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Understanding Alcohol Abuse Symptoms

The study investigates a theoretical model linking five predictors to alcohol abuse and dependence symptoms among college students. It finds that social norms, perceived utility of alcohol, and family history of alcohol problems indirectly influence alcohol consumption, while poor behavioral control and affective lability have direct effects on abuse and dependence symptoms. The research highlights the importance of understanding these distinct psychological mechanisms for preventing alcohol-related issues in college populations.

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0% found this document useful (0 votes)
7 views24 pages

Understanding Alcohol Abuse Symptoms

The study investigates a theoretical model linking five predictors to alcohol abuse and dependence symptoms among college students. It finds that social norms, perceived utility of alcohol, and family history of alcohol problems indirectly influence alcohol consumption, while poor behavioral control and affective lability have direct effects on abuse and dependence symptoms. The research highlights the importance of understanding these distinct psychological mechanisms for preventing alcohol-related issues in college populations.

Uploaded by

bharathymahesh20
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

NIH Public Access

Author Manuscript
Psychol Addict Behav. Author manuscript; available in PMC 2010 September 1.
Published in final edited form as:
NIH-PA Author Manuscript

Psychol Addict Behav. 2009 September ; 23(3): 415–427. doi:10.1037/a0016003.

Alcohol Abuse and Dependence Symptoms: A Multidimensional


Model of Common and Specific Etiology

Jeffrey S. Simons,
The University of South Dakota
Kate B. Carey, and
Syracuse University
Thomas A. Wills
Albert Einstein College of Medicine of Yeshiva University

Abstract
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This study tested a theoretical model hypothesizing differential pathways from five predictors to
alcohol abuse and dependence symptoms. The participants were college students (N= 2,270)
surveyed on two occasions in a 6-month prospective design. Social norms, perceived utility of alcohol
use, and family history of alcohol problems were indirectly associated with Time 2 (T2) abuse and
dependence symptoms through influencing level of alcohol consumption. Poor behavioral control
had a direct effect on alcohol abuse but not dependence symptoms at T2, whereas affective lability
exhibited a direct prospective effect on alcohol dependence but not abuse symptoms. A multigroup
analysis showed that high levels of poor control increased the strength of paths from both
consumption level and affective lability to abuse symptoms. Implications for prevention of alcohol
problems among college students are discussed.

Keywords
Alcohol abuse and dependence; self-control; affect regulation; etiology

This study tests a theoretical model positing that alcohol abuse and dependence have
differential relationships with five conceptual domains of variables: affective lability, poor
NIH-PA Author Manuscript

behavioral control, social norms, personal utility of alcohol use, and family history of alcohol
problems. Alcohol-related problems are multifaceted with a complex etiology and course
(American Psychiatric Association, 2000; Baer, 2002; Schulenberg & Maggs, 2002).
Understanding alcohol use and misuse requires identifying factors that support the initiation
and maintenance of alcohol use patterns, account for the plasticity of behavior while intoxicated
(e.g., type and likelihood of abuse symptoms, negative consequences), and contribute to
progression to alcohol dependence (Edwards, 1974, 1986; Jackson, Sher, & Park, 2005;
Leonard & Blane, 1999; Zucker, 1994). Our theory suggests that alcohol consumption and

Jeffrey S. Simons, Ph.D. Department of Psychology The University of South Dakota 414 E. Clark Street, Vermillion, SD 57069 Office:
(605) 677-5353 Fax: (605) 677-3195 jsimons@[Link] Correspondence concerning this article should be addressed to Jeffrey S. Simons,
Department of Psychology, The University of South Dakota, 414 East Clark St., Vermillion, SD 57069. Electronic mail may be sent to
jsimons@[Link]. .
Publisher's Disclaimer: The following manuscript is the final accepted manuscript. It has not been subjected to the final copyediting,
fact-checking, and proofreading required for formal publication. It is not the definitive, publisher-authenticated version. The American
Psychological Association and its Council of Editors disclaim any responsibility or liabilities for errors or omissions of this manuscript
version, any version derived from this manuscript by NIH, or other third parties. The published version is available at
[Link]/journals/adb.
Simons et al. Page 2

symptoms of abuse and dependence arise, in part, from theoretically distinct psychological
mechanisms. Examining these mechanisms in a multivariate model can improve our
understanding of these constructs, their etiology, and course.
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Alcohol Abuse and Dependence


Alcohol-related problems have historically been divided into abuse symptoms (e.g., associated
adverse consequences, conduct problems) and dependence symptoms (e.g., compulsive use
behavior, craving, withdrawal, tolerance). The distinction between abuse and dependence as
qualitatively distinct constructs has an extensive background (Edwards, Gross, Keller, &
Moser, 1976) and this qualitative distinction has been supported by factor analytic studies in
adolescent and adult samples (Grant et al., 2007; Harford & Muthen, 2001; Wills et al.,
2002). Furthermore, though results have been mixed, the dimensions have been differentially
associated with variables such as alcohol consumption and family history of alcohol problems,
both being more strongly related to dependence than to abuse (Hasin, van Rossem, McCloud,
& Endicott, 1997; Knight et al., 2002; Schuckit & Smith, 2001).

