Effect of exposure to evening light on sleep initiation in the elderly: A longitudinal analysis for repeated measurements in home settings

Epidemiologic data have demonstrated associations of sleep-onset insomnia with a variety of diseases, including depression, dementia, diabetes and cardiovascular diseases. Sleep initiation is controlled by the suprachiasmatic nucleus of the hypothalamus and endogenous melatonin, both of which are influenced by environmental light. Exposure to evening light is hypothesized to cause circadian phase delay and melatonin suppression before bedtime, resulting in circadian misalignment and sleep-onset insomnia; however, whether exposure to evening light disturbs sleep initiation in home settings remains unclear. In this longitudinal analysis of 192 elderly individuals (mean age: 69.9 years), we measured evening light exposure and sleep-onset latency for 4 days using a wrist actigraph incorporating a light meter and an accelerometer. Mixed-effect linear regression analysis for repeated measurements was used to evaluate the effect of evening light exposure on subsequent sleep-onset latency. The median intensity of evening light exposure and the median sleep-onset latency were 27.3?lux (interquartile range, 17.9–43.4) and 17?min (interquartile range, 7–33), respectively. Univariate models showed significant associations between sleep-onset latency and age, gender, daytime physical activity, in-bed time, day length and average intensity of evening and nighttime light exposures. In a multivariate model, log-transformed average intensity of evening light exposure was significantly associated with log-transformed sleep-onset latency independent of the former potential confounding factors (regression coefficient, 0.133; 95% CI, 0.020–0.247; p?=?0.021). Day length and nighttime light exposure were also significantly associated with log-transformed sleep-onset latency (p?=?0.001 and p?<?0.001, respectively). In conclusion, exposure to evening light in home setting prolongs subsequent sleep-onset latency in the elderly.     

EEG power density during nap sleep: reflection of an hourglass measuring the duration of prior wakefulness

The relation between the duration of prior wakefulness and EEG power density during sleep in humans was assessed by means of a study of naps. The duration of prior wakefulness was varied from 2 to 20 hr by scheduling naps at 1000 hr, 1200 hr, 1400 hr, 1600 hr, 1800 hr, 2000 hr, and 0400 hr. In contrast to sleep latencies, which exhibited a minimum in the afternoon, EEG power densities in the delta and theta frequencies were a monotonic function of the duration of prior wakefulness. The data support the hypothesis that EEG power density during non-rapid eye movement sleep is only determined by the prior history of sleep and wakefulness and is not determined by clock-like mechanisms.     

Influence of the level of trait anxiety on sleep EEG of men and women

Psychophysiological tests for identifying the level of trait anxiety and polysomnology have been used in this study. Gender differences in the organization of sleep phases during the first three cycles and the spectral density of sleep EEGs for persons with high and low levels of trait anxiety have been studied.     

Effects of red ginseng extract on sleep architecture and electroencephalogram power spectra in rats

Sleep and Biological Rhythms - We evaluated the ability of the ethanol extract of red ginseng (RGE) to regulate sleep architecture. Adult rats were chronically fitted with sleep-wake recording...     

Interhemispheric EEG asymmetries during unilateral bright-light exposure and subsequent sleep in humans

We tested whether evening exposure to unilateral photic stimulation has repercussions on interhemispheric EEG asymmetries during wakefulness and later sleep. Because light exerts an alerting response in humans, which correlates with a decrease in waking EEG theta/alpha-activity and a reduction in sleep EEG delta activity, we hypothesized that EEG activity in these frequency bands show interhemispheric asymmetries after unilateral bright light (1,500 lux) exposure. A 2-h hemi-field light exposure acutely suppressed occipital EEG alpha activity in the ipsilateral hemisphere activated by light. Subjects felt more alert during bright light than dim light, an effect that was significantly more pronounced during activation of the right than the left visual cortex. During subsequent sleep, occipital EEG activity in the delta and theta range was significantly reduced after activation of the right visual cortex but not after stimulation of the left visual cortex. Furthermore, hemivisual field light exposure was able to shift the left predominance in occipital spindle EEG activity toward the stimulated hemisphere. Time course analysis revealed that this spindle shift remained significant during the first two sleep cycles. Our results reflect rather a hemispheric asymmetry in the alerting action of light than a use-dependent recovery function of sleep in response to the visual stimulation during prior waking. However, the observed shift in the spindle hemispheric dominance in the occipital cortex may still represent subtle local use-dependent recovery functions during sleep in a frequency range different from the delta range.     

