The Effects of Alcohol on Long-term Memory - Research Paper Example

INTRODUCTION Alcohol is a substance that brings threat to the health of an individual globally and may result to multiple organ system dysfunctions; however, alcohol remains to be a part of the culture of mankind despite of its deleterious long term effects (Lee, et al., 2009). Alcohol poses varied effects not only in the brain, but also, to other parts of the body (Lee, et al., 2009). The effects of alcohol that can be deleterious to the body include difficulty in walking, blurring of vision, slurring of speech, slowing of reaction time, and impairment of memory (National Institute on Alcohol Abuse and Alcoholism, 2004). The ability of alcohol to impair the brain can be detected only after one or two bouts of drinking alcoholic beverages; however, this can be resolved quickly as soon as the person stops drinking alcohol (National Institute on Alcohol Abuse and Alcoholism, 2004). Among heavy drinking individuals, brain deficits may persist when drinking goes on for a long period of time even after that individual becomes sober. The topic on the effects of alcohol to the brain remains as a hot subject matter in research even to this date (National Institute on Alcohol Abuse and Alcoholism, 2004). One must note that the ability of the brain to form a new long – term memories is hampered primarily by alcohol; however, the previously established long – term memories and its ability in keeping new information active in the memory box for a short period remains intact (White, 2003). As the consumption of alcohol is increased, the memory impairment magnitude does also increases. Hence, alcohol consumed in large amount rapidly produces partial or complete blackouts described as period of loss of memory for events that just transpired while in beige drinking (White, 2003). Among social drinkers, in addition to college drinkers, blackouts were found to encompass events ranging from minor conversation to its worst sequelae of doing sexual intercourse. In alcohol induced impairments of memory, a disrupted hippocampal activity was noted to play a central role in the new memory information (White, 2003). The effect of the long – term use of alcohol results to the damage of the nerve cell connections causing irreversible damage to the brain exhibited as loss of memory as well as personality changes (VirginiaTech, 2012). To perform activities of daily living, proper functioning of the memory is essential since it is necessary in the individual’s ability to learn and remember things (Verster, et al., 2003). However, during episodes of alcohol intoxication, an impairment of memory and psychomotor activity has been reported consistently. Ultimately, it was reported that serious deficits of memory were noted among individuals who engages in frequent binge drinking. Verster, et al. (2003) reported that a study performed in rats showed a significant corticolimbic neural cell loss after a 4 – day continuous binge drinking. Verster, et al. also noted that alcohol hangover affects not only people who indulge in drinking but also results to serious consequences in the economy. In the United States (US), absenteeism reported as hangover – related results to poor performance at work that wasted a yearly expenditure to the economy of the US to about 148 billion USD (Verster, et al., 2003). With regards to their relationships with the co – workers and superiors, conflicts of alcoholics with their supervisors and co – workers were noted among individuals who previously had alcohol hangover (Verster, et al., 2003). They were also noted to feel miserable in the job with a significant tendency to fall asleep during working hours. Hence, a reduction in the physical performance among health volunteers and the athletes during hangover were also reported (Verster, et al., 2003). Wernicke – Korsakoff Syndrome Aside from long – term memory loss, a deficiency in thiamine was seen in about 80 percent of alcoholics, and these individuals are projected to develop Wernicke – Korsakoff Syndrome, a serious disorder of the brain consisting of two syndromes known as Wernicke’s encephalopathy and Wernicke’s psychosis (National Institute on Alcohol Abuse and Alcoholism, 2004). Individuals with Wernicke’s encephalopathy exhibit either of the following signs and symptoms of mental confusion, nerve paralysis such as oculomotor disturbances and difficulty in coordinating the muscles (National Institute on Alcohol Abuse and Alcoholism, 2004). An example of a person with Wernicke’s encephalopathy exhibit confusion in finding their way out or has inability to walk. In some cases, the classic signs and symptoms of Wernicke’s encephalopathy were left undiagnosed until after death only after finding out that patients are having thiamine deficiency – related encephalopathy (National Institute on Alcohol Abuse and Alcoholism, 2004). On the other hand, about 80 to 90 percent of alcoholic individuals also develop a chronic and debilitating syndrome that is characterized with persistent problems in