousal positive and high arousal negative emotions. This concept needs to be investigated. Therefore, the figure may/may not be an accurate mathematical representation of learning with regards to the intensities of positive and negative emotions. In actuality, the scaling and intensities of emotions on the negative and positive sides of the scale may not be equal, particularly in reference to the position of optimal learning on the scale. Furthermore, upon plotting the 3rd dimension, which could be one or more of the regulatory factors discussed here might alter the position and shape of the optimal learning peak.

Moreover, the intensity of positive emotions does not show direct mathematical proportionality to learning/achievement. In other words, the concept of ‘higher the intensity of positive emotions, higher the achievement’ is not applicable. Low-intensity positive emotions such as satisfaction and relaxedness may be potentially dysregulating and high-intensity positive emotions may hamper achievement (Figs. 2b and 3 ). Optimal achievement is likely to be associated with low to medium level intensity of positive emotions like pleasantness (Valiente et al., 2012 ) (Fig. 3 ). Therefore, it has been proposed that both positive and negative high arousal emotions impair cognitive ability (Figs. 2b and 3 ) whereas low-arousal emotions could enhance behavioural performance (Miller et al., 2018 ).

Interestingly, some studies have indicated that emotions do not play a significant role in context. For example, a study showed that there was no evidence that negative emotions in depressed participants showed negative interpretations of ambiguous information (Bisson and Sears, 2007 ). In another study, improvements in visuomotor skills happened regardless of perturbation or mood states (Kaida et al., 2017 ). Thus, mood can either impair, enhance or have no effect on cognition. The effect of mood on cognition and learning can be variable and depend on the complexity of the task (Martin and Kerns, 2011 ) and/or other factors. Some of these factors have been discussed in the following section. The discrepancies in the data on the effects of mood on cognition and learning may be partly attributed to the influence of these factors on cognitive functions.

Factors affecting cognition and its relationships with sleep and mood/emotion

The relationship of cognition with sleep and mood is confounded by the influence of various factors (Tyng et al., 2017 ) such as diet, hydration level, metabolic disorders (e.g., obesity), sex hormones and gender, sleep, circadian rhythm, age and genetics (Fig. 1 ). These factors and their relationships with learning are discussed in this section.

A healthy diet is defined as eating many servings per day of fruits and vegetables, while maintaining a critical view of the consumption of saturated fat, sugar and salt (Healthy Diet—an Overview|ScienceDirect Topics, n.d.). It is also about adhering to two or more of the three healthy attributes with regards to food intake, namely, sufficiently low meat, high fish and high fruits and vegetables (Sarris et al., 2020 ). Another definition of a healthy diet is the total score of the healthy eating index >51 (Zhao et al., 2021 ).

The association between an unhealthy diet and the development of metabolic disorders has been long established. In addition, food affects both cognition and emotion (Fig. 1 ) (Spencer et al., 2017 ). Food and mood show a bidirectional relation whereby food affects mood and mood affects the choice of food made by the individual. Alongside, poor diet can lead to depression while a healthy diet reduces the risk of depression (Francis et al., 2019 ). A high-fat diet stimulates the hippocampus to initiate neuroinflammatory responses to minor immune challenges and this causes memory loss. Likewise, low intake of omega-3 polyunsaturated fatty acids can affect endocannabinoid and inflammatory pathways in the brain causing microglial phagocytosis, i.e., engulfment of synapses by the brain microglia in the hippocampus, eventually leading to memory deficits and depression. On the other hand, vegetables and fruits rich in polyphenolics can lower oxidative stress and inflammation, and thereby avert and/or reverse age-related cognitive dysfunctionality (Spencer et al., 2017 ). Fruits and vegetables, fish, eggs, nuts, and dairy products found in the Mediterranean diet can reduce the risk of developing depression and promote better mental health than sugar-sweetened beverages and high-fat food found in Western diets. Consumption of dietary antioxidants such as the polyphenols in green tea has shown a negative correlation with depression-like symptoms (Firth et al., 2020 ; Huang et al., 2019 ; Knüppel et al., 2017 ). Likewise, chocolate or its components have been found to reduce negative mood or enhance mood, and also enhance or alter cognitive functions temporarily (Scholey and Owen, 2013 ). Alcohol consumption is prevalent amongst university students including those who report feelings of sadness and hopelessness (Htet et al., 2020 ). It can lead to poor academic performance, hamper tasks that require a high degree of cognitive control, dampen emotional responsiveness, impair emotional processing, and generally cause emotional dysregulation (Euser and Franken, 2012 ). Further details on the effects of diet on mood have been discussed elsewhere (Singh, 2014 ). Diet also affects sleep (Binks et al., 2020 ), which in turn affects learning and academic performance. Thus, diet is linked with sleep, mood, and brain functionality (Fig. 1 ).

Water is a critical nutrient accounting for about 3/4th of the brain mass (N. Zhang et al., 2019 ). Unlike the previously thought deficit of 2% or more in body water levels, loss of about 1–2% can be detrimental and hinder normal cognitive functionality (Riebl and Davy, 2013 ). Thus, mild dehydration can disrupt cognitive functions and mood; particularly applicable to the very old, the very young and those living in hot climatic conditions or those exercising rigorously. Dehydration diminishes alertness, concentration, short-term memory, arithmetic ability, psychomotor skills and visuomotor tracking. This is possibly due to the dehydration-induced physiological stress which competes with cognitive processes. In children, voluntary water intake has been shown to improve visual attention, enhance memory performance (Popkin et al., 2010 ) and generally improve memory and attention (Benton, 2011 ). In adults, dehydration can elevate anger, fatigue and depression and impair short-term memory and attention, while rehydration can alleviate or significantly improve these parameters (Popkin et al., 2010 ; N. Zhang et al., 2019 ). Thus, dehydration causes alterations in cognition and emotions, thereby showcasing the impact of hydration levels on both learning and emotional status (Fig. 1 ).

Interestingly, when older persons are deprived of water, they are less thirsty and less likely to drink water than water-deprived younger persons. This can be due to the defective functionality of baroreceptors, osmoreceptors and opioid receptors that alter thirst regulation with aging (Popkin et al., 2010 ). Since water is essential for the maintenance of memory and cognitive performance, the decline of cognitive functionality in the elderly could be partly attributed to their lack of sufficient fluid/water intake when dehydrated.

Obesity and underweightness

Normal weight is defined as a body mass index between 18.5 and 25 kg/m 2 (McGee and Diverse Populations Collaboration, 2005 ) or between 22 and 26.99 kg/m 2 (Nösslinger et al., 2021 ). Being underweight reflects rapid weight loss or an inability to increase body mass and is defined through grades (1–3) of thinness. In children, these are associated with poor academic performance in reading and writing skills, and mathematics (Haywood and Pienaar, 2021 ). Basically, underweight children may have health issues and this could affect their academic abilities (Zavodny, 2013 ). Also, malnourished children tend to show low school attendance and may show poor concentration and impaired motor functioning and problem-solving skills that could collectively lead to poor academic performance at school (Haywood and Pienaar, 2021 ). Malnourished children can show poor performance on cognitive tasks that require executive function. Executive functions could be impaired in overweight children too and this may lead to poor academic performance (Ishihara et al., 2020 ). The negative relation between overweightness and academic performance also implies that the reverse may be true. Poor academic outcome may cause children to overeat and reduce exercise or play and this could lead to them being overweight (Zavodny, 2013 ).

The influence of weight on academic performance is reiterated in observations that in children independent of socioeconomic and other factors, weight loss in overweight/obese children and weight gain in underweight children positively influenced their academic performance (Ishihara et al., 2020 ). Interestingly, independent of the BMI classification, perceptions of underweight and overweight can predict poorer academic performance. In youth, not only larger body sizes but perceptions about deviating from the “correct weight” can impede academic success. This clearly indicates an impact of overweight and underweight perceptions on the emotional and physical health of adolescents (Fig. 1 ) (Livermore et al., 2020 ).

Cognitive and mood disorders are common co-morbidities associated with obesity. Compared to people with normal weight, obese individuals frequently show some dysfunction in learning, memory, and other executive functions. This has been partly attributed to an unhealthy diet, which causes a drift in the gut microbiota. In turn, the obesity-associated microbiota contributes to obesity-related complications including neurochemical, endocrine and inflammatory changes underlying obesity and its comorbidities (Agustí et al., 2018 ). The exacerbated inflammation in obesity may impair the functionality of the region in the brain that is associated with learning, memory, and mood regulation (Castanon et al., 2015 ).

Obesity and mood appear to have a reciprocal relationship whereby obesity is highly prevalent amongst individuals with major depressive disorder and obese individuals are at a high risk of developing anxiety, depression and cognitive malfunction (Restivo et al., 2017 ). In patients with major depressive disorder, obesity has been associated with reduced cognitive functions, likely due to the reduction in grey matter and impaired integrity of white matter in the brain, particularly in areas related to cognition (Hidese et al., 2018 ). Obesity has been shown to be a predictor of depression and the two are linked via psychobiological mechanisms (LaGrotte et al., 2016 ). Notably, sleep deprivation increases the risk of obesity (Beccuti and Pannain, 2011 ) and sleep helps evade obesity (Pearson, 2006 ). Collectively, this links cognition and academic achievement with sleep, obesity, and mood.

Sex hormones and gender

According to the Office of National Statistics, the UK government defines sex as that assigned at birth and which is generally male or female, whereas gender is where an individual may see themselves as having no gender or non-binary gender or on a spectrum between man and woman. The following section discusses both sex and gender in context, as addressed within the cited studies.

Studies show that females outperform males in most academic subjects (Okano et al., 2019 ) and show more sustained performance in tests than male peers (Balart and Oosterveen, 2019 ). This indicates that biological sex may play a role in academic performance. The hormone oestrogen helps develop and maintain female characteristics and the reproductive system. Oestrogen also affects hippocampal neurogenesis, which involves neural stem cells proliferation and survival, and this contributes to memory retention and cognitive processing. Generally, on average, females show higher levels of oestrogen than males. This may partly explain the observed sex-based differences in academic achievement. Administration of oestrogen in females has been proposed to positively affect cognitive behaviour as well as depressive-like and anxiety-like behaviours (Hiroi et al., 2016 ). Clinical trials can establish whether there are any sex-based differences in cognition following oestrogen administration in males and females.

Progesterone, the hormone released by ovaries in females is also produced by males to synthesise testosterone. It affects some non-reproduction functions in the central nervous system in both males and females such as neural circuits formation, and regulates memory, learning and mood (González-Orozco and Camacho-Arroyo, 2019 ). The menstrual cycle in females shows alterations in oestrogen and progesterone levels and is broadly divided into early follicular, mid ovulation and late luteal phase. It is believed that the low-oestrogen-low-progesterone early follicular phase relates to better spatial abilities and “male favouring” cognitive abilities, whereas the high-oestrogen-high-progesterone late follicular or mid-luteal phases relate to verbal fluency, memory and other “female favouring” cognitive abilities (Sundström Poromaa and Gingnell, 2014 ). Thus, sex-hormone derivatives (salivary oestrogen and salivary progesterone) can be used as predictors of cognitive behaviour (McNamara et al., 2014 ). These ovarian hormones decline with menopause, which may affect cognitive and somatosensory functions. However, ovariectomy of rats, which depleted ovarian hormones, caused depression-like behaviour in rats but did not affect spatial performance (Li et al., 2014 ). While this suggests a positive effect of these hormones on mood, it questions their function in cognition and proposes activity-specific functions, which need to be investigated.

