Effects of alcohol on polysomnographically recorded sleep in healthy subjects

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.     

Sleep electroencephalographic spectral power after withdrawal from alcohol in alcohol-dependent patients

BACKGROUND: Dysfunctional hyperarousal is suspected to be a neurophysiological determinant of relapse in abstinent alcohol-dependent patients. In the present study, we used spectral power analysis of the sleep electroencephalographic (EEG) to quantify brain activity during sleep in patients during subacute withdrawal as well as in control subjects. Our hypothesis was that the subgroup of patients who relapsed within the 3 months to follow-up would exhibit-increased dysfunctional arousal manifested by higher-frequency (beta) EEG power during sleep. METHODS: Twenty-six alcohol-dependent in-patients were examined with polysomnography over 2 nights 2 to 3 weeks after withdrawal. At the 3-month clinical follow-up assessment, 12 of them had relapsed and 14 abstained. The control group consisted of 23 healthy subjects similar to the patients with alcohol dependence in age and gender distribution. Spectral sleep EEG analysis was performed on both nights (adaptation and baseline) of all subjects. Logarithmic artifact-controlled spectral band power of sleep stage 2 and rapid eye movement (REM) sleep was analyzed for Group, Gender, and Age effects using multiple analyses of covariance. Three groups were compared with the Group factor: relapsers, abstainers, and controls. RESULTS: Generally, both Group and Age effects were significant for the second, baseline night for the visually scored sleep parameters, while spectral EEG parameters showed significant differences in the adaptation night. In the adaptation night, a significant enhancement in the beta2 band (24-32 Hz) was seen in REM sleep in relapsers relative to both abstainers and controls. CONCLUSIONS: The beta2 increase could be interpreted as a sign of dysfunctional arousal during REM sleep "unmasked" by the additional stressor of sleep environment adaptation. Its determinants are likely to be both premorbid and drinking history related.     

Effects of acamprosate on sleep during alcohol withdrawal: A double-blind placebo-controlled polysomnographic study in alcohol-dependent subjects

BACKGROUND: Sleep disturbances are frequently encountered in alcohol-dependent patients. Drugs improving sleep during abstinence from alcohol may play an important role in the recovery process. METHODS: In the present study, the effects of acamprosate, a drug successfully used in maintaining abstinence following alcohol withdrawal, were assessed by polysomnographic recordings. A parallel double-blind placebo-controlled study was conducted in 24 male DSM-IV alcohol-dependent subjects aged 35.9+/-1.2 years. Treatments (2 tablets of 333 mg acamprosate vs placebo t.i.d.) were initiated 8 days before alcohol withdrawal and continued during the 15 days following alcohol withdrawal. Polysomnographic assessments were recorded during acute withdrawal (the first 2 nights following withdrawal) and during postwithdrawal abstinence (the last 2 nights of the trial). RESULTS: Results show that, compared with placebo, acamprosate decreased wake time after sleep onset and increased stage 3 and REM sleep latency (all treatment effects with a p < 0.05 significance). Withdrawal effects themselves were also demonstrated as sleep efficiency (p < 0.01) and total sleep time (p < 0.05) were lower in abstinence nights versus withdrawal nights, whereas no significant treatment x withdrawal effect could be evidenced. Acamprosate was well tolerated during the entire course of the study. CONCLUSIONS: The present study shows that acamprosate ameliorates both sleep continuity and sleep architecture parameters classically described as disturbed in alcohol-dependent patients. From a clinical perspective, it suggests that an 8-day acamprosate prewithdrawal treatment is well tolerated and can attenuate the sleep disturbances engendered by alcohol withdrawal in alcohol-dependent subjects.     

Effect of moderate alcohol upon obstructive sleep apnoea.

