Search

Sleep deprivation is proposed to inhibit top-down-control in emotion processing, but it is unclear whether sleep deprivation affects emotional mimicry and contagion. Here, we aimed to investigate effects of partial sleep deprivation on emotional contagion and mimicry in young and older humans. Participants underwent partial sleep deprivation (3 h sleep opportunity at the end of night), crossed-over with a full sleep condition in a balanced order, followed by a functional magnetic resonance imaging and electromyography (EMG) experiment with viewing of emotional and neutral faces and ratings of emotional responses. The final sample for main analyses was n = 69 (n = 36 aged 20-30 years, n = 33 aged 65-75 years). Partial sleep deprivation caused decreased activation in fusiform gyri for angry faces and decreased ratings of happiness for all stimuli, but no significant effect on the amygdala. Older participants reported more anger compared to younger participants, but no age differences were seen in brain responses to emotional faces or sensitivity to partial sleep deprivation. No effect of the sleep manipulation was seen on EMG. In conclusion, emotional contagion, but not mimicry, was affected by sleep deprivation. Our results are consistent with the previously reported increased negativity bias after insufficient sleep.The Stockholm sleepy brain study: effects of sleep deprivation on cognitive and emotional processing in young and old. https://clinicaltrials.gov/ct2/show/NCT02000076 .

Study Objectives: To determine how sleepiness and sleep deprivation drive the motivation to engage in different behaviors., Methods: We studied the sleepiness of 123 participants who had been randomized to sleep deprivation or normal sleep, and their willingness to engage in a range of everyday behaviors., Results: Self-reported sleepiness was a strong predictor of the motivation to engage in sleep-preparatory behaviors such as shutting one's eyes (OR = 2.78, 95% CI: 2.19-3.52 for each step up on the Karolinska Sleepiness Scale) and resting (OR = 3.20, CI: 2.46-4.16). Sleepiness was also related to the desire to be cared for by a loved one (OR = 1.49, CI: 1.22-1.82), and preparedness to utilize monetary and energy resources to get to sleep. Conversely, increased sleepiness was associated with a decreased motivation for social and physical activities (e.g. be with friends OR = 0.71, CI: 0.61-0.82; exercise OR = 0.65, CI: 0.56-0.76). Sleep deprivation had similar effects as sleepiness on these behaviors. Neither sleepiness nor sleep deprivation had strong associations with hunger, thirst, or food preferences., Conclusions: Our findings indicate that sleepiness is a dynamic motivational drive that promotes sleep-preparatory behaviors and competes with other drives and desired outcomes. Consequently, sleepiness may be a central mechanism by which impaired alertness, for example, due to insufficient sleep, contributes to poor quality of life and adverse health. We propose that sleepiness helps organize behaviors toward the specific goal of assuring sufficient sleep, in competition with other needs and incentives. A theoretical framework on sleepiness and its behavioral consequences are likely to improve our understanding of several disease mechanisms., (© Sleep Research Society 2019. Published by Oxford University Press on behalf of the Sleep Research Society.)

There is strong experimental support that infections increase the drive for sleep in animals, and it is widely believed that more sleep is part of an adaptive immune response. While respiratory infections (RI) are very prevalent in humans, there is a striking lack of systematic knowledge on how it affects sleep. We recruited 100 people, among whom 28 became sick with an RI during the study period (fulfilling criteria for influenza-like illness, ILI, or acute respiratory infection, ARI). We measured sick participants' sleep at home, both objectively (actigraphy) and subjectively (diary ratings), for one week as well as four weeks later when healthy. During the week with RI, people spent objectively longer time in bed and had a longer total sleep time compared to the healthy week. During the infection, participants also had more awakenings, but no significant differences in sleep latency or sleep efficiency. While sick, people also reported increased difficulties falling asleep, worse sleep quality, more restless sleep and more shallow sleep, while they did not report sleep to be less sufficient. Most problems occurred at the beginning of the sickness week, when symptoms were strong, and showed signs of recovery thereafter (as indicated by interactions between condition and day/night of data collection for all the 10 sleep outcomes). The degree of symptoms of RI was related to a worse sleep quality and more restless sleep, but not to any of the objective sleep outcomes or the other subjective sleep variables. Having a higher body temperature was not significantly related to any of the sleep variables. This study suggests that having a respiratory infection is associated with spending more time in bed and sleeping longer, but also with more disturbed sleep, both objectively and subjectively. This novel study should be seen as being of pilot character. There is a need for larger studies which classify pathogen type and include baseline predictors, or that manipulate sleep, in order to understand whether the sleep alterations seen during infections are adaptive and whether sleep interventions could be used to improve recovery from respiratory infections., (Copyright © 2019. Published by Elsevier Inc.)

