Alcoholic Dementia: Definition, Causes, Symptoms, and Treatment

Alcoholic dementia (AD) occurs due to chronic alcohol misuse, leading to cognitive decline and memory impairment. Alcohol dementia is associated with prolonged nutrient deficiencies, especially thiamine (vitamin B1), and direct toxic effects of alcohol on brain cells. The global prevalence of dementia has seen a substantial surge in recent decades, rising from an estimated 20.2 million cases in 1990 to 57.4 million in 2019, according to the report “Estimation of the Global Prevalence of Dementia in 2019 and Forecasted Prevalence in 2050” conducted by the Global Burden of Disease 2019 Dementia Forecasting Collaborators.

The primary cause includes long-term alcohol abuse, which disrupts the absorption of essential nutrients like thiamine (vitamin B1), resulting in brain damage and related complications. Other contributing factors are liver damage, repeated head trauma, and a genetic predisposition to alcohol dependence. The 2020 report by the Lancet Commission for Dementia Prevention, Intervention, and Care estimated that 40% of global dementia cases are able to be prevented or delayed by addressing 12 key modifiable risk factors, including alcohol addiction, as highlighted by Livingstone et al. in “Dementia Prevention, Intervention, and Care: 2020 Report of the Lancet Commission.”

Symptoms of alcohol dementia manifest as memory loss, difficulty with decision-making, impaired motor coordination, and behavioral changes, which severely affect daily functioning. By 2050, the global population of individuals living with dementia is expected to rise to 152 million, as outlined by Patterson C. in “The State of the Art of Dementia Research: New Frontiers,” published in the World Alzheimer Report 2018.

Treatment focuses on halting alcohol consumption through structured rehabilitation programs, alongside nutritional supplementation, particularly thiamine, and cognitive rehabilitation therapies to manage and ameliorate symptoms. Alcohol-related dementia is linked to low survival rates. 

What Is Alcoholic Dementia?

Alcoholic dementia is a severe cognitive disorder directly caused by prolonged excessive alcohol consumption. Also known as alcohol-related brain damage, this condition affects millions of individuals worldwide, progressively deteriorating brain function and cognitive abilities. Alcohol abuse precipitates major neurological impairments that dramatically diminish an individual’s quality of life. Cognitive impairments in alcohol-dependent patients without other neurological complications are drawing increased focus from addiction medicine professionals due to their influence on treatment outcomes. Research indicates that 50% to 80% of these patients experience cognitive deficits, as noted by Bernardin et al. 2014 in “Cognitive Impairments in Alcohol-Dependent Subjects.”

A Korean cohort study of 3,933,382 individuals found that sustained mild drinking (<15 g/day) minimized dementia risk by 21%, moderate drinking (15–29.9 g/day) by 17%, while heavy drinking (≥30 g/day) increased it by 8%. Declining heavy to moderate drinking lowered dementia risk by 8%, and starting mild drinking cut it by 7%. Elevated drinking or quitting was associated with higher risks. This suggests even low alcohol consumption thresholds affect dementia risk, as observed by Jeon et al. 2023, in “Changes in Alcohol Consumption and Risk of Dementia in a Nationwide Cohort in South Korea.”

At What Age Does Alcoholic Dementia Occur?

Alcoholic dementia occurs in individuals aged 40 to 70, though it appears earlier in severe cases of prolonged alcohol abuse. Not all individuals who consume alcohol develop alcoholic dementia; however, heavy, chronic alcohol use raises the risk. Alcohol-related brain damage, including dementia, is influenced by the duration and intensity of alcohol consumption as well as other factors like nutritional deficiencies.

A study published in Eur J Epidemiol examined the long-term association between alcohol consumption and dementia risk in a Norwegian cohort from the HUNT study. An analysis of 40,435 participants over 27 years, identified 1,084 dementia cases. Frequent alcohol consumption (≥5 times/14 days) was associated with a 40% higher dementia risk compared to infrequent drinking. Abstinence initially showed a 30% increased risk, but this was nonsignificant after adjustment. Findings were consistent for Alzheimer’s and vascular dementia, as concluded by Langballe et al. 2015 in “Alcohol Consumption and Risk of Dementia Up to 27 Years Later in a Large, Population-Based Sample: The HUNT Study, Norway.”

