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“Sleep Duration and Brain Structure—phenotypic Associations and Genotypic Covariance”, Fjell et al 2022

“Sleep duration and brain structure—phenotypic associations and genotypic covariance”⁠, Anders Fjell, Oystein Sorensen, Yunpeng Wang, Inge K. Amlien, William Baare, David Bartres-Faz, Lars Bertram et al (2022-02-17; ⁠, ; similar):

The question of how much sleep is best for the brain attracts scientific and public interest, and there is concern that insufficient sleep leads to poorer brain health. However, it is unknown how much sleep is sufficient and how much is too much. We analyzed 51,295 brain magnetic resonance images from 47,039 participants, and calculated the self-reported sleep duration associated with the largest regional volumes and smallest ventricles relative to intracranial volume (ICV) and thickest cortex. 6.8 hours of sleep was associated with the most favorable brain outcome overall. Critical values, defined by 95% confidence intervals, were 5.7 and 7.9 hours. There was regional variation, with for instance the hippocampus showing largest volume at 6.3 hours. Moderately long sleep (> 8 hours) was more strongly associated with smaller relative volumes, thinner cortex and larger ventricles than even very short sleep (< 5 hours), but effect sizes were modest. People with larger ICV reported longer sleep (7.5 hours), so not correcting for ICV yielded longer durations associated with maximal volume. Controlling for socioeconomic status⁠, body mass index and depression symptoms did not alter the associations. Genetic analyses showed that genes related to longer sleep in short sleepers were related to shorter sleep in long sleepers. This may indicate a genetically controlled homeostatic regulation of sleep duration. Mendelian randomization analyses did not suggest sleep duration to have a causal impact on brain structure in the analyzed datasets. The findings challenge the notion that habitual short sleep is negatively related to brain structure.

“Genetic and Environmental Influences on Sleep-Wake Behaviours in Adolescence”, O''Callaghan et al 2021

“Genetic and Environmental Influences on Sleep-Wake Behaviours in Adolescence”⁠, Victoria S. O''Callaghan, Narelle K. Hansell, Wei Guo, Joanne S. Carpenter, Haochang Shou, Lachlan T. Strike et al (2021-10-22; ; similar):

Objectives: To investigate the influence of genetic and environmental factors on sleep-wake behaviours across adolescence.

Methods: 495 participants (aged 9 to 17; 55% females), including 93 monozygotic (MZ) and 117 dizygotic (DZ) twin pairs, and 75 unmatched twins, wore an accelerometry device and completed a sleep diary for 2 weeks.

Results: Individual differences in sleep onset, wake time, and sleep midpoint were influenced by both additive genetic (44–50% of total variance) and shared environmental (31–42%) factors, with a predominant genetic influence for sleep duration (62%) and restorative sleep (43%). When stratified into younger (aged 9–14) and older (aged 16–17) subsamples, genetic sources were more prominent in older adolescents. The moderate correlation between sleep duration and midpoint (rp = −0.43, rg = 0.54) was attributable to a common genetic source. Sleep-wake behaviours on school and non-school nights were correlated (rp = 0.44–0.72) and influenced by the same genetic and shared environmental factors. Genetic sources specific to night-type were also identified, for all behaviours except restorative sleep.

Conclusions: There were strong genetic influences on sleep-wake phenotypes, particularly on sleep timing, in adolescence. Moreover, there may be common genetic influences underlying both sleep and circadian rhythms. The differences in sleep-wake behaviours on school and non-school nights could be attributable to genetic factors involved in reactivity to environmental context.

[Keywords: sleep, adolescence, heritability, twins, genetics, actigraphy]

“Evening Home Lighting Adversely Impacts the Circadian System and Sleep”, Cain et al 2020

“Evening home lighting adversely impacts the circadian system and sleep”⁠, Sean W. Cain, Elise M. McGlashan, Parisa Vidafar, Jona Mustafovska, Simon P. N. Curran, Xirun Wang, Anas Mohamed et al (2020-11-05; ; backlinks; similar):

The regular rise and fall of the sun resulted in the development of 24-h rhythms in virtually all organisms. In an evolutionary heartbeat, humans have taken control of their light environment with electric light. Humans are highly sensitive to light, yet most people now use light until bedtime.

We evaluated the impact of modern home lighting environments in relation to sleep and individual-level light sensitivity using a new wearable spectrophotometer. We found that nearly half of homes had bright enough light to suppress melatonin by 50%, but with a wide range of individual responses (0–87% suppression for the average home). Greater evening light relative to an individual’s average was associated with increased wakefulness after bedtime.

Homes with energy-efficient lights had nearly double the melanopic illuminance of homes with incandescent lighting. These findings demonstrate that home lighting substantially affects sleep and the circadian system, but the impact of lighting for a specific individual in their home is highly unpredictable.

“Glymphatic Failure As a Final Common Pathway to Dementia”, Nedergaard & Goldman 2020

2020-nedergaard.pdf: “Glymphatic failure as a final common pathway to dementia”⁠, Maiken Nedergaard, Steven A. Goldman (2020-10-02; similar):

Sleep is evolutionarily conserved across all species, and impaired sleep is a common trait of the diseased brain. Sleep quality decreases as we age, and disruption of the regular sleep architecture is a frequent antecedent to the onset of dementia in neurodegenerative diseases.

The glymphatic system⁠, which clears the brain of protein waste products, is mostly active during sleep. Yet the glymphatic system degrades with age, suggesting a causal relationship between sleep disturbance and symptomatic progression in the neurodegenerative dementias. The ties that bind sleep, aging, glymphatic clearance, and protein aggregation have shed new light on the pathogenesis of a broad range of neurodegenerative diseases, for which glymphatic failure may constitute a therapeutically targetable final common pathway.

