Does Alcohol Make You Stupid?

Does Alcohol Make You Stupid
Is booze killing your brain cells? Not exactly. We’ve all heard the old warning from a parent, a friend, or a spouse before a night out on the town: Drinking alcohol kills brain cells. If you’re like me, you’ve probably believed it for awhile. Who hasn’t woken up after a long night of boozing feeling like less of a man than you are? You can’t think straight, your reflexes are slow, your senses foggy; even when the hangover fades, you feel like a complete mess of a person.

  • Here’s the hard truth: Alcohol may make you dumber, but it most certainly doesn’t kill your brain cells.
  • Let’s take a look at the science, shall we? After comparing the brains of dead alcoholics and nonalcoholics, scientists at the Bartholin Institute in Denmark found that, surprise!, the total number of neurons to be the same.

“Alcohol, like other substances, can kill brain cells at high doses, but moderate alcohol use does not,” explains Popular Science ‘s Megan Scudellari. “It does interfere with how neurons communicate, affecting one’s ability to perform tasks like walking, speaking, and making decisions.” So no, brain cell death isn’t the culprit when you find yourself a total blubbering mess, but a lack of communication between the neurons that make you the charming fella you are.

  1. When alcohol reaches the brain, it disables function by damaging the connective tissue at the end of neurons.
  2. This disrupts communication among neurons and makes it harder for an individual to focus or complete minor tasks,” explained Dana Dovey in Medical Daily in 2014.
  3. Our bodies are incredibly resilient and for the most part forgiving works of nature.

This alcohol-induced cell rampage does minor damage and most definitely does not result in the cell’s death.” But what if I drink enough booze to kill a Russian platoon? Even that won’t wipe our your brain’s contingent of cells, apparently: Researchers at Washington University in St.

  • Louis found that even when they applied alcohol directly to your neurons (I don’t even want to know how they did this), the cells didn’t die but started producing steroids that messed with communication.
  • Who started this stupid rumor, anyway? You can thank the American Temperance movement that turned the entire country into a bunch of teetotaling goons during the U.S.

Prohibition with the passage of the 18th Amendment. It took nearly 60 years for a groundbreaking 1993 study in The Lancet ​ to finally bust this dangerous myth. In fact, more recent studies have shown that moderate alcohol consumption can actually have a positive impact on your long-term cognitive health.

Does alcohol affect intelligence?

Conclusions – We found that lower results on IQ tests are associated with higher consumption of alcohol measured in terms of both total alcohol intake and binge drinking in Swedish adolescent men. Keywords: IQ, Alcohol Consumption Intelligence has been shown to be associated with various health-related outcomes in several studies (Andersson et al., 2008 ; Calvin et al., 2011 ; David et al., 1997 ; Gale et al., 2010 ; Hart et al., 2004 ; Hemmingsson et al., 2007 ; Martin et al., 2004 ).

  1. However, previous findings on cognitive ability and alcohol-related problems have not been consistent, possibly due to differences between the outcomes assessed.
  2. One suggested explanation for the association between intelligence and health is that cognitive skills enhance possibilities to make healthy lifestyle choices.

Cognitive ability has been found to be associated with several health-related behaviors, such as smoking, food intake, and physical activity (Batty et al., 2007b, c ; Hemmingsson et al., 2008 ). The scientific literature on intelligence and alcohol consumption in adolescence, measured as total intake and type of drinking, is scarce.

A twin study from the United States showed that a high IQ assessed at age 17 was associated with heavier alcohol use as measured by an alcohol use composite, taking into account symptoms of alcohol abuse/dependence, number of intoxications, frequency of use and number of drinks during a year, and maximum number of drinks within 24 hours (Johnson et al., 2009 ).

A study from Switzerland investigated how IQ test results from conscription were associated with frequency of drinking, defined as nondrinking, rare drinking (1 to 5 times/y), occasional drinking (1 to 5 times/month), moderate drinking (1 to 5 times/wk), and daily drinking.

  1. It showed that high performance on IQ tests had a positive association with moderate drinking (Muller et al., 2013 ).
  2. In the 1970 British Cohort Study, it was found that higher childhood mental ability was associated with higher alcohol intake as an adult (Batty et al., 2008 ).
  3. Another study from the United States, of a population 14 to 21 years of age, showed, on a measure of verbal intelligence, that lower verbal intelligence was associated with lower alcohol consumption, but also with a higher risk of alcohol-related problems among those who consumed alcohol (Windle and Blane, 1989 ).

Intelligence is commonly defined as “a very general mental capability that, among other things, involves the ability to reason, plan, solve problems, think abstractly, comprehend complex ideas, learn quickly, and learn from experience” (Gottfredson, 1997 ).

There are several tests of intelligence available, and the main difference between them lies in the recognition, or not, of a general factor, “g,” as introduced by Spearman. The “g” factor theory addresses the positive correlations found between tests designed to capture different suggested areas of intelligence, for example, verbal, logical, and spatial.

Instead of 1 “g” factor, Horn and Cattell suggested 5 “general” factors, of which those concerned with “fluid” and “crystallized” abilities are the most influential. The first is a matter of basic ability to reason ( g f ), while the latter ( g c ) concerns how well the individual has invested his/her fluid ability in society to gain knowledge of value.

These 2 theories are often contrasted with that of Thurstone, in whose model primary mental abilities are expected to explain test results more independently (Carlstedt, 2000 ; Gustafsson, 1984 ; Nisbett et al., 2012 ). However, as concluded by Deary ( 2012 ), there are few empirical grounds for considering intelligence without the “g”-factor.

Studies on alcohol consumption should consider both total alcohol intake and pattern of drinking (Rehm et al., 2003 ). Although few studies have been performed on patterns of drinking, they have been shown to be of importance for certain diagnoses, for example, ischemic heart disease, fetal alcohol syndrome, and injury (Plunk et al., 2014 ; Rehm et al., 2010 ).

  1. There are different definitions of patterns of drinking in the literature.
  2. Normally, binge drinking is contrasted with a moderate or steady type of drinking, but there is a lack of distinct and broadly acknowledged measures of the different patterns of consumption (Field et al., 2008 ).
  3. It is, however, known, that binge drinking is more common among young adults and adolescents (Kuntsche et al., 2004 ).

Further, a systematic review by McCambridge and colleagues ( 2011 ) showed that high alcohol consumption in late adolescence is carried into adulthood and as too are the problems associated with alcohol. The aim of this study was to examine the association between intelligence and total alcohol intake during a specific time period and pattern of drinking.

  1. Is there an association between intelligence and total alcohol intake in adolescence?
  2. Is there an association between intelligence and pattern of drinking in adolescence?
  3. Are there differences in the associations between different the cognitive factors measured in an IQ test and total alcohol intake and pattern of drinking in adolescence?
  4. Does any association between IQ test results and total alcohol intake in adolescence persist into adulthood?

Do intelligent people get drunk?

Evolutionary psychologist Dr. Satoshi Kanazawa indicates that intelligent people use alcohol more unhealthily than dumb people by drinking excessively rather than moderately. What are the public health implications of such a finding? The Stanton Peele Addiction Website, February 14, 2011.

  • This blog post also appeared on Stanton’s Addiction in Society blog at PsychologyToday.com,
  • This post is a response to More Intelligent People Are More Likely to Binge Drink and Get Drunk by Satoshi Kanazawa Dr.
  • Anazawa has reissued his assertion that more intelligent people binge drink and get drunk more, according to the National Longitudinal Study of Adolescent Health (Add Health).

The following data from that study relate childhood IQ to binge drinking and drunkenness: “Very dull” Add Health respondents (with childhood IQ 125) engage in binge drinking roughly once every other month. The association between childhood intelligence and adult frequency of getting drunk is equally clear and monotonic.

