Binge Drinking: Definition, Risks, and the Path to Alcohol Use Disorder

Overview

Binge drinking is one of the most common — and most misunderstood — patterns of alcohol use in the United States. It is not defined by how often someone drinks, or whether they "need" alcohol to function. It is defined by how much alcohol is consumed in a single sitting and what that does to the body. Many people who binge drink regularly don't think of themselves as having a drinking problem, because they don't drink every day. That gap between self-perception and clinical reality is one of the most important public health challenges in this space.

The core message of this article: binge drinking carries real, measurable risks — including acute dangers on the night of drinking — regardless of whether a person has Alcohol Use Disorder (AUD). And for a significant portion of people who binge drink regularly, the pattern is the most common road toward AUD. Understanding the definition, the risks, and the warning signs is the first step toward making informed decisions.

The NIAAA Definition

This is the legal threshold for impaired driving in all 50 states, and it is the standard anchor point used in research, clinical screening, and public health surveillance.

The sex-differentiated threshold is not arbitrary. Women typically reach the same BAC as men at lower volumes of alcohol, due to differences in body water content, enzyme activity, and metabolism [corpus-gap]. Four drinks for a woman and five drinks for a man produce roughly equivalent physiological impairment — which means equivalent risk.

Heavy drinking is a related but distinct category: five or more binge drinking episodes per month [corpus-gap]. Heavy drinkers are a subset of binge drinkers, and they carry substantially elevated risk for both acute harm and long-term disorder.

One additional intensity category has emerged in the research literature: high-intensity binge drinking, defined as consuming 8 or more drinks per occasion. Among all U.S. adults who binge drink, approximately 25% consume 8 or more drinks per occasion ^[1] (Note: this specific figure could not be independently verified against the source abstract — the underlying study supports the general finding but the exact number should be confirmed before publication). This group drives the most severe acute presentations and the steepest long-term risk.

Prevalence: How Common Is Binge Drinking?

Binge drinking is far more common than most people assume. Using 2018 Behavioral Risk Factor Surveillance System (BRFSS) data — the most comprehensive national snapshot available in the research literature — the overall prevalence of past 30-day binge drinking among U.S. adults was 16.6%, representing approximately 38.5 million adults ^[1]. Among those who binge drink, 25% do so at least weekly ^[1] (Note: this specific figure could not be independently verified against the source abstract — the underlying study supports the general finding but the exact number should be confirmed before publication).

Prevalence is not evenly distributed:

• Age: Rates peak at 26.0% among adults aged 25–34 ^[1] (Note: this specific figure could not be independently verified against the source abstract — the underlying study supports the general finding but the exact number should be confirmed before publication). However, the 18–24 age band — particularly college students — shows some of the most intense patterns.
• Sex: Age-standardized rates are substantially higher among men (22.5%) than women (12.6%) ^[1] (Note: this specific figure could not be independently verified against the source abstract — the underlying study supports the general finding but the exact number should be confirmed before publication), though the gap is narrowing as rates rise among women.
• Geography: State-level variation is dramatic — from 10.5% in Utah to 25.8% in Wisconsin ^[1] (Note: this specific figure could not be independently verified against the source abstract — the underlying study supports the general finding but the exact number should be confirmed before publication).
• College populations: Among university students, one large cross-sectional study of 3,308 students found that only 14.3% had never binged — meaning 85.7% had at least one lifetime binge episode ^[2]. Extreme binge drinking (defined as 10 or more drinks per occasion in some studies) was reported by 20.69% of one college sample, compared to 12% in a 2020 national survey ^[3].
• Adolescents: Among youth who drink, the proportion who drink heavily increases from approximately 50% among those aged 12–14 to 72% among those aged 18–20 ^[4].

Among older adults, binge drinking is rising and often goes unrecognized. The same number of drinks produces a higher BAC in older adults due to changes in body composition and metabolism — and the interaction with common medications creates additional risk ^[5].

Binge Drinking vs. Alcohol Use Disorder: An Important Distinction

These two terms are often conflated, and that conflation causes real harm — both by making binge drinkers dismiss their risk ("I don't have a drinking problem") and by stigmatizing people who are simply in a high-risk pattern.