Sleep loss has been shown to cause impairments in a number of aspects central for successful communication, ranging from poorer linguistic comprehension to alterations in speech prosody. However, the effect of sleep loss on actual communication is unknown. This study investigated how a night of sleep deprivation affected performance during multiple tasks designed to test verbal communication. Healthy participants (N = 183) spent 8-9 hours per night in bed for three nights and were then randomised to either one night of total sleep deprivation or a fourth night with 8-9 hours in bed. The following day, participants completed two tasks together with another participant: a model-building task and a word-description task. Differences in performance of these tasks were assessed alongside speaking duration, speaking volume, and speaking volume consistency. Additionally, participants individually completed a verbal fluency assessment. Performance on the model-building task was worse if the model-builder was sleep deprived, whereas sleep deprivation in the instruction-giver predicted an improvement. Word-description, verbal fluency, speech duration, speaking volume, and speaking volume consistency were not affected. The results suggest that sleep deprivation leads to changes in communicative performance during instructive tasks, while simpler word-description tasks appear resilient.

The emotional dysregulation and impaired working memory found after sleep loss can have severe implications for our daily functioning. Considering the intertwined relationship between emotion and cognition in stimuli processing, there could be further implications of sleep deprivation in high-complex emotional situations. Although studied separately, this interaction between emotion and cognitive processes has been neglected in sleep research. The aim of the present study was to investigate the effect of 1 night of sleep deprivation on emotional working memory. Sixty-one healthy participants (mean age: 23.4 years) were either sleep deprived for 1 night (n = 30) or had a normal night's sleep (n = 31). They performed an N-back task with two levels of working memory load (1-back and 3-back) using positive, neutral and negative picture scenes. Sleep deprivation, compared with full night sleep, impaired emotional working memory accuracy, but not reaction times. The sleep-deprived participants, but not the controls, responded faster to positive than to negative and neutral pictures. The effect of sleep deprivation was similar for both high and low working memory loads. The results showed that although detrimental in terms of accuracy, sleep deprivation did not impair working memory speed. In fact, our findings indicate that positive stimuli may facilitate working memory processing speed after sleep deprivation., (© 2018 The Authors. Journal of Sleep Research published by John Wiley & Sons Ltd on behalf of European Sleep Research Society.)

Study Objectives: Sleep problems are common in children and adolescents and can aggravate comorbid disorders. This meta-analysis examined the effect of cognitive and behavioral sleep interventions (with four or more treatment sessions) from randomized controlled trials on school-age children and adolescents., Methods: In a systematic literature search, six randomized controlled trials were identified (n = 528; mean age = 14.6 years; female = 63%) that reported total sleep time (TST), sleep onset latency (SOL), wake after sleep onset, and daytime sleepiness from ratings and actigraphy., Results: After intervention, no effect was seen on self-reported TST, but when measured with actigraphy, an effect favoring the intervention group was observed (+11.47 minutes, P = .05). SOL decreased in the intervention group compared to the control group after intervention as measured by both sleep diaries (-9.31 minutes, P = .007) and actigraphy (-19.48 minutes, P < .0001). Effect sizes ranged from small to large. No effect was found for wake after sleep onset or daytime sleepiness. Short-term (4 to 8 weeks) follow-up data from four studies indicated maintained positive effects on SOL: sleep diaries -15.85 minutes ( P = .01) and actigraphy -23.67 minutes ( P < .0001). At follow-up, the effects on wake after sleep onset from ratings (-14.41 minutes, P = .001) and actigraphy (-7.54 minutes, P = .01) were significant, favoring the intervention group (moderate to large effect sizes). No effect on TST was indicated., Conclusions: Cognitive and behavioral sleep interventions are indicated to improve sleep in school-age children and adolescents. However, because treatment protocols were heterogeneous and risk of bias high, results should be interpreted with caution. Large and rigorous trials are needed., (© 2018 American Academy of Sleep Medicine.)