What Are the Causes of Alcoholic Dementia?

The causes of alcoholic dementia include Wernicke-Korsakoff syndrome, neurotoxicity, nutritional deficiencies, liver disease, and brain atrophy. Chronic alcohol consumption damages brain cells disrupts nutrient absorption, and impedes organ function, producing progressive cognitive decline. These factors collectively breed brain dysfunction and memory debilitation.

Common causes of alcoholic dementia include:

• Wernicke-Korsakoff Syndrome: A severe neurological condition caused by thiamine (vitamin B1) deficiency, leading to memory loss and cognitive dysfunction. A study analyzing thiamine supplementation among 14,998 ICU patients with alcohol use disorder (AUD) from 2010 to 2017 revealed that 51% received supplementation. Rates varied by condition: 59% for alcohol withdrawal, 26% for septic shock, 41% for traumatic brain injury (TBI), and 24% for diabetic ketoacidosis (DKA). Notably, 52% of patients received thiamine within 12 hours, primarily through enteral routes (41%), emphasizing a care gap, particularly for AUD patients with conditions other than alcohol withdrawal, as explained by Pawar et al. 2021 in “Thiamine Supplementation in Patients with Alcohol Use Disorder Presenting with Acute Critical Illness.”
• Neurotoxicity: Direct damage to brain cells from prolonged alcohol exposure, impairing neural communication. Seven studies and data from 33 European countries were analyzed, highlighting sex differences in alcohol-related dementia risk where moderate alcohol use was connected to lower dementia risk in men (3 studies) and women (4 studies). High-risk alcohol use escalated the risk, especially for early-onset dementia, spawning 3.2% of dementia cases in women and 7.8% in men aged 45–64. Findings emphasize the need for sex-specific research while relying on established guidelines for alcohol consumption, as stated by Kilian et al. 2023 in “Alcohol Use, Dementia Risk, and Sex: A Systematic Review and Assessment of Alcohol-Attributable Dementia Cases in Europe.”
• Nutritional Deficiencies: Alcohol interferes with absorbing essential nutrients like thiamine, which is critical for brain health. A study involving 105 male alcoholics demonstrated that combining nutritional therapy with conventional treatment boosted long-term sobriety outcomes. Six months post-treatment, 81.3% of participants receiving both therapies remained sober, compared to 37.8% in the conventional treatment group. This suggests that nutritional therapy enhances long-term recovery from alcoholism, as recounted by Guenther (1983) in “The Role of Nutritional Therapy in Alcoholism Treatment.”
• Liver Disease: Alcohol-induced liver damage results in toxins accumulating in the bloodstream, affecting brain function. In a clinical study of 9,635 patients with alcohol use disorder (AUD), 60.4% were men, with an average age of 54.8 years. The findings revealed that 11.8% (1,135) of the patients had alcohol-related liver disease (ALD), while 40.5% (3,906) received medical addiction therapy. Notably, medical addiction therapy was associated with a 63% reduction in the risk of developing ALD, as mentioned by Vannier et al. 2022 in “Incidence and Progression of Alcohol-Associated Liver Disease After Medical Therapy for Alcohol Use Disorder.”
• Brain Atrophy: Shrinkage of brain tissue due to long-term alcohol use, contributing to terrible cognitive deficits. The brains of individuals with alcohol dependence are 3–9% smaller than those of healthy individuals, with volume loss affecting regions such as the hippocampus, putamen, pallidum, thalamus, corpus callosum, and cerebellar gray matter. This reduction in brain size is directly linked to the quantity of alcohol consumed, as detailed by Daviet et al. (2022) in “Associations Between Alcohol Consumption and Gray and White Matter Volumes in the UK Biobank.”