“The Effects of Blue-Light Filtration on Sleep and Work Outcomes”, Guarana et al 2020

2021-guarana.pdf: “The Effects of Blue-Light Filtration on Sleep and Work Outcomes”⁠, Cristiano L. Guarana, Christopher M. Barnes, Wei Jee Ong (2020-07-13; ; similar):

In this article, we investigate the effects of blue-light filtration on broad attitudinal and behavioral outcomes (ie. work engagement, organizational citizenship behavior, and counterproductive work behavior).

Drawing on recent developments in the circadian process literature and its related research on chronobiology⁠, we propose that a cost-effective sleep intervention can improve multiple organizationally relevant outcomes. Specifically, we theorize that wearing blue-light filtering glasses creates a form of physiologic darkness, thus improving both sleep quantity and quality. We then argue that wearing blue-light filtering glasses is related to work engagement, task performance, and nontask performance via sleep quantity and sleep quality. Considering that individuals vary in the timing of their circadian process, we propose that chronotype is a first-stage moderator for our theoretical model.

We tested these theoretical expectations in 2 experimental experience sampling studies. In Study 1a, we collected data from 63 managers (519 daily observations) and found that wearing blue-light filtering glasses is an effective intervention to improve physiological (sleep), attitudinal (work engagement), and behavioral (task performance, organizational citizenship behavior, and counterproductive work behavior) outcomes. In general, the effects were stronger for employees who tend to have sleep periods later in the day.

In Study 1b, we collected data from 67 call center representatives (529 daily observations) and measured task performance from clients. We replicated most of the findings except for the interactions.

Our model highlights how and when wearing blue-light filtering glasses can help employees to live and work better.

[Keywords: circadian process, sleep, well-being, work engagement, task and nontask performance]

“Sleep Loss Can Cause Death through Accumulation of Reactive Oxygen Species in the Gut”, Vaccaro et al 2020

2020-vaccaro.pdf: “Sleep Loss Can Cause Death through Accumulation of Reactive Oxygen Species in the Gut”⁠, Alexandra Vaccaro, Yosef Kaplan Dor, Keishi Nambara, Elizabeth A. Pollina, Cindy Lin, Michael E. Greenberg et al (2020-06-11; similar):

Highlights:

  • Sleep deprivation leads to ROS accumulation in the fly and mouse gut
  • Gut-accumulated ROS trigger oxidative stress in this organ
  • Preventing ROS accumulation in the gut allows survival without sleep in flies

The view that sleep is essential for survival is supported by the ubiquity of this behavior, the apparent existence of sleep-like states in the earliest animals, and the fact that severe sleep loss can be lethal. The cause of this lethality is unknown. Here we show, using flies and mice, that sleep deprivation leads to accumulation of reactive oxygen species (ROS) and consequent oxidative stress, specifically in the gut. ROS are not just correlates of sleep deprivation but drivers of death: their neutralization prevents oxidative stress and allows flies to have a normal lifespan with little to no sleep. The rescue can be achieved with oral antioxidant compounds or with gut-targeted transgenic expression of antioxidant enzymes. We conclude that death upon severe sleep restriction can be caused by oxidative stress, that the gut is central in this process, and that survival without sleep is possible when ROS accumulation is prevented.

[Keywords: sleep, sleep deprivation, reactive oxygen species, oxidative stress, free radicals, gut, survival, antioxidants]

“Sleep Deprivation Hormesis: The Shift That Doesn't Kill You Makes You Stronger”, Huecker et al 2020

2020-huecker.pdf: “Sleep deprivation hormesis: The shift that doesn't kill you makes you stronger”⁠, Martin R. Huecker, Jacob Shreffler, Brian Ferguson (2020; ; similar):

Google “hormesis” + an adversary in nature, and you will see positive benefits: bitter plant toxins, extreme heat/​cold, intense exercise, ethanol⁠, hypoxia⁠, nicotine⁠, even ionizing radiation.4,5 Almost every stress that evolving humans inevitably encountered has a favorable effect in small doses. But one unavoidable “toxin”, encountered by most of us in the emergency department⁠, is accused of being harmful in all cases: Sleep deprivation⁠. …what if sleep deprivation were not always bad?

…Depression also responds to acute sleep deprivation [see Boland et al 2017], with robust evidence that one all-nighter elevates the mood.6 Sleep deprivation may prophylax against PTSD after a fear-inducing situation.7 Sleep deprivation mitigates inflammation and ischemic insult in brain cells, protecting hippocampal neurons from damage.8 12 hours of lost sleep appears to not just protect the hippocampus⁠, but also induces neurogenesis that persists 15–30 days later.9 Yes, sleep loss increases oxidative stress and free radical formation,10 but so do exercise, fasting, and plant polyphenols⁠.5

Sleep researchers allow a biased hypothesis to direct research. Most protocols test individuals immediately after deprivation, neglecting measurements after adequate recovery sleep. Elite athletes immediately after a competition meet criteria for ICU admission. Lactate⁠, creatine kinase⁠, free radicals, electrolyte abnormalities, cortisol levels and other markers appear dangerously deranged. Similarly, subjects’ psychomotor vigilance and emotional liability after staying up all night suggest severe acute stress.

…Human subjects allowed ample recovery sleep resemble subjects who did not experience sleep deprivation, trending toward better response time and less sleepiness12. What if this paradigm were applied to shift workers? What if people who undergo small doses of sleep deprivation respond like athletes—stronger? By conducting systematic and longitudinal studies on effects of sleep deprivation and optimization of the recovery process, new studies could elucidate the complete picture of human resilience.