learning and memory known as Wernicke’s psychosis (National Institute on Alcohol Abuse and Alcoholism, 2004). Patients with this syndrome are oftentimes forgetful, frustrated quickly and are having walking and coordination difficulty. What is striking most in this type of syndrome is the patient’s difficulty in putting on new information, otherwise known as anterograde amnesia; however, in some cases, the ability of the patient to remember old information (retrograde amnesia) is also notably reduced (National Institute on Alcohol Abuse and Alcoholism, 2004). Alcohol and Fetal Alcohol Syndrome During pregnancy, drinking can also lead to a collection of serious symptoms of fetal alcohol syndrome, and its effects lead to physical, learning, and behavioural effects in a brain that is still developing (National Institute on Alcohol Abuse and Alcoholism, 2004). Children with fetal alcohol syndrome are remarkably smaller and posses a distinct feature in their faces. In worst cases, long – term problems in learning and behaviour are developed due to less number of brain cells or neurons that leads a child not to function correctly as expected (National Institute on Alcohol Abuse and Alcoholism, 2004). BODY OF TEXT Tsambazis and Stough published in the year 2000 a paper entitled Alcohol Impairs Speed of Information Processing and Simple and Choice Reaction Time and Differentially Impairs Higher – Order Cognitive Abilities. This study was done to prove whether alcohol impairs processing of information in all stages of information processing from the earlier to the later stage of processing information. Although previous studies were done on the impairment of information among alcoholics, it somehow failed to classify what stage of impairment the patients were classified at. As a result, this study is aimed to examine the effects oral intake of alcohol to information processing from the earliest to its latest stages. There were sixteen (16) adults who participated in the study in both alcohol and placebo, which were assessed for inspection time, simple reaction time, choice reaction time, and cognitive ability using Wechsler Adult Intelligence Scale – Revised (WAIS – R). In this study, the inspection time was used “as a predictor variable in a linear regression to examine whether a disruption of the early stages of information processing accounted for changes in total information processing after alcohol administration (Tsambazis and Stough, 2000). Because this was the first study that uses the WAIS – R subtests to examine the effects of alcohol, the point of comparison of the results from other studies using varied tasks was notably difficult to compare. Hence, the authors of this research recommended that further research must be done to examine the influence of alcohol that uses the WAIS – R subtest performance to replicate the existing result. The results obtained from this study indicated that during the early stages of information processing, the total information processing was significantly slowed by alcohol. From this study, it was concluded that based on the information measured by WAIS - R, alcohol impairs processing of visual information, attention, abstract reasoning, and visuo – motor condition among individuals. The results were consistent with observed impairment on the inspection time as well as simple and complex reaction time. However, the effects of alcohol on the inspection time were not able to foresee the result of alcohol on simple and complex reaction time as well as on the WAIS – R subtest, which only suggests that on the early stages of information processing, the effect of alcohol was not determined to be the cause of decreased total information processing performance. To find out more on the effects of alcohol in long – term memory, another study by Verster, et al. (2003) on Alcohol Hangover Effects on Memory Functioning and Vigilance Performance after an Evening of Binge Drinking was reviewed in this paper. It was noted in this paper that the impairing after effects of acute alcohol intoxication on the memory functioning among health volunteers after chronic alcohol use are established well; however, a research that determines the next morning effect showed scarce results on the effect on the memory functioning after a single episode of binge drinking. In a single – blind study that comprises an evening session as its baseline, a total of 48 healthy volunteers were asked to participate in the study followed by the administration of 1.4 grams per kilogram of ethanol or placebo as its treatment, and a morning sessions. The effect of alcohol in the memory is tested by performing a word – learning test, which include the immediate and delayed recall as well as the recognition test. Included in the investigation is a 45 – minute Mackworth clock test used in measuring vigilance as well as the alertness of the subject. Mackworth clock test is done to conclude whether or not the findings in the word – learning test suggest sedation or specific impairments in the memory. In this study, the results