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Psychol Bull. Author manuscript; available in PMC 2009 September 22.
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PMCID: PMC2748736

Binge Drinking in Young Adults: Data, Definitions, and Determinants


Binge drinking is an increasingly important topic in alcohol research, but the field lacks empirical cohesion and definitional precision. The present review summarizes findings and viewpoints from the scientific binge-drinking literature. Epidemiological studies quantify the seriousness of alcohol-related problems arising from binge drinking, with a growing incidence reported in college-age men over the last 2 years. Experimental studies have found neurocognitive deficits for frontal lobe processing and working memory operations in binge-drinking compared with nonbinge alcohol drinkers. The findings are organized with the goals of providing a useful binge-drinking definition in the context of the empirical results. Theoretical implications are discussed on how binge drinking may alter neurophysiological and neurocognitive function.

Keywords: binge drinking, epidemiology, neuropsychological, review, definitions

Alcohol consumption in humans is the third leading preventable cause of death in the United States (McGinnis & Foege, 1993). A common abuse pattern called binge drinking contributes to a substantial portion of alcohol-related deaths (Chikritzhs, Jonas, Stockwell, Heale, & Dietze, 2001). This type of drinking also is associated with alcohol poisoning, unintentional injuries, suicide, hypertension, pancreatitis, sexually transmitted diseases, and meningitis, among other disorders. As binge drinking is relatively common, it underlies many negative social costs, including interpersonal violence, drunk driving, and lost economic productivity, as reported by the National Institute on Alcohol Abuse and Alcoholism (NIAAA, 2000). These statistics have attracted increased attention from a variety of perspectives.

The term “binge” originated as a clinical description of alcoholics and was defined by periods of heavy drinking followed by abstinence (Tomsovic, 1974). The word is distinct from the expression “binge drinking” that, since its conception, has engendered a wide array of definitional elements. This definitional difficulty originates from two different but related uses of the phrase: (1) epidemiological studies that emphasize isolated excessive drinking episodes, and (2) experimental studies that evaluate behavioral drinking patterns (Lange & Voas, 2000a). The present review was undertaken to bridge these approaches and to provide a comprehensive, integrative, and useful portrait of the binge-drinking literature with a focus on young adult humans. We obtained studies through literature searches using “binge drinking,” “alcohol binging,” and “college drinking.” Ancillary terms, such as light or social drinking and alcohol dependence, were included when they occurred within the binge framework (Boyd, McCabe, & Morales, 2005). The goals were to characterize the primary data and definitional attributes of binge drinking as delineated by current scientific findings.

Table 1 summarizes the binge-drinking studies identified. Although the conceptual and empirical views of an operational definition have been slow to coalesce, technical agreement about binge drinking has evolved appreciably over the last 10 years. Specific reports are used to illustrate how the definition, its rationale, and utility have developed. The approach considers both quantity and frequency of consumption as defining characteristics of binge drinking. The review is organized into three sections: (1) Issues underlying the concept of binge drinking are outlined; (2) the relationship of alcohol consumption to binge drinking is highlighted; (3) binge drinking and its cognitive, physiological, and withdrawal effects are examined, with the influence of alcoholism, family history for alcoholism, and other determinants sketched. In the Discussion section, we review the implications of the findings and suggest future research directions.

Table 1
Summary of Binge Drinking Studies

Definitional Background


An initial view defined binge drinking as at least five alcoholic drinks consumed during the same session (Cahalan, Cisin, & Crossley, 1969). However, the comprehensive College Alcohol Study (CAS) conducted by the Harvard School of Public Health characterized binge drinking as five drinks for men and four drinks for women on a single occasion within the past 2 weeks (Wechsler, Davenport, Dowdall, Moeykens, & Castillo, 1994). The adjustment to the four-drink cutoff for women was based on their lower rate of gastric metabolism for alcohol, which leads to higher blood alcohol levels compared with men for the same quantity (Wechsler, Dowdall, Davenport, & Rimm, 1995). The 5/4 definition is consistent with findings that after consumption of this amount or more, individuals are at greater risk for exhibiting serious alcohol-related problems (e.g., vandalism, fights, injuries, drunk driving, trouble with police, etc.) and subsequent negative health, social, economic, or legal consequences (Wechsler, 2000).

Despite the intended practicality of the CAS and other large scale survey definitions, characterizing binge drinking using only a “single occasion” within a specified time-frame may conflate the estimates of binge drinkers as defined by a pattern of behavior (Naimi et al., 2003; Substance Abuse and Mental Health Services Administration [SAMHSA], 2007; Wechsler et al., 1994), as both drinking quantity and frequency have been shown to be important indictors of risky drinking in college students (Presley & Pimentel, 2006). Additional issues include how a single “drink” is defined, consumption amount, and alcohol tolerance contribute to individual inebriation levels (Jaccard & Turrisi, 1987).

One attempt to quantify behavioral drinking employed blood alcohol concentration (BAC) level, such that a 0.08 gram percent—now the legal intoxication level in all 50 states (Alcohol Policy Information System, 2007)—for a given occasion indicated binge-drinking patterns (Lange & Voas, 2000b). Another approach developed a Binge-Drinking Score from three questions of the Alcohol Use Questionnaire (Mehrabian & Russell, 1978; Townshend & Duka, 2002). This method used quantifiable assessments of drinks per hour, times drunk within the last 6 months, and percentage of time being intoxicated when drinking to calculate a summary score unrelated to the weekly consumption of alcohol (Townshend & Duka, 2005).

A standardized conceptual definition of binge drinking was proposed by the NIAAA in 2004:

A “binge” is a pattern of drinking alcohol that brings BAC to 0.08 gram percent or above. For the typical adult, this pattern corresponds to consuming five or more drinks (male), or four or more drinks (female), in about two hours. (p. 3)

A standard drink equals 0.5 oz of alcohol as is found in one 12-oz beer, one 5-oz glass of wine, or one 1.5-oz shot of distilled spirits (NIAAA, 2004). This definition of binge drinking is similar to many used in epidemiological studies, which employ quantity (BAC), consumption amounts, and episode duration. The definition does not specify, however, the time period or number of binging occurrences that would describe a long-term binge-drinking practice. Thus, NIAAA's definition characterizes single binge episodes but does not capture the consumption pattern associated with serious health and social consequences.


The inclusion of a past time-frame to quantify frequency of binging episodes is necessary to differentiate “binge drinking” from “alcoholism” or “alcohol dependence.” This temporal aspect of a binge-drinking pattern has been variably defined as the past week (Kokavec & Crowe, 1999), past 2 weeks (Wechsler et al., 1994), past 30 days/month (Okoro et al., 2004; SAMHSA, 2007; Zeigler et al., 2005), past 6 months (Hartley, Elsabagh, & File, 2004; Townshend & Duka, 2002, 2005; Weissenborn & Duka, 2003), and past year (Cranford, McCabe, & Boyd, 2006). These different time-frames emphasize various aspects of binge-drinking patterns, but their use inhibits direct comparison among findings.

The most informative time-frame appears to be within the past 6 months, as it is an optimal period to link alcohol consumption and alcohol-related problems (Hartley et al., 2004; Townshend & Duka, 2002, 2005; Weissenborn & Duka, 2003). Longitudinal studies of binge drinking have established that college students inconsistently report heavy episodic drinking across time (Schulenberg, O'Malley, Bachman, Wadsworth, & Johnston, 1996; Weingardt et al., 1998), so that a 2-week time-frame would underestimate binging prevalence (Vik, Tate, & Carrello, 2000). A recent study found that nearly one third of those classified as nonbinge drinkers (<5/4 drinks) during a 2-week time period in the middle of the month were classified as either binge drinkers (≥5/4 drinks, 1 or 2 times during the past 2 weeks) or frequent binge drinkers (≥5/4 drinks, ≥3 times in past 2 weeks) during the first 2 weeks of the month (LaBrie, Pedersen, & Tawalbeh, 2007). Use of a 2-week time period, therefore, would yield approximately 30% of heavy binge drinkers being excluded. A past 6 months time-frame for college samples captures the vacation time of the academic calendar during which students would be more apt to binge drink. Although longer time frames have yet to be analyzed, the ability to recall consumption amounts and frequencies accurately (e.g., recall bias) would seem to diminish with extended time frames. The goal in selecting an optimal time frame associated with a binge-drinking pattern is to optimize the accuracy of self-reported drinking amounts, while also capturing an accurate representation of this problematic drinking pattern. Further, employing a multiple binging occurrences evaluation strengthens the definition as these attributes together integrate the quantifiable dimensions of binge drinking.