“A Rare Mutation of Β1-Adrenergic Receptor Affects Sleep/Wake Behaviors”, Shi et al 2019

2019-shi.pdf: “A Rare Mutation of β1-Adrenergic Receptor Affects Sleep / Wake Behaviors”⁠, Guangsen Shi, Lijuan Xing, David Wu, Bula J. Bhattacharyya, Christopher R. Jones, Thomas McMahon, S. Y. Christin Chong et al (2019-08-28; )

“ZMA Sleep Experiment”, Branwen 2017

ZMA: “ZMA Sleep Experiment”⁠, Gwern Branwen (2017-03-13; ⁠, ⁠, ⁠, ; backlinks; similar):

A randomized blinded self-experiment of the effects of ZMA (zinc+magnesium+vitamin B6) on my sleep; results suggest small benefit to sleep quality but are underpowered and damaged by Zeo measurement error/​data issues.

I ran a blinded randomized self-experiment of 2.5g nightly ZMA powder effect on Zeo-recorded sleep data during March-October 2017 (n = 127). The linear model and SEM model show no statistically-significant effects or high posterior probability of benefits, although all point-estimates were in the direction of benefits. Data quality issues reduced the available dataset, rendering the experiment particularly underpowered and the results more inconclusive. I decided to not continue use of ZMA after running out; ZMA may help my sleep but I need to improve data quality before attempting any further sleep self-experiments on it.

“Meta-Analysis of the Antidepressant Effects of Acute Sleep Deprivation”, Boland et al 2017

2017-boland.pdf: “Meta-Analysis of the Antidepressant Effects of Acute Sleep Deprivation”⁠, Elaine M. Boland, Hengyi Rao, David F. Dinges, Rachel V. Smith, Namni Goel, John A. Detre, Mathias Basner et al (2017-01-01; ⁠, ; backlinks)

“The Effect of Vitamin D Supplement on the Score and Quality of Sleep in 20–50 Year-old People With Sleep Disorders Compared With Control Group”, Shahi et al 2017

2017-majid.pdf: “The effect of vitamin D supplement on the score and quality of sleep in 20–50 year-old people with sleep disorders compared with control group”⁠, Majid Mohammad Shahi, Ahmad Hosseini Seyed, Bizhan Helli, Mohammad Hosein Haghighi Zade, Mohammad Abolfathi et al (2017; ; backlinks; similar):

Objectives: Sleep quality may be directly related with vitamin D serum level. Some studies found that people with lower vitamin D serum level experienced a lower sleep quality. Consequently, this study aimed at determining the effect of vitamin D supplements on sleep score and quality in 20–50 year-old people with sleep disorders.

Methods: This double blind, clinical trial was performed in November 2015–February 2016 on 89 people with sleep disorders based on Petersburg’s Sleep Index. Patient samples were divided randomly into 2 groups: intervention and placebo. At the end of the study, the data on 89 subjects (44 in intervention group and 45 people in placebo group) were examined. Intervention group received a 50 000-unit vitamin D supplement, one in a fortnight for 8 weeks. Meanwhile, placebo group received placebo. Before and after intervention, Petersburg’s Sleep Quality Questionnaire, International Physical Activity Questionnaire, general information questionnaire, sun exposure, vitamin D serum level and 3-day food record questionnaire were assessed and recorded for all participants. To analyze data, t-test, chi square, ANCOVA, U-Mann-Whitney and Wilcoxon statistical tests were used.

Findings: Based on the results of the present study, at the end of the study sleep score (PSQI) reduced statistically-significantly in vitamin recipients as compared with placebo recipients (p < 0.05). This difference was statistically-significant even after modifying confounding variables (p < 0.05).

Conclusion: This study shows that the use of vitamin D supplement improves sleep quality, reduces sleep latency, raises sleep duration and improves subjective sleep quality in people of 20–50 year-old with sleep disorder.

[Keywords: Vitamin D supplement, serum vitamin D, sleep disorders]

“CO2/ventilation Sleep Experiment”, Branwen 2016

CO2: “CO2/ventilation sleep experiment”⁠, Gwern Branwen (2016-06-05; ⁠, ⁠, ⁠, ; backlinks; similar):

Self-experiment on whether changes in bedroom CO2 levels affect sleep quality

Some psychology studies find that CO2 impairs cognition, and some sleep studies find that better ventilation may improve sleep quality. Use of a Netatmo air quality sensor reveals that closing my bedroom tightly to reduce morning light also causes CO2 levels to spike overnight to 7x daytime levels. To investigate the possible harmful effects, I run a self-experiment randomizing an open bedroom door and a bedroom box fan (2x2) and analyze the data using a structural equation model of air quality effects on a latent sleep factor with measurement error⁠.

“Sleep Disturbance, Sleep Duration, and Inflammation: A Systematic Review and Meta-Analysis of Cohort Studies and Experimental Sleep Deprivation”, Irwin et al 2016

“Sleep Disturbance, Sleep Duration, and Inflammation: A Systematic Review and Meta-Analysis of Cohort Studies and Experimental Sleep Deprivation”⁠, Michael R. Irwin, Richard Olmstead, Judith E. Carroll (2016; ; similar):

Background: Sleep disturbance is associated with inflammatory disease risk and all-cause mortality. Here, we assess global evidence linking sleep disturbance, sleep duration, and inflammation in adult humans.

Methods: A systematic search of English language publications was performed, with inclusion of primary research articles that characterized sleep disturbance and/​or sleep duration or performed experimental sleep deprivation and assessed inflammation by levels of circulating markers. Effect sizes (ES) and 95% confidence intervals (CI) were extracted and pooled using a random effect model.

