Adolescent binge drinking alters adult brain neurotransmitter gene expression, behavior, brain regional volumes, and neurochemistry in mice

Background: Binge drinking is common in human adolescents. The adolescent brain is undergoing structural maturation and has a unique sensitivity to alcohol neurotoxicity. Therefore, adolescent binge ethanol may have long‐term effects on the adult brain that alter brain structure and behaviors that are relevant to alcohol‐use disorders. Methods: To determine whether adolescent ethanol (AE) binge drinking alters the adult brain, male C57BL/6 mice were treated with either water or ethanol during adolescence (5 g/kg/d, i.g., postnatal days P28 to P37) and assessed during adulthood (P60 to P88). An array of neurotransmitter‐specific genes, behavioral tests (i.e., reversal learning, prepulse inhibition, and open field), and postmortem brain structure using magnetic resonance imaging (MRI) and immunohistochemistry, were employed to assess persistent alterations in adult brain. Results: At P38, 24 hours after AE binge, many neurotransmitter genes, particularly cholinergic and dopaminergic, were reduced by ethanol treatment. Interestingly, dopamine receptor type 4 mRNA was reduced and confirmed using immunohistochemistry. Normal control maturation (P38 to P88) resulted in decreased neurotransmitter mRNA, e.g., an average decrease of 56%. Following AE treatment, adults showed greater gene expression reductions than controls, averaging 73%. Adult spatial learning assessed in the Morris water maze was not changed by AE treatment, but reversal learning experiments revealed deficits. Assessment of adult brain region volumes using MRI indicated that the olfactory bulb and basal forebrain were smaller in adults following AE. Immunohistochemical analyses found reduced basal forebrain area and fewer basal forebrain cholinergic neurons. Conclusions: Adolescent binge ethanol treatment reduces adult neurotransmitter gene expression, particularly cholinergic genes, reduces basal forebrain and olfactory bulb volumes, and causes a reduction in the density of basal forebrain acetylcholine neurons. Loss of cholinergic neurons and forebrain structure could underlie adult reversal learning deficits following adolescent binge drinking.     

Adult transition from at-risk drinking to alcohol dependence: the relationship of family history and drinking motives

Background:  Prospective studies have not previously examined whether a family history of alcoholism and drinking motives conjointly predict a diagnosed DSM-IV alcohol abuse or dependence in adults, despite a large literature that each is associated with alcohol consumption. The focus of this study is the conjoint, prospective examination of these risk factors in a 10-year longitudinal study of adults who were at-risk drinkers at baseline.
Methods:  Prospective, population-based cohort of drinkers aged 18 or older from a Northeastern U.S. area initially evaluated for history of alcohol use disorders and drinking motives in 1991 to 1992. New onset dependence was studied in those who never met the criteria for alcohol dependence at baseline ( n  = 423), and new onset abuse was studied in those who never met the criteria for alcohol abuse at baseline ( n  = 301) and who did not develop dependence during the follow-up.
Results:  Family history significantly interacted with 2 baseline drinking motives in predicting new onsets of DSM-IV alcohol dependence: drinking to reduce negative affect (OR 3.38; 95% CI 1.05, 10.9) and drinking for social facilitation (OR 3.88; CI 1.21, 12.5). Effects were stronger after conditioning the drinking motives on having a positive family history of alcoholism. In contrast, in predicting new onsets of alcohol abuse, drinking motives did not have direct effects or interact with family history.
Conclusions:  Those who drank to reduce negative affect or for social facilitation at baseline were at greater risk of alcohol dependence 10 years later if they also had a family history of alcoholism. These results suggest an at-risk group that can be identified prior to the development of alcohol dependence. Further, the findings suggest utility in investigating the interaction of drinking motives with measured genetic polymorphisms in predicting alcohol dependence.     