The age of onset of regular (> once a month) drinking has been reported to be “15.2 ± 1.2 years old (M ± SD) for high-risk children and 16.5 ± 1.2 years old for low-risk children” on the basis of a sample of 125 children (Hill, Shen, Lowers, & Locke, 2000, p. 269). Of the total 10.8 million underage Americans (12–20 years) who reported consuming alcohol in the past 30 days, 7.2 million (or 19%) were binge drinkers (≥5 drinks on the same occasion on ≥1 day in past 30 days) as defined by National Survey on Drug Use and Health (SAMHSA, 2007). Early onset of binge drinking or exposure to binging has been linked to the increased risk of binging in adulthood (Wechsler, Dowdall, Davenport, & Castillo, 1995; Weitzman, Nelson, & Wechsler, 2003). Other factors that predict binging include the following: never being married, having a grade point average of B or less, and placing little importance on religion.

The CAS study found that for a sample of 140 colleges nationwide, 44% of the responding students were binge (≥5/4 successive drinks) drinkers (Wechsler et al., 1994). The Behavioral Risk Factor Surveillance System (BRFSS) study assessed adults who were 18 years of age or greater through a random-digit telephone survey across the United States between 1993 and 2001 (Naimi et al., 2003). The number of binge episodes (≥5 alcoholic beverages in one sitting) among adults in the United States increased from about 1.2 billion to 1.5 billion. The younger adults in this sample (18–25 years) evinced the highest rate of binge-drinking episodes in the year 2001, whereas individuals older than 55 years had the lowest rate of binge-drinking episodes (Naimi et al., 2003). Differences in the prevalence estimates (CAS vs. BRFSS) may be due to different populations, with the CAS targeting college students and the BRFSS targeting the general community.

Most epidemiological reports indicate that men account for the majority of binge drinkers (Cranford et al., 2006; Wechsler et al., 1994; Wechsler, Dowdall, Davenport, & Castillo, 1995). The CAS study found that approximately 50% of the male and 39% of the female students were binge drinkers, with the BRFSS study concluding that men accounted for 81% of all binge-drinking episodes (Naimi et al., 2003). Furthermore, bingers in the BRFSS study were less likely to report any college education compared with nonbingers, although the opposite outcome also has been reported (Dawson, Grant, Stinson, & Chou, 2004; Slutske, 2005).

Racial differences were reported. Being White accounted for 78% of all binge-drinking episodes, and Hispanics demonstrated the highest rate of binge-drinking episodes per person for most of the years examined. African Americans constituted the lowest binge-drinking racial group, with fewer than five episodes per person per year (Naimi et al., 2003). Another large scale survey (N = 4,580) found a 33.2% prevalence estimate for binging (≥5/4 drinks in a row during past 2 weeks) for Asians compared with a 60.7% prevalence estimate for Whites (Cranford et al., 2006). The high frequency of a “flushing response” after alcohol ingestion has been theorized to account for the lower binging rates in Asians. The aldehyde dehydrogenase gene (ALDH2, Chromosome 12) that is prevalent in Asian populations fosters severe and predominately negative reactions to a moderate dose of alcohol compared with a heterozygous or individual without the allele (Cook et al., 2005).

Alcohol Consumption

Alcohol's effect on individuals stems from a variety of cognitive, biological, and social factors. The propensity to binge drink may arise from a combination of these factors, which could contribute to the underlying “cause” of binge drinking. Studies of these factors typically employ drinking definitions that are specialized for the particular variable or measure used, so that result comparisons need to be made from this perspective. However, these variables taken in the context of their roles as mediators and moderators of alcohol consumption are potentially important indices of future binge drinking and are reviewed here to provide appropriate background for their effects.

Alcohol Expectancies

Alcohol impairs the functioning of a variety of domains, including memory, judgment, and behavior (Nelson et al., 1998; Sayette, 1999). It diminishes eye movements (Blekher et al., 2002; Holdstock & de Wit, 1999; Moser, Heide, & Kömpf, 1998), short-term memory (Chait & Perry, 1994; Heishman, Arasteh, & Stitzer, 1997; Mattila et al., 1996), and motor performance (Fogarty & Vogel-Sprott, 2002). These direct influences of alcohol consumption, however, vary in magnitude as a function of amount ingested and individual differences in alcohol expectancies. A study of 302 undergraduates found that mood was affected by alcohol intake: Men more often reported social-situational enhancements (e.g., meeting people), whereas women often reported physical (e.g., falling asleep) effects (Goldstein, Wall, McKee, & Hinson, 2004). Alcohol-related memories can account for as much as 50% of the variance in predicting concurrent and prospective drinking (Wiers et al., 2002), and expectances can predict as well as demographic variables, such as social and problem drinking (Christiansen & Goldman, 1983).

Expectancy effects can be manipulated: Drinkers instructed to “try and stay sober” demonstrated superior hand coordination and recall memory performance compared with those not so motivated (Young & Pihl, 1980). Lower numbers of positive alcohol expectancies and reduced consumption have been linked to fewer binge-drinking episodes, whereas negative expectancies were not (Blume, Schmaling, & Marlatt, 2003). Alcohol expectancies and drinking refusal self-efficacy have been proposed to be significant predictors of drinking styles. Binge drinkers (≥6/4 drinks per drinking period) were characterized as either having positive (are able to refuse drinks easily) or negative (unable to stop drinking) drinking refusal self-efficacy. A model derived from these observations “predicts that social and binge drinkers can be discriminated on the basis of their alcohol expectancies, while binge drinkers and alcoholics can be discriminated on the basis of drinking refusal self-efficacy” (Oei & Morawska, 2004, p. 173). Thus, beliefs about alcohol effects appear to contribute to the experience of drinking.

Perception of Drunkenness

Inebriation is another important factor related to binge drinking, and it is often reported as the basis for binging (Wechsler et al., 1994). However, alcohol drinkers misbelieve that standard mixed drinks are more potent than standard servings of wine or beer. These individuals also believe that each additional drink they consumed had a decreasing impact on BAC (Jaccard & Turrisi, 1987). Sober adolescents were asked to estimate their perceived level of simulated drunkenness as quantified by whether their BAC was under or over the legal limit while they were exposed to external cues that systematically described drinking scenarios (Turrisi & Wiersma, 1999). The young people underestimated their “perceived” level of inebriation during 19% of the experimental scenarios, suggesting that their judgment was affected by the cues.

Induced public self-awareness (stimulated by exposure to mirrors and a camera) was hypothesized to increase salience of the situational behavioral standard (i.e., sober comportment), which increased motivation toward effortful performance. Shorter response time was obtained for the self-aware compared with the control group on a task that required the participant to identify correct and misspelled words (Ross & Pihl, 1988). This expectancy effect also was observed for at-risk college drinkers trained to reduce consumption by demonstrating that the students experienced enhanced mood and conviviality when they were induced to think they were consuming alcohol but were not (Fromme, Marlatt, Baer, & Kivlahan, 1994). As greater positive expectancies have been associated with binge drinking, expectancy differences appear to be a strong influence on alcohol's individual effects (Blume et al., 2003).

Tolerance to Alcohol

Individual responsivity or “tolerance” to alcohol also is important and has been assessed by the BAC curve changes with consumption (Fillmore & Vogel-Sprott, 1998). The rising limb theory supposes that heavy drinkers are more sensitive than light drinkers to the subjective positive euphorigenic effects during the early portion of the BAC curve but less sensitive to the sedative-like effects during both the rising and declining phases (Holdstock, King, & de Wit, 2000). Young adult heavy binge drinkers (≥5/4 drinks on one occasion at least once a week) were found to produce this biphasic response on a battery of behavioral scales. An initial pattern of positive reinforcement and absence of negative effects was obtained for the binge compared with nonbinge drinkers (<5/4 drinks per occasion), who did not show a biphasic alcohol response and reported heightened sedation throughout both limbs of the BAC curve (King, Houle, de Wit, Holdstock, & Schuster, 2002). Although the biphasic response may have been produced by the binge pattern of consumption, the authors speculated that the differential sensitivity between binge and nonbinge drinkers may have contributed to the enhanced risk for the development of alcohol-use disorders and the acquisition of binge-drinking patterns.