Results: A total of 72 studies (n > 50,000) were analyzed with assessment of C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor α (TNFα). Sleep disturbance was associated with higher levels of CRP (ES .12; 95% CI = 0.05-.19) and IL-6 (ES .20; 95% CI = 0.08-.31). Shorter sleep duration, but not the extreme of short sleep, was associated with higher levels of CRP (ES .09; 95% CI = 0.01-.17) but not IL-6 (ES .03; 95% CI: -.09 to .14). The extreme of long sleep duration was associated with higher levels of CRP (ES .17; 95% CI = 0.01-.34) and IL-6 (ES .11; 95% CI = 0.02–20). Neither sleep disturbances nor sleep duration was associated with TNFα. Neither experimental sleep deprivation nor sleep restriction was associated with CRP, IL-6, or TNFα. Some heterogeneity among studies was found, but there was no evidence of publication bias.

Conclusions: Sleep disturbance and long sleep duration, but not short sleep duration, are associated with increases in markers of systemic inflammation.

“Effects of Lunar Phase on Sleep in Men and Women in Surrey”, Monica et al 2015

“Effects of lunar phase on sleep in men and women in Surrey”⁠, Ciro Della Monica, Giuseppe Atzori, Derk-Jan Dijk (2015-06-12; backlinks; similar):

Recently, evidence has emerged that the phases of the moon may modulate subjective sleep quality and polysomnographically assessed sleep structure in humans. We aimed to explore further the putative effects of circa-lunar periodicity (~29.5 days) on subjective and objective parameters of human sleep in a retrospective analysis. The baseline sleep recordings of 205 (91 males and 114 females; mean age = 47.47 years, standard deviation = 19.01; range: 20–84 years) healthy and carefully screened participants who participated in two clinical trials in the Surrey Clinical Research Centre were included in the analyses. Sleep was recorded in windowless sleep laboratories. For each study night, we calculated the distance, in days, to the date of the closest full moon phase and based on this distance, classified sleep records in three lunar classes. Univariate analysis of variance with factors lunar class, age and sex was applied to each of 21 sleep parameters. No statistically-significant main effect for the factor lunar class was observed for any of the objective sleep parameters and subjective sleep quality but some statistically-significant interactions were observed. The interaction between lunar class and sex was statistically-significant for total sleep time, Stage 4 sleep and rapid eye movement (REM) sleep. Separate analyses for men and women indicated that in women total sleep time, Stage 4 sleep and REM sleep were reduced when sleep occurred close to full moon, whereas in men REM duration increased around full moon. These data provide limited evidence for an effect of lunar phase on human sleep.

“Human Sleep and Cortical Reactivity Are Influenced by Lunar Phase”, Smith et al 2014

“Human sleep and cortical reactivity are influenced by lunar phase”⁠, Michael Smith, Ilona Croy, Kerstin Persson Waye (2014-06-16; backlinks; similar):

Various human biological functions adhere to a circadian rhythm that to some extent may be affected by environmental factors, including light and temperature 1. Recent evidence from Cajochen et al2 indicates that human sleep is influenced by the cycle of the moon, measured in conditions precluding the potential impact of nocturnal lunar illumination Here in a similarly retrospective study of 47 healthy volunteers (mean age 23.3, S.D. ±2.9 years) we demonstrate that total sleep time decreases by 25 minutes and cortical reactivity to environmental stimuli during sleep increases around full moon, and rapid eye movement (REM) sleep latency lengthens by 30 minutes around new moon. The findings strengthen the notion that human sleep is modulated by lunar phase but point to important deviations from the study of Cajochen et al that need to be addressed, particularly with regard to individual susceptibility.

“Lunar Cycle Effects on Sleep and the File Drawer Problem”, Cordi et al 2014

“Lunar cycle effects on sleep and the file drawer problem”⁠, Maren Cordi, Sandra Ackermann, Frederik W. Bes, Francina Hartmann, Boris N. Konrad, Lisa Genzel, Marcel Pawlowski et al (2014-06-16; backlinks; similar):

Popular beliefs about the influence of the full moon on humans exist, although no solid evidence has so far confirmed these ideas1. Cajochen et al2 recently presented fascinating data on lunar cycle effects on human sleep. However, in a re-analysis of sleep electroencephalography (EEG) data in three large samples, we were unable to replicate their findings. In addition, we identified further mostly unpublished null findings, suggesting that the conflicting results might be an example of a publication bias (ie. the file drawer problem).

“Bacopa Quasi-Experiment”, Branwen 2014

Bacopa: “Bacopa Quasi-Experiment”⁠, Gwern Branwen (2014-05-06; ⁠, ⁠, ⁠, ⁠, ; backlinks; similar):

A small 2014-2015 non-blinded self-experiment using Bacopa monnieri to investigate effect on memory/​sleep/​self-ratings in an ABABA design; no particular effects were found.

Bacopa is a supplement herb often used for memory or stress adaptation. Its chronic effects reportedly take many weeks to manifest, with no important acute effects. Out of curiosity, I bought 2 bottles of Bacognize Bacopa pills and ran a non-randomized non-blinded ABABA quasi-self-experiment from June 2014 to September 2015, measuring effects on my memory performance, sleep, and daily self-ratings of mood/​productivity. For analysis, a multi-level Bayesian model on two memory performance variables was used to extract per-day performance, factor analysis was used to extract a sleep index from 9 Zeo sleep variables, and the 3 endpoints were modeled as a multivariate Bayesian time-series regression with splines. Because of the slow onset of chronic effects, small effective sample size, definite temporal trends probably unrelated to Bacopa, and noise in the variables, the results were as expected, ambiguous, and do not strongly support any correlation between Bacopa and memory/​sleep/​self-rating (+/​-/​- respectively).