Moderate-to-large quantities of alcohol are known to aggravate severe obstructive sleep apnoea (OSA), however, the reported effects of moderate alcohol consumption upon mild-to-moderate OSA are inconsistent. Given the reported benefits of moderate alcohol consumption on cardiovascular mortality, recommendations regarding the management of patients with OSA are difficult to formulate. The aim of this study was to evaluate the effects of moderate alcohol on sleep and breathing in subjects with mild-to-moderate OSA. Twenty-one male volunteers, who snored habitually, underwent polysomnography with and without 0.5 g alcohol x kg body weight (BW)(-1) consumed 90 min prior to sleep time, in random order. The mean blood alcohol concentration (BAC) following alcohol at the time of lights out was 0.07 g x dL(-1). The distribution amongst the various sleep stages was not significantly altered by alcohol. The mean apnoea/hypopnoea index rose from 7.1+/-1.9 to 9.7+/-2.1 events x h(-1) (mean+/-SEM, p=0.017); however, there was no significant change in the minimum arterial oxygen saturation measured by pulse oximetry Sp,O2, apnoea length or snoring intensity. Mean sleep cardiac frequency rose significantly from 53.9+/-1.4 to 59.9+/-1.9 beats x min(-1) (P<0.001) and overnight urinary noradrenalin increased from 14.9+/-2.3 to 18.8+/-2.3 nmol x mmol creatinine(-1) (p=0.061) on the alcohol night compared to the nonalcohol night. To conclude, modest alcohol consumption, giving a mean blood alcohol concentration of 0.07 g x dL(-1), significantly increases both obstructive sleep apnoea frequency and mean sleep cardiac frequency.     

Effect of ethanol on the efficacy of nasal continuous positive airway pressure as a treatment for obstructive sleep apnea

The effect of ethanol ingestion on the efficacy of nasal continuous positive airway pressure (nasal CPAP) as a treatment for the obstructive sleep apnea (OSA) syndrome was studied in ten obese male subjects undergoing this therapy. On the first night of polysomnography, the lowest level of CPAP that maintained airway patency was determined (critical level). On the second (control) night (C), subjects slept the entire night on this level of CPAP. On the third night (E), subjects ingested either 1.5 ml/kg (part A, N = 6) or 2.0 ml/kg (part B, N = 4) of 50 percent ethanol (100 proof vodka) over one half-hour starting 1 h before bedtime. A serum ethanol level was obtained at bedtime (part A: 63.7 +/- 17.3 mg/dl; part B: 108.6 +/- 20.6 mg/dl), and subjects were monitored on the critical level of CPAP. Comparison of nights C and E for parts A + B showed no difference in total sleep time (TST) or the amount of different sleep stages as an absolute time or a percentage of TST except that there was more stage 2 (as a percent of TST) on E nights. The apnea + hypopnea index and C and E nights did not differ and was quite low (3.6 +/- 3.7/h vs 1.9 +/- 2.7/h). Similarly, ethanol ingestion did not increase the number of desaturations to at or below 90 and 85 percent, or lower the mean arterial oxygen saturation in NREM or REM sleep. Analysis of parts A and B separately also showed no differences with respect to the apnea + hypopnea index or the number of desaturations on control and ethanol nights. We conclude that acute moderate ethanol ingestion does not decrease the efficacy of an optimum level of nasal CPAP.     

Effects of alcohol on sleep and the sleep electroencephalogram in healthy young women

BACKGROUND: Although the association between sleep and alcohol has been of interest to scientists for decades, the effects of alcohol on sleep and sleep electroencephalogram (EEG) have not been extensively studied in women. Our specific aim was to determine whether sleep stage variables and/or spectral characteristics of the sleep EEG are altered by alcohol administration in women. METHODS: Changes of sleep and the sleep EEG were investigated after administration of a moderate dose of alcohol (0.49 g/kg) in the hour before bedtime compared with placebo in young healthy women. After approximately 2 weeks at home on a fixed 8.5- or 9-hour stabilization sleep schedule, sleep was continuously recorded by polysomnography for 3 consecutive nights [adaptation, placebo, alcohol (mean breath alcohol concentration 0.043 g/% before bedtime)] in the laboratory in 7 women (ages 22-25, mean=23.5, SD=1 year). Sleep stages were scored according to conventional criteria. Electroencephalogram power spectra of the bipolar derivations Fz/Cz (anterior) and Pz/Oz (posterior) were calculated using a fast Fourier transform routine. RESULTS: Only few changes in sleep and the sleep EEG were observed. Across the entire night rapid eye movement (REM) sleep decreased, while minutes of stage 4 sleep were increased in the first 2-hour interval on alcohol nights compared with placebo nights. Spectral analysis of the EEG showed increased power in the alpha range (9-11 Hz) during all-night non-REM (NREM) sleep in anterior derivations after alcohol compared with placebo. Differences in spectral EEG power were also present in 2-hour intervals of NREM sleep; in particular, EEG power was increased on the alcohol night for frequency bins within the alpha range in anterior derivations and within the delta range (3-4 Hz) in posterior derivations during the initial part of the night. CONCLUSIONS: A moderate dose of alcohol just before bedtime resulted in a short-lived increase in sleep intensity. A limitation of the study, however, was that only a single dose of alcohol was used to examine the effects of alcohol on sleep.     

