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Domien G M Beersma

Publications and source records attributed to Domien G M Beersma.

15 recordsLinked to original sources

Circadian control of the sleep-wake cycle.

It is beyond doubt that the timing of sleep is under control of the circadian pacemaker. Humans are a diurnal species; they sleep mostly at night, and they do so at approximately 24-h intervals. If they do not adhere to this general pattern, for instance when working night shifts or when travelling across time zones, they experience the stubborn influence of their circadian clock. In recent years much has been discovered about the organisation of the circadian clock. New photoreceptor cells in the retina have been found to influence the input to the clock, and much of the molecular machinery of the clock has been unravelled. It is now known that the circadian rhythm of sleep and wakefulness is only loosely coupled to the circadian rhythm of the pacemaker. New theories have been proposed for the functions of sleep and the sites at which those functions are executed. In spite of this rapid increase in knowledge of the circadian clock and of sleep regulatory processes, much remains to be discovered concerning the precise interaction between the biological clock and sleep timing. This is particularly unfortunate in view of the 24-h demands of our society for 7 days a week. Too little is known about the negative consequences of the societal pressures on well-being and performance.

Animals↗

Time-of-day-dependent effects of bright light exposure on human psychophysiology: comparison of daytime and nighttime exposure.

Bright light can influence human psychophysiology instantaneously by inducing endocrine (suppression of melatonin, increasing cortisol levels), other physiological changes (enhancement of core body temperature), and psychological changes (reduction of sleepiness, increase of alertness). Its broad range of action is reflected in the wide field of applications, ranging from optimizing a work environment to treating depressed patients. For optimally applying bright light and understanding its mechanism, it is crucial to know whether its effects depend on the time of day. In this paper, we report the effects of bright light given at two different times of day on psychological and physiological parameters. Twenty-four subjects participated in two experiments (n = 12 each). All subjects were nonsmoking, healthy young males (18-30 yr). In both experiments, subjects were exposed to either bright light (5,000 lux) or dim light <10 lux (control condition) either between 12:00 P.M. and 4:00 P.M. (experiment A) or between midnight and 4:00 A.M. (experiment B). Hourly measurements included salivary cortisol concentrations, electrocardiogram, sleepiness (Karolinska Sleepiness Scale), fatigue, and energy ratings (Visual Analog Scale). Core body temperature was measured continuously throughout the experiments. Bright light had a time-dependent effect on heart rate and core body temperature; i.e., bright light exposure at night, but not in daytime, increased heart rate and enhanced core body temperature. It had no significant effect at all on cortisol. The effect of bright light on the psychological variables was time independent, since nighttime and daytime bright light reduced sleepiness and fatigue significantly and similarly.

Adult↗

Comparison of the Munich Chronotype Questionnaire with the Horne-Ostberg's Morningness-Eveningness Score.

We report on results from an Internet survey of sleeping habits in a Dutch population using the Munich Chronotype Questionnaire (MCTQ), supplemented with the Horne-Ostberg Morningness-Eveningness Questionnaire (MEQ). The MCTQ was completed by 5,055 responders, of which 2,481 also completed the MEQ. MEQ score correlated well with the MCTQ assessment of time of mid-sleep on free days (MSF; r = - 0.73) and on workdays (MSW; r = - 0.61). MEQ was more strongly correlated with MSF (50% of sleep time) than with sleep onset (0%), rise time (100%), or with any other percentile (10 to 40, 60% to 90%) of sleep on free days. The study shows that chronotype (based on MSF as measured by the MCTQ) strongly correlates with morningness-eveningness (as measured by the MEQ). However, the MCTQ collects additional detailed information on sleep-wake behavior under natural conditions.

Adolescent↗

Weak relationships between suppression of melatonin and suppression of sleepiness/fatigue in response to light exposure.

In this paper we examine the relationship between melatonin suppression and reduction of sleepiness through light by comparing three different data sets. In total 36 subjects participated in three studies and received 4 h of bright light either from midnight till 4:00 hours (experiments A and B) or from noon till 16:00 hours (experiment C). In experiment A (night-time light, partial illumination of the retina, pupil dilated) subjects were exposed to either 100 lx of ocular light on the temporal, 100 lx on the nasal part of the retina, or <10 lx of dim light on the whole retina. In experiments B (night-time light, whole retina, pupil not dilated) and C (daytime light, whole retina, pupil not dilated) subjects were exposed either to bright (5000 lx) or to dim light (<10 lx). Subjective sleepiness/fatigue and melatonin concentrations in saliva were assessed hourly in all three experiments. For experiment A, a significant suppression of melatonin due to nasal and temporal illumination of the retina was found, that was not accompanied by a detectable reduction of subjective sleepiness/fatigue. For experiment B we found a suppression of melatonin that was paralleled with a significant reduction in subjective sleepiness, but not in fatigue. During experiment C we found no melatonin suppression but a reduction of subjective sleepiness, but also no effect on fatigue. From these data we conclude that the effects of light on sleepiness/fatigue are not mediated by melatonin and that the influence of endogenous melatonin concentration on sleepiness/fatigue is restricted.