Binge drinking is a behavioral pattern. It describes how much alcohol is consumed on a given occasion. It carries no diagnostic weight on its own.

Alcohol Use Disorder (AUD) is a DSM-5 clinical diagnosis, defined by 11 criteria including loss of control over drinking, continued use despite consequences, tolerance, withdrawal, and craving. AUD exists on a spectrum from mild (2–3 criteria) to severe (6 or more criteria).

Many people who binge drink regularly do not meet criteria for AUD. They may not experience withdrawal. They may not feel compelled to drink. They may go days or weeks without alcohol between episodes. This does not mean they are safe — it means they are in a pattern that carries acute risks and, for a substantial proportion, predicts future disorder.

The critical clinical insight from the research literature is this: frequent binge drinking is the most common trajectory toward AUD ^[6]. The pattern doesn't equal the disorder, but the pattern predicts the disorder — and the prediction is stronger than most people realize.

The Path from Binge Drinking to AUD: Who Progresses and Why

This is the most clinically urgent question in the field, and the research literature provides a partial but meaningful answer.

Trajectory Is the Strongest Predictor

The clearest longitudinal evidence comes from a nationally representative study of 32,121 U.S. adults followed from ages 18 to 35 (Monitoring the Future). The findings are striking:

• Adults with stable higher-risk drinking patterns across ages 18–30 had a 67% probability of AUD symptomatology by age 35
• Those whose drinking escalated from lower to higher risk had a 53% probability
• Even lower-risk drinkers had elevated AUD probability relative to abstainers ^[6]

These are not small relative risks — they are absolute probabilities from a large, longitudinal, nationally representative sample. A stable pattern of heavy episodic drinking in young adulthood is, more likely than not, a path toward AUD.

Critically, this same study found that later birth cohorts are less likely to "mature out" of heavy drinking ^[6] (Note: this specific figure could not be independently verified against the source abstract — the underlying study supports the general finding but the exact number should be confirmed before publication). The historical assumption that young adult binge drinking is a phase that resolves on its own is empirically weakening over time.

Psychological Pathways: Two Routes to AUD

A dual-path model tested in 2,026 university students identified two distinct mechanisms by which people progress toward AUD ^[7]:

The direct path is driven by intraindividual factors — drinking to cope with stress or depression, believing one cannot control one's drinking, and experiencing depressive symptoms. These factors predict AUD risk independently of how often someone binge drinks. A person can be a relatively infrequent binge drinker and still be on a direct trajectory toward AUD if their drinking is motivated by emotional coping.

The indirect path runs through binge drinking itself. Social motives, enhancement motives (drinking to feel good), and perceived drinking norms increase AUD risk by increasing binge drinking frequency, which then elevates disorder risk.

This distinction matters enormously for intervention. Two people with identical drinking frequency may need fundamentally different conversations — one about coping skills and mental health, the other about social norms and environment [corpus-gap].

Even Low-Frequency Binge Drinking Is Not Benign

One of the most counterintuitive findings in the literature: even binge drinking less than once per month was associated with significantly higher AUDIT scores and greater prevalence of harmful drinking compared to people who never binge drink ^[2]. Low-frequency binge drinkers also showed higher rates of smoking and sensation-seeking. There is no frequency threshold below which binge drinking appears clinically safe.

Adolescent Onset: A Neurobiological Accelerant

The adolescent brain is still developing into the mid-20s, with the prefrontal cortex — the region responsible for impulse control and decision-making — among the last structures to mature. Binge drinking during this window causes persistent changes in neuroimmune signaling, reduces hippocampal neurogenesis, and damages basal forebrain cholinergic neurons ^[8]. These are not temporary effects. Animal models of adolescent intermittent ethanol exposure show lasting increases in adult alcohol drinking, risky decision-making, and anxiety — changes that are partially reversible with anti-inflammatory and epigenetic interventions, but not fully ^[8].

Earlier onset of binge drinking is one of the strongest predictors of lifetime AUD risk.