Social Issues

Drinking in a group leads to the experience of greater euphoria than drinking the same quantity alone (Pliner & Cappell, 1974), and drinking in a social setting facilitates more consumption than solitary drinking (Storm & Cutler, 1981). A survey of 409 college students found that a drinking event with many people intoxicated and having school friends present were factors predictive of binge drinking with five or more drinks (Clapp & Shillington, 2001). Students often seek out environments that facilitate binge drinking (Clapp et al., 2003; Lange & Voas, 2000b). Indeed, peer relationships can be a risk factor for increased alcohol consumption, as collegiate living arrangements—especially fraternities and sororities—are a significant correlate of binge drinking. Other factors include living with a roommate, stressing the importance of parties, and having five or more close student friends (Wechsler, Dowdall, Davenport, & Castillo, 1995).

Binge drinking can affect quality of life in terms of general health. After adjustment for age, frequent binge drinkers (≥5 drinks on one occasion > 3 times in last 30 days) compared with infrequent binge drinkers (≥5 drinks on one occasion < 3 times in the last 30 days) were more likely than nonbinge drinkers to report fair or poor health and experience more sick days. These findings appear to reflect the generally negative consequences of alcohol abuse but at an earlier stage in poor health development (Okoro et al., 2004).

In contrast, the benefits of light and moderate alcohol consumption have been well documented for stress reduction, mood enhancement, reduced depression symptoms, improved functioning in the elderly (Baum-Baicker, 1985; Pernanen, 1991), as well as for protection against coronary artery disease (Sacco et al., 1999). These issues often are reported as reasons for consuming alcohol. Only when the perceived drinking effects are detached from personal experience are harmful effects of drinking cited as “objective” assessments (Peele & Brodsky, 2000). The term “moderate” drinking, therefore, should not be confused with “binge drinking,” as the latter implies irregular intake and withdrawal from large quantities of alcohol and often leads to different outcomes than the positive ones associated with moderate drinking.

Binge Drinking

The current binge-drinking literature varies widely on the nature of the individual studies and definitions used to categorize alcohol consumption. Interpreting the results of these studies, therefore, requires a perspective that includes comparative awareness of sample characteristics, binge-drinking definition, and the control/nonbinge-drinking group inclusion criteria. Important too is to maintain the distinction between human and animal studies, as the former are typically much less specific than the later with respect to the neurophysiological underpinnings of binge-drinking effects. However, an overview of the general findings helps provide a fundamental grounding in what is known about binge-drinking outcomes at different levels of effect.

Cognitive Effects

Binge-drinking studies that measure cognitive function have found frontal lobe and working memory deficits, although an empirical definition of binging has not been used consistently. Heavy social drinkers, defined to include those who engaged in binge-drinking episodes, demonstrated delayed auditory and verbal memory deficits that were related to task difficulty. These deficits were not found for the light social drinkers. The findings implied that “frequent intake of large amounts of alcohol in any one sitting (i.e., ‘binge’ drinking) may place individuals at an increased risk for suffering alcohol-related cognitive impairment” (Nichols & Martin, 1997, p. 455). However, the conflation of participant drinking levels with descriptive labels colors statements about binge-drinking effects, thereby making comparisons unclear.

In Table 2, we summarize neurocognitive studies of binge-drinking studies using standard neuropsychological tests. The Binge-Drinking Score method was employed in several of these to define research participant drinking groups (Townshend & Duka, 2005). Binge drinkers compared with nonalcohol drinkers evinced cognitive impairments in the Paced Auditory Serial Addition Test, executive planning function, and episodic memory tasks—findings similar to frontal function deficits found in Korsakoff alcoholics (Hartley et al., 2004). Another report found that binge drinkers relative to nonbinging drinkers produced errors in a spatial working memory and pattern recognition tasks (Weissenborn & Duka, 2003). Furthermore, female compared with male binge drinkers were more impaired on these paradigms and unable to inhibit their response to an alerting stimulus in a vigilance task. Thus, binge drinking may be associated with deficits in frontal inhibitory control (Townshend & Duka, 2005).

Table 2
Neuropsychological Studies of Binge Drinking

It is important in this context to distinguish binge drinking from alcohol dependence. For example, alcohol dependent individuals who did binge drink—that is, regularly consumed more than 10 successive drinks—were compared with an alcohol dependent group who did not binge drink. No differences in performance were found for visuo-motor speed, visuo-spatial organization/planning, learning, proactive/retroactive interference, and item retrieval efficiency (Kokavec & Crowe, 1999). Comparable executive functioning results were obtained for both groups, and binge drinkers performed better than nonbinge drinkers on memory tasks. Although binge drinking was associated with impaired performance on immediate and delayed recall of verbal and visual information (Wechsler Memory Scale–Revised), retrieval ability was similar so that semantic organizational ability may be superior in binge compared with nonbinge drinkers. The pattern of binge versus nonbinge findings is likely affected by the inclusion of alcohol dependence criteria and the disproportionate number of drinks required in the binge definition.

Physiological Factors

The consensus from animal model studies is that “binge” effects require a long-term (multiple days) exposure to alcohol (e.g., Greiffenstein, Mathis, Stouwe, & Molina, 2007; Moore et al., 2007; Wezeman, Juknelis, Himes, & Callaci, 2007)—a viewpoint similar to the clinical alcoholic binge but quite different from the most common interpretations of binge drinking discussed above. Moreover, animal studies of alcohol binge exposure have led to the conclusion that such ethanol intake can lead to neurodegeneration in corticolimbic areas linked to learning and spatial memory (Aggleton, Hunt, & Rawlins, 1986; Haberly, 1998; Jarrard, 1993), such as the olfactory bulb, piriform cortex, perirhinal cortex, entorhinal cortex, and the hippocampal dentate gyrus (Collins, Corso, & Neafsey, 1996; Collins, Zou, & Neafsey, 1998; Corso, Mostafa, Collins, & Neafsey, 1998; Crews, Braun, Switzer, & Knapp, 2000; Zou, Martinez, Neafsey, & Collins, 1996). Researchers have found extensive neurodegeneration of the entorhinal cortex in rats after 2 days of “binge” alcohol exposure using stomach catheters that produced learning deficits (Obernier, White, Swartzwelder, & Crews, 2002). The vulnerability of this region after a single “binge” episode (i.e., 2 days of alcohol exposure) implies that long-term ethanol exposure may not produce the neurotoxicity commonly associated with heavy alcohol use. However, the duration of alcohol exposure time that leads to neurotoxicity is still unknown.

The Iowa Gambling Task (IGT) has been used to measure decision making skills in a sample of human binge (≥5 drinks on one occasion, more than one time in the past 30 days) and nonbinge alcohol drinkers. Diminished IGT performance was found in chronic high-binge drinkers (binge drinking 2 or more times a week 95% of the time) compared with low-binge drinkers (binge drinking 2 or more times a week 3% of the time). Heavy drinkers and possible alcohol dependent/abusers were included, and it was acknowledged that the findings did not permit differentiation of whether the quantity/frequency of drinking or the pattern of drinking was the cause of the diminished IGT performance (Goudriaan, Grekin, & Sher, 2007).

Magnetic resonance imaging measures of regional white and gray matter regional volumes were used to quantify N-acetylaspartate (NAA) concentrations—a metabolite biomarker of neural integrity. For bingers (> 100/80 alcohol drinks/month on <21 days in the past 3 years) compared with nonbingers, decreased NAA concentrations were associated with increased metabolism and frontal white matter loss, with higher parietal gray matter NAA. Consumption amount for heavy drinkers (> 100/80 drinks per month over past 3 years, which included binge drinkers) was correlated with lower executive functioning and working memory test scores. In addition, their relative frontal NAA loss was associated with impaired executive functioning and processing speed. Taken together, the results imply that these bingers have less parietal neuron damage than continual heavy drinkers (Meyerhoff et al., 2004), and that binge drinking may result in relatively specific neural deficits that differ from those associated with continual drinking levels.