Alcohol increases sleep apnea and oxygen desaturation in asymptomatic men

Using standard sleep techniques, we performed a placebo-controlled and randomized study to assess the effect of alcohol ingestion (2 ml/kg of body weight) on breathing and oxygen saturation during sleep. Twenty asymptomatic men volunteered for the two-night study: 11 were given a placebo on night 1, and alcohol on night 2 (group A); nine were given alcohol on night 1 and a placebo on night 2 (group B). We compared the incidence of sleep events (apnea, hypopnea and arterial oxygen desaturation) during the nights the subjects received alcohol and during the nights they received the placebo.Alcohol was associated with significant increases in the occurrence of the following: the number of sleep events (207 to 383, p < 0.01), the events of arterial oxygen desaturation (118 to 226, p < 0.01) and the number of apneic events (20 to 110, p < 0.01). Alcohol had no significant effects on the number of times hypopnea occurred. Values obtained during sleep on the control night after alcohol ingestion also showed that the episodes of arterial oxygen desaturation remained statistically increased over control values before the ingestion of any alcohol (p = 0.01). These results show that in asymptomatic men alcohol ingestion increases the incidence of arterial oxygen desaturation and disordered breathing during sleep and that the increase in arterial oxygen desaturation persists for an additional night, even when no alcohol is consumed.     

Moderate alcohol ingestion increases upper airway resistance in normal subjects

Apnea during sleep has been associated with both increased pharyngeal resistance and nasal obstruction. Alcohol can worsen obstructive sleep apnea, but its influence on pharyngeal resistance and nasal patency has not been evaluated. Accordingly, we determined the effects of alcohol on pharyngeal and nasal resistances in 11 normal awake subjects on 2 separate days. Baseline pharyngeal resistance prior to placebo and alcohol was not significantly different. After placebo, pharyngeal resistance did not change significantly. However, after alcohol, pharyngeal resistance increased from 1.9 +/- 0.5 (SEM) to 3.3 +/- 0.8 cm H2O/L/s at 45 min (p less than 0.05) and returned to near baseline level by 90 min. Baseline nasal resistance varied considerably within subjects on the 2 days, but the mean values for baseline nasal resistance on alcohol and placebo days were not significantly different. Nasal resistance did not change after placebo, but after alcohol, nasal resistance increased from 2.4 +/- 0.9 at baseline to 3.7 +/- 0.8 at 45 min (NS) and to 4.3 +/- 1.2 cm H2O/L/s at 90 min (p less than 0.05). We conclude that a decrease in pharyngeal airway size and an increase in nasal resistance may account for alcohol's ability to worsen obstructive sleep apnea.     

Low-flow oxygen and bilevel ventilatory support: effects on ventilation during sleep in cystic fibrosis

