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Alcohol and Sleep Review: Sound Statistics and Valid Conclusions
... An acute prebedtime dose of alcohol in non-alcohol-dependent individuals deteriorates REM sleep (97,98). There is debate about its effect: several studies have observed longer latency in REM sleep and decreased REM sleep only in the first half of the night, while other studies find this effect across the whole night (99)(100)(101). The link between alcohol at bedtime in non-alcoholic people and DRF does not seem to have been studied. Alcohol-dependent subjects report more negative dreams than those who are non-alcoholdependent (102), with an increase in dream emotional negativity during the first weeks of abstinence (103). ...
In order to ensure robust relationships between the dependent and independent variables in clinical dream/nightmare studies, the major factors which influence the frequency of reported dreams must be controlled. This article sets out methodological recommendations to both researchers seeking to ensure the equivalence of experimental groups of participants in group-matching designs, and to clinicians who wish to check that any change in frequency of reported nightmares over the course of a psychological or a pharmacological intervention is not caused by factors other than the experimental treatment itself. The main factors influencing the frequency of dream recall are presented: demographic variables, psychological characteristics, pathological dimensions, and substance consumption. A series of questionnaires is proposed for easily measuring these control variables.
... In particular, the relationship between seizures, sleep and alcohol is a complicated and much-debated issue (Ebrahim et al., 2015(Ebrahim et al., , 2013Pressman et al., 2015). Seizures and sleep disturbances are common during phases of active drinking and abstinence among individuals with alcohol-use disorders, while the situation is different after occasional alcohol intake because alcohol is a frequently used tranquilizer and sleep inducer with probable effects upon the seizure threshold in patients and susceptible individuals. ...
Purpose:
The relationship between sleep and seizures is intricate. The aim of this study was to assess whether sleep loss is an independent seizure precipitant in a clinical setting.
Methods:
In this prospective, observational cross-over study, 179 consecutive hospital admissions for epileptic seizures were included. A semi-structured interview regarding several seizure precipitants was performed. The sleep pattern prior to the seizure, as well as alcohol, caffeine and drug use, were recorded. The interview was repeated by telephone covering the same weekday at a time when there had been no recent seizure. The Hospital Anxiety and Depression Scale (HADS) and a visual analogue scale for perceived stress were applied at admission. Student's t-test, Fisher exact test and ANOVA were used for statistical analyses.
Results:
Complete data for analysis were retrieved in 144 patients. The sleep-time during the 24h prior to the seizure was lower (7.3h) compared to follow-up (8.3h; p<0.0005). Caffeine consumption and use of relevant non antiepileptic drugs (AED) were not different. HADS and stress scores at admission did not correlate with sleep-time difference. In ANOVA, controlled for alcohol consumption and AED use, the sleep-time difference remained significant (p=0.008). The interaction with alcohol intake was high, but the sleep-time difference remained highly significant also for the non- and low-consumption (≤2 units per day) subgroup (n=121, 7.50h vs 8.42h, p=0.001).
Conclusion:
Epileptic seizures are often precipitated by a combination of various clinical factors, but sleep loss stands out as an independent seizure trigger.
To assess the effect of 3 oz of 80-proof alcohol on the frequency and severity of obstructive sleep apnea (OSA), we studied six OSA patients and six healthy subjects on 2 nights. During the 1st night, when no alcohol was given, five patients demonstrated mild and one severe OSA episodes associated with a decline in arterial oxygen saturation to at least 92% (hypoxic event). On the 2nd night after ingesting 3 oz of alcohol just prior to bedtime, all the patients demonstrated a significant increase in the number and/or severity of hypoxic events compared with the no-alcohol night. Furthermore, the most severe hypoxic events occurred within 80 to 160 min after sleep onset, a significantly shorter latency after sleep onset than on the no-alcohol night. In contrast, the healthy subjects had no incidents of hypoxic events or breathing abnormalities during sleep after ingesting 0.8 gm/kg of alcohol. Possible mechanisms for these results are discussed. An OSA provocation test using alcohol is proposed during a 2nd night of evaluation for patients with mild to moderate or intermittent OSA conditions, but not for patients demonstrating severe hypoxic events or with alcohol intolerance. The alcohol provocation test would serve to determine the influence of alcohol on the frequency and severity of hypoxic events, providing the patient with a measure of the adverse effects of social drinking on their condition.