Serotonin is a neurotransmitter. Reduced serotonin is correlated with cognitive dysfunctions. Tryptophan hydroxylase-2 is the rate-limiting enzyme in serotonin synthesis. Polymorphisms of this enzyme have been implicated in cognitive disorders. Women have a lower rate of serotonin synthesis and are more susceptible to such dysfunctions than men (Hiroi et al., 2016 ; Nishizawa et al., 1997 ), implying a greater impact of serotonin reduction on cognitive functions in women than in men. Central serotonin also helps to maintain the feeling of happiness and wellbeing, regulates behaviour, and suppresses appetite, thereby modulating nutrient intake. Additionally, it has the ability to promote the wake state and inhibit rapid eye movement sleep (Arnaldi et al., 2015 ; Yabut et al., 2019 ). Thus, any sex-based differences in serotonin levels may affect cognitive functions directly or indirectly via the aforementioned parameters.

Interestingly, data on the relationship between sex and sleep have been ambiguous. While in one study, female students at a university showed less sleep difficulties than male peers (Assaad et al., 2014 ), other studies showed that female students were at a higher risk of presenting sleep disorders related to nightmares (Toscano-Hermoso et al., 2020 ) and insomnia was significantly associated with the risk of poor academic performance only in females (Marta et al., 2020 ). Collectively, sex and gender may influence learning directly, or indirectly by affecting sleep and mood; the other two factors that affect cognitive functions (Fig. 1 ).

Circadian rhythm

Circadian rhythm is a biological phenomenon that lasts for ~24 hours and regulates various physiological processes in the body including the sleep–wake cycles. Circadian rhythm is linked with memory formation, learning (Gerstner and Yin, 2010 ), light, mood and brain circuits (Bedrosian and Nelson, 2017 ). We use light to distinguish between day and night. Interestingly, light stimulates the expression of microRNA-132, which is the sole known microRNA involved in photic regulation of circadian clock in mammals (Teodori and Albertini, 2019 ). The photosensitive retinal ganglions that express melanopsin in eyes not only orchestrate the circadian rhythm with the external light-dark cycle but also influence the impact of light on mood, learning and overall health (Patterson et al., 2020 ). For example, we frequently experience depression-like feelings during the dark winter months and pleasantness during bright summer months. This can be attributed to the circadian regulation of neural systems such as the limbic system, hypothalamic–pituitary–adrenal axis, and monoamine neurotransmitters. Mistimed light in the night disturbs our biological judgement leading to a negative impact on health and mood. Thus, increased incidence of mood disorders correlates with disruption of the circadian rhythm (Walker et al., 2020 ). Interestingly, a study involving university students showed the significance of short-wavelength light, specifically, blue-enriched LED light in reducing melatonin levels [best circadian marker rhythm (Arendt, 2019 )], and improved the perception of mood and alertness (Choi et al., 2019 ). While these examples depict the effect of circadian rhythm on mood, the reverse is also true. Individuals who demonstrate depression show altered circadian rhythm and disturbances in sleep (Fig. 1 ) (Germain and Kupfer, 2008 ). Also, since circadian rhythm regulates physiological and metabolic processes, disruption in circadian rhythm can cause metabolic dysfunctions like diabetes and obesity (Shimizu et al., 2016 ), eventually affecting cognition and learning (Fig. 1 ).

Delayed circadian preference including a tendency to sleep later in the night is common amongst young adults and university students (Hershner and Chervin, 2014 ). This delayed sleep phase disorder, often seen in adolescents, negatively impacts academic achievement and is frequently accompanied by depression (Bartlett et al., 2013 ; Sivertsen et al., 2015 ). Alongside, there is a positive correlation between sleep regularity and academic grades, implying that irregularity in sleep–wake cycles is associated with poor academic performance, delayed circadian rhythm and sleep and wake timings (Phillips et al., 2017 ). Even weekday-to-weekend discrepancy in sleeping patterns has been associated with impaired academic performance in adolescents (Sun et al., 2019 ). Further connection between sleep pattern, circadian rhythm, alertness, and the mood was observed in adolescents aged 13–18 where evening chronotypes showed poor sleep quality and low alertness. In turn, sleep quality was associated with poor outcomes including low daytime alertness and depressed mood. Evening chronotypes and those with poor sleep quality were more likely to report poor academic performance via association with depression. Strangely, sleep duration did not directly affect their functionality (Short et al., 2013 ). Contrastingly, in adults aged 40–69 years, the evening and morning chronotypes were associated with superior and poor cognitive performance, respectively, relative to intermediate chronotype (Kyle et al., 2017 ). In addition to this age-specific effect, the effect of chronotype can be subject-specific. For example, in subjects involving fluid cognition for example science, there was a significant correlation between grades and chronotype, implying that late chronotypes would be disadvantaged in exams of scientific subjects if examined early in the day. This was distinct from humanistic/linguistic subjects in which no correlation with chronotype was observed (Zerbini et al., 2017 ). These observations question the “one size fits all” approach of assessment strategies.

Daytime nap

The benefits of daytime napping in healthy adults have been discussed in detail elsewhere (Milner and Cote, 2009 ). In children, daytime nap facilitates generalisation of word meanings (Horváth et al., 2016 ) and explicit memory consolidation but not implicit perceptual learning (Giganti et al., 2014 ). A 90-min nap increases hippocampal activation, restores its function and improves declarative memory encoding (Ong et al., 2020 ). Generally, daytime napping has been found to be beneficial for memory, alertness, and abstraction of general concepts, i.e. creating relational memory networks (Lau et al., 2011 ). Delayed nap following a learning activity helps in the retention of declarative memory (Alger et al., 2010 ) and exercising before the daytime nap is thought to benefit memory more than napping or exercising alone (Mograss et al., 2020 ). Also, napping for 0.1–1 hour has been associated with a reduced prevalence of overweightness (Chen et al., 2019 ).

Contrastingly, in some studies, napping has been found to impart no substantial benefits to cognition. For example, despite the daytime nap of 1 hour, procedural performance remained impaired after total deprivation of night sleep (Kurniawan et al., 2016 ), indicating that daytime nap may not always be reparative. In other studies, 4 weeks of 90-minute nap intervention (napping or restriction) did not alter behavioural performance or brain activity during sleep in healthy adults aged 18–35 (McDevitt et al., 2018 ) and enhancements in visuomotor skills occurred regardless of daytime nap (Kaida et al., 2017 ). Age is a factor in relishing the benefits of napping. A 90-min nap can benefit episodic memory retention in young adults but these benefits decrease with age (Scullin et al., 2017 ) and may be harmful in the older population, particularly in those getting more than 9 hours of sleep (Mantua and Spencer, 2017 ; Mehra and Patel, 2012 ).

Napping can increase the risk for depression (Foley et al., 2007 ) and show a positive association with depression, i.e., napping is associated with greater likelihood of depression (Y. Liu et al., 2018 ). Cardiovascular diseases, cirrhosis and kidney disease have been linked with both daytime napping and depression (Abdel-Kader et al., 2009 ; Hare et al., 2014 ; Ko et al., 2013 ). While a previous study indicated that the time of nap, morning or afternoon, made no difference to its effect on mood (Gillin et al., 1989 ), a subsequent study suggested that the timing of nap influenced relapses into depression. Specifically, in depressed individuals, morning naps caused a higher propensity of relapse into depression than afternoon naps, thereby proposing the involvement of circadian rhythm in this process. Apart from depression, studies have struggled to identify the direct effect of nap on mood (Gillin et al., 1989 ; Wiegand et al., 1993 ). As daytime napping has been associated with poor sleep quality (Alotaibi et al., 2020 ), it may lead to irregular sleep–wake patterns and thereby alter circadian rhythm (Phillips et al., 2017 ). Also, nap duration was found to be important. In patients with affirmed depression, shorter naps were found to be more detrimental than longer naps (Wiegand et al., 1993 ), whereas, in the elderly, more and longer naps were associated with increased risk of mortality amongst the cognitively impaired individuals (Hays et al., 1996 ). Thus, daytime napping can affect cognitive processes directly or indirectly via its association with circadian rhythm, metabolic dysfunctions, mood, or sleep (Fig. 1 ).

Aging is associated with decreased neurogenesis and structural changes in the hippocampus amongst other neurophysiological effects. This in turn is associated with age-related mood and memory impairments (Kodali et al., 2015 ). Study on the effect of age on mood and emotion regulation in adults aged 20–70 years showed that older participants had a higher tendency to use cognitive reappraisal while reducing negative mood and enhancing positive mood. Interestingly, while women did not show correlations between age and reappraisal, men showed an increment in cognitive reappraisal with age. This indicates gender-based differences in the effect of aging on emotion regulation (Masumoto et al., 2016 ). The influence of age on sleep is well known. Older people that have sleep patterns like the young demonstrate stronger cognitive functions and lesser health issues than those whose sleep patterns match their age (Djonlagic et al., 2021 ). Collectively, this interlinks age, cognition, mood, and sleep.

Apparently, there is a genetic influence on learning and emotions. Approximately 148 independent genetic loci have been identified that influence and support the notion of heritability of general cognitive functions (Davies et al., 2018 ). This indicates the role of genetics in cognition (Fig. 1 ). The α-7 nicotinic acetylcholine receptor (encoded by the gene CHRNA7 ) is expressed in the central and peripheral nervous systems and other peripheral tissues. It has been implicated in various behavioural and psychiatric disorders (Yin et al., 2017 ) and recognised as an important receptor of the cholinergic anti-inflammatory pathway that exhibits a neuroprotective role. Its activation has been shown to improve learning, working memory and cognition (Ren et al., 2017 ). However, there have been some contrasting results related to this receptor. While its deletion has been linked with cognitive impairments, aggressive behaviours, decreased attention span and epilepsy, Chrna7 deficient mice have shown normal learning and memory, and the gene was not deemed essential for the control of emotions and behaviour in mice. Thus, the role of α-7 nicotinic acetylcholine receptor in maintaining mood and cognitive functions, although indicative, is yet to be fully deciphered in humans (Yin et al., 2017 ). Similarly, the gene Slitrk6 , which plays a role in the development of neural circuits in the inner ear may also play a role in some cognitive functions, but it does not appear to play a clear role in mood or memory (Matsumoto et al., 2011 ). Notably, inborn errors of metabolism, i.e., rare inherited disorders may show psychiatric manifestations even in the absence of obvious neurological symptoms. These manifestations could involve impairments in cognitive functions, and/or in the regulation of learning, mood and behaviour (Bonnot et al., 2015 ).