However, recent studies using item response theory have focused on identifying a
unidimensional model of alcohol problem severity (Martin, Chung, Kirisci, & Langenbucher,
2006; Saha, Chou, & Grant, 2006). This research indicates that some symptoms are not
uniformly predictive of degree of alcohol involvement across demographic groups, suggesting
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that they are indicators of another related process instead of alcohol problem severity. For
example, abuse symptoms of hazardous use, legal problems, and getting in physical fights are
more likely to be endorsed by men than women, and represent less severe alcohol involvement
for men (Kahler & Strong, 2006; Martin et al., 2006). These symptoms may be indicators of
self-control deficits rather than specific symptoms of alcohol use disorder (Martin et al.,
2006; Mason & Windle, 2002). Recently, Martin and colleagues have suggested that alcohol
use disorder be defined by a single dimension of alcohol dependence and that clinically
significant, but non-criterion, associated consequences be described and possibly shifted to V
codes in the DSM-V (Martin, Chung, & Langenbucher, 2008). They argue that these associated
consequences (e.g., some problem behavior symptoms) should not be considered a disorder or
criterion symptoms. This differentiation between alcohol use disorder and associated
consequences is particularly relevant to the study of alcohol-related problems in college
students. For many college students, heavy alcohol use and associated consequences appear to
be a time-limited developmental process that may be a function of the unique social and
environmental factors of college (Schulenberg et al., 2001; Schulenberg & Maggs, 2002).
Students often have new-found levels of freedom, limited social responsibilities, and are in an
environment where alcohol is often readily available, and its use (at times heavy use) is socially
promoted.
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In summary, both multidimensional factor models and unidimensional item response models
suggest that some abuse symptoms represent a potentially different type of alcohol-related
problem that may be qualitatively different from level of alcohol involvement and dependence.
College students may exhibit patterns of hazardous drinking and associated problems that,
while risky, may not be signs of an alcohol disorder per se. This underscores the importance
of examining psychological mechanisms specific to the development of alcohol abuse (i.e.,
negative consequences) or dependence, independent of their common association with heavy
alcohol consumption.

Affective Lability and Alcohol Dependence


Affective lability may be differentially associated with alcohol abuse and dependence.
Affective lability refers to the frequency, speed, and range of changes in affective states. The
affective processing model of negative reinforcement posits that fluctuation in negative affect

Psychol Addict Behav. Author manuscript; available in PMC 2010 September 1.


Simons et al. Page 3

is the core mechanism driving substance dependence (Baker, Piper, McCarthy, Majeskie, &
Fiore, 2004). This model integrates the role of both “external” (e.g., stress) and “internal” (e.g.,
withdrawal) sources of negative affect in influencing cognitive processing, creating response
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biases, and as a stimulus for drug consumption. The model suggests that subtle withdrawal
symptoms (e.g., hangover) can occur relatively early in a use trajectory and are important initial
determinants of continued use behavior. Repeated use and withdrawal cycles sensitize the
individual to stimuli that signal negative affect. At low levels of negative affect, early signals
of impending negative affect or signs of dropping levels of the drug may be detected and
motivate drug use outside of conscious awareness. In contrast, high levels of negative affect
promote “hot” information processing (Metcalfe & Mischel, 1999). The “hot” system is
characterized as an emotion-based, reflexive system, optimized for quick processing and
stimulus response. High negative affect is posited to reduce deliberative cognitive control
processes and create strong response biases, which greatly increase the incentive value of drug
use and decrease the incentive value of non-drug alternatives. Importantly, negative affect
driving this process and influencing cognitive processing and responses may arise from either
acute withdrawal or other external or internal determinants of negative affective states.

Given the importance of sensitization to negative affective states, high levels of negative affect,
and rapid changes in negative affect in this model, we propose that individuals characterized
by high levels of affective lability are at increased risk for the compulsive drinking patterns
characteristic of dependence. Although lability per se is not central to Baker and colleagues’
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model, lability is positively associated with negative affectivity and fluctuation in negative
affective states that are central to the negative reinforcement model. Indeed, affective lability
was significantly associated with alcohol dependence but not abuse symptoms in an inpatient
substance use treatment sample (Simons, Oliver, Gaher, Ebel, & Brummels, 2005c). For
college students, affective lability is frequently unrelated or negatively associated with level
of drinking but is positively associated with composite measures of alcohol-related problems
(Simons & Carey, 2006; Simons, Gaher, Correia, Hansen, & Christopher, 2005a). We
hypothesized that affective lability is a factor contributing specifically to the development of
a pattern of consumption indicative of alcohol dependence.

Poor Control and Alcohol Abuse


Poor control of behavior (e.g., impulsivity) has been linked to alcohol use in several populations
(Brody & Ge, 2001; Miller & Brown, 1991; Patock-Peckham, Cheong, Balhorn, & Nagoshi,
2001), and here we propose that it will increase the conduct problems characteristic of alcohol
abuse. Poor behavioral control is characterized by lack of restraint, planning, and forethought;
exhibiting premature responding and poor delay of gratification; difficulty in fitting behavior
to situational demands; and failure to consider risks (Daruna, Barnes, McCown, Johnson, &
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Shure, 1993; Plutchik & Van Praag, 1995; Wills, Walker, Mendoza, & Ainette, 2006). Poor
control may lead to a variety of deleterious outcomes as behavior may be governed more by
immediate “hot” cognition and relatively less by deliberative controlled processing of distal
consequences (Carver, 2005; Metcalfe & Mischel, 1999). Problems such as interpersonal
conflict, assault and other illegal behavior, and neglecting social responsibilities all occur at
increased rates among people characterized by impulsiveness and poor control (Carver,
2005; Mason & Windle, 2002; Sher & Trull, 1994; Wills & Dishion, 2004). Whereas alcohol
intoxication may increase the likelihood of these behaviors, poor control may also increase the
likelihood of these behaviors independent of consumption. We hypothesized that poor control
is a factor contributing to abuse symptoms, independent of level of alcohol consumption.