We measured ventilation in all sleep stages in patients with cystic fibrosis (CF) and moderate to severe lung disease, and compared the effects of low-flow oxygen (LFO2) and bilevel ventilatory support (BVS) on ventilation and gas exchange during sleep. Thirteen subjects, age 26 +/- 5.9 yr (mean +/- 1 SD), body mass index (BMI) 20 +/- 3 kg/m2, FEV1 32 +/- 11% predicted, underwent three sleep studies breathing, in random order, room air (RA), LFO2, and BVS +/- O2 with recording of oxyhemoglobin saturation (SpO2) (%) and transcutaneous carbon dioxide (TcCO2) (mm Hg). During RA and LFO2 studies, patients wore a nasal mask with a baseline continuous positive airway pressure (CPAP) of 4 to 5 cm H2O. Minute ventilation (V I) was measured using a pneumotachograph in the circuit and was not different between wake and non-rapid eye movement (NREM) sleep on any night. However, V I was reduced on the RA and LFO2 nights from awake to rapid eye movement (REM) (p < 0.01) and from NREM to REM (p < 0.01). On the BVS night there was no significant difference in V I between NREM and REM sleep. Both BVS and LFO2 improved nocturnal SpO2, especially during REM sleep (p < 0.05). The rise in TcCO2 seen with REM sleep with both RA and LFO2 was attenuated with BVS (p < 0.05). We conclude that BVS leads to improvements in alveolar ventilation during sleep in this patient group.     

Effect of theophylline on sleep and sleep-disordered breathing in patients with chronic obstructive pulmonary disease

To investigate the effect of theophylline on sleep and sleep-disordered breathing in patients with chronic obstructive pulmonary disease (COPD), we studied 12 male nonhypercapnic subjects with a mean +/- SEM age of 62.8 +/- 2.5 yr and a FEV1 of 1.36 +/- 0.11 L using a randomized double-blind crossover protocol. Sustained-action theophylline (250 mg three times or four times a day) or placebo was administered for 2 days, and the alternate drug was administered on the following 2 days. Sleep studies were performed on Nights 2 and 4 with spirometry at 9:00P.M. and 7:00A.M. Two puffs of metaproterenol or albuterol were administered at 10:00P.M. on both study nights. A theophylline level, drawn at bedtime (10:00 to 11:00P.M.), was 14.2 +/- 0.78 micrograms/ml on the theophylline nights and less than 2 on placebo nights. The morning FEV1 was significantly better during theophylline administration (1.27 +/- 0.12 versus 1.00 +/- 0.11 L, p less than 0.001). The mean arterial oxygen saturation (SaO2) and transcutaneous carbon dioxide pressure (PCO2) were also better during NREM sleep on theophylline nights. Neither the mean SaO2 and transcutaneous PCO2 during REM sleep nor the apnea plus hypopnea index (events per hour of sleep) differed between placebo and theophylline nights. Theophylline administration did not impair the amount or architecture of sleep as neither total sleep time nor the fraction of time spent in Stages 1, 2, and 3/4 and REM differed between the two regimens. The number of arousals per hour of sleep was slightly less on theophylline nights (19.9 +/- 1.7 versus 24.9 +/- 2.7, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Short-term use of fluoxetine in asymptomatic obese subjects with sleep-related hypoventilation.

Disordered nocturnal breathing with significant arterial oxygen desaturation and sleep apnoea is a feature of extreme obesity which is often difficult to manage in the short term. We have evaluated the effect of fluoxetine, a centrally acting 5-HT re-uptake inhibitor, on sleep-breathing patterns in asymptomatic extremely obese subjects. A double-blind cross-over study was used to compare fluoxetine (60 mg for three days) to placebo. Eleven obese subjects (ten males, one female, mean weight +/- s.d. 131 +/- 2 kg) slept overnight in a sleep laboratory with the polysomnographic study recorded after an initial acclimatization night. The obese subjects had normal respiratory function and normal fully awake arterial oxygen saturation (%SaO2 97 +/- 1). Marked O2 desaturation was seen in all the subjects during sleep but the average asleep %SaO2 did not differ between the two treatment phases (placebo 90 +/- 5; fluoxetine 92 + 2%). However, fluoxetine significantly increased the minimum %SaO2 recorded during the study night either by abolishing or reducing REM sleep (placebo 73 +/- 2%; fluoxetine 81 +/- 8%; P < 0.05, 95% CI -12.3 to -2.03). Frequent hypopnoea was observed in all subjects in both REM and non-REM sleep whereas apnoea was uncommon. The total apnoea/hypopnoea index fell in six subjects during the fluoxetine night, the largest reduction being seen in the most severely affected. In five of the six the improvement was associated with the abolition of REM sleep. Total sleep time did not differ between the placebo and fluoxetine nights nor did a qualitative assessment of sleep using a visual analogue score.(ABSTRACT TRUNCATED AT 250 WORDS)     