Other factors and associations

Indeed, optimal learning is additionally influenced by factors beyond those discussed here. These factors could be adequate meal frequency, physical activity and low screen time (Adelantado-Renau, Jiménez-Pavón, et al., 2019 ; Burns et al., 2018 ). In adolescents, the time of internet usage was identified as a factor that mediated the association between sleep quality (but not duration) and academic performance (Adelantado-Renau, Diez-Fernandez, et al., 2019 ; Evers et al., 2020 ). Self-perception is another determinant of performance. The American Psychological Association defines self-perception as “person’s view of his or herself or of any of the mental or physical attributes that constitute the self. Such a view may involve genuine self-knowledge or varying degrees of distortion”. Compared to other residents, surgery residents indicated the less perceived impact of sleep-loss on their performance (Woodrow et al., 2008 ). This may be related to specific work culture or profession where there is the reluctance of acceptance of natural human limitations posed by sleep deprivation. Whether there is real resistance to sleep deprivation amongst such professional groups or a misconception requires investigation. Exercise affects both sleep and mood; the latter probably affects in a sex-dependent manner. Thus, moderate exercise has been proposed as a therapy for treating mood disorders (Lalanza et al., 2015 ).

Sleep and mood: a bidirectional but unequal relationship

While the cause of the relationship between sleep and mood is not fully understood, adequate quality and quantity of sleep has shown physiological benefits and may enhance mood (Scully, 2013 ). Sleep encourages insightful behaviour (Wagner et al., 2004 ) and regulates mood (Vandekerckhove and Wang, 2017 ). Sleeping and dreaming activate emotional and reward systems that help process information, and consolidate memory “with high emotional or motivational value”. Inevitably, sleep disturbances can dysregulate these motivational and emotional processes and cause predisposition to mood disorders (Perogamvros et al., 2013 ). Sleep loss can reinforce negative emotions, reduce positive emotions, and increase the risk for psychiatric disorders. In children and adolescents, it can increase anger, depression, confusion and aggression (Vandekerckhove and Wang, 2017 ). Thus, sleep disorder has been associated with depression, where the former can predict the latter (LaGrotte et al., 2016 ). Sleep deprivation and daytime sleepiness amongst adolescents and college students cause mood deficits, negatively affect their mood and learning, and lead to poor academic performance (Hershner and Chervin, 2014 ; Short and Louca, 2015 ). Thus, disrupted sleep acts as a diagnostic factor for mood disorders, including post-traumatic stress disorder, major depression and anxiety (Walker et al., 2020 ).

In turn, mood affects sleep quality. Emotional events and stress during the daytime can affect sleep physiology. Negative states such as sadness, loneliness, and grief are related to sleep impairments, whereas positive states like love can be associated with lessened sleep duration but better sleep quality; the latter needs further evidence. Although dysregulation of emotion relates to poor sleep quality (Vandekerckhove and Wang, 2017 ), the effect of mood on sleep can be modulated by our approach of coping with our emotions (Vandekerckhove and Wang, 2017 ). Therefore, this effect is significantly smaller than the reverse (Triantafillou et al., 2019 ).

Summary and future direction

Sleep and mood influence cognitive functions and thereby affect academic performance. In turn, these are influenced by a network of regulatory factors that directly or indirectly affect learning. The compilation of observations clearly demonstrates the complexity and multifactorial dependence of academic achievement on students’ lifestyle and physiology, as discussed in the form of effectors like age, gender, diet, hydration level, obesity, sex hormones, circadian rhythm, and genetics (Fig. 1 ).

The emerged picture brings forth two points. First, it partly explains the ambiguous and conflicting data on the effects of sleep and mood on academic performance. Second, these revelations collectively question the ‘one-size fits all’ approach in implementing education strategies. It urges to explore formulating bespoke group-specific or subject-specific strategies to optimise teaching–learning approaches. Knowledge of these factors and their associations with each other can aid in forming these groups and improving educational strategies to better support students. However, it is essential to retain parity in education, and this would be the biggest challenge while formulating bespoke approaches.

In the context of sleep, studies could be conducted that first establish standardised means of measuring sleep quality and then measure sleep quality and quantity simultaneously in individuals of different ages groups, sex, and professions. This could then be related to their performance in their respective fields/professions; academic or otherwise. Such studies will help to better understand these interrelationships and address some discrepancies in the data.

Limitations

One limitation of this review is that it addresses only academic performance. Performance should be viewed broadly and be inclusive of all types, for example, athletic performance, dance performance or performance at work on a desk job that may include creative work or financial/mathematical calculations. It would be interesting to investigate the effect of alterations in sleep and mood on various types of performances and those results will be able to provide us with a much broader picture than the one depicted here. Notably, while learning can be assessed, it is difficult to quantify emotions (Ayaz‐Alkaya, 2018 ; Nieh et al., 2013 ). As such, it is believed that qualitative research is a better approach for studying emotional responses than quantitative research (Ayaz‐Alkaya, 2018 ).

Another point of limitation is related to the proposed models in Figs. 2 and 3 . These show hypothetical mathematical scales of learning and emotion where emotions are placed on a scale of learning, and learning is placed on the scale of emotions, respectively. While these models certainly help to better visualise and understand the interrelationships, these scales show only 2-dimensions. There could be a 3rd dimension, and this could be either one of the factors or a combination of the several factors discussed here (and beyond) that determine the effect of mood/emotion on learning/cognition. Additionally, the depicted scales and their interpretations may vary between individuals because the intensity of the same emotion felt by different individuals may differ. Figure 3 depicts emotions and learning. Based on the studies so far, here, negative emotions have been shown to stimulate learning, but which negative emotions these would be (for e.g., shame or anxiety), at what intensities these would stimulate optimal learning if at all, and how this compares with optimal learning induced by positive emotions remains to be investigated. Therefore, the extent to which these scales can be applied in real-life needs to be verified.

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Zhu Y, Gao H, Tong L, Li Z, Wang L, Zhang C, Yang Q, Yan B (2019) Emotion regulation of hippocampus using real-time fMRI neurofeedback in healthy human. Front Hum Neurosci 13. https://doi.org/10.3389/fnhum.2019.00242

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Mehta, K.J. Effect of sleep and mood on academic performance—at interface of physiology, psychology, and education. Humanit Soc Sci Commun 9 , 16 (2022). https://doi.org/10.1057/s41599-021-01031-1

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Sleep Deprivation’s Effect on Your Brain

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When you don’t get enough good quality sleep, you may feel a little dazed and confused. This is partly due to decreased signaling across your brain, diminishing functions like movement, mood, attention, and memory. Over multiple sleepless nights, sleep deprivation reduces your ability to form long-term memories and makes it harder for your brain to dispose of waste products.

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You watched cat videos all night. Now, you can’t seem to shake the grogginess and struggle to complete [splash] basic tasks.

[Rustle] Your sluggishness mimics your brain’s performance after a night [zip] of no sleep. [Woosh] As you try to stay alert after little sleep, regions across [whirring] your cortex, or the outermost layer of your brain, are not as active [beeping] as normal.

Lower activity in your prefrontal cortex makes it harder to process moment-to-moment information [doorbell buzzes, phone rings] and react to your surroundings. What’s more, reduced signaling in the visual [zip] cortex and intraparietal [zip] sulcus challenges your ability to integrate visual information [zip up] and coordinate it [zip down] with your movements.

Diminished activation across the parietal cortex hinders [clink] your capacity [tick-tock] to keep track of temporary information [zip]. It also disrupts your ability to retrieve [swish] old memories and learn new [woosh] information. When all these areas slow down, it may be harder to complete tasks that require your attention and stay [banging] in a good mood.

[Crickets chirping] Sleep deprivation over longer periods of time can reduce your brain’s ability to form long-term memories and hinder your ability to dispose of waste products [bubbling] building up in your brain.

Even if you may not [beeping] feel tired or sleepy, it could take days [swishing] for your body to fully recover from lost sleep, which may be a good enough reason to stop scrolling and [crickets chirping] aim for a full, seven-to-eight-hour night’s rest.

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5 Ways Sleep Deprivation Affects Your Brain and Mood, According to Sleep Doctors

Your mind needs sleep just as much as your body does.

Lindsay is a freelance travel and lifestyle journalist covering topics from love, marriage, fitness, wellness, psychology, and entrepreneurism.

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Parents of newborns, students cramming for exams, overworked professionals pushed to their max, insomniacs, caffeine dependents, night-shift workers, and menstruating people—at some point, we all know how getting less than enough sleep feels (very bad). Though it’s normal to have trouble falling asleep and/or staying asleep occasionally, prolonged periods of sleepless nights and chronic sleep deprivation can harm not only our bodies, but our minds.

Sleep is essential for brain development, wellness, and functioning, explains Heidi Riney, MD, board-certified sleep medicine and neurology psychologist and the chief medical officer of Nox Health . “Sleep has long been thought to be a passive process, but it’s actually an active state, and the quality and duration of our sleep impacts crucial brain functions,” she says, including memory storage, attention maintenance and arousal, learning new material/tasks, mood stability, the ability to read social cues, problem-solving, executive functioning, and impulse control.

So what happens to your brain health and mental capacities if you consistently don’t get enough sleep? And how can you power through on days when you didn’t get enough shut-eye the night before? We asked sleep specialists and mental health experts to weigh in.

How Much Sleep Do You Need for Optimal Brain Health? 

Though it seems like a straightforward question, it’s somewhat complicated to understand how much sleep your mind needs to perform well and stay well. The human brain is as different from one person to the next as fingerprints. Because of this, the specific amount of optimal sleep one brain needs isn’t the same for everyone, says licensed clinical psychologist Bethany Cook, PsyD .

Generally speaking, Cook says, scientists have found that most adults need around 8 or 9 hours of sleep to perform and feel their best. However, since this estimate is a bell curve, some people need more, and some need less to feel great. 

Though without undergoing formal sleep analysis, it’s difficult to know exactly how much sleep you need, there are a few things that can help guide your body’s natural cues. Quality and quantity of hours sleep do matter, but so does how you feel in the morning.

“The only way of knowing if you’re getting ‘quality sleep’ is if you typically wake up feeling rested, refreshed, and revitalized,” Cook says. “Our brains need around four to six full sleep cycles a night to wake [feeling] rested. If you're sleeping for 10 hours every night, but not waking up feeling refreshed, you’re getting poor sleep quality.” She adds that it can be helpful to visit a clinic for a sleep study to identify and fix the problems in your sleep cycle.

The Mental Health Effects of Sleep Deprivation

A slower response time.

Even if you didn’t have a single sip of wine last night, you might wake up feeling foggy and sluggish, unable to respond to questions or respond to things happening around you quickly, explains Nicole Avena, PhD , research neuroscientist, psychologist, and a wellness ambassador for Nature Made. 

“Lack of sleep, short term, has been linked to poor response times and processing,” she says. “This not only can impair your awareness, but it can also harm others around you. Demanding cognitive functions, for example, driving, cannot be performed adequately when sleep is hindered.”