“Caffeine Wakeup Experiment”, Branwen 2013

Caffeine: “Caffeine wakeup experiment”⁠, Gwern Branwen (2013-04-07; ⁠, ⁠, ⁠, ⁠, ⁠, ; backlinks; similar):

Self-experiment on whether consuming caffeine immediately upon waking results in less time in bed & higher productivity. The results indicate a small and uncertain effect.

One trick to combat morning sluggishness is to get caffeine extra-early by using caffeine pills shortly before or upon trying to get up. From 2013-2014 I ran a blinded & placebo-controlled randomized experiment measuring the effect of caffeine pills in the morning upon awakening time and daily productivity. The estimated effect is small and the posterior probability relatively low, but a decision analysis suggests that since caffeine pills are so cheap, it would be worthwhile to conduct another experiment; however, increasing Zeo equipment problems have made me hold off additional experiments indefinitely.

“Bayesian Estimation Supersedes the t Test”, Kruschke 2013

2012-kruschke.pdf: “Bayesian estimation supersedes the t test”⁠, John J. Kruschke (2013; ; backlinks; similar):

Bayesian estimation for 2 groups provides complete distributions of credible values for the effect size, group means and their difference, standard deviations and their difference, and the normality of the data. The method handles outliers. The decision rule can accept the null value (unlike traditional t-tests) when certainty in the estimate is high (unlike Bayesian model comparison using Bayes factors). The method also yields precise estimates of statistical power for various research goals. The software and programs are free and run on Macintosh, Windows, and Linux platforms.

[Keywords: Bayesian statistics, effect size, robust estimation, Bayes factor, confidence interval]

“Zeo_DataDownload™_Help_Sheet”, Tata 2013

2013-zeo-exportdatasheet.pdf: “Zeo_DataDownload™_Help_Sheet”⁠, Emily Tata (2013-01-01; backlinks)

“Polysomnographic Validation of a Wireless Dry Headband Technology for Sleep Monitoring in Healthy Young Adults”, Tonetti et al 2013

2013-tonetti.pdf: “Polysomnographic validation of a wireless dry headband technology for sleep monitoring in healthy young adults”⁠, Lorenzo Tonetti, Nicola Cellini, Massimiliano de Zambotti, Marco Fabbri, Monica Martoni, Stephan E. Fábregas et al (2013-01-01; backlinks)

“Evidence That the Lunar Cycle Influences Human Sleep”, Cajochen et al 2013

2013-cajochen.pdf: “Evidence that the Lunar Cycle Influences Human Sleep”⁠, Christian Cajochen, Songül Altanay-Ekici, Mirjam Münch, Sylvia Frey, Vera Knoblauch, Anna Wirz-Justice et al (2013-01-01; backlinks)

“Potassium Sleep Experiments”, Branwen 2012

Potassium: “Potassium sleep experiments”⁠, Gwern Branwen (2012-12-21; ⁠, ⁠, ⁠, ; backlinks; similar):

2 self-experiments on potassium citrate effects on sleep: harm to sleep when taken daily or in the morning

Potassium and magnesium are minerals that many Americans are deficient in. I tried using potassium citrate and immediately noticed difficulty sleeping. A short randomized (but not blinded) self-experiment of ~4g potassium taken throughout the day confirmed large negative effects on my sleep. A longer followup randomized and blinded self-experiment used standardized doses taken once a day early in the morning, and also found some harm to sleep, and I discontinued potassium use entirely.

“Redshift Sleep Experiment”, Branwen 2012

Redshift: “Redshift sleep experiment”⁠, Gwern Branwen (2012-05-09; ⁠, ⁠, ⁠, ⁠, ⁠, ; backlinks; similar):

Self-experiment on whether screen-tinting software such as Redshift/​f.lux affect sleep times and sleep quality; Redshift lets me sleep earlier but doesn’t improve sleep quality.

I ran a randomized experiment with a free program (Redshift) which reddens screens at night to avoid tampering with melatonin secretion & the sleep from 2012–2013, measuring sleep changes with my Zeo⁠. With 533 days of data, the main result is that Redshift causes me to go to sleep half an hour earlier but otherwise does not improve sleep quality.

“Vitamin D Sleep Experiments”, Branwen 2012

Vitamin-D: “Vitamin D sleep experiments”⁠, Gwern Branwen (2012; ⁠, ⁠, ⁠, ; backlinks; similar):

Self-experiment on vitamin D effects on sleep: harmful taken at night, no or beneficial effects when taken in the morning.

Vitamin D is a hormone endogenously created by exposure to sunlight; due to historically low outdoors activity levels, it has become a popular supplement and I use it. Some anecdotes suggest that vitamin D may have circadian and zeitgeber effects due to its origin, and is harmful to sleep when taken at night. I ran a blinded randomized self-experiment on taking vitamin D pills at bedtime. The vitamin D damaged my sleep and especially how rested I felt upon wakening, suggesting vitamin D did have a stimulating effect which obstructed sleep. I conducted a followup blinded randomized self-experiment on the logical next question: if vitamin D is a daytime cue, then would vitamin D taken in the morning show some beneficial effects? The results were inconclusive (but slightly in favor of benefits). Given the asymmetry, I suggest that vitamin D supplements should be taken only in the morning.