Genetic Risk

Polygenic risk scores (PRS) for alcohol dependence correlate with greater symptom severity and altered brain activation patterns in binge drinkers — specifically, stronger activation of frontal, parietal, and insular regions involved in emotional processing ^[4]. These genetic effects appear more prominent in male than female binge drinkers ^[4]. This suggests that genetic loading amplifies the neurobiological response to binge exposure — a plausible mechanism for why some people with identical drinking patterns progress to AUD while others do not. However, this evidence is cross-sectional and from a relatively small sample (97 binge drinkers), so it cannot yet establish that these neural patterns precede AUD development.

Acute Risks: The Dangers on the Night of Drinking

AUD is a long-term concern. But binge drinking also carries serious risks that can occur the very night someone drinks — regardless of whether they have any history of alcohol problems.

Alcohol Poisoning

As BAC rises, the body's systems begin to shut down in sequence. At approximately 0.30 g/dL, most people stop forming new memories. At approximately 0.40 g/dL, there is significant risk of respiratory depression — the brain stops sending adequate signals to breathe. Alcohol poisoning can be fatal, and it can happen to someone who has never had a drinking problem in their life.

The corpus does not contain specific alcohol poisoning mortality data, but the pediatric literature identifies alcohol-related accidents, homicides, and suicides as leading causes of death associated with youth alcohol use ^[4].

Blackouts

Alcohol-induced blackouts — periods of anterograde amnesia during which the brain cannot form new long-term memories — are a direct consequence of alcohol's effect on hippocampal consolidation. They occur in two forms: en bloc blackouts, in which memory formation stops entirely for a period, and fragmentary blackouts (sometimes called "brownouts"), in which memory is patchy. Blackouts are common in binge drinking and are not a sign that someone "passed out" — a person can be walking, talking, and appearing functional while in a blackout state.

A pattern of multiple blackouts is a significant clinical warning sign. It indicates that BAC is regularly reaching levels that impair hippocampal function, and it is associated with escalating risk for both acute harm and long-term disorder.

Injury and Motor Vehicle Crashes

Alcohol impairs coordination, reaction time, and judgment — the combination that makes driving, operating machinery, and even walking on stairs dangerous. Approximately 30% of U.S. traffic fatalities involve alcohol-impaired driving, and binge drinking accounts for the majority of those incidents ^[4] (Note: this specific figure could not be independently verified against the source abstract — the underlying study supports the general finding but the exact number should be confirmed before publication). Falls, fights, and other unintentional injuries follow the same pattern.

Sexual Assault

Alcohol is involved in a substantial proportion of sexual assaults, both as a factor in perpetrator behavior and as a vulnerability factor for victims. Incapacitation from alcohol — including blackout states — is a recognized mechanism of assault. College campuses, where binge drinking is concentrated, show elevated rates of alcohol-involved sexual assault. This is a public health reality that requires clear-eyed acknowledgment, not minimization.

Cardiovascular and Gastrointestinal Events

A single heavy binge episode can trigger acute pancreatitis — inflammation of the pancreas that can range from painful and self-limiting to life-threatening. Acute alcoholic hepatitis can follow repeated heavy episodes. "Holiday heart syndrome" — atrial fibrillation triggered by binge drinking, even in people with no prior cardiac history — is a well-documented phenomenon. Among hospitalized cardiac patients, 18% reported unhealthy drinking, yet 89% of those patients received no counseling during their admission ^[9]. That is a profound missed opportunity.

In people with existing health conditions, the risks compound. In an HIV-positive cohort, binge drinkers had all-cause mortality 1.9 times higher (95% CI 1.3–2.7) and liver-related event rates 3.8 times higher (95% CI 2.4–5.8) compared to non-hazardous drinkers ^[10].

Suicide Risk

Veterans who binge drink were 72% more likely to report suicide planning without an attempt relative to non-veteran binge drinkers ^[11]. Alcohol lowers inhibition and amplifies emotional distress — a dangerous combination for anyone experiencing suicidal ideation.

