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Alcohol affects the brain based on a person’s drinking habits. Occasional and moderate drinkers can suffer effects such as memory impairment, recklessness, and impaired decision making. Heavy drinkers tend to suffer from memory loss, loss of attention span, Wernicke-Korsakoff syndrome, loss of visuospatial abilities, and the ability to think abstractly.
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Consuming large amounts of alcohol quickly and/or on an empty stomach can cause a blackout or periodic memory lapses. Blackouts are more prevalent among social drinkers, regardless of factors like age or dependence. They also affect all genders; however, women tend to get blackouts more easily than men.
ARBD (alcohol-related brain damage) is a serious condition that occurs as a result of drinking too much alcohol over a prolonged period.
Unlike dementia, individuals with ARBD can recover partially or fully if they get support and stop taking alcohol.
To better understand the process of what alcohol does to the brain, we have issued a list below which describes the seven stages of alcoholic intoxication. They are as follows:
BAC, or Blood Alcohol Concertation of (0.01 to 0.05) can impair reaction time and judgment slightly depending on the person (factors like gender and weight). [1]
This phase occurs when the BAC ranges from 0.03 – 0.12. Euphoria occurs after 1 to 4 drinks for women and 2 to 5 drinks for men depending on factors like body size. This phase is signified by talkativeness, poor inhibition, and slight feelings of euphoria.
While this phase is pleasurable to a drinker, it has negative effects like impaired memory, judgment, and coordination. The risk of getting into an accident at phase 2 increases fourfold. Driving with a blood alcohol concentration of 0.08 or more is illegal. [2]
This phase is characterised by excitement. As the BAC increases from 0.09 up to 0.25, other effects like emotional instability, significantly delayed reaction time, and lack of critical judgment set in.
Other effects include nausea and vomiting, loss of balance, drowsiness, and vision, memory, and perception impairment.
This phase begins when the BAC level reaches 0.18 and lasts all the way to a BAC of 0.30 and includes disorientation and emotional upheaval. Individuals at this stage tend to feel very dizzy.
They may stagger if they are walking or have difficulty standing up if they are seated. They also exhibit other symptoms like forgetfulness, loss of memory, and increased pain threshold. [3]
This phase begins and ends at a BAC level of 0.25 and 0.40, respectively. This stage presents the highest risk of suffering from alcohol poisoning. The extreme intoxication causes excessive vomiting, inability to stand/walk, difficulty maintaining continence. [4]
Risk of getting into a coma increases when the BAC level ranges from 0.35 to 0.45. This phase is characterised by severely depressed circulation and respiration. A person can also suffer from body temperature drops, poor reflexes, and motor responses. [5]
Phase 7 is characterised by a BAC of 0.45 and above. At this BAC, the body can’t sustain vital functions resulting in death. However, death can still occur at lower BACs.
In the short-term, alcohol alters neurotransmitter levels in the brain. Neurotransmitters are critical for sending signals around the body. They also play a critical role in controlling emotion, behaviour, and physical activity.
In the short-term, alcohol alters the work of the neurotransmitter GABA producing effects like slurred speech and sluggish movement. Alcohol also increases the work of glutamate, a neurotransmitter that regulates dopamine levels in the brain.
The resulting effects include feelings of pleasure. Alcohol also clouds judgment and lowers inhibitions in the short-term, resulting in effects such as engaging in risky behaviour.
1. Thiamine deficiency is among the most common long-term effects of taking alcohol. As mentioned above Vitamin B1 or thiamine is critical for bodily and brain functions.
The body’s thiamine “stores” include the liver and kidneys, which are damaged by excessive alcohol consumption over a long time.
2. Delirium tremens is another long-term effect of alcohol consumption. The condition is characterised by confusion, shaking, and hallucinations. Delirium tremens is triggered when individuals who have abused alcohol for a long time try quitting.
3. Wernicke-Korsakoff syndrome: Long-term alcohol consumption also causes WKS, or chronic memory disorder linked to thiamine deficiency.
4. Foetal alcohol syndrome: Long-term alcohol consumption can expose unborn babies to alcohol-related brain damage. Symptoms of this syndrome include weak coordination, hearing and vision problems, poor memory, concentration problems, hyperactivity, and intellectual disabilities.
5. ARBI: Alcohol-related brain impairment is common among individuals who have drunk alcohol heavily for many years. The impairment decreases thinking abilities gradually depending on the years of alcohol abuse.
Evidence shows that the disorder affects 1 in every 200 adults in the UK. The prevalence is higher among individuals with alcohol addiction i.e. 1 in every 3.
The disorder is also more prevalent in middle-aged individuals between 40 and 50 years. However, younger and older individuals can also be affected. In regards to gender, men are affected more than women. The disorder is more common among individuals in poorer communities.
This is due to many reasons, significantly so the lack of education about the consequences of drinking and the health implications of excessive consumption. This fact also relates to the socio-economic status of those living in poorer communities (unemployment, lack of social activity, domestic issues.)
Individuals with ARBI need to feel understood. Some reassurance is important. Also, reinforcing and rewarding appropriate behaviour helps. You should avoid arguing, ordering the person, taking their behaviour personally, or reacting to provocation.
Below is a list of some of the most common and unfortunate signs of alcohol-related brain damage. If you suspect that you, or someone you know who is struggling with alcoholism, is exhibiting any of these signs, it’s important you seek professional help immediately.