Although smarter people (as measured in childhood) get drunk more, they are less likely than dull people to become alcoholics. Does that mean that they are inured against alcoholism? The dominant theory here would be that being smart is a protective life asset. They are just as likely to become alcoholics. Which would still be somewhat counterintuitive, since despite getting drunk far more often than dull people, they are no more likely to succumb to alcoholism. Smart people are more likely to be alcoholics. This could follow from several theories of behavior: smart people tempt fate by drinking more, and thus they are more likely to become alcoholics. Or, smart people are inherently more likely to be alcoholics – perhaps being smart makes them more acutely aware of the world’s problems, or creates other damaging emotional states.

These different possibilities offer different perspectives on attacking alcoholism and addiction. If smart kids are significantly more likely to become alcoholics, childhood intelligence is a risk factor for alcoholism. Should parents and society therefore be wary of – even strive against – kids being smart? Perhaps you have heard people who say things like that they hope their kids aren’t smart for reasons like this – although the dominant striving-parent culture in America is certainly not oriented that way.

  1. Or should this not be a concern for parents of smart kids – or at least no more of a concern than it is for all parents? What a quandary – something most people generally value leads to a behavior of which we disapprove – and possibly to a permanent disease state. But Dr.
  2. Anazawa goes beyond suggesting childhood intelligence is more likely to entail adult difficulties of the type coded in DSM’s categories of emotional disorders (I mean alcohol dependence, et al.).

He says that smarter people are not likely to behave more healthily in regards to intoxicants, if moderate drinking is such a healthy behavior. Dr. Kanazawa notes “There are occasional medical reports and scientific studies which tout the health benefits of mild alcohol consumption, such as drinking a glass of red wine with dinner every night” (it’s not clear from this statement whether Dr.

  1. Anazawa accepts or rejects this claim).
  2. While, he continues, “it may be tempting to conclude that more intelligent individuals are more likely to engage in such mild alcohol consumption than less intelligent individuals.
  3. Unfortunately for the intelligent individuals, this is not the case.” This follows, for Dr.

Kanazawa, since “more intelligent children are more likely to grow up to engage in binge drinking and getting drunk,” In Dr. Kanasawa’s view, occasional drunkenness (once every other month or so) is incompatible with regular moderate drinking. Which would mean that, as a rule of thimb, intelligent people overall behave less healthily with alcohol and drugs.

Do guys mean what they say when drunk?

Do people mean what they say when drunk? Yes, sometimes people mean what they say when they are drunk. But most of the time, people say whatever comes to mind when drinking without any concern if it’s genuinely how they feel. Alcohol lowers inhibition and makes people feel talkative, extroverted, and emboldened.

Does alcohol make you braver?

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One reason many people drink is to boost their confidence. Alcohol is often used to remove inhibitions and make you feel more self-assured, brave and confident in yourself. You may drink at parties to feel more relaxed or down a beer before talking to someone you’re attracted to.

  1. Yet does alcohol truly increase your confidence? The simple answer is no.
  2. It’s true that alcohol directly affects the brain, but not in positive ways.
  3. While drinking may make you feel a little more confident, it’s just a mask that you can hide behind.
  4. Self-acceptance without alcohol is the real way to find the strength to be yourself.

Alcohol courage, or liquid courage, is a term that originated in the 17th century. Soldiers heading to the front lines to face cannons and gunfire were given a good dose of gin, which was thought to boost their confidence. Today, people use alcohol courage for other purposes.

Drinking gives them the confidence to do things they are otherwise too scared to do — flirting, fighting, singing karaoke at a bar. Alcohol causes our brain to release a flood of dopamine. This chemical is associated with pleasure and can make you feel confident and powerful. Alcohol also directly impacts the part of the brain associated with good judgment.

This reduces your inhibitions and fears, making you more likely to make an impulsive decision without thinking things through.

Does alcohol affect thinking?

Image Diffusion tensor imaging (DTI) of fiber tracks in the brain of a 58-year-old man with alcohol use disorder. DTI maps white-matter pathways in a living brain. Image courtesy of Drs. Adolf Pfefferbaum and Edith V. Sullivan. Alcohol interferes with the brain’s communication pathways and can affect the way the brain looks and works.

Does alcohol sharpen your mind?

A glass of wine after a long day can feel like the perfect thing to clear your mind. Based on this new study, it actually is clearing your mind – of damaging toxins and inflammation. Published in Scientific Reports, the research showed that low levels of alcohol, equivalent to two glasses of wine or a pint and a half of beer, can flush these damaging substances from your brain and help stave off Alzheimer’s,

Just make sure you stop at just two glasses. A bottle a day isn’t so helpful, as the researchers are sure to clarify. And excessive alcohol consumption can have the opposite effect. The experiment was conducted on mice. One group abstained from drinking completely (such responsible mice!) and the other group kicked back with the equivalent of a couple drinks.

The group consuming alcohol proved to be more efficient at clearing waste from their brains than the teetotalers. However, “prolonged intake of excessive amounts of ethanol is known to have adverse effects on the central nervous system,” Maiken Nedergaard, lead author of the study, told The Irish Times,

  • When mice were exposed to large amounts of alcohol over a long period of time, they experienced enough inflammation to erode their cognitive abilities and motor skills.
  • The ones who took it easy on the booze, however, performed just as well on cognitive tests as those who didn’t drink at all.
  • Their motor skills remained intact and their ability to clear out toxins improved.

Drinking a glass or two of wine every day might do well to keep one’s memory sharp. So perhaps his abstinence from alcohol isn’t the healthiest thing about President Trump’s diet after all. View slideshow related to drinking

Guinness Is Healthier Than Your Light Beer World’s Oldest Man Dies at 113 After a Lifetime of Fresh Vegetables and Red Wine 25 Fascinating Mid-Winter Wines – Pricey Whites, Affordable Reds

What is drinking IQ?

DRINKiQ: sharing the facts and promoting moderation DRINKiQ is our dedicated responsible drinking online platform that provides facts about alcohol, the effects of drinking on the body and the mind, and the impact of harmful drinking on individuals and society.

Do highly successful people drink alcohol?

Author: Claudia M. Elsig, MD – When we think of Ultra-High-Net-Worth Individuals (UHNWIs), the image we most commonly conjure is of a smartly dressed man on his superyacht with a glass of whisky in his hand. It is cliched but dangerously close to the truth.

Is alcohol good for the memory?

Aaron M. White, Ph.D. – Aaron M. White, Ph.D., is an assistant research professor in the Department of Psychiatry, Duke University Medical Center, Durham, North Carolina. This work was supported by the National Institute on Alcohol Abuse and Alcoholism grant AA–12478 and the Institute for Medical Research at the VA Medical Center in Durham, North Carolina.

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.
  • Blackouts are much more common among social drinkers—including college drinkers—than was previously assumed, and have been found to encompass events ranging from conversations to intercourse.

Mechanisms underlying alcohol–induced memory impairments include disruption of activity in the hippocampus, a brain region that plays a central role in the formation of new auotbiographical memories. Key words: alcoholic blackout; memory interference; AOD (alcohol and other drug) intoxication; AODE (alcohol and other drug effects); AODR (alcohol and other drug related) mental disorder; long–term memory; short–term memory; state–dependent memory; BAC level; social AOD use; drug interaction; disease susceptibility; hippocampus; frontal cortex; neuroimaging; long–term potentiation If recreational drugs were tools, alcohol would be a sledgehammer.

  1. Few cognitive functions or behaviors escape the impact of alcohol, a fact that has long been recognized in the literature.
  2. As Fleming stated nearly 70 years ago, “the striking and inescapable impression one gets from a review of acute alcoholic intoxication is of the almost infinite diversity of symptoms that may ensue from the action of this single toxic agent” (1935) (pp.94–95).

In addition to impairing balance, motor coordination, decisionmaking, and a litany of other functions, alcohol produces detectable memory impairments beginning after just one or two drinks. As the dose increases, so does the magnitude of the memory impairments.

  1. Under certain circumstances, alcohol can disrupt or completely block the ability to form memories for events that transpire while a person is intoxicated, a type of impairment known as a blackout.
  2. This article reviews what is currently known regarding the specific features of acute alcohol–induced memory dysfunction, particularly alcohol–induced blackouts, and the pharmacological mechanisms underlying them.