Effects of mild heat exposure on sleep stages and body temperature in older men

The purpose of this study was to examine the effects of mild heat exposure on sleep stages and body temperature in older men. Ten healthy male volunteers with a mean age of 69.2 ± 1.35 years served as subjects. The experiments were carried out under two different sets of conditions: 26 °C 50% relative humidity (RH) and 32 °C 50% RH. The subjects slept from 2200 hours to 0600 hours with a cotton blanket and wearing short-sleeve pajamas and shorts on a bed covered by a sheet. Electroencephalogram, electro-occulogram and mental electromyogram recordings were made through the night. Rectal and skin temperatures were measured continuously. No significant differences were observed in sleep onset latency. In time spent in each sleep stage, wakefulness was significantly increased at 32 °C than at 26 °C. The total amount of wakefulness increased and rapid eye movement sleep (REM) decreased at 32 °C compared to 26 °C. The fall in rectal temperature was significantly suppressed and the mean skin temperature was significantly higher at 32 °C than at 26 °C. These results suggest that, for older men, even mild heat exposure during the nighttime sleep period may increase thermal load, suppress the decrease of rectal temperature, decrease REM, and increase wakefulness and whole-body sweat loss.     

Enhancement of REM sleep during extraocular light exposure in humans

This study examined the effects on sleep of light administered to an extraocular site. A 3-h photic stimulus was applied to the popliteal region during sleep in 14 human subjects. Each subject also underwent a control stimulus condition during a separate laboratory session. The proportion of rapid eye movement (REM) sleep during the 3-h light administration session increased by an average of 31% relative to the control condition. The frequency but not the duration of REM episodes was altered during light exposure, thereby shortening the REM/non-REM (NREM) cycle length. No other sleep stages were significantly affected during light administration nor was sleep architecture altered after the light-exposure interval. These results confirm that extraocular light is transduced into a signal that is received and processed by the human central nervous system. In addition, they expand to a novel sensory modality previous findings that REM sleep can be enhanced by sensory stimulation.     

Effect of evening exposure to dim or bright light on the digestion of carbohydrate in the supper meal

In a previous study we found that daytime exposure to bright as compared to dim light exerted a beneficial effect on the digestion of the evening meal. This finding prompted us to examine whether the digestion of the evening meal is also affected by evening light intensity. Subjects lived in light of 200 lux during the daytime (08:00-17:00 h) and took their evening meal at 17:00 h under 20 lux (evening dim-light condition: 17:00-02:00 h) or 2000 lux (evening bright-light condition: 17:00-02:00 h) until retiring at 02:00 h. Assessment of carbohydrate digestion of the evening meal was accomplished by a breath hydrogen test that is indicative of the malabsorption of dietary carbohydrate. Hydrogen excretion in the breath in the evening under the dim-light condition was significantly less than under the bright-light condition (p < 0.05). This finding is the opposite to that obtained in previous experiments in which subjects were exposed to the different intensities of light during the daytime, and indicates that the exposure to dim light in the evening exerts a better effect on carbohydrate digestion in the evening meal than does the exposure to bright light.     

Independent associations of exposure to evening light and nocturnal urinary melatonin excretion with diabetes in the elderly