The acute and chronic effects of alcohol and alcohol withdrawal on sleep patterns and plasma GH and cortisol fluctuations occurring during sleep were studied. Five healthy men, aged 21-26 yr, consumed a placebo drink for 3 baseline nights, alcohol (0.8 g/kg) for 9 nights, and a placebo drink on final withdrawal night. All-night polygraphic sleep recordings and blood samples (every 20 min with a venous catheter) were collected for 1 placebo, 1 acute alcohol, 1 chronic alcohol (night 9), and 1 alcohol withdrawal night. Acute and chronic alcohol consumption reduced rapid eye movement sleep nonsignificantly during the first half of the night, whereas slow wave sleep (stages 3 and 4) was increased significantly after acute alcohol, returning to baseline values on the chronic alcohol night. On the withdrawal night, rapid eye movement sleep and slow wave sleep were not significantly different from placebo sleep. Alcohol significantly suppressed plasma GH values (70-75%) on acute and chronic nights. All measures of GH, including total integral for bedtime hours, mean hourly rate, and peak level, were similarly affected by alcohol. GH returned to placebo values on the withdrawal night. Measures of nighttime plasma cortisol were not significantly altered by alcohol or alcohol withdrawal at this dose level.
Introduction And I see men become mad and demented from no manifest cause and at the same time doing many things out of place, and I have known many persons in sleep groaning and crying out, some in a state of suffocation, some jumping up and fleeing out of doors, and deprived of their reason till they awaken and afterwards becoming well and rational as before, although they be pale and weak. The parasomnias most frequently associated with forensic consequences are the disorders of arousal – confusional arousals, sleepwalking/sleep terrors – and their variant sexsomnia, parasomnia due to drug or substance and REM sleep behavior disorder (RBD). Most of these come to the attention of the courts because of a violent act resulting in injury, disability or death for which the accused claims amnesia. The violence may take the form of verbal, physical or sexual acts, or alternatively, the individual may be charged with acts of endangerment, e.g. dangerous driving, reckless endangerment, driving under the influence of drugs and/or alcohol, etc.Violent behaviors arising from the sleep period are reported by about 2% of the adult population. Chapter 2 provides a thorough review of the epidemiology of parasomnias. The first systematic literature review on sleepwalking violence was published in 1974 by Alexander Bonkalo, an eminent forensic psychiatrist who reviewed 50 historical reports of adult sleepwalking violence, 20 cases of murder and 30 related to other criminal acts.
