Melbourne School of Psychological Sciences - Theses

Permanent URI for this collection

Search Results

Now showing 1 - 1 of 1
  • Item
    Thumbnail Image
    The effects of acute alcohol consumption on sleep and memory in young adults
    Chan, Julia Kheng Mei ( 2013)
    Sleep is a basic physiologic drive fundamental to human survival. Adequate sleep is particularly important for maturation of biological and neuronal processes. Adolescence and young adulthood are unique developmental periods characterised by numerous changes to neural physiology, as reflected in dramatically altered sleep behaviour. These biological changes are accompanied by a tendency for increased alcohol consumption due to social and environmental changes occurring during this time. These neuronal changes may result in the brains of adolescents and young adults being at a heightened vulnerability for alcohol related disruption. Thus, the consequences of acute alcohol consumption may be particularly relevant to these developmentally unique age groups. Patterns of alcohol consumption during adolescence and young adulthood are often characterised by repeated acute exposure to high concentrations of alcohol. Acute consumption of alcohol has been linked to numerous cognitive deficits including disruptions to memory. Alcohol consumption has also been linked to disruptions in the continuity and architecture of sleep in adults. Specifically, alcohol is known to act initially as a sedative, reducing sleep onset latency. It also increases slow wave sleep (SWS) and decreases rapid eye movement (REM) sleep early in the sleep period. However, subsequently it decreases SWS, increases REM sleep and also increases sleep disruptions in the second half of the sleep period. Sleep disruptions have been linked to memory deficits and it is thought that sleep processes may play an important role in memory consolidation. In particular, SWS and REM sleep have been highlighted as being particularly important for sleep related memory consolidation. Although the independent relationships between alcohol and memory deficits, alcohol and sleep disruption, and sleep and improved memory are well researched in adults, less is known about adolescents and young adults. Additionally, no studies to date have assessed the effects of alcohol on sleep related memory consolidation in any age group. Adolescents and young adults are increasingly reliant on memory processes as they transition from high school, and are exposed to challenging tertiary education and workplace environments. Given that they are also in the midst of rapid physiological development, alcohol related disruptions to sleep and memory may be particularly detrimental to this age group. In light of the limited knowledge about the impact of acute alcohol use on young adult sleep and memory, the present investigation had two aims. The first experiment aimed to characterise the effects of acute alcohol consumption on sleep quality and architecture in young adults, and secondarily, to assess whether the half night sleep architecture effects seen in previous literature may be as a result of changes to sleep cycle length, rather than changes to sleep architecture. In accordance with the adult literature, it was hypothesised that alcohol would act initially as a sedative, being associated with shorter sleep onset latencies, but subsequently disrupt sleep, with more sleep disturbances in the second half of the sleep period. It was also hypothesised that alcohol would alter sleep architecture, being associated with more SWS and less REM sleep in the first half, but less SWS and more REM sleep in the second half of the sleep period. The second experiment aimed to elucidate whether any sleep disruptions found would disrupt sleep related memory processes in this age group. It was hypothesised that alcohol would disrupt memory directly, being associated with decreased performance on a procedural memory task in a daytime waking condition. It was also expected that alcohol would disrupt sleep related memory consolidation by disrupting sleep, resulting in an absence of improvement in the performance of a procedural memory task following a night of sleep when compared to a night of sleep deprivation. Placebo administration, however, was expected to be associated with enhanced performance on the procedural memory task following a night of sleep when compared with sleep deprivation. Participants for the first experiment were 24 (12 female) 18-21 year old light drinking volunteers. All underwent three nights of polysomnography (PSG) in a sleep laboratory- an adaptation night followed by alcohol and placebo nights counterbalanced over participants. All participants received a standardised meal 5 hours before lights out and were allowed to sleep from their normal bedtime until natural awakening from sleep. On alcohol nights, in the half hour starting one hour before lights out, participants were dosed with vodka mixed with orange juice in order to achieve a breath alcohol concentration (BrAC) of .1% on the basis of weight, height and total body water. On placebo nights, participants received an equivalent volume of orange juice with a straw dipped in