Moderate Ethylic Alcohol Consumption Memory Impact

Research on Whether Moderate Ethylic Alcohol Consumption Impairs the Formation and Retrieval of Long-Term Memories

Subject: Psychology

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The aim of this research was to investigate if there could be any potential beneficial effects of consuming a moderate amount of ethylic alcohol on the cognitive process of memory formation and retrieval in the long-term. Thus, the research question explored was ‘Research on whether moderate ethylic alcohol consumption impairs the formation and retrieval of long-term memories’.

The investigation tried to confront the common belief of alcohol (moderate or excessive) being associated with a decline of cognitive capabilities. Recent research suggested that a moderate alcohol consumption in late life results in better episodic memory and larger hippocampal area (Downer, Jiang, Zanjani, & Fardo, 2014). The research firstly explored how ethylic alcohol affects different areas responsible for memory like the hippocampus and the amygdala and also looked at the effects upon neurotransmitters in the brain. Secondly, the research compared studies suggesting alcohol impaired memory formation and retrieval and research looking at the contrary. Research implying alcohol can be harmful for memory looked only at the effects of excessive drinking and there did not seem to be a downside of drinking moderately. It is difficult to establish what moderate consumption is due to the fact that it differs everywhere around the globe and often varies from men to women. In order to avoid taking a reductionist point of view, the research explored other factors that could have an effect on memory such as sleep, stress and nutrition.

In conclusion, excessive drinking could be associated with an early onset of dementia whilst a moderate consumption seemed to prevent the appearance of Alzheimer’s disease due to the antioxidants found in beverages. Additionally, even if blackouts may occur due to drinking excessively, long-term memories remain intact unless there is a persistent abuse over time. However, in that case, the brain is able to recover itself by abstaining.

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Abstract word count: 297

The consumption of ethylic alcohol can damage different parts of the brain like the hippocampus and the amygdala which are responsible for memory. Heavy drinking can also affect neurotransmitters levels like glutamate (McEntee & Crook, 1993), GABA (National Institute on Alcohol Abuse and Alcoholism, 2015), serotonin (National Institute on Alcohol Abuse and Alcoholism, 2015), dopamine (Mandal, 2015) and acetylcholine (Alban, 2016; Arendt, Schugens, & Bigl, 1990) which are intertwined with keeping memory processes. White (2003) suggested that alcohol interrupts memory processing which is why blackouts occur (not being able to remember bits of information after being intoxicated). Further research obtained a correlation between heavy drinking and poorer performance on memory tasks (Parada et al., 2011). Nevertheless, these issues are associated with excessive drinking and the effect should be the contrary with moderate drinking as suggested by Sabia et al. (2014) who found out that heavy drinkers experienced memory loss six years sooner than moderate drinkers.

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Moderate consumption is defined as less than 14 units per week for both men and women in the UK, taking one unit to be 8 grams of pure alcohol (drinkaware.co.uk, 2016). However, it is difficult to determine what moderate drinking really is since the value changes in different places around the globe and research assessing the positive and negative effects of moderate drinking use different amounts of alcohol in their investigation. According to Weyerer et al. (2011), a moderate intake seems to decrease dementia risk which was further investigated by Wheeler (2008) who found out that the antioxidant polyphenols found in red wine remove protein that accumulates in Alzheimer’s patients as well as resveratrol (in champagne) which improves memory and protects against impairment (Alzheimer’s Drug Discovery Foundation, 2014). Surprisingly, abstainers had a lower cognitive performance compared to moderate drinkers in a study by Arntzen, Schirmer, Wilsgaard and Mathiesen (2010). A review study suggested that there is substantial evidence to say that light to moderate red wine intake decreases dementia and cognitive decline (Neafsey & Collins, 2011).

Henceforward, the aim of this paper is to investigate if there are any beneficial effects of moderate consumption on the formation and retrieval of long-term memory.

The hippocampus seems to be highly involved with memory consolidation. It is important for the transference from short-term (STM) to long-term (LTM). Additionally, the hippocampus is able to grow new neurons (thus, if there was alcohol damage it would not be as severe) although it can be impaired by glucocorticoids (Kühn et al., 2014). The importance of the hippocampus in memory is supported by the case study of HM (Scoville & Milner, 1957) who had epileptic seizures due to brain damage. Consequently, surgeons removed tissue from the medial temporal lobe including the hippocampus to try to stop the seizures. As a result, HM suffered anterograde amnesia, meaning that he could not create new episodic or semantic memories but memories from before the operation remained intact. Hence, the hippocampus was shown to be a temporary store.