EFFECTS OF ALCOHOL ON MEMORY 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. One classic, often–cited model, initially proposed by Atkinson and Shiffrin (1968), posits that memory formation and storage take place in several stages, proceeding from sensory memory (which lasts up to a few seconds) to short–term memory (which lasts from seconds to minutes depending upon whether the information is rehearsed) to long–term storage.

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. In the modal model of memory, when one attends to sensory information, it is transferred from a sensory memory store to short–term memory.

The likelihood that information will be transferred from short–term to long–term storage, or be encoded into long–term memory, was once thought to depend primarily on how long the person keeps the information active in short–term memory via rehearsal.

Although rehearsal clearly influences the transfer of information into long–term storage, it is important to note that other factors, such as the depth of processing (i.e., the level of true understanding and manipulation of the information), attention, motivation, and arousal also play important roles (Craik and Lockhart 1972; Otten et al.2001; Eichenbaum 2002).1 ( 1 It is well beyond the scope of this review to assess the impact of alcohol on memory utilizing multiple perspectives on information processing and storage.

For simplicity, this review will characterize the effects of alcohol on memory using a three–stage process of memory formation akin to the modal model. The interpretation of the effects of alcohol on memory likely would vary somewhat depending on the memory model one uses.) Variability in the use of terms, particularly in operational definitions of short–term memory, makes it difficult to formulate a simple synopsis of the literature on alcohol–induced memory impairments.

As Mello (1973) stated three decades ago with regard to the memory literature in general, “The inconsistent use of descriptive terms has been a recurrent source of confusion in the ‘short–term’ memory literature and ‘short–term’ memory has been variously defined as 5 seconds, 5 minutes, and 30 minutes” (p.333).

In spite of this inconsistency, several conclusions can be drawn from research on alcohol–induced memory impairments. One conclusion is that the impact of alcohol on the formation of new long–term “explicit” memories—that is, memories of facts (e.g., names and phone numbers) and events—is far greater than the drug’s impact on the ability to recall previously established memories or to hold new information in short–term memory (Lister et al.1991).

(See figure 1 for a diagram depicting the stages of memory and where alcohol interferes with memory.) Intoxicated subjects are typically able to repeat new information immediately after its presentation and often can keep it active in short–term storage for up to a few minutes if they are not distracted (for an early review, see Ryback 1971), though this is not always the case (Nordby et al.1999).

Similarly, subjects normally are capable of retrieving information placed in long–term storage prior to acute intoxication. In contrast, alcohol impairs the ability to store information across delays longer than a few seconds if subjects are distracted between the time they are given the new information and the time they are tested.

In a classic study, Parker and colleagues (1976) reported that when intoxicated subjects were presented with “paired associates”—for example, the letter “B” paired with the month “January”—they were impaired when asked to recall the items after delays of a minute or more. However, subjects could recall paired associates that they had learned before becoming intoxicated.

More recently, Acheson and colleagues (1998) observed that intoxicated subjects could recall items on word lists immediately after the lists were presented but were impaired when asked to recall the items 20 minutes later.

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Figure 1 A general model of memory formation, storage, and retrieval based on the modal model of memory originally proposed by Atkinson and Shiffrin (1968). Alcohol seems to influence most stages of the process to some degree, but its primary effect appears to be on the transfer of information from short–term to long–term storage. Intoxicated subjects are typically able to recall information immediately after it is presented and even keep it active in short–term memory for 1 minute or more if they are not distracted. Subjects also are normally able to recall long–term memories formed before they became intoxicated; however, beginning with just one or two drinks, subjects begin to show impairments in the ability to transfer information into long–term storage. Under some circumstances, alcohol can impact this process so severely that, once sober again, subjects are unable to recall critical elements of events, or even entire events, that occurred while they were intoxicated. These impairments are known as blackouts.

Ryback (1971) characterized the impact of alcohol on memory formation as a dose–related continuum, with minor impairments at one end and large impairments at the other, all impairments representing the same fundamental deficit in the ability to transfer new information from short–term to long–term storage.

  1. When doses of alcohol are small to moderate (producing blood alcohol concentrations below 0.15 percent), memory impairments tend to be small to moderate as well.
  2. At these levels, alcohol produces what Ryback (1971) referred to as cocktail party memory deficits, lapses in memory that people might experience after having a few drinks at a cocktail party, often manifested as problems remembering what another person said or where they were in conversation.

Several studies have revealed that alcohol at such levels causes difficulty forming memories for items on word lists or learning to recognize new faces (Westrick et al.1988; Mintzer and Griffiths 2002). As the dose increases, the resulting memory impairments can become much more profound, sometimes culminating in blackouts—periods for which a person is unable to remember critical elements of events, or even entire events, that occurred while he or she was intoxicated.

Alcohol–Induced Blackouts Blackouts represent episodes of amnesia, during which subjects are capable of participating even in salient, emotionally charged events—as well as more mundane events—that they later cannot remember (Goodwin 1995). Like milder alcohol–induced memory impairments, these periods of amnesia are primarily “anterograde,” meaning that alcohol impairs the ability to form new memories while the person is intoxicated, but does not typically erase memories formed before intoxication.

Formal research into the nature of alcohol–induced blackouts began in the 1940s with the work of E.M. Jellinek (1946). Jellinek’s initial characterization of blackouts was based on data collected from a survey of Alcoholics Anonymous members. Noting that recovering alcoholics frequently reported having experienced alcohol–induced amnesia while they were drinking, Jellinek concluded that the occurrence of blackouts is a powerful indicator of alcoholism.

  1. In 1969, Goodwin and colleagues published two of the most influential studies in the literature on blackouts (Goodwin et al.1969 a,b ).
  2. Based on interviews with 100 hospitalized alcoholics, 64 of whom had a history of blackouts, the authors posited the existence of two qualitatively different types of blackouts: en bloc and fragmentary blackouts.

People experiencing en bloc blackouts are unable to recall any details whatsoever from events that occurred while they were intoxicated, despite all efforts by the drinkers or others to cue recall. Referring back to our general model of memory formation, it is as if the process of transferring information from short–term to long–term storage has been completely blocked.

  • En bloc memory impairments tend to have a distinct onset.
  • It is usually less clear when these blackouts end because people typically fall asleep before they are over.
  • Interestingly, people appear able to keep information active in short–term memory for at least a few seconds.
  • As a result, they can often carry on conversations, drive automobiles, and engage in other complicated behaviors.

Information pertaining to these events is simply not transferred into long–term storage. Ryback (1970) wrote that intoxicated subjects in one of his studies “could carry on conversations during the amnesic state, but could not remember what they said or did 5 minutes earlier.

  1. Their immediate and remote memory were intact” (p.1003).
  2. Similarly, in their study of memory impairments in intoxicated alcoholics, Goodwin and colleagues (1970) reported that subjects who experienced blackouts for testing sessions showed intact memory for up to 2 minutes while the sessions were taking place.

Unlike en bloc blackouts, fragmentary blackouts involve partial blocking of memory formation for events that occurred while the person was intoxicated. Goodwin and colleagues (1969 a ) 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 2003 b ; Goodwin et al.1969 b ). Blackouts: State–Dependent Memory Formation? Early anecdotal evidence suggested that blackouts might actually reflect state–dependent information storage—that is, people might be able to remember events that occurred while they were intoxicated if they returned to that state (e.g., Goodwin et al.1969 a ).

State–dependent memory can be viewed as a special case of a broader category known as context–dependent memory (e.g., White et al.2002 a ), in which cues that are associated with an event when a memory is formed tend to help trigger recall for that event at a later time.

For instance, in a classic study by Godden and Baddeley (1975) divers who learned word lists either on land or under water remembered more words when tested in the same context in which learning took place (i.e., land–land or water–water). Likewise, returning to the same emotional or physiological state that was present when a memory was formed often can facilitate recall of that memory.

It is not uncommon to hear stories of drinkers who stash alcohol or money while intoxicated and can locate the hiding places only after becoming intoxicated again (Goodwin 1995). Regardless of how compelling such stories can be, clear evidence of state–dependent learning under the influence of alcohol is lacking.

