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Sleep reactivation did not boost suppression-induced forgetting.
Schechtman, E, Lampe, A, Wilson, BJ, Kwon, E, Anderson, MC, Paller, KA
Scientific reports. 2021;(1):1383
Abstract
Sleep's role in memory consolidation is widely acknowledged, but its role in weakening memories is still debated. Memory weakening is evolutionary beneficial and makes an integral contribution to cognition. We sought evidence on whether sleep-based memory reactivation can facilitate memory suppression. Participants learned pairs of associable words (e.g., DIET-CREAM) and were then exposed to hint words (e.g., DIET) and instructed to either recall ("think") or suppress ("no-think") the corresponding target words (e.g., CREAM). As expected, suppression impaired retention when tested immediately after a 90-min nap. To test if reactivation could selectively enhance memory suppression during sleep, we unobtrusively presented one of two sounds conveying suppression instructions during sleep, followed by hint words. Results showed that targeted memory reactivation did not enhance suppression-induced forgetting. Although not predicted, post-hoc analyses revealed that sleep cues strengthened memory, but only for suppressed pairs that were weakly encoded before sleep. The results leave open the question of whether memory suppression can be augmented during sleep, but suggest strategies for future studies manipulating memory suppression during sleep. Additionally, our findings support the notion that sleep reactivation is particularly beneficial for weakly encoded information, which may be prioritized for consolidation.
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Early Morning Food Intake as a Risk Factor for Metabolic Dysregulation.
Stothard, ER, Ritchie, HK, Birks, BR, Eckel, RH, Higgins, J, Melanson, EL, Wright, KP, McHill, AW
Nutrients. 2020;(3)
Abstract
Increased risk of obesity and diabetes in shift workers may be related to food intake at adverse circadian times. Early morning shiftwork represents the largest proportion of shift workers in the United States, yet little is known about the impact of food intake in the early morning on metabolism. Eighteen participants (9 female) completed a counterbalanced 16 day design with two conditions separated by ~1 week: 8 h sleep opportunity at habitual time and simulated early morning shiftwork with 6.5 h sleep opportunity starting ~1 h earlier than habitual time. After wake time, resting energy expenditure (REE) was measured and blood was sampled for melatonin and fasting glucose and insulin. Following breakfast, post-prandial blood samples were collected every 40 min for 2 h and the thermic effect of food (TEF) was assessed for 3.25 h. Total sleep time was decreased by ~85 min (p < 0.0001), melatonin levels were higher (p < 0.0001) and post-prandial glucose levels were higher (p < 0.05) after one day of simulated early morning shiftwork compared with habitual wake time. REE was lower after simulated early morning shiftwork; however, TEF after breakfast was similar to habitual wake time. Insufficient sleep and caloric intake during a circadian phase of high melatonin levels may contribute to metabolic dysregulation in early morning shift workers.
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Post-Hoc Analyses of the Effects of Baseline Sleep Quality on SHP465 Mixed Amphetamine Salts Extended-Release Treatment Response in Adults with Attention-Deficit/Hyperactivity Disorder.
Surman, CBH, Robertson, B, Chen, J, Cortese, S
CNS drugs. 2019;(7):695-706
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OBJECTIVE Sleep problems are common in adults with attention-deficit/hyperactivity disorder (ADHD). The presence of sleep problems at the time of presentation for ADHD treatment could impact the level of improvement in ADHD symptoms or executive function occurring with ADHD pharmacotherapy. Therefore, we examined the influence of baseline sleep quality on the effects of SHP465 mixed amphetamine salts (MAS) extended-release. METHODS Adults (18-55 years) with Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision-defined ADHD and baseline ADHD Rating Scale IV (ADHD-RS-IV) total scores ≥ 24 were randomized to once-daily SHP465 MAS (12.5-75 mg) or placebo in a 7-week, double-blind, dose-optimization study. Post-hoc analyses evaluated SHP465 MAS treatment effects on ADHD symptoms, using the ADHD-RS-IV, and executive function, using the Brown Attention-Deficit Disorder Scale (BADDS), based on baseline sleep quality as defined by Pittsburgh Sleep Quality Index (PSQI) scores [sleep quality impaired (PSQI total score > 5; PSQI component scores 2 or 3) versus not impaired (PSQI total score ≤ 5; PSQI component scores 0 or 1)]. Analyses were conducted in the intent-to-treat population. RESULTS Of 280 enrolled participants, 272 were randomized (placebo, n = 135; SHP465 MAS, n = 137). The intent-to-treat population consisted of 268 participants (placebo, n = 132; SHP465 MAS, n = 136), and 170 participants (placebo, n = 76; SHP465 MAS, n = 94) completed the study. Treatment differences nominally favored SHP465 MAS over placebo in both sleep impairment groups regarding ADHD-RS-IV total score changes (all nominal p < 0.05), except for those with impairment defined by sleep efficiency (p = 0.2696), and regarding BADDS total score changes (all nominal p < 0.05), except for those with impairment defined by sleep duration (p = 0.1332) and sleep efficiency (p = 0.8226). There were no statistically significant differences in SHP465 MAS treatment effects between sleep impairment groups. CONCLUSIONS Improvements in ADHD symptoms and executive function occurred with dose-optimized SHP465 MAS, regardless of baseline impairment in some aspects of sleep in adults with ADHD, with no significant differences observed as a function of sleep impairment. CLINICAL TRIALS REGISTRATION ClinicalTrials.gov identifier-NCT00150579.
