Daniel Aeschbach

Evening use of light-emitting eReaders negatively affects sleep, circadian timing, and next-morning alertness

Significance The use of light-emitting electronic devices for reading, communication, and entertainment has greatly increased recently. We found that the use of these devices before bedtime prolongs the time it takes to fall asleep, delays the circadian clock, suppresses levels of the sleep-promoting hormone melatonin, reduces the amount and delays the timing of REM sleep, and reduces alertness the following morning. Use of light-emitting devices immediately before bedtime also increases alertness at that time, which may lead users to delay bedtime at home. Overall, we found that the use of portable light-emitting devices immediately before bedtime has biological effects that may perpetuate sleep deficiency and disrupt circadian rhythms, both of which can have adverse impacts on performance, health, and safety. In the past 50 y, there has been a decline in average sleep duration and quality, with adverse consequences on general health. A representative survey of 1,508 American adults recently revealed that 90% of Americans used some type of electronics at least a few nights per week within 1 h before bedtime. Mounting evidence from countries around the world shows the negative impact of such technology use on sleep. This negative impact on sleep may be due to the short-wavelength–enriched light emitted by these electronic devices, given that artificial-light exposure has been shown experimentally to produce alerting effects, suppress melatonin, and phase-shift the biological clock. A few reports have shown that these devices suppress melatonin levels, but little is known about the effects on circadian phase or the following sleep episode, exposing a substantial gap in our knowledge of how this increasingly popular technology affects sleep. Here we compare the biological effects of reading an electronic book on a light-emitting device (LE-eBook) with reading a printed book in the hours before bedtime. Participants reading an LE-eBook took longer to fall asleep and had reduced evening sleepiness, reduced melatonin secretion, later timing of their circadian clock, and reduced next-morning alertness than when reading a printed book. These results demonstrate that evening exposure to an LE-eBook phase-delays the circadian clock, acutely suppresses melatonin, and has important implications for understanding the impact of such technologies on sleep, performance, health, and safety.

All-night dynamics of the human sleep EEG

SUMMARY  The dynamics of the sleep EEG were investigated by all‐night spectral analysis of 51 sleep records. Power density was calculated for 1‐Hz bins in the 0.25–25.0 Hz range. Values in non‐rapid‐eye‐movement sleep (NREMS) were higher than in REMS in the 0.25–16.0 Hz range, and lower in the 18.25–22.0 Hz range. Power density in the 0.25–12.0 Hz range showed a declining trend over the first four NREMS episodes, which, depending on the frequency bin, could be approximated by non‐linear or linear decay functions. In the frequency range of sleep spindles (12.25–15.0 Hz), power density in the 13.25–15.0 Hz band showed an increasing trend between NREMS episode 2 and NREMS episode 4. A correlation matrix of 25 1‐Hz bins revealed for NREMS a negative correlation between slow‐wave activity (SWA; 0.25–4.0 Hz) and activity in the spindle frequency range. This negative correlation was highest in the first NREMS episode and diminished progressively over the subsequent NREMS episodes. Within NREMS episodes, the values in the spindle frequency range showed a U‐shaped time course, the trough coinciding with a high level of SWA. By contrast, in both the early and late part of the episode the two types of activity changed in the same direction. The results are consistent with recent electrophysiological studies indicating that the establishment of NREMS is associated with a progressive hyperpolarization of thalamocortical neurons during which the membrane potential exhibits oscillations first in the spindle frequency range and then in the range of SWA.

Short-Wavelength Light Sensitivity of Circadian, Pupillary, and Visual Awareness in Humans Lacking an Outer Retina

Summary As the ear has dual functions for audition and balance, the eye has a dual role in detecting light for a wide range of behavioral and physiological functions separate from sight [1–11]. These responses are driven primarily by stimulation of photosensitive retinal ganglion cells (pRGCs) that are most sensitive to short-wavelength (∼480 nm) blue light and remain functional in the absence of rods and cones [8–10]. We examined the spectral sensitivity of non-image-forming responses in two profoundly blind subjects lacking functional rods and cones (one male, 56 yr old; one female, 87 yr old). In the male subject, we found that short-wavelength light preferentially suppressed melatonin, reset the circadian pacemaker, and directly enhanced alertness compared to 555 nm exposure, which is the peak sensitivity of the photopic visual system. In an action spectrum for pupillary constriction, the female subject exhibited a peak spectral sensitivity (λmax) of 480 nm, matching that of the pRGCs but not that of the rods and cones. This subject was also able to correctly report a threshold short-wavelength stimulus (∼480 nm) but not other wavelengths. Collectively these data show that pRGCs contribute to both circadian physiology and rudimentary visual awareness in humans and challenge the assumption that rod- and cone-based photoreception mediate all “visual” responses to light.