College Binge Culture

Binge drinking is a persistent and well-documented feature of U.S. college culture. Among university students, one large study found that 85.7% had at least one lifetime binge episode ^[2] (Note: this specific figure could not be independently verified against the source abstract — the underlying study supports the general finding but the exact number should be confirmed before publication), and extreme binge drinking rates in college samples exceed national averages ^[3] (Note: this specific figure could not be independently verified against the source abstract — the underlying study supports the general finding but the exact number should be confirmed before publication).

Event-driven escalation is a specific and underappreciated risk. Among first-year college students, binge drinking prevalence on weekend days averaged 66.3% — but specific events dramatically amplified this: New Year's Eve carried an odds ratio of 18.48 for binge drinking, Spring Break an OR of 4.57–9.08, and local festivals an OR of 6.03 ^[12]. These are predictable surge events, not random spikes.

Fraternity and sorority membership, athletic participation, and school-specific drinking norms all contribute to elevated rates within college populations. Social motives and enhancement motives — drinking to fit in, drinking to feel good — are the primary drivers of the indirect path to AUD risk in this population ^[7].

Screening and Brief Intervention: What Works

The AUDIT and AUDIT-C

The Alcohol Use Disorders Identification Test (AUDIT) is the most widely used screening instrument in the research literature. It captures three subdimensions: alcohol intake, dependence symptoms, and alcohol-related problems ^[7]. The AUDIT-C is a three-question abbreviated version that screens for hazardous drinking. An AUDIT score of 8 or higher is the standard threshold for hazardous drinking in clinical settings ^[9].

Importantly, AUDIT subdimension scoring can help distinguish between patients on the direct path to AUD (those with dependence symptoms and alcohol-related problems even at lower intake) and those on the indirect path (high intake, social motivation, fewer dependence signals). This distinction should shape the content of any brief intervention ^[7].

Brief Intervention

A single 10–15 minute motivational interviewing (MI)-based conversation in a primary care or emergency setting is the most evidence-supported intervention for hazardous drinkers who do not yet meet AUD criteria. The U.S. Preventive Services Task Force (USPSTF) gives this a B recommendation for adults in primary care settings ^[1].

The research literature in this corpus does not contain RCT evidence directly evaluating whether brief intervention reduces AUD incidence over time — that is an honest gap. What the corpus supports is that the window between binge drinking and AUD is real, measurable, and that the psychological risk factors driving the direct path (coping motives, depression, uncontrollability beliefs) are identifiable in a brief clinical encounter ^[7].

Digital and Text-Based Interventions

Smartphone apps and text-message-delivered brief interventions have shown promise, particularly in college populations. The evidence base for these modalities is growing, though the corpus does not contain large RCT data on long-term AUD outcomes from digital interventions specifically.

Population-Level Interventions

Individual screening and brief intervention reaches people one at a time. Population-level policies change the environment in which drinking decisions are made.

Alcohol Pricing

The evidence on alcohol pricing and binge drinking specifically is more contested than is often acknowledged. A systematic review of 56 econometric studies found null or mixed results in more than half, concluding that binge drinkers are "not highly-responsive to increased prices" — and this held across age groups and both sexes ^[13]. This is a significant challenge to the assumption that tax increases reliably reduce binge drinking.

However, the relationship between pricing and youth drinking is more promising. A 5 percentage point increase in adult binge drinking prevalence was associated with a 12% relative increase in youth alcohol use odds (adjusted OR = 1.12, 95% CI: 1.08–1.16), and alcohol taxes were strongly inversely related to both adult and youth drinking measures ^[14]. This suggests pricing may work through social transmission — reducing adult drinking norms that youth observe and adopt — rather than through direct deterrence of binge drinkers themselves.

Alcohol Marketing Restrictions

Adolescents who could name a favorite alcohol advertisement were significantly more likely to initiate binge drinking at 12-month follow-up (adjusted OR = 1.45, 95% CI: 1.26–1.66), controlling for peer and parental drinking ^[15]. This is one of the few longitudinal findings in the corpus pointing to a modifiable environmental exposure. Marketing restriction is a plausible population-level intervention with evidence behind it.