Circadian misalignment between internal and environmental rhythms dysregulates glucose homeostasis because of disruption of the biological clock, and increases risk of diabetes. Although exposure to evening light and decreased melatonin secretion are both associated with the circadian misalignment, it remains unclear whether they are associated with diabetes. In this cross-sectional study on 513 elderly individuals (mean age, 72.7 years), we measured ambulatory light intensity during the 4?h prior to bedtime at 1-min intervals during two consecutive days and overnight urinary 6-sulfatoxymelatonin excretion (UME) along with glucose metabolism. The median average intensity of evening light exposure and UME were 25.4?lux (interquartile range 17.5–37.6) and 6.6?μg (interquartile range 3.9–9.7), respectively. Both log-transformed average intensity of evening light exposure and log-transformed UME were significantly associated with diabetes in a multivariate logistic regression model adjusted for covariates, including gender, body mass index, duration in bed, and night-time light exposure [adjusted odds ratio (OR), 1.72; 95% confidence interval (CI), 1.12–2.64; p?=?0.01; and adjusted OR, 0.66; 95% CI, 0.44–0.97; p?=?0.04; respectively]. An increase in evening light exposure from 17.5 to 37.6?lux (25–75th percentiles) was associated with a 51.2% (95% CI, 8.2–111.4%) increase in prevalent diabetes, and an increase in UME from 3.9 to 9.7?μg (25–75th percentiles) was associated with a 32.0% (95% CI, 1.9–52.8%) decrease in prevalent diabetes. In conclusion, this study in elderly individuals demonstrated that evening light exposure in home settings and UME were significantly and independently associated with diabetes.     

The relationship between short-term memory capacity and EEG power spectral density

Multiplying memory span by mental speed, we obtain the information entropy of short-term memory capacity, which is rate-limiting for cognitive functions and corresponds with EEG power spectral density. The number of EEG harmonics (n = 1, 2,, 9) is identical with memory span, and the eigenvalues of the EEG impulse response are represented by the zero-crossings up to the convolved fundamental, the P300. In analogy to quantum mechanics the brain seems to be an ideal detector simply measuring the energy of wave forms. No matter what the stimulus is and how the brain behaves, the metric of signal and memory can always be understood as a superposition of n states of different energy and their eigenvalues.     

Chronic exposure to ELF magnetic fields during night sleep with electric sheet: effects on diurnal melatonin rhythms in men

The possible effects of repeated night-time exposure to an extremely low frequency magnetic field (ELF-MF) on melatonin were investigated in nine healthy male subjects aged 23-37 yr. The 16-week experiment consisted of 3 weeks of pre-exposure, 11 weeks of night-time exposure to MF generated from a nonheated electric sheet (ES), and 2 weeks of post-exposure recovery observation. The average MF intensity (rms, mainly 50 Hz AC) on the surface of the sheet was 0.7 microT at the head, 8.3 microT at the waist, and 3.5 microT at the feet of the subject. For each of the urine samples collected 5 times a day on scheduled sampling days, the urinary excretion rate (ng/h) of melatonin was determined, and 24 h rhythms were extracted for each subject and each experimental period (pre-exposure, first half and latter half exposure, and post-exposure periods) by the method of complex cosine curve fitting. Although estimates of the peak height, acrophase, and total daily amount of melatonin were characterized by significant variations among individual subjects, they did not reveal any statistically significant difference between exposure periods and nonexposure periods. Thus, the present study indicates that any profound effect of the MF originating from an ES on nocturnal melatonin production and its circadian rhythm is unlikely.     

Effects of exercise with or without light exposure on sleep quality and hormone reponses

[Purpose]

The objectives of the present study were to determine the effect of sun exposure and aerobic exercise on quality of sleep and investigate sleep-related hormonal responses in college-aged males.

[Methods]

In this study, the cross-over design was utilized. The subjects (N = 10) without any physical problems or sleep disorders participated in the experimental performed 4 protocols in only sun exposure (for 30 minutes, EG1) protocol, only aerobic exercise (walking and jogging for 30 minutes, EG2) protocol, aerobic exercise with sun exposure (EG3) protocol, and control (no exercise and no sun exposure, EG4) protocol. Each protocol was 5 times per week with one-week break (wash-out period) between protocols to prevent the effects of the previous protocol. Total test period was should be 7 weeks (one week of protocol and one week of break). Before and after each aerobic exercise session, the subjects completed stretching to warm up for 5 to 10 minutes. Surveys consisting of (bedtime, wake-up time, sleep onset latency, and (Pittsburgh Sleep Quality Index (PSQI) were obtained before the test and after each protocol. After each protocol, the following sleep-related hormonal responses were measured: blood concentrations of melatonin, cortisol, epinephrine, and norepinephrine. One-way ANOVA was used to determine differences between protocols. Statistical significance was set at p < 0.05.

