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A High Price to Pay: The Relationship Between Alcoholism, Memory Loss, and Dementia

The blackout is often invoked as a comic punchline for a night of overindulgence. Movies and television shows often depict their well-meaning but misguided protagonists in pain and confusion following a night of binge drinking, desperately regretting their misadventures while fearing the fallout from actions they have no memory of. The consequences of an alcohol-induced blackout in movies and sitcoms usually drive the comedic plot, as characters find themselves unexpectedly married or pregnant or covered in face tattoos and tending a tiger they somehow purchased the night before.

However, real life is very different than an episode of Friends and it rarely resembles the plotline of The Hangover. The consequences of a binge blackout are no laughing matter. In fact, the effects of alcohol exposure on the brain and memory are by no means limited to the short term. Rather, alcohol abuse is strongly linked to significant, enduring, and often irreversible brain damage, including various forms of dementia. But how, exactly, does alcohol abuse impact the brain in general and the memory in particular?

Understanding the Neurological Impacts of Alcohol Exposure

Chronic alcohol abuse has long been associated with significant changes to brain structures and functioning, with a particularly strong impact on both short-term and long-range memory (1, 2, 3). However, the exact mechanisms of these neuropathologies have been relatively little understood until recently, thanks in large measure to advances in neuroimaging.

Researchers have found that there are, in fact, multiple processes involved in creating the structural and functional changes that lead to memory and cognitive impairment in the alcohol abuser’s brain (3, 4). The research also suggests that a myriad of factors determine which neurological structures are most impacted and how. Considerations such as age, disease severity, alcohol exposure type and frequency, and genetic vulnerability play a substantial role in determining how the brain will be affected by alcohol misuse (2, 4, 5).

Short-Term Effects: Blackouts and “Brownouts”

Although the alcohol blackout is often the classic cultural stereotype of the night of binge drinking, research shows that even short-term memory loss due to heavy, acute alcohol exposure is far more complicated than it may initially seem and that the damage done by alcohol exposure may be far more significant and enduring. For instance, not everyone who experiences memory loss due to a heavy drinking episode will have a full “blackout.” Some people will, indeed, have no memory of the episode, referred to as “en bloc” memory loss. Others will experience “fragmentary” amnesia, meaning that the loss of memory is partial rather than complete. Still others will experience episodic memory loss, which refers to the learning and recall of the processes required to complete a given task and signifies deficiencies in the encoding, storage, and retrieval of new information in the “contextual memory” (6).

Neuroimaging suggests that the impacts on short-term memory, whether leading to fragmentary, en bloc, or episodic memory loss appears to relate to changes in the deep structures of the brain, and particularly those associated with memory and information processing. The most significant of these structures is the hippocampus, which, the researchers found, showed signs of atrophy in neurological scans (6, 7). Importantly, these same studies show that short-term memory loss and related declines in cognitive function, don’t just occur during the alcohol exposure, but can linger for several days after the event (6).

In addition to the impacts of acute and heavy alcohol exposure on the deep structures of the brain, the wide variations in the forms that blackouts may take also illuminate the complex and diverse processes through which alcohol-induced brain damage occurs. For example, studies suggest that those with genetic vulnerabilities are more likely than the general population to experience binge drinking blackouts, brownouts, and episodic memory loss (2, 4).

Thiamine Deficiency

The hippocampus is not the only deep brain structure to be adversely affected by alcohol exposure. It’s the impact on the thalamus which may lead to the most devastating, long-term effects (1, 4, 8). Chronic alcohol abuse has been strongly linked to malnutrition and, more specifically, to thiamine deficiency (1, 3). In the short-term, severe thiamine deficiency can lead to a reversible but serious condition known as Wernick encephalopathy (WE), which is associated with lesions in the thalamus and is an inflammation of the brain that can lead to confusion, loss of motor control, vision and eye movement disordereds and, in severe cases, coma and death (1, 3). When this condition persists or is left untreated, or if underlying alcohol use disorder (AUD) continues, then WE can progress to a diagnosis of Korsakoff syndrome, a condition leading to irreversible brain damage charactrized by significant memory loss (1).