经鼻持续气道正压通气对阻塞性睡眠呼吸暂停低通气综合征患者睡眠结构近远期的影响

目的　观察经鼻持续气道正压 (nCPAP)通气对阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者睡眠结构近远期的影响。方法　 17例对照者行多导睡眠图 (PSG)监测 ,对 30例经PSG诊断的OSAHS患者行nCPAP治疗 ,治疗第 1夜行PSG监测 ,连续家庭nCPAP治疗 6个月后行第 2次PSG监测 ,分析比较睡眠结构的变化。结果　OSAHS患者治疗前睡眠转换次数、1期、2期睡眠比例较对照组增加 (P <0 0 5 ) ,慢波睡眠期、快动眼 (REM )期比例较对照组低 (P <0 0 5 ) ;nCPAP治疗第 1夜睡眠转换次数、1期、2期睡眠比例较治疗前降低 (P <0 0 5 ) ,慢波睡眠期、REM期比例较治疗前升高 (P <0 0 5 ) ;nCPAP治疗 6个月后睡眠转换次数、1期、2期、慢波睡眠期比例与治疗第 1夜比较差异均无显著性 (P >0 0 5 ) ,而REM期比例较治疗第 1夜降低 (P <0 0 5 )。结论　OSAHS患者睡眠转换次数明显增多 ,1期睡眠增加而REM期睡眠减少 ,睡眠结构紊乱。nCPAP治疗第 1夜及6个月后睡眠结构得到有效纠正 ,是OSAHS长期有效的治疗方法之一。     

Effects of a moderate evening alcohol dose. I: sleepiness

Background: Few studies examining alcohol's effects consider prior sleep/wake history and circadian timing. We examined introspective and physiological sleepiness on nights with and without moderate alcohol consumption in well-rested young adults at a known circadian phase.
Methods: Twenty-nine adults (males=9), ages 21 to 25 years ( M =22.6, SD=1.2), spent 1 week on an at-home stabilized sleep schedule (8.5 or 9 hours), followed by 3 in-lab nights: adaptation, placebo, and alcohol. Alcohol (vodka; 0.54 g/kg for men; 0.49 g/kg for women) or placebo beverage was consumed over 30 minutes ending 1 hour before stabilized bedtime. In addition to baseline, 3 sleep latency tests (SLTs) occurred after alcohol/placebo ingestion (15, 16.5, and 18 hours after waking). Stanford Sleepiness Scales (SSS) and Visual Analog Scales (VAS) of sleepiness were completed before each SLT and approximately every 30 minutes. The Biphasic Alcohol Effects Scale (BAES) was administered a total of 4 times (baseline, 5, 60, and 90 minutes postalcohol/placebo). Subjects' circadian phase was determined from melatonin levels in saliva samples taken at approximately 30-minute intervals.
Results: All sleepiness and sedation measures increased with time awake. Only SSS and BAES sedation measures showed higher levels of sleepiness and sedation after alcohol compared with placebo. The mean circadian phase was the same for assessments at both conditions.
Conclusions: Alcohol did not increase physiological sleepiness compared with placebo nor was residual sedation evident under these conditions. We conclude that the effects on sleepiness of a moderate dose of alcohol are masked when sleep–wake homeostatic and circadian timing influences promote high levels of sleepiness.     

Positive nasal airway pressure eliminates snoring as well as obstructive sleep apnea

Nine men who were habitual snorers were studied during a control and a treatment night (in random order) to assess the effect of nasal continuous positive airway pressure (CPAP) on snoring, sleep-disordered breathing, and nocturnal oxygen desaturation. Four subjects had symptoms suggestive of the sleep apnea syndrome, but the other five were asymptomatic. Polysomnography and recordings of snores were obtained on both nights. On the treatment night, the subjects wore a customized infant anesthesia mask over their noses, and CPAP was applied and adjusted upward from 4 cm H2O to a level that obliterated snoring. Nasal CPAP (range 4 to 13 cm H2O) reduced the mean number of snores per night from 1,015 per subject to 23 per subject (p less than 0.01). Mean numbers of episodes of apnea, hypopnea, and desaturation were also significantly reduced. Analysis of sleep structure showed no significant differences in sleep period time, total sleep time, or the percentages of stages 3 and 4 sleep. The percentage of stages 1 and 2 was significantly greater on control nights, and the percentage of REM sleep was greater on treatment nights. On the control nights, snoring was common in stages 3 and 4 and least common during REM sleep.     