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The amygdala is located at the end of the hippocampus. It is responsible for the processing of emotional memories. The case study of B.P. (Cahill, Babinsky, Markowitsch, & McGaugh, 1995) who had a damaged amygdala due to a disease highlights its importance. Psychological tests showed he was in the normal range for cognitive functions including attention, intelligence and STM. B.P. was told a story about a boy walking with his mother to visit his father at work (phase 1). Then, emotional events were introduced with graphic pictures of the boy being injured in a car accident (phase 2). He did not show an enhanced memory for phase 2 although presented normal memory for phase 1 and reported a high emotional reaction to the story. Thus, findings suggest that influence of emotional arousal on LTM is mediated by the amygdala; if there is a higher emotional arousal, it is remembered better.

Information processing requires an input, encoding, storage, retrieval and an output. Excessive drinking interrupts the process and does not allow the input to be stored which is why blackouts occur (White, 2003). Atkinson & Shiffrin (1968) proposed the multi-store model which suggests that there are three main separate stores (see Figure 1) and the memory processes are sequential.

Sensory memory registers sensory information and stores it for around one to four seconds. The information is captured by the senses and so, it is modality specific (e.g. hearing, vision). Only a small part continues into short-term memory store, which depends on whether the individual was paying attention or not. In case one was not paying attention, the information will be filtered out. The next stage is short-term memory. It has a limited capacity of around seven items and a limited duration of about six to twelve seconds. In order to transfer information processed in STM to the LTM store, it must be rehearsed otherwise, the information will be forgotten. If there is an elevated alcohol intake, it will interrupt the process here as the input will not be rehearsed and thus, will not be transferred into LTM (White, 2003). LTM is the final destination of memories, according to the multi-store model, it has indefinite duration and unlimited capacity. Although it is the “permanent” storage, some memories can be forgotten due to interference or retrieval failure (Hannibal & Crane, 2012a).

Alcohol intake affects the levels of different neurotransmitters that play a role in the formation and retrieval of memories. Glutamate is an excitatory neurotransmitter that affects cognition, memory and learning. It is needed for long term potentiation (LTP) (McEntee & Crook, 1993) which is the process by which learning occurs as the result of the synapse of one neuron being repeatedly fired and excited by another neuron (Yue, 2013).

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GABA is an inhibitory neurotransmitter that can be very powerful in intensifying the responses of the body, feelings and mood which is also affected by the intake of alcohol. In a sober state, the brain works to balance the neurotransmitters that excite with the ones that inhibit in order to keep the body balanced (National Institute on Alcohol Abuse and Alcoholism, 2015). Alcohol disrupts the communication between nerve cells which is what truly underlies memories, meaning that memories will not be saved in LTM (Tokuda, Izumi, & Zorumski, 2011). Ethylic alcohol increases the levels of the inhibitory neurotransmitter GABA by binding to the receptor sites of neurons, reducing energy levels and calming everything down. Since it is an inhibitory neurotransmitter, it decreases the communication between neurons and decreases the levels of glutamate. As previously mentioned, glutamate plays an important role in LTP therefore, not having enough glutamate will interrupt LTP and as a result, memories from the STM will not be able to be transferred into the LTM storage (MacDonald, 2016). Glutamate is also responsible for increasing brain activity and increasing energy levels but because alcohol suppresses glutamate, brain functions slow down. Ethylic alcohol is a depressant in the brain because it reduces excitatory neurotransmitters and increases inhibitory neurotransmitters (DiSalvo, 2012).