[Results]

Bedtime of EG4 was significantly later than that of the EG1 or EG3. Wake-up time in the EG4 was significantly later than that of the EG1 or the EG3. Sleep onset latency in the EG4 was longer than that of the EG3. The quality of sleep in the EG4 was lower than that of the EG3. Sleep cycle in the EG4 was significantly shorter than that of the EG1. Blood melatonin concentrations of the EG3 was significantly higher than that of the EG4. There were no significant differences in blood concentrations of cortisol, epinephrine, or norepinephrine among protocols, with the order from the lowest to the highest values of EG1 < EG2 < EG3 < EG4.

[Conclusion]

The present data found that EG1 and EG3 showed positive sleep-related hormonal responses, sleep habits, and quality of sleep, indicating that sun exposure or exercise with sun exposure may improve the physical status and quality of life.     

Adenosine deaminase polymorphism affects sleep EEG spectral power in a large epidemiological sample

Slow wave oscillations in the electroencephalogram (EEG) during sleep may reflect both sleep need and intensity, which are implied in homeostatic regulation. Adenosine is strongly implicated in sleep homeostasis, and a single nucleotide polymorphism in the adenosine deaminase gene (ADA G22A) has been associated with deeper and more efficient sleep. The present study verified the association between the ADA G22A polymorphism and changes in sleep EEG spectral power (from C3-A2, C4-A1, O1-A2, and O2-A1 derivations) in the Epidemiologic Sleep Study (EPISONO) sample from São Paulo, Brazil. Eight-hundred individuals were subjected to full-night polysomnography and ADA G22A genotyping. Spectral analysis of the EEG was carried out in all individuals using fast Fourier transformation of the signals from each EEG electrode. The genotype groups were compared in the whole sample and in a subsample of 120 individuals matched according to ADA genotype for age, gender, body mass index, caffeine intake status, presence of sleep disturbance, and sleep-disturbing medication. When compared with homozygous GG genotype carriers, A allele carriers showed higher delta spectral power in Stage 1 and Stages 3+4 of sleep, and increased theta spectral power in Stages 1, 2 and REM sleep. These changes were seen both in the whole sample and in the matched subset. The higher EEG spectral power indicates that the sleep of individuals carrying the A allele may be more intense. Therefore, this polymorphism may be an important source of variation in sleep homeostasis in humans, through modulation of specific components of the sleep EEG.     

The impact of experimental instruction on changes in EEG power during verbal creative thinking in men and women

Features of EEG pattern during verbal creative thinking depending on experimental instruction were studied in men and women. Spectral power density was analyzed in six frequency bands (4-30 Hz). Performance of a creative task produced an increase in the power of theta (4-6 Hz) and beta2 (20-40 Hz) components and decrease in the power of alpha (8-13 Hz) and betal (13-20 Hz). Changes in the alpha and betal bands were observed, predominantly, in the posterior areas, whereas power of the thetal and beta2 bands increased in the anterior areas. Independently of instruction, women demonstrated greater synchronization in the theta1 band than men, whereas in men the desynchronization in the alpha2 band (10-13 Hz) was more pronounced. When the subjects were instructed to create original sentences, a widespread decrease in the EEG power was observed in the band of 8-30 Hz as compared to instruction "to create sentences". Thus, the instruction-related changes in EEG power were not gender-specific. They may reflect neural activity mediating selective attention.     