How Does Alcohol Addiction Lead to Dementia?

Alcohol addiction leads to dementia by causing extensive damage to the brain through multiple mechanisms. Chronic alcohol use chops gray matter volume, which is brain tissue that processes information and controls memory, senses, and decision-making. specifically in regions critical for memory and decision-making, such as the hippocampus and prefrontal cortex. It also sparks vitamin B1 (thiamine) deficiency, a vital nutrient for brain function, resulting in conditions like Wernicke-Korsakoff syndrome, which severely destroys cognitive abilities. Moreover, alcohol’s neurotoxic effects damage brain cells and disrupt neural communication pathways, exacerbating cognitive decline.

A meta-analysis examining 12 cognitive functions in individuals with alcohol dependence made known streamlining in cognitive performance across all areas after one year of continuous abstinence. Analyzing 62 studies, the research revealed moderate impairment across 11 cognitive domains during short-term abstinence (<1 month) and 10 domains during intermediate-term abstinence (2-12 months), supporting the notion of widespread brain impairment in alcoholism, as noted by Stavro et al. 2013 in “Widespread and Sustained Cognitive Deficits in Alcoholism: A Meta-analysis.”

What Are the Effects of Alcoholic Dementia on the Brain?

The effects of alcoholic dementia on the brain are brain atrophy, impairing memory, motor functions, and executive abilities. These effects worsen over time, generating greater cognitive and functional decline in individuals with alcoholic dementia.

The effects of alcoholic dementia include:

• Brain Atrophy: Prolonged alcohol consumption leads to the shrinking of brain tissue, particularly in areas responsible for memory and cognition, such as the hippocampus. This atrophy disrupts cognitive processes and accelerates the progression of dementia. A study comparing 42 abstinent alcohol-dependent (AD) patients and 34 healthy controls found that AD patients exhibited impaired cognitive performance, particularly in attention, visual memory, and working memory. Patients who had been abstinent for less than a year showed more deficits relative to those with longer abstinence and the control group, as expressed by Kopera et al. 2012 in “Cognitive Functions in Abstinent Alcohol-dependent Patients.”
• Impaired Memory: Alcohol damages neural pathways involved in memory formation and recall. The consequences are severe short-term and long-term memory loss, which is a hallmark of alcoholic dementia. Drinking alcohol is associated with a reduction in the brain’s white matter volume, which transmits signals between different brain regions, thus, impairing brain function. Long-term alcohol consumption above the recommended limit of 14 units per week shrinks areas of the brain involved in memory. Drinking more than 28 units per week accelerates cognitive decline as individuals age, as explained by the Alzheimer’s Society in “Alcohol and the Risk of Dementia.”
• Reduced Executive Function: Alcohol-related damage to the frontal lobe impairs decision-making, planning, and problem-solving skills. Individuals with alcoholic dementia struggle with tasks requiring focus, organization, and complex thought.
• Motor Dysfunction: Alcohol abuse disrupts coordination and balance by damaging the cerebellum, leading to motor difficulties such as poor gait and tremors, common in alcoholic dementia patients.
• Mood and Behavioral Changes: Chronic alcohol use alters the brain’s regulation of emotions, leading to depression, irritability, and aggression. These changes worsen with the progression of alcoholic dementia. Two epidemiological studies conducted diagnostic interview surveys in representative community samples to examine the prevalence of psychiatric and substance use disorders. The National Institute of Mental Health Epidemiologic Catchment Area (ECA) Study found that 16.5% of individuals with lifetime major depression also had an alcohol use disorder, as noted by Quello et al. 2005 in “Mood Disorders and Substance Use Disorder: A Complex Comorbidity.”

What Are the Symptoms of Alcoholic Dementia?

The symptoms of alcoholic dementia are memory loss, challenge concentrating, impaired goal-setting, poor decision-making, lack of motivation, and hallucinations. These cognitive and behavioral disruptions differ in severity, progressively worsening as the dementia advances, posing massive hurdles to daily functioning.