Serotonin, another neurotransmitter in charge of regulating emotional expressions also increases in the brain, as well as endorphins which induce feeling of relaxation and euphoria (National Institute on Alcohol Abuse and Alcoholism, 2015). Dopamine increases in the reward centre, the place that creates a gratifying feeling when doing a pleasurable activity e.g. spending time with friends. Dopamine helps to improve STM and is in charge of deciding what stays in STM and what is transferred to LTM. Low levels of dopamine in the frontal lobes lead to an impairment on cognitive functions (Mandal, 2015). As a result of an increased level of dopamine, ethylic alcohol makes one feel good and therefore, one keeps drinking in order to obtain more dopamine and carry on feeling good. At the same time dopamine is released, an alteration is caused among the other brain chemicals that enhance feelings of depression. After drinking for a long period of time, the effect of dopamine diminishes but the drinker is addicted to the feeling even though they are no longer getting more dopamine released (DiSalvo, 2012). The brain tries to adapt and compensate for this disruptions however this can help to build ethanol tolerance that could result in having a strong dependency towards alcohol and having withdrawal symptoms (National Institute on Alcohol Abuse and Alcoholism, 2015). Acetylcholine, another neurotransmitter found in the hippocampal region, plays a major role in the ability to learn and form episodic memories. It is necessary to have a sufficient level of acetylcholine to have good memory and is needed to convert short-term memories into long-term. Deficiencies of acetylcholine commonly results in dementia and Alzheimer’s disease, individuals with Alzheimer’s can have 90% lower levels of this neurotransmitter than usual (Alban, 2016). According to research (Arendt et al., 1990), excessive alcohol induces a decrease of acetylcholine whilst moderate intake seems to release more acetylcholine and other neurotransmitters involved in cognitive functions (Downer et al., 2014). Nevertheless, when drinking moderately, there should not be a significant variation in the number of neurotransmitters.

Ethylic alcohol seems damage memory if it is consumed excessively (more than 14 units per week for both men and women in the UK; taking one unit to be 8g of pure alcohol (drinkaware.co.uk, 2016)). Excessive drinking affects declarative memory. It causes damage to the hippocampus, resulting in anterograde amnesia (Parada et al., 2011), like the previously mentioned case of patient HM.

Parada et al. (2011) found a clear connection between excessive drinking and a lower ability to learn new verbal information. They examined 122 Spanish university students and divided them into those who abstained from drinking and those who took part in intensive alcohol consumption. Parada et al. subjected the students to a neuropsychological assessment using a logical memory assessment to test verbal declarative memory and tests to measure visual declarative memory. The results enabled them to establish a link between heavy drinking patterns and poorer performance on memory tasks. Intensive drinkers recalled fewer words than abstainers in the verbal declarative memory test and also displayed more difficulties recalling verbal material in the logical memory test but there was no significant difference in the visual memory test. Although this study does support that heavy drinkers can have more difficulties than those who abstain, it is an ethnocentric piece of research as all the participants were Spanish students and perhaps the results would be different elsewhere in the world if other ethnicities had a stronger tolerance to alcohol. Moreover, the sample is also biased as they are all university students and their brains could be more susceptible to alcohol abuse than maybe an older adult aged 35. Parada et al. did not look at the effects of moderate drinking and perhaps, the results could have been better than for abstainers.

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Intensive ethanol intake impairs the activity in brain receptors responsible for learning, putting younger individuals at a higher risk for memory loss. The damage caused is not immediately visible but memory loss increases in later life. Similarly, heavy drinking in seniors also results in experiencing memory loss six years sooner than for those elders who drink moderately (Sabia et al., 2014). Ethylic alcohol is responsible for alcohol related dementia which is 10% of all dementia cases (Gupta & Warner, 2008). Nonetheless, it is hard to say that it is just alcohol responsible for this memory loss as there could be other factors or health conditions affecting their memory.

Alcohol-related brain impairment (ARBI) is a common outcome of ethanol abuse. The issues it presents are memory loss, inability to learn new things, inability to follow conversations coherently and often becoming mentally confused and confounding pieces of information (Better Health Channel, 2015) with the potential of evolving into Wernicke and Korsakoff’s syndrome by producing a thiamine (vitamin B1) deficiency. If this syndrome is left untreated, the consequence is a severe anterograde amnesia (Zahr, Kaufman, & Harper, 2011).

Although frequent excessive alcohol intake can cause the hippocampus to lose its ability to perform cognitive functions and retain new information, abstaining from drinking can help the brain to restore itself. Kühn et al., (2014) investigated the effects of abstinence on the brain by using MRI brain scans to see if there was any change in the hippocampus of an individual abstaining as part of the treatment for alcoholism. The scans generated information regarding the size and the level of function inside the hippocampus. Kühn et al. selected 42 subjects affected by alcoholism and 32 unaffected. They conducted two MRIs. The first one was at the first stage of the treatment right after alcohol withdrawal had taken place. The second one was two weeks in the treatment. The results obtained from the first set of scans showed that people with alcoholism had damages to the hippocampus compared to individuals without alcoholism but still displayed a slight increase of grey matter. The results after two weeks in the process exhibited a substantial regain in hippocampus functions including an increased volume. It could therefore be inferred that after longer periods of abstinence, the brain will grow new cells (neurogenesis) and will heal itself by strengthening the connections between neurons through the process known as neuroplasticity, and eventually, will return to its normal state (HAMS Network, 2015). Yet, damage to the hippocampus could have been the result of factors other than alcohol. Perhaps the alcoholics had a more stressful life and the damage was caused by glucocorticoids and repaired leading a stress-free lifestyle during the treatment. However, contrary to the popular belief that alcohol kills brain cells, unless there is a thiamine deficiency (vitamin B1), brain cells are intact even if the brain shrinks. The same number of grey cells (responsible for thinking, feeling and decisions) was found in heavy drinkers and non-drinkers. A long period of abstinence or moderate drinking can restore the brain volume of heavy drinkers to nearly the same size as non-drinkers and hence cognitive functioning returns to normal (Jensen & Pakkenberg, 1993; Pfefferbaum et al., 1995).

