What Causes Alcohol-Induced Blackouts?

When this happens, memories do not form or store, so they can’t necessarily be recovered. A person with a total blackout feels like the events that occurred while intoxicated never occurred. Research also indicates that a person who has experienced one blackout is more likely to have blackouts in the future. The long-term effects of a blackout are unknown, but they may cause the brain to be more susceptible to memory losses in the future.

Indirect Effects of Alcohol on Hippocampal Function

Binging, pre-partying, and alcohol games, especially on an empty stomach, all produce a rapid rise in blood alcohol levels that make blackouts more likely. Because blackouts tend to occur at high BACs, they commonly stem from binge drinking, defined as a pattern of drinking that increases a person’s BAC to 0.08 percent or higher. This typically occurs after 4 drinks for women and 5 drinks for men—in about 2 hours. In fact, many people who have a potential case of acute ketamine withdrawal blackouts do so after engaging in a behavior known as high-intensity drinking, which is defined as drinking at levels that are at least twice as high as the binge-drinking thresholds for women and men. 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.

When Do Blackouts Occur?

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. Studies also suggest that prenatal exposure to alcohol increases a person’s chance of experiencing blackouts in the future, and certain genes may increase a person’s likelihood to black out. Passing out means a person has either fallen asleep or lost consciousness from too much drinking. In contrast, a person is awake during a blackout, but their brain is not creating new memories. Sometimes a person can transition from having a blackout to passing out. Considerable evidence suggests that chronic alcohol use damages the frontal lobes and leads to impaired performance of tasks that rely on frontal lobe functioning (Kril and Halliday 1999; Moselhy et al. 2001).

Experienced Drinkers Don’t Black Out

BrACs of 20 g/dl and above are typically required to induce a blackout, thereby limiting the ability to safely dose research participants to the point of blackout. Finally, given the growing literature on alcohol-induced memory impairments and blackouts, a standardized assessment for alcohol-induced blackouts is sorely needed. Most of the existing research on alcohol-induced blackouts either uses a single item from the Rutgers Alcohol Problem Index or the investigator’s own description/definition of an alcohol-induced blackout. Moreover the frequency of occurrence for blackouts is currently measured in widely different ways, including dichotomous measures (e.g., Yes/No blackouts) and proportion of times drinking that blackouts were experienced (e.g., always, sometimes, never). In an effort to better characterize blackouts, researchers should collect detailed information about past and current alcohol consumption patterns, as well as other illicit drug use. Optimally, actual BrACs or blood draws could be collected to back-extrapolate peak BACs to the time of blackout.

1. Risk Factors

Alcohol-induced blackouts can lead to impaired memory of events that transpired while intoxicated, and a drastically increased risk of injuries and other harms. They can occur in anyone who drinks alcohol, no matter their age or level of experience with drinking. In this factsheet, we will take a sober look at this common but deeply concerning consequence of alcohol misuse. However in a four year follow up of young blackout drinkers, only 32% of respondents that were experiencing blackouts in the initial survey continued to experience them four years later. Alcoholic blackouts in this group appeared to have resolved spontaneously when the subjects graduated college, got married, or successfully entered the adult work force. Spontaneous resolution of blackout drinking appears to result from an interaction between informal support and objective social conditions such as full-time employment and a positive financial situation.

  1. You may not have any memory of the time that’s passed when your blood alcohol content is above that threshold.
  2. Knight and colleagues (1999) observed that 35 percent of trainees in a large pediatric residency program had experienced at least one blackout.
  3. This means that even after a blackout occurs, you can continue to experience memory loss and other difficulties recalling memories.
  4. In the short-term, drinking enough to blackout means the brain is not making memories or storing them.
  5. (Six? My quota was more like 16.) I told myself this report was just another form of woman-shaming by our patriarchal society.