Effect of three alcohol doses on breathing during sleep in 30-49 year old nonobese snorers and nonsnorers

To test the effect of alcohol ingestion and snoring on sleep-disordered breathing (SDB), the sleep and respiration of 31 nonobese healthy males ages 30-49 (15 snorers, 16 nonsnorers) were studied overnight after alcohol ingestion. Subjects received placebo, 0.32, 0.65, and 0.81 g alcohol/kg body weight prior to their evening bedtime, with each dose given on one of four nonconsecutive nights in a repeated-measures counterbalanced design. On each night, respiration was assessed by recording respiratory effort from intercostal surface electromyography (EMG), ventilation from oral and nasal thermistors, and arterial oxygen saturation (SaO2) from an ear oximeter (BIOX III). Snorers had significantly: (a) more total SDB, (b) more obstructive sleep apnea (OSA), and (c) lower minimum SaO2 than nonsnorers after the placebo and each alcohol dose. Snorers had more hypoxic events than nonsnorers after each alcohol dose but not after placebo. Increasing alcohol dose caused a statistically significant (p = 0.0004) decrease in minimum SaO2 in snorers only, but this decrease was small and probably not clinically important. Alcohol did not cause significant increases in SDB and hypoxic events, and did not have different effects on SDB and hypoxic events for snorers versus nonsnorers. Because this experiment included only nonobese 30-49-year-old males, these results do not imply that alcohol has no significant effects on obese subjects or those older than 50.     

Impaired objective daytime vigilance in obesity-hypoventilation syndrome: impact of noninvasive ventilation

BACKGROUND: Obesity-hypoventilation syndrome (OHS) is efficiently treated by noninvasive ventilation (NIV). Sleep respiratory disturbances, reduced ventilatory drive, and excessive daytime sleepiness (EDS) are commonly reported, but their relationships remain unclear. OBJECTIVES: To characterize sleep breathing disorders encountered in patients with OHS, to compare low and normal CO(2) responders in terms of sleep abnormalities, subjective and objective measures of EDS, and to measure the changes induced by NIV on these parameters. METHODS: At baseline and after 5 nights of NIV, 15 consecutive patients (mean [+/- SD] age, 55 +/- 9 years; mean body mass index, 38.7 +/- 6.1 kg/m(2); Paco(2), 47.3 +/- 2.3 mm Hg) prospectively underwent polysomnography, CO(2) ventilatory response testing, Epworth sleepiness scale scoring, and the Oxford Sleep Resistance (OSLER) test, which is an objective vigilance test. RESULTS: OHS patients exhibited obstructive sleep apnea syndrome (mean apnea-hypopnea index, 62 +/- 32 events per hour) and rapid eye movement (REM) sleep hypoventilation (mean REM sleep time, 35 +/- 33%). Baseline CO(2) sensitivity was significantly related to the proportion of hypoventilation during REM sleep (r = 0.54; p = 0.037). Six patients showed abnormal sleep latencies during the OSLER test (71% of the low CO(2) responders vs 14% of the normal CO(2) responders). Low CO(2) responders exhibited significantly shorter sleep latencies during the OSLER test (23 +/- 14 vs 37 +/- 8 min, respectively; p = 0.05). Using NIV, diurnal blood gas levels were improved and REM sleep hypoventilation were suppressed. Objective sleepiness was improved in low CO(2) responders (p = 0.04). CONCLUSION: In OHS patients, the lower the daytime CO(2) response, the higher the proportion of REM sleep hypoventilation and daytime sleepiness. Short-term therapy with NIV improves all of these parameters.     