According to Arendt, Schugens, & Bigl (1990) alcohol decreases acetylcholine levels. Some rats were treated with a solution of ethanol for 28 weeks, whilst controls had water. They found that levels of acetylcholine decreased in the cortex and hippocampus four weeks after alcohol withdrawal. The rats presented an impaired performance in a spontaneous alternation task tested at long acquisition-retention intervals. Ethylic alcohol was responsible for memory impairment in the rats. Injecting physostigmine (0.45 g/kg) could inhibit the enzyme responsible for the breakdown of acetylcholine, meaning that there was more acetylcholine available at the receptor sites.

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Although the outcome of an impaired memory seems to apply when the alcohol intake is excessive, it does not mean that the effect will be the same if intaking a moderate amount. Moreover, other factors also have a role to play in the complex cognitive process of memory, meaning that a direct cause and effect cannot be established.

After previously discussing whether alcohol was harmful for memory, the opposite needs to be discussed to determine if moderate alcohol intake could be beneficial for memory formation and retrieval.

Downer et al. (2014) found a correlation between moderate alcohol consumption and better memory. They defined the terms moderate as 7 to 14 drinks per week and heavy as 15 to 34 per week. The researchers collected data from 660 patients asking them to complete surveys, assessing their neuropsychological state, looking at whether they had Alzheimer’s risk factor and taking MRIs of their brains’ activity. They found that moderate alcohol consumption in late life (60 years and older) is associated with better episodic memory and larger hippocampal volume in comparison to late life abstainers but perhaps, they already had a larger hippocampal volume due to other factors like healthier nutrition or stress-free lifestyle. This study just shows a correlation, not necessarily a causation. It could be argued that individuals who were able to drink in their late life were healthier in general and had better episodic memory than those who had to abstain due to a medical condition. Also, the validity of the data is questionable as they used surveys and individuals might have tried to make themselves look better by giving false responses.

Similarly, German researchers (Weyerer et al., 2011) discovered that moderate alcohol consumption also decreases dementia risk as opposed to heavy drinking which can be responsible for the contrary (Alzdiscovery, 2016). Weyerer et al. carried on a longitudinal study. They interviewed 3,327 individuals aged 75 and over and followed up with them collecting information from doctors and family members. They also looked at other factors like depression and smoking. At the end of the three years, 217 developed dementias, of which 111 developed Alzheimer’s disease. Half of those declared that they did not intake any form of alcohol regularly. Participants who had a moderate consumption of maximum two drinks of 10 grams, were 29% less prone to develop dementia and 38 percent less likely to suffer from Alzheimer’s. The validity of the data is still questionable since individuals tend to lie in interviews to make themselves look better however, it is more reliable than Downer et al. (2014) as information was also collected from doctors and family members. The study is ethnocentric since it took place in Germany where moderate drinking is defined slightly differently than in the UK (20-29 drinks of 10g as opposed to 14 drinks of 8g in the UK per week).

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Red wine has been shown to have antioxidant polyphenols in charge of removing protein plaque that accumulate in the brain of Alzheimer’s disease patients (Wheeler, 2008). Red wine also contains another antioxidant called resveratrol which improves memory and helps to protect against late life mental impairment (Alzheimer’s Drug Discovery Foundation, 2014). Arntzen et al. (2010) seem to have found evidence supporting red wine intake being good for memory. They tested 5033 older adults on learning, memory and attention tasks after seven years. The results obtained illustrated that moderate wine consumption was associated with better performance on all cognitive tests on men and women. They found no correlation between other alcoholic beverages and cognitive test results. Alcohol abstention was associated with lower cognitive performance in women.