  • In one recent study, Weissenborn and Duka (2000) examined whether subjects who learned word lists while intoxicated could recall more items if they were intoxicated again during the testing session.
  • No such state–dependency was observed.
  • Similarly, Lisman (1974) tried unsuccessfully to help subjects resurrect lost information for events occurring during periods of intoxication by getting them intoxicated once again.

Blood Alcohol Concentrations and Blackouts Drinking large quantities of alcohol often precedes blackouts, but several other factors also appear to play important roles in causing such episodes of memory loss. As Goodwin and colleagues (1969 a ) stated with regard to subjects in one of their studies, “Although blackouts almost always were associated with heavy drinking, this alone seemed insufficient to produce one.

On many other occasions, subjects said they had drunk as much or more without memory loss” (p.195). Among the factors that preceded blackouts were gulping drinks and drinking on an empty stomach, each of which leads to a rapid rise in BAC. Subsequent research provided additional evidence suggesting a link between blackouts and rapidly rising BACs.

Goodwin and colleagues (1970) examined the impact of acute alcohol exposure on memory formation in a laboratory setting. The author recruited 10 male subjects for the project, all but one through the unemployment office in St. Louis, Missouri. Most subjects met diagnostic criteria for alcoholism and half had a history of frequent blackouts.

The men were asked to consume roughly 16 to 18 ounces of 86–proof bourbon in approximately 4 hours. Beginning 1 hour after subjects began drinking, memory was tested by presenting subjects with several different stimuli, including a series of children’s toys and scenes from erotic films. Subjects were asked to recall details regarding these stimuli 2 minutes, 30 minutes, and 24 hours after the stimuli were shown.

Half of the subjects reported no recall for the stimuli or their presentation 30 minutes and 24 hours after the events, though most seemed to recall the stimuli 2 minutes after presentation. Lack of recall for the events 24 hours later, while sober, represents clear experimental evidence for the occurrence of blackouts.

  1. 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.
  2. 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. In a similar study, Ryback (1970) examined the impact of alcohol on memory in seven hospitalized alcoholics given access to alcohol over the course of several days.

All subjects were White males between the ages of 31 and 44. Blackouts occurred in five of the seven subjects, as evidenced by an inability to recall salient events that occurred while drinking the day before (e.g., one subject could not recall preparing to hit another over the head with a chair). Estimates of BAC levels during blackout periods suggested that they often began at levels around 0.20 percent and as low as 0.14 percent.

The duration of blackouts ranged from 9 hours to 3 days. Based on his observations, Ryback concluded that a key predictor of blackouts was the rate at which subjects consumed their drinks. He stated, “It is important to note that all the blackout periods occurred after a rapid rise in blood alcohol level” (p.622).

The two subjects who did not black out, despite becoming extremely intoxicated, experienced slow increases in blood alcohol levels. Blackouts Among Social Drinkers Most of the research conducted on blackouts during the past 50 years has involved surveys, interviews, and direct observation of middle–aged, primarily male alcoholics, many of whom were hospitalized.

Researchers have largely ignored the occurrence of blackouts among young social drinkers, so the idea that blackouts are an unlikely consequence of heavy drinking in nonalcoholics has remained deeply entrenched in both the scientific and popular cultures.

  • Yet there is clear evidence that blackouts do occur among social drinkers.
  • Night and colleagues (1999) observed that 35 percent of trainees in a large pediatric residency program had experienced at least one blackout.
  • Similarly, Goodwin (1995) reported that 33 percent of the first–year medical students he interviewed acknowledged having had at least one blackout.

“They were inexperienced,” he wrote. “They drank too much too quickly, their blood levels rose extremely quickly, and they experienced amnesia” (p.315). In a study of 2,076 Finnish males, Poikolainen (1982) found that 35 percent of all males surveyed had had at least one blackout in the year before the survey.

As might be expected given the excessive drinking habits of many college students (Wechsler et al.2002), this population commonly experiences blackouts. White and colleagues (2002 c ) recently surveyed 772 undergraduates regarding their experiences with blackouts. Respondents who answered yes to the question “Have you ever awoken after a night of drinking not able to remember things that you did or places that you went?” were considered to have experienced blackouts.

Fifty–one percent of the students who had ever consumed alcohol reported blacking out at some point in their lives, and 40 percent reported experiencing a blackout in the year before the survey. Of those who had consumed alcohol during the 2 weeks before the survey, 9.4 percent reported blacking out during this period.

Students in the study reported that they later learned that they had participated in a wide range of events they did not remember, including such significant activities as vandalism, unprotected intercourse, driving an automobile, and spending money. During the 2 weeks preceding the survey, an equal percentage of males and females experienced blackouts, despite the fact that males drank significantly more often and more heavily than females.

This outcome suggests that at any given level of alcohol consumption, females—a group infrequently studied in the literature on blackouts—are at greater risk than males for experiencing blackouts. The greater tendency of females to black out likely arises, in part, from well–known gender differences in physiological factors that affect alcohol distribution and metabolism, such as body weight, proportion of body fat, and levels of key enzymes.

  1. There also is some evidence that females are more susceptible than males to milder forms of alcohol–induced memory impairments, even when given comparable doses of alcohol (Mumenthaler et al.1999).
  2. In a subsequent study, White and colleagues (2004) interviewed 50 undergraduate students, all of whom had experienced at least one blackout, to gather more information about the factors related to blackouts.

As in the previous study, students reported engaging in a range of risky behaviors during blackouts, including sexual activity with both acquaintances and strangers, vandalism, getting into arguments and fights, and others. During the night of their most recent blackout, most students drank either liquor alone or in combination with beer.

  1. Only 1 student out of 50 reported that the most recent blackout occurred after drinking beer alone.
  2. On average, students estimated that they consumed roughly 11.5 drinks before the onset of the blackout.
  3. Males reported drinking significantly more than females, but they did so over a significantly longer period of time.

As a result, estimated peak BACs during the night of the last blackout were similar for males (0.30 percent) and females (0.35 percent). As Goodwin observed in his work with alcoholics (1969 b ), fragmentary blackouts occurred far more often than en bloc blackouts, with four out of five students indicating that they eventually recalled bits and pieces of the events.

Roughly half of all students (52 percent) indicated that their first full memory after the onset of the blackout was of waking up in the morning, often in an unfamiliar location. Many students, more females (59 percent) than males (25 percent), were frightened by their last blackout and changed their drinking habits as a result.

Use of Other Drugs During Blackouts Alcohol interacts with several other drugs, many of which are capable of producing amnesia on their own. For instance, diazepam (Valium ® ) and flunitrazepam (Rohypnol) are benzodiazepine sedatives that can produce severe memory impairments at high doses (White et al.1997; Saum and Inciardia 1997).

Alcohol enhances the effects of benzodiazepines (for a review, see Silvers et al.2003). Thus, combining these compounds with alcohol could dramatically increase the likelihood of experiencing memory impairments. Similarly, the combination of alcohol and THC, the primary psychoactive compound in marijuana, produces greater memory impairments than when either drug is given alone (Ciccocioppo et al.2002).

Given that many college students use other drugs in combination with alcohol (O’Malley and Johnston 2002), some of the blackouts reported by students may arise from polysubstance use rather than from alcohol alone. Indeed, based on interviews with 136 heavy–drinking young adults (mean age 22), Hartzler and Fromme (2003 b ) concluded that en bloc blackouts often arise from the combined use of alcohol and other drugs.

  1. White and colleagues (2004) observed that, among 50 undergraduate students with a history of blackouts, only 3 students reported using other drugs during the night of their most recent blackout, and marijuana was the drug in each case.
  2. Are Some People More Likely Than Others to Experience Blackouts? In classic studies of hospitalized alcoholics by Goodwin and colleagues (1969 a,b ), 36 out of the 100 patients interviewed indicated that they had never experienced a blackout.

In some ways, the patients who did not experience blackouts are as interesting as the patients who did. What was it about these 36 patients that kept them from blacking out, despite the fact that their alcoholism was so severe that it required hospitalization? Although they may actually have experienced blackouts but simply were unaware of them, there may have been something fundamentally different about these patients that diminished their likelihood of experiencing memory impairments while drinking.

