The brain recovers from alcohol abuse by returning cells to their normal size once the patient has stopped drinking.
The absence of alcohol allows the brain to repair itself through cellular re-growth.
How Different Areas Of The Brain Recover
How Long Does It Take?
The length of recovery depends on how much damage has already been done.
If the over-consumption of alcohol is severe, then the length of time to recover will match that intensity.
For some people a few weeks is all that’s needed to return the brain chemistry back to its original state.
For others, months of recovery are required.
This timescale depends on how long the abuse has been going on, and how well recovery is going.
Vulnerable Areas And How They Recover
The cerebral cortex processes higher-level information such as memory, reasoning, decision-making, emotions, and personality.
Alcohol is a depressant, which means it slows down the functions of the body.
In the cerebral cortex, this means information processing and sensory processing take longer.
Through slow processing and reaction times, secondary damage can be caused to the body – for example a car accident.
This makes the cerebral cortex a vulnerable area of the brain.
In a 2009 study, the experiment showed that patients with alcohol dependence (PAD) showed less activity in their subcortical and cortical structures.
This was in comparison to the healthy control subjects (HC).
In the experiment, PAD had a longer reaction time than HC when they needed to distinguish a stop sign signal.
This was due to impaired prefrontal cortex activation.
A different study, published in 2011, looked at how the cerebral cortex recovered after alcohol abuse.
The study followed patients who abstained, who were detoxified and who had acute withdrawal symptoms along with a healthy control group.
Those with withdrawal symptoms and those who were detoxified had less fluency in their frontal lobe activation in comparison to the control group.
This was due to the increased monoamine and glucocorticoid releases.
Those who abstained and the HC had similar levels of fluency.
As the detoxified group moved further away from their intoxication state, their brain activity reached levels of HC.
This was all due to the recovering ventromedial prefrontal cortex (VmPFC) explained in more detail below.
The ventromedial prefrontal cortex is part of the prefrontal striatal limbic circuit (PSL), in which the frontal lobe controls reason and decision-making.
A hypoactive VmPFC is more likely to respond to carvings than a non-hypoactive VmPFC.
Repeated excess alcohol use disrupts the VmPFC regulation creating high emotional arousal and high cravings.
The patient’s heart rate showed 1, 51=8.3; p<0.006 while their salivary cortisol recorded 1, 54=4.8; p=0.03.
This shows that those in the neurobiologically vulnerable state will likely compromise their ability to control their drinking cravings.
Using the information above, the withdrawal group and detoxified group had less fluency in their frontal lobe and therefore had less control over their cravings.
To recover, they need to maintain an intact PSL circuit to control their decision-making.
To do this alpha1-adrenergic antagonists need to be included in the patient’s withdrawal plan.
Common versions of these include Prazosin.
This drug reduces the amount of glucocorticoid and monoamine release, thereby allowing increased performance and fluency in the PSL circuit, which in turn leads to better decision-making and fewer relapses.
The limbic system controls the brain’s concept of reward.
The PSL is partly made up of the limbic system.
Although the frontal lobe controls reason and decision-making, the limbic system provides stress and reward.
The two work together to create the prefrontal striatal limbic circuit.
When impaired by alcohol, the limbic system produces fear and arousal responses at a reduced rate.
When presented with reward cues such as compliments, money or alcohol, patients of alcohol abuse have a stronger response to alcohol than any other offering.
Completely abstaining from alcohol created a dysfunction in the reward system, leading to a lack of control over the patient’s awareness and an increase in alcohol cravings.
To recover, the limbic system needs to be rewarded with alcohol less frequently, to create resistance.
However, it cannot completely abstain due to the high possibility of a relapse.
When an acute level of alcohol is in the system, this can affect the way the thalamus controls motion and collects data.
In a 2017 study, heavy drinkers (HD) and normal controls (NM) participated in an experiment which asked NM to not drink before the study and HD to not drink 3 days before the study.
They were studied using functional connectivity density mapping and found that NM had higher FCD (functional connectivity density) visual in multiple areas of the brain, including the thalamus.
HD and NM were then split into placebo groups (PLC) and drinking groups (ALC).
PLC was given diet soda caffeine free. ALC was given 0.75g kg -1 of alcohol mixed with the same soda.
Each was given 3 drinks per 50kg of the person’s weight.
Results showed that irritability, restlessness and low performance were greater in ALC HD.
This was the group that started off with the lowest thalamus rating, and did not recover from the 3 day abstinence due to the soda mix given during the experiment.