Early adult outcomes of adolescent binge drinking: person- and variable-centered analyses of binge drinking trajectories

BACKGROUND: Many studies of the consequences of binge drinking take a variable-centered approach that may mask developmentally different trajectories. Recent studies have reported qualitatively different binge drinking trajectories in young adulthood. However, analyses of developmental trajectories of binge drinking have not been examined for an important period of drinking development: adolescence. The purpose of this study was to examine young adult outcomes of adolescent binge drinking using an approach that combines person-centered and variable-centered methods. METHODS: Data were from the Seattle Social Development Project, an ethnically diverse, gender balanced sample (n = 808) followed prospectively from age 10 to age 21. Semiparametric group-based modeling was used to determine groups of binge drinking trajectories in adolescence. Logistic regression was used to examine how well the trajectory groups predicted young adult outcomes after demographics, childhood measures, and adolescent drug use were considered. RESULTS: Four distinct trajectories of binge drinking during adolescence were identified: Early Highs, Increasers, Late Onsetters, and Nonbingers. These trajectories significantly predicted positive and negative outcomes in adulthood after controlling for demographic characteristics, early proxy measures of the outcome, and adolescent drug use. CONCLUSIONS: This integrated person- and variable-centered approach provides more information about the effects of specific patterns of binge drinking than studies that employ variable-centered methods alone.     

Striatal dopamine release and family history of alcoholism

BACKGROUND: The offspring of alcohol-dependent individuals are at increased risk for alcoholism. The present study was designed to determine whether mesolimbic dopamine binding potential (BP), dopamine release, stress hormones, and subjective responses to intravenous amphetamine are different in nonalcoholic offspring from families with a history of alcohol dependence [family history positive (FHP)] than in nonalcoholic offspring without a family history of alcohol dependence [family history negative (FHN)]. METHODS: Participants were 41 healthy men and women (11 FHP, 30 FHN; age range 18-29). After completing baseline psychiatric symptom and personality measures, striatal D2/D3 dopamine BP and dopamine release in response to an amphetamine challenge were measured with positron emission tomography (PET) using the D2/D3 dopamine (DA) receptor radioligand [11C]raclopride. Binding potential was defined as Bmax/KD, percent change in BP from baseline defined dopamine release. During the scans, subjects rated the degree to which they were experiencing each of 10 possible drug effects. Plasma cortisol and growth hormone (GH) were also measured at scheduled intervals during the scans. RESULTS: Neither baseline BP nor dopamine release differed by family history. Similarly, subjective responses to amphetamine did not differ by a family history of alcoholism. Although both cortisol and GH increased following administration of amphetamine, these increases did not differ between family history groups. CONCLUSIONS: Using amphetamine to provoke mesolimbic dopamine, we did not show significant differences in dopamine release, subjective responses, or stress hormone measures as a function of family history of alcoholism.     

Lateral asymmetries in the frontal brain: effects of depression and a family history of alcoholism in female adolescents

BACKGROUND: Subtle electroencephalographic (EEG) abnormalities have been detected among subjects with depressed affect. The present study attempted to discern whether these abnormalities reflect a main effect or an interaction between depression and either of two family history variables--a family history of alcoholism or a family history of depression. METHODS: The subjects were 151 adolescent females, aged 14 to 20 years, of whom 58 met DSM-III-R diagnostic criteria for a lifetime history of a major depressive episode. The electroencephalogram was recorded from 31 electrode sites while the subjects sat relaxed, with their eyes open, for 5 min. RESULTS: Analyses of EEG data revealed that a personal history of depression and a family history of alcoholism had opposite effects on the EEG power spectrum. Depression was associated with an increase in alpha power (7.5-12.5 Hz). In contrast, a family history of alcoholism was associated with an increase in fast beta power (19-30 Hz) and a decrease in theta power (4-7 Hz). There were no significant main or interactive effects of a family history of depression. Current source density topographic analyses of the significant group differences in alpha and fast beta power demonstrated that the effects of depression could be localized to the right frontal brain, whereas the effects of a family history of alcoholism were localized to the left frontal area. CONCLUSIONS: The laterally opposite effects of depression and a family history of alcoholism suggest a high level of functional differentiation of the frontal brain. They also suggest that the different neurophysiological substrates of depression and familial risk can be distinguished through the use of modern methods of EEG source localization.     