Withdrawal Effects

A related issue is whether binge drinking causes permanent cognitive deficits. Previous studies of alcohol dependent adolescents suggest that frequent heavy drinking produces long-term memory deficits (Tapert et al., 2001). A study of nondependent binge drinkers examined hangover effects from binge drinking (≥5 drinks on a single occasion), which were assessed with memory tasks to determine whether cognitive deficits were related to the hangover episode or long-term neural damage. Encoding and consolidation processes were impaired, but delayed recall was intact, suggesting that retrieval processes were affected only during the hangover (Verster, van Duin, Volkerts, Schreuder, & Verbaten, 2003). The implications of these findings may be best described by the Federal Aviation Administration's Pilot Safety Guidelines on alcohol and flying: “eight hours from bottle to throttle” (Salazar & Antuñano, 2008, p. 3). Moreover, hours from last drink appear unrelated to cognitive performance (Townshend & Duka, 2005), and neuropsychological impairment from heavy social drinking over 6 months has not been observed (Alterman & Hall, 1989). Thus, the relationship between heavy alcohol consumption and subsequent cognitive capability is unclear.

Another interpretation suggests that increased binging causes a greater number of withdrawals, which produce the long-term deficits (Glenn, Parsons, Sinha, & Stevens, 1988; Parsons & Stevens, 1986; Stephens et al., 2005). The number of alcohol withdrawals has been linked to impairments of long-term nonverbal memory in adolescents and to poor memory in adult alcoholics (Glenn et al., 1988). Alcoholic patients with two or more medically supervised alcohol detoxifications demonstrated more frontal lobe cognitive dysfunction than patients with a single or no previous detoxification (Duka, Townshend, Collier, & Stephens, 2003).

Neural “kindling” has been proposed as the mechanism by which alcohol ingestion and subsequent withdrawal produce cognitive damage (Ballenger & Post, 1978). Repeated withdrawals are thought to generate an accumulative adaptive process that underlies the “advancing pathogenesis associated with the development of alcoholism [such that] continued alcohol abuse could be related to an avoidance of distress from worsening acute withdrawal symptoms induced by a kindling process that advances the course of alcoholism” (Breese, Overstreet, & Knapp, 2005, pp. 371–372). This view is consistent with an increased risk for brain damage from binge drinking and subsequent withdrawal (Hunt, 1993; Wechsler et al., 1994).

The occurrence of “blackouts” in which complex activities are performed with no recollection of the behavior available may be a related phenomenon and perhaps a biomarker for the mechanism of neurotoxicity observed in binge drinkers. Blackouts occur often in binge drinkers and could originate from reduced activity of N-methyl-D-aspartate (NMDA) receptors in the hippocampus, which would impair long-term potentiation (Izumi, Nagashima, Murayama, & Zorumski, 2005; for a review, see Allgaier, 2002). Excessive glucocorticoid release induced by the withdrawal stress could intensify the responses of already overactive NMDA receptors, thereby initiating blackouts (Hunt, 1993). Periods of binging followed by abstinence then trigger a neural cycle that leads to increased neurotoxicity of structures involved in learning and memory.

Alcoholism, Alcohol Dependence, and Other Determinants

Table 3 summarizes the definitions of alcohol abuse and dependence from the Diagnostic and Statistical Manual of Mental Disorders (4th ed.; American Psychiatric Association, 1994). Inclusion of frank alcoholism in binge samples may result in biased drinking correlates stemming from the negative consequences of alcoholism as well as binging. Alcohol dependence also can alter binge-drinking outcomes. College students who are frequent heavy episodic drinkers (5/4 or more drinks on three or more occasions in the past 2 weeks) had 19 times greater odds of being classified with alcohol dependence and 13 times greater odds of being classified with alcohol abuse compared with nonheavy episodic drinkers. The occasional episodic drinkers (heavy drinking on one or two occasions during the past 2 weeks) were found to have 4 times greater odds of dependence or abuse compared with the nonheavy episodic drinkers (Knight et al., 2002). However, earlier reports suggest that the comorbidity of binge drinking (periodic heavy drinking followed by a period of abstinence), with alcohol addiction or dependence, is not clinically supported (Levy, 1988; Levy & Kunitz, 1974).

Table 3
Definitions of Alcohol Abuse, Dependence, and Binge Drinking

Parental history for alcoholism and binge drinking (≥5 drinks per occasion) in a sample of alcohol dependent individuals both have been found to influence short-term outcome of alcohol dependence (Hasin, Paykin, & Endicott, 2001). An additional factor is gender, because as many as 81% of all binge-drinking episodes are attributed to men (Naimi et al., 2003), but men also demonstrate increased frequency of alcohol dependence (Robin, Long, Rasmussen, Albaugh, & Goldman, 1998). These data suggest that the relationships among binge-drinking definitions, epidemiological findings, and alcohol-related diagnostic categories need additional refinement.

Family History

Presence of alcoholism in the family covaries with behavioral and neuroimaging measures of binge drinking (Ehlers et al., 2007; Kokavec & Crowe, 1999). Alcohol expectancies have been shown to be a genetically influenced characteristic having a heritability between 0.4 and 0.6 (Heath et al., 1999; Schuckit et al., 2001), with greater alcohol consumption in high-risk than in low-risk control families (Newlin & Thomson, 1990). After the consumption of the lower or higher ethanol dose (approximately three or five drinks, respectively), men with high risk for alcoholism reported significantly less intense feelings of intoxication compared with low-risk men (Ehlers & Schuckit, 1988; O'Malley & Maisto, 1988; Schuckit, 1980, 1984, 1988). As outlined above, individuals who are homozygous for the ALDH2 gene are less likely to binge drink (Luczak, Wall, Shea, Byun, & Carr, 2001), which needs to be considered in such studies.

These associations have spurred the search for a binge-drinking gene. College students with the short version of the serotonin transporter gene (5-HTT) consumed more alcohol per occasion, more often drank expressly to become inebriated, and were more likely to engage in binge drinking than college students without the 5-HTT variant (Herman, Philbeck, Vasilopoulos, & Depetrillo, 2003). The 5-HTT gene is thought to be involved in serotonin reuptake, and the students who were homozygotic for the short version of 5-HTT were more likely to report troublesome drinking patterns. Students with at least one copy of the 5-HTT long variant gene consume fewer alcoholic drinks per episode but are equal in the number of episodes. Individuals who are homozygous for the short version are also at risk for higher levels of anxiety and depression and may use alcohol to reduce tension (Mazzanti et al., 1998).

Event-Related Potentials (ERPs)

ERPs are sensitive to the neural effects of alcohol intake (Porjesz & Begleiter, 1996). Several studies have reported decreases in ERP component (N1, MMN, P300) amplitudes with ethanol doses ranging from 0.50 g/kg to 0.85 g/kg (Campbell & Lowick, 1987; Grillon, Sinha, & O'Malley, 1995; Jääskeläinen et al., 1995, 1998; Rohrbaugh et al., 1987; Sommer, Leuthold, & Hermanutz, 1993). The P300 component reflects attention and memory operations engaged when stimulus change occurs (Polich, 2007). P300 variation with ethanol ingestion has been interpreted as demonstrating adverse effects on perceptual processing resources, a measure of central nervous system disinhibition, or frontal executive dysfunction (Begleiter & Porjesz, 1999; George, Potts, Kothman, Martin, & Mukundan, 2004; Kim, Kim, & Kwon, 2001).

ERPs also have been used to assess familial history as a neural signature or “marker” of alcoholism (Begleiter, Porjesz, Bihari, & Kissin, 1984; Hill et al., 1998; Hill & Steinhauer, 1993; O'Connor, Hesslebrock, Tasman, & DePalma, 1987; Porjesz & Begleiter, 1990). A meta-analysis of the early studies found that these effects were variable (Polich, Pollock, & Bloom, 1994), and that difficult visual discrimination tasks produced the strongest family history effects (e.g., Carlson, Iacono, & McGue, 2002; Iacono, Carlson, Malone, & McGue, 2002; Reese & Polich, 2003). These findings suggest that the P300 component in particular can index the effects of alcohol intake and may reflect the genetic background of alcoholism.

ERPs are just beginning to be used to assay binge drinking. A facial discrimination task yielded P300 amplitudes that were smaller for adolescents exposed to alcohol (i.e., ≥5 drinks per occasion), with a positive family history for alcohol dependence acting as a significant covariate. Further, P300 latency was decreased for alcohol and drug-exposed young adults in the absence of an alcohol challenge relative to control participants (Ehlers et al., 2007). Recent ERP studies suggest that high-binge compared with low-binge college student groups can be differentiated with tasks requiring strong visual stimulus processing: P300 amplitude tends to be smaller for the high- compared with the low-binge groups, although the quantity and frequency of alcohol intake that produces these effects are still unclear (Courtney & Polich, 2008).