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Simons et al. Page 4

Moderation Effects of Poor Control


Both alcohol intoxication and the heightened emotional arousal associated with labile affect
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can reduce deliberative cognitive control processes (Baker et al., 2004; Curtin & Fairchild,
2003; Fillmore, Carscadden, & Vogel-Sprott, 1998; Metcalfe & Mischel, 1999; Steele &
Josephs, 1990). Consequences of such reduced deliberative control effects may be most
pronounced among individuals with a high level of poor control. The affective processing
model of dependence discussed above posits that heightened negative affect reduces conscious
cognitive control processes leading to compulsive consumption. Poor control may amplify this
process due to pre-existing deficits in deliberative cognitive processing. For example, though
support has been mixed, some research suggests that poor control may increase associations
between affective lability and alcohol problems as well as negative affect and both heavy use
and problems (Hussong, Hicks, Levy, & Curran, 2001; Simons, Carey, & Gaher, 2004; Simons
et al., 2005b). Affective lability and poor behavioral control are moderately to strongly
correlated and thus may be expected to have some common effects on both abuse and
dependence (Simons & Carey, 2006; Wills et al., 2006). Thus, we are not proposing that there
should be a clear demarcation of associations. For example, in addition to poor control, lability
may be relevant to interpersonal conflicts or assault characteristic of abuse. Such effects may
be most pronounced in individuals with a higher level of poor control.

Similarly, some alcohol-related problems including both abuse and dependence symptoms may
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derive, in part, from an effect of alcohol for reducing information processing and cognitive
control processes, hence narrowing response options and increasing focus on immediate cues
(Baker et al., 2004; Curtin & Fairchild, 2003; Fillmore et al., 1998; Metcalfe & Mischel,
1999; Steele & Josephs, 1990). Poor control may amplify this process as well. Poor control
has been found to moderate the relationship between alcohol use and related problems,
increasing the strength of associations (Neal & Carey, 2007; Simons et al., 2005b), and research
has provided some evidence of greater moderating effects of poor control on the relationship
between substance use and abuse rather than dependence symptoms (Wills et al., 2002).

Indirect Predictors of Problems via Alcohol Consumption


While affective lability and poor behavioral control may be particularly relevant for the
development of abuse and dependence symptoms, it should be recognized that alcohol
consumption among college students is a highly social activity (Schulenberg & Maggs,
2002). Socio-cultural factors such as social norms, fraternity/sorority membership, or
perceived utility of alcohol for attaining personal goals are important factors supporting the
initiation and maintenance of drinking patterns (Park, Sher, & Krull, 2008; Read, Wood,
Kahler, Maddock, & Palfai, 2003; Simons & Carey, 2006). The associations of these factors
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with problems are often indirect, through influencing level of consumption, rather than directly
predictive of use-related problems (Read et al., 2003; Simons & Carey, 2006; Wills et al.,
2002).

In addition, several studies have observed elevated rates of alcohol use disorders and alcohol-
related problems among children of alcoholics (Jackson, O’Neill, & Sher, 2006; Kushner &
Sher, 1993; Perkins & Berkowitz, 1991; VanVoorst & Quirk, 2003). Among adolescents, the
association between family history and alcohol problems is mediated by level of alcohol use
(Stice et al., 1998). Recent longitudinal research with adolescents revealed that family history
of alcoholism was positively associated with trajectory groups defined by either adolescent-
limited problem drinking or escalating (into adulthood) problem drinking, compared with a
low- or no-problem-drinking group (Warner, White, & Johnson, 2007). However, family
history did not differentiate the two problem drinking groups. Family history may be associated

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Simons et al. Page 5

primarily with rates of drinking rather than a specific risk for developing a persistent alcohol
use disorder.
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Present Research
This prospective study tested antecedents and moderators of alcohol consumption, abuse, and
dependence. Some variables (alcohol norms, utility, and family history) were hypothesized to
act primarily by promoting a higher level of alcohol consumption, itself a risk factor for abuse
or dependence. Other variables (affective lability, poor behavioral control) were hypothesized
to have direct effects to abuse or dependence symptomatology. In addition, poor control was
hypothesized to moderate the effects of several other variables. A heuristic model of the
primary hypotheses is presented in Figure 1.

Methods
Participants
Participants were 2270 college students recruited from a state university. Women made up
64% of the sample. The sample ranged in age from 18-25 years (M = 19.59, SD = 1.51). Ninety-
four percent of the participants were White, 1% Asian, 1% Black, 1% Native American/
Alaskan Native, and 3% other or did not respond. Ninety-eight percent were non-Hispanic.
These demographic characteristics are comparable to the university population (Regents
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Information Systems, 2006). Participants were recruited through e-mail, fliers, and
advertisements in the student newspaper. The study was described as a study of emotions,
personal goals, and alcohol and other risk behavior. All enrolled undergraduates were eligible
for recruitment. Eighty-seven percent of the baseline sample returned for a 6-month follow-up
(T2), and 94% of returning participants were successfully matched to their baseline (T1) data.
Missing data were replaced as needed by best subsets regression imputation using the Stata
9.0 impute module using existing Time 1 (T1) or Time 2 (T2) data as predictors (StataCorp,
2005). Specifically, partially completed scales had items imputed before creating total scores
and scale scores required for defining the analysis groups (i.e., poor control and T2 six-month
drinking) were imputed. However, the structural equation models were conducted with missing
data modeled through Full Information Maximum Likelihood (FIML; (Enders & Bandalos,
2001; Muthen & Muthen, 2006). One previous manuscript has been published from this dataset
(Simons, Dvorak, & Batien, 2008).