In support of this possibility, a recent study by Hartzler and Fromme (2003 a ) suggests that people with a history of blackouts are more vulnerable to the effects of alcohol on memory than those without a history of blackouts. 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. There are two possible interpretations for these data, both of which support the hypothesis that some people are more susceptible to blackouts than others.

  • One plausible interpretation is that subjects in the fragmentary blackout group always have been more vulnerable to alcohol–induced memory impairments, which is why they performed poorly during testing under alcohol, and why they are members of the blackout group in the first place.
  • 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).

Similar results have been observed in animal studies (White et al.2000 a ). The argument for an inherent vulnerability to alcohol–induced memory impairments, including blackouts, is strengthened by two recent studies. In an impressive longitudinal study, Baer and colleagues (2003) examined the drinking habits of pregnant women in 1974 and 1975, and then studied alcohol use and related problems in their offspring at seven different time points during the following 21 years.

These authors observed that prenatal alcohol exposure was associated with increased rates of experiencing alcohol–related consequences, including blackouts, even after controlling for the offsprings’ general drinking habits. In addition, a recent report by Nelson and colleagues (2004) suggests that there might actually be a genetic contribution to the susceptibility to blackouts, indicating that some people simply are built in a way that makes them more vulnerable to alcohol–induced amnesia.

As discussed in the section below on the potential brain mechanisms underlying alcohol–induced amnesia, it is easy to imagine that the impact of alcohol on brain circuitry could vary from person to person, rendering some people more sensitive than others to the memory–impairing effects of the drug. HOW DOES ALCOHOL IMPAIR MEMORY? During the first half of the 20th century, two theoretical hurdles hampered progress toward an understanding of the mechanisms underlying the effects of alcohol on memory.

More recent research has cleared away these hurdles, allowing for tremendous gains in the area during the past 50 years. 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.

In 1953, large portions of H.M.’s medial temporal lobes, including most of his hippocampus, were removed in an effort to control intractable seizures (Scoville and Milner 1957). Although the frequency and severity of H.M.’s seizures were significantly reduced by the surgery, it soon became clear that H.M.

suffered from a dramatic syndrome of memory impairments. He still was able to learn basic motor skills, keep information active in short–term memory for a few seconds or more if left undistracted, and remember episodes of his life from long ago, but he was unable to form new long–term memories for facts and events.

The pattern of H.M.’s impairments also forced a re–examination of models of long–term memory storage. Specifically, although H.M. was able to retrieve long–term memories formed roughly a year or more before his surgery, he could not recall events that transpired within the year preceding his surgery. This strongly suggests that the transfer of information into long–term storage actually takes place over several years, with the hippocampus being necessary for its retrieval for the first year or so.

Subsequent research with other patients confirmed that the hippocampus, an irregularly shaped structure deep in the forebrain, is critically involved in the formation of memories for events (see figure 2 for a depiction of the brain, with the hippocampus and other relevant structures highlighted).

Patient R.B. lost a significant amount of blood as a result of heart surgery. He survived but showed memory impairments similar to those exhibited by H.M. Upon his death, histology revealed that the loss of blood to R.B.’s brain damaged a small region of the hippocampus called hippocampal area CA1, which contains neurons known as pyramidal cells because of the triangular shape of their cell bodies (Zola–Morgan et al.1986).

Hippocampal CA1 pyramidal cells assist the hippocampus in communicating with other areas of the brain. The hippocampus receives information from a wide variety of brain regions, many of them located in the tissue, called the neocortex, that blankets the brain and surrounds other brain structures.

(Neocortex literally means “new bark” or “new covering.” When one looks at a picture of the human brain, most of what is visible is neocortex.) The hippocampus somehow ties information from other brain regions together to form new autobiographical memories, and CA1 pyramidal cells send the results of this processing back out to the neocortex.

As is clear from patient R.B., removing CA1 pyramidal cells from the circuitry prevents the hippocampal memory system from doing its job.

Figure 2 The human brain, showing the location of the hippocampus, the frontal lobes, and the medial septum.

The second barrier to understanding the mechanisms underlying alcohol’s effects on memory was an incomplete understanding of how alcohol affects brain function at a cellular level. Until recently, alcohol was assumed to affect the brain in a general way, simply shutting down the activity of all cells with which it came in contact.

  1. The pervasiveness of this assumption is reflected in numerous writings during the early 20th century.
  2. For instance, Fleming (1935) wrote, “The prophetic generalization of Schmiedeberg in 1833 that the pharmacological action of alcohol on the cerebrum is purely depressant has been found, most pharmacologists will agree, to characterize its action in general on all tissues” (p.89).
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During the 1970s, researchers hypothesized that alcohol depressed neural activity by altering the movement of key molecules (in particular, lipids) in nerve cell membranes. This change then led to alterations in the activity of proteins, including those that influence communication between neurons by controlling the passage of positively or negatively charged atoms (i.e., ions) through cell membranes (e.g., Chin and Goldstein 1977).

This view persisted into the late 1980s, at which time the consensus began to shift as evidence mounted that alcohol has selective effects on the brain’s nerve–cell communication (i.e., neurotransmitter) systems, altering activity in some types of receptors but not others (e.g., Criswell et al.1993).

Substantial evidence now indicates that alcohol selectively alters the activity of specific complexes of proteins embedded in the membranes of cells (i.e., receptors) that bind neurotransmitters such as gamma–aminobutyric acid (GABA), glutamate, serotonin, acetylcholine, and glycine (for a review, see Little 1999).

In some cases, only a few amino acids appear to distinguish receptors that are sensitive to alcohol from those that are not (Peoples and Stewart 2000). It remains unclear exactly how alcohol interacts with receptors to alter their activity. Alcohol, Memory, and the Hippocampus More than 30 years ago, both Ryback (1970) and Goodwin and colleagues (1969 a ) speculated that alcohol might impair memory formation by disrupting activity in the hippocampus.

This speculation was based on the observation that acute alcohol exposure (in humans) produces a syndrome of memory impairments similar in many ways to the impairments produced by hippocampal damage. Specifically, both acute alcohol exposure and hippocampal damage impair the ability to form new long–term, explicit memories but do not affect short–term memory storage or, in general, the recall of information from long–term storage.

Research conducted in the past few decades using animal models supports the hypothesis that alcohol impairs memory formation, at least in part, by disrupting activity in the hippocampus (for a review, see White et al.2000 b ). Such research has included behavioral observation; examination of slices of and brain tissue, neurons in cell culture, and brain activity in anesthetized or freely behaving animals; and a variety of pharmacological techniques.

As mentioned above, damage limited to the CA1 region of the hippocampus dramatically disrupts the ability to form new explicit memories (Zola–Morgan et al.1986). In rodents, the actions of CA1 pyramidal cells have striking behavioral correlates. Some cells tend to discharge electrical signals that result in one cell communicating with other cells (i.e., action potentials) when the rodent is in a distinct location in its environment.

  • The location differs for each cell.
  • For instance, while a rat searches for food on a plus–shaped maze, one pyramidal cell might generate action potentials primarily when the rat is at the far end of the north arm, while another might generate action potentials primarily when the rat is in the middle of the south arm, and so on.

Collectively, the cells that are active in that particular environment create a spatial, or contextual map that serves as a framework for event memories created in that environment. Because of the location–specific firing of these cells, they often are referred to as “place–cells,” and the regions of the environment in which they fire are referred to as “place–fields” (for reviews, see Best and White 1998; Best et al.2001).

Given that CA1 pyramidal cells are critically important to the formation of memories for facts and events, and the clear behavioral correlates of their activity in rodents, it is possible to assess the impact of alcohol on hippocampal output in an intact, fully functional brain by studying these cells.

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.

  1. Figure 3 displays the activity of an individual CA1 pyramidal cell.
  2. 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).
  3. 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 figure illustrates, the cell’s activity was essentially shut off by alcohol. Neural activity returned to near–normal levels within about 7 hours of alcohol administration.