N A RECENT publication, Ebrahim and colleagues state in their abstract that they have provided an assessment of “all known scientific studies of the effects of alcohol on the nocturnal sleep of healthy volunteers” (Ebrahim et al., 2013, p. 539). Our review of this article found it to be seriously flawed by research design and statistical problems. Ebrahim and colleagues (2013) selected 20 published articles concerned with the effects of alcohol on sleep in humans. Numerous articles were excluded from consideration. Within these articles are 38 groups of subjects based on other criteria such as sex or dose of alcohol administered. Although all sleep stages were addressed, Ebrahim and colleagues (2013) focus on the effects of alcohol on slow-wave sleep (SWS); variously known as or abbreviated as SWS, deep sleep, Stages 3 + 4. Current nomenclature combines stages 3 and 4 sleep and renames them “N3”(Iber et al., 2007). As noted in their conclusion, One area of debate and sometimes controversy has been the issue of the impact of alcohol on SWS. For the first time, all the available data are presented here and based on the findings from all available studies, and in the majority, alcohol clearly increases SWS in the first part of sleep at all doses, across gender and ages. Data for the impact of alcohol on total night SWS display a dose dependent effect with low doses showing no clear trend, moderate doses show a trend toward an increase in SWS and with high doses there is a significant and clear effect of increasing total SWS. This effect is consistent across gender and age groups. (Ebrahim et al., 2013, pp. 547–548)
This review provides a qualitative assessment of all known scientific studies on the impact of alcohol ingestion on nocturnal sleep in healthy volunteer's. At all dosages, alcohol causes a reduction in sleep onset latency, a more consolidated first half sleep and an increase in sleep disruption in the second half of sleep. The effects on rapid eye movement (REM) sleep in the first half of sleep appear to be dose related with low and moderate doses showing no clear trend on REM sleep in the first half of the night whereas at high doses, REM sleep reduction in the first part of sleep is significant. Total night REM sleep percentage is decreased in the majority of studies at moderate and high doses with no clear trend apparent at low doses. The onset of the first REM sleep period is significantly delayed at all doses and appears to be the most recognizable effect of alcohol on REM sleep followed by the reduction in total night REM sleep. The majority of studies, across dose, age and gender, confirm an increase in slow wave sleep (SWS) in the first half of the night relative to baseline values. The impact of alcohol on SWS in the first half of night appears to be more robust than the effect on REM sleep and does not appear to be an epiphenomenon REM sleep reduction. Total night SWS is increased at high alcohol doses across gender and age groups.
This study evaluated sex and family history of alcoholism as moderators of subjective ratings of sleepiness/sleep quality and polysomnography (PSG) following alcohol intoxication in healthy, young adults.
Ninety-three healthy adults [mean age 24.4 ± 2.7 years, 59 women, 29 subjects with a positive family history of alcoholism (FH+)] were recruited. After screening PSG, participants consumed alcohol (sex/weight adjusted dosing) to intoxication [peak breath alcohol concentration (BrAC) of 0.11 ± 0.01 g% for men and women] or matching placebo between 20:30 and 22:00 hours. Sleep was monitored using PSG between 23:00 and 07:00 hours. Participants completed the Stanford Sleepiness Scale and Karolinska Sleepiness Scale at bedtime and on awakening and a validated post-sleep questionnaire.
Following alcohol, total sleep time, sleep efficiency, nighttime awakenings, and wake after sleep onset were more disrupted in women than men, with no differences by family history status. Alcohol reduced sleep onset latency, sleep efficiency, and rapid eye movement sleep while increasing wakefulness and slow wave sleep across the entire night compared with placebo. Alcohol also generally increased sleep consolidation in the first half of the night, but decreased it during the second half. Sleepiness ratings were higher following alcohol, particularly in women at bedtime. Morning sleep quality ratings were lower following alcohol than placebo.
Alcohol intoxication increases subjective sleepiness and disrupts sleep objectively more in healthy women than in men, with no differences evident by family history of alcoholism status. Evaluating moderators of alcohol effects on sleep may provide insight into the role of sleep in problem drinking.
To explore the time of day effects of alcohol on sleep, we examined sleep following alcohol administered at four times of day and three homeostatic loads during a 20-hr forced desynchrony (FD) protocol.
Twenty-six healthy young adults (21-25 yrs) were studied.
Participants were dosed at 4 clock times: 0400 (n = 6; 2 females), 1600 (n = 7; 4 females), 1000 (n = 6; 1 female) or 2200 (n = 7; 2 females). Participants slept 2300 to 0800 for at least 12 nights before the in-lab FD study. Double blind placebo and alcohol (vodka tonic targeting 0.05g% concentration) beverages were each administered three times during FD at different homeostatic loads: low (4.25 or 2.24 hrs awake), medium (8.25 or 6.25 hrs awake), high (12.25 or 10.25 hrs awake) in the 0400 and 1600 or 1000 and 2200 groups, respectively. Sleep was staged and subjected to spectral analysis.