Procedure
Participants completed on-line questionnaires under the supervision of a research assistant.
Participants had adequate space to protect their privacy and provided informed consent for
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participation. Participation took approximately 45 minutes. The study was approved by the
human subjects institutional review board. Responses were identified by a user-defined code,
ensuring participants’ anonymity. Participants received $20 for the baseline assessment and
$30 for a 6-month follow-up assessment. Average time interval was 203 days (SD = 50.35).

Measures
Alcohol consumption was assessed by three indicators. First, the Modified Daily Drinking
Questionnaire (DDQ-M; Dimeff, Baer, Kivlahan, & Marlatt, 1999) consisted of a grid
representing the seven days of the week. The grid assessed participants’ typical daily alcohol
consumption for a typical week during the last six months. Weekly consumption was calculated
by summing the number of standard drinks (one standard drink is equal to 12 oz. beer, 5 oz.
wine, or 1.5 oz. liquor) across the number of drinking days reported by the participant. Second,
frequency of use of alcohol in the past six months was assessed with a 9-point anchored rating
scale (0 = no use, 8 = more than once a day). Third, quantity of alcohol consumed per drinking

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day in the last six months was assessed by an 11-point scale (0 = no drinks [i.e., non-drinker],
10 = 19 or more drinks). This scale was adapted from (Dimeff, Baer, Kivlahan, & Marlatt,
1999). The DDQ-M, the frequency rating scale, and the quantity rating scale were indicators
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of an alcohol consumption latent variable.

Abuse and dependence symptoms in the last 6 months were assessed by a DSM-IV alcohol
abuse and dependence symptom checklist (Knight et al., 2002). The 10-item abuse checklist
assesses each abuse symptom with multiple items, resulting in a summary score that ranges
from 0 – 4 indicating the number of DSM-IV abuse symptoms endorsed. Dependence
symptoms were assessed by a 7-item checklist corresponding to DSM-IV criteria (Knight et
al., 2002). These have been used previously with college students and have expected
associations with alcohol-related variables (Knight et al., 2002).

Affective lability was a latent variable assessed by three indicators derived from subscales of
the Affective Lability Scale – Short form (Oliver & Simons, 2004). Items are rated on 4-point
scales (1) Very Undescriptive - (4) Very Descriptive; sample item: “I switch back and forth
between being extremely energetic and having so little energy that it’s a huge effort just to get
where I am going.” The three subscales assess affective lability in respect to depression/elation
(8 items, α = .87), anxiety/depression (5 items, α = .86) and anger (5 items, α = .83).

Poor control was a latent variable assessed by three indicators. First, seven items from the
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Eysenck impulsivity scale I7 (Eysenck, Pearson, Easting, & Allsopp, 1985) assessing difficulty
in controlling behavior (α = .75). Sample item; “Do you generally do and say things without
stopping to think”. In addition, two scales were derived from a measure of self-regulation
(Kendall & Williams, 1982); impatience (three items, e.g., “I have to have everything right
away,” α = .52) and distractibility (6 items, e.g., “I like to switch from one thing to another,”
α = .81). Items are rated on 5-point scales (1) = Not At All True Of Me, (5) = Very True Of
Me. Previous studies indicate that these measures of impulsivity, impatience, and distractibility
form a replicable subscale structure and load significantly on a factor of poor control (Wills et
al., 2001; Wills et al., 2002; Wills & Stoolmiller, 2002). High scores indicate poor behavioral
control.

Social norms was a latent variable assessed by three indicators: (a) Number of friends who
drink alcohol (7-point anchored rating scale [0] none – [6] all); (b) Friends’ attitude toward
participant using alcohol once a week or more (9-point anchored rating scale [1] Strongly
disapprove – [9] Strongly approve); (c) Friends’ attitude toward participant getting drunk (9-
point anchored rating scale [1] Strongly disapprove – [9] Strongly approve).

Alcohol use utility was a latent variable defined by five indicators. Personal strivings are “goals
that lie directly behind individuals’ behavioral choices” (Emmons & King, 1988), and are
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relatively stable in college students (Emmons, 1989). In the assessment, the participant first
lists 10 personal strivings, each representing “an objective you are typically trying to
accomplish.” The remainder of the assessment focuses on the five strivings that the participant
identifies as most descriptive. The five strivings were entered into a matrix that included five
columns that represent levels of alcohol use (1) abstinence - (5) most every day. The participant
rates the extent to which each level of use would help or hinder the attainment of each personal
striving using a 5-point scale (−2= very harmful effect, +2 = very helpful effect). An alcohol
use utility score was created for each personal striving (reverse scoring the abstinence column)
and these five scores were indicators of the latent alcohol use utility variable. The resulting
utility score reflects both individual differences in types of valued goals as well as individual
differences in perceived utility of substance use for goal attainment (Simons & Carey, 2003;
Simons, Christopher, Oliver, & Stanage, 2006).

