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The Connection Between Alcohol and Memory Loss

Written by Jonathan Strum

& Medically Reviewed by Dr. Deep Shukla, PhD, MS

Medically Reviewed

Up to Date

This article was reviewed by a medical professional to guarantee the delivery of accurate and up-to- date information. View our research policy.

Last Updated - 6/17/2022

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Alcohol use can negatively impact cognitive functions in the brain, including learning and memory. Intoxication can lead to a temporary inability to form new memories, known as short-term memory loss. This is often referred to as a “blackout” and is caused by a rapid increase in blood alcohol levels.

Long-term, excessive alcohol use can directly damage brain regions involved in cognitive function. It can also cause damage to other organ systems and indirectly impair cognitive brain regions. Chronic alcohol use can lead to brain damage, resulting in a permanent or long-term inability to form new memories.

Signs of Alcohol-Induced Memory Loss

Alcohol can cause cognitive deficits after only one or two drinks, and the level of memory impairment increases with the amount of alcohol consumed. Symptoms of memory loss due to alcohol intoxication may include:

  • Difficulty remembering recent events or conversations
  • Difficulty keeping track of a conversation
  • Difficulty concentrating
  • Inability to understand normal speech

The effects of alcohol-induced blackouts are accompanied by side effects of intoxication, including reduced motor coordination, balance and decision-making abilities. A combination of these factors may lead to reckless and risky behaviors.

Symptoms of memory loss due to long-term alcohol intake may be long-lasting, such as:

  • Inability to form new memories and retrieve old memories
  • Impaired ability to carry out motor activities
  • Impaired visuospatial abilities — difficulty recognizing or identifying objects
  • Deficits in executive function, including decision-making, planning and processing complex information

Alcohol Blackouts

Consuming large amounts of alcohol can impair the ability to form new memories, resulting in a memory blackout.

New information is initially stored in short-term memory and then transferred to long-term memory. Short-term memory has a limited capacity and stores information for a very short period of time (between 5 to 30 minutes). This information may either be transferred to long-term memory or forgotten. In contrast, long-term memory includes memories that are stored for anywhere between a few days to many years.

Alcohol intake disrupts the transfer of memories from short-term memory to long-term memory. Alcohol intake does not impair memories that were acquired before drinking (long-term memory), nor does it impair the retention of information for a few minutes (short-term memory). However, people tend to forget this newly acquired information because the transfer to long-term memory is disrupted.

Alcohol intoxication may result in a partial or complete inability to form new memories. In a partial or fragmentary blackout, the person is able to remember some information after being reminded of the events. In a complete blackout, the person is unable to recall any information from when they were intoxicated. Although people with an alcohol use disorder often experience blackouts, they are also common in social drinkers who rapidly consume large amounts of alcohol.

Wernicke-Korsakoff Syndrome

Chronic alcohol use can impair cognitive function directly by causing brain damage or indirectly by affecting other body systems. Vitamin B1 (thiamine) deficiency is one of the biggest causes of cognitive deficits in chronic alcohol users. Thiamine must be obtained from food sources, and alcohol directly interferes with the absorption and processing of thiamine. Chronic alcohol users also tend to have a poor diet, which can cause a thiamine deficiency.

Thiamine is important for the synthesis of brain neurotransmitters, and it is also necessary for metabolizing sugars in the brain. Prolonged thiamine deficiency can interfere with neuron function and result in Wernicke-Korsakoff syndrome. Wernicke-Korsakoff syndrome consists of two separate conditions: Wernicke’s encephalopathy and Korsakoff’s psychosis.

Thiamine deficiency initially leads to Wernicke’s encephalopathy, which is a short-lived and life-threatening condition. The symptoms of Wernicke’s encephalopathy include:

  • Paralysis of muscles controlling eye movements
  • Altered mental state (confusion)
  • Impaired motor control

Wernicke’s encephalopathy can be reversed by thiamine treatment. If it is not treated, however, the condition progresses to Korsakoff’s psychosis. This can cause memory loss but generally involves only a limited decline of intellectual abilities. Wernicke-Korsakoff syndrome involves an impaired ability to form new memories, but it may also cause difficulty retrieving memories that were formed before the condition.

Prevention of Alcohol-Induced Memory Loss

Alcohol use, in general, is associated with impairment of cognitive function. However, regular alcohol intake at low levels is associated with a reduced risk of dementia when compared to abstinence or moderate-to-heavy alcohol intake. From a long-term perspective, people should limit their amount of alcohol use and avoid alcohol abuse.

Excessive alcohol intake may result in intoxication without causing a blackout. Other interacting factors such as rapid intake are often necessary to cause a blackout. Some of these factors include:

  • Consuming large amounts of alcohol
  • Using alcohol on an empty stomach
  • Rapid alcohol consumption

Aside from avoiding excessive amounts of alcohol, people can take a few measures to prevent alcohol-induced blackouts. It can be helpful to stay hydrated and eat a meal before starting to drink. Avoiding rapid intake of alcohol and pacing the rate of alcohol consumption is also recommended. People should also limit the number of drinks they consume that have high alcohol content.

If you or a loved one suffers from alcohol misuse or addiction, The Recovery Village Ridgefield can help. Contact us today to learn about treatment options that can address substance use and co-occurring mental health disorders.

Sources

Moriyama, Yasushi; Mimura, Masaru; Kato, Motoichiro; Kashima, Haruo. “Primary alcoholic dementia and alcohol‐related dementia.” Psychogeriatrics, September 2006. Accessed August 31, 2019.

White, Aaron M. “What happened? Alcohol, memory blackouts, and the brain.” Alcohol Research & Health, 2003. Accessed August 31, 2019.

Martin, Peter R.; Singleton, Charles K.; Hiller-Sturmhöfel, Susanne. “The role of thiamine deficiency in alcoholic brain disease.” Alcohol Research & Health, 2003. Accessed August 31, 2019.

View Sources

Moriyama, Yasushi; Mimura, Masaru; Kato, Motoichiro; Kashima, Haruo. “Primary alcoholic dementia and alcohol‐related dementia.” Psychogeriatrics, September 2006. Accessed August 31, 2019.

White, Aaron M. “What happened? Alcohol, memory blackouts, and the brain.” Alcohol Research & Health, 2003. Accessed August 31, 2019.

Martin, Peter R.; Singleton, Charles K.; Hiller-Sturmhöfel, Susanne. “The role of thiamine deficiency in alcoholic brain disease.” Alcohol Research & Health, 2003. Accessed August 31, 2019.

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