Through the MRI scan, this correlated with the lower Mean IFCD (local functional connectivity density) of 20 or less.
If this level of degradation continues, it can lead to Wernicke-Korsakoff Syndrome – a memory disorder which can also cause confusion and tremors.
To recover this area of the brain, the patient needs to abstain from drinking alcohol and maintain a healthy diet.
Oral supplements of thiamine (Vitamin B1) can repair FCD.
It helps the thalamus ingest the vitamins and magnesium needed to reduce the effects of Korsakoff syndrome.
Through thiamine supplementation, the patient will receive the nutrient needed to convert food into energy, which in turn creates power to grow and develop functional cells.
During stress or exercise β-endorphin is released or secreted into the bloodstream.
Its job is to prolong feelings of euphoria and inhibit the feelings of pain.
Alcohol produces β-endorphin secretion, but it also produces the corticotropin-releasing hormone.
This secondary response is a stress hormone, released like a timescale after β-endorphin secretion, proving negative feedback and causing cravings for β-endorphin secretion once more.
This creates a cycle of addiction.
Through a mathematical equation in a 2021 study, the researchers found a snowball-like effect as more alcohol intake created a shorter cycle time, producing more negative feedback requiring more alcohol to produce β-endorphin.
Through withdrawal, β-endorphin levels decline while corticotropin-releasing hormone levels continue but at a reduced rate.
The negative response follows the positive response but through a delay. This showed that the hypothalamus is at risk of creating an unending cycle of addiction without support.
Through corticotropin-releasing hormone suppressants, the stress hormone can be diluted causing greater room for recovery.
The Brain’s Grey Matter
How Is It Harmed From Alcohol Abuse?
The main association between alcohol abuse and the brain is the reduction in grey matter volume.
The reduction of grey matter is called atrophy.
These impairments create difficulties in social relationships, feelings of aggression, evaluation of risk or injury, and value towards responsibilities.
A 2021 meta-research paper, showed how different research studies identified variations in atrophy impact.
The common denominators were the anterior cingulate cortices (ACC), prefrontal cortices, posterior cingulate cortices (PCC) and striatal and insular regions.
Each of these sections of the brain contains grey matter and becomes significantly reduced in comparison to healthy control groups.
A Harvard study showed these findings in real terms.
The research found that those who drank 4 or more times a day received 6 times more atrophy impact than non-drinkers.
As the brain shrinks, its functionality shrinks too. It loses its ability to recall memories, to concentrate, and its reasoning capabilities are diminished too.
Is The Damage Permanent?
Depending on the intensity of the abuse and the area of the brain most affected, the damage will either be persistent or permanent.
Wernicke-Korsakoff Syndrome, for example, is a chronic memory disorder, which can be reversed if caught early enough.
If the patient abstains for 1 year, the nerve damage markers can return to normal.
A 2016 study showed that 85% of traumatic brain injuries created through alcohol abuse are mild, and with treatment can be healed.
Other motor neuron disorders such as Parkinson’s cannot be reserved.
Although these disorders’ leading risk factor is age, alcohol abuse can progress the disease’ development causing the effects to begin earlier or the patient to deteriorate faster.
Ethanol can stimulate inhibitory γ-aminobutyric acid (GABA) receptors as well as suppress the excitatory glutamate receptors.
The increase in glutamate-induced excitotoxicity creates permanent neuronal damage normally connected to malnutrition.
This means the patient’s cognitive skills, nerve growth and intracellular signalling pathways become disrupted.
What To Expect In Recovery
Dopamine Levels Begin To Normalise
Alcohol increases a patient’s dopamine levels. Drinking too much alcohol overloads the brain’s dopamine levels, creating a delay in dopamine production.
A 2006 study, showed that an initial increase in ethanol of 2g/kg in male rats caused an increase in dopamine by 40%.
With just 0.25g/kg the increase was only 20%.
However the 0.25g/kg rats returned to baseline dopamine levels after 90 mins, but the 2g/kg rats continued to have high dopamine levels.
The results showed that the brain does not respond linearly, meaning the increase in alcohol doesn’t create an increase in dopamine.
The rats developed a tolerance to dopamine.
Due to the persistent dopamine release, patients experience abnormal emotional responses.
Dopamine levels can return to normal after 4 weeks of abstinence, however, a 1999 study showed that some recovery in dopamine transport binding can occur as early as 4 days from abstinence.