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Association of serum BDNF levels and the BDNF Val66Met polymorphism with the sleep pattern in healthy young adults.
Saitoh, K, Furihata, R, Kaneko, Y, Suzuki, M, Takahashi, S, Uchiyama, M
PloS one. 2018;(6):e0199765
Abstract
BACKGROUND Brain-derived neurotrophic factor (BDNF) is widely expressed in the brain and plays an important role in neuronal maintenance, plasticity, and neurogenesis. Prior studies have found that decreased serum BDNF levels are associated with perceived stress, depression, or sleep disturbances in humans. STUDY OBJECTIVES To elucidate whether the serum BDNF levels and BDNF genotype were associated with the sleep pattern in healthy young adults. METHODS The study group consisted of 79 healthy paid volunteers (45 men, 34 women) aged 20 to 29 years. Serum BDNF levels were measured with an enzyme-linked immunosorbent assay, and a single-nucleotide polymorphism (Val66Met) in the BDNF gene was assessed with a TaqMan assay. Details of the sleep pattern were obtained from 1-week sleep/wake records. RESULTS Serum BDNF levels were significantly associated with sleep parameters on weekends, whereas no such association was found on weekdays. On weekends, longer total sleep time and time in bed, and later mid-sleep time were associated with lower serum BDNF levels. The difference between mid-sleep time on weekdays and that on weekends, otherwise known as social jetlag, was negatively associated with serum BDNF levels. Met/Met homozygotes of the BDNF Val66Met polymorphism had significantly longer time in bed on weekends than Val/Val homozygotes. Heterozygotes did not differ from Val/Val homozygotes. CONCLUSIONS We first found that serum BDNF levels and the BDNF Val66Met polymorphism in healthy young adults were associated with the sleep pattern on weekends but not with that on weekdays, suggesting that the systems involved in BDNF control may be linked to endogenous sleep characteristics rather than the socially constrained sleep schedule in healthy young adults.
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Comparison of the Effect of Two Kinds of Iranian Honey and Diphenhydramine on Nocturnal Cough and the Sleep Quality in Coughing Children and Their Parents.
Ayazi, P, Mahyar, A, Yousef-Zanjani, M, Allami, A, Esmailzadehha, N, Beyhaghi, T
PloS one. 2017;(1):e0170277
Abstract
Coughing in a child induced by upper respiratory tract infections (URTIs) can be a problem, both for the child and its parents. Current studies show a lack of proven efficacy for over-the counter (OTC) medications, but promising data support the use of honey for children. The aim of this study was to compare the effects of two kinds of Iranian honey with diphenhydramine (DPH) on nocturnal pediatric coughs and the sleep quality of children and their parents. This was a clinical trial (registered in IRCT; No.: 28.20.7932, 15 October 2013). The study consisted of 87 patients. All the parents completed a standard previously validated questionnaire. The children were randomly assigned to one of three treatment groups: Group 1, Honey type 1 (Kimia Company, Iran) (n = 42), Group 2, Honey type 2 (Shahde-Golha, Iran) (n = 25), and Group 3, DPH (n = 20). Each group received double doses of the respective treatments on two successive nights. A second survey was then administered via a telephone interview in which the parents were asked the same questions. The mean scores for all aspects of coughs were significantly decreased in each group before and after the treatment. All three treatments improved the cough and sleep scores. Honey type 1 was superior to DPH in improving all aspects of coughs, except the frequency, and Honey type 2 was more effective than DPH in improving all aspects of coughs, except the sleep quality of the child. There was no significant difference between Honey type 1 and 2 in any aspects of cough relief in the present study. The results suggest that honey may provide better cough relief than DPH in children and improve the sleep quality of children and their parents.