Figure 3 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. Neural activity returned to near normal levels within roughly 7 hours after alcohol administration.

White and Best administered several doses of alcohol in this study, ranging from 0.5 g/kg to 1.5 g/kg. (Only one of the experiments is represented in figure 3.) They found that the dose affected the degree of pyramidal cell suppression. Although 0.5 g/kg did not produce a significant change in the firing of hippocampal pyramidal cells, 1.0 and 1.5 g/kg produced significant suppression of firing during a 1–hour testing session following alcohol administration.

The dose–dependent suppression of CA1 pyramidal cells is consistent with the dose–dependent effects of alcohol on episodic memory formation. Alcohol and Hippocampal Long–Term Potentiation In addition to suppressing the output from pyramidal cells, alcohol has several other effects on hippocampal function.

For instance, alcohol severely disrupts the ability of neurons to establish long–lasting, heightened responsiveness to signals from other cells (Bliss and Collinridge 1993). 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.

  • In a typical LTP experiment, two electrodes (A and B) are lowered into a slice of hippocampal tissue kept alive by bathing it in oxygenated artificial cerebral spinal fluid (ACSF).
  • A small amount of current is passed through electrode A, causing the neurons in this area to send signals to cells located near electrode B.

Electrode B then is used to record how the cells in the area respond to the incoming signals. This response is the baseline response. Next, a specific pattern of stimulation intended to model the pattern of activity that might occur during an actual learning event is delivered through electrode A.

When the original stimulus that elicited the baseline response is delivered again through electrode A, the response recorded at electrode B is larger (i.e., potentiated). In other words, as a result of the patterned input, cells at position B now are more responsive to signals sent from cells at position A.

The potentiated response often lasts for an extended period of time, hence the term long–term potentiation, Alcohol interferes with the establishment of LTP (Morrisett and Swartzwelder 1993; Givens and McMahon 1995; Pyapali et al.1999; Schummers and Browning 2001), and this impairment begins at concentrations equivalent to those produced by consuming just one or two standard drinks (e.g., a 12–oz beer, 1.5–oz of liquor in a shot or mixed drink, or a 5–oz glass of wine) (Blitzer et al.1990).

If sufficient alcohol is present in the ACSF bathing the slice of hippocampal tissue when the patterned stimulation is given, the response recorded later at position B will not be larger than it was at baseline (that is, it will not be potentiated). And, just as alcohol tends not to impair recall of memories established before alcohol exposure, alcohol does not disrupt the expression of LTP established before alcohol exposure.

One of the key requirements for the establishment of LTP in the hippocampus is that a type of signal receptor known as the NMDA 2 receptor becomes activated. ( 2 N –methyl–D–aspartate is a receptor for the neurotransmitter glutamate.) Activation of the NMDA receptor allows calcium to enter the cell, which sets off a chain of events leading to long–lasting changes in the cell’s structure or function, or both.

  • Alcohol interferes with the activation of the NMDA receptor, thereby preventing the influx of calcium and the changes that follow (Swartzwelder et al.1995).
  • This is believed to be the primary mechanism underlying the effects of alcohol on LTP, though other transmitter systems probably are also involved (Schummers and Browning 2001).

Indirect Effects of Alcohol on Hippocampal Function Like other brain regions, the hippocampus does not operate in isolation. Information processing in the hippocampus depends on coordinated input from a variety of other structures, which gives alcohol and other drugs additional opportunities to disrupt hippocampal functioning.

One brain region that is central to hippocampal functioning is a small structure in the fore brain known as the medial septum (Givens et al.2000). The medial septum sends rhythmic excitatory and inhibitory signals to the hippocampus, causing rhythmic changes in the activity of hippocampal pyramidal cells.

In electroencephalograph recordings, this rhythmic activity, referred to as the theta rhythm, occurs within a frequency of roughly 6 to 9 cycles per second (hertz) in actively behaving rats. The theta rhythm is thought to act as a gatekeeper, increasing or decreasing the likelihood that information entering the hippocampus from cortical structures will be processed (Orr et al.2001).

(For more information on the role of electrophysiology in diagnosing alcohol problems, see the article in this issue by Porjesz and Begleiter.) Information entering the hippocampus when pyramidal cells are slightly excited (i.e., slightly depolarized) has a better chance of influencing hippocampal circuitry than signals that arrive when the cells are slightly suppressed (i.e., slightly hyperpolarized).

Manipulations that disrupt the theta rhythm also disrupt the ability to perform tasks that depend on the hippocampus (Givens et al.2000). Alcohol disrupts the theta rhythm in large part by suppressing the output of signals from medial septal neurons to the hippocampus (Steffensen et al.1993; Givens et al.2000).

Given the powerful influence that the medial septum has on information processing in the hippocampus, the impact of alcohol on cellular activity in the medial septum is likely to play an important role in the effects of alcohol on memory. Indeed, in rats, putting alcohol directly into the medial septum alone produces memory impairments (Givens and McMahon 1997).

Other Brain Regions Involved in Alcohol–Induced Memory Impairments The hippocampus is not the only structure involved in memory formation. A host of other brain structures also are involved in memory formation, storage, and retrieval (Eichenbaum 2002).

  1. Recent research with humans has yielded compelling evidence that key areas of the frontal lobes play important roles in short–term memory and the formation and retrieval of long–term explicit memories (e.g., Shastri 2002; Curtis and D’Esposito 2003; Ranganath et al.2003).
  2. Damage to the frontal lobes leads to profound cognitive impairments, one of which is a difficulty forming new memories.

Recent evidence suggests that memory processes in the frontal lobes and the hippocampus are coordinated via reciprocal connections (Wall and Messier 2001; Shastri 2002), raising the possibility that dysfunction in one structure could have deleterious effects on the functioning of the other.

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). “Shrinkage” in brain volume, changes in gene expression, and disruptions in how performing certain tasks affects blood flow in the brain all have been observed in the frontal lobes of alcohol–dependent subjects (Kril and Halliday 1999; Lewohl et al.2000; Tapert et al.2001; Kubota et al.2001; Desmond et al.2003).

Although much is known about the effects of chronic (i.e., repeated) use of alcohol on frontal lobe function, little is known about the effects of one–time (i.e., acute) use of alcohol on activity in the frontal lobes, or the relationship of such effects to alcohol–induced memory impairments.

Compelling evidence indicates that acute alcohol use impairs the performance of a variety of frontal lobe–mediated tasks, like those that require planning, decisionmaking, and impulse control (Weissenborn and Duka 2003; Burian et al.2003), but the underlying mechanisms are not known. Research also suggests that baseline blood flow to the frontal lobes increases during acute intoxication (Volkow et al.1988; Tiihonen et al.1994), that metabolism in the frontal lobes decreases (Wang et al.2000), and that alcohol reduces the amount of activity that occurs in the frontal lobes when the frontal lobes are exposed to pulses from a strong magnetic field (Kahkonen et al.2003).

Although the exact meaning of these changes remains unclear, the evidence suggests that acute intoxication alters the normal functioning of the frontal lobes. Future research is needed to shed more light on this important question. In particular, research in 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.

  • SUMMARY AND CONCLUSIONS As detailed in this brief review, alcohol can have a dramatic impact on memory.
  • Alcohol primarily disrupts the ability to form new long–term memories; it causes less disruption of recall of previously established long–term memories or of the ability to keep new information active in short–term memory for a few seconds or more.

At low doses, the impairments produced by alcohol are often subtle, though they are detectable in controlled conditions. As the amount of alcohol consumed increases, so does the magnitude of the memory impairments. Large quantities of alcohol, particularly if consumed rapidly, can produce a blackout, an interval of time for which the intoxicated person cannot recall key details of events, or even entire events.

  1. En bloc blackouts are stretches of time for which the person has no memory whatsoever.
  2. Fragmentary blackouts are episodes for which the drinker’s memory is spotty, with “islands” of memory providing some insight into what transpired, and for which more recall usually is possible if the drinker is cued by others.