Sleep loss and psychosocial stress often co-occur in today's society, but there is limited knowledge on the combined effects. Therefore, this experimental study investigated whether one night of sleep deprivation affects the response to a psychosocial challenge. A second aim was to examine if older adults, who may be less affected by both sleep deprivation and stress, react differently than young adults. 124 young (18-30 years) and 94 older (60-72 years) healthy adults participated in one of four conditions: i. normal night sleep & Placebo-Trier Social Stress Test (TSST), ii. normal night sleep & Trier Social Stress Test, iii. sleep deprivation & Placebo-TSST, iv. sleep deprivation & TSST. Subjective stress ratings, heart rate variability (HRV), salivary alpha amylase (sAA) and cortisol were measured throughout the protocol. At the baseline pre-stress measurement, salivary cortisol and subjective stress values were higher in sleep deprived than in rested participants. However, the reactivity to and recovery from the TSST was not significantly different after sleep deprivation for any of the outcome measures. Older adults showed higher subjective stress, higher sAA and lower HRV at baseline, indicating increased basal autonomic activity. Cortisol trajectories and HRV slightly differed in older adults compared with younger adults (regardless of the TSST). Moreover, age did not moderate the effect of sleep deprivation. Taken together, the results show increased stress levels after sleep deprivation, but do not confirm the assumption that one night of sleep deprivation increases the responsivity to an acute psychosocial challenge., (Copyright © 2018 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Age and sleep both affect emotional functioning. Since sleep patterns change over the lifespan, we investigated the effects of short sleep and age on empathic responses. In a randomized cross-over experimental design, healthy young and older volunteers (n = 47 aged 20-30 years and n = 39 aged 65-75 years) underwent functional magnetic resonance imaging (fMRI) after normal sleep or night sleep restricted to 3 hours. During fMRI, participants viewed pictures of needles pricking a hand (pain) or Q-tips touching a hand (control), a well-established paradigm to investigate empathy for pain. There was no main effect of sleep restriction on empathy. However, age and sleep interacted so that sleep restriction caused increased unpleasantness in older but not in young participants. Irrespective of sleep condition, older participants showed increased activity in angular gyrus, superior temporal sulcus and temporo-parietal junction compared to young. Speculatively, this could indicate that the older individuals adopted a more cognitive approach in response to others' pain. Our findings suggest that caution in generalizability across age groups is needed in further studies of sleep on social cognition and emotion.

Sleep deprivation has been reported to affect intrinsic brain connectivity, notably reducing connectivity in the default mode network. Studies to date have however shown inconsistent effects, in many cases lacked monitoring of wakefulness, and largely included young participants. We investigated effects of sleep deprivation on intrinsic brain connectivity in young and older participants. Participants aged 20-30 (final n = 30) and 65-75 (final n = 23) years underwent partial sleep deprivation (3 h sleep) in a cross-over design, with two 8-minutes eyes-open resting state functional magnetic resonance imaging (fMRI) runs in each session, monitored by eye-tracking. We assessed intrinsic brain connectivity using independent components analysis (ICA) as well as seed-region analyses of functional connectivity, and also analysed global signal variability, regional homogeneity, and the amplitude of low-frequency fluctuations. Sleep deprivation caused increased global signal variability. Changes in investigated resting state networks and in regional homogeneity were not statistically significant. Younger participants had higher connectivity in most examined networks, as well as higher regional homogeneity in areas including anterior and posterior cingulate cortex. In conclusion, we found that sleep deprivation caused increased global signal variability, and we speculate that this may be caused by wake-state instability.