Breath Alcohol Concentration (BrAC) confirmed targeted maximal levels. At bedtime, BrAC was 0 in the low and medium homeostatic load conditions; however, at high homeostatic load, BrAC was still measurable. Spectral characteristics of sleep were unaffected with alcohol at any time of day. Few alcohol related changes were seen for sleep stages; however, with alcohol given at 0400 at a high homeostatic load there was an increase in wake.
These data lend support to the idea that alcohol may be disruptive to sleep; however, our findings are inconsistent with the idea that a low dose of alcohol is a useful sleep aid when attempting to sleep at an adverse circadian phase.
This study assessed the effects of heavy drinking with high or low congener beverages on next-day neurocognitive performance, and the extent to which these effects were mediated by alcohol-related sleep disturbance or alcoholic beverage congeners, and correlated with the intensity of hangover.
Healthy heavy drinkers age 21 to 33 (n = 95) participated in 2 drinking nights after an acclimatization night. They drank to a mean of 0.11 g% breath alcohol concentration on vodka or bourbon one night with matched placebo the other night, randomized for type and order. Polysomnography recordings were made overnight; self-report and neurocognitive measures were assessed the next morning.
After alcohol, people had more hangover and more decrements in tests requiring both sustained attention and speed. Hangover correlated with poorer performance on these measures. Alcohol decreased sleep efficiency and rapid eye movement sleep, and increased wake time and next-day sleepiness. Alcohol effects on sleep correlated with hangover but did not mediate the effects on performance. No effect of beverage congeners was found except on hangover severity, with people feeling worse after bourbon. Virtually no sex differences appeared.
As drinking to this level affects complex cognitive abilities, safety could be affected, with implications for driving and for safety-sensitive occupations. Congener content affects only how people feel the next day so does not increase risk. The sleep disrupting effects of alcohol did not account for the impaired performance so other mechanisms of effect need to be sought. As hangover symptoms correlate with impaired performance, these might be contributing to the impairment.
In healthy young women, rapid eye movement sleep decreased, slow-wave sleep increased, sleep-onset latency decreased and late-night disturbance of sleep increased with increasing doses of alcohol.
The purpose of this study was to assess the effects of low ethanol doses on sleep and mood and to assess its reinforcing effects used as a hypnotic. Twenty healthy adults, aged 21-45 yrs, all moderate social drinkers, were studied: eleven subjects had insomnia and nine were normal sleepers, as documented by clinical polysomnography. On two sampling nights each, ethanol (0.5 g/kg) or placebo was administered before sleep in color-coded cups presented in three doses (0.2, 0.2, and 0.1 g/kg) separated by 15 min. On three subsequent nights subjects chose their preferred presleep beverage (0.2 g/kg ethanol or placebo) based on cup color and were given an opportunity for 3 additional refills (0.2 g/kg each) of the chosen beverage at 15 min intervals, yielding a total possible dose of 0.8 g/kg. Insomniacs chose ethanol 67% of nights and normals 22%. Insomniacs chose significantly more ethanol refills than normals for an average nightly dose of 0.45 g/kg and normals took significantly more placebo refills. On the sampling nights 0.5 g/kg ethanol reduced REM sleep for both groups for the 8-hr sleep period and in insomniacs increased stage 3-4 sleep and reduced stage 1 sleep during the first half of the night to the level seen in the normals. Other sleep variables were not altered in either group or halves of the night. Presleep improvements in the Profile of Mood States tension and concentration factors were also associated with ethanol administration. Thus, acutely, both sleep and mood effects appear to be associated with the reinforcing effects of ethanol as a hypnotic for insomniacs.
Background:
After studying the sleep of alcohol-dependent patients at the beginning and over the course of abstinence in earlier studies, our interest in the current study focused on the direct effect of 2 doses of alcohol [0.03 and 0.1% blood alcohol level (BAL)] on healthy sleep. This is the first polysomnographic study testing the impact of 2 doses of alcohol ingestion (thus reflecting "normal" social drinking and alcohol abuse) in a single-blind randomized design in healthy volunteers. The study evaluated a short-term acute drinking period for 3 and 2 days of withdrawal from alcohol not only for polysomnographic variables but also for subjective estimates of sleep quality.