Blackouts are much more common among social drinkers than previously assumed and should be viewed as a potential consequence of acute intoxication regardless of age or whether one is clinically dependent upon alcohol. Tremendous progress has been made toward an understanding of the mechanisms underlying alcohol–induced memory impairments.

Alcohol disrupts activity in the hippocampus via several routes—directly, through effects on hippocampal circuitry, and indirectly, by interfering with interactions between the hippocampus and other brain regions. The impact of alcohol on the frontal lobes remains poorly understood, but probably plays an important role in alcohol–induced memory impairments.

Modern neuroimaging techniques, such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI), provide incredible opportunities for investigating the impact of drugs like alcohol on brain function during the performance of cognitive tasks.

  1. The use of these techniques will no doubt yield important information regarding the mechanisms underlying alcohol–induced memory impairments in the coming years.
  2. Memory formation and retrieval are highly influenced by factors such as attention and motivation (e.g., Kensinger et al.2003).
  3. With the aid of neuroimaging techniques, researchers may be able to examine the impact of alcohol on brain activity related to these factors, and then determine how alcohol contributes to memory impairments.

Despite advances in human neuroimaging techniques, animal models remain absolutely essential in the study of mechanisms underlying alcohol–induced memory impairments. Hopefully, future work will reveal more regarding the ways in which the effects of alcohol on multiple transmitter systems interact to disrupt memory formation.

Similarly, recent advances in electrophysiological recording techniques, which allow for recordings from hundreds of individual cells in several brain regions simultaneously (Kralik et al.2001), could provide much–needed information regarding the impact of alcohol on the interactions between disparate brain regions involved in the encoding, storage, and retrieval of information.

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Why do I lie when I’m drunk?

So, Do Drunk People Lie? – Alcohol overloads working memory, impairs judgment, causes primary inhibitory impairment surrounding social situations and affects social rationalization or the ability to tell whether something is socially acceptable. So, with lowered inhibitions and social rationalization, an individual may say what’s on their mind without filters — some deeply personal information may be true, while other boisterous comments, a lie.

  • Context can help determine whether drunks mean what they say.
  • For example, heartfelt emotions are often genuine because people lack the rationalization skills to be devious and contriving.
  • On the other hand, negative comments or anger may be a defense mechanism and not necessarily stem from truth.
  • This is because a drunk brain may use anything it can to defend against perceived attackers — and this includes lying.

Intoxicated individuals are more likely to respond emotionally in social situations due to inhibited emotional processing,

Does true feelings come out when drunk?

Why do people drink to affect their emotions? – Do people drink to forget their emotions? Yes, some people drink to forget or avoid their emotions. Human beings instinctively want to reduce the experience of negative emotions and escape from feelings that we don’t want to have.

challenging life events a break-up the loss of a loved one Illness memories of trauma

However, these short-term positive emotions come at a cost. Getting rid of your inhibitions for a night might make it easier to face tough social situations. However, intentionally worsening your decision-making skills can also result in a lot of regret once the buzz wears off.

  1. Do true feelings come out when you’re drunk? True feelings may come out when you’re drunk, but this isn’t necessarily true all the time.
  2. Instead, alcohol can make people make fake stories and react with emotions they don’t feel,
  3. As it turns out, lowered inhibitions and impaired judgment aren’t exactly a recipe for truth-telling — drunk words are not sober thoughts.

What are the long-term effects of alcohol on emotions? The long-term effects of alcohol on emotions include:

learning deficits increased stress social anxiety aggressive behavior impaired memory mental disorders sleep disturbances other cognitive damage

Are people flirty when drunk?

Model Chrissy Teigen recently got candid about what her husband John Legend is really like after a few drinks. Her only complaint? Legend gets “way too loving” when he’s drunk. (But honestly, aww.) “He’ll be like, ‘Let’s go in the closet!'” Teigen said in an interview with Cosmopolitan, explaining that her bed and closet are near each other.

  1. He just gets very, very touchy, and he’s like a little baby—it’s really sweet.” Teigen’s description of this kind of tipsy physical affection is something many of us are familiar with.
  2. Let’s be honest, Legend’s not the only one who gets a little sweet after a few cocktails.
  3. And Suzette Glasner, Ph.D., associate professor of psychiatry at UCLA and author of The Addiction Recovery Skills Workbook, tells SELF there are a few reasons why this alcohol-induced affection can happen.

Part of the reason why alcohol has this effect is chemical. For starters, research shows that in the short-term, low doses of alcohol can reduce tension, lower inhibitions, and increase relaxation. Because we’re feeling less self-conscious, we might act more impulsively when it comes to intimacy—sharing personal things, being more forward, and doing other things that aren’t normally as easy to do.

  1. All around, we’re less cautious.
  2. And sometimes that leads us to (literally) lean on our friends a little more than usual.
  3. These effects are often magnified when someone’s had a lot to drink.
  4. With larger doses of alcohol, not only can a person lower their inhibitions, but their emotions can also be altered,” Glasner explains.

This combination of decreased inhibition and increased emotion can create a perfect storm for physical affection. And if this is happening to you, a lot of what you’re experiencing is chemical. ” Alcohol has well documented effects on brain chemicals and structures that us control our impulses and suppress or deliberately hold back on certain behaviors,” Glasner says.

  • Beyond simple physiology, there’s a psychological reason why you may be extra snuggly after you’ve been drinking.
  • Plus, expecting to act more touchy-feely while tipsy can actually cause you to act more touchy-feely while tipsy, David J.
  • Hanson, Ph.D., professor emeritus of sociology of the State University of New York at Potsdam, tells SELF.

It’s kind of a self-fulfilling prophecy: “We have expectations as to what alcohol’s going to do to us, and we tend to comply with those expectations,” Hanson explains. “When a person thinks alcohol is going to make them more enamored, they’re going to act that way—it’s psychological.” And Glasner agrees, explaining that our expectations can actually have a pretty big impact on our behaviors.

If a person who is ordinarily shy or reserved drinking will loosen them up and give them the courage to act differently toward another person, then that expectation alone can lead to a change in behavior,” she says. Odds are, it’s a combination of physiology and psychology: The chemical effects of alcohol plus your expectations equal a whole bunch of physical affection.

If you’re a little freaked out about your tendencies toward physical affection when you’re drinking, there’s only one real solution. Glasner’s only recommendation: Drink less. Since this is an a+b=c scenario (you+alcohol=lots of snuggles), the move is to cut back on your alcohol intake at a given time.

Is alcohol making me lazy?

Alcohol and fatigue – Harvard Health Does Alcohol Make You Stupid Image: KatarzynaBialasiewicz/Thinkstock Many people think that a little nightcap will help them sleep soundly through the night. Although alcohol’s sedative effects can make you drowsy, they also have other effects that can interfere with quality sleep.

  • Several hours after that nightcap, the alcohol raises the body’s level of epinephrine, a stress hormone that increases the heart rate and generally stimulates the body, which can result in nighttime awakenings.
  • Indeed, alcohol may account for 10% of cases of persistent insomnia.
  • Alcohol also relaxes throat muscles, and this relaxation can worsen sleep-related breathing problems and contribute to sleep apnea.

What’s more, alcohol may increase the need to urinate during the night — just another way in which it can disrupt sleep. Alcohol’s sedative quality can rob you of energy in another way. Drinking wine, beer, or hard liquor during the day can make you feel drowsy or lethargic.

Does alcohol mess with you mentally?

The relationship between alcohol and mental health is complex. Some people may drink alcohol to relax or help cope with daily stresses; however, alcohol is a depressant drug 1 that can cause anxiety and increase stress. Alcohol can negatively affect thoughts, feelings and actions, and contribute to the development of, or worsen, existing mental health issues over time.

Does alcohol stop you from overthinking?

How alcohol affects anxiety – Alcohol is a depressant. It slows down processes in your brain and central nervous system, and can initially make you feel less inhibited.10,11 In the short-term, you might feel more relaxed – but these effects wear off quickly.

Is alcohol good for overthinkers?

Social embarrassment – Alcohol is a natural disinhibitor — meaning it can cause you to make choices you may not make while sober. This is why some people can wake up feeling embarrassed about things they said or did. This can definitely cause anxiety and worsen any existing phobias or overthinking tendencies you may already have.