The present review highlights issues that contribute to the definition of binge drinking, with the main variables centering on the quantity consumed and the time-frame of consumption. However, alcohol consumption effects are modulated by individual variation with respect to expectancy, how expectations influence the perception of inebriation, tolerance to alcohol ingestion, and the social environment. These factors contribute to the characterization of binge drinking in relation to its cognitive, physiological, and withdrawal effects. Moreover, the relevant findings empirically differentiate binge drinking from clinical alcoholism by defining how these variables influence alcohol effects. Thus, the interactive milieu of alcohol's internal determinants is complex and surprisingly subtle, so that binging to some is not necessarily binging to others.

An Operational Definition

Epidemiological reports of binge drinking vary in definitional consistency, but for young adults they indicate a large prevalence and imply a clear burden of suffering. The individual and social costs associated with binge drinking—such as drunken driving, induced violence, and personal injury—are profound. The cognitive damage that may be inflicted by binge drinking appears to involve alteration in critical neural mechanisms. However, experimental binge-drinking studies vary in their definitional approaches so that the what, where, and when of the neurocognitive insult is uncertain. Functional magnetic resonance imaging and ERP methods are beginning to assay such outcomes, but these approaches require sustained definitional rigor to inform public health policies.

The current NIAAA (2004) definition has provided a structure for binge drinking, but scientific and clinical assessments would benefit from the formation of a definition that facilitates comparison among studies. Given the findings outlined above, this definition should encompass three factors: alcohol quantity consumed, time-frame of consumption, and time period of past binging episodes. A definition of binge drinking that integrates these issues is as follows: A pattern of drinking alcohol that brings BAC to 0.08 gram percent or above (≥5/4 for men/women in 2 hr) on more than one occasion within the past 6 months. This definition (1) is operational in structure, (2) delimits consumption amount and time-frame (taking into account gender), and (3) specifies a time period that encompasses individual variation.

Future Directions

The intriguing hints provided by initial genetic studies may ultimately identify the neural origins of propensity to binge drink, which likely reflect fundamental individual differences to alcohol intake and interact with the wider context of personality or psychiatric variables. Searching for the primary reasons why some young adults binge would foster genetic links between binge drinking and subsequent alcohol dependence. Characterizing the association between binge-drinking mechanisms and the development of alcoholism could reveal a means to pursue and evaluate treatment interventions before the addictive disease is fully developed.

Neurophysiological and neurocognitive assessments of binge drinking are demonstrating promise in specifying biological differences between bingers and controls. The biphasic alcohol response exhibited by young binge drinkers and the associated neuropsychological impairments found for frontal lobe processing provide clues to the origins of binge drinking. Preliminary findings suggest working memory deficits in binge drinkers, but whether these are long-term or abate after withdrawal is unknown. Although difficult to execute, longitudinal studies of adolescent binge drinking could establish whether and how future alcohol dependence and abuse originates from this pattern of alcohol consumption while controlling for family history. Addressing these issues with a quantifiable and consistent binge-drinking definition would encourage comparisons among studies and increase their societal impact.


Scientific understanding of how alcohol produces reactions that vary across individuals from pleasurable to deadly requires clear observation of the phenomena and definitional agreement about what is observed. The public health concerns about young adult binge drinking have helped to motivate refinement of its definition. The implications of the empirical framework outlined here can be used to evaluate the proposed quantities, time-frame, and consumption frequencies as factors that may contribute to subsequent alcohol-related problems. The proposed binge-drinking definition should therefore help provide the operational utility that will facilitate inferences across studies.


This work was supported by National Institute on Alcohol Abuse and Alcoholism Grant AG10604. This article is 19458-MIND (Molecular and Integrative Neuroscience Department) from The Scripps Research Institute. We thank Shirley Y. Hill and Brian Lopez for very helpful comments on earlier versions of this article.

Contributor Information

Kelly E. Courtney, Department of Psychology, San Diego State University, La Jolla, California.

John Polich, Molecular and Integrative Neurosciences Department, The Scripps Research Institute, La Jolla, California.