After a single alcoholic drink, the body produces an increase in serotonin.
Serotonin latches on to receptors such as 5-HT3 which sends electrical signals.
Alcohol enhances these signals, causing excessive stimulation.
Excessive stimulation leads to tolerance development.
Withdrawal symptoms are a common side effect of abstinence.
These symptoms are triggered by enhanced serotonin activity reduction.
To reduce mood disorders such as depression, created as a side effect of withdrawal symptoms, agents called selective serotonin reuptake inhibitors (SSRIs) are offered to patients.
A commonly known SSRI is Prozac.
As with dopamine, consistent excessive serotonin creates a delay in natural production.
Through abstinence, it takes on average 24 weeks for serotonin levels to reach normalised levels.
However, if the patient is born with less natural serotonin than others, fewer depression-free days will occur during and after recovery.
These patients will benefit from SSRI medication to increase serotonin levels and prevent relapse.
Frontal Lobe Regeneration
People who abuse alcohol show significant shrinkage in their subcortical and cortical brain structures.
The frontal lobes are the most affected by shrinkage.
Through abstinence, the frontal lobe can regenerate the lost grey matter.
After 1 month of abstinence, the cortical grey matter will increase.
After 1 year of abstinence, the regeneration process begins to enlarge the third ventricle.
This increases working memory, as well as spatial, visual and motor abilities.
The regeneration process is due to the production of new neurons.
Production Of New Neurons
People who drink to excess develop neurodegeneration.
Neurodegeneration is when the number of brain cells or neurons decreases or becomes damaged.
Neurodegeneration begins subtly, has a varied effect on the brain, and can cause widespread bodily harm.
In a study conducted in 1980, rats were fed a liquid diet which fulfilled their nutritional needs but also contained alcohol.
They were on this diet for 5 months.
After 5 months, the rats went through forced abstinence.
The results of the test showed a loss of neurons in the hippocampal pyramidal and dentate granule cells.
A 2005 study showed that butylated hydroxytoluene (BHT) given to rat subjects taking the Binge Alcohol-Induced Brain Damage (BIBD) model, prevented the loss of neurodegeneration.
This means that BHT antioxidants can block neurodegeneration.
In a 2004 study, researchers found that abstinence increased their test subject’s new stem cell proliferation throughout all regions of the brain.
The effects were noticeable after 1 day and continued for weeks.
This means that new neurons will start producing again, after 1 day of abstinence.
Improvement To Tissue Surrounding The Brain
The amount of brain tissue in a chronic drinker is lower than in other people affected by the same factors minus alcohol abuse.
The most dramatic loss can be found in the corpus callosum, which connects the hemispheres.
In a 1989 study, patients were scanned using an MRI scanner within 10 days of their last drink, and then re-scanned after 4 weeks of abstinence.
The MRI readings showed that within this short period of time, the patient’s ventricles (fluid) were rapidly smaller.
This shows that structural brain tissue can regrow after alcohol-related trauma.
In a 1995 study, researchers aimed to redo this experiment and extend it.
After 2 months of abstinence, the ventricle sizes continued to reduce, while the brain tissue developed and improved.
This shows that the tissue surrounding the brain improves its structure through abstinence.
Communication Skills Increase
During the degradation of the cerebral cortex, a person’s ability to use a large vocabulary and piece together complex thoughts becomes diminished.
This doesn’t mean that speech is removed completely, but an individual may realise that they cannot grasp a word they once knew, or that they cannot string together a sentence that truly represents their thoughts.
With fewer concepts being represented, this leads to a struggle to understand emotional communication and non-verbal communication.
In turn, this can lead to aggression through frustration and confusion.
When recovery has been completed, and the individual has moved past withdrawal, they will start to develop new neurons.
With these new neurons, the capability to understand communication (written, spoken, emotional, and nonverbal) begins to increase.
The most severe impairment caused by alcohol abuse is memory dysfunction.
Between 75% and 100% of people treated for alcoholism in a dedicated facility perform under the average for their age group when their memory and cognitive functions are tested.
In a 1983 study, the researchers found that short-term memory functions remain impaired after 5 years.
However, a 2016 study showed that patients who completed cognitive therapy alongside work therapy were 55.9% more likely to retain verbal memory than those without therapy.
However, this figure was still 58.5% lower than someone of the same age who doesn’t have a drinking disorder.
This showed that with therapy, long-term and short-term memory functions can be returned, but not to the same extent as HC.