Can I drink while studying?

Does Alcohol Make You Stupid Lauren Grant/Iowa State Daily According to Science Daily, alcohol is a better drink of choice than caffeine while studying. Alcohol enhances learning while caffeine gives a more short-lived adrenaline effect. Alcohol makes you feel more relaxed and more creative at the same time.

  • Did you know that drinking beer while studying is more beneficial than drinking caffeine while studying? It can easily be assumed that drinking alcohol while studying is distracting, but much to our surprise it is actually more useful.
  • Here are some facts that prove alcohol is a better choice than caffeine according to Science Daily: • Helps the brain remember facts more efficiently • Improves problem-solving skills • Social and intellectual lubricant to studying • Complete tests faster than sober test-takers would Combining alcohol and studying can help students increase their learning in many different ways.

Alcohol enhances the learning while caffeine gives more of a short-lived adrenaline effect. Of course, there are some benefits to caffeine. According to Study Magazine, caffeine gives you that boost of energy to either start your day or finish it off strong.

Is vodka good for the brain?

Health Benefits of Vodka – Does Alcohol Make You Stupid Check out amazing benefits of drinking Vodka and how this effect your helath in good terms. Also list some advantages, you can get after drinking Vodka. Vodka has a dilating effect on the arteries which stimulates the blood to flow freely. This free flow of blood to the heart inhibits the risks of major illnesses such as strokes and cardiac arrests.

Vodka is also very useful in increasing the amount of HDL (good cholesterol) in the body and balancing the overall cholesterol level. Vodka is known for its sleep-inducing properties and has a calming effect on the brain. Out of all the alcoholic drinks even the red wine, vodka has far more impact in decreasing the stress factor of the body.

Moderate consumption of vodka helps in relaxing the mind and body.

Does alcohol reduce ability?

A few more drinks, a big difference – It might not take as many drinks as you think to slow your reaction time and make safe driving harder. For the purposes of standardization, a drink is defined as 12 ounces of 5% alcohol beer; five ounces of 12% alcohol wine; or one and a half ounces of 80 proof (40% alcohol) liquor.

  • To account for an individual imbibing over a longer period of time, subtract about 0.01% for each 40 minutes of drinking time.
  • A 160-pound man that consumes two alcoholic beverages will experience some loss of judgment, decreased ability to rapidly track a moving target and reduced multitasking ability, according to the Centers for Disease Control and Prevention.

Women, who generally weigh less than men, would see a higher BAC per drink. Three alcoholic drinks will bring a person’s blood alcohol level to approximately 0.05%, which can impair the ability to rapidly focus vision, lower alertness and decrease coordination — to the point that steering becomes difficult and response to driving emergencies becomes blunted.

  • After approximately four alcoholic drinks, one’s balance, vision and reaction time are often affected.
  • It becomes harder to detect roadway dangers.
  • Reasoning and information processing are often measurably impaired.
  • This corresponds most closely to a BAC of 0.08%.
  • A blood alcohol concentration of 0.10% is generally associated with a clear loss of reaction time and control.

There will be a reduced ability to maintain proper lane position or to brake appropriately.

What does alcohol do to your brain dopamine?

How Does Alcohol Affect Dopamine Levels? – When you drink, the brain’s reward system is flooded with dopamine, producing the euphoric “buzz.” In fact, dopamine production can increase with the first sip of alcohol, or even just by thinking about drinking because your brain has probably associated pleasure with alcohol.

Alcohol increases dopamine production, so you feel good and, generally, relaxed. In order to keep the good feelings going, your brain prompts you to continue drinking. However, when it comes to dopamine levels and addictive substances, alcohol behaves somewhat differently than other substances or pharmaceuticals.

Alcohol does not prevent the reuptake of dopamine while other substances do, So, in effect, your brain reabsorbs the dopamine the alcohol made it create. Your brain adapts to the sudden increase in the neurotransmitter by producing less dopamine, but because of the link to pleasure, it doesn’t want you to stop after a few drinks — even when your dopamine levels start to deplete.

Dopamine levels fall, and the euphoric buzz goes with it, but your brain is looking to regain the feeling caused by the increased level of dopamine. You compensate for this by drinking more. Eventually, you rely fully on alcohol to generate dopamine release, and without it, you experience withdrawal symptoms,

In other words, you are addicted. Often, the only way to break this cycle is through rehab and therapy. Some addictive substances affect dopamine directly, whereas alcohol and other drugs have an indirect effect. Alcohol is a small molecule, so it interacts with many neurotransmitters in the brain.

Large molecules, like opiates or amphetamines, only stimulate a specific neurotransmitter. Thus, the actions of alcohol in the brain are quite complex in comparison. Alcohol also interacts with other neurotransmitters, producing a variety of effects: adrenaline (acts as a stimulant); endorphins (similar to opiates and can act as a pain-killer and produce an endorphin “high”); GABA (similar to Valium in causing relaxation and drowsiness); glutamate (leads to staggering, slurred speech and memory blackouts); and norepinephrine/noradrenaline (also acts as a stimulant), among others.

Alcohol has such a wide variety of effects, affecting the parts of your brain that control speech, movement, memory, and judgment. This is why the signs of overindulgence include slurred speech, bad or antisocial behavior, trouble walking, and difficulty performing manual tasks.

  1. Research has shown that the brains of alcoholics have dopamine levels that are significantly below average.
  2. This explains why alcoholics would continue to seek more and more alcohol in order to achieve the same pleasure.
  3. Dopamine deficiencies are also associated with depression and other psychological disorders.

Even with alcohol’s effect on dopamine production, you don’t have to continue drinking. Rehab programs will help break the cycle through detox and therapy — either one-on-one or group sessions. Detox will clear the alcohol from your system, helping your brain to re-achieve balance,

  1. Dopamine production will return to normal, and other parts of the recovery program will offer things that will help your brain boost dopamine levels without chemicals.
  2. Therapy sessions will teach you coping techniques to deal with the triggers that fuel drinking,
  3. You may also receive treatment for depression at the same time, as it is one of the primary withdrawal symptoms.

While drinking initially boosts a person’s dopamine levels, the brain adapts to the dopamine overload with continued alcohol use. It produces less of the neurotransmitter, reducing the number of dopamine receptors in the body and increasing dopamine transporters, which carry away the excess dopamine.

Does alcohol increase dopamine?

Alcohol’s Actions as a Reinforcer: Dopamine’s Role – Although numerous studies have attempted to clarify dopamine’s role in alcohol reinforcement by manipulating dopaminergic signal transmission, these investigations do not allow any firm conclusions (for a review, see Di Chiara 1995 ).

The comparison of alcohol’s effects with the effects of conventional reinforcers, such as food, however, provides some clues to dopamine’s role in mediating alcohol reinforcement. Palatable food activates dopaminergic signal transmission in the NAc shell, for example, by exerting specific sensory (e.g., taste, or gustatory) stimuli.

Orally administered alcohol similarly activates taste receptors, thereby increasing dopamine release in the NAc. In contrast to food, however, alcohol also can modify the function of dopaminergic neurons more directly by entering the brain. Accordingly, oral alcohol administration influences dopamine release in the NAc both through its gustatory properties (i.e., as a conventional reinforcer) and through its direct actions on the brain (i.e., as a drug reinforcer).

Consistent with this hypothesis, two peaks of dopamine release occur in the NAc. The first peak results from the alcohol-related gustatory stimuli; the second results from alcohol’s actions within the brain. Consequently, alcohol-induced direct activation of dopaminergic signal transmission might reinforce the motivational properties of the gustatory stimuli associated with alcohol.

As a result of this mechanism, the alcohol-related gustatory stimuli acquire strong incentive properties (i.e., they become motivational stimuli that induce the drinker to seek even more alcohol). Similarly, appetitive stimuli related to alcohol (e.g., extrinsic stimuli, such as the sight of a certain brand of an alcoholic beverage or the sight of a bar) also acquire incentive properties and promote the search for and consumption of alcohol.

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