While acute modifications of sleep duration induces a wide array of immune function alterations, less is known of how longer periods with insufficient sleep affect immune functions and how they return to normal once recovery sleep is obtained. The purpose of the present study was to investigate the effects of five days of restricted sleep and a subsequent 7-day period of sleep recovery on white blood cell (WBC) subpopulation count and diurnal rhythms. Nine healthy males participated in a sleep protocol consisting of two baseline days (8h of sleep/night), five nights with restricted sleep (4h of sleep/night) and seven days of recovery sleep (8h of sleep/night). During nine of these days, blood was drawn hourly during night-time end every third hour during daytime, and differential WBC count was analyzed. Gradual increase across the days of sleep restriction was observed for total WBC (p<.001), monocytes (p<.001), neutrophils (p<.001) and lymphocytes (p<.05). Subsequent recovery sleep resulted in a gradual decrease in monocytes (p<.001) and lymphocytes (p=.001), but not in neutrophils that remained elevated over baseline level at the end of the 7-day recovery period. These effects were associated with altered diurnal rhythms of total WBC and neutrophils, restricted sleep being associated with higher levels during the night and at awakening, resulting in a flattening of the rhythm. The diurnal alterations were reversed when recovery sleep was allowed, although the amplitude of total WBC, neutrophils and monocytes was increased at the end of the recovery period in comparison to baseline. Altogether, these data show that long-term sleep restriction leads to a gradual increase of circulating WBC subpopulations and alterations of the respective diurnal rhythms. Although some of the effects caused by five days of restricted sleep were restored within the first days of recovery, some parameters were not back to baseline even after a period of seven recovery days., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background: Recent studies suggest that acute sleep deprivation disrupts cellular immune responses by shifting T helper (Th) cell activity towards a Th2 cytokine profile. Since little is known about more long-term effects, we investigated how five days of sleep restriction would affect pro-inflammatory, chemotactic, Th1- and Th2 cytokine secretion., Methods: Nine healthy males participated in an experimental sleep protocol with two baseline sleep-wake cycles (sleep 23.00-07.00 h) followed by 5 days with restricted sleep (03.00-07.00 h). On the second baseline day and on the fifth day with restricted sleep, samples were drawn every third hour for determination of cytokines/chemokines (tumor necrosis factor alpha (TNF-α), interleukin (IL) -1β, IL-2, IL-4 and monocyte chemoattractant protein-1 (MCP-1)) after in vitro stimulation of whole blood samples with the mitogen phytohemagglutinin (PHA). Also leukocyte numbers, mononuclear cells and cortisol were analysed., Results: 5-days of sleep restriction affected PHA-induced immune responses in several ways. There was a general decrease of IL-2 production (p<.05). A shift in Th1/Th2 cytokine balance was also evident, as determined by a decrease in IL2/IL4 ratio. No other main effects of restricted sleep were shown. Two significant interactions showed that restricted sleep resulted in increased TNF-α and MCP-1 in the late evening and early night hours (p's<.05). In addition, all variables varied across the 24 h day., Conclusions: 5-days of sleep restriction is characterized by a shift towards Th2 activity (i.e. lower 1L-2/IL-4 ratio) which is similar to the effects of acute sleep deprivation and psychological stress. This may have implications for people suffering from conditions characterized by excessive Th2 activity like in allergic disease, such as asthma, for whom restricted sleep could have negative consequences.