Common symptoms of alcoholic dementia include:

• Memory loss: Individuals struggle to recall recent events or remember familiar information, which hampers their ability to perform daily tasks and maintain social connections.
• Difficulty concentrating: Alcoholic dementia causes an inability to focus on conversations or complete simple tasks, reducing efficiency and accelerating frustration in daily activities.
• Impaired goal-setting: The cognitive deficits prevent individuals from planning or following through with long-term objectives, making it difficult to maintain a career, relationships, or personal growth.
• Poor decision-making: Alcoholic dementia results in a heightened inability to assess situations clearly, leading to poor judgment and risky behaviors, which further complicates recovery or stability.
• Lack of motivation: Apathy and loss of interest in activities that once brought joy or fulfillment are common, contributing to social withdrawal and a decline in physical health.
• Hallucinations: Individuals with alcoholic dementia experience visual or auditory hallucinations, causing confusion and distress, which facilitates a breakdown in their sense of reality.
• Disorientation: A person loses track of time or becomes confused about their surroundings, leading to increased vulnerability, especially when unsupervised.
• Mood swings: Fluctuations in mood, ranging from irritability to deep depression, fracture interpersonal relationships, and emotional instability. In a clinical study, the most prevalent psychiatric disorders were depression (8.3%), anxiety disorder (7.5%), and bipolar disorder (0.8%), with all other disorders showing a prevalence of 0.2% or lower. Depression and anxiety were notably more common in individuals who consumed alcohol more frequently, with a 9.5% prevalence of depression and 8.3% for anxiety among those drinking “weekly or more,” and 8.8% and 8.9% in the “both” category, as reported by Palvez et al. 2020 in “Associations Between Psychiatric Disorders and Alcohol Consumption Levels in an Adult Primary Care Population.”

What Are the Stages of Alcoholic Dementia?

The stages of alcoholic dementia are early, middle, and late. Each stage is marked by the gradual worsening of symptoms, starting with mild cognitive impairments and progressing to severe neurological and behavioral dysfunctions. 

Early-stage symptoms are relatively subtle, while middle and late stages involve more pronounced deficits that affect daily life. 313,958 White British current drinkers in the UK Biobank were followed for 13.2 years, during which 1.7% (5,394) developed dementia. Conventional analysis showed a J-shaped relationship, with the lowest dementia risk at 12.2 units of alcohol per week.

However, Mendelian Randomization (MR) analyses identified a linear causal relationship, indicating that higher genetically predicted alcohol consumption growing dementia risk by 122% (HR: 2.22), challenging the notion of a safe alcohol threshold for dementia prevention as demonstrated by Zheng et al. 2024 in “Association Between Alcohol Consumption and Incidence of Dementia in Current Drinkers: Linear and Non-Linear Mendelian Randomization Analysis.”

The stages of alcoholic dementia are given below:

• Early stage:
  • Mild memory loss, especially short-term memory.
  • Difficulty concentrating and focusing on tasks.
  • Occasional confusion or disorientation, especially in unfamiliar settings.
  • Social withdrawal and mood alterations, like irritability or anxiety.
• Middle stage:
  • Severe memory impairment, with increasing difficulty recalling past events and recognizing familiar faces.
  • Impaired decision-making and problem-solving abilities.
  • Disorientation to time and place becomes more frequent.
  • Apathy and reduced motivation for personal activities or responsibilities.
  • Hallucinations or delusions start to appear.
• Late stage:
  • Profound memory loss, including long-term memories, with patients unable to recognize close family members or their surroundings.
  • Complete loss of independent functioning and severe confusion about basic concepts like time and place.
  • Inability to communicate effectively, with frequent nonsensical speech or loss of speech altogether.
  • Physical decline due to poor self-care and loss of motor skills, such as difficulty walking or eating.
  • Frequent behavioral changes, including aggression, agitation, or severe depression.

How Is Alcoholic Dementia Diagnosed?

To diagnose alcoholic dementia, a comprehensive evaluation is required, which includes a detailed medical history, cognitive assessments, and neuropsychological tests. These tests focus on memory, attention, problem-solving, and executive functions. 