Methods:
In a crossover design with a 1-week interval, healthy subjects received alcohol to raise their blood alcohol to either 0.03 or 0.1% BAL at bedtime for 3 consecutive nights after an alcohol-free baseline night. Objective (polysomnography) and subjective sleep (questionnaires) was recorded each night. During the following 2 days, alcohol was discontinued with simultaneous measurements of sleep to gauge withdrawal effects.
Results:
At a dose of alcohol leading to BAL of 0.03%, no clear effects could be detected. Following an evening BAL of 0.1%, a hypnotic-like effect (shortened sleep latency, reduced number of wake periods, decreased stage 1 sleep) occurred primarily during the first half of the night with signs of rebound effects being already present during the second half of the night (increased stage 1 sleep). At this dose, alcohol significantly increased slow-wave sleep (SWS) in the first half of the night and reduced REM density in the beginning of the night. After discontinuation of the higher alcohol dose, REM sleep amount increased. No significant withdrawal or rebound effects could be observed for parameters of sleep continuity during the 2 nights after discontinuation from alcohol at a BAL of 0.1%.
Conclusions:
Owing to the small sample size, the results of this study need to be interpreted with caution. Short-term moderate alcohol consumption (BAL 0.03%) did not significantly alter objective or subjective parameters of sleep. Higher doses of alcohol resulting in a BAL level of 0.10% immediately before going to bed mainly influenced sleep in the first half of the night, resembling the effects of a short-acting hypnotic drug, including a suppression of phasic aspects of REM sleep (REM density). Interestingly, analysis of the latter part of these nights indicated the immediate presence of withdrawal effects (increased light sleep). No statistically significant effects on sleep parameters were observable during the 2 nights of withdrawal from alcohol at the higher BAL. Interpreted carefully, our data indicate that negative effects on sleep occur already with short-term use of alcohol at doses of BAL of 0.10%, despite hypnotic-like effects during the first hours of sleep, especially during the latter part of the night.
United Kingdom; and Department of Psychiatry and Ophthalmology (CS)
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From the Department of Neuropsychiatry (IE, PF, AJW), London Sleep Centre, London, United Kingdom; and Department of Psychiatry and Ophthalmology (CS), University of Toronto, Toronto, Ontario, Canada. Received for publication November 11, 2014; accepted February 26, 2015. Reprint requests: Irshaad Ebrahim, Neuropsychiatry, London Sleep Centre, 137 Harley Street, London W1G 6BF, UK; Tel.: +44 (0) 20
Medico-legal consequences of parasomnias Review: alcohol and sleep I: effects on normal sleep
- Ebrahim
- Io
- Shapiro
Ebrahim IO, Shapiro CM (2010) Medico-legal consequences of parasomnias, in Parasomnias and Other Movement Disorders (Thorpy M, Plazzi G eds), pp 81–98. Cambridge University Press, Cambridge, UK. Ebrahim IO, Shapiro CM, Williams AJ, Fenwick PB (2013) Review: alcohol and sleep I: effects on normal sleep. Alcohol Clin Exp Res 37:539–549.
Review: alcohol and sleep I: effects on normal sleep
- Ebrahim IO
- Shapiro CM
- Williams AJ
- Fenwick PB
Ebrahim IO, Shapiro CM, Williams AJ, Fenwick PB (2013) Review:
alcohol and sleep I: effects on normal sleep. Alcohol Clin Exp Res
37:539–549.
Parasomnias and Other Movement Disorders
- Ebrahim IO
- Shapiro CM
Review: alcohol and sleep I: effects on normal sleep
- I O Ebrahim
- C M Shapiro
- A J Williams
- P B Fenwick
Ebrahim IO, Shapiro CM, Williams AJ, Fenwick PB (2013) Review:
alcohol and sleep I: effects on normal sleep. Alcohol Clin Exp Res
37:539-549.