Ethanol Toxicity

Alcohol-related thiamine deficiency and subsequent Wernick encephalopathy and Korsakoff syndrome are leading causes of long-term memory loss and cognitive impairment, but exposure to ethanol in and of itself can have highly destructive impacts on brain structures and functioning (3). Indeed, ethanol toxicity has been linked to severe, long-term cognitive decline as well as the development of Alzheimer’s and other forms of dementia (1, 3, 4).

Thiamine deficiency takes its most significant toll on the thalamus, the deep brain structure responsible not only for sensory and motor regulation but also for consciousness and alertness (including memory and cognition) (8). Ethanol toxicity, however, seems to have more complex, more wide-ranging, and less well understood impacts on the brain. What is currently known about ethanol toxicity, though, is nothing good for brain health and longevity. For example, chronic and excessive exposure to alcohol can lead to severe inflammation of the brain (neuroinflammation), particularly of the hippocampus and frontal cortex (4).

At the same time, intermittent binge drinking, even in adolescence, can lead to significant changes in the brain that persist throughout adulthood, contributing to memory loss and cognitive impairment and increasing the risk for dementia later in life (4). This includes changes to the structures of the hippocampus, the basal forebrain, and the frontal cortex (4). The brain also begins to lose its capacity to repair itself, to create new neurons and neuropathways (neurogenesis) (3, 4).

What this means, ultimately, is that not only is the brain altered by ethanol toxicity, but the brain’s circuitry is also significantly impaired (8). Neurons cannot communicate effectively, and the individual’s ability to think, to learn, and to remember can be severely compromised, even before dementia or Alzheimer’s develop.

How Bayshore Can Help

If you or someone you love is experiencing alcohol use disorder (AUD), cognitive decline, memory loss, and dementia do not have to be the future. Our multidisciplinary team of experts can help you regain your sobriety and protect brain health through a holistic treatment plan that includes diet, exercise, and mental and physical healthcare. Contact us today to discuss how we can help you or your loved one live a long, healthy life free of alcohol dependency and its threat to your mind and memory.

At Bayshore Retreat we have extensive knowledge in treating substance abuse and co-occurring mental health issues. We understand that Mental Health Disorders can be the root cause of substance abuse. We use the latest scientific research and holistic approach for drug and alcohol addiction treatment.

  1. Zahr, N. M., Kaufman, K. L., & Harper, C. G. (2011). Clinical and pathological features of alcohol-related brain damage. Nature reviews. Neurology, 7(5), 284–294.
  2. Miller, M. B., Merrill, J. E., DiBello, A. M., & Carey, K. B. (2018). Distinctions in Alcohol-Induced Memory Impairment: A Mixed Methods Study of En Bloc Versus Fragmentary Blackouts. Alcoholism, clinical and experimental research, 42(10), 2000–2010.
  3. Diamond, I., & Messing, R. O. (1994). Neurologic effects of alcoholism. The Western journal of medicine, 161(3), 279–287.
  4. Nunes, P. T., Kipp, B. T., Reitz, N. L., & Savage, L. M. (2019). Aging with alcohol-related brain damage: Critical brain circuits associated with cognitive dysfunction. International review of neurobiology, 148, 101–168.
  5. Rehm, J., Hasan, O., Black, S. E., Shield, K. D., & Schwarzinger, M. (2019). Alcohol use and dementia: a systematic scoping review. Alzheimer’s research & therapy, 11(1), 1.
  6. Pitel, A. L., Beaunieux, H., Witkowski, T., Vabret, F., Guillery-Girard, B., Quinette, P., Desgranges, B., & Eustache, F. (2007). Genuine episodic memory deficits and executive dysfunctions in alcoholic subjects early in abstinence. Alcoholism, clinical and experimental research, 31(7), 1169–1178.
  7. Reitz, N. L., Nunes, P. T., & Savage, L. M. (2021). Adolescent Binge-Type Ethanol Exposure in Rats Mirrors Age-Related Cognitive Decline by Suppressing Cholinergic Tone and Hippocampal Neurogenesis. Frontiers in behavioral neuroscience, 15, 772857.
  8. Chanraud, S., Pitel, A. L., Rohlfing, T., Pfefferbaum, A., & Sullivan, E. V. (2010). Dual tasking and working memory in alcoholism: relation to frontocerebellar circuitry. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 35(9), 1868–1878.
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