Effects of cigarette smoking and family history of alcoholism on sweet taste perception and food cravings in women

BACKGROUND: Despite popular beliefs that smoking affects the sensitivity and liking of sweet-tasting foods and beverages, few psychophysical studies have examined this phenomenon and none have taken into account the individual's family history of alcoholism (FH+), a predictor of heightened sweet preferences. METHODS: A within- and between-subjects study was conducted to determine the effect of both cigarette smoking and an acute exposure to nicotine on sweet taste sensitivity and preferences in women. Two groups were studied on 2 days separated by 1 week: women who were current smokers (n = 27, 18 were FH+) and those who never smoked in their lifetime (n = 22, 9 were FH+). Current smokers smoked nicotine-containing cigarettes during 1 test session and nicotine-free cigarettes during the other. The procedures were identical during both test sessions for the group of never smokers, with the exception that they did not smoke. Two-alternative staircase methods and forced-choice tracking procedures were used to assess sucrose thresholds and preferences, respectively, during both test session. Standardized questionnaires were administered to assess food cravings as well as smoking and alcohol usage and dependence. The Family Interview for Genetic Studies was used to detect alcoholism according to the DSM III criteria for family members up to second-degree relatives. RESULTS: Acute exposure to nicotine did not affect sucrose detection thresholds or preferences, but smokers had significantly higher sucrose detection thresholds than never smokers. The greater the smoking dose in pack-years, the lower the sucrose sensitivity. Regardless of smoking status, women who were FH+ preferred significantly higher sucrose concentrations and craved sweets more often than women who were not. CONCLUSIONS: Both smoking and having a family history of alcoholism had differential effects on sweet taste. Smoking was associated with decreased sweet taste sensitivity whereas having a family history of alcoholism was associated with heightened sweet preferences. These findings suggests that future research on the effects of smoking on food habits and cravings should take into account family history of alcoholism given its association with sweet liking and the increased likelihood to develop a tobacco disorder.     

Course of DSM-IV alcohol dependence in a community sample: effects of parental history and binge drinking

BACKGROUND: The role of positive family history in the etiology of alcohol dependence has been demonstrated repeatedly but little is known about the effect of this risk factor on the chronicity of alcohol dependence once it has begun. METHODS: We studied the effects of parental and sibling history in conjunction with frequency of binge drinking in a sample of 169 community residents who met criteria for DSM-IV alcohol dependence at the baseline interview. Subjects were re-interviewed approximately 1 year later and the status of their alcohol-dependence disorders (remitted or chronic) was determined. RESULTS: Parental history of alcoholism was significantly related to chronicity of alcohol dependence, as was frequency of binge drinking. CONCLUSIONS: Failure to find an effect for family history on chronicity would have suggested that the effect was transient, perhaps interacting with time-limited environmental vulnerability. The finding of a positive relationship between family history and chronicity suggests that the relationship between familial/ genetic background and alcohol dependence is stable.     

Altered emotion-modulated startle in young adults with a family history of alcoholism

BACKGROUND: Alcoholism risk may be accompanied by poor regulation of emotions, signaling altered central nervous system processes. This study used the emotion-modulated startle paradigm to test the hypothesis that young adults with a positive paternal history of alcoholism (FH+), relative to family-history-negative persons (FH-), have altered emotional reactivity to environmental cues. METHODS: We tested 30 FH+ and 30 FH-, 15 males and 15 females in each group. Participants completed self-report instruments and interviews and had eye blink electromyograms (EMG) measured to acoustic startle probes while viewing color photographs rated as affectively pleasant, neutral, and unpleasant. RESULTS: FH- had the expected linear increase in startle magnitude, with eye blink EMG gaining in strength (F = 18, p < 0.0002) from pleasant to neutral to unpleasant slides. In contrast, FH+ did not show EMG potentiation to the unpleasant slides and therefore lacked the same linear trend (F < 1, p > 0.4). Notably, FH groups rated the emotional valence and arousal of the photographs in similar ways. Self-reported negative affect partly accounted for the lack of startle potentiation in FH+, suggesting that startle modulation differences between the groups may be associated with underlying psychological characteristics. CONCLUSIONS: These findings implicate altered limbic outputs to the startle pathway in FH+ despite normal conscious evaluation of emotional arousal and pleasantness of the slides. This method may provide a useful paradigm for testing processing of emotionally relevant stimuli in relation to risk for alcohol use disorders.     