Circadian System, Sleep and Endocrinology

Levels of numerous hormones vary across the day and night. Such fluctuations are not only attributable to changes in sleep/wakefulness and other behaviors but also to a circadian timing system governed by the suprachiasmatic nucleus of the hypothalamus. Sleep has a strong effect on levels of some hormones such as growth hormone but little effect on others which are more strongly regulated by the circadian timing system (e.g., melatonin). Whereas the exact mechanisms through which sleep affects circulating hormonal levels are poorly understood, more is known about how the circadian timing system influences the secretion of hormones. The suprachiasmatic nucleus exerts its influence on hormones via neuronal and humoral signals but it is now also apparent that peripheral tissues contain circadian clock proteins, similar to those in the suprachiasmatic nucleus, that are also involved in hormone regulation. Under normal circumstances, behaviors and the circadian timing system are synchronized with an optimal phase relationship and consequently hormonal systems are exquisitely regulated. However, many individuals (e.g., shift-workers) frequently and/or chronically undergo circadian misalignment by desynchronizing their sleep/wake and fasting/feeding cycle from the circadian timing system. Recent experiments indicate that circadian misalignment has an adverse effect on metabolic and hormonal factors such as circulating glucose and insulin. Further research is needed to determine the underlying mechanisms that cause the negative effects induced by circadian misalignment. Such research could aid the development of novel countermeasures for circadian misalignment.

Dynamics of the human EEG during prolonged wakefulness: evidence for frequency-specific circadian and homeostatic influences

The electroencephalogram (EEG) of nine healthy individuals was recorded at half-hourly intervals during approximately 40 h of sustained wakefulness in a constant routine protocol. EEG power density in the 0.75-9.0 Hz range exhibited a global increasing trend, and a local trough in the evening, centered approximately 6 h prior to the temperature minimum. The former could be attributed to a wake-dependent influence, and the latter to a circadian influence. Power density in the 9.25-12.0 Hz band showed a circadian modulation, the trough coinciding with the minimum of the endogenous rhythm of body temperature, whereas a wake-dependent influence was not evident. Power density in the 12.25-25.0 Hz range exhibited a wake-dependent increase, whereas a circadian modulation was absent. It is concluded that the circadian pacemaker and the wake-dependent (i.e. homeostatic) process affect the waking EEG in a frequency-specific manner.

Evidence for a biological dawn and dusk in the human circadian timing system

1 Because individuals differ in the phase angle at which their circadian rhythms are entrained to external time cues, averaging group data relative to clock time sometimes obscures abrupt changes that are characteristic of waveforms of the rhythms in individuals. Such changes may have important implications for the temporal organization of human circadian physiology. 2 To control for variance in phase angle of entrainment, we used dual internal reference points ‐ onset and offset of the nocturnal period of melatonin secretion ‐ to calculate average profiles of circadian rhythm data from five previously published studies. 3 Onset and/or offset of melatonin secretion were found to coincide with switch‐like transitions between distinct diurnal and nocturnal periods of circadian rhythms in core body temperature, sleepiness, power in the theta band of the wake EEG, sleep propensity and rapid eye movement (REM) sleep propensity. 4 Transitions between diurnal and nocturnal periods of sleep‐wake and cortisol circadian rhythms were found to lag the other transitions by 1‐3 h. 5 When the duration of the daily light period was manipulated experimentally, melatonin‐onset‐related transitions in circadian rhythms appeared to be entrained to the light‐to‐dark transition, while melatonin‐offset‐related transitions appeared to be entrained to the dark‐to‐light transition. 6 These results suggest a model of the human circadian timing system in which two states, one diurnal and one nocturnal, alternate with one another, and in which transitions between the states are switch‐like and are separately entrained to dawn and dusk. 7 This description of the human circadian system is similar to the Pittendrigh‐Daan model of the rodent circadian system, and it suggests that core features of the system in other mammals are conserved in humans.