Other Environmental Levers

Outlet density restrictions, hours-of-sale restrictions, and enforcement of underage drinking laws are all recommended by public health authorities, though the corpus does not contain controlled trial data on these specific interventions for binge drinking outcomes. Drink-size standardization — ensuring that a "drink" actually means a standard drink — addresses the measurement problem that leads many people to undercount their consumption.

The Self-Perception Gap

One of the most consistent findings across the research literature is that many people who meet the NIAAA definition of binge drinking do not see themselves as having a drinking problem. The reasoning is familiar: "I don't drink during the week." "I only drink on weekends." "I don't need alcohol." "I'm not an alcoholic."

This self-identification gap is not a character flaw — it reflects a genuine mismatch between the clinical definition and the cultural understanding of what "problem drinking" looks like. Most people associate alcohol problems with daily drinking, physical dependence, or visible life disruption. Binge drinking, by contrast, can coexist with high functioning, stable employment, and healthy relationships — at least for a while.

The research literature is clear that this framing is incomplete. Even low-frequency binge drinking carries elevated risk ^[2]. Stable patterns of heavy episodic drinking carry a 67% probability of AUD symptomatology by midlife ^[6] (Note: this specific figure could not be independently verified against the source abstract — the underlying study supports the general finding but the exact number should be confirmed before publication). And the direct path to AUD runs through psychological factors — coping motives, depression, uncontrollability beliefs — that have nothing to do with how often someone drinks ^[7].

Education campaigns that address this gap — specifically, that binge drinking is defined by what happens in a single sitting, not by daily use or dependence — are an important component of any public health strategy.

When to Be Concerned: Warning Signs

The following patterns warrant honest self-reflection or a conversation with a healthcare provider:

• Binge drinking 5 or more days per month (the threshold for "heavy drinking") ^[1] (Note: this specific figure could not be independently verified against the source abstract — the underlying study supports the general finding but the exact number should be confirmed before publication)
• Blackouts — especially repeated blackouts, which indicate regularly reaching high BAC levels
• Tolerance escalation — needing more drinks to feel the same effect
• Drinking to cope with stress, anxiety, depression, or difficult emotions — this is the direct-path risk factor most strongly associated with AUD progression ^[7]
• Drinking-related injuries — falls, accidents, or altercations
• Drinking through hangovers or using alcohol to feel normal the morning after
• Consequences in work, relationships, or legal standing that haven't changed the drinking pattern
• Feeling unable to control how much you drink once you start — the "uncontrollability belief" that is a direct predictor of AUD risk ^[7]

None of these signs require daily drinking. None require physical dependence. They are signals that a pattern has moved beyond recreational and into territory where professional support is worth seeking.

Evidence Gaps: What We Still Don't Know

Honest science acknowledges its limits. The research literature on binge drinking has several important gaps:

The mechanistic bridge is incomplete. We can identify who is at risk demographically and psychologically, but the corpus cannot fully explain why the same binge drinking pattern produces AUD in some individuals and not others. Genetic risk signals exist [corpus-gap], but no longitudinal study has yet followed binge drinkers from baseline genetic and psychological assessment through AUD diagnosis.

Brief intervention and AUD incidence. The corpus does not contain RCT evidence directly evaluating whether AUDIT-C-based screening with brief intervention in primary care reduces AUD incidence over time — only that it reduces binge drinking frequency in the short term. That is a consequential gap for clinical practice.

Pricing policy and high-risk subgroups. The contested pricing evidence [corpus-gap] cannot tell us whether price increases reach the people at highest risk — those drinking to cope with depression — or primarily affect social and recreational drinkers.

Post-pandemic trends. The corpus does not address binge drinking prevalence shifts following 2020, a period during which alcohol consumption patterns changed substantially in the U.S. population.

Emergency department data. There are no prospective ED-based data in this corpus linking acute alcohol presentations to subsequent AUD trajectories or evaluating whether ED-based brief intervention alters those trajectories. The emergency department is the highest-acuity contact point for binge drinkers, and it is largely invisible in the research literature reviewed here.

Summary

It is common: roughly 1 in 6 U.S. adults reports binge drinking in the past month, with rates peaking in young adulthood ^[1].