Short-Term Memory Disruption

When you miss your date with Mr. Sandman, the next day may likely bring a struggle to remember much of anything: your keys, your wallet, your phone, you name it. According to Taz Bhatia, MD , board-certified integrative medicine physician and OLLY ambassador, this is because there is a connection between sleep and its impact on memory retention. “Sleep is essential in consolidating memories and allowing us to retain and recall information,” she says. “However, this process can be disrupted without enough sleep, leading to difficulties forming, keeping, and calling back memories.”

Increased Appetite and Cravings

After tossing and turning for hours, you finally leave your bed and head straight to the kitchen. What do you reach for? Probably simple carbohydrates and sugar, since one common effect of sleep deprivation is increased hunger by 24 percent, says Melissa Halas, MA, RDN, CDE , registered dietitian and brain health expert for Neauriva.  

“Often, the carbohydrates consumed aren’t nutrient-dense foods like apples, or whole grains, but rather simple carbs like snack foods high in refined sugars or refined grains,” she says. So if you’re wondering why you can’t stop craving sugar , maybe you should take a look at your sleep patterns first.

Trouble Making Decisions (Large or Small)

Depending on what type of career path you’re on, the ability to make fast decisions is vital to your success. Think: operating heavy machinery, responding to an emergency, or managing a large team with many moving parts. (And let’s not even get started on all the decision-making that also needs to happen at home.) Even if you don’t have a high-stakes job, being able to make simple decisions, like what to wear for the day, is impacted by sleep. Avena explains that our brains process things differently when we don’t get enough sleep. “What’s called ‘naturalistic decision making,’ or being able to make everyday decisions, like what to have for lunch, can be altered,” she says. “This is due to the prefrontal cortex lacking adequate rest.”

Difficulty Regulating Emotions

Maybe you don’t usually have a short fuse with your partner and friends, but every interaction might feel tense and irritating when you’re running on only two hours of rest. This is because people who don’t sleep well or enough often feel snappy, depressed, and more likely to make risky choices, according to Avena. “There’s no need to break up with your boyfriend after days of not sleeping properly, but your brain may think otherwise,” she says. “Sleep plays a role in the brain to regulate and process emotions, which affects how we react and manage emotions every day.” If you’re mood seems like it’s on a chaotic roller coaster, part of the reason may be that you (and your brain) are under-slept, leading to quick tears, more flashes of frustration, negative reactions, and the like.

How to Cope if You're Running on Little Sleep

We all have our reasons for sleepless nights once in a while, and in these cases, while making sure to prioritize your sleep again is the best solution, it's not always an immediate possibility. Here are some of the healthiest and most effective ways to power through and compensate for any mental glitches that come with occasional sleep deprivation. But don't rely on these tips as an excuse to skimp on sleep! They're temporary bandages, not the final fix for sleepiness.

Get outside.

You might want to crawl under the covers and hide from the world after a restless night, but you should do the opposite, as sunlight and fresh air are both great for triggering endorphins and serotonin , Avena says. “ Serotonin , in particular, is a melatonin precursor and can help fight insomnia together,” she says. “It can be as easy as sitting on your porch for your morning coffee.”

Listen to music to wake up your brain.

Taylor Swift can get you through a breakup, and she might also help your brain power through a tough day. When you need an energy boost on sleepy mornings, turn up the volume on your favorite, upbeat playlist while driving or taking a shower. Believe it or not, when you listen to music, your entire brain lights up with neuronal activity, getting the entire brain ‘online.' Cook says: “While all the parts are awake and working, music’s vibrational energy will inevitably sync your own body's internal energy to match the faster, higher and happy vibrations.”

Caffeinate (responsibly).

Although turning to too much caffeine habitually to make up for poor sleep isn’t wise, there’s little downside to using it as a wakefulness tool every now and then, says Valerie Ulene, MD, MPH, cofounder of Boom Home Medical . “A caffeinated beverage early in the day will almost certainly help keep you more alert for a few hours,” she says. “Just remember to avoid caffeine after about mid-day as consuming it too close to bedtime will likely cause more problems than it solves.”

Try to find the root issue.

Though you may need to power through the day after a poor night of sleep, it's crucial to try to identify the reason you’re not sleeping the night before and address it before it becomes a chronic issue. 

“It can take days to catch up from even losing one hour of sleep the night before, so it’s best to try and maintain a consistent sleep and wake schedule and allow yourself to get at least seven hours of sleep each night,” Dr. Riney says. “If you feel you’re experiencing poor quality sleep or have daytime dysfunction that may be attributed to poor sleep, it’s important to seek out a sleep specialist for further evaluation.”

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Your First Step Toward a Better Mood

Poor sleep can make anxiety, depression and other mental health issues worse. Here’s what to do about it.

An illustration of a person lying on their back in a bed with eyes open. The bedroom walls and floor tiles are deteriorating, breaking off and floating away.

By Christina Caron

It started with mild anxiety.

Emily, who asked to be identified only by her first name because she was discussing her mental health, had just moved to New York City after graduate school, to start a marketing job at a big law firm.

She knew it was normal to feel a little on edge. But she wasn’t prepared for what came next: chronic insomnia.

Operating on only three or four hours of sleep, it didn’t take long for her anxiety to ramp up: At 25, she was “freaking nervous all the time. A wreck.”

When a lawyer at her firm yelled at her one day, she experienced the first of many panic attacks. At a doctor’s suggestion, she tried taking a sleeping pill, in the hopes that it might “reset” her sleep cycle and improve her mood. It didn’t work.

Americans are chronically sleep deprived: one-third of adults in the United States say they get less than 7 hours a night. Teenagers fare even worse: About 70 percent of high school students don’t get enough sleep on school nights.

And it is having a profound effect on mental health.

An analysis of 19 studies found that while sleep deprivation worsened a person’s ability to think clearly or perform certain tasks, it had a greater negative effect on mood. And when the National Sleep Foundation conducted a survey in 2022, half of those who said they slept less than 7 hours each weekday also reported having depressive symptoms. Some research even indicates that addressing insomnia may help prevent postpartum depression and anxiety .

Clearly, sleep is important. But despite the evidence, there continues to be a shortage of psychiatrists or other doctors trained in sleep medicine, leaving many to educate themselves. So what happens to our mental health if we aren’t getting enough sleep, and what can be done about it?

How does poor sleep affect your mood?

When people have trouble sleeping, it changes how they experience stress and negative emotions, said Aric Prather, a sleep researcher at the University of California, San Francisco, who treats patients with insomnia. “And for some, this can have a feed-forward effect — feeling bad, ruminating, feeling stressed can bleed into our nights,” he said.

Carly Demler, 40, a stay-at-home mother in North Carolina, said she went to bed one night and never fell asleep . From that point onward, she would be up at least once a week until 3 or 4 a.m. It continued for more than a year.

She became irritable, less patient and far more anxious.

Hormone blood work and a sleep study in a university lab offered her no answers. Even after taking Ambien, she stayed up most of the night. “It was like my anxiety was a fire that somehow jumped the fence and somehow ended up expanding into my nights,” she said. “I just felt I had no control.”

In the end, it was cognitive behavioral therapy for insomnia , or C.B.T.-I., that brought Ms. Demler the most relief. Studies have found that C.B.T.-I. is more effective than sleep medications are over the long term: As many as 80 percent of the people who try it see improvements in their sleep.

Ms. Demler learned not to “lay in bed and freak out.” Instead, she gets up and reads so as not to associate her bedroom with anxiety, then returns to bed when she’s tired.

“The feeling of gratitude that I have every morning, when I wake up and feel well rested, I don’t think will ever go away,” she said. “That’s been an unexpected silver lining.”

Adults need between 7 and 9 hours of sleep a night, according to the Centers for Disease Control and Prevention . Teenagers and young children need even more.

It’s not just about quantity. The quality of your sleep is also important. If it takes more than 30 minutes to fall asleep, for example, or if you regularly wake up in the middle of the night, it is harder to feel rested, regardless of the number of hours you spend in bed.

But some people “have a tendency to think they’re functioning well even if they’re sleepy during the day or having a harder time focusing,” said Lynn Bufka, a clinical psychologist and spokeswoman for the American Psychological Association.

Ask yourself how you feel during the day: Do you find that you’re more impatient or quick to anger? Are you having more negative thoughts or do you feel more anxious or depressed? Do you find it harder to cope with stress? Do you find it difficult to do your work efficiently?

If so, it’s time to take action.

How to stop the cycle.

We’ve all heard how important it is to practice good sleep hygiene , employing the daily habits that promote healthy sleep. And it’s important to speak with your doctor, in order to rule out any physical problems that need to be addressed, like a thyroid disorder or restless legs syndrome.

But this is only part of the solution.

Conditions like anxiety, post-traumatic stress disorder and bipolar disorder can make it harder to sleep, which can then exacerbate the symptoms of mental illness, which in turn makes it harder to sleep well.

“It becomes this very difficult to break cycle,” Dr. Bufka said.

Certain medications, including psychiatric drugs like antidepressants, can also cause insomnia. If a medication is to blame, talk to your doctor about switching to a different one, taking it earlier in the day or lowering the dose, said Dr. Ramaswamy Viswanathan, a professor of psychiatry and behavioral sciences at State University of New York Downstate Health Sciences University and the incoming president of the American Psychiatric Association.

The cycle can afflict those without mental health disorders too, when worries worsen sleep and a lack of sleep worsens mood.

Emily, who worked in the big law firm, would become so concerned about her inability to sleep that she didn’t even want to get into bed.

“You really start to believe ‘I’m never going to sleep,’” she said. “The adrenaline is running so high that you can’t possibly do it.”

Eventually she came across “Say Goodnight to Insomnia” by Gregg D. Jacobs. The book, which uses C.B.T.-I. techniques, helped Emily to reframe the way she thought about sleep. She began writing down her negative thoughts in a journal and then changing them to positive ones. For example: “What if I’m never able to fall asleep again?” would become “Your body is made to sleep. If you don’t get enough rest one night, you will eventually.” These exercises helped her stop catastrophizing.

Once she started sleeping again, she felt “way happier.”

Now, at 43, nearly 20 years after she moved to New York, she is still relying on the techniques she learned, and brings the book along whenever she travels. If she doesn’t sleep well away from home, “I catch up on sleep for a few days if necessary,” she said. “I’m way more relaxed about it.”

Christina Caron is a Times reporter covering mental health. More about Christina Caron

Managing Anxiety and Stress

Stay balanced in the face of stress and anxiety with our collection of tools and advice..

These simple and proven strategies will help you manage stress , support your mental health and find meaning in the new year.

First, bring calm and clarity into your life with these 10 tips . Next, identify what you are dealing with: Is it worry, anxiety or stress ?

Persistent depressive disorder is underdiagnosed, and many who suffer from it have never heard of it. Here is what to know .

If you notice drastic shifts in your mood during certain times of the year, you could have seasonal affective disorder. Here are answers to your top questions about the condition .

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Drawing, music and writing can elevate your mood and benefit your mental health. Here are some easy ways to welcome them into your life .