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The role of melatonin to attain electroencephalograms in children in a sub-Saharan African setting.
Ibekwe, R, Jeaven, L, Wilmshurst, JM
Seizure. 2017;:87-94
Abstract
PURPOSE Limited access to electroencephalograms (EEGs) in sub-Saharan Africa results in a high patient load attending the few neurophysiology units. The state of sleep in children improves yield and reduces artefact of EEGs. Melatonin induces "natural sleep" without the risk of airway compromise. This study evaluated the effectiveness of oral melatonin to attain electroencephalograms in South African children. METHOD Children undergoing EEG who were unable to cooperate or required sleep EEG, received oral melatonin (3mg<15kg; 6mg>15kg). A retrospective control group received chloral hydrate. Outcome measures were the proportion of children who slept, useful EEG study data, sleep latency and duration, artefacts and EEG study abnormalities. RESULTS 173 children were recruited, 88 (51%) male, median age 4 years 9 months (range 0-14 years). 87% achieved stage 2 sleep. Median sleep latency was 44.5min and duration of sleep was 25min (range 18.5-29min). Children had no post-sedation irritability, persistent drowsiness, nor any other adverse events or deferments for inter-current illnesses. Sedation with melatonin was less successful in children with developmental and behavioural problems (χ2=6.18, P=0.046), with a higher rate of artefacts (χ2=5.83, P=0.05). 33.5% (n=58) had abnormal EEG studies, which was comparable to a historical cohort sedated with chloral hydrate (45.5%) (χ2=1.22, P=1.27). Also for artefacts (79% melatonin group versus 86% chloral hydrate group) (χ2=0.63, P=0.42). CONCLUSIONS Melatonin is effective and safe in inducing sleep for EEG recording in our setting.
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The Sleep/Wake Cycle is Directly Modulated by Changes in Energy Balance.
Collet, TH, van der Klaauw, AA, Henning, E, Keogh, JM, Suddaby, D, Dachi, SV, Dunbar, S, Kelway, S, Dickson, SL, Farooqi, IS, et al
Sleep. 2016;(9):1691-700
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STUDY OBJECTIVES The rise in obesity has been paralleled by a decline in sleep duration in epidemiological studies. However, the potential mechanisms linking energy balance and the sleep/wake cycle are not well understood. We aimed to examine the effects of manipulating energy balance on the sleep/wake cycle. METHODS Twelve healthy normal weight men were housed in a clinical research facility and studied at three time points: baseline, after energy balance was disrupted by 2 days of caloric restriction to 10% of energy requirements, and after energy balance was restored by 2 days of ad libitum/free feeding. Sleep architecture, duration of sleep stages, and sleep-associated respiratory parameters were measured by polysomnography. RESULTS Two days of caloric restriction significantly increased the duration of deep (stage 4) sleep (16.8% to 21.7% of total sleep time; P = 0.03); an effect which was entirely reversed upon free feeding (P = 0.01). Although the apnea-hypopnea index stayed within the reference range (< 5 events per hour), it decreased significantly from caloric restriction to free feeding (P = 0.03). Caloric restriction was associated with a marked fall in leptin (P < 0.001) and insulin levels (P = 0.002). The fall in orexin levels from baseline to caloric restriction correlated positively with duration of stage 4 sleep (Spearman rho = 0.83, P = 0.01) and negatively with the number of awakenings in caloric restriction (Spearman rho = -0.79, P = 0.01). CONCLUSIONS We demonstrate that changes in energy homeostasis directly and reversibly impact on the sleep/wake cycle. These findings provide a mechanistic framework for investigating the association between sleep duration and obesity risk.
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Beneficial impact of sleep extension on fasting insulin sensitivity in adults with habitual sleep restriction.