  • Aggleton JP, Hunt PR, Rawlins JN. The effects of hippocampal lesions upon spatial and non-spatial tests of working memory. Behavioural Brain Research. 1986;19:133–146. [PubMed]
  • Alcohol Policy Information System. Adult operator blood alcohol concentration limit laws as of January 1, 2007. 2007. Retrieved July 07, 2008, from{85AC5A78–16B8–444A–95BE-BA2A10EEE53A}&DE={9F60E063–02C1–46B2–8AF0–8F".
  • Allgaier C. Ethanol sensitivity of NMDA receptors. Neurochemistry International. 2002;41:377–382. [PubMed]
  • Alterman AI, Hall JG. Effects of social drinking and familial alcoholism risk on cognitive functioning: Null findings. Alcoholism: Clinical and Experimental Research. 1989;13:799–803. [PubMed]
  • American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th. Washington, DC: Author; 1994.
  • Ballenger JC, Post RM. Kindling as a model for alcohol withdrawal syndromes. British Journal of Psychiatry. 1978;133:1–14. [PubMed]
  • Baum-Baicker C. The psychological benefits of moderate alcohol consumption: A review of the literature. Drug and Alcohol Dependence. 1985;15:305–322. [PubMed]
  • Begleiter HH, Porjesz BB. What is inherited in the predisposition toward alcoholism? A proposed model. Alcoholism: Clinical and Experimental Research. 1999;23:1125–1135. [PubMed]
  • Begleiter H, Porjesz B, Bihari B, Kissin B. Event-related brain potentials in boys at risk for alcoholism. Science. 1984 September 28;225:1492–1496. [PubMed]
  • Blekher T, Beard JD, O'Connor S, Orr WE, Ramchandani VA, Miller K, et al. Response of saccadic eye movements to alcohol in African American and non-Hispanic White college students. Alcoholism: Clinical and Experimental Research. 2002;26:232–238. [PubMed]
  • Blume AW, Schmaling KB, Marlatt AG. Predictors of change in binge drinking over a 3-month period. Addictive Behaviors. 2003;28:1007–1012. [PubMed]
  • Boyd CJ, McCabe SE, Morales M. College students' alcohol use: A critical review. Annual Review of Nursing Research. 2005;23:179–211. [PubMed]
  • Breese GR, Overstreet DH, Knapp DJ. Conceptual framework for the etiology of alcoholism: A “kindling”/stress hypothesis. Psychopharmacology. 2005;178:367–380. [PMC free article] [PubMed]
  • Cahalan D, Cisin IH, Crossley HM. American drinking practices: A national study of drinking behavior and attitudes. New Brunswick, NJ: Rutgers Center of Alcohol Studies; 1969.
  • Campbell KB, Lowick BM. Ethanol and event-related potentials: The influence of distractor stimuli. Alcohol. 1987;4:257–263. [PubMed]
  • Carlson SR, Iacono WG, McGue M. P300 amplitude in adolescent twins discordant and concordant for alcohol use disorders. Biological Psychology. 2002;61:203–227. [PubMed]
  • Chait LD, Perry JL. Acute and residual effects of alcohol and marijuana, alone and in combination, on mood and performance. Psychopharmacology. 1994;115:340–349. [PubMed]
  • Chikritzhs TN, Jonas HA, Stockwell TR, Heale PF, Dietze PM. Mortality and life-years lost due to alcohol: A comparison of acute and chronic causes. Medical Journal of Australia. 2001;174:281–284. [PubMed]
  • Christiansen BA, Goldman MS. Alcohol-related expectancies versus demographic/background variables in the prediction of adolescent drinking. Journal of Consulting and Clinical Psychology. 1983;51:249–257. [PubMed]
  • Clapp JD, Lange J, Min JW, Shillington A, Johnson M, Voas R. Two studies examining environmental predictors of heavy drinking by college students. Prevention Science. 2003;4:99–108. [PubMed]
  • Clapp JD, Shillington AM. Environmental predictors of heavy episodic drinking events. American Journal of Drug and Alcohol Abuse. 2001;27:310–313. [PubMed]
  • Collins MA, Corso TD, Neafsey EJ. Neuronal degeneration in rat cerebrocortical and olfactory regions during subchronic “binge” intoxication with ethanol: Possible explanation for olfactory deficits in alcoholics. Alcoholism: Clinical and Experimental Research. 1996;20:284–292. [PubMed]
  • Collins MA, Zou JY, Neafsey EJ. Brain damage due to episodic alcohol exposure in vivo and in vitro: Furosemide neuroprotection implicates edema-based mechanism. The FASEB Journal. 1998;12:221–230. [PubMed]
  • Cook TA, Luczak SE, Shea SH, Ehlers CL, Carr LG, Wall TL. Associations of ALDH2 and ADH1B genotypes with response to alcohol in Asian Americans. Journal of Studies on Alcohol. 2005;66:196–204. [PubMed]
  • Corso TD, Mostafa HM, Collins MA, Neafsey EJ. Brain neuronal degeneration caused by episodic alcohol intoxication in rats: Effects of nimodipine, 6,7-dinitro-quinoxaline-2,3-dione, and MK-801. Alcoholism: Clinical and Experimental Research. 1998;22:217–224. [PubMed]
  • Courtney KE, Polich J. Neuroelectric assessment of binge drinking [Abstract] Psychophysiology. 2008;45:S50.
  • Cranford JA, McCabe SE, Boyd CJ. A new measure of binge drinking: Prevalence and correlates in a probability sample of undergraduates. Alcoholism: Clinical and Experimental Research. 2006;30:1896–1905. [PMC free article] [PubMed]
  • Crews FT, Braun CJ, Switzer RC, Knapp DJ. Binge ethanol causes differential brain damage in young adolescent rats compared to adult rats. Alcoholism: Clinical and Experimental Research. 2000;24:1712–1723. [PubMed]
  • Dawson DA, Grant BF, Stinson FS, Chou PS. Another look at heavy episodic drinking and alcohol use disorders among college and noncollege youth. Journal of Studies on Alcohol. 2004;65:477–488. [PubMed]
  • Duka T, Townshend JM, Collier K, Stephens DN. Impairment in cognitive functions after multiple detoxifications in alcoholic inpatients. Alcoholism: Clinical and Experimental Research. 2003;27:1563–1572. [PubMed]
  • Ehlers CL, Phillips E, Finnerman G, Gilder D, Lau P, Criado J. P3 components and adolescent binge drinking in Southwest California Indians. Neurotoxicology and Teratology. 2007;29:153–163. [PubMed]
  • Ehlers CL, Schuckit MA. EEG response to ethanol in sons of alcoholics. Psychopharmacology Bulletin. 1988;24:434–437. [PubMed]
  • Fillmore MT, Vogel-Sprott M. Behavioral impairment under alcohol: Cognitive and pharmacokinetic factors. Alcoholism: Clinical and Experimental Research. 1998;22:1476–1482. [PubMed]
  • Fogarty JN, Vogel-Sprott M. Cognitive processes and motor skills differ in sensitivity to alcohol reinforcement. Journal of Studies on Alcohol. 2002;63:404–411. [PubMed]
  • Fromme K, Marlatt GA, Baer JS, Kivlahan DR. The Alcohol Skills Training Program: A group intervention for young adult drinkers. Journal of Substance Abuse Treatment. 1994;11:143–154. [PubMed]
  • George MR, Potts G, Kothman D, Martin L, Mukundan CR. Frontal deficits in alcoholism: An ERP study. Brain and Cognition. 2004;54:245–247. [PubMed]
  • Glenn SW, Parsons OA, Sinha R, Stevens L. The effects of repeated withdrawals from alcohol on the memory of male and female alcoholics. Alcohol and Alcoholism. 1988;23:337–342. [PubMed]
  • Goldstein AL, Wall A, McKee SA, Hinson RE. Accessibility of alcohol expectancies from memory: Impact of mood and motives in college drinkers. Journal of Studies on Alcohol. 2004;65:95–104. [PubMed]
  • Goudriaan AE, Grekin ER, Sher KJ. Decision making and binge drinking: A longitudinal study. Alcoholism: Clinical and Experimental Research. 2007;31:928–938. [PMC free article] [PubMed]
  • Greiffenstein P, Mathis KW, Stouwe CV, Molina PE. Alcohol binge before trauma/hemorrhage impairs integrity of host defense mechanisms during recovery. Alcoholism: Clinical and Experimental Research. 2007;31:704–715. [PubMed]
  • Grillon C, Sinha R, O'Malley SS. Effects of ethanol on the processing of low probability stimuli: An ERP study. Psychopharmacology. 1995;119:455–465. [PubMed]
  • Haberly L. The synaptic organization of the brain. In: Shepherd GM, editor. Olfactory cortex. New York: Oxford University Press; 1998. pp. 377–416.
  • Hartley DE, Elsabagh S, File SE. Binge drinking and sex: Effects on mood and cognitive function in healthy young volunteers. Pharmacology, Biochemistry and Behavior. 2004;78:611–619. [PubMed]
  • Hasin SS, Paykin A, Endicott J. Course of DSM–IV alcohol dependence in a community sample: Effects of parental history and binge drinking. Alcoholism: Clinical and Experimental Research. 2001;25:411–414. [PubMed]
  • Heath AC, Madden PA, Bucholz KK, Dinwiddie SH, Slutske WS, Bierut LJ, et al. Genetic differences in alcohol sensitivity and the inheritance of alcoholism risk. Psychological Medicine. 1999;29:1069–1081. [PubMed]
  • Heishman SJ, Arasteh K, Stitzer ML. Comparative effects of alcohol and marijuana on mood, memory, and performance. Pharmacology, Biochemistry and Behavior. 1997;58:93–101. [PubMed]