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The Effects of Sleep Deprivation

For this assignment, I have watched a TED Talk video in which Wendy Troxel explains the impact of the lack of sleep on teenagers. The author argues that the role of sleep is significantly underrated, which leads to many issues with health, both physical and mental (Troxel, 2016). I agree with this fact, as I have experienced the adverse effects caused by the lack of sleep myself. I regularly observe these effects in my classmates, which leaves me no doubt that this is indeed an epidemic, as Troxel stated in her TED Talk.

The effects of sleep deprivation are well-studied, however, they are often ignored by the majority during schedule planning. Shattuck et al. (2019) state that the lack of sleep leads to “adverse health outcomes, including weight gain and obesity, diabetes, hypertension, heart disease and stroke, depression, and increased risk of death” (p. 205). Chronic sleep deprivation increases the chances for severe mental issues, including dementia and Alzheimer’s’s disease (Bobić et al., 2016). and During the exams, sleep is always hard to come by for me. Due to the stress, I often find myself studying past my regular bedtime, sleeping for about 5 hours a day. While the effects of this behavior harmed my performance, I was unable to prevent myself from doing so.

If I had to define sleep without referencing other sources, I would say that it is a state of unconsciousness during which an organism restores its energy reserves over time. For humans, a complete sleep cycle improves cognitive abilities, decreases chances to develop conditions that plague modern society, lowers the occurrence of mental health disorders, and alleviates logistical issues. A full night’s sleep plays a crucial role in human development, and it is necessary for educational facilities to review their approach to schedule planning.

Bobić, T., Šečić, A., Zavoreo, I., Matijević, V., Filipović, B., Kolak, Z., Kes, V., Ciliga, D., & Sajković, D. (2016). The impact of sleep deprivation on the brain. Acta Clinica Croatica , 55 , 469-473. Web.

Shattuck, N. L., Matsangas, P., Mysliwiec, V., & Creamer, J. L. (2019). The role of sleep in human performance and well-being. Human Performance Optimization , 200-233. Web.

Troxel, W. (2016). Transcript of “Why school should start later for teens” . TED: Ideas worth spreading. Web.

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Sleep Deprivation and Its Detrimental Effects

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Sleep Deprivation

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Table of Contents

Physical health consequences, cognitive impairment and reduced productivity, emotional well-being and mental health, impact on quality of life, counterarguments and solutions.

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Sleep deprivation as treatment for depression: Systematic review and meta‐analysis

Michael ioannou.

1 Region Västra Götaland, Psykiatri Affektiva, Department of Psychiatry, Sahlgrenska University Hospital, Gothenburg Sweden

2 Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg Sweden

Constanze Wartenberg

3 Region Västra Götaland, HTA‐centrum, Gothenburg Sweden

Josephine T. V. Greenbrook

4 School of Law, Mason Institute for Medicine, Life Science and the Law, University of Edinburgh, Edinburgh Scotland

5 Department of the Life Context and Health Promotion, Institute of Health and Care Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg Sweden

Tomas Larson

Kajsa magnusson.

6 Region Västra Götaland, Medical Library, Sahlgrenska University Hospital, Gothenburg Sweden

Linnea Schmitz

Petteri sjögren, zoltán szabó, steinn steingrimsson, associated data.

The data that support the findings of this study are available in the Supporting Information of this article.

To systematically review evidence on the efficacy and safety of sleep deprivation (SD) as a treatment option for patients with unipolar or bipolar depression.

A systematic review according to PRISMA guidelines was conducted. The certainty of evidence was assessed using the GRADE approach. Controlled trials were included in efficacy analysis, case series for evaluating complications and qualitative studies for patients’ experiences.

Eight controlled studies (368 patients), one qualitative study and seven case series (825 patients) were included. One week after treatment start, SD combined with standard treatment did not reduce depressive symptoms compared with standard treatment (standardized mean difference, SMD = −0.29, [95% confidence interval, CI: −0.84 to 0.25], p  = 0.29). When excluding a study in elderly patients in a post hoc analysis, the difference was statistically significant (SMD = −0.54 ([95% CI: −0.86 to −0.22], p  < 0.001)) but it diminished two weeks after treatment start. No superiority of SD was found compared with antidepressants, but SD may be superior to exercise in certain settings. It is uncertain whether SD affects quality of sleep, quality of life, everyday functioning or length of stay. Apart from switch to mania (ranging between 2.7% and 10.7%), no other serious complications were reported.

Sleep deprivation has been studied in a wide range of settings resulting in divergent results for the short‐term efficacy on depressive symptoms. Post hoc analyses indicated that there may be a significant but transient effect in certain populations. Further studies should focus on identifying subgroups of responders as well as examining feasibility in routine clinical care.

  • Sleep deprivation may have a transient effect on depressive symptoms in a subgroup of patients.
  • It is uncertain whether sleep deprivation affects the health‐related quality of life, everyday functioning, quality of sleep and length of hospital stay.
  • The transient effect of sleep deprivation limits its clinical relevance as an add‐on treatment to current antidepressants.

Limitations

  • The meta‐analysis was based on post‐treatment assessments only, as information regarding mean change from baseline and the corresponding standard deviations was missing in almost all included studies.
  • Differences in several aspects of the included studies (mostly on study population, comparators, treatment protocols, and subsequent maintenance strategies) limited the certainty of evidence.

1. INTRODUCTION

Depression is a leading cause of disability worldwide, 1 causing a high burden of disease and substantial societal cost. 2 , 3 It is a major contributor to death by suicide 1 and is highly correlated with cardiovascular and other chronic disease‐related mortality. 4

Although antidepressant medications are more efficacious than placebo, a significant number of treatment‐seeking patients with depression do not respond sufficiently and even for responders several weeks may pass before an optimal therapeutic effect is reached. 5 , 6 , 7 This latency period (between start of medication to its full effect) is critical, as it has been found to be related to both increased risk for suicidal behaviour and poor treatment response. 8 , 9 Thus, identifying treatment options for alleviating depressive symptoms rapidly should be regarded as a prioritized goal in clinical psychiatric research.

A treatment method of interest is sleep deprivation (SD) or wake therapy, where a patient intentionally remains awake during one or more nights in order to regulate the diurnal rhythm and thereby alleviate depressive symptoms. Although instantaneous overnight remission of depressive symptoms after SD has been widely reported, relapse after recovery sleep is common. 10 In order to improve the effect of SD and to achieve maintained effect, several chronotherapeutic protocols have been developed. These protocols vary in several aspects: the type of SD (total, ie complete SD for a whole night or partial, ie parts of the night); the number of nights awake (single or repeated with intermittent nights with sleep); sleep management after SD (eg the length of recovery sleep, strategies for sleep phase advances and sleep time stabilization); maintenance strategies (eg concurrent light therapy or pharmacotherapy) and strategies for protocol adherence (eg hospital setting, various monitoring methods, availability of physical and social activities during the SD). When systematically evaluating the efficacy of SD as treatment of depression, it is important to take into account the heterogeneity of the treatment protocols as well as the instruments and timing of the clinical assessments. The effect of SD also needs to be evaluated in relation to the time period for which an additional treatment option is urgently needed (ie the time to response or remission of depression after start of treatment with the current antidepressants), a latency period of presumably more than two weeks. 8 A recent meta‐analysis suggests that SD may have an antidepressant effect in the first week of treatment in bipolar depression, 11 but a comprehensive review of SD for the whole spectrum of depressive disorders is warranted.

1.1. Aims of the review

The main objective of this review was to assess whether SD with or without subsequent light therapy is an effective treatment option by itself or in addition to standard treatment for patients with unipolar or bipolar depression compared with no SD or other treatment. In addition, the safety of SD was investigated.

A systematic review was conducted as part of a health technology assessment (HTA) performed at HTA‐centrum, Sahlgrenska University Hospital in Gothenburg, Sweden. 12 The methods are based on the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA). 13 The PICO process (Population, Intervention, Comparator, Outcome) was used to define the research question and eligibility criteria for the literature search. The review was not registered in a prospective register prior to the literature search. However, the selection and analysis of the articles were based on the initially defined PICO and performed according to the current praxis at the HTA‐centrum.

2.1. Eligibility criteria

To be eligible, studies had to meet the following criteria:

  • Population: Study participants were adult patients (≥18 years old) with depression including bipolar depression (defined according to DSM criteria). 14
  • Intervention: SD for at least one night under supervision in an inpatient setting (with or without subsequent light therapy).
  • Comparator: (i) no SD with or without underlying standard treatment or (ii) other treatment (eg medication, exercise) than SD with or without standard treatment. Studies in which electroconvulsive therapy (ECT) was used as a standard treatment or comparator to SD were not eligible for inclusion.
  • Outcomes: The outcomes of primary interest were mortality (including suicide), self‐harm and depressive symptoms (assessed by validated instrument). Additional important outcomes were quality of sleep, health‐related quality of life measured with validated instruments, medication use, everyday functioning (activities of daily living, return to work) according to validated scales or administrative data, length of hospital stay, patients’ experience during treatment (based on qualitative studies), diurnal rhythm and complications. Eventual worsening in depressive symptoms was to be evaluated as part of effect measures rather than complications.
  • Types of study included the following: randomized controlled trials (RCTs) with at least five patients per group, cohort studies (with at least 10 patients per group), case series with at least 50 patients (for analysis of complications) and qualitative studies (for information on patients’ experience during treatment, with at least five patients). Studies had to be published in English or Scandinavian languages (Danish, Norwegian or Swedish). No restriction was applied to the date of publication.

2.2. Patient involvement

The PICO was reviewed by representatives from a local patient organization (Intresseförening Bipolär Sjukdom, IBIS) who confirmed the relevance of the outcomes at issue as well as emphasizing the importance of rapid relief of depressive symptoms from the patient's perspective.

2.3. Data sources and study selection

During March 2019, two authors (KM and IS) performed systematic searches in PubMed, EMBASE, the Cochrane Library, CINAHL, PsycInfo and a number of HTA databases. In June 2019, ClinicalTrials.gov was searched for relevant completed and ongoing trials. The details of the search strategy for each database are reported in Appendix S1 . As a complement to this search, we also reviewed the reference lists of relevant articles. These two authors conducted the literature searches, selected studies, and independently of one another assessed the obtained abstracts and made a first selection of full‐text articles for inclusion or exclusion. Any disagreements were resolved in consensus. All remaining articles were sent to all authors who read the full‐text articles independently of one another and decided in a consensus meeting which articles should be included in the review. Excluded studies and reasons for exclusion are presented in the Appendix S2 . The search was repeated in all the above databases in March 2020. Additional 139 abstracts were assessed by CW and MI without meeting the inclusion criteria.