Leproult, R, Deliens, G, Gilson, M, Peigneux, P
Sleep. 2015;(5):707-15
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STUDY OBJECTIVES A link between sleep loss and increased risk for the development of diabetes is now well recognized. The current study investigates whether sleep extension under real-life conditions is a feasible intervention with a beneficial impact on glucose metabolism in healthy adults who are chronically sleep restricted. DESIGN Intervention study. PARTICIPANTS Sixteen healthy non-obese volunteers (25 [23, 27.8] years old, 3 men). INTERVENTIONS Two weeks of habitual time in bed followed by 6 weeks during which participants were instructed to increase their time in bed by one hour per day. MEASUREMENTS AND RESULTS Continuous actigraphy monitoring and daily sleep logs during the entire study. Glucose and insulin were assayed on a single morning blood sample at the end of habitual time in bed and at the end of sleep extension. Home polysomnography was performed during one weekday of habitual time in bed and after 40 days of sleep extension. Sleep time during weekdays increased (mean actigraphic data: +44 ± 34 minutes, P < 0.0001; polysomnographic data: +49 ± 68 minutes, P = 0.014), without any significant change during weekends. Changes from habitual time in bed to the end of the intervention in total sleep time correlated with changes in glucose (r = +0.53, P = 0.041) and insulin levels (r = -0.60, P = 0.025), as well as with indices of insulin sensitivity (r = +0.76, P = 0.002). CONCLUSIONS In healthy adults who are chronically sleep restricted, a simple low cost intervention such as sleep extension is feasible and is associated with improvements in fasting insulin sensitivity.
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Timing and intensity of light correlate with body weight in adults.
Reid, KJ, Santostasi, G, Baron, KG, Wilson, J, Kang, J, Zee, PC
PloS one. 2014;(4):e92251
Abstract
Light exposure can influence sleep and circadian timing, both of which have been shown to influence weight regulation. The goal of this study was to evaluate the relationship between ambient light, sleep and body mass index. Participants included 54 individuals (26 males, mean age 30.6, SD = 11.7 years). Light levels, sleep midpoint and duration were measured with wrist actigraphy (Actiwatch-L) for 7 days. BMI was derived from self-reported height and weight. Caloric intake was determined from 7 days of food logs. For each participant, light and activity data were output in 2 minute epochs, smoothed using a 5 point (10 minute) moving average and then aggregated over 24 hours. The mean light timing above 500 lux (MLiT500) was defined as the average clock time of all aggregated data points above 500 lux. MLiT500 was positively correlated with BMI (r = 0.51, p<0.001), and midpoint of sleep (r = 0.47, p<0.01). In a multivariable linear regression model including MLiT500 and midpoint of sleep, MLiT500 was a significant predictor of BMI (B = 1.26 SE = 0.34, β = 0.53 p = 0.001, r2Δ = 0.22). Adjusting for covariates, MLiT500 remained an independent predictor of BMI (B = 1.28 SE = 0.36, β = 0.54, p = 0.002, r2Δ = 0.20). The full model accounted for 34.7% of the variance in BMI (p = 0.01). Exposure to moderate levels of light at biologically appropriate times can influence weight, independent of sleep timing and duration.
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Sleep duration and risk of atrial fibrillation (from the Physicians' Health Study).
Khawaja, O, Sarwar, A, Albert, CM, Gaziano, JM, Djoussé, L
The American journal of cardiology. 2013;(4):547-51
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Although sleep quality and duration have been related to cardiovascular end points, little is known about the association between sleep duration and incident atrial fibrillation (AF). Hence, we prospectively examined the association between sleep duration and incident AF in a cohort of 18,755 United States male physicians. Self-reported sleep duration was ascertained during a 2002 annual follow-up questionnaire. Incident AF was ascertained through annual follow-up questionnaires. Cox regression analysis was used to estimate the relative risks of AF. The average age at baseline was 67.7 ± 8.6 years. During a mean follow-up of 6.9 ± 2.1 years, 1,468 cases of AF occurred. Using 7 hours of sleep as the reference group, the multivariate adjusted hazard ratio for AF was 1.06 (95% confidence interval 0.92 to 1.22), 1.0 (reference), and 1.13 (95% confidence interval 1.00 to 1.27) from the lowest to greatest category of sleep duration (p for trend = 0.26), respectively. In a secondary analysis, no evidence was seen of effect modification by adiposity (p for interaction = 0.69); however, prevalent sleep apnea modified the relation of sleep duration with AF (p for interaction = 0.01). From the greatest to the lowest category of sleep duration, the multivariate-adjusted hazard ratio for AF was 2.26 (95% confidence interval 1.26 to 4.05), 1.0 (reference), and 1.34 (95% confidence interval 0.73 to 2.46) for those with prevalent sleep apnea and 1.01 (95% confidence interval 0.87 to 1.16), 1.0 (reference), and 1.12 (95% confidence interval 0.99 to 1.27) for those without sleep apnea, respectively. Our data showed a modestly elevated risk of AF with long sleep duration among United States male physicians. Furthermore, a shorter sleep duration was associated with a greater risk of AF in those with prevalent sleep apnea.