Restored Fine Motor Skills
When dopamine transporters are lost or damaged, the effects reduce the function of motor speed and verbal learning.
In a 2001 study, researchers tested a healthy control group and an alcohol abuse group by asking them to put pegs into a hole as quickly as possible while conducting a PET scan.
The study showed that the lack of dopamine correlated with slower reaction times.
In a 2015 study, researchers used a device called the Talking Pen to assist people with alcohol-caused fine motor skill impairment.
In the study, they asked their subjects to follow a fine line drawing, with and without the pen.
On the base test, the patients scored Mean ± SD = 24.00 ± 7.81, while in their Talking Pen assignment this reduced to 11.71 ± 2.49, Z score = 2.37.
This showed that their competition time and error times were reduced due to the help of the pen.
This pen was triangular and had a laser pointer which could buzz if the pen went outside the line.
The pen can talk, buzz or change colours to encourage the user through their fine motor skills.
It acts as a reward stimulator which helps to release dopamine.
As the patient abstains from alcohol abuse and develops neurons which create new dopamine transporters, they can use techniques such as a Talking Pen.
This will encourage a higher dopamine level, which will restore fine motor skills.
Promote New Cell Growth
Excessive alcohol usage results in the degeneration of neurons.
Abstinence from alcohol can contribute to cellular regrowth, however, the mechanics which drive this change are still largely unknown.
A 2018 study wanted to see how long it takes for new cell growth to occur.
They tested rats after they had been exposed to alcohol for 4 days.
The tests used fluorescent labelling to examine Type-1, -2a, -2b and −3 progenitor cells.
The study showed that cell proliferation began 5 days after abstinence, but only Type 2 progenitors were actively dividing.
For all cell proliferation to return to normal, abstinence of 28 days was needed.
As the rats were only exposed to alcohol for 4 days, the process may take longer than a month in long term alcohol abuse patience.
Addiction is considered a disorder of motivational behaviour.
Either positive reinforcement encourages continued unhealthy drinking due to unstable dopamine levels, or negative reinforcement encourages continued unhealthy drinking due to medical self-administration.
Self-administered medical use of alcohol occurs in 44% of anxiety or depression, and 50% of people with bipolar disorder.
Self-medication may also be used to avoid withdrawal symptoms.
These are motivations to continue chronic drinking.
As chronic drinking change’s the brain’s ability to produce neural stem cells and reduces proliferation, the prefrontal cortex becomes damaged.
From the damage, the ability to control impulsive behaviour diminishes.
A 1995 study showed that motivation towards heavy drinking continued after withdrawals through abstinence, as relapse most commonly occurred after 9 months of abstinence.
This shows that motivation towards drinking is continuous in alcohol abusers, and even after long periods of abstinence, relapse is likely.
Who Is At Risk?
Children who have experienced traumatic brain injuries before the age of 5 are 3.6 times more likely to become alcohol dependent during their adolescence.
A 2015 study showed that adolescents with traumatic brain injuries were 2 to 4 times more likely to binge drink than their classmates.
In a 2013 study, researchers found that 20% of patients within a rehabilitation centre experienced a traumatic brain injury before the age of 16.
A 1992 study showed that those with traumatic brain injuries were more likely to develop seizures when drinking, while a 1997 study indicated that those with traumatic brain injuries experienced higher levels of cognitive impairment than those who abstained and alcoholics without TBIs.
This shows that trauma at a young age is more likely to create binge drinking, and those who binge drink with traumatic brain injuries are more likely to develop cognitive impairment.
A 2013 study which looked at this specific correlation between children with TBIs and alcohol abuse found that those within this category were 3 times more likely to develop long-term and permanent damage to their brains.
This means that children with traumatic brain injuries are the most at risk of suffering permanent brain damage through alcohol abuse.
Chronic alcohol abuse leads to neurodegeneration through the oxidative stress caused by neuroimmune gene induction.
Through neurodegeneration, neuroimmune signalling is activated. Drinking alcohol increases the signals, causing increases in risky decision-making and inflexible behaviour.
This is because the areas of the brain most affected by neurodegeneration are the prefrontal cortex and the limbic system.
Through postmortem studies on human brains, studies have shown that lifelong alcohol consumption correlates with persistent neuroimmune signalling, which in turn contributes to chronic relapsing.
This is a sign of permanent neurodegeneration damage through long-term binge drinking.
In a 2004 study, researchers studied the effects of long-term sobriety and recovery, tracking alcoholic women over 4 years.