They can still eat, walk, hold conversations, have sex, drive, and get into fights. Be prepared to give medical professionals any information you know about the person who needs help. Try to figure out what they’ve been drinking and how much they’ve consumed. You may be worried about getting them in trouble, but any information you share can be life-saving, so don’t omit any details that could help emergency responders provide care. Without help, addiction can dismantle a person’s life, health, and relationships. Fortunately, with the right combination of treatments, recovery from an alcohol addiction is possible.

During a blackout, an entire section of the brain (the hippocampus, which is responsible for long-term memories) experiences a neurophysiological, chemical disruption and completely shuts down. “Alcohol reduces the amount of information that makes it to the hippocampus and shuts down neurons in the hippocampus that make memories,” Aaron White, Ph.D., senior scientific advisor to the NIAAA director and one of the country’s leading experts on blackouts, tells SELF. “This creates a temporary void in the record-keeping system.” Memories lost in a blackout will never come back, because the information wasn’t stored in the first place. A person should speak to a doctor if they believe that they are experiencing symptoms of syncope, epileptic blackouts, or blackouts that are the result of medication. In cases of severe alcohol intoxication, a person may need emergency assistance. We are currently investigating which substances strengthen long-term potentiation under the influence of alcohol and thus support the formation of memories.

The NMDA receptor is necessary for LTP induction in area CA1 of the hippocampus. Ethanol’s effect on LTP in area CA1 of the hippocampus is thought to involve both inhibition of the NMDA receptor and potentiation of the biofeedback γ-aminobutyric acid A (GABAA) receptor transmission, which leads indirectly to further NMDA receptor inhibition [7,35,36]. Also known as an “en bloc” blackout, this refers to a total blackout that usually spans hours.

This heightened responsiveness is known as long-term potentiation (LTP). Because researchers have theorized that something like LTP occurs naturally in the brain during learning (for a review, see Martin and Morris 2002), many investigators have used LTP as a model for studying the neurobiology underlying the effects of drugs, including alcohol, on memory. The difference between a brownout and a blackout is that brownouts involve partial memory loss. With a brownout, you may be able to remember certain details from the period of time you were affected, but other portions of time can’t be recalled. Blackouts involve complete memory loss caused by your brain’s inability to record new memories for a period of time due to the effects of excessive alcohol, substance misuse or some other condition.

Specifically, it appears alcohol impairs the so-called long-term potentiation of synapses at the pyramidal cells in the hippocampus. Alcohol alters the activity of certain glutamate receptors, thereby boosting the production of specific steroid hormones. Normally this mechanism, responsible for strengthening the synaptic transfer of information between neurons, is the basis of memory formation. Alcohol can affect brain function and memory.1  While the exact ways alcohol affects brain chemistry can be complex, heavy alcohol use can have negative short-term and long-term health outcomes regarding one’s memory. The first hurdle concerned scientists’ understanding of the functional neuroanatomy of memory. In the 1950s, following observations of an amnesic patient known as H.M., it became clear that different brain regions are involved in the formation, storage, and retrieval of different types of memory.

Additionally, blackouts may occur at far lower thresholds among younger populations. That’s largely because the parts of your brain responsible for fentanyl laced weed decision-making aren’t fully matured until around age 25. Despite this, intentional binge drinking has been a common practice among young adults.

Alcohol suppresses hippocampal pyramidal cell activity in an awake, freely behaving rat. Pyramidal cells often fire when the animal is in discrete regions of its environment, earning them the title “place-cells.” The specific areas of the environment where these cells fire are referred to as place-fields. The figure shows the activity of an individual pyramidal cell before alcohol administration (baseline), 45 to 60 minutes after alcohol administration, and 7 hours after alcohol administration (1.5 g/kg). Each frame in the figure shows the firing rate and firing location of the cell across a 15-minute block of time during which the rat was foraging for food on a symmetric, Y-shaped maze. White pixels are pixels in which the cell fired at very low rates, and darker colors represent higher firing rates (see key to the right of figure). As is clear from a comparison of activity during baseline and 45 to 60 minutes after alcohol administration, the activity of the cell was essentially shut off by alcohol.

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