Sleep following alcohol intoxication in healthy, young adults: effects of sex and family history of alcoholism

Background: This study evaluated sex and family history of alcoholism as moderators of subjective ratings of sleepiness/sleep quality and polysomnography (PSG) following alcohol intoxication in healthy, young adults. Methods: Ninety‐three healthy adults [mean age 24.4 ± 2.7 years, 59 women, 29 subjects with a positive family history of alcoholism (FH+)] were recruited. After screening PSG, participants consumed alcohol (sex/weight adjusted dosing) to intoxication [peak breath alcohol concentration (BrAC) of 0.11 ± 0.01 g% for men and women] or matching placebo between 20:30 and 22:00 hours. Sleep was monitored using PSG between 23:00 and 07:00 hours. Participants completed the Stanford Sleepiness Scale and Karolinska Sleepiness Scale at bedtime and on awakening and a validated post‐sleep questionnaire. Results: Following alcohol, total sleep time, sleep efficiency, nighttime awakenings, and wake after sleep onset were more disrupted in women than men, with no differences by family history status. Alcohol reduced sleep onset latency, sleep efficiency, and rapid eye movement sleep while increasing wakefulness and slow wave sleep across the entire night compared with placebo. Alcohol also generally increased sleep consolidation in the first half of the night, but decreased it during the second half. Sleepiness ratings were higher following alcohol, particularly in women at bedtime. Morning sleep quality ratings were lower following alcohol than placebo. Conclusions: Alcohol intoxication increases subjective sleepiness and disrupts sleep objectively more in healthy women than in men, with no differences evident by family history of alcoholism status. Evaluating moderators of alcohol effects on sleep may provide insight into the role of sleep in problem drinking.     

A new measure of binge drinking: prevalence and correlates in a probability sample of undergraduates

BACKGROUND: A standard measure defines binge drinking as the consumption of 5 or more drinks in a row for men (4 or more drinks for women) on at least 1 occasion during the past 2 weeks. A revised operational definition of binge drinking was developed by the National Institute on Alcohol Abuse and Alcoholism in 2004 and incorporated the duration of the drinking episode in addition to the quantity of alcohol consumed. This study compares the standard and new binge measures for overall and subgroup prevalence rates; associations with gender, race/ethnicity, and age of drinking onset; and associations with negative drinking consequences. METHODS: A probability sample of 4,580 randomly selected college students (50.3% female, M age=19.9, SD=2.0) at a large Midwestern university in the United States completed a Web-based survey of alcohol and other drug use. Participants reported on past 2-week binge drinking using the standard measure and past-year binge drinking using the new measure. RESULTS: The longer past-year time frame of the new measure yielded a higher prevalence estimate of binge drinking (63.6%) compared with the 2-week standard measure (53.2%). Approximately 9.9% of those who were classified as binge drinkers using the 2-week standard measure were classified as non-binge drinkers using the new measure specification of a 2-hour duration for the drinking episode. The past-year new binge measure was positively associated with negative drinking consequences even when the 2-week measure was statistically controlled. CONCLUSIONS: Using a longer time frame and incorporating the duration of the drinking episode, the new measure of binge drinking appears to capture an important element of risky alcohol involvement in college students that is not fully assessed by the standard measure.     