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Family history of alcohol problems was assessed by 9-item versions of the Short Michigan
Alcohol Screening Test (SMAST) that have been adapted to assess participants’ biological
father’s (F-SMAST) and mother’s (M-SMAST) alcohol abuse (Crews & Sher, 1992). The
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correlation between the 9-item version and parent SMAST scores are .73 (F-SMAST) and .76
(M-SMAST). These scales have demonstrated good reliability and validity in college student
samples, and the recommended cut score of 3 was used (Crews & Sher, 1992). Alcohol
problems for participants’ maternal and paternal grandparents were assessed by four single-
item questions (e.g., Do you think your paternal grandfather (i.e., your biological father’s
father) has or had problems because of drinking?). Single-item assessments of college students’
parent’s alcoholism have demonstrated reasonably good psychometrics in regard to sensitivity,
specificity, and test-retest reliability (Crews & Sher, 1992). The family history density (FHD)
method was used to code family history. This method is recommended when both men and
women are being assessed (Stoltenberg, Mudd, Blow, & Hill, 1998). FHD is based upon degree
of family relatedness including both parents and all four grandparents. Relatives without
history of alcohol problems receive a score of zero. Each parent with evidence of alcohol
problems contributes 0.5 and each grandparent with evidence of alcohol problems contributes
0.25 to the total score, which can range from 0-2.

Analysis Plan
Structural equation models were estimated using Mplus 5.1 (Muthén & Muthén, 2008) with
Full Information Maximum Likelihood (FIML) estimation, which models the complete dataset
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allowing the inclusion of cases with missing data. Missing data are assumed to be missing at
random (MAR) but not necessarily missing completely at random (MCAR; Enders &
Bandalos, 2001). Covariances among all exogenous variables were included in the model. All
variables were measured at T1 and alcohol consumption and problems were measured at both
T1 and T2. Correlations between error variances for paired T1 and T2 indicators were specified
in the model. We tested two measurement models, one for the continuous predictors and one
to examine the factor structure of the binary DSM criteria. We used maximum likelihood
estimation for the former and the WLSMV estimator (Muthén & Muthén, 2008) for the latter.
We then combined these into an overall measurement model and estimated it using WLSMV.
Incremental fit indexes (e.g., CFI) greater than or equal to .95 represent acceptable fit (Hu &
Bentler, 1999). SRMR values less than or equal to .08 and RMSEA values less than or equal
to .06 represent acceptable fit (Hu & Bentler, 1999). For modeling categorical data with
WLSMV, CFI ≥ .96 and WRMR of approximately 1.0 indicate good fit (Yu, 2002). To our
knowledge, there are not clear guidelines for fit indices for models with a combination of
continuous and categorical data.

We tested two structural models. All participants who reported alcohol use during the follow-
up period were included (N = 2084). The first model examined the hypothesized direct effects
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of affective lability and poor control, and indirect effects of alcohol use utility, family history,
and social norms. Gender was included as a covariate. The second model was a multigroup
analysis that examined the moderating effects of poor control. Poor control was removed from
the previous model and used as a grouping variable, comparing effects across the upper (n =
1042) and lower (n = 1042) halves. In the multigroup analysis, factor loadings were constrained
to be equal across groups and the fit of this model was compared to the fit of an unconstrained
model. All observed variable error variances and covariances, the variances and covariances
of exogenous latent variables, and the disturbance term variances and covariances of
endogenous latent variables were freely estimated across groups

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Results
Attrition Analyses
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Attrition analyses indicated that participants with matched T2 assessments (n = 1851) reported
slightly less alcohol use and problems. For example, they tended to report fewer drinks per
week on the DDQ-M (M = 13.14, SD =13.73 vs. M = 15.92, SD =16.37), lower scores on the
abuse symptoms checklist (M = 0.70, SD =0.92 vs. M = 0.89, SD =1.04), and lower scores on
the dependence symptom checklist (M = 0.78, SD =1.23 vs. M = 0.96, SD =1.34). A logistic
regression analysis indicated that all study variables accounted for approximately 3% of the
variance in attrition, with LR χ2 (30) = 68.36, p < .001, Cragg-Uhler R2 = .03. This magnitude
of differential attrition is comparable to that found in other longitudinal studies conducted in
this age range (e.g., Newcomb & Bentler, 1988) and the longitudinal sample was similar in
basic characteristics to the baseline sample.

Descriptive Statistics
At T2, approximately 92% of the total sample reported drinking at least once in the past six
months. Table 1 presents summary statistics for the analytic sample (i.e., reported drinking at
least once in the past six months). At T2, approximately 52% of drinkers (47% of the full T2
sample) reported one or more abuse symptoms, 47% reported one or more abuse symptoms
and less than three dependence symptoms, and 11% reported 3 or more dependence symptoms
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in the past 6-months. Abuse and dependence symptoms were moderately correlated at T1 (r
= .48, p < .001) and T2 (r = .50, p < .001). Participants in the analytic sample reported drinking
a mean of 14.27 (SD = 13.33) drinks per week and 7-8 drinks per drinking day (rating scale
M = 3.84, SD = 2.36) at T2. The sample is thus characterized by rates of drinking and related
problems that are relatively high compared to national samples and congruent with the elevated
rates of heavy drinking among young adults in this region (Knight et al., 2002;Wright & Sathe,
2006).