Two circadian rhythms in the human electroencephalogram during wakefulness

The influence of the circadian pacemaker and of the duration of time awake on the electroencephalogram (EEG) was investigated in 19 humans during approximately 40 h of sustained wakefulness. Two circadian rhythms in spectral power density were educed. The first rhythm was centered in the theta band (4.25-8.0 Hz) and exhibited a minimum approximately 1 h after the onset of melatonin secretion. The second rhythm was centered in the high-frequency alpha band (10.25-13.0 Hz) and exhibited a minimum close to the body temperature minimum. The latter rhythm showed a close temporal association with the rhythms in subjective alertness, plasma melatonin, and body temperature. In addition, increasing time awake was associated with an increase of power density in the 0.25- to 9.0-Hz and 13.25- to 20. 0-Hz ranges. It is concluded that the waking EEG undergoes changes that can be attributed to circadian and homeostatic (i.e., sleep-wake dependent) processes. The distinct circadian variations of EEG activity in the theta band and in the high-frequency alpha band may represent electrophysiological correlates of different aspects of the circadian rhythm in arousal.The influence of the circadian pacemaker and of the duration of time awake on the electroencephalogram (EEG) was investigated in 19 humans during ∼40 h of sustained wakefulness. Two circadian rhythms in spectral power density were educed. The first rhythm was centered in the theta band (4.25-8.0 Hz) and exhibited a minimum ∼1 h after the onset of melatonin secretion. The second rhythm was centered in the high-frequency alpha band (10.25-13.0 Hz) and exhibited a minimum close to the body temperature minimum. The latter rhythm showed a close temporal association with the rhythms in subjective alertness, plasma melatonin, and body temperature. In addition, increasing time awake was associated with an increase of power density in the 0.25- to 9.0-Hz and 13.25- to 20.0-Hz ranges. It is concluded that the waking EEG undergoes changes that can be attributed to circadian and homeostatic (i.e., sleep-wake dependent) processes. The distinct circadian variations of EEG activity in the theta band and in the high-frequency alpha band may represent electrophysiological correlates of different aspects of the circadian rhythm in arousal.

Evidence from the waking electroencephalogram that short sleepers live under higher homeostatic sleep pressure than long sleepers

We used the waking electroencephalogram to study the homeostatic sleep regulatory process in human short sleepers and long sleepers. After sleeping according to their habitual schedule, nine short sleepers (sleep duration < 6 h) and eight long sleepers (> 9 h) were recorded half-hourly during approximately 40 h of wakefulness in a constant routine protocol. Within the frequency range of 0.25-20.0 Hz, spectral power density in the 5.25-9.0 and 17.25-18.0 Hz ranges was higher in short sleepers than in long sleepers. In both groups, increasing time awake was associated with an increase of theta/low-frequency alpha activity (5.25-9.0 Hz), whose kinetics followed a saturating exponential function. The time constant did not differ between groups and was similar to the previously obtained time constant of the wake-dependent increase of slow-wave activity (0.75-4.5 Hz) in the sleep electroencephalogram. In addition, the time constant of the decrease of slow-wave activity during extended recovery sleep following the constant routine did not differ between groups. However, short sleepers showed an abiding enhancement of theta/low-frequency alpha activity during wakefulness after recovery sleep that was independent of the homeostatic process. It is concluded that, while the kinetics of the homeostatic process do not differ between the two groups, short sleepers live under and tolerate higher homeostatic sleep pressure than long sleepers. The homeostat-independent enhancement of theta/low-frequency alpha activity in the waking electroencephalogram in the short sleepers may be genetically determined or be the result of long-term adaptation to chronically short sleep.

Dynamics of slow-wave activity and spindle frequency activity in the human sleep EEG: effect of midazolam and zopiclone.

Electroencephalographic slow-wave activity (SWA; power density in the 0.75 to 4.5 Hz band) and spindle frequency activity (SFA; 11.25 to 15.0 Hz) exhibit a typical time course and a distinct mutual relationship during sleep. Because benzodiazepines (BDZ) suppress SWA and enhance SFA, we investigated the effect of two BDZ-receptor agonists on the dynamics of these EEG parameters. A single dose of midazolam (15 mg), zopiclone (7.5 mg), or placebo was administered before bedtime to healthy young men. Although the two drugs reduced SWA and enhanced SFA, their time course across and within sleep cycles as well as their mutual relationship were little affected. The results constitute further evidence that hypnotics acting as BDZ-receptor agonists do not substantially interfere with the homeostatic aspect of sleep regulation.

A role for non-rapid-eye-movement sleep homeostasis in perceptual learning.

Slow-wave activity (SWA; EEG power density in the 0.75–4.5 Hz range) in non-rapid-eye-movement (NREM) sleep is the primary marker of sleep homeostasis and thought to reflect sleep need. But it is unknown whether the generation of SWA itself serves a fundamental function. Previously, SWA has been implicated in brain plasticity and learning, yet the evidence for a causal role remains correlative. Here, we used acoustic slow-wave suppression to test whether overnight improvement in visual texture discrimination, a form of perceptual learning, directly depends on SWA during sleep. Two groups of subjects were trained on a texture discrimination task (TDT) after baseline sleep, and were tested 24 h later, after a 4 h experimental (EX) sleep episode (with or without SWA suppression), and again after a night of recovery sleep. In the suppression group, SWA during EX sleep was reduced by 30% compared with the control group, whereas total sleep time and REM sleep were not affected. Texture discrimination improved after EX sleep in the control group but not in the suppression group. Moreover, overnight improvement in TDT performance correlated with EEG power density during NREM sleep in the frequency range of SWA (maximum r = 0.75 at 0.75–1.0 Hz) over brain areas involved in TDT learning. We conclude that SWA is an important determinant of sleep-dependent gains in perceptual performance, a finding that directly implicates processes of sleep homeostasis in learning.