“The World Epidemic of Sleep Disorders Is Linked to Vitamin D Deficiency”, Gominak & Stumpf 2012

2012-gominak.pdf: “The world epidemic of sleep disorders is linked to vitamin D deficiency”⁠, S. C. Gominak, W. E. Stumpf (2012-01-01; backlinks)

“The Midpoint of Sleep Is Associated With Dietary Intake and Dietary Behavior among Young Japanese Women”, Sato-Mito et al 2011

2011-satomito.pdf: “The midpoint of sleep is associated with dietary intake and dietary behavior among young Japanese women”⁠, Natsuko Sato-Mito, Satoshi Sasaki, Kentaro Murakami, Hitomi Okubo, Yoshiko Takahashi, Shigenobu Shibata et al (2011-01-01; backlinks)

“Zeo Sleep Self-experiments”, Branwen 2010

Zeo: “Zeo sleep self-experiments”⁠, Gwern Branwen (2010-12-28; ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ; backlinks; similar):

EEG recordings of sleep and my experiments with things affecting sleep quality or durations: melatonin, potassium, vitamin D etc

I discuss my beliefs about Quantified Self⁠, and demonstrate with a series of single-subject design self-experiments using a Zeo. A Zeo records sleep via EEG; I have made many measurements and performed many experiments. This is what I have learned so far:

  1. the Zeo headband is wearable long-term
  2. melatonin improves my sleep
  3. one-legged standing does little
  4. Vitamin D at night damages my sleep & Vitamin D in morning does not affect my sleep
  5. potassium (over the day but not so much the morning) damages my sleep and does not improve my mood/​productivity
  6. small quantities of alcohol appear to make little difference to my sleep quality
  7. I may be better off changing my sleep timing by waking up somewhat earlier & going to bed somewhat earlier
  8. lithium orotate does not affect my sleep
  9. Redshift causes me to go to bed earlier
  10. ZMA: inconclusive results slightly suggestive of benefits

“Nootropics”, Branwen 2010

Nootropics: “Nootropics”⁠, Gwern Branwen (2010-01-02; ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ⁠, ; backlinks; similar)

“Melatonin”, Branwen 2008

Melatonin: “Melatonin”⁠, Gwern Branwen (2008-12-19; ⁠, ⁠, ⁠, ⁠, ⁠, ; backlinks; similar):

Melatonin improves sleep, & sleep is valuable

I discuss melatonin’s effects on sleep & its safety with research up to 2015; I segue into the general benefits of sleep and the severely disrupted sleep of the modern Western world, the cost of melatonin use and the benefit (eg. enforcing regular bedtimes), followed by a basic cost-benefit analysis of melatonin concluding that the net profit is large enough to be worth giving it a try barring unusual conditions or very pessimistic safety estimates.

“Sleep and Sex: What Can Go Wrong? A Review of the Literature on Sleep Related Disorders and Abnormal Sexual Behaviors and Experiences”, Schenck et al 2007

“Sleep and sex: what can go wrong? A review of the literature on sleep related disorders and abnormal sexual behaviors and experiences”⁠, Carlos H. Schenck, Isabelle Arnulf, Mark W. Mahowald (2007-06-01; backlinks; similar):

To formulate the first classification of sleep-related disorders and abnormal sexual behaviors and experiences. A computerized literature search was conducted, and other sources, such as textbooks, were searched. Many categories of sleep related disorders were represented in the classification: parasomnias (confusional arousals/​sleepwalking, with or without obstructive sleep apnea; REM sleep behavior disorder); sleep related seizures; Kleine-Levin syndrome (KLS); severe chronic insomnia; restless legs syndrome; narcolepsy; sleep exacerbation of persistent sexual arousal syndrome; sleep related painful erections; sleep related dissociative disorders; nocturnal psychotic disorders; miscellaneous states.

Kleine-Levin syndrome (78 cases) and parasomnias (31 cases) were most frequently reported. Parasomnias and sleep related seizures had overlapping and divergent clinical features. 31 cases of parasomnias (25 males; mean age, 32 years) and 7 cases of sleep related seizures (4 males; mean age, 38 years) were identified.

A full range of sleep related sexual behaviors with self and/​or bed partners or others were reported, including masturbation, sexual vocalizations, fondling, sexual intercourse with climax, sexual assault/​rape, ictal sexual hyperarousal, ictal orgasm, and ictal automatism. Adverse physical and/​or psychosocial effects from the sleepsex were present in all parasomnia and sleep related seizure cases, but pleasurable effects were reported by 5 bed partners and by 3 patients with sleep related seizures. Forensic consequences were common, occurring in 35.5% (11⁄31) of parasomnia cases, with most (9⁄11) involving minors. All parasomnias cases reported amnesia for the sleep-sex, in contrast to 28.6% (2⁄7) of sleep related seizure cases. Polysomnography (without penile tumescence monitoring), performed in 26 of 31 parasomnia cases, documented sexual moaning from slow wave sleep in 3 cases and sexual intercourse during stage 1 sleep/​wakefulness in one case (with sex provoked by the bed partner). Confusional arousals (CAs) were diagnosed as the cause of “sleepsex” (“sexsomnia”) in 26 cases (with obstructive sleep apnea [OSA] comorbidity in 4 cases), and sleepwalking in 2 cases, totaling 90.3% (28⁄31) of cases being NREM sleep parasomnias. REM behavior disorder was the presumed cause in the other 3 cases.

Bedtime clonazepam therapy was effective in 90% (9⁄10) of treated parasomnia cases; nasal continuous positive airway pressure therapy was effective in controlling comorbid OSA and CAs in both treated cases. All 5 treated patients with sleep related sexual seizures responded to anticonvulsant therapy. The hypersexuality in KLS, which was twice as common in males compared to females, had no reported effective therapy.