Brain imaging, such as MRI or CT scans, assists in identifying physical changes in the brain, such as shrinkage in areas like the hippocampus and cortex, which are common in alcohol-related brain damage. Diagnosing alcoholic dementia is difficult due to its similarities with other conditions, including alcohol use disorder and other forms of dementia. There are no specific tests designed solely for alcoholic dementia, so diagnosis relies on exclusion and a thorough review of the patient’s alcohol consumption history and cognitive decline patterns.

How Is Alcoholic Dementia Treated?

To treat alcoholic dementia, the primary approach involves abstinence from alcohol, as continued consumption worsens cognitive decline.

Nutritional support is important, particularly thiamine (Vitamin B1) supplementation, as deficiencies in this vitamin are common among individuals with alcohol dependence and contribute to cognitive impairments. Thiamine supplementation precludes or alleviates brain damage, uniquely in cases concerning Wernicke-Korsakoff syndrome, a condition related to alcohol use and thiamine deficiency. 

Cognitive remediation therapy (CRT) is another pillar component, aimed at boosting percipient functions such as memory, attention, and executive functions through structured therapeutic exercises. CRT promotes improvements in cognitive abilities and well-being for individuals with alcohol-related cognitive impairments. Social support, such as participation in counseling and rehabilitation programs, also encourages long-term recovery and bolsters treatment outcomes.

A study involving 41 alcohol-dependent patients revealed that those who received cognitive remediation (CR) therapy in addition to conventional treatment showed huge advancements in cognitive functions, particularly in attention (alertness, divided attention), working memory, and delayed memory (recall). Patients who received CR also illustrated greater betterments in psychological well-being and drops in alcohol craving, distinctly in the compulsion aspect of craving, as proposed by Rupp et al. 2012 in “Cognitive Remediation Therapy During Treatment for Alcohol Dependence published in the Journal of Studies on Alcohol and Drugs.”

Does Cognitive Behavioral Therapy Help with Alcoholic Dementia?

Yes, Cognitive Behavioral Therapy (CBT) does help with alcoholic dementia, explicitly in addressing the psychological aspects of the condition. While CBT is not a direct treatment for the cognitive impairments associated with alcoholic dementia, it manages the underlying issues such as alcohol dependence, anxiety, depression, and other emotional challenges that aggravate cognitive weakness. Cognitive Behavioral Therapy (CBT) has been proven to decrease substance use and support long-term recovery in 50–75% of cases, establishing it as a fundamental aspect of addiction treatment programs, as explored in a large-scale study by Pybis et al. 2017.

How to Prevent Alcoholic Dementia

To prevent alcoholic dementia, adopting lifestyle changes and avoiding harmful alcohol consumption are the most important actions. Abstaining from excessive drinking, staying physically active, and maintaining a nutritious diet are core factors in brain health. Support from peers or support groups also aids individuals to stay on track and handle their alcohol use. 

Tips and strategies to prevent alcoholic dementia include:

• Avoid drinking alcohol: Limiting or completely avoiding alcohol consumption heads off alcohol-related brain damage and cognitive fallout.
• Engage in regular exercise: Physical activity enhances blood flow to the brain, jumpstarts memory, and pivots cognitive health.
• Maintain a healthy diet: A balanced diet rich in vitamins and minerals, especially vitamin B1, helps nourish the brain and cut down risks of neurodegenerative diseases.
• Join support groups: Participating in alcohol support groups furnishes emotional support, encouragement, and practical strategies to avoid relapse. Research shows that 42% of participants in Alcoholics Anonymous (AA) maintain complete abstinence after one year, compared to 35% of those undergoing other treatments, such as Cognitive Behavioral Therapy (CBT), as spotlighted by Kelly et al. 2020 in “Alcoholics Anonymous and Other 12-Step Programs for Alcohol Use Disorder,” published in the Cochrane Library. This highlights that AA shows a higher long-term abstinence rate than other therapeutic approaches for alcohol use disorder.
• Seek professional help when needed: Early intervention from addiction specialists or therapists hinders the onset or progression of alcohol-related cognitive impairments.