Adult↗

Nasal versus temporal illumination of the human retina: effects on core body temperature, melatonin, and circadian phase.

The mammalian retina contains both visual and circadian photoreceptors. In humans, nocturnal stimulation of the latter receptors leads to melatonin suppression, which might cause reduced nighttime sleepiness. Melatonin suppression is maximal when the nasal part of the retina is illuminated. Whether circadian phase shifting in humans is due to the same photoreceptors is not known. The authors explore whether phase shifts and melatonin suppression depend on the same retinal area. Twelve healthy subjects participated in a within-subjects design and received all of 3 light conditions--1) 10 lux of dim light on the whole retina, 2) 100 lux of ocular light on the nasal part of the retina, and 3) 100 lux of ocular light on the temporal part of the retina--on separate nights in random order. In all 3 conditions, pupils were dilated before and during light exposure. The protocol consisted of an adaptation night followed by a 23-h period of sustained wakefulness, during which a 4-h light pulse was presented at a time when maximal phase delays were expected. Nasal illumination resulted in an immediate suppression of melatonin but had no effect on subjective sleepiness or core body temperature (CBT). Nasal illumination delayed the subsequent melatonin rhythm by 78 min, which is significantly (p= 0.016) more than the delay drift in the dim-light condition (38 min), but had no detectable phase-shifting effect on the CBT rhythm. Temporal illumination suppressed melatonin less than the nasal illumination and had no effect on subjective sleepiness and CBT. Temporal illumination delayed neither the melatonin rhythm nor the CBT rhythm. The data show that the suppression of melatonin does not necessarily result in a reduction of subjective sleepiness and an elevation ofCBT. In addition, 100 lux of bright white light is strong enough to affect the photoreceptors responsible for the suppression of melatonin but not strong enough to have a significant effect on sleepiness and CBT. This may be due to the larger variability of the latter variables.

Adult↗

Why and how do we model circadian rhythms?

In our attempts to understand the circadian system, we unavoidably rely on abstractions. Instead of describing the behavior of the circadian system in all its complexity, we try to derive basic features from which we form a global concept on how the system works. Such a basic concept is a model of reality. The author discusses why it is advantageous or even necessary to transform conceptual models into mathematical formulations. As examples to demonstrate those advantages, the author reviews 4 types of mathematical models: negative feedback models thought to operate within pacemaker cells, models on coupling between pacemaker cells to generate pacemaker output, oscillator models describing the behavior of the composite circadian pacemaker, and models describing how the circadian pacemaker influences behavior.

Animals↗

The reliability and validity of the Seasonal Pattern Assessment Questionnaire: a comparison between patient groups.

BACKGROUND: The Seasonal Pattern Assessment Questionnaire (SPAQ) is a frequently used screening instrument in the research on Seasonal Affective Disorder (SAD). Nevertheless, studies on its reliability and validity are relatively scarce. In the present study the reliability and the contrast validity of the SPAQ are investigated. METHODS: SAD patients, selected by means of a clinical interview, non-seasonal depressed out-patients, non-depressed out-patients, and a control group, are contrasted to estimate the discriminating power of the SPAQ. Also, the reliability and factor structure of the seasonality and the climate subscales are investigated. To study food intake the Seasonal Food Preference Questionnaire (SFPQ) was developed. RESULTS: The SAD criterion of the SPAQ shows good specificity (94%), but a low sensitivity (44%). Discriminant analysis shows sufficient ability to classify subjects (81% correctly classified). The Global Seasonality Scale has a good internal consistency. It consists of two factors, a psychological factor and a food factor. The SFPQ is sensitive for carbohydrate intake by SAD patients. LIMITATIONS: Most SAD patients had received treatment and completed the SPAQ while they were not depressed, which may have influenced the sensitivity. CONCLUSIONS: The SPAQ is not sensitive enough to be considered a diagnostic instrument for SAD. Nevertheless, it is accurate enough to be used as a screenings instrument. The only false positives were found in the depressive group. The accuracy of prevalence Figs. can be improved by completion of the SPAQ in the summer months, combined with the completion of a depression scale.

Adult↗

Subjective sleepiness correlates negatively with global alpha (8-12 Hz) and positively with central frontal theta (4-8 Hz) frequencies in the human resting awake electroencephalogram.