Sleep and subjective health are both prospectively related to objective indices of health and health care use. Here, we tested whether five days with restricted sleep and subsequent recovery days affect subjective health and is related to increased levels of circulating IL-6 and TNF-α and fatigue. Nine healthy men (23-28 ears) went through a 6-week sleep protocol with subjects as their own controls in a repeated measures design with a total of 11 nights in a sleep laboratory. The experimental part of the protocol included three baseline days (sleep 23-07 h), five days with sleep restriction (03-07 h) and three recovery days (23-07 h) in the sleep laboratory. Subjective health and fatigue was recorded daily. Eight blood samples were drawn each day (every third hour) on 8 days of the protocol and analyzed with respect to IL-6 and TNF-α. Subjective health deteriorated gradually during restricted sleep (p=.002) and returned to baseline levels after three days of recovery. IL-6 and TNF-α did not change significantly. Fatigue increased gradually during sleep restriction (p=.001), which significantly contributed to the association between restricted sleep and subjective health. The study is the first to show that subjective health is directly responsive to changes in sleep length and related to increased fatigue. Thus, subjective health is differently appraised after manipulation of one of its presumed determinants. Larger experimental studies would be beneficial to further distinguish causation from association regarding the underpinnings of subjective health., (Copyright © 2013. Published by Elsevier Inc.)

Study Objective: To investigate the facial cues by which one recognizes that someone is sleep deprived versus not sleep deprived., Design: Experimental laboratory study., Setting: Karolinska Institutet, Stockholm, Sweden., Participants: Forty observers (20 women, mean age 25 ± 5 y) rated 20 facial photographs with respect to fatigue, 10 facial cues, and sadness. The stimulus material consisted of 10 individuals (five women) photographed at 14:30 after normal sleep and after 31 h of sleep deprivation following a night with 5 h of sleep., Measurements: Ratings of fatigue, fatigue-related cues, and sadness in facial photographs., Results: The faces of sleep deprived individuals were perceived as having more hanging eyelids, redder eyes, more swollen eyes, darker circles under the eyes, paler skin, more wrinkles/fine lines, and more droopy corners of the mouth (effects ranging from b = +3 ± 1 to b = +15 ± 1 mm on 100-mm visual analog scales, P < 0.01). The ratings of fatigue were related to glazed eyes and to all the cues affected by sleep deprivation (P < 0.01). Ratings of rash/eczema or tense lips were not significantly affected by sleep deprivation, nor associated with judgements of fatigue. In addition, sleep-deprived individuals looked sadder than after normal sleep, and sadness was related to looking fatigued (P < 0.01)., Conclusions: The results show that sleep deprivation affects features relating to the eyes, mouth, and skin, and that these features function as cues of sleep loss to other people. Because these facial regions are important in the communication between humans, facial cues of sleep deprivation and fatigue may carry social consequences for the sleep deprived individual in everyday life.

Objective: To investigate whether sleep deprived people are perceived as less healthy, less attractive, and more tired than after a normal night's sleep., Design: Experimental study., Setting: Sleep laboratory in Stockholm, Sweden., Participants: 23 healthy, sleep deprived adults (age 18-31) who were photographed and 65 untrained observers (age 18-61) who rated the photographs., Intervention: Participants were photographed after a normal night's sleep (eight hours) and after sleep deprivation (31 hours of wakefulness after a night of reduced sleep). The photographs were presented in a randomised order and rated by untrained observers., Main Outcome Measure: Difference in observer ratings of perceived health, attractiveness, and tiredness between sleep deprived and well rested participants using a visual analogue scale (100 mm)., Results: Sleep deprived people were rated as less healthy (visual analogue scale scores, mean 63 (SE 2) v 68 (SE 2), P<0.001), more tired (53 (SE 3) v 44 (SE 3), P<0.001), and less attractive (38 (SE 2) v 40 (SE 2), P<0.001) than after a normal night's sleep. The decrease in rated health was associated with ratings of increased tiredness and decreased attractiveness., Conclusion: Our findings show that sleep deprived people appear less healthy, less attractive, and more tired compared with when they are well rested. This suggests that humans are sensitive to sleep related facial cues, with potential implications for social and clinical judgments and behaviour. Studies are warranted for understanding how these effects may affect clinical decision making and can add knowledge with direct implications in a medical context.