had shown that in alcohol group, it is expected that delayed recall in the morning session was worse compared to the placebo group. On the other hand, an unimpaired immediate recall and recognition were noted in the alcohol group, which is unlikely in the morning session group noted in the alcohol group who exhibited a significantly reduced alertness of the subject under placebo group before and after the study. Conversely, there was no significant difference observed in the morning session between the alcohol group and placebo group using the Macworth clock test. Verster, et al (2003) concluded in their study of impaired delayed recall that during alcohol hangover, a significant impairment of the memory retrieval process was shown. However, there was no significant effect on the vigilance performance indicating that this particular impairment in memory “does not reflect sedation.” In another study that correlates the of alcohol in memory is done by White (2003), which explained that blackouts are amnestic episodes wherein an individual is capable of participating in the most salient to the most mundane events that they cannot remember later. This is best explained with memory impairments as a result of milder alcohol intake which blocks the ability of an individual in forming new memory while he is still under the influence of alcohol. This is due to the ability of alcohol to impair the ability of an individual to form memory; however the ability to recall memories prior to its intoxication is typically intact. White (2003) added that several other factors play an important role in memory loss/blackouts aside from drinking large quantities of alcohol. White quoted Goodwin and colleagues (1969) in their studies noting that heavy drinking alone is not sufficient in producing blackouts, but rather, it is associated with other factors such as “gulping drinks and drinking on an empty stomach.” In some cases, the combination of alcohol with high doses of other sedative drugs such as diazepam (Valium) and flunitrazepam (Rohypnol) may also produce severe impairment of memory since alcohol has the capacity to augment the effects of benzodiazepines. Thus, the likelihood of memory impairment is increased dramatically when alcohol is combined with the aforementioned drugs. Moreover, a greater impairment of memory is produced when alcohol is combined with psychoactive compounds such as marijuana than taking it alone. This was proven by O’Malley and Johnston in their literature noting that a more emphasized effect on blackouts is increased among students who were using the combination of alcohol and polysubstance than the effect of taking alcohol alone. On alcohol, memory, and hippocampus, White (2003) noted that a disruption of the hippocampal activity was speculated as the mechanism that had caused memory impairment secondary to alcohol. The aforementioned speculation came from the observation noting that a syndrome of memory impairment is caused by the acute exposure to alcohol producing a syndrome of impairments of memory that is in various ways, similar with that was produced in hippocampal damage. Hence, an individuals’ ability to form a new long term and explicit memories are impaired by both acute exposure to alcohol and damage to the hippocampus; but not the storage recall of short – term and long – term memories. White (2003) added that from the research previously conducted using animal models to support the hypothesis suggested that the impairment of memory formation by alcohol were supported by the disrupting activity noted in the hippocampus. This research were supported by the “behavioural observation, examination of slices of and brain tissue, neurons in cell culture, and brain activity in anesthetized or freely behaving animals.” To conclude the study, White (2003) noted that a dramatic impact on the memory was observed among alcoholic individuals since alcohol disrupts primarily the formation of new long – term memories as well as less disruption of recall of long – term memories that were previously established, and the individual’s ability in keeping “new information active in short term memory.” Although it can be detected in controlled conditions, the impairment caused by alcohol at low doses is often subtle; however, if the amount of consumed alcohol is increased, the magnitude in the impairment of memory is also increased as well. In severe cases, when alcohol is consumed in large quantity and rapidly, a condition termed as blackout, which is the time interval where an intoxicated person is unable to recall the details or the entire key events, is produced. On the other hand, a certain type of blackout known as en bloc blackouts is a condition where an individual has definitely “no memory whatsoever.” An episode known as fragmentary blackouts is noted when the memory of that certain alcoholic drinker is “spotty with islands” where the memory is only cued by other drinkers as to what had transpired. White (2003) stated that blackouts are commonly found among social drinkers as a consequence of