What Is the Life Expectancy of People with Alcoholic Dementia?

The life expectancy of individuals with alcoholic dementia is between 5-10 years, specifically, those with Wernicke-Korsakoff syndrome (WKS). 

About 50% of individuals diagnosed with WKS die within 8 years following the onset of Wernicke’s encephalopathy, with the chief causes of death being cancer and bacterial infections as seen in a large epidemiological study that deduced five-year survival rates of 53.4% for men and 63.4% for women. At 10 years, survival dropped to 29.5% for men and 38.3% for women, reflecting the condition’s severe prognosis as claimed by Palm et al. 2022 in “Incidence and Mortality of Alcohol-Related Dementia and Wernicke-Korsakoff Syndrome: A Nationwide Register Study.”

These figures differ widely depending on factors such as the severity of the condition, the presence of other health complications, and whether the individual stops drinking alcohol and receives early intervention. On average, life expectancy oscillates from several years to a decade, with men experiencing a slightly shorter lifespan in comparison to women​.

Individuals with alcoholic dementia must receive proper care and medical treatment, as early intervention and alcohol cessation augment the quality of life and possibly extend life expectancy.

Is Alcoholic Dementia Reversible?

Yes, alcoholic dementia is relatively reversible, decidedly in its early stages. Some cognitive refinement takes place with abstinence from alcohol and adequate nutritional support, set in the early stages, the destruction of brain cells, especially in areas for memory and cognition, is permanent. Abstaining from alcohol and addressing deficiencies such as vitamin B1 (thiamine) forestalls further deterioration, but structural damage to the brain whose ramification is lasting cognitive degradation has already occurred, which makes recovery not guaranteed.

A case report of a 42-year-old patient with alcohol-related dementia (ARD) revealed cognitive improvements after a period of abstinence from alcohol. Initially, neuropsychological tests showed severe verbal memory disturbance, and early Alzheimer’s disease was suspected. However, after disclosing his excessive alcohol consumption, the patient’s cognitive function improved markedly. FDG-PET imaging initially showed glucose hypometabolism in the diencephalon and basal forebrain, which recovered over a five-year follow-up period. This case suggests that hypofunction in these regions is associated with reversible ARD according to Asada et al. (2010) in “Reversible Alcohol-related dementia: A Five-year Follow-up Study Using FDG-PET and Neuropsychological Tests.”

Another piece of research intimates that the encouraging aspect of Alcohol-Related Brain Damage (ARBD) is that, unlike other forms of dementia such as Alzheimer’s disease, it does not inevitably worsen over time. The progression of ARBD is halted, and in some cases, even reversed with appropriate treatment. Indeed, no treatment guarantees 100% effectiveness, research suggests that an estimated 75% of individuals with ARBD who receive treatment show some degree of recovery. Specifically, 25% achieve a complete picking up, another 25% experience considerable convalescence, 25% see only a slight upgrade, and 25% show no recuperation at all, according to the charity Alcohol Change UK.

What Is the Difference Between Alcoholic Dementia and Alzheimer’s Disease?

The main difference between alcoholic dementia (or alcohol-related brain damage, ARBD) and Alzheimer’s disease lies in their causes and progression. Alcoholic dementia is principally caused by long-term excessive alcohol consumption, which ensues in brain damage, notably in areas associated with memory and cognition. This damage is accelerated by nutritional deficiencies, particularly a lack of vitamin B1 (thiamine).

The damage is relatively reversed or at least stabilized if alcohol use is stopped and nutritional support is granted early enough In contrast, Alzheimer’s disease is a neurodegenerative condition characterized by the accumulation of amyloid plaques and tau tangles in the brain, inducing irreversible cell death and progressive cognitive depreciation. Unlike alcoholic dementia, Alzheimer’s disease worsens with time without any potential for reversal.