Future research is needed to shed more light on this important question. In particular, research in what are whippets animals will be an important supplement to studies in humans, affording a better understanding of the underlying prefrontal circuitry involved in alcohol-induced memory impairment. Alcohol-related blackouts are gaps in a person’s memory for events that occurred while they were intoxicated. These gaps happen when a person drinks enough alcohol to temporarily block the transfer of memories from short-term to long-term storage—known as memory consolidation—in a brain area called the hippocampus. The authors concluded that the blackouts were caused by an inability to transfer information from short-term to long-term memory when blood alcohol levels were rising. The results were published in the Quarterly Journal of Studies on Alcohol.
This is because blacking out typically involves dangerous drinking behaviors, such as binge drinking and heavy drinking. The term for the type of memory loss individuals experience when they black out is called anterograde amnesia, which means they can’t form or store new memories but they have previous memories. People who experience an alcohol-related blackout may keep walking, talking, making decisions, and drinking, but they don’t remember some or all of what happened. These people may seem relatively fine to those around them despite their memory impairment.
The activity—which corresponds to the middle portion of the lower left arm of the maze—is shown before alcohol administration (A), 45 to 60 minutes after alcohol administration (B), and 7 hours after alcohol administration (C). The dose of alcohol used in the testing session was 1.5 grams per kilogram of body weight— enough to produce a peak BAC of about 0.16 percent. (A corresponding BAC in humans would be twice the legal driving limit in most States.) As the how to wean off alcohol figure illustrates, the cell’s activity was essentially shut off by alcohol.
These authors recruited 108 college students, half of whom had experienced at least one fragmentary blackout in the previous year. While sober, members of the two groups performed comparably in memory tasks. However, when they were mildly intoxicated (0.08 percent BAC) those with a history of fragmentary blackouts performed worse than those without such a history.
This heightened responsiveness is known as long-term potentiation (LTP). In recent work with awake, freely behaving rats, White and Best (2000) showed that alcohol profoundly suppresses the activity of pyramidal cells in region CA1. The researchers allowed the rats to forage for food for 15 minutes in a symmetric, Y-shaped maze and measured the animals’ hippocampal activity using tiny wires (i.e., microelectrodes) implanted in their brains.
And the higher blood alcohol levels reach, the more likely a person will black out. The more genetically susceptible rhinophyma and alcoholism an individual is, the less alcohol is required to black out. You may feel fine or functional while drinking and will only realize you have memory loss after the fact.
We do know that women are more likely to experience other effects of alcohol, such as liver cirrhosis, heart damage, nerve damage and other diseases caused by alcohol. However, scientists at the Washington University School of Medicine found in a 2011 study that alcohol didn’t kill brain cells. Instead, they found that alcohol interfered with receptors in the brain, making them produce steroids that interrupted the learning and memory-building process. Take our free, 5-minute alcohol abuse self-assessment below if you think you or someone you love might be struggling with alcohol abuse. The evaluation consists of 11 yes-or-no questions that are intended to be used as an informational tool to assess the severity and probability of an alcohol use disorder. The test is free and confidential, and no personal information is needed to receive the results.
There are two possible interpretations for these data, both of which support the hypothesis that some people are more susceptible to blackouts than others. A second interpretation is that subjects in the blackout group performed poorly during testing as a result of drinking enough in the past to experience alcohol-induced memory impairments. In other words, perhaps their prior exposure to alcohol damaged the brain in a way that predisposed them to experiencing future memory impairments. This latter possibility is made more likely by recent evidence that students who engage in repeated episodes of heavy, or binge, drinking are more likely than other students to exhibit memory impairments when they are intoxicated (Weissenborn and Duka 2000).
Unlike en bloc blackouts, fragmentary blackouts involve partial blocking of memory formation for events that occurred while the person was intoxicated. Goodwin and colleagues (1969a) reported that subjects experiencing fragmentary blackouts often become aware that they are missing pieces of events only after being reminded that the events occurred. Interestingly, these reminders trigger at least some recall of the initially missing information. Research suggests that fragmentary blackouts are far more common than those of the en bloc variety (White et al. 2004; Hartzler and Fromme 2003b; Goodwin et al. 1969b). He survived but showed memory impairments similar to those exhibited by H.M.
Several factors affect the likelihood that information will be transferred into long-term memory. For decades, researchers have known that alcohol disrupts the brain’s ability to transfer memories from short-term to long-term memory, but they didn’t know how. The common consensus was that alcohol killed brain cells, causing memory loss and other cognitive impairments. The term “blackout” refers to the loss of memory caused by a fast spike in blood alcohol level (BAC). It may also be referred to as “alcohol-induced amnesia.” Want to know what causes a drunk blackout?
The fact that subjects could remember aspects of the events 2 minutes after they occurred but not 30 minutes or 24 hours afterward provides compelling evidence that the blackouts stemmed from an inability to transfer information from short-term to long-term storage. For all but one subject in the blackout group, memory impairments began during the first few hours of drinking, when BAC levels were still rising. The average peak BAC in this group, which was roughly 0.28 percent, occurred approximately 2.5 hours after the onset of drinking. Alcohol primarily interferes with the ability to form new long-term memories, leaving intact previously established long-term memories and the ability to keep new information active in memory for brief periods. As the amount of alcohol consumed increases, so does the magnitude of the memory impairments. Large amounts of alcohol, particularly if consumed rapidly, can produce partial (i.e., fragmentary) or complete (i.e., en bloc) blackouts, which are periods of memory loss for events that transpired while a person was drinking.
Neural activity returned to near-normal levels within about 7 hours of alcohol administration. To evaluate the effects of alcohol, or any other drug, on memory, one must first identify a model of memory formation and storage to use as a reference. This model often is referred to as the modal model of memory, as it captures key elements of several other major models. Indeed, elements of this model still can be seen in virtually all models of memory formation.
He is the author of numerous books, including From Bud to Brain and Marijuana on My Mind. Some groups have a higher risk and should use special care when consuming alcoholic beverages.