By year 4, 13 of the 14 subjects maintained their sobriety and showed recovered levels of psychomotor speed and memory, but continued impairment to standing balance.
This showed that temporal lobe recovery and the frontal lobe are possible through long-term abstinence, however, the cerebellum damage in long-term alcoholics may be permanent.
Alcoholics And Deficiencies
Cirrhosis of the liver is a common injury occurring through alcohol abuse.
The impact changes the brain structure and develops deficiencies in nutritional states such as vitamin B1.
These deficiencies can cause brain dysfunction and brain damage to a severe level.
People with nutritional deficiencies caused by alcohol abuse are known as “complicated alcoholics” while those without this damage are known as “uncomplicated alcoholics”.
Complicated alcoholics show more major white matter loss than uncomplicated alcoholics.
In uncomplicated alcoholics, studies show that there are no obvious white matter lesions to identify, meaning that white matter loss is a complicated alcoholic issue.
A 2005 study showed that white matter loss through alcohol disrupts axonal and myelination integrity.
While a 1999 study showed that alcohol creates a permanent reduction in the thickness of myelin sheaths.
Myelin sheaths allow electrical impulses to be transmitted quickly, and so the thinning of this insulating layer means slower responses. This means that alcoholics with nutritional deficiencies are more likely to develop permanently slowed reaction times.
How To Help Your Brain Recover
A 2022 meta-study created the Exercise Intervention Habit Mechanism which aimed to manipulate the plasticity of positive and negative rewards needed to create habits.
They found a simple neurological circuit which surrounds the creation of habits – suggestion, behaviour, and reward.
They found that changing the behaviour while keeping to the same pattern can help replace old habits with new ones.
For example, if the subject normally starts drinking after work, replacing this drinking time with a workout allows them to exhibit the behaviour and receive a dopamine reward at the same time as their previous habit.
This allows the dopamine levels to continue thereby reducing the likelihood of relapsing.
A Balanced Diet
Alcohol can affect a person’s metabolism which in turn prevents them from absorbing or digesting nutrients needed to be nourished.
Due to this alcoholics are often malnourished, and lacking essential nutrients such as proteins and vitamins.
Those who drink more than 30% of their daily calorie intake in the form of alcohol ingest less than the recommended amount of nutritional value.
Because of these deficiencies, the lack of nutrients can lead to liver disease.
To prevent these deficiencies from causing permanent damage, people with an alcohol abuse disorder need to eat a balanced diet to help ingest as many nutritional minerals as possible.
To repair the brain, the most important foods include those with thiamine (also known as vitamin B1). This will help prevent conditions such as Wernicke-Korsakoff syndrome.
Thiamine can be found in:
- Green peas
Relapsing is a chronic condition created by strong negative reinforcement caused by craving and withdrawal.
In an attempt to avoid these states of mind, relapsing occurs, however behavioural treatment aims to prevent relapsing through mindfulness.
Mindfulness is the ability to experience the good, bad and neutral as it is without reacting to it. In mindfulness behavioural therapy, patients are taught how to recognize their emotional states and regulate the positives and the negatives.
This allows the patients to accept the uncomfortable state of withdrawal or cravings without instinctively reacting to it.
The emotional response can be explained by the change in grey matter through mindfulness.
A 2012 study showed that 45 minutes of meditation a day over 8 weeks, increases the amount of grey matter in the brain.
Create A Regular Sleep Cycle
Alcohol affects the gamma-aminobutyric acid neurotransmitter system.
This means that it acts like a sedative, allowing people to sleep faster and reducing the amount of REM sleep overall.
It does this by damaging nerve cells and fibres connected to synchronous neuronal firing across the cortex.
Due to this, insomnias and PTSD patients are likely to develop an alcohol abuse disorder to aid sleep.
Treating sleeping problems as part of the alcohol abuse recovery can prevent the risk of relapse.
Cognitive behavioural therapy is currently the main treatment for insomnia as 80% of patients benefit from the practice.
As part of the practice of patience, patients limit the amount of time awake they spend in bed, creates a comfortable bedtime environment to promote only sleep and avoids stimulants such as alcohol and caffeine.
This allows the patient to create a regular sleep cycle.
During a successful sleep cycle, cellular repair can take place in the brain.
It does this by removing the cerebrospinal fluid, which in turn removes toxins in the brain. With the toxins and dead cells removed, new stem cell proliferation can continue and repair damaged cells.