The symptoms are as follows:
There is a clear link between regular excessive drinking and the risk of developing dementia. This type of brain disorder is known as ‘alcoholic dementia’ and is signified by a person’s lack of ability to make plans, follow through and make decisions, and assessing risks in day-to-day life.
This condition is signified by an alteration in the person’s personality, with diminished emotional and impulse control. This is often signified by socially suspicious behaviour that the person may not have exhibited in the past. Memory and attention problems, as well as noticeable difficulty in concentrating, are also signs of dementia.
ARBD encompasses the damage that takes place because of excessive long-term drinking. It is also known as wet brain or Wernicke-Korsakoff Syndrome caused by excessive drinking over a long time, which changes the structure and shape of the brain.
Korsakoff’s condition gradually occurs with symptoms becoming apparent such as problems with concentration and attention, memory gaps which are often defended by false accounts (confabulation) and an inability to learn new information, however minor.
The brain disorder is caused by a lack of thiamine (Vitamin B1) coupled with the damaging effects of alcohol. Vitamin deficiency is common among long-term heavy drinkers since alcohol interferes with the absorption of some vitamins. ARBD symptoms include; confabulation, difficulty learning/remembering/thinking, altered personality, and mood problems.
Wet brain or Wernicke-Korsakoff syndrome refers to a special type of brain damage caused by heavy repeated exposure to alcohol. The syndrome occurs because of thiamine deficiency. Levels of the vitamin diminish with poor diet common among individuals who abuse alcohol regularly.
Alcohol also hinders thiamine absorption by interfering with the enzyme responsible for activating thiamine. The vitamin is required for many functions, including the synthesis of neurotransmitters.
This condition is the most serious of the three syndromes relating to alcohol and brain damage. Wernicke’s encephalopathy is characterised by a sudden change in movement, speech, ability to concentrate and recall information, and is considered fatal due to the dangerously low levels of thiamine present in the body.
Doctors will diagnose this condition judging on the way the patient presents themselves during diagnosis, and if suspected, tests will follow to gauge the thiamine and B-1 levels in the blood. But mainly, this condition is confirmed by what is referred to as ‘the triad’ – by the – ophthalmoplegia, ataxia, and confusion.
Individuals who have learning disabilities or related conditions like ADHD have a higher likelihood of substance abuse. Depression, loneliness, poor academic achievements, and lowered self-esteem are shared attributes of learning difficulties and alcoholic disposition.
Alcohol-related brain damage can’t be diagnosed before a person stops drinking. Persons with ARBD follow the same assessment as that for individuals with dementia.
Diagnosis starts with a physical examination followed by a record of a person’s detailed history of alcohol use and mental abilities. A brain scan rules out stroke, tumours among other possible causes of ARBD-related symptoms.
Diagnosis also includes monitoring the person when they are alcohol-free to see if the condition worsens or stabilises. Worsening may be an indication of diseases like Alzheimer’s. ARBD improves or stabilises with alcohol abstinence.
Diagnosis can include alcoholic dementia, Korsakoff’s alcoholic psychosis, Wernicke-Korsakoff syndrome, chronic alcoholic brain syndrome, alcohol amnestic syndrome, or other conditions.
Alcohol-related brain damage can be reversed by quitting alcohol altogether. Shrinkage in some parts of the brain caused by alcohol can be reversed by abstaining from alcohol for a prolonged time.
Fortunately, there are medications that can be administered to help combat the consequences of chronic alcohol consumption. Below is a list of the most commonly prescribed medications:
Drugs like Acamprosate (brand name: Campral) are common in treating alcohol dependence. Acamprosate stabilizes chemical balance inside the brain that was previously disrupted by alcoholism.
The drug should be used alongside drug rehab treatment services like group therapy and total abstinence from alcohol. The drug shouldn’t be prescribed to individuals with kidney problems or possible allergies to ingredients used to make the drug.
Benzodiazepines treat alcohol withdrawal symptoms by enhancing neurotransmitter activity that was previously compromised by alcoholism. This, in turn, restores memory, alertness, coordination, muscle tone, among other previous impairments.
Alcohol withdrawal sets in when a person who is dependent on alcohol tries quitting abruptly. Benzos address the resulting withdrawal effects like headaches, irritability, panic, pain, chills, restlessness, tremors, seizures, nausea, and vomiting.
Disulfiram treats chronic alcohol dependence. The drug was the first FDA-approved drug for treating chronic alcohol dependence. The drug is soluble in alcohol and water. Disulfiram is an alcohol-sensitizing or alcohol-aversive agent that can cause acute toxic physical reactions when taken alongside alcohol.
Naltrexone is an FDA approved drug that treats alcohol dependence. The drug also works for individuals dependent on drugs like heroin. People taking naltrexone should stop taking alcohol and other drugs.
The drug shouldn’t be taken by individuals who rely on opioid painkillers to treat chronic pain or individuals with acute hepatitis or liver failure.
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[1] http://www.drugdetection.net/PDF%20documents/Dubowski%20-%20stages%20of%20alcohol%20effects.pdf
[2] https://www.scientificamerican.com/article/scientists-pinpoint-brain-region-that-may-be-center-of-alcohol-addiction/
[3] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3625995/
[4] https://www.bmj.com/content/357/bmj.j2645
[5] https://academic.oup.com/alcalc/article/44/2/136/184817