Alcohol Problem Analyses


Measurement model for abuse and dependence symptoms—The hypothesized 2-
factor measurement model (based on 4 items for abuse and 7 items for dependence) provided
good fit to the data, with χ2 (116, N =2,080) = 222.88, p < .001; RMSEA = 0.021; CFI = .98;
and WRMR = 1.028. Standardized factor loadings ranged from .45 - .81 (p’s < .001). A single-
factor alcohol problem model had adequate fit (χ2 (118, N =2,080) = 252.70, p < .001; RMSEA
= 0.023; CFI = .97; and WRMR = 1.108). However, the two-factor model had significantly
better fit than the one-factor model (Δχ2 (5, N =2,080) = 35.32, p < .0001). The chi-square
difference and degrees of freedom are estimated by Mplus for comparison of models estimated
by WLSMV. Abuse and dependence latent factors were highly correlated (r = .87 at T1 and
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r = .85 at T2).

Measurement model for continuous predictors—The hypothesized measurement


model provided a good fit to the data, with χ2 (152, N =2,084) = 831.98, p < .001; RMSEA =
0.046; CFI = .96; and SRMR = 0.038. Standardized factor loadings ranged from .60 - .89
(p’s < .001).

Measurement model respecification—Error term covariances with modification indices


greater than 50 were sequentially freed and the model re-estimated (there were no modification
indices greater than 20 in the problems analysis). This resulted in two correlated errors
(distractability with ALS-depression/elation, social norms 1 with T1 alcohol use frequency).
For the final measurement model, χ2 (150, N =2,084) = 645.38, p < .001; RMSEA = 0.040;
CFI = .97; and SRMR = 0.036. Standardized factor loadings ranged from .61 - .89 (p’s < .001).
Table 2 presents the correlations between the constructs in the measurement model.

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Simons et al. Page 9

Full measurement model—The measurement model combining all latent constructs fit
well χ2 (258, N =2,084) = 875.10, p < .001; RMSEA = 0.034; CFI = .94; and WRMR = 1.35.
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Structural model—The hypothesized structural model fit the data well, with χ2 (278, N
=2,084) = 977.70, p < .001; RMSEA = 0.035; CFI = .93; and WRMR = 1.40.

Model respecification—We considered adding non-hypothesized structural paths to the


model based on the modification indices and substantive interpretation. A path from T1
dependence symptoms to T2 alcohol consumption was added. In the initial model, neither
affective lability or poor control was prospectively associated with T2 abuse. We thus dropped
the weaker and non-hypothesized lability path. For the final model, χ2 (278, N =2,084) =
973.22, p < .001; RMSEA = 0.035; CFI = .93; and WRMR = 1.39.

The model is presented in Figure 2. As shown, the analysis tests the hypothesized structural
associations at T1, models the stability of the criterion variables over the follow-up period, and
then tests prospective associations of the T1 predictors on T2 consumption, abuse and
dependence symptoms. It is thus a test of prospective associations that partials out the cross-
sectional associations and explicitly models the stability of the criterion variables as well as
the errors of their indicators. Abuse and dependence symptoms are modeled with a correlated
disturbance term to account for their residual covariation.
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As hypothesized, family history of alcohol problems, alcohol use utility, and social norms were
each associated with T1 alcohol consumption but only indirectly associated with T1 abuse and
dependence symptoms via this association. In contrast, affective lability exhibited cross-
sectional associations with dependence symptoms that did not go through level of use, but was
unrelated to abuse symptoms at T1. Poor control exhibited a significant cross-sectional
association with both dependence and abuse symptoms. These effects represent significant
associations between these constructs after partialing out the strong effect of consumption on
both abuse and dependence symptoms as well as the common variance with the other
exogenous variables. The model thus shows unique cross-sectional associations between both
affective lability and poor control and the criterion variables, abuse and dependence symptoms,
independent of the rate of alcohol consumption or the other covariates.

Furthermore, prospective paths indicated that affective lability had a direct effect on T2
dependence symptoms and poor control had a direct effect on T2 abuse symptoms. These
effects are significant after partialing out all of the cross-sectional associations depicted in the
model. Male gender, social norms, and T1 dependence symptoms exhibited significant positive
prospective associations with level of alcohol consumption at T2. The significant effects of the
other variables on T2 consumption were all indirect via cross-sectional associations with T1
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consumption. Total and indirect effects of the exogenous variables on T2 consumption, abuse,
and dependence are presented in Table 3.

In respect to differential direct predictors of alcohol abuse and dependence symptoms, affective
lability was significantly associated with T2 dependence but not abuse symptoms. In contrast,
poor control exhibited significant direct prospective associations with abuse but not
dependence. At T1, affective lability was associated with dependence symptoms but not abuse
symptoms, while poor control was associated with both abuse and dependence symptoms at
T1.