  • Herman AI, Philbeck JW, Vasilopoulos NL, Depetrillo PB. Serotonin transporter promoter polymorphism and differences in alcohol consumption behavior in a college student population. Alcohol and Alcoholism. 2003;38:446–449. [PubMed]
  • Hill SY, Locke J, Zezza N, Kaplan B, Neiswanger K, Steinhauer SR, et al. Genetic association between reduced P300 amplitude and the DRD2 dopamine receptor A1 allele in children at high risk for alcoholism. Biological Psychiatry. 1998;43:40–51. [PubMed]
  • Hill SY, Shen S, Lowers L, Locke J. Factors predicting the onset of adolescent drinking in families at high risk for developing alcoholism. Biological Psychiatry. 2000;48:265–275. [PubMed]
  • Hill SY, Steinhauer S. Assessment of prepubertal and postpubertal boys and girls at risk for developing alcoholism with P300 from a visual discrimination task. Journal of Studies on Alcohol. 1993;54:350–358. [PubMed]
  • Holdstock L, de Wit H. Ethanol impairs saccadic and smooth pursuit eye movements without producing self-reports of sedation. Alcoholism, Clinical and Experimental Research. 1999;23:664–672. [PubMed]
  • Holdstock L, King AC, de Wit H. Subjective and objective responses to ethanol in moderate/heavy and light social drinkers. Alcoholism: Clinical and Experimental Research. 2000;24:789–794. [PubMed]
  • Hunt WA. Are binge drinkers more at risk of developing brain damage? Alcohol. 1993;10:559–561. [PubMed]
  • Iacono WG, Carlson SR, Malone SM, McGue M. P3 event-related potential amplitude and the risk for disinhibitory disorders in adolescent boys. Archives of General Psychiatry. 2002;59:750–751. [PubMed]
  • Izumi Y, Nagashima K, Murayama K, Zorumski CF. Acute effects of ethanol on hippocampal long-term potentiation and long-term depression are mediated by different mechanisms. Neuroscience. 2005;136:509–517. [PubMed]
  • Jääskeläinen IP, Hirvonen J, Kujala T, Alho K, Eriksson CJ, Lehtokoski A, et al. Effects of naltrexone and ethanol on auditory event-related brain potentials. Alcohol. 1998;15:105–111. [PubMed]
  • Jääskeläinen IP, Lehtokoski A, Alho K, Kujala T, Pekkonen E, Sinclair JD, et al. Low dose of ethanol suppresses mismatch negativity of auditory event-related potentials. Alcoholism: Clinical and Experimental Research. 1995;19:607–610. [PubMed]
  • Jaccard J, Turrisi R. Cognitive processes and individual differences in judgments relevant to drunk driving. Journal of Personality and Social Psychology. 1987;53:135–145. [PubMed]
  • Jarrard LE. On the role of the hippocampus in learning and memory in the rat. Behavioral and Neural Biology. 1993;60:9–26. [PubMed]
  • Kim MS, Kim JJ, Kwon JS. Frontal P300 decrement and executive dysfunction in adolescents with conduct problems. Child Psychiatry and Human Development. 2001;32:93–106. [PubMed]
  • King AC, Houle T, de Wit H, Holdstock L, Schuster A. Biphasic alcohol response differs in heavy versus light drinkers. Alcoholism: Clinical and Experimental Research. 2002;26:827–835. [PubMed]
  • Knight JR, Wechsler H, Kuo M, Seibring M, Weitzman ER, Schuckit MA. Alcohol abuse and dependence among U.S. college students. Journal of Studies on Alcohol. 2002;63:263–270. [PubMed]
  • Kokavec A, Crowe SF. A comparison of cognitive performance in binge versus regular chronic alcohol misusers. Alcohol and Alcoholism. 1999;34:601–608. [PubMed]
  • LaBrie J, Pedersen ER, Tawalbeh S. Classifying risky-drinking college students: Another look at the two-week drinker-type categorization. Journal of Studies on Alcohol and Drugs. 2007;68:1–5. [PubMed]
  • Lange JE, Voas RB. Defining binge drinking quantities through resulting BACs. Annual Proceedings/Association for the Advancement of Automotive Medicine. 2000a;44:389–404. [PMC free article] [PubMed]
  • Lange JE, Voas RB. Youth escaping limits on drinking: Binging in Mexico. Addiction. 2000b;95:521–528. [PubMed]
  • Levy JE. The effects of labeling on health behavior and treatment programs among North American Indians [Monograph] American Indian and Alaska Native Mental Health Research. 1988;1:211–231. [PubMed]
  • Levy JE, Kunitz SJ. Indian drinking: Navajo practices and Anglo-American theories. New York: Wiley; 1974.
  • Luczak SE, Wall TL, Shea SH, Byun SM, Carr LG. Binge drinking in Chinese, Korean, and White college students: Genetic and ethnic group differences. Psychology of Addictive Behaviors. 2001;15:306–309. [PubMed]
  • Mattila MJ, Patat A, Seppälä T, Kalska H, Jalava ML, Vanakoski J, et al. Single oral doses of amisulpride do not enhance the effects of alcohol on the performance and memory of healthy subjects. European Journal of Clinical Pharmacology. 1996;51:161–166. [PubMed]
  • Mazzanti CM, Lappalainen J, Long JC, Bengel D, Naukkarinen H, Eggert M, et al. Role of the serotonin transporter promoter polymorphism in anxiety-related traits. Archives of General Psychiatry. 1998;55:936–940. [PubMed]
  • McGinnis JM, Foege WH. Actual causes of death in the United States. Journal of the American Medical Association. 1993;270:2207–2212. [PubMed]
  • Mehrabian A, Russell JA. A questionnaire measure of habitual alcohol use. Psychological Reports. 1978;43:803–806. [PubMed]
  • Meyerhoff DJ, Blumenfeld R, Truran D, Lindgren J, Flenniken D, Cardenas V, et al. Effects of heavy drinking, binge drinking, and family history of alcoholism on regional brain metabolites. Alcoholism: Clinical and Experimental Research. 2004;28:650–661. [PMC free article] [PubMed]
  • Miller JW, Naimi TS, Brewer RD, Jones SE. Binge drinking and associated health risk behaviors among high school students. Pediatrics. 2007;119(1):76–85. [PubMed]
  • Moore EM, Serio KM, Goldfarb KJ, Stepanovska S, Linsenbardt DN, Boehm SL., II GABAergic modulation of binge-like ethanol intake in C57BL/6J mice. Pharmacology, Biochemistry and Behavior. 2007;88:105–113. [PMC free article] [PubMed]
  • Moser A, Heide W, Kömpf D. The effects of oral ethanol consumption on eye movements in healthy volunteers. Journal of Neurology. 1998;245:542–559. [PubMed]
  • Naimi TS, Brewer RD, Mokdad A, Denny C, Serdula MK, Marks JS. Binge drinking among U.S. adults. Journal of the American Medical Association. 2003;289:70–75. [PubMed]
  • National Institute on Alcohol Abuse and Alcoholism. Tenth special report to the US Congress on alcohol and health. Bethesda MD: National Institutes of Health; 2000.
  • National Institute on Alcohol Abuse and Alcoholism. National Institute of Alcohol Abuse and Alcoholism Council approves definition of binge drinking. NIAAA Newsletter. 2004. Winter. Retrieved October 25, 2007, from
  • Nelson TO, Graf A, Dunlosky J, Marlatt A, Walker D, Luce K. Effect of acute alcohol intoxication on recall and on judgments of learning during the acquisition of new information. In: Mazzoni G, Nelson TO, editors. Metacognition and cognitive neuropsychology: Monitoring and control processes. Mahwah, NJ: Erlbaum; 1998. pp. 161–180.
  • Newlin DB, Thomson JB. Alcohol challenge with sons of alcoholics: A critical review and analysis. Psychological Bulletin. 1990;108:383–402. [PubMed]
  • Nichols JM, Martin F. The effect of lorazepam on long-term verbal recall in heavy and light social drinkers. Alcohol. 1997;14:455–461. [PubMed]
  • Obernier JA, White AM, Swartzwelder HS, Crews FT. Cognitive deficits and CNS damage after a 4-day binge ethanol exposure in rats. Pharmacology, Biochemistry and Behavior. 2002;72:521–532. [PubMed]
  • O'Connor S, Hesslebrock V, Tasman A, DePalma N. P3 amplitude in two distinct tasks is decreased in young men with a history of paternal alcoholism. Alcohol. 1987;4:323–330. [PubMed]
  • Oei TPS, Morawska A. A cognitive model of binge drinking: The influence of alcohol expectancies and drinking refusal self-efficacy. Addictive Behaviors. 2004;29:159–179. [PubMed]
  • Okoro CA, Brewer RD, Naimi TS, Moriarty DG, Giles WH, Mokdad AH. Binge drinking and health-related quality of life: Do popular perceptions match reality? American Journal of Preventive Medicine. 2004;26:230–233. [PubMed]
  • O'Malley SS, Maisto SA. Effects of family drinking history and expectancies on responses to alcohol in men. Journal of Studies on Alcohol. 1988;46:289–297. [PubMed]
  • Parsons OA, Stevens L. Previous alcohol intake and residual cognitive deficits in detoxified alcoholics and animals. Alcohol and Alcoholism. 1986;21:137–157. [PubMed]
  • Peele S, Brodsky A. Exploring psychological benefits associated with moderate alcohol use: A necessary corrective to assessments of drinking outcomes? Drug and Alcohol Dependence. 2000;60:221–247. [PubMed]
  • Pernanen K. Alcohol in human violence. New York: Guilford Press; 1991.