Healthy subjects with a family history of alcoholism show increased stimulative subjective effects of alcohol

Background: Research has shown that subjects with a family history positive (FHP) of alcoholism are at increased risk for alcoholism and that this group reacts differently to alcohol than family history negative (FHN) subjects. These different levels of sensitivity may make FHP persons more likely to consume alcohol. Here, we tested the hypothesis that subjects FHP for type 1 alcoholism (according to Cloninger) are more sensitive than control subjects to the stimulative, properties of alcohol following a single moderate dose of alcohol. Methods: Fifty‐one healthy men and women (22 FHP and 29 FHN) participated in 2 laboratory sessions, in which they consumed a beverage containing ethanol (0.6 g/kg in juice) or placebo (juice alone) in a randomized order. Primary dependent measures were self‐report questionnaires of mood states. Results: Subjects with family history of type 1 alcoholism showed increased stimulative responses and an elevated positive mood state after ethanol compared to controls. Conclusions: At this moderate dose, ethanol increased stimulative subjective responses in individuals who were “family history positive.” This enhanced sensitivity could motivate to exaggerated drinking and thereby increase the risk for developing alcoholism.     

Risky decision-making: an FMRI study of youth at high risk for alcoholism

Background: Adolescents with a family history of alcoholism (FHP) are at risk for developing an alcohol use disorder (AUD), and some studies indicate that FHP individuals show deficits in executive functioning. The ability to make adaptive decisions is one aspect of successful executive functioning that is often measured during risk‐taking tasks; however, this behavior has not been examined in FHP youth. As impaired decision‐making could predispose FHP youth to make poor choices related to alcohol use, the current study examined the neural substrates of risk‐taking in FHP adolescents and their family history negative (FHN) peers. Methods: Thirty‐one (18 FHP, 13 FHN) youth between 13 and 15 years old were included in this study. All youth had used little to no alcohol prior to study involvement. Functional magnetic resonance imaging was used to examine the neural substrates of risk‐taking during the Wheel of Fortune (WOF) decision‐making task ( Ernst et al., 2004 ) in FHP and FHN youth. Results: FHP youth did not differ from FHN youth in risk‐taking behavior, but showed less brain response during risky decision‐making in right dorsolateral prefrontal cortex and right cerebellar regions compared with FHN peers. Conclusions: Despite no behavioral differences on the WOF decision‐making task, FHP youth exhibited atypical neural response during risk‐taking compared with FHN peers. Atypical brain activity, in regions implicated in executive functioning could lead to reduced cognitive control, which may result in risky choices regarding alcohol use. This could help explain the higher rates of AUDs seen in FHP adolescents. Further examination of risky behavior and associated brain response over the course of adolescence is necessary to characterize the vulnerabilities of FHP youth in the absence of alcohol abuse.     

Parental history of alcoholism and problem behaviors in Native-American children and adolescents

BACKGROUND: A positive family history of alcoholism is one of the most consistent and powerful predictors of a person's risk for developing this disorder. This finding has stimulated much research on etiological vulnerability factors and mechanisms by which children of alcoholic parents are at high risk for developing alcohol-related problems. In primarily Euro-American samples, parental alcoholism has been associated with a variety of negative outcomes for children and adolescents, including problematic behavior. Native-American Indians, in addition to high rates of alcoholism and alcohol-related mortality, have the highest prevalence of a positive family history for alcoholism of all ethnic groups in the United States. METHODS: This study used the Achenbach Child Behavior Checklist (CBCL) to evaluate behavioral problems in 96 Mission Indian children and adolescents based on the presence or absence of parental alcohol dependence and sex of the offspring. RESULTS: Consistent with previous research, results indicated a high prevalence of a positive family history of alcoholism in these Native-American youths. Seventy-four percent of the offspring had either one or both parents with alcohol dependence (children of alcoholics). Only 7% had no first- or second-degree alcoholic relatives. Results indicated that sons of alcoholics scored significantly higher on the Total Behavior Problem scale, as well as the Internalizing and Externalizing scales, of the CBCL than sons of nonalcoholics, whereas there were no significant differences in CBCL scores between daughters of alcoholics and daughters of nonalcoholics. It is noteworthy that scores on the CBCL for Mission Indian children of alcoholics were comparable to scores in the published literature of children of alcoholics of other ethnicities. In addition, a relatively low percentage of youths were identified with significant levels of behavioral problems. CONCLUSIONS: These findings suggest that sons of alcoholics of Mission Indian heritage experience more problems than sons of nonalcoholics, but also suggest that Mission Indian children of alcoholics are not more vulnerable to behavioral problems than children of alcoholic parents of other ethnic backgrounds.     

