Risk-taking behavior: effects of ethanol, caffeine, and basal sleepiness (original) (raw)
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Ethanol and caffeine effects on daytime sleepiness/alertness
Sleep, 1987
Eighteen normal-sleeping young (mean age 25.6 years) volunteers received either ethanol (0.75 g/kg producing blood ethanol concentrations of 71.1 +/- 24.3 mg/100 ml on average) or caffeine (4.0 mg/kg dissolved in 300 ml of 97% caffeine-free instant coffee) at 0920-0950 h after spending 5, 8, or 11 h time in bed (TIB) the previous night. Latency to sleep onset was tested at 1000, 1200, 1400, and 1600 h. Mean sleep latency differed significantly between drugs on each day of testing, with subjects being sleepier after ethanol than caffeine. On day 2 the TIB manipulation produced significant differences in latency, with the 11-h condition differing from both the 8- and 5-h conditions. The significant interaction revealed that in fully rested subjects (11-h TIB), ethanol did not produce sleepiness to the degree it did after 5 or 8 h in bed. In this condition latencies were similar to those of the caffeine and 5- or 8-h TIBs.
2003
Caffeine has been shown to reverse some of the performance-impairing effects of ethanol. However, it is not known whether this antagonistic effect of caffeine is mediated by a reduction in sleepiness. The present study assessed physiological alertness/sleepiness, memory, and psychomotor performance following the administration of placebo, ethanol, and caffeine+ethanol combinations. A total of 13 healthy individuals (21-35 years old) underwent four conditions presented in a Latin Square Design: placebo-placebo, ethanol (0.5 g/kg)-placebo, ethanol (0.5 g/kg)-caffeine 150 mg, and ethanol (0.5 g/kg)-caffeine 300-mg. The Multiple Sleep Latency Test (MSLT), psychomotor performance battery, memory test, and mood/sleepiness questionnaires were administered following each condition. The peak breadth ethanol concentration (BrEC) was 0.043 7 0.0197% and did not differ among the three caffeine treatments. As expected, ethanol reduced mean latency on the MSLT. The lowest caffeine dose reversed this effect and the highest dose increased mean latency (greater alertness) significantly beyond placebo levels. Ethanol also impaired psychomotor performance and memory. The 300-mg caffeine dose restored performance and memory measures to placebo levels. Although visual analog ratings of dizziness were increased by ethanol, they were not diminished by either caffeine dose. In conclusion, Low-dose caffeine prevented the sleepiness and performance impairment associated with a moderate dose of ethanol. Thus, caffeine, similar to other stimulants, can reverse the physiologically sedating effects of ethanol, although other negative effects remain.
Sleep extension, enhanced alertness and the sedating effects of ethanol
Pharmacology Biochemistry and Behavior, 1989
Sleep extension, enhanced alertness and the sedating effects of ethanol. PHARMACOL BIOCHEM BEHAV 34(2) 321-324, 1989.-Twelve, healthy young men (mean age 25.6 years) consumed either ethanol (0.75 g/kg producing a peak breath ethanol concentration, BEC, of 0.060% on average) or placebo at 0900-0930 hr after spending 8 hr time-in-bed (TIB) the previous night and once again after 7 or 8 consecutive nights of 10 hr TIB. Latency to sleep onset (on the Multiple Sleep Latency Test, a standard measure of daytime sleepiness/alertness) was tested at 1000. 1200, 1400 and 1600 hr and divided attention performance was assessed at 1100 hr. Ethanol reduced sleep latency and divided attention performance and the sleep extension improved both sleep latency and divided attention performance. Sleep extension attenuated the sedating effects of ethanol; sleep latency after extending sleep did not differ between placebo and ethanol. While the effects of ethanol on performance still were detectable after sleep extension, the level of performance was at the 8-hr TIB placebo level. BEC peak and decline (determined before each latency test) did not change with the sleep extension. Hence, reduced BECs do not account for the reduction in the disruptive effects of ethanol with sleep extension.