Multigroup Analysis
Measurement model—The hypothesized measurement model with factor loadings
constrained to be equal across groups (defined by median split on poor control) provided a

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Simons et al. Page 10

good fit to the data, with χ2 (320, N =2084) = 677.24, p < .001; RMSEA = 0.033; CFI = .96;
and WRMR = 1.59.1
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Structural model—We first tested the hypothesized model with paths unconstrained across
groups χ2 (345, N =2084) = 723.18, p < .001; RMSEA = 0.032; CFI = .96; WRMR = 1.60.
We estimated a model with four specific paths constrained to test the hypothesized moderating
effects of poor control on associations between T1 consumption and T1 abuse, T2 consumption
and T2 abuse, and T1 lability and T1 and T2 abuse symptoms. These constraints significantly
worsened the model fit, Δχ2 (4, N = 2084) = 13.33, p = .0098. As hypothesized, in each case
the effects were stronger in the high poor control group. We then tested the four hypothesized
moderating effects of poor control on the associations with dependence symptoms (i.e., T1
lability to T1 and T2 dependence symptoms, T1 consumption to T1 dependence, T2
consumption to T2 dependence). These constraints did not significantly worsen the model fit
(compared to the initial unconstrained model) Δχ2 (4, N = 2084) = 3.56, p = .4694. To create
a more parsimonious model, we constrained all structural paths aside from the four moderation
effects identified above. This partially constrained model did not fit significantly worse than
the fully unconstrained model Δχ2 (15, N = 2084) = 17.23, p = .305; Final model χ2 (338, N
= 2084) = 694.38, p < .001; RMSEA = 0.032; CFI = .96; WRMR = 1.62.2 See Figure 3.

Discussion
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The purpose of this prospective study was to test a theoretical model that generated several
hypotheses about the etiology of alcohol abuse and dependence symptoms. The results were
consistent with both main-effect and moderation hypotheses in almost all respects. Alcohol
abuse and dependence symptoms exhibited a two-factor structure with both common and
unique antecedents. In addition, the identification of predicted antecedents for abuse and
dependence provided support for the proposed etiological processes manifesting in
meaningfully distinct classes of alcohol-related outcomes.

Associations between Affective Lability and Dependence Symptoms


In the main-effect model, affective lability exhibited significant direct cross-sectional and
prospective associations with dependence but not abuse and this did not occur through level
of use. This finding lends support for the proposed theoretical mechanism based on the affective
processing model of negative reinforcement (Baker et al., 2004). We propose that the speed,
frequency, and intensity of affective shifts experienced by individuals with labile affect places
them at increased risk for the process of the development of drug addiction. Thus the dynamics
of affect regulation become central to addiction etiology, contrasting with earlier formulations
of self-medication models that posit that negative affective states act simply as aversive stimuli
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to be coped with (Khantzian, 1985). This perspective is consistent with recent research on
smoking, which indicated that negative mood variability predicted escalation in smoking
among adolescents (Weinstein, Mermelstein, Shiffman, & Flay, 2008). Importantly, Weinstein
and colleagues demonstrated that negative mood variability predicted escalation independent
of effects of mean negative mood level. Dvorak and Simons (2008) similarly demonstrated
that lability, but not negative affect, differentiated daily from occasional smokers. Affect

1The initial measurement model with correlated errors across time for all indicators resulted in a non-positive definite matrix for the high
poor control group. This was corrected by constraining a correlated error across time on the abuse and dependence factors in each group.
Following the recommendations of Hoyle and Smith (1994), we examined the assumption of measurement invariance in factor loadings.
We tested a model with factor loadings freely estimated across groups. The unconstrained model did not fit significantly better than the
constrained model (Δχ2 (18, N = 2084) = 8.11, p = .98. Chi-square difference and degrees of freedom are estimated by Mplus for WLSMV.
2We examined the moderated paths across alternative groupings by conducting a tertile split of the sample based on poor control scores.
The tertile analysis (Δχ2 (8, N = 2084) = 17.46, p = .026) indicated that the paths significantly varied across groups. Inspection of the
coefficients revealed a pattern basically consistent with the median split analysis. Thus the observed moderation effects are consistent
across multiple splits of the data.

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lability is significantly associated with negative affectivity. Future research jointly examining
the role of mean levels of negative affect as well as affect variability in predicting substance
dependence and accounting for associations between internalizing disorders and substance
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dependence is warranted.

Consistent with previous research, affective lability did not correlate significantly with level
of alcohol consumption and was in fact negatively associated with T1 consumption in the
structural model, indicating a suppression effect (Simons & Carey, 2006). It did, however, have
direct effects to dependence symptoms at T1 and T2 when consumption was controlled. This
suggests that labile affect may be specifically associated with the development of a pattern of
drinking that is compulsive and characterized by the hallmark symptoms of dependence. The
direct unique relation between affective lability and dependence symptoms, combined with the
lack of a significant total effect on T2 abuse symptoms, supports its proposed role specifically
in the development of alcohol dependence, and the findings emphasize the importance of this
pathway to the development of alcohol problems. Affective lability may thus be a marker
variable that can help to identify persons who will be at risk for alcohol problems even after
they leave the college environment.

Although affective lability plays a potentially important role in the etiology of dependence, it
is not necessarily more influential than other variables. For example, social norms, due to its
strong relation to T1 consumption, ultimately had a large indirect effect on T2 dependence
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symptoms because of the linkage between norms, consumption, and dependence. In this
environmental context, social influences can present a significant adverse effect through
promoting frequent and unconstrained drinking, which sets up a pathway to dependence among
the more vulnerable individuals in the college population. Thus we would emphasize the
implications of social context factors for prevention of alcohol problems among college
students. The findings, we think, support programs to address both the subtle influence of
normative factors (through correcting erroneous perceptions about the prevalence and
acceptability of binge drinking) and situational factors that directly encourage high levels of
consumption (e.g., parties with large amounts of alcohol easily available). Programs using
motivational interviewing to reduce consumption among current heavy drinkers can also help
achieve this goal through counseling at the individual level (Carey, Henson, Carey, & Maisto,
2007; Carey, Scott-Sheldon, Carey, & DeMartini, 2007).