Subjective perceptions associated with the ascending and descending slopes of breath alcohol exposure vary with recent drinking history

Background: The differentiator model predicts that individuals with a positive family history of alcoholism (FHA) or heavy alcohol consumers will feel more sensitive to the effects of alcohol on the ascending phase of the blood alcohol content while feeling less sedated on the descending phase. This study tested whether subjective perceptions are sensitive to the slope of breath alcohol concentration (BrAC) and whether that sensitivity is associated with an FHA and/or recent drinking history (RDH). Methods: Family‐history‐positive (FHP, n = 27) and family‐history‐negative (FHN, n = 27) young adult nondependent drinkers were infused intravenously with alcohol in 2 sessions separated by 1 week. After 20 minutes, one session had an ascending BrAC (+3.0 mg%/min), while the other session had a descending BrAC (?1 mg%/min). The BrAC for both sessions at this point was approximately 60 mg%, referred to as the crossover point. Subjective perceptions of intoxication, high, stimulated, and sedation were sampled frequently and then interpolated to the crossover point. Within‐subject differences between ascending and descending responses were examined for associations with FHA and/or RDH. Results: Recent moderate drinkers reported increased perceptions of feeling intoxicated (p < 0.023) and high (p < 0.023) on the ascending slope compared with the descending slope. In contrast, recent light drinkers felt more intoxicated and high on the descending slope. Conclusions: Subjective perceptions in young adult social drinkers depend on the slope of the BrAC when examined in association with RDH. These results support the differentiator model hypothesis concerning the ascending slope and suggest that moderate alcohol consumers could be at risk for increased alcohol consumption because they feel more intoxicated and high on the ascending slope. Subjects did not feel less sedated on the descending slope, contrary to the differentiator model but replicating several previous studies.     

ADH1B polymorphism, alcohol consumption, and binge drinking in Slavic Caucasians: results from the Czech HAPIEE study

Background: Several genetic polymorphisms influence the risk of heavy alcohol consumption but it is not well understood whether the genetic effects are similar in different populations and drinking cultures, nor whether the genetic influences on binge drinking are similar to those seen for alcoholism. Methods: We have analyzed the effect of the Arg47His (rs1229984) variant within the alcohol dehydrogenase (ADH1B) gene on a range of drinking related variables in a large Eastern European Slavic population (Czech HAPIEE study), which recruited random samples of men and women aged 45–69 years in 7 Czech towns (3,016 males and 3,481 females with complete data). Drinking frequency, annual alcohol intake, prevalence of binge drinking (≥100 g in men and ≥60 g in women at least once a month) and the mean dose of alcohol per occasion were measured by the graduated frequency questionnaire. Alcohol intake in a typical week was used to define heavy drinking (≥350 g/wk in men and ≥210 g in women). Problem drinking (≥2 positive answers on CAGE) and negative consequences of drinking on different aspects of life were also measured. Results: The frequency of the His47 allele carriers was 11%. Homozygotes in the common allele (Arg47Arg), among both males and females, had significantly higher drinking frequency, and annual and weekly intake of alcohol than His47 carriers. The odds ratio of heavy drinking in Arg47Arg homozygotes versus His47 carriers was 2.1 (95% confidence intervals 1.1–3.2) in men and 2.2 (1.0–4.7) in women. In females, but not in males, Arg47Arg homozygotes had marginally significantly higher prevalence of binge drinking and mean alcohol dose per drinking session. There was no consistent association with problem drinking and negative consequences of drinking. Conclusions: The ADH1B genotype was associated with the frequency and volume of drinking but its associations with binge drinking and problem drinking were less consistent.     