vodka. Results indicated that young adult sleep was altered by alcohol, in a pattern broadly consistent with the adult literature. Slow wave sleep was increased and REM sleep was decreased in the first half of the sleep period, and particularly in the first sleep cycle, while SWS was decreased and sleep disturbances were increased in the second half of the sleep period, and particularly very late in the night. Unexpectedly, however, there was no effect of alcohol on sleep onset latency and no rebound of REM sleep late in the sleep period- findings that are discrepant with the adult literature on alcohol and sleep, and may reflect developmental differences in sleep systems. Sleep cycle analysis also showed that the half night sleep architecture changes observed were not due to changes in sleep cycle length. Further, spectral analyses indicated that alcohol simultaneously promoted delta and alpha activity in the electroencephalogram (EEG) at frontal sites in the first sleep cycles. This finding is suggestive either of an arousal influence which may compete with the sleep maintenance influence of delta sleep, or of a phenomenon similar to, or the same as, alpha-delta sleep- an EEG pattern that indicates the presence of an extremely disruptive stimulus during sleep. Given the disruptive influence of alcohol observed in this experiment, the second experiment examined the possible cognitive consequences of this sleep disturbance. Participants for the second experiment were 36 (18 female) 18-21 year old right handed young adults selected using the same criteria as experiment one, and randomly assigned to one of three groups- normal sleep, sleep deprivation or daytime waking groups. They participated in two experimental nights- one alcohol and one placebo- each preceded by an adaptation night of PSG. Alcohol dosing procedures were identical to experiment one. Normal sleep and sleep deprivation participants learned a procedural memory task 3 hours prior to their normal bedtimes before 8 hours of sleep (with PSG) or sleep deprivation and were retested on the memory task the morning after the condition. Daytime waking participants learned the memory task one hour after awakening but underwent the same sequence of events in the same length of time as the other participants, being tested on the task after 8 hours of daytime wakefulness. Contrary to predictions, results indicated that there were significant improvements in performance on the memory task from the test to the subsequent retest in all three groups with no differences between groups or alcohol condition. This indicated that memory was consolidated over time, regardless of whether that time was spent asleep or awake, and irrespective of alcohol consumption. In other words, results showed no evidence of sleep related memory consolidation and so the effect of alcohol on this process could not be assessed. In summary, findings confirmed that similar to adults, alcohol consumption in young adulthood drastically disrupts the continuity and architecture of subsequent sleep. Additionally, they highlighted the rationale of examining sleep in this age group, as the absence of a shortened sleep onset latency and a REM sleep rebound after alcohol is uncharacteristic of findings in adults. We speculate that these findings may indicate that alcohol may have some unique effects on young adult sleep due to maturational differences in the sleep system. Results further extend previous findings indicating the presence of increased alpha and delta activity at frontal EEG sites, which may suggest an impairment of sleep’s restorative qualities after alcohol use. Regardless of these impacts, results also indicate no evidence of a sleep related memory enhancement effect and no direct effect of alcohol on memory. Therefore, there was no opportunity to assess the effects of alcohol on sleep related memory consolidation. These findings are discrepant with the adult literature, and suggest that procedural memory consolidation may be robust to alcohol related interference in young adults, and be time dependent rather than state dependent, happening independently of sleep-wake states. These findings make important contributions to the field’s understanding of the independent relationships between alcohol and sleep, sleep and memory and alcohol use and memory. They highlight the disruptive influence of pre sleep alcohol use on young adult sleep, particularly very late in the sleep period, and extend previous literature, pointing to more subtle alcohol-related disruptions in the sleep EEG. They also highlight the importance of distinguishing between memory consolidation and sustained performance enhancements when assessing the sleep related memory consolidation effect. Future investigations into these effects should include an older comparison group and utilise alternative types of memory tasks (e.g. declarative or episodic tasks), allowing for a more direct assessment of age related differences and of the possible existence of the sleep related memory enhancement for different types of memory. This would assist educational opportunities for young adults- a developmentally unique age group known to engage in risky drinking.