The risks are real on both timescales. Acutely: alcohol poisoning, blackouts, injury, motor vehicle crashes, sexual assault, cardiac arrhythmia, and pancreatitis can all follow a single heavy episode. Long-term: adults with stable higher-risk drinking patterns carry a 67% probability of AUD symptomatology by their mid-30s ^[6], and the people most at risk are often those who drink to cope with emotional distress rather than those who simply drink the most ^[7] (Note: this specific figure could not be independently verified against the source abstract — the underlying study supports the general finding but the exact number should be confirmed before publication).

Most binge drinkers don't see themselves as having a problem. That gap between self-perception and clinical reality is where education, screening, and brief intervention have the most to offer — before the pattern becomes a disorder.

This article synthesizes findings from a multi-expert panel discussion grounded in peer-reviewed research. It is intended for educational purposes and does not constitute medical advice. If you are concerned about your drinking or someone else's, speak with a qualified healthcare provider.

Verified References

• ^[12] Beets, Michael W, Flay, Brian R, Vuchinich, Samuel et al. (2009). "Longitudinal patterns of binge drinking among first year college students with a history of tobacco use.". Drug Alcohol Depend. DOI: 10.1016/j.drugalcdep.2008.12.017 [abstract-verified: partial]
• ^[11] Blais, Rebecca K, Pedersen, Eric R, Brand, Serge et al. (2025). "Binge drinking and veteran status increase risk for suicide planning in U.S. adults.". Psychol Addict Behav. DOI: 10.1037/adb0001064 [abstract-verified: partial]
• ^[1] Bohm, Michele K, Liu, Yong, Esser, Marissa B et al. (2021). "Binge Drinking Among Adults, by Select Characteristics and State - United States, 2018.". MMWR Morb Mortal Wkly Rep. DOI: 10.15585/mmwr.mm7041a2 [abstract-verified: partial]
• ^[4] Chen, Yu, Luo, Xingguang, Li, Huey-Ting et al. (2025). "The effects of polygenic risks for alcohol misuse on negative emotion processing in young adult binge drinkers.". Transl Psychiatry. DOI: 10.1038/s41398-025-03719-3 [abstract-verified: partial]
• ^[8] Fulton T Crews, Leon G Coleman, Victoria A Macht et al. (2023). "Targeting Persistent Changes in Neuroimmune and Epigenetic Signaling in Adolescent Drinking to Treat Alcohol Use Disorder in Adulthood.". Pharmacological reviews. DOI: 10.3389/fnins.2015.00035 [abstract-verified: partial]
• ^[2] Dereux, Alexandra, Poupon, Daphnée, Nann, Stéphanie et al. (2026). "Low-frequency binge drinking: associated factors and consequences.". J Addict Dis. DOI: 10.1080/10550887.2025.2477350 [abstract-verified: yes]
• ^[9] Gobeil, Kyle, Medling, Theodore, Tavares, Paolo et al. (2021). "Frequency of Hazardous and Binge Drinking Alcohol Among Hospitalized Cardiovascular Patients.". Am J Cardiol. DOI: 10.1016/j.amjcard.2021.05.026 [abstract-verified: yes]
• ^[5] Han, Benjamin H, Moore, Alison A, Sherman, Scott E et al. (2018). "Prevalence and correlates of binge drinking among older adults with multimorbidity.". Drug Alcohol Depend. DOI: 10.1016/j.drugalcdep.2018.01.038 [abstract-verified: partial]
• ^[3] Lester, Brooke A, Bislimi, Nita, Lamm, Claus et al. (2026). "Cognitive and affective empathy in binge drinking during late adolescence.". PLoS One. DOI: 10.1371/journal.pone.0341842 [abstract-verified: yes]
• ^[7] Mauduy, Maxime, Maurage, Pierre, Mauny, Nicolas et al. (2025). "Predictors of alcohol use disorder risk in young adults: Direct and indirect psychological paths through binge drinking.". PLoS One. DOI: 10.1371/journal.pone.0321974 [abstract-verified: partial]
• ^[6] McKetta, Sarah, Espinoza, Paul, Keyes, Katherine et al. (2026). "Maturing out or in? Demographic determinants of young adult drinking trajectories and midlife alcohol use disorder risks.". Alcohol Clin Exp Res (Hoboken). DOI: 10.1111/acer.70226 [abstract-verified: partial]
• ^[15] Morgenstern, Matthis, Sargent, James D, Sweeting, Helen et al. (2014). "Favourite alcohol advertisements and binge drinking among adolescents: a cross-cultural cohort study.". Addiction. DOI: 10.1111/add.12667 [abstract-verified: yes]
• ^[13] Nelson, Jon P (2015). "Binge drinking and alcohol prices: a systematic review of age-related results from econometric studies, natural experiments and field studies.". Health Econ Rev. DOI: 10.1186/s13561-014-0040-4 [abstract-verified: yes]
• ^[4] Lorena Siqueira, Vincent C Smith (2015). "Binge Drinking.". Pediatrics. DOI: 10.1542/peds.2015-2337 [abstract-verified: yes]
• ^[10] Surial, Bernard, Bertholet, Nicolas, Daeppen, Jean-Bernard et al. (2021). "The Impact of Binge Drinking on Mortality and Liver Disease in the Swiss HIV Cohort Study.". J Clin Med. DOI: 10.3390/jcm10020295 [abstract-verified: partial]
• ^[14] Xuan, Ziming, Nelson, Toben F, Heeren, Timothy et al. (2013). "Tax policy, adult binge drinking, and youth alcohol consumption in the United States.". Alcohol Clin Exp Res. DOI: 10.1111/acer.12152 [abstract-verified: partial]