2.4. Data extraction

Two reviewers (MI and LS) extracted data for each eligible study, and another author (CW or PS) verified the data extraction. We retrieved information on study design, location, clinical and demographic population data (including type of depression, gender and age distribution), treatment protocols, outcome measures and main findings. When needed, outcome values were retrieved from diagrams or calculated with help of online calculators. Additional study data were retrieved for three studies, after contacting the corresponding authors. 15 , 16 , 17

2.5. Assessment of quality

The risk of bias was evaluated by all authors using a checklist for assessment of RCTs from the Swedish Agency for Health Technology Assessment and Assessment of Social Services (SBU). 18 This checklist, based on the Cochrane risk of bias tool, 19 assesses selection bias, performance bias, detection bias, attrition bias, reporting bias and conflicts of interest. Any discrepancies in assessments were resolved in consensus meetings. For qualitative studies, the tool of SBU for assessment of qualitative studies was used. 20

The certainty of evidence was assessed at outcome level using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system. 21 The following factors were assessed: study limitations/risk of bias (including randomization, blinding, follow‐up, dropouts, compliance and intention‐to‐treat analysis); consistency (including direction and magnitude of effect across studies and overlap of confidence intervals); directness (including setting, population, intervention, control, outcome and comparison–in other words the generalizability); and precision (including sample size and width of confidence intervals). We initially assigned a high certainty level, but downgraded one or more levels to moderate, low or very low if issues with GRADE criteria regarding study quality, directness or precision were detected.

2.6. Publication bias

Potential publication bias was assessed by searching ClinicalTrials.gov and by visual inspection of funnel plots. The main strategy was to search for relevant studies that had been listed as completed on ClinicalTrials.gov but had not been published.

2.7. Statistics

When possible, data were combined in meta‐analysis for investigation of the aggregated effect. The meta‐analysis was performed with Review Manager (RevMan) [Computer program] version 5.3. Copenhagen: The Nordic Cochrane Centre, The Cochrane Collaboration: Copenhagen, Denmark, 2014. Notably, the meta‐analysis had to be based on post‐treatment assessments only, as information regarding mean change from baseline and the corresponding standard deviation is missing in almost all publications. This implies less statistical power to detect treatment effects, compared to the analysis in terms of change from baseline, which is used in the publications. Because different versions of Hamilton depression rating scale (HDRS) 22 were used for assessment of depression symptoms, we calculated standardized mean differences (SMD) and their 95% confidence intervals (CI). The level of statistical significance was set to p  < 0.05. Effect sizes were pooled in a random‐effects model given expected heterogeneity between studies. Statistical heterogeneity was assessed with the χ 2 and I 2 statistics. When warranted, post hoc analyses were conducted for clarification, but not contributed in the overall conclusions of evidence synthesis (which were based on the PICO). No ethical approval was needed prior to the study as the analysed data were retrieved from previous published studies in which informed consent was obtained by primary investigators.

3.1. Search results

The literature search identified 2133 articles after removal of duplicates. After reading the abstracts, 2055 articles were excluded with additional 43 articles excluded after reading the articles in full text. The remaining 35 articles were sent to all participants of the project group to read in full text out of which 19 articles were finally included in the analysis. A flowchart of the study selection process is presented in Figure  1 . No unpublished studies were found on our search on ‘ClinicalTrials.gov’.

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Flow diagram of selection process (PRISMA chart)

3.2. Characteristics of included studies

The included studies, their design and patient characteristics are presented in Table  1 . In all, seven RCTs were included, 15 , 16 , 17 , 26 two of which had three treatment arms and contributed to both comparison of SD as add‐on to standard treatment and SD to other treatments. 14 , 22 The studies by Kundermann et al and by Martiny et al were reported in two 17 , 27 and three publications, 25 , 28 , 29 respectively. Six RCTs ( n  = 215 patients) and one cohort study ( n  = 41) investigated SD as add‐on compared with standard treatment. Three RCTs ( n  = 148 patients) compared SD with other treatment. 15 , 23 , 25 The characteristics of the included controlled trials and the results for each outcome are presented below separately for the comparison of i) SD as add‐on compared with standard treatment ii) for the comparison of SD versus other treatment. Apart from the studies above, seven case series 30 , 31 , 32 , 33 , 34 , 35 , 36 were included for the evaluation of rate of complications following SD and one qualitative study 37 contributed information regarding patients’ experience during treatment. Total rather than partial SD was used in all the included studies.

Characteristics of included studies

Abbreviations: C, control group; ca, circa (approximately); CBT, cognitive behavioural therapy; HDRS, Hamilton depression rating scale; HrQoL, health‐related quality of life; I, intervention group; LT, light therapy; RCT, randomized controlled trial; SD, standard deviation; SPA, sleep phase advance; STS, sleep time stabilization; TSD, total sleep deprivation.

3.2.1. SD as add‐on compared to standard treatment

Six RCTs with a total of 215 patients 15 , 16 , 17 , 23 , 24 , 26 , 27 and one cohort study 38 in 49 patients compared SD as add‐on to standard treatment. Antidepressant medication was used as standard treatment in all studies except in one RCT where CBT was used. 17 , 27 Only one of these studies had no limitations regarding directness, precision and risk of bias. 16 All other studies had minor or major risk of bias—mainly due to limitations in blinding, and high or incompletely described dropout rates. The directness was limited in four of the studies, for example due to differing SD protocols (1 up to 6 wake nights) and patient populations (eg one study in elderly patients with late‐onset depression). 15 , 17 , 24 , 38 Furthermore, two studies had small sample sizes limiting the precision. 17 , 24 Two studies combined SD with chronotherapeutic interventions (light therapy, sleep time stabilization). 16 , 26

3.2.2. SD compared with other treatment

Three RCTs were included with a total of 148 patients comparing SD with other active treatment. Two studies compared SD with medication. 15 , 23 The third study compared SD combined with subsequent chronotherapeutic maintenance (light therapy and sleep time stabilization) with exercise as active comparator. 25 , 28 , 29 The risk of bias was judged to be minor in all three studies (some limitations in blinding, and some questions regarding the control treatments). Questions regarding directness were raised for two studies (one study only included elderly patients, and for the study comparing SD with exercise, the latter was of limited duration and intensity). Furthermore, one of these three studies had a small sample size limiting the precision. 23 The quality assessment of RCTs and the cohort study is presented in the outcome tables.

3.3. Outcomes

A summary of key findings is presented in Table  2 .

Summary of findings, by comparison

Abbreviations: CI, confidence interval; GAF, global assessment of functioning; GRADE, grading of recommendations, assessment, development and evaluations; HDRS, Hamilton depression rating scale; HRQL, health‐related quality of life; n.s., not significant; RCT, randomized controlled trials; sign., significant; SMD, standardized mean difference; TSD, total sleep deprivation; vs, versus.

3.4. Mortality (including suicide) and self‐harm

None of the included studies reported data regarding mortality or self‐harm.

3.5. Depressive symptoms

In all the included studies, depressive symptoms were assessed using the HDRS at baseline and several subsequent times during the studies. The HDRS ratings were assessed by clinicians/raters in all studies, but different versions of the scale have been used.

3.5.1. SD as add‐on compared with standard treatment

Six RCTs 15 , 16 , 17 , 23 , 24 , 26 , 27 and one cohort study 38 investigated the effect of SD as add‐on to standard treatment on depressive symptoms. Depressive symptoms were assessed for a study duration of 2–9 weeks (Appendix S3 ).

Effects of SD during the first week after treatment start

Four RCTs reported statistically significant differences between the treatment groups regarding depressive symptoms during the first week. In three studies, results were in favour of SD 16 , 24 , 26 and in one study in favour of the comparator. 15 A meta‐analysis of the post‐treatment HDRS data during the first week was statistically non‐significant for SD combined with standard treatment compared with standard treatment only (SMD = −0.29 [95% CI: −0.84 to 0.25], p  = 0.29), with substantial heterogeneity in the analysis ( I 2  = 70%) (Figure ​ (Figure2 2 ).

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Meta‐analysis of the Hamilton depression rating scale (HDRS) scores during the first week after start of treatment with sleep deprivation as add‐on to standard treatment compared with standard treatment only

The RCT by Reynolds et al 15 was found to be the main source of the statistical heterogeneity. In a post hoc sensitivity analysis excluding Reynolds et al 15 , and thereby the only study specifically conducted in elderly patients, the heterogeneity resolved ( I 2  = 0%) and the overall effect was statistically significantly different with a standardized mean difference of SMD = ‐0.54 [95% CI: −0.86 to −0.22], p  = 0.0009 in favour of SD.

Given the idea to offer SD as an add‐on treatment to psychopharmacological treatment alone, an additional post hoc analysis of the five RCTs ( n  = 196 patients) with this design was conducted. The overall effect was not statistically significant one week after the start of treatment (SMD = −0.32 [95% CI −0.97 to 0.32]; p  = 0.32) but showed statistically significant difference when excluding Reynolds et al 15 as above (SMD = −0.59 [95% CI: −0.94 to −0.25], p  = 0.0007).

Further post hoc analyses were conducted by separating bipolar and unipolar depression. The RCT by Kragh et al 16 was excluded from these analyses because of mixed population. Thus, three studies were included in the meta‐analysis for unipolar depression 15 , 17 , 23 and two for bipolar depression. 24 , 26 One week after treatment start, the effects of SD were not statistically significant in studies on unipolar depression (SMD = −0.10 [95% CI −1.16 to 0.96], p  = 0.85, I 2  = 81%). For studies on bipolar depression, there was a tendency towards significance at the same time point (SMD = −0.54 [95% CI −1.08 to 0.00], p  = 0.05, I 2  = 0%).

When excluding the RCT on late‐life depression by Reynolds et al 15 , the effect size of SD in unipolar depression was numerically similar to bipolar depression but still not statistically significant (SMD = −0.59 [95% CI −1.44 to 0.25], p  = 0.17, I 2  = 40%). Note, these analyses regarding subgroups of patients were conducted post hoc and are thus merely explorative.

Based on the GRADE assessment (Table  2 ), we conclude that SD given in addition to standard treatment, in patients with depression, may result in little or no difference in depressive symptoms compared with no add‐on treatment during the first week after treatment start (low certainty of evidence).

Effects of SD more than one week after treatment start

In five out of the six RCTs, no statistically significant effect of SD was observed in the subsequent weeks after SD. 15 , 16 , 17 , 23 , 24 One RCT reported a maintained effect of SD. 26 Meta‐analysis of the HDRS scores two to three weeks after first SD did not show any statistically significant differences (SMD = 0.13 [95% CI −0.38 to 0.64]; p  = 0.61), I 2  = 63%. No reliable variability data were available for one of the studies 23 which therefore does not contribute to the meta‐analysis on the effect of SD more than one week after treatment start (Appendix S4 ). When excluding the study by Reynolds et al 15 , as above, the heterogeneity resolved ( I 2  = 0%) but the comparison was not statistically different (SMD = −0.07 [95% CI −0.40 to 0.27], p  = 0.70, I 2  = 0%). Stratified post hoc analyses did not reveal notable differences for bipolar depression (SMD = −0.33 [95% CI −0.87 to 0.20], p  = 0.22, I 2  = 0%) or unipolar depression (SMD = 0.43 [95% CI −0.66 to 1.51], p  = 0.44, I 2  = 76%). Inspection of the funnel plots based on the meta‐analyses of the post‐treatment HDRS data revealed no evidence of publication bias. Based on our GRADE assessment (Table  2 ), we conclude that SD given in addition to standard treatment, in patients with depression or bipolar depression, may have little or no persisting effect on depressive symptoms, after more than one week, compared with no add‐on treatment (low certainty of evidence).