acute alcohol intoxication. From the previously reviewed studies, it can be seen that the understanding towards the mechanism of alcohol induced impairment of memory has progressed tremendously. This includes the understanding towards the mechanism of hippocampal disruption of activity secondary to alcoholism through various routes that may directly affect the circuitry of the hippocampus or through indirectly interfering between the hippocampus and other regions in the brain’s communication. In contrast, White (2003) noted that although frontal lobe may probably play an important role in alcohol – induced impairments in memory, the alcohol impact on the frontal lobe regions remains understood poorly. A journal by Lee, et al. (2009) noted that it was thought for a long time that generally, alcohol brings forth an antidepressant effect on the central nervous system; however, this concept was refuted by Lee, et al., noting that alcohol only affects selectively certain parts of the brain. As an example, a condition known as alcohol – induced blackout is emphasized noting a temporary inability of the subject to form new long – term memories while maintaining other skills. Current studies reported that retrograde memory impairment caused by alcohol was reported specifically as blackouts secondary to impairments in retrieval of information and encoding deficits. In these study, depending on the severity of impairment of memory, alcoholic blackouts is classified as complete or partial; otherwise known as en bloc or fragmentary, respectively. Impairment of memory in acute intoxication causes a type of “memory encoded with spatial and social context” known as dysfunction of episodic memory. Currently, studies noted that discrete regions in the brain support the multiple memory systems; however, alterations of the hippocampus and its related structures in the learning and memory may be caused by the acute effects of the alcohol. The likelihood of acquiring blackout is due to the blood alcohol concentration’s rapid increase. On the other hand, Lee, et al. noted that genetic factors may also play an important role in the vulnerability of the CNS on the effects of the alcohol since not all subjects in their study experienced blackouts. Genetic factor reportedly predisposed individuals to alcoholism. Lee, et al suggested that to further learn on the mechanism and impact associated with the alcohol induced blackout, extensive research on memory and learning must be correlated with the acute effects of alcohol on the brain. Norton and Rape (2011) in a literature review entitled Brain Cognitive Deficits Associated with Alcohol Abuse notes that frontal cortex region, an area which is responsible in executive implementation, is highly susceptible to alcohol damage. The damage of the frontal cortex results to an individual’s compromise on their ability to plan in advance, on inhibition as well as on their ability to think on the outcome of their action. These cognitive deficits continue even after the individual gains sobriety. Treatment starts from educating the patient as well as the family members that may eventually improve cognitive deficits. CONCLUSION From the collection of studies of various journals and researchers, it can be concluded that the effect of alcohol to an alcoholic is variable and the degree of impairment and disease that may be experienced by an alcoholic may differ since these people may came from different origin (National Institute on Alcohol Abuse and Alcoholism, 2004). Hence, an inconclusive evidence were reported by most of the researchers noting that alcohol is the sole and only variable made to be responsible in brain deficiencies. It is therefore recommended that further research must be made to characterize the vulnerability of alcoholics to damages to the brain (National Institute on Alcohol Abuse and Alcoholism, 2004). REFERENCES Lee, H., Roh, S., and Kim, D. 2009. Alcohol Induced Black – out. International Journal of Environmental Research and Public Health, 6(11), 2783-2792 National Institute on Alcohol Abuse and Alcoholism. 2004. Alcohol Alert. Retrieved from http://pubs.niaaa.nih.gov/publications/aa63/aa63.htm Norton, F. and Rape, L. 2011. Brain Cognitive Deficits Associated with Alcohol Abuse. The American Association of Behavioral and Social Sciences Journal, 2011(15): 1-18. Tzambazis, K. And Stough C. 2000. Alcohol Impairs Speed of Information Processing and Simple and Choice Reaction Time and Differentially Impairs Higher – Order Cognitive Abilities. Alcohol and Alcoholism, 35(2): 197-201. Verster, J., van Duin, D., Volkerts, E., Schreuder, A., and Verbaten, M. 2003. Alcohol Hangover Effects on Memory Functioning and Vigilance Performance after an Evening of Binge Drinking. Neuropsychopharmacology, 2003(28), 740 – 746. VirginiaTech. 2012. Alcohol’s Effect on the Brain and Body. Retrieved from http://www.alcohol.vt.edu/students/alcoholeffects/brainbody.htm White, A. 2003. What Happened? Alcohol, Memory Blackouts, and the Brain. Alcohol Research and Health, 27(2): 186-196. Read More