Familial transmission of alcoholism among nonalcoholics and mild, severe, and dyssocial subtypes of alcoholism

BACKGROUND: In the field of alcohol studies, there are many typologies attempting to reduce the heterogeneity of expression of this complex disorder to better understand its natural history and etiology. However, few typologies have included empirical assessment of the degree of familial liability. To the extent there is variability in genetic vulnerability to alcoholism, inclusion of measures of this variability in proposed typologies is important to their validity and utility. We test whether the mild, severe, and dyssocial typology distinguished cases of alcohol dependence with high familial liability from those with low familial liability to alcoholism. METHODS: Data came from the National Longitudinal Alcohol Epidemiologic Survey-1992, a household probability sample representative of those 18 years of age and older in the contiguous US Response rate was 92%. Only whites were included here because the typology under study has been successfully applied to this race/ethnic group only. The total number of respondents were 32,447 and included 13,825 men and 18,622 women. Identification of a biological relative as alcoholic was based on the proband's report. All analyses were weighted to adjust for sampling under a multistage stratified design. RESULTS: Familial density of alcoholism (number of alcoholics/number of adult family members) substantially differed by proband alcohol dependence status for both men and women (male probands-nonalcoholics 7%, mild 13%, severe 25%, dyssocial 19%; female probands-nonalcoholics 8%, mild 18%, severe 33%, dyssocial 24%; p <.001). Cross-fostering analysis of the probands with adoptive/stepparents indicated little difference between nonalcoholic and mild alcoholic probands and suggests greater influence of biological parents for severe subtype probands compared to other probands. CONCLUSIONS: These results suggest construct validity for the alcoholism typology as distinguishing subtypes with differing degrees of familial liability to alcoholism. The typology may be useful when employing an extreme comparison strategy in genetic studies of alcohol dependence.     

Item response theory analysis of binge drinking and its relationship to lifetime alcohol use disorder symptom severity in an American Indian community sample

Background: Item response theory (IRT) has been used to examine alcohol use disorder (AUD) symptoms and their psychometric properties but has not been previously applied to AUD symptoms from an American Indian sample. Methods: Lifetime DSM‐IV AUD symptoms and binge drinking (5+ drinks men/4+ drinks women) at ≥1, ≥4, ≥8, and ≥15 days per month during the period of heaviest lifetime drinking criteria were assessed in 530 American Indian participants. Exploratory factor analysis was used to examine the factor structure of the 10 AUD symptoms and each alcohol consumption criterion. Two‐parameter IRT models generated marginal maximum likelihood estimates for discrimination (a) and threshold (b) parameters for 10 DSM‐IV AUD symptoms and each consumption criterion. Differential item functioning (DIF) analysis was used to assess AUD symptom severity in groups defined by gender and age at interview. Results: The AUD symptoms of “Withdrawal” and “Activities Given Up” were the most severe symptoms. “Tolerance” and “Social/Interpersonal Problems” were the least severe. All AUD symptoms fell on the moderate portion of the severity continuum, except “Withdrawal,” which fell at the lower end of the severe portion. The consumption criterion of 5+/4+ (male/female) at ≥8 times per month demarcated the portion of the severity continuum where AUD symptoms began to occur at a probability of 50%. DIF analysis showed significant gender and age at interview differences for “Hazardous Use,”“Tolerance,” and “Activities Given Up,” but not for the other AUD symptoms. Conclusions: In this American Indian community sample, alcohol abuse and dependence did not represent distinct disorders. Only one AUD symptom was found outside the moderate portion of the underlying AUD severity continuum. Drinking 5+/4+ (male/female) drinks at a frequency of ≥8 times per month during the period of heaviest lifetime drinking was found to function well as both a risk and a diagnostic criterion for lifetime DSM‐IV AUD. DSM‐IV AUD symptom criteria, as currently assessed, may be limited in their ability to capture the full range of symptom severity of AUDs, at least in this high‐risk population.