A broad range of sleep related disorders associated with abnormal sexual behaviors and experiences exists, with major clinical and forensic consequences.

“Positive Sleep State Misperception—A New Concept of Sleep Misperception”, Trajanovic et al 2007

2007-trajanovic.pdf: “Positive sleep state misperception—A new concept of sleep misperception”⁠, Nikola N. Trajanovic, Vlada Radivojevic, Yulia Kaushansky, Colin M. Shapiro (2007-03-01)

“The Dynamics of Neurobehavioural Recovery following Sleep Loss”, Lamond et al 2007

2007-lamond.pdf: “The dynamics of neurobehavioural recovery following sleep loss”⁠, Nicole Lamond, Sarah M. Jay, Jillian Dorrian, Sally A. Ferguson, Christopher Jones, Drew Dawson (2007-02-19; backlinks; similar):

Rate of recovery of daytime performance and sleepiness following moderate and severe sleep deprivation (SD) was examined when recovery opportunity was either augmented or restricted.

30 healthy non-smokers, aged 18–33 years, participated in one of 3 conditions: moderate SD with augmented (9-h) recovery opportunities, moderate SD with restricted (6-h) recovery opportunities, or severe SD with augmented recovery opportunities. Each participant attended the laboratory for 8–9 consecutive nights: an adaptation and baseline night (23:00–08:00 hours), one or 2 night(s) of wakefulness, and 5 consecutive recovery sleep opportunities (23:00–08:00 hours or 02:00–08:00 hours). On each experimental day, psychomotor vigilance performance (PVT) and subjective sleepiness (SSS) were assessed at 2-hourly intervals, and MSLTs were performed at 10:00h. PSG data was collected for each sleep period.

For all groups, PVT performance statistically-significantly deteriorated during the period of wakefulness, and sleepiness statistically-significantly increased. Statistically-significant differences were observed between the groups during the recovery phase. Following moderate SD, response speed, lapses and SSS returned to baseline after one 9-h sleep opportunity, while sleep latencies required 2 9-h opportunities. When the recovery opportunity was restricted to 6 hours, neither PVT performance nor sleepiness recovered, but stabilized at below-baseline levels. Following severe SD, sleepiness recovered after one (SSS) or 2 (physiological) 9-h sleep opportunities, however PVT performance remained statistically-significantly below baseline for the entire recovery period.

These results suggest that the mechanisms underlying the recovery process may be more complicated than previously thought, and that we may have underestimated the impact of sleep loss and/​or the restorative value of subsequent sleep.

[Keywords: neurobehavioural recovery, performance, recovery opportunity, sleep deprivation, sleep restriction, sleepiness]

“Meditation Practices for Health: State of the Research”, Center 2007

“Meditation Practices for Health: State of the Research”⁠, University of Alberta Evidence-based Practice Center (2007; backlinks; similar):

Many uncertainties surround the practice of meditation. Scientific research on meditation practices does not appear to have a common theoretical perspective and is characterized by poor methodological quality. Firm conclusions on the effects of meditation practices in healthcare cannot be drawn based on the available evidence. Future research on meditation practices must be more rigorous in the design and execution of studies and in the analysis and reporting of results.

“Sleep Function and Synaptic Homeostasis”, Tononi & Cirelli 2006

2006-tononi.pdf: “Sleep function and synaptic homeostasis”⁠, Giulio Tononi, Chiara Cirelli (2006-02-01; backlinks; similar):

This paper reviews a novel hypothesis about the functions of slow wave sleep—the synaptic homeostasis hypothesis. According to the hypothesis, plastic processes occurring during wakefulness result in a net increase in synaptic strength in many brain circuits. The role of sleep is to downscale synaptic strength to a baseline level that is energetically sustainable, makes efficient use of gray matter space, and is beneficial for learning and memory. Thus, sleep is the price we have to pay for plasticity, and its goal is the homeostatic regulation of the total synaptic weight impinging on neurons. The hypothesis accounts for a large number of experimental facts, makes several specific predictions, and has implications for both sleep and mood disorders.

[Keywords: Long-term depression, Synaptic scaling, Learning, Consolidation, Delta sleep, Slow waves, Slow oscillation]

“Self-management of Fatal Familial Insomnia. Part 2: Case Report”, Schenkein & Montagna 2006

“Self-management of fatal familial insomnia. Part 2: case report”⁠, Joyce Schenkein, Pasquale Montagna (2006; ⁠, ; similar):

Context: Fatal familial insomnia (FFI) is a genetically transmitted neurodegenerative prion disease that incurs great suffering and has neither a treatment nor cure. The clinical literature is devoid of management plans (other than palliative). Part 1 of this article reviews the sparse literature about FFI, including case descriptions. Part 2 describes the efforts of one patient (with the rapid-course Met-Met subtype) who contended with his devastating symptoms and improved the quality of his life.

Design: Interventions were based on the premise that some symptoms may be secondary to insomnia and not a direct result of the disease itself. Strategies (derived by trial and error) were devised to induce sleep and increase alertness. Interventions included vitamin supplementation, narcoleptics, anesthesia, stimulants, sensory deprivation, exercise, light entrainment, growth hormone, and electroconvulsive therapy (ECT).

Results: The patient exceeded the average survival time by nearly 1 year, and during this time (when most patients are totally incapacitated), he was able to write a book and to successfully drive hundreds of miles.

Conclusion: Methods to induce sleep may extend and enhance life during the disease course, although they do not prevent death. It is hoped that some of his methods will inspire further clinical studies.