Effect of alcohol ingestion on breathing and oxygenation during sleep. Analysis of the influence of age and sex

Breathing and oxygenation were monitored in 78 asymptomatic volunteers on two successive nights of sleep. Four groups of subjects were recruited: 20 young men, 20 young women, 20 men older than 40 years, and 18 postmenopausal women. In random order, subjects ingested either 2 ml/kg (body weight) of 100-proof vodka in orange juice or a similar amount of water in orange juice before bedtime. Alcohol ingestion shortened sleep in the older men and in the postmenopausal women. No effect of alcohol ingestion on breathing or oxygenation during sleep was seen in any group of women. In men, alcohol ingestion increased the numbers of desaturation episodes and caused more severe oxygen desaturation during sleep. The effect of alcohol ingestion on breathing and oxygenation during the sleep of asymptomatic volunteers appears to be limited to men.     

Effect of moderate alcohol consumption on hypertriglyceridemia: a study in the fasting state.

BACKGROUND: Patients with hypertriglyceridemia (HTG) are generally advised to avoid alcohol, even though moderate alcohol consumption is cardioprotective. Alcohol increases plasma triglyceride concentration transiently in normolipidemic subjects, but whether alcohol consumption per se increases triglyceride concentrations in patients with HTG is unclear. OBJECTIVE: To assess whether baseline fasting triglyceride concentration determines plasma triglyceride concentration after acute oral alcohol intake. METHODS: Twelve persons with fasting triglyceride concentrations of 2.3 to 8.5 mmol/L (200-750 mg/dL) and 12 persons as a non-HTG group were enrolled. Obesity, current smoking, and history of hypertension, diabetes, or excessive alcohol use were exclusionary. Fasted subjects consumed 38 mL of ethanol in water (equivalent, 2 alcoholic drinks); blood samples were collected at baseline and at intervals thereafter for 10 hours. No less than 1 week later, the subjects consumed water alone in a control test. RESULTS: Mean triglyceride values were 4.04+/-0.41 mmol/L (358+/-36.9 mg/dL) and 1.00+/-0.11 mmol/L (89+/-10.2 mg/dL) for the HTG and non-HTG groups, respectively. Despite similar changes with alcohol feeding in plasma ethanol, nonesterified fatty acid, and acetate concentrations, the groups differed in triglyceride response. At 6 hours (peak) compared with baseline, triglyceride concentration increased only 3% in the HTG group but 53% in the non-HTG group. The former change was not significantly different from the effect with water alone (-9.2% from baseline; P = .43), whereas the latter was (-8.0%; P = .003). CONCLUSIONS: Acute alcohol intake alone is not an important determinant of plasma triglyceride concentration in individuals with HTG. Other factors, such as the contemporaneous consumption of fat and alcohol, known to increase triglyceride concentrations synergistically in non-HTG individuals, may be more important.     

Sleep following alcohol intoxication in healthy, young adults: effects of sex and family history of alcoholism

Background: 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. Methods: 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. Results: 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. Conclusions: 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.     

Prediction of the degree of nocturnal oxygen desaturation in sleep apnea syndrome by estimating the testosterone level

We studied the influence of hypoxia due to sleep apnea on testosterone (T) secretion. It was conducted on the basis of an idea that sustained hypoxia may depress T secretion. The subjects consisted of 15 male patients with no drug administration whose complaints were snoring and/or obesity. The subjects participated in a sleep study on two consecutive nights. During the first night we collected blood samples starting every 4 hours from 10 PM via a catheter and measured T. From the data of the second night, we calculated total desaturation time with more than 4% from the baseline SaO2. According to the amount of this desaturation time, the subjects were divided into 2 groups; desaturation time less than 80 min in group 1 and longer in group 2, respectively. The peak value was seen at 6 AM in group 1 and at 10 AM in group 2. We investigated the correlation between the ratio of T10/T6, which is the ratio of T level at 10 AM to that at 6 AM, and parameters of sleep disorders related to oxygen desaturation. Total 4% desaturation time in total sleep period and non REM period significantly correlated with this ratio. From the diagram illustrating the correlation between the ratio and total 4% desaturation time in total sleep period, we could assume that if the ratio is beyond 1, the subject may have had more than about 80 min of total 4% desaturation time.