3.5.2. SD compared with other treatment

Two RCTs with minor study limitations including 73 patients compared SD and concurrent administration of placebo with initiation of antidepressant medication. 15 , 23 No difference was found between SD compared with antidepressant medication during the two‐week follow‐up in the studies (Appendix S5 ). Based on our GRADE assessment (Table  2 ), we conclude that it is uncertain whether SD compared with medication affects depressive symptoms in patients with depression (very low certainty of evidence).

One study with minor study limitations (described in three publications focusing on different length of follow‐up) 25 , 28 , 29 compared SD followed by chronotherapeutic maintenance with exercise of limited duration and intensity. Patients in the SD group showed a rapid, statistically significant and larger reduction in depression scores than patients in the exercise group one week after start of treatment with SD (SMD = −0.83 [95% CI −1.30 to −0.36]; p  = 0.06). The between‐group difference diminished over the 29 weeks of follow‐up (Appendix S5 ). Based on our GRADE assessment (Table  2 ), we conclude that SD with subsequent chronotherapeutic maintenance may result in reduced depressive symptoms compared with exercise in patients with depression starting antidepressant medication (low certainty of evidence).

Taken altogether, a meta‐analysis of the overall post‐treatment HDRS data during the first week showed no statistically significant superiority of SD compared with other treatment (antidepressants or exercise) (SMD = −0.18 ([95% CI: −0.92 to 0.55], p  = 0.63). However, the heterogeneity in the analysis was substantial ( I 2   =  77%) (Appendix S6 ).

3.6. Quality of sleep

The outcome quality of sleep was investigated in one RCT comparing SD as add‐on versus no add‐on treatment 16 and in one RCT comparing SD with exercise 25 , 28 , 29 (Appendix S7 ). In both studies, quality of sleep was self‐reported using non‐validated instruments. Both studies reported positive effects of the combination of SD, light therapy and sleep time stabilization on patients’ sleep duration, sleep maintenance and self‐reported sleep quality. A statistically significant advance of the sleep‐wake cycle was observed in one study, 29 indicating less problems falling asleep. Kragh et al 16 report a decrease in awakenings during the night and less day time sleeping in the first weeks after SD. Based on our GRADE assessment (Table  2 ), we conclude that it is uncertain whether SD affects the quality of sleep in patients with depression compared with no or other treatment (very low certainty evidence).

3.7. Health‐related quality of life (HRQL)

HRQL was measured with validated instruments in one RCT 16 comparing SD as add‐on versus no add‐on treatment and in one RCT 29 comparing SD to exercise (Appendix S8 ). Both studies 16 , 29 evaluated similar chronotherapeutic interventions (combination of SD, light therapy and sleep time stabilization) and measured HRQL with the WHO‐5 scale. Only one study 29 showed statistically significantly better self‐reported HRQL in the SD treatment group than in the control group. Based on our GRADE assessment (Table  2 ), we conclude that it is uncertain SD affects the health‐related quality of life measured in patients with depression compared with no or other treatment (very low certainty evidence).

3.8. Everyday functioning

Everyday functioning was investigated by using GAF assessments in one RCT 16 comparing SD as add‐on to medication with no add‐on treatment and in one RCT 29 comparing SD to exercise (Appendix S9 ). The two studies had similar intervention protocols for the SD groups, but they report GAF scores in different post‐treatment time periods (9 weeks and 29 weeks after SD, respectively). 16 , 29 No statistically significant effect on everyday functioning was found. Based on our GRADE assessment (Table  2 ), we conclude that it is uncertain whether SD affects the everyday functioning in patients with depression compared with no or other treatment (very low certainty evidence).

3.9. Length of hospital stay

One RCT 16 investigated the length of hospital stay in patients treated with SD as add‐on compared with no add‐on treatment (Appendix S10 ). No statistically significant difference was found between groups. Noticeably, the median length of hospital stay was numerically longer for the SD group. No studies investigated this outcome in comparison of SD to other treatment. Based on our GRADE assessment (Table  2 ), we conclude that it is uncertain whether SD in addition to standard treatment affects the length of hospital stay compared with no add‐on treatment in patients with depression (very low certainty of evidence).

3.10. Medication use

None of the included studies investigated the need for or changes in medication use before and after intervention. Data on psychotropic medication were reported in two studies 16 , 29 mainly serving as control information for a possible cofounder. No statistically significant differences between intervention and control groups were reported (very low certainty evidence).

3.11. Patient‐reported experience

Only one qualitative study was found to focus on patients’ experiences of SD when taking part in an RCT. 37 The quality of the study was evaluated as moderate because of lack of information on ethical rational (ie power imbalances during interviewing) and theoretical foundation (ie insufficient presentation of manifest analysis). The participants’ overall experiences were reported to be positive. A rapid but transient antidepressant effect was experienced by some patients whereas others described long‐term benefits, such as improved sleep and diurnal rhythms. Negative experiences were limited, and mostly related to disappointment surrounding inadequate or transient responses.

3.12. Complications

The systematic documentation of complications is limited in the included studies. Data are provided in three RCTs, 16 , 26 , 29 one cohort study 38 and seven case series 30 , 31 , 32 , 33 , 34 , 35 , 36 (Appendix S11 ).

The switch rate to manic state in patients with depression was reported in eight studies. 16 , 25 , 26 , 30 , 31 , 32 , 33 , 36 Summarized over all included studies above, the average switch rate in patients with bipolar disorder during SD treatment (650 patients with bipolar disorder) was 5.5% (ranging between 2.7% and 10.7%). The publications do not provide any information as to when the switch to mania occurred in relation to the SD. No conclusive data could be retrieved on mood switching in SD‐treated patients with unipolar depression.

Regarding the tolerability and feasibility of the treatment, relevant data were retrieved from three RCTs 26 , 29 , 38 and one cohort study. 38 Of the 152 patients who were treated with SD, 17 (11.2%) were reported as dropouts. The reasons for dropout were not specified in all cases, but ECT treatment and failure to adhere to study protocol were mentioned. A comparison with the control groups is not possible, since information on dropouts in the control groups is very limited. One patient in the control group developed polarity switch. 29 Two studies 16 , 29 described development or worsening of anxiety in a small number of patients following SD.

4. DISCUSSION

The primary aim of the systematic review was to assess the efficacy and safety of SD with or without subsequent chronotherapeutic maintenance in patients with depressive symptoms including bipolar depression. In summary, the meta‐analysis showed no statistically significant difference one week following start of intervention. However, in post hoc analyses excluding a study focusing on elderly patients, the effect size was moderate and statistically significant. Given the limited data available, treatment effect on other relevant outcomes is uncertain. Furthermore, no superiority of SD was found compared with antidepressants. Finally, one study suggested that SD with subsequent chronotherapeutic maintenance may be superior to exercise in patients with depression starting antidepressant medication and the superiority could be maintained for several weeks. 29 However, these findings based on a single study need replication for a thorough evaluation.

Boland et al 39 reported a meta‐analysis of the antidepressant effects of SD with focus on short‐term response rates and correlations of response to factors such as medication status, type of SD, age and gender. That review has a methodological approach that does not meet PRISMA guidelines. 13 A major limitation of that review article is the lack of comparison to a control group. Boland et al 39 observe that the response to SD was not correlated with the type of SD, medication status, diagnosis, age or gender of the study population. A more recent meta‐analysis supported that chronotherapy (SD combined with other interventions) has a rapid effect on depression. 40 However, our review had more stringent inclusion criteria focused on SD and we included RCTs that are not included in the meta‐analysis by Humptson et al 40 Moreover, the present analysis distinguished between different comparators (add‐on vs no add‐on, SD vs medication and SD vs exercise), include several outcomes and followed a different statistical approach. Ramirez‐Mahaluf et al 11 conducted a meta‐analysis on SD effect in bipolar depression, including exclusively studies on patients with bipolar disorder. In their efficacy analysis of SD as an add‐on treatment, two studies were included, both of which are covered in our analysis. 24 , 26 Ramirez‐Mahaluf et al 11 argue for a statistically significant effect of SD after one week. However, in our post hoc analyses, we found only a tendency towards significance ( p  = 0.05) for the same time period. Namely, Ramirez‐Mahaluf et al 11 measured time from the initiation of the study treatment protocol (including drug titration periods) and not specifically from the treatment start with SD. Thus, different baseline time points were used, leading to different conclusions on the short‐term effects of SD.

The effects of SD on unipolar compared with bipolar depression are worth further discussion. Circadian rhythm disruptions are common both in unipolar and bipolar depression. 41 Despite common mechanism‐of‐action targets for unipolar and bipolar depression, it has been debated whether the polarity of depression affects the response to SD, eventually in favour of bipolar depression. 42 In our post hoc analyses, we found similar numerical yet not statistically significant effect sizes for patients with bipolar depression and non‐elderly patients with unipolar depression. However, these considerations are merely explorative as they build on post hoc analyses of studies which in addition have methodological limitations (see below).

Total SD was used in all the included studies. Although total SD is the most established method in research and clinical praxis, different types of SD, such as late partial SD and selective Rapid Eye Movement‐SD (REM‐SD), have been presumed to have antidepressant effects. 43 , 44 However, a single study did not show any advantages of late partial compared to total SD regarding efficacy or adherence. 45 Moreover, Grözinger et al 46 compared REM‐SD to non‐REM‐SD without finding any significant difference on the alleviation of depressive symptoms.

4.1. Limitations

A key limitation of the present review was that the meta‐analysis was based on post‐treatment assessments only, as information regarding mean change from baseline and the corresponding standard deviation was missing in almost all publications. This approach is less powerful than the statistical analyses used in the individual publications, which consider repeated measures at different time points. Further limitations were the heterogeneity between studies in the study population (eg either or both unipolar and bipolar depressions), SD protocols (eg number of wake nights, use of other subsequent chronotherapeutic interventions) concurrent treatment (ongoing or starting antidepressant medication, other standard treatments) and outcome measures (eg different versions of the HDRS). In order to take both heterogeneity and differences in the included studies into account, we analysed the data using a random‐effects model, which is more conservative.

The study population varied across the included studies—mainly in terms of the diagnoses and suicidality of the included patients. Regarding diagnoses: two studies included patients with bipolar disorder 24 , 26 ; three studies recruited only patients with unipolar depression 15 , 17 , 38 ; two studies included patients with either unipolar or bipolar depression 16 , 25 ; and in one study, no exact information regarding the kind of depression was available. 23 All but two studies listed suicidality as an exclusion criterion. 24 , 38 It should be noted that the variety in sleep disturbances in patients with depression—ranging from insomnia to hypersomnia—has not been considered explicitly in the included studies. Moreover, anxiety is a common, agonizing symptom of depression and Martiny et al 25 commented that a high level of anxiety may be a contraindication for SD. For the other studies, it is unclear how many patients suffered from anxiety.