The link between cardiac autonomic activity and sleep delta power is altered in men with sleep apnea-hypopnea syndrome

We hypothesize that sleep apnea-hypopnea alters interaction between cardiac vagal modulation and sleep delta EEG. Sleep apnea-hypopnea syndrome (SAHS) is related to cardiovascular complications in men. SAHS patients show higher sympathetic activity than normal subjects. In healthy men, non-rapid eye movement (NREM) sleep is associated with cardiac vagal influence, whereas rapid eye movement (REM) sleep is linked to cardiac sympathetic activity. Interaction between cardiac autonomic modulation and delta sleep EEG is not altered across a life span nor is the delay between appearances of modifications in both signals. Healthy controls, moderate SAHS, and severe SAHS patients were compared across the first three NREM-REM cycles. Spectral analysis was applied to ECG and EEG signals. High frequency (HF) and low frequency (LF) of heart rate variability (HRV), ratio of LF/HF, and normalized (nu) delta power were obtained. A coherency analysis between HF(nu) and delta was performed, as well as a correlation analysis between obstructive apnea index (AI) or hypopnea index (HI) and gain, coherence, or phase shift. HRV components were similar between groups. In each group, HF(nu) was larger during NREM, while LF(nu) predominated across REM and wake stages. Coherence and gain between HF(nu) and delta decreased from controls to severe SAHS patients. In SAHS patients, the delay between modifications in HF(nu) and delta did not differ from zero. AI and HI correlated negatively with coherence, while HI correlated negatively with gain only. Apneas-hypopneas affect the link between cardiac sympathetic and vagal modulation and delta EEG demonstrated by the loss of cardiac autonomic activity fluctuations across shifts in sleep stages. Obstructive apneas and hypopneas alter the interaction between both signals differently.     

The impact of sleep timing and bright light exposure on attentional impairment during night work

The prevalence of hazardous incidents induced by attentional impairment during night work and ensuing commute times is attributable to circadian misalignment and increased sleep pressure. In a 10-day shift work simulation protocol (4 day shifts and 3 night shifts), the efficacies of 2 countermeasures against nighttime (2300 to 0700 h) attentional impairment were compared: (1) Morning Sleep (0800 to 1600 h; n = 18) in conjunction with a phase-delaying light exposure (2300 to 0300 h), and (2) Evening Sleep (1400 to 2200 h; n = 17) in conjunction with a phase-advancing light exposure (0300 to 0700 h). Analysis of the dim light salivary melatonin onset indicated a modest but significant circadian realignment in both sleep groups (evening sleep: 2.27 +/- 0.6 h phase advance, p < 0.01; morning sleep: 4.98 +/- 0.43 h phase delay, p < 0.01). Daytime sleep efficiency and total sleep time did not differ between them or from their respective baseline sleep (2200 to 0600 h; p > 0.05). However, on the final night shift, the evening sleep subjects had 37% fewer episodes of attentional impairment (long response times: 22 +/- 4 vs. 35 +/- 4; p = 0.02) and quicker responses (p < 0.01) on the Psychomotor Vigilance Task than their morning sleep counterparts. Their response speed recovered to near daytime levels (p = 0.47), whereas those of the morning sleep subjects continued to be slower than their daytime levels (p = 0.008). It is concluded that partial circadian realignment to night work in combination with reduced homeostatic pressure contributed to the greater efficacy of a schedule of Evening Sleep with a phase-advancing light exposure as a countermeasure against attentional impairment, over a schedule of Morning Sleep with a phase-delaying light exposure. These results have important implications for managing patients with shift work disorder.     

Psychophysiological effects of a brief nocturnal light exposure

This study compared the effects of a brief pulse (60-minute) of three full spectrum light intensities (1000, 500 and 30 lux) and two green light intensities (1000 and 500 lux) administered between 0200 and 0300 hrs. Ten participants were involved in this repeated measures study. Each participant experienced one condition every week for five weekends. Sessions began at 1800 hours and ended at 0600 hours the following day. Outside of the 60-minute exposure period, each session was spent in 30 lux white light. Oral temperature, salivary melatonin, cognitive performance and subjective mood were sampled throughout the sessions. Analysis revealed that all of the experimental light conditions significantly reduced salivary melatonin concentrations immediately following the pulse. This effect was not maintained beyond the duration of the light pulse. There was no significant effect on oral temperature. There were also no significant effects on cognitive performance and subjective mood, though some positive trends were observed. These results argue that brief, moderate intensity, pulses of either green or full spectrum light are sufficient to suppress the normal nocturnal rise in melatonin. However, the level of suppression obtained does not translate into significant improvement in cognitive performance or subjective mood.