Interactions between alcohol and caffeine in relation to psychomotor speed and accuracy
… : Clinical and Experimental, 2002
Unlike other CNS depressants, alcohol intoxication can be associated with increased error rates, coupled with unaffected (or speeded) response rates during psychomotor and cognitive processing. The present study examined whether concurrent consumption of caffeine may differentially affect these aspects of alcohol and performance.A randomised, double-blind, placebo-controlled design was utilised in which 64 healthy young volunteers received either 0.66 g/kg alcohol, caffeine (110–120 mg), both or neither. Performance was assessed using a four choice reaction time task (FCRT) with elements of repetitive (predictable) and random stimuli sequences and the digit symbol substitution task (DSST).Individuals on alcohol made significantly more errors during both fixed and random FCRT sequences, and there was evidence of weak antagonism of these effects by caffeine on the latter measure. On the DSST test of psychomotor speed, alcohol was associated with a significant slowing, the caffeine group were significantly faster and there was clear antagonism of the effects of alcohol by caffeine. These findings confirm that alcohol consumption is associated a greater number of errors and provide some evidence for task-specific antagonism of alcohol's cognitive effects by caffeine. Copyright © 2002 John Wiley & Sons, Ltd.
Sleepiness and Ethanol Effects on Simulated Driving
Alcoholism: Clinical and Experimental Research, 1994
Twelve healthy young men were assessed in each of four experimental conditions presented in a Latin Square design: 8-hr time in bed (TIB) and placebo, 4-hr TIB and placebo, 8-hr TIB and ethanol, and 4-hr TIB and ethanol. After consuming ethanol (0.6 g/kg) or placebo (0900-0930 hr) with 20% supplements at 1030 and 1100 hr, subjects were tested for sleepiness (Multiple Sleep Latency Test at 1000, 1200, 1400, and 1600 hr) and divided attention (1030 hr) performance on day 1, and for simulated driving and divided attention (1000-1200 and 1400-1600 hr) performance on day 2. In the morning testing, with breath ethanol concentrations (BECs) averaging 0.049%, sleepiness was increased, divided attention reaction times increased (on both days), and simulated driving performance was disturbed in the ethanol and 4-hr TIB relative to placebo. Similarly in the afternoon, with BECs averaging 0.013%, the ethanol and 4-hr TIB condition increased sleepiness and disrupted divided attention and simulated driving performance. The results show that sleepiness and low-dose ethanol combine to impair simulated automobile driving, an impairment that extends beyond the point at which BEC reaches zero. They provide a possible explanation for the incidence of alcohol-related automobile accidents at low BECs.
Addiction, 2011
Aims Marketing that promotes mixing caffeinated 'energy' drinks with alcoholic beverages (e.g. Red Bull with vodka) targets young drinkers and conveys the expectation that caffeine will offset the sedating effects of alcohol and enhance alertness. Such beliefs could result in unwarranted risk taking (e.g. driving while intoxicated). The aim of this study was to assess the acute effects of caffeinated versus non-caffeinated alcoholic beverages on a simulated driving task and attention/reaction time. Design We conducted a 2 ¥ 2 between-groups randomized trial in which participants were randomized to one of four conditions: beer and non-alcoholic beer, with and without caffeine added. Caffeine was added in the same proportion as found in a commercially available caffeinated beer (69 mg/12 oz of beer at 4.8% alc. by vol). Participants Participants were 127 non-dependent, heavy episodic, young adult drinkers (age 21-30) who were college students or recent graduates. The target breath alcohol level was 0.12 g%. Measures Driving performance was assessed with a driving simulator; sustained attention/reaction with the Psychomotor Vigilance Task (PVT). Findings Across the driving and attention/reaction time we found main effects for alcohol, with alcohol significantly impairing driving and sustained attention/reaction time, with mainly large statistical effects; however, the addition of caffeine had no main or interaction effects on performance. Conclusion The addition of caffeine to alcohol does not appear to enhance driving or sustained attention/reaction time performance relative to alcohol alone.
Sleep, sleepiness, and alcohol use
Alcohol research & health : the journal of the National Institute on Alcohol Abuse and Alcoholism, 2001
The study of alcohol's effects on sleep dates back to the late 1930s. Since then, an extensive literature has described alcohol's effects on the sleep of healthy, nonalcoholic people. For example, studies found that in nonalcoholics who occasionally use alcohol, both high and low doses of alcohol initially improve sleep, although high alcohol doses can result in sleep disturbances during the second half of the nocturnal sleep period. Furthermore, people can rapidly develop tolerance to the sedative effects of alcohol. Researchers have investigated the interactive effects of alcohol with other determinants of daytime sleepiness. Such studies indicate that alcohol interacts with sleep deprivation and sleep restriction to exacerbate daytime sleepiness and alcohol-induced performance impairments. Alcohol's effects on other physiological functions during sleep have yet to be documented thoroughly and unequivocally.
Effects of a Moderate Evening Alcohol Dose. I: Sleepiness
Alcoholism: Clinical and Experimental Research, 2007
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 5 9), ages 21 to 25 years (M 5 22.6, SD 5 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.