“The Impact of Sleep Deprivation on Decision Making: A Review”, Harrison & Horne 2000

2000-harrison.pdf: “The Impact of Sleep Deprivation on Decision Making: A Review”⁠, Yvonne Harrison, James A. Horne (2000-09-01; ⁠, ; backlinks; similar):

Few sleep deprivation (SD) studies involve realism or high-level decision making, factors relevant to managers, military commanders, and so forth, who are undergoing prolonged work during crises. Instead, research has favored simple tasks sensitive to SD mostly because of their dull monotony. In contrast, complex rule-based, convergent, and logical tasks are unaffected by short-term SD, seemingly because of heightened participant interest and compensatory effort.

However, recent findings show that despite this effort, SD still impairs decision making involving the unexpected, innovation, revising plans, competing distraction, and effective communication. Decision-making models developed outside SD provide useful perspectives on these latter effects, as does a neuropsychological explanation of sleep function.

SD presents particular difficulties for sleep-deprived decision makers who require these latter skills during emergency situations.

“We Are Chronically Sleep Deprived”, Bonnet & Arand 1995

1995-bonnet.pdf: “We are Chronically Sleep Deprived”⁠, Michael H. Bonnet, Donna L. Arand (1995-12-01; backlinks):

Data from recent laboratory studies indicate that nocturnal sleep periods reduced by as little as 1.3 to 1.5 hours for 1 night result in reduction of daytime alertness by as much as 32% as measured by the Multiple Sleep Latency Test (MSLT).

Other data document that (1) 17%–57% of normal young adults have MSLT latencies of ≤5.5 minutes, whereas ≤50% have MSLT values of ≥ 10 minutes and (2) 28%–29% of young adults reported normally sleeping ≤6.5 hours on each weeknight. More extensive reduction of daily sleep amount is seen in night-shift workers.

A minimum of 2%–4% of middle-aged adults have hypersomnolence associated with sleep apnea⁠.

Together, these data show that substantial sleep loss exists in 1⁄3rd or more of normal adults, that the effects are large and replicable and that similar effects can be produced in just 1 night in the laboratory.

In light of the magnitude of this sleep debt⁠, it is not surprising that fatigue is a factor in 57% of accidents leading to the death of a truck driver and in 10% of fatal car accidents and results in costs of up to $121.2$56.01995 billion dollars per year. A recent sleep extension study suggests that the average underlying sleep tendency in young adults is about 8.5 hours per night. By comparison, the average reported sleep length of 7.2–7.4 hours is deficient, and common sleep lengths of ≤6.5 hours can be disastrous.

We must recognize the alertness function of sleep and the increasing consequences of sleepiness with the same vigor that we have come to recognize the societal impact of alcohol.

[Keywords: sleep deprivation⁠, sleepiness, sleep disorders, work schedule tolerance]

“Functional Consequences of Sustained Sleep Deprivation in the Rat”, Everson 1995

1995-everson.pdf: “Functional consequences of sustained sleep deprivation in the rat”⁠, Carol A. Everson (1995-07-01; ; backlinks; similar):

Sleep deprivation disrupts vital biological processes that are necessary for cognitive ability and physical health, but the physiological changes that underlie these outward effects are largely unknown.

The purpose of the present studies in the laboratory rat is to prolong sleep deprivation to delineate the pathophysiology and to determine its mediation.

In the rat, the course of prolonged sleep deprivation has a syndromic nature and eventuates in a life-threatening state. An early and central symptom of sleep deprivation is a progressive increase in peripheral energy expenditure to nearly double normal levels.

An attempt to alleviate this negative energy balance by feeding rats a balanced diet that is high in its efficiency of utilization prolongs survival and attenuates or delays development of malnutrition-like symptoms, indicating that several symptoms can be manipulated to some extent by energy and nutrient consumption. Most changes in neuroendocrine parameters appear to be responses to metabolic demands, such as increased plasma catecholamines indicating sympathetic activation. Plasma total thyroid hormones⁠, however, decline to severely low levels; a metabolic complication that is associated with other sleep deprivation-induced symptoms, such as a decline in body temperature to hypothermic levels despite increased energy expenditure. Metabolic mapping of the brain revealed a dissociation between the energy metabolism of the brain and that of the body.

Sleep deprivation’s effects on cerebral structures are heterogeneous and unidirectional toward decreased functional activity. The hypometabolic brain structures are concentrated in the hypothalamus⁠, thalamus and limbic system⁠, whereas few regions in the rest of the brain and none in the medulla⁠, are affected. Correspondence can be found between some of the affected cerebral structures and several of the peripheral symptoms, such as hyperphagia and possible heat retention problems.

The factor predisposing to mortality is a decreased resistance to infection. Lethal opportunistic organisms are permitted to infect the bloodstream, which presumably results in a cascade of toxic-like reactions. Host defense is thus the first system to fail. There is neither fever nor marked tissue inflammatory reactions typical of infectious disease states, suggesting that sleep deprivation is immunosuppressive.

Each of the 4 major abnormalities identified—(1) a deep negative energy balance and associated malnutrition; (2) heterogeneous decreases in cerebral function; (3) low thyroid hormone concentrations; and (4) decreased resistance to infection—can be viewed as having an early origin during the sleep deprivation process to signify the foremost pathogenic situation to which the other abnormalities might be secondarily related.

The findings therefore remain somewhat equivocal for an unitary function for sleep, but can support putative roles for sleep in thermoregulation⁠, energy conservation, immune system integrity and tissue restoration.

[Keywords: sleep deprivation, metabolism, nutrition, thyroxine, cerebral glucose utilization, thermoregulation, host defense, immune function]

Fatal insomnia

Wikipedia

Miscellaneous