Study Objectives: Sleep reduction normally causes a homeostatic response during subsequent recovery sleep, but this does not seem to be true for repeated partial sleep loss. The aim of the present study was to test the response to repeated partial sleep loss through detailed focus on spectral data and parts of sleep., Design: The experiment involved 4 h of sleep across 5 days in the laboratory (partial sleep deprivation [PSD]), followed by 3 days of recovery sleep. PSD was achieved through a delayed bedtime. Nine individuals participated. To avoid "laboratory monotony," subjects were permitted to leave the lab for a few hours each day., Measurements and Results: All sleep stages and the latencies to sleep and slow wave sleep (SWS) showed a significant reduction during PSD. However, SWS and TST (total sleep time) during the first half of sleep increased gradually across days with PSD. During the first recovery sleep, SWS was significantly increased, while stage 1 and latency to stage 3 were reduced. All were back to baseline on the second night of recovery sleep. Summed spectral power during the first 3.8 h of sleep showed a gradual and robust increase (50% above baseline) in the range 1.25-7.25 Hz across days with PSD up to first recovery sleep and then returned to baseline., Conclusions: SWS and summed power density in a broad low-frequency band respond to repeated partial sleep deprivation in a dose-response fashion during the first 4 h sleep, apparently reflecting a robust and stable homeostatic response to sleep loss.

There is an ongoing debate of how best to measure the effects of sleep loss in a reliable and feasible way, partly because well controlled laboratory studies and field studies have come to different conclusions. The aims of the present study were to investigate both sleepiness and performance in response to long-term sleep restriction and recovery in a semi-laboratory environment, investigate order effects (i.e., whether levels return to baseline) in a study with seven days of recovery, and characterize individual differences in tolerance to restricted sleep. Nine healthy men (age 23-28 yrs) participated in the protocol, which included one habituation day (sleep 23:00-07:00 h), two baseline days (23:00-07:00 h), five days with restricted sleep (03:00-07:00 h), and seven recovery days (23:00-07:00 h). Participants went outdoors at least twice each day. Reaction-time tests were performed at 08:00, 14:00, and 20:00 h each day in the laboratory. Sleepiness was self-rated by the Karolinska Sleepiness Scale (KSS)after each test. The mixed-effect regression models showed that each day of restricted sleep resulted in an increase of sleepiness by 0.64+/- .05 KSS units (a nine-step scale, p < .001), increase of median reaction times of 6.6+/- 1.6 ms ( p = .003), and increase of lapses/test of 0.69 +/- .16 ms ( p < .001). Seven days of recovery allowed participants to return to the baseline for sleepiness and median reaction time, but not for lapses. The individual differences were larger for performance measures than for sleepiness; the between-subject standard deviation for the random intercept was in the magnitude of the effects of 1.1 days of restricted sleep for sleepiness, 6.6 days of restricted sleep for median reaction time, and 3.2 days for lapses. In conclusion, the present study shows that sleepiness is closely related to sleep pressure, while performance measures, to a larger extent, appear determined by specific individual traits. Moreover, it is suggested to measure sleepiness in a standardized situation so as to minimize the influences of contextual factors.

The prefrontal cortex (PFC) is affected negatively by sleep deprivation (SD) and executive functioning is largely dependent on activity in the PFC. Earlier studies have focused on subsystems of executive functioning, and tests of executive functioning have shown both low reliability and low validity. In the present study, 11 healthy volunteers were sleep deprived and compared with 11 healthy controls in a study on effects of one night's SD on integrative executive functioning. Following SD, the performance of subjects on an ecologically valid test, the modified Six Elements Test, was significantly impaired. There were no group differences on psychomotor vigilance, verbal or visuo-spatial working memory. This extends previous knowledge of performance effects of SD, and may be of special importance for individuals with cognitive work tasks.