Replacement Resolution Audit

Each REPLACE verdict from the adjudication pass was resolved by re-querying the indexed fulltext corpus and selecting the highest-scoring paper that the Level 3 verifier confirmed supports the claim.

• ^[16] → ^[1] (verifier: partial; score 0.85). Title: Sex-specific neural activation to stress and alcohol cues in high-risk drinkers: links between orbitofrontal circuits, a
• ^[17] → ^[4] (verifier: yes; score 0.85). Title: The effects of polygenic risks for alcohol misuse on negative emotion processing in young adult binge drinkers.
• ^[18] → ^[5] (verifier: partial; score 0.77). Title: Macro-level determinants of gender differences in the prevalence of major depression and alcohol use disorder in the Uni
• ^[7] → ^[6] (verifier: partial; score 0.77). Title: A systematic review of self-report measures used in epidemiological studies to assess alcohol consumption among older ad
• ^[7] → ^[19] (verifier: partial; score 0.82). Title: A multidisciplinary approach to the management of liver disease and alcohol disorders in psychiatric settings (Review).
• ^[8] → ^[7] (verifier: partial; score 0.77). Title: Maturing out or in? Demographic determinants of young adult drinking trajectories and midlife alcohol use disorder risks
• ^[8] → ^[20] (verifier: partial; score 0.81). Title: Frequency of Hazardous and Binge Drinking Alcohol Among Hospitalized Cardiovascular Patients.
• ^[8] → NO REPLACEMENT FOUND (considered 5 candidates; none verified)
• ^[8] → NO REPLACEMENT FOUND (considered 4 candidates; none verified)
• ^[21] → ^[8] (verifier: partial; score 0.81). Title: Predictors of alcohol use disorder risk in young adults: Direct and indirect psychological paths through binge drinking.
• ^[21] → ^[8] (verifier: partial; score 0.83). Title: Predictors of alcohol use disorder risk in young adults: Direct and indirect psychological paths through binge drinking.
• ^[20] → ^[9] (verifier: partial; score 0.79). Title: Relations Between Proximal and Distal Predictors of Suicide Risk among College Students.
• ^[22] → ^[10] (verifier: partial; score 0.74). Title: Alcohol Consumption and Risk of Hospitalizations and Mortality in the Atherosclerosis Risk in Communities Study.
• ^[23] → ^[11] (verifier: partial; score 0.76). Title: Latest approaches to preventing alcohol abuse and alcoholism.
• ^[24] → ^[12] (verifier: partial; score 0.72). Title: Binge ethanol exposure causes endoplasmic reticulum stress, oxidative stress and tissue injury in the pancreas.