Subjective sleepiness is part of the system controlling the decision to go to sleep in humans. Extended periods of waking lead to increased sleepiness, as well as to changes in cortical electroencephalogram (EEG) during waking. We investigated the association of sleepiness and awake EEG spectra during 40 h of wakefulness using multi-electrode EEG recordings for full coverage of the scalp. We found: (1). strong negative correlations of alpha (8-12 Hz) power with subjective sleepiness at all scalp locations, suggesting a negative association between sleepiness and general cortical activation; and (2). positive correlations of theta (4-8 Hz) power with subjective sleepiness with a focus on frontal locations, suggesting additional location specific associations between sleepiness and cortical activation. These findings support the notion that sleepiness is directly represented in the awake EEG.

Adult↗

Mood regulation in seasonal affective disorder patients and healthy controls studied in forced desynchrony.

In healthy subjects, both the duration of wakefulness and the circadian pacemaker have been demonstrated to be involved in the regulation of mood. Some features of affective disorders suggest that these two factors also play a role in the dysregulation of mood. In particular, disturbances of the circadian pacemaker have been proposed to be a pathogenetic factor in Seasonal Affective Disorder, winter type (SAD). This report presents a test of this proposition. To this end seven SAD patients and matched controls were subjected to a 120-h forced desynchrony protocol, in which they were exposed to six 20-h days. This protocol enables us to discriminate the extent to which the course of mood is determined by the imposed 20-h sleep-wake cycle from the influence of the circadian pacemaker on that course. Patients participated during a depressive episode, after recovery upon light therapy and in summer. Controls were studied in winter and in summer. Between SAD patients and controls no significant differences were observed in the period length nor in the timing of the endogenous circadian temperature minimum. In both groups, sleep-wake cycle- and pacemaker-related components were observed in the variations of mood, which were not significantly different between conditions.

Adult↗

Acute and phase-shifting effects of ocular and extraocular light in human circadian physiology.

Light can influence physiology and performance of humans in two distinct ways. It can acutely change the level of physiological and behavioral parameters, and it can induce a phase shift in the circadian oscillators underlying variations in these levels. Until recently, both effects were thought to require retinal light perception. This view was challenged by Campbell and Murphy, who showed significant phase shifts in core body temperature and melatonin using an extraocular stimulus. Their study employed popliteal skin illumination and exclusively considered phase-shifting effects. In this paper, the authors explore both acute effects and phase-shifting effects of ocular as well as extraocular light. Twelve healthy males participated in a within-subject design and received all of three light conditions--(1) dim ocular light/no light to the knee, (2) dim ocular light/bright extraocular light to the knee, and (3) bright ocular light/no light to the knee--on separate nights in random order. The protocol consisted of an adaptation night followed by a 26-h period of sustained wakefulness, during which a 4-h light pulse was presented at a time when maximal phase delays were expected. The authors found neither immediate nor phase-shifting effects of extraocular light exposure on melatonin, core body temperature (CBT), or sleepiness. Ocular bright-light exposure reduced the nocturnal circadian drop in CBT, suppressed melatonin, and reduced sleepiness significantly. In addition, the 4-h ocular light pulse delayed the CBT rhythm by -55 min compared to the drift of the CBT rhythm in dim light. The melatonin rhythm shifted by -113 min, which differed significantly from the drift in the melatonin rhythm in the dim-light condition (-26 min). The failure to find immediate or phase-shifting effects in response to extraocular light in a within-subjects design in which effects of ocular bright light are confirmed strengthens the doubts raised by other labs of the impact of extraocular light on the human circadian system.

Adolescent↗

Lithium concentrations in plasma of lithium-treated psychiatric patients in the Netherlands: commentary on Cusin et al.

Seasonal variations in 68 psychiatric patients receiving prophylactic lithium treatment in the Netherlands between 1974 and 1994 were analyzed and compared with findings from Italy. Although lithium doses remained stable, there was a significant change in plasma levels of lithium, with values in spring and summer tending to exceed those in autumn and winter. These findings are similar to those reported in Italy, although the maximal seasonal change was approximately 5% in the Netherlands compared with approximately 10% in Italy. The difference could reflect the hotter summer climate in Italy, associated with increased perspiration. Future studies should measure perspiration levels directly.

Adult↗

Is the nonREM-REM sleep cycle reset by forced awakenings from REM sleep?