The treatment protocol varied from a single wake night 15 up to six wake nights within three weeks. 17 Subsequent maintenance strategies varied the following: some studies combined SD with medication only, whilst three trials 16 , 26 , 29 provided additional chronotherapeutic interventions (light therapy, sleep phase advance and/or sleep time stabilization). Overall, the most favourable results were reported after SD for three wake nights within one week in combination with medication and other chronotherapeutic interventions. It should be emphasized that the support offered to patients during wake nights differed considerably—in some studies various activities (requiring room and personnel) were offered, whereas patients in other studies merely were instructed to stay awake with very limited further support.

The limitation of using HDRS as depression rating scale is worth consideration—especially when investigating the effect of SD. The scale has been criticized, as changes in HDRS score may be observed even if a clinically relevant change in cardinal symptoms of depression is lacking. 47 , 48 , 49 Namely, the HDRS score may decrease due to changes in a subset of items related to sleep or appetite without corresponding changes in core symptoms such as depressed mood, and anhedonia. Moreover, a modified version of HDRS has been used in three of the included studies 17 , 23 , 26 and the comparability of these results may be affected.

4.1.1. Implication to practice

The paramount question is whether SD has a clinically relevant effect. In evaluating placebo‐controlled clinical trials of antidepressant medication, the American Food and Drug Administration (FDA) and European Medicines Agency (EMA) considered an average two‐point difference in HDRS‐17 score as a minimal clinically significant difference (comparing an active substance to placebo). 50 , 51 Meta‐analyses of currently used antidepressant medication compared with placebo regarding HDRS reported an SMD of −0.35 to −0.30 in patients with mild‐to‐moderate depression. 52 In this context, the effect size in the post hoc meta‐analysis of SD as add‐on treatment in non‐elderly psychiatric population would qualify as clinically relevant. However, the confidence interval is wide and the overall confidence in this finding from a post hoc analysis is low. Furthermore, the included studies reported transient effects that lasted for some days after SD—this duration needs to be evaluated in relation to the need for additional treatment options during the first weeks it takes until antidepressant medication gains effect. Still, even if SD only reduces depression symptoms for a limited duration, this may be of clinical value in the absence of other treatment options. Also, it remains to be seen, if SD may be repeated for renewed effect in patients who respond to this treatment.

Another important question regarding the clinical practice is the risk of complications because of the treatment. Apart from the risk of switch to mania, no other serious complication has been reported in the included studies. Switch from depression to mania is regarded as a fundamental and defining feature of bipolar disorder. 53 It may occur spontaneously or precipitated by stress or concurrent treatment. 54 The switch rate to mania during treatment with placebo has been estimated to 4.2% for patients with bipolar disorder. 55 According to Benedetti 56 , the switch rate to mania may rise to 15‐40% during treatment with antidepressants. There is also evidence that the study design, the type of antidepressants and the age of the participants may explain the variance in switch rate. 57 In the studies included in this review, a switch rate around 5.5% was reported. Yet, this observation is limited by the heterogeneity of treatment modalities and insufficient reporting of complications in most of the publications. Moreover, no study was specifically designed to assess the risk of manic switch meaning that a meta‐analysis of risk for patients with bipolar disorder was not possible. With respect to the clinical relevance, the risk of switch to mania should not be considered as an absolute contraindication for inpatient SD treatment of patients with bipolar disorder.

4.1.2. Implication for research

As conclusions are limited by the heterogeneity of treatment modalities and study population, further well‐designed RCTs are required to investigate the optimal treatment protocol and patient subgroups who could benefit from the treatment. A major issue in investigating the effects of SD is the impossibility of double‐blinded studies—thus, head‐to‐head to other treatment methods may be preferable.

The heterogeneity in the clinical response to SD may partly reflect the heterogeneous nature of depression 58 , 59 , 60 . The differentiation of unipolar and bipolar depression should as in most previous studies be considered in future research. Moreover, neuroimaging may improve the selection of patients who respond to SD although further research is required. 61 , 62 , 63

The age of the participants may play role in the heterogeneity in the clinical response to SD. Ageing affects namely the circadian rhythms as changes occur in seminal parts of the circadian system such as the retina and the suprachiasmatic nucleus in hypothalamus. 10 , 64 Moreover, late‐life depression may differ from early‐life depression in aetiology and response to treatment. 65 Thus, elderly depressed patients may respond differently to chronotherapies as also indicated by the not replicated study on elderly depressed patients. 15 Further studies need to evaluate the impact of ageing on sleep and the circadian system and on the efficacy of SD.

In conclusion, SD may have a role in the rapid relief of depression; however, the certainty of evidence is low. Furthermore, it is uncertain whether SD affects quality of sleep, health‐related quality of life, everyday functioning or length of hospital stay. Generally, the method is well‐tolerated, although the risk of switch to mania exists. Albeit the low grade of evidence, the treatment method of SD should be considered an important part of the future research in rapid relief of depression.

CONFLICT OF INTEREST

The authors have no conflict of interest to declare in relation to the present work.

PEER REVIEW

The peer review history for this article is available at https://publo ns.com/publo n/10.1111/acps.13253.

Supporting information

Appendix S1

Appendix S2

Appendix S3

Appendix S4

Appendix S5

Appendix S6

Appendix S7

Appendix S8

Appendix S9

Appendix S10

Appendix S11

ACKNOWLEDGEMENTS

The authors wish to acknowledge Ulla Wide and Ludger Grote for valuable comments on the HTA report upon which this systematic review is based.

DATA AVAILABILITY STATEMENT

Home — Essay Samples — Nursing & Health — Sleep Deprivation — The Effects Of Sleep Deprivation On Memory

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The Effects of Sleep Deprivation on Memory

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Published: Feb 8, 2022

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Introduction, sleep’s role in memory, effects on semantic memory, effects on emotional working memory, effects on procedural memory.

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sleep deprivation effects essay

FOX News

Sleep deprivation dangers: How pulling an all-nighter affects your physical and mental health

Most people have sacrificed sleep at some point, but those extra waking hours could come at a price.

While it can be tempting to burn the midnight oil — whether it’s to get some work done, knock out a home project or care for a loved one — forgoing rest can wreak havoc on your health .

Fox News Digital spoke to experts about the short- and long-term effects of pulling an all-nighter — and how to rebound after a period of missed sleep.

DOES THE 'SLEEPY GIRL MOCKTAIL' REALLY WORK? EXPERT WEIGHS IN ON THE VIRAL SLEEP TREND

Here's a deep dive.

Pulling an all-nighter can have several impacts on the body, both physically and mentally, according to Dr. Leah Joseph, a primary care physician with New York-based Teladoc Health. 

READ ON THE FOX NEWS APP

"The physical effects include weakening your immune system, which makes you more susceptible to illnesses," she told Fox News Digital. 

"Your body may also release a higher level of cortisol, which leads to elevated stress levels ."

In addition, sleep deprivation can result in impaired memory, concentration and overall cognitive function, Joseph noted.

GOOGLE SEARCHES FOR 'SLEEP' REACHED ALL-TIME HIGH IN 2023, NEW STUDY NOTES

"The mental effects include mood changes, which can contribute to irritability, anxiety or depression," she said. 

"It also affects your decision-making, as your judgment may be negatively affected."

Alex Dimitriu, M.D., who is double board-certified in psychiatry and sleep medicine and is founder of Menlo Park Psychiatry & Sleep Medicine in California, also warned of adverse effects.

"There is evidence that even a single night of insufficient — or worse yet, absent — sleep leads to a buildup of toxins in the brain similar to those seen in people with Alzheimer's disease ," he told Fox News Digital. 

"Similar to Alzheimer's, even one night of lost sleep can cause fatigue, impaired impulse control, mood instability, diminished attention and memory — all symptoms similar to ADHD."

"Underslept" people are more likely to suffer from a variety of psychiatric conditions , Dimitriu said. 

Those include depression, anxiety, substance use, memory impairment and possibly an eventual increased risk of dementia. 

"The brain needs sleep to clean up and reset," he said.

Physically, lost sleep causes increased carb craving, diminished immunity and increased stress hormones, such as cortisol and adrenaline, he added. 

"The increased stress hormones, in turn, can elevate heart rate, blood pressure and blood sugar."

While pulling an occasional all-nighter may include include fatigue , irritability, impaired cognitive function and a temporary disruption of the sleep-wake cycle, Joseph said it may not cause significant long-term damage on its own.

"Occasional all-nighters may not cause significant long-term damage if followed by sufficient recovery sleep," she said. "The human body is resilient and can generally recover from short-term sleep deprivation."

Consistently skipping sleep over an extended period can lead to chronic sleep deprivation, however, which can have more severe consequences over time. 

Those impacts can include an increased risk of cardiovascular disease , diabetes, obesity, impaired immune function and mental health issues, Joseph said.

NEW YEAR CAN BRING BETTER SLEEP AT NIGHT IF YOU FOLLOW THESE 9 SMART STEPS

Sleep deprivation will affect different people in different ways, she noted, as individual factors and resilience play a role. 

"An all-nighter never killed anyone," Dimitriu agreed. "However, they add up, and you will still feel miserable after a night of no sleep, and will not perform at your best."

Staying up all night can significantly disrupt your sleep schedule and circadian rhythm, Joseph said.

"The circadian rhythm is a natural, internal process that regulates the sleep-wake cycle and repeats roughly every 24 hours," the doctor said. 

"When you stay up all night, you throw off this cycle, leading to several potential effects on your sleep schedule."

SLEEPING LONGER OVER THE WEEKEND COULD HELP PREVENT HEART ATTACKS, SAYS STUDY

After pulling an all-nighter, it may take some time for the body to readjust, and this can lead to temporary insomnia or difficulties falling asleep at the usual time, according to Joseph. 

"Some potential effects that someone can suffer from include delayed sleep onset, irregular sleep patterns, increased sleep debt and difficulty regaining normalcy," she said.

To mitigate the impact on your sleep schedule, prioritize getting back on track as soon as possible, said Joseph. 

Some strategies include shifting to an earlier bedtime, spending time outdoors during daylight hours to help regulate your circadian rhythm, and establishing a consistent sleep routine by going to bed and waking up at the same time each day, according to Joseph.

"Personally, I also like to limit caffeine close to bedtime and stay hydrated," she said. "If I do need a nap, I limit it to 20 to 30 minutes."

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Dimitriu also recommended getting some sunlight exposure in the morning to reset your rhythm.

"Morning light is really important to getting you to bed at night," he said.

Getting outdoor physical activity during the day, eating a light dinner and going to bed a little earlier than usual can also help regulate sleep cycles, the doctor advised.

Both experts agreed that the best strategy is to plan for healthy sleep and avoid all-nighters.

"Your performance after a night of not sleeping can be markedly diminished," Dimitiu said. "All-nighters are often the result of poor planning, so try to plan ahead and avoid nights of lost sleep."

Joseph added, "While occasional all-nighters may not have severe long-term consequences, making them a habit can contribute to health issues over time."

"Prioritizing regular, sufficient sleep is essential for your overall well-being ."

For more Health articles, visit www.foxnews.com/health .

Original article source: Sleep deprivation dangers: How pulling an all-nighter affects your physical and mental health

Consistently skipping sleep over an extended period can lead to chronic sleep deprivation, which can have severe consequences over time. iStock

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