Neafsey & Collins (2011) conducted a review study of research carried out over the last few years. They came to the conclusion that excessive drinking is associated with a higher risk of dementia and cognitive impairment. Nonetheless, there is substantial evidence that light to moderate alcohol intake, especially wine, decreases the risk of dementia and cognitive decline. However, they did not state what was considered as moderate.

Trying to find a relationship between alcohol consumption and its effects on memory is taking a rather reductionist perspective. It is not possible to ignore all the other factors that could also play a role in the formation and retrieval of long-term memories.

Sleep deprivation is one of the causes that leads to poorer memory. Humans need to have enough sleep during the night in order to consolidate memories. Also, having a bad sleep causes fatigue which interferes with the ability to consolidate and retrieve memories (WebMD, 2015). Sleep deprivation disrupts hippocampal function responsible for memory consolidation. Activation of cortical regions for consolidation appears to happen during periods of inactivity and sleep which could may be attributed to not paying attention to anything else and non-REM sleep plays a large role in incorporating memories to cortical areas. An increase of GABA neurotransmitters affects sleep features and hippocampus dependent memory consolidation (Prince & Abel, 2013). Since alcohol increases the production of GABA, could there be a correlation suggesting that alcohol is helpful in consolidating memories?

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Factors such as depression and stress have an effect on memory. Depression creates a difficulty to pay attention and focus which impairs memory processing directly. Stress and anxiety cause the brain to be overstimulated and distracted therefore, the ability to remember is affected. Post-traumatic stress can also lead to memory deficiency (WebMD, 2015). Kirschbaum, Wolf, May, Wippich, & Hellhammer (1996) investigated if there was a correlation between cortisol levels and memory by selecting 40 healthy subjects and giving them either 10mg of cortisol or a placebo. After one hour, participants were tested on procedural and declarative memory and spatial thinking. Those who had cortisol showed worse performance in the declarative memory and spatial thinking tasks. Thus, high cortisol appears to lead to impaired memory function.

Additionally, physiological issues like complex B vitamin deficiency (especially B1 and B12) often result in memory loss (WebMD, 2015). Early life iron deficiency has been suggested to affect speed of processing, and learning and memory. It alters the structure and physiology of the developing hippocampus and therefore, can cause memory issues in the long-term (Fretham, Carlson, & Georgieff, 2011). Perrig, Perrig, & Stahelin (1997) illustrated that plasma antioxidant levels correlate with cognitive performance in healthy elders. 442 subjects aged 65-94 were tested for memory and plasma vitamin levels were measured. Results showed higher ascorbic acid and β-carotene were associated with better free recall, recognition and vocabulary. Since antioxidants may play a role in the prevention of progressive cognitive impairments, the polyphenols found in red wine could indeed ameliorate memory decline.

Due to all these factors being linked with having worse memory, it can simply be argued that those who intake moderate amounts of alcohol also have good sleep, no depression, stress or anxiety, and good health in general. Therefore, alcohol might not be responsible for better memory, but many other factors can be linked with a person that is overall healthy and also consumes alcohol.

Although heavy drinking can be associated with an early onset of dementia, moderate drinking seems to be safe and even prevents dementia and Alzheimer’s disease due to the polyphenols antioxidants found in beverages like wine. Even if blackouts may occur as a result of excessive alcohol intake, long-term memories are left unchanged and unharmed unless the abuse is persistent over a long term. If the abuse has been persistent, the brain is able to repair itself by neuroplasticity if one abstains for a period of at least two weeks.

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At the moment, it appears that moderate amounts of alcohol intake can be beneficial in the formation and retrieval of long-term memories taking into consideration the ability of the brain to heal itself through neuroplasticity and return to a normal state.

Other factors could also interfere with any possible correlation between alcohol and memory such as sleep, stress or nutrition.

In conclusion, more research would need to be executed specifically addressing whether a moderate amount of alcohol intake impairs the formation and retrieval of long-term memories. Ideally, it would be carried out with different beverages to compare if the polyphenols in red wine truly prevent Alzheimer’s disease compared to other antioxidants found in whiskey, for example. Other factors like sleep, nutrition and stress should be taken into consideration in further research by comparing all this factors in different participants and having them to be between a specified limit to make sure that the findings support it is just the moderate amount of alcohol intake affecting long-term memory and no other random factors.

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Kühn, S., Charlet, K., Schubert, F., Kiefer, F., Zimmermann, P., Heinz, A., & Gallina

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