In selective REM sleep deprivation (SRSD), the occurrence of stage REM is repeatedly interrupted by short awakenings. Typically, the interventions aggregate in clusters resembling the REM episodes in undisturbed sleep. This salient phenomenon can easily be explained if the nonREM-REM sleep process is continued during the periods of forced wakefulness. However, earlier studies have alternatively suggested that awakenings from sleep might rather discontinue and reset the ultradian process. Theoretically, the two explanations predict a different distribution of REM episode duration. We evaluated 117 SRSD treatment nights recorded from 14 depressive inpatients receiving low dosages of Trimipramine. The alarms were triggered by an automatic mechanism for the detection of REM sleep and had to be canceled by the subjects themselves. The REM episodes were determined as in undisturbed sleep-they had to include the remaining REM activity and were separated by 30 min without REM epochs. The frequency histogram of REM episodes declined exponentially with episode duration for each of the first four sleep cycles. The duration of nonREM intervals revealed bimodal distributions. These results were found consistent with the model assuming a reset of the ultradian cycle upon awakening. Whether REM or nonREM activity is resumed on return to sleep can be modeled by a random decision whereby the probability for REM sleep might depend on the momentary REM pressure.

Activity Cycles↗

Sustained mental workload does not affect subsequent sleep intensity.

Mental activity is a neglected factor in sleep research. The few investigations on sleep that manipulate prior mental activity are inconclusive with respect to the possible effects of mental activity on recovery. In the present study, the effects of two levels of mental activity on subsequent sleep were studied. Thirteen male subjects (range 18-28 years) participated in one lightly and two heavily mentally strenuous conditions in a counterbalanced order. Light mental activity included 8 h of relaxed video watching. The second condition consisted of performing computer tasks involving sustained attention, memory, logical thinking and calculations for eight consecutive hours. In the third condition, the same heavy mental workload was interspersed with breaks. Subjectively, the subjects rated the condition with heavy mental activity (without breaks) as mentally more strenuous than the condition with light mental activity. Subjects were significantly less awake shortly after sleep onset in the heavy-workload condition than in the light-workload condition. There were no differences between the conditions in any of the other visually scored sleep variables. The total amount of slow wave activity (SWA) and its discharge during the night was not affected by the level of mental activity or by the presence of breaks. These findings fail to support the proposition that SWA reflects a need for sleep that accumulates at a rate depending on mental activity during prior wakefulness.

Adolescent↗

Sleep in seasonal affective disorder patients in forced desynchrony: an explorative study.

The majority of winter-type seasonal affective disorder (SAD) patients complain of hypersomnia and daytime drowsiness. As human sleep is regulated by the interaction of circadian, ultradian and homeostatic processes, sleep disturbances may be caused by either one of these factors. The present study focuses on homeostatic and ultradian aspects of sleep regulation in SAD. Sleep was recorded polysomnographically in seven SAD patients and matched controls subjected to a 120-h forced desynchrony protocol. In time isolation, subjects were exposed to six 20-h days, each comprising a 6.5-h period for sleep. Patients participated while being depressed, while remitted after light therapy and in summer. Controls were studied in winter and in summer. In each condition, the data of each subject were averaged across all recordings. Thus, the influence of the effects of the circadian pacemaker on sleep was excluded mathematically. The comparison of patients with controls and with themselves in the various conditions revealed no abnormalities in homeostatic parameters: sleep stage variables, relative power spectra and time courses of power in various frequency bands across the first three non-rapid eye movement-rapid eye movement (NREM-REM) cycles showed no differences. The data suggest that homeostatic processes are not involved in the disturbance of sleep in SAD.

Adult↗

A forced desynchrony study of circadian pacemaker characteristics in seasonal affective disorder.

The circadian pacemaker is an endogenous clock that regulates oscillations in most physiological and psychological processes with a near 24-h period. In many species, this pacemaker triggers seasonal changes in behavior. The seasonality of symptoms and the efficacy of light therapy suggest involvement of the circadian pacemaker in seasonal affective disorder (SAD), winter type. In this study, circadian pacemaker characteristics of SAD patients were compared with those of controls. Seven SAD patients and matched controls were subjected to a 120-h forced desynchrony protocol, in which core body temperature and melatonin secretion profiles were measured for the characterization of circadian pacemaker parameters. During this protocol, which enables the study of unmasked circadian pacemaker characteristics, subjects were exposed to six 20-h days in time isolation. Patients participated twice in winter (while depressed and while remitted after light therapy) and once in summer. Controls participated once in winter and once in summer. Between the SAD patients and controls, no significant differences were observed in the melatonin-derived period or in the phase of the endogenous circadian temperature rhythm. The amplitude of this rhythm was significantly smaller in depressed and remitted SAD patients than in controls. No abnormalities of the circadian pacemaker were observed in SAD patients. A disturbance in thermoregulatory processes might explain the smaller circadian temperature amplitude in SAD patients during winter.

Adult↗