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How Alcohol Affects Cognition

Updated on March 21, 2018
Charlotte Doyle profile image

Charlotte is an artist, freelance writer, wife, homeschooling mother, and college student pursuing a Master's degree in psychology.

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This article is concerning alcohol-related dementia and a related condition known as Wernicke-Korsakoff syndrome. Dementia can happen due to the toxins held within alcohol itself. Alcohol dementia causes damage to different areas of the brain, and usually, this kind of damage occurs due to alcohol abuse. It is known that the human brain is extremely vulnerable to alcohol, and its neurotoxic effects. A direct result of this is cognitive disorders. The cognitive complications may occur due to an imbalance of the electrolytes, toxicity of a metabolite nature, or even malnutrition.

Alcohol-related dementia is correlated with drinking heavily throughout several years. While it's not actual dementia in itself, the person experiencing alcohol-related dementia may suffer from memory loss that is short term. By the Alzheimer’s Society, about ten percent of people who are quite young are already affected severely by this condition.

It has been found that the neuropathological studies, as well as the imaging findings, discovered that alcohol abuse (prolonged and excessive use) causes functional damage to the brain that is quite permanent. It also creates structural damage as well, which is also permanent. Alcohol appears to lower the amount of thiamine within the body. (Ridley, 2013) Thiamine is essential, as it is a B-complex vitamin. Those who do not have enough thiamine in their body have a condition called beriberi. Thiamin diphosphate is associated with glucose metabolism, and its essential enzymes. Thiamin Triphosphate is a bit chemically different but helps the body at the neuronal membrane level. The brain's Thiamin metabolism occurs between the glial cells and the associated neurons. Thiamin deficiency, caused by alcohol abuse, usually results in a condition known as Wernicke-Korsakoff syndrome. (Butterworth, 2003)

Imaging has shown that there brain's ventricular that is bilateral is usually enlarged. Other evidence has been seen that lessened thiamin related functioning within the brain are associated with the disease like Parkinson's or even Alzheimer's, which are neurodegenerative. Eventually, alcohol's toxicity and even the oxidative stress causes cell death, which increases neurological disorders, such as dementia and dementia-like symptoms. The deficits, of a cognitive nature that are evident with alcohol-related dementia, are issues regarding "visuospatial functions, memory, and executive tasks, with a potential for partial recovery if abstinence is maintained." (Sachdeva, 2016)

I would like to further expand on the syndrome known as Wernicke-Korsakoff, as it's usually found near research regarding alcohol-related dementia. According to the DSM-IV (the mental health disorder category literature, fourth edition), Wernicke-Korsakoff is also known as an alcohol-induced persisting amnestic disorder. This condition is usually discovered by those who have chronically abused alcohol. This condition itself is caused by a thiamine deficiency, and the lack then creates an issue of encephalopathy. Encephalopathy means a disease which negatively affects the brain through a toxin or infection, such as a virus.

This condition has its symptoms, such as confusion, deficits with learning and difficulties with memories. An individual may have a mental status that is altered, like symptoms of dementia or even confusion. They may also suffer from ataxia, which is balance or coordination that is impaired, usually due to a neurological issue. The patient may also present symptoms of nystagmus, which is also known as ophthalmoplegia. This is a situation where person's eye moves in strange directions without the person want it to. The eye may move in a circular motion, up and down and the vision may also blur. As mentioned before, this condition can also be caused without alcohol and may be present in those who suffer from anorexia, starvation, poor nutrition, and even schizophrenia. Women who are pregnant and in their first trimester may show symptoms of Wernicke-Korsakoff syndrome if they have already developed a condition known as hyperemesis gravidarum. This is when a woman has severe vomiting and nausea when they are pregnant. This is a significant difference between alcohol-induced dementia and Wernicke-Korsakoff syndrome. While they are similar, and may both have to do with a reduction in thiamin within the body, WKS may happen to a variety of people. Alcohol-related dementia only occurs to those who have abused alcohol.

There are a few barriers when it comes to associating alcohol with dementia. Usually, the lifestyle that comes with excessive alcohol use creates a situation where the person is more prone to brain-related injuries, such as falling or driving drunk, resulting in an accident. Sometimes, alcohol abuse is also associated with abuse or other drugs as well, which could complicate or even exacerbate existing neurological brain-related issues. The debate that exists has to do with whether or not it's possible to obtain dementia as alcoholism's direct result. Does neurotoxicity, or an ethanol nature, primarily cause alcohol-related dementia, or does the manifestation of dementia show up due to another issue created by alcoholism, such as lessened thiamin levels? Again, the lifestyles of alcohol abusers create a problematic situation when it comes to directly connecting alcohol abuse to dementia.

The outlook is somewhat positive, as it appears that about twenty-five percent of those who are affected by alcohol-related dementia may eventually make a good recovery. Half of these individuals may achieve what is known as a 'partial recover,' and these people will need much support to carry on with activities of daily living. Another twenty-five percent, unfortunately, will not recover and these individuals will require long-term care, indefinitely. To recover from this, the individual has to catch dementia or dementia-like symptoms early enough, cease drinking entirely, and replace current diet with a healthier diet. They have to take supplements to replace vitamins that have been neglected, especially thiamine.

As of now, alcohol-related dementia has been relatively quiet but is an issue that will get progressively worse, especially with the increasing incidence of the condition within young people. Many countries may call the situation as alcohol amnesia or alcohol-related brain injury, as dementia has not been entirely proven, due to the barriers mentioned above.

References:

Butterworth, R. (2003) Thiamin deficiency and brain disorders. Nutr Res Rev. 2003 Dec; 16(2):277-84. doi: 10.1079/NRR200367.

Ridley, N. J., Draper, B., & Withall, A. (2013). Alcohol-related dementia: an update of the evidence. Alzheimer’s Research & Therapy, 5(1), 3. http://doi.org/10.1186/alzrt157

Sachdeva, A., Chandra, M., Choudhary, M., Dayal, P., & Anand, K. S. (2016). Alcohol-Related Dementia and Neurocognitive Impairment: A Review Study. International Journal of High-Risk Behaviors & Addiction, 5(3), e27976.http://doi.org/10.5812/ijhrba.27976

© 2018 Charlotte Doyle

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