  • Pliner P, Cappell H. Modification of affective consequences of alcohol: A comparison of social and solitary drinking. Journal of Abnormal Psychology. 1974;83:418–425. [PubMed]
  • Polich J. Updating P300: An integrative theory of P3a and P3b. Clinical Neurophysiology. 2007;118:2128–2148. [PMC free article] [PubMed]
  • Polich J, Pollock V, Bloom FE. Meta-analysis of P300 amplitude from males at-risk for alcoholism. Psychological Bulletin. 1994;115:55–73. [PubMed]
  • Porjesz B, Begleiter H. Event-related potentials in individuals at risk for alcoholism. Alcohol. 1990;7:465–469. [PubMed]
  • Porjesz B, Begleiter H. Effects of alcohol on electrophysiological activity of the brain. In: Begleiter H, Kissin B, editors. The pharmacology of alcohol and alcohol dependence. 2nd. New York: Oxford University Press; 1996. pp. 207–247.
  • Presley CA, Pimentel ER. The introduction of heavy and frequent drinker: A proposed classification to increase accuracy of alcohol assessments in postsecondary educational settings. Journal of Studies on Alcohol. 2006;67:324–332. [PubMed]
  • Read JP, Beattie M, Chamberlain R, Merrill JE. Beyond the “binge” threshold: Heavy drinking patterns and their association with alcohol involvement indices in college students. Addictive Behaviors. 2008;33:225–234. [PubMed]
  • Reese C, Polich J. Alcoholism risk and the P300 event-related brain potential: Modality, task, and gender effects. Brain and Cognition. 2003;53:46–57. [PubMed]
  • Robin RW, Long JC, Rasmussen JK, Albaugh B, Goldman D. Relationship of binge drinking to alcohol dependence, other psychiatric disorders, and behavioral problems in an American Indian tribe. Alcoholism: Clinical and Experimental Research. 1998;22:518–523. [PubMed]
  • Rohrbaugh JW, Stapleton JM, Parasuraman R, Zubovic EA, Frowein HW, Varner JL, et al. Dose-related effects of ethanol on visual sustained attention and event-related potentials. Alcohol. 1987;4:293–300. [PubMed]
  • Ross DF, Pihl RO. Alcohol, self-focus and complex reaction-time performance. Journal of Studies on Alcohol. 1988;49:115–125. [PubMed]
  • Sacco RL, Elkind M, Boden-Albala B, Lin IF, Kargman DE, Hauser WA, et al. The protective effect of moderate alcohol consumption on ischemic stroke. Journal of the American Medical Association. 1999;281:53–60. [PubMed]
  • Salazar GJ, Antunano MJ. Alcohol and flying: A deadly combination. 2008. Retrieved March 17, 2008,
  • Sayette MA. Psychological theories of drinking and alcoholism. In: Leonard KE, Blane HT, editors. Cognitive theory and research. 2nd. New York: Guilford Press; 1999. pp. 247–291.
  • Schuckit MA. Self-rating of alcohol intoxication by young men with and without family histories of alcoholism. Journal of Studies on Alcohol. 1980;41:242–249. [PubMed]
  • Schuckit MA. Subjective response to alcohol in sons of alcoholics and controls. Archives of General Psychiatry. 1984;41:879–884. [PubMed]
  • Schuckit MA. Reactions to alcohol in sons of alcoholics and controls. Alcoholism: Clinical and Experimental Research. 1988;12:465–470. [PubMed]
  • Schuckit MA, Edenberg HJ, Kalmijn J, Flury L, Smith TL, Reich T, et al. A genome-wide search for genes that relate to a low level of response to alcohol. Alcoholism: Clinical and Experimental Research. 2001;25:323–329. [PubMed]
  • Schulenberg J, O'Malley PM, Bachman JG, Wadsworth KN, Johnston LD. Getting drunk and growing up: Trajectories of frequent binge drinking during the transition to young adulthood. Journal of Studies on Alcohol. 1996;57:289–304. [PubMed]
  • Slutske WS. Alcohol use disorders among U.S. college students and their non-college-attending peers. Archives of General Psychiatry. 2005;62:321–327. [PubMed]
  • Sommer W, Leuthold H, Hermanutz M. Covert effects of alcohol revealed by event-related potentials. Perception & Psychophysics. 1993;54:127–135. [PubMed]
  • Stephens DN, Ripley TL, Borlikova G, Schubert M, Albrecht D, Hogarth L, et al. Repeated ethanol exposure and withdrawal impairs human fear conditioning and depresses long-term potentiation in rat amygdala and hippocampus. Biological Psychiatry. 2005;58:392–400. [PubMed]
  • Storm T, Cutler RE. Observations of drinking in natural settings: Vancouver beer parlors and cocktail lounges. Journal of Studies on Alcohol. 1981;42:972–997. [PubMed]
  • Substance Abuse and Mental Health Services Administration. Results from the 2006 National Survey on Drug Use and Health: National findings (Office of Applied Studies, NSDUH Series H-32, DHHS Publication No SMA 07–4293) Rockville, MD: Author; 2007.
  • Tapert SF, Brown GG, Kindermann SS, Cheung EH, Frank LR, Brown SA. fMRI measurement of brain dysfunction in alcohol-dependent young women. Alcoholism: Clinical and Experimental Research. 2001;25:236–245. [PubMed]
  • Tomsovic M. “Binge” and continuous drinkers: Characteristics and treatment follow-up. Quarterly Journal of Studies on Alcohol. 1974;35:558–564. [PubMed]
  • Townshend JM, Duka T. Patterns of alcohol drinking in a population of young social drinkers: A comparison of questionnaire and diary measures. Alcohol and Alcoholism. 2002;37:187–192. [PubMed]
  • Townshend JM, Duka T. Binge drinking, cognitive performance and mood in a population of young social drinkers. Alcoholism: Clinical and Experimental Research. 2005;29:317–325. [PubMed]
  • Turrisi R, Wiersma K. Examination of judgments of drunkenness, binge drinking, and drunk-driving tendencies in teens with and without a family history of alcohol abuse. Alcoholism: Clinical and Experimental Research. 1999;23:1191–1198. [PubMed]
  • Verster JC, van Duin D, Volkerts ER, Schreuder AH, Verbaten MN. Alcohol hangover effects on memory functioning and vigilance performance after an evening of binge drinking. Neuropsychopharmacology. 2003;28:740–746. [PubMed]
  • Vik PW, Tate SR, Carrello P. Detecting college binge drinkers using an extended time frame. Addictive Behaviors. 2000;25:607–612. [PubMed]
  • Wechsler H. Binge drinking: Should we attack the name or the problem? [Electronic version] The Chronicle of Higher Education, B12. 2000. Oct 20, Retrieved October 15, 2007, from
  • Wechsler H, Davenport A, Dowdall G, Moeykens B, Castillo S. Health and behavioral consequences of binge drinking in college: A national survey of students at 140 campuses. Journal of the American Medical Association. 1994;272:1672–1677. [PubMed]
  • Wechsler H, Dowdall GW, Davenport A, Castillo S. Correlates of college student binge drinking. American Journal of Public Health. 1995;85:921–926. [PubMed]
  • Wechsler H, Dowdall GW, Davenport A, Rimm EB. A gender-specific measure of binge drinking among college students. American Journal of Public Health. 1995;85:982–985. [PubMed]
  • Wechsler H, Nelson TF. Binge drinking and the American college student: What's five drinks? Psychology of Addictive Behaviors. 2001;15:287–291. [PubMed]
  • Wechsler H, Nelson TF. Relationship between level of consumption and harms in assessing drink cut-points for alcohol research: Commentary on “Many college freshmen drink at levels far beyond the binge threshold” by White et al. Alcoholism: Clinical and Experimental Research. 2006;30:922–927. [PubMed]
  • Weingardt KR, Baer JS, Kivlahan DR, Roberts LJ, Miller ET, Marlatt GA. Episodic heavy drinking among college students: Methodological issues and longitudinal perspectives. Psychology of Addictive Behaviors. 1998;12:155–167.
  • Weissenborn R, Duka T. Acute alcohol effects on cognitive function in social drinkers: Their relationship to drinking habits. Psychopharmacology. 2003;165:306–312. [PubMed]
  • Weitzman ER, Nelson TF, Wechsler H. Taking up binge drinking in college: The influences of person, social group, and environment. Journal of Adolescent Health. 2003;32:26–35. [PubMed]
  • Wezeman FH, Juknelis D, Himes R, Callaci JJ. Vitamin D and ibandronate prevent cancellous bone loss associated with binge alcohol treatment in male rats. Bone. 2007;41:639–645. [PMC free article] [PubMed]
  • Wiers RW, Stacy AW, Ames SL, Noll JA, Sayette MA, Zack M, et al. Implicit and explicit alcohol-related cognitions. Alcoholism: Clinical and Experimental Research. 2002;26:129–137. [PubMed]
  • Young JA, Pihl RO. Self-control of the effects of alcohol intoxication. Journal of Studies on Alcohol. 1980;41:567–571. [PubMed]
  • Zeigler DW, Wang CC, Yoast RA, Dickinson BD, McCaffree MA, Robinowitz CB, et al. The neurocognitive effects of alcohol on adolescents and college students. Preventive Medicine. 2005;40:23–32. [PubMed]
  • Zou JY, Martinez DB, Neafsey EJ, Collins MA. Binge ethanol-induced brain damage in rats: Effects of inhibitors of nitric oxide synthase. Alcoholism: Clinical and Experimental Research. 1996;20:1406–1411. [PubMed]