Poor Control and Alcohol Abuse


Main-effect results showed that poor behavioral control had a prospective direct effect on abuse
(but not dependence) symptoms, in addition to its relations with baseline drinking and
symptomatology. Abuse symptoms include failure to fulfill social responsibilities, reckless
hazardous behavior, socially disruptive illegal activity, and interpersonal conflicts such as
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physical fights (American Psychiatric Association, 2000). The results of the current study
demonstrate that poor control contributes to these problems indirectly, through its positive
relation to alcohol consumption, and also contributes directly to these problems even after
controlling for consumption. Assessment measures typically ask whether these behaviors have
occurred “while drinking” or “because of drinking.” Without explicitly modeling the
occurrence of these behaviors while sober as well as intoxicated it is difficult to determine the
extent to which such behaviors are a symptom of alcohol abuse or due to preexisting personal
characteristics correlated with consumption (Neal & Fromme, 2007). Our results are consistent
with recent item-response studies that suggest some symptoms of “alcohol problems” may be
indexing the existence of another correlated process, in this case, poor behavioral control
(Martin et al., 2006). Edwards’ (1974, 1986) concept of plasticity and the biaxial model of
dependence and disability (e.g., abuse symptoms) is a useful heuristic for conceptualizing the
effects of poor control. Poor control may be conceived of as a pathoplastic agent that affects

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Simons et al. Page 12

intoxicated behavior, promoting a range of socially deleterious and risky behavior commonly
grouped under the rubric of alcohol abuse.
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Moderation Effects of Poor Control


Moderation hypotheses were mostly supported, as poor control interacted with both affective
lability and alcohol consumption in the prediction of abuse symptoms. Consistently, high levels
of poor control increased the strength of the associations. This may occur because poor control
is associated with decreased deliberative cognitive processing and an increased emphasis on
immediate salient cues guiding behavior (Carver, 2005; Wills & Dishion, 2004). Alcohol
intoxication itself is associated with a decrease in information processing speed and inhibition,
and an overall narrowing of cognitive focus (Fillmore, 2003; Fillmore et al., 1998; Steele &
Josephs, 1990). Also, the intense emotional arousal characteristic of labile affect is associated
with a decrease in deliberative “cool” cognitive processing (Baker et al., 2004; Metcalfe &
Mischel, 1999). The “cool” system is posited to be associated with declarative knowledge,
slower acting, reflective, and contributes to the inhibition of prepotent responses (Baker et al.,
2004; Lieberman, 2007; Metcalfe & Mischel, 1999). Thus, we believe these interactions
represent a similar process whereby preexisting poor control combined with intoxication or
affective lability leads to enhanced alcohol-related problems. Moderating effects of poor
control may result from an over-reliance on immediate affective and environmental cues and
a decreased awareness of alternative behaviors, solutions, and potential consequences (Curtin
& Fairchild, 2003; Steele & Josephs, 1990).
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Clinical Implications
Heavy drinking among college students is associated with both acute and long-term negative
consequences (Jackson et al., 2005), so prevention programs during the college years are clearly
warranted (Baer et al., 2002). Though students in college may drink more than their same aged
non-college peers, college attendance overall is associated with less risk for alcohol
dependence in later life (Harford, Yi, & Hilton, 2006; SAMHSA 2006), so consideration should
be given to identifying which students are more at risk for long-term alcohol problems. The
results of the present study suggest that affective lability may be a factor that differentiates
students who will develop long-standing problems with alcohol dependence from persons who
are experiencing a time-limited period of heavy drinking. Both secondary and tertiary
interventions may benefit from including components designed to reduce volatile negative
affect and poor behavioral control as well as to reduce alcohol consumption. Poor control had
multiple direct, indirect, and interactive effects on alcohol outcomes. The direct effects on
alcohol abuse suggest that there may be value in conceptualizing such problems as reflecting
general deficits in self-control rather than solely a problem of excessive alcohol use. The
prospective association between social norms and alcohol consumption as well as the strong
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cross-sectional associations with both alcohol use utility and social norms are supportive of
the emphasis on these or related constructs in college alcohol interventions (e.g., Dimeff et al.,
1999). Interventions to foster improved self-control across the lifespan may be beneficial in
not only reducing alcohol use but also reducing a range of problematic social behaviors, using
either targeted programs for high-risk students or broader general-population approaches
(Miller, Leckman, Delaney, & Tinkcom, 1992; Rehm, Kaslow, & Rabin, 1987; Watson &
Tharp, 2002).

Structure of Alcohol Use Disorder


The better fit of a 2-factor model to the data, the differential associations with lability and poor
control, and the unique prospective association from T1 dependence symptoms to T2
consumption, each support the differentiation of alcohol abuse and dependence symptoms in
this population. However, the factors were highly correlated and a parsimonious 1-factor model

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Simons et al. Page 13

fit the data adequately. Though our results support the differentiation of abuse and dependence
symptoms, this is not to suggest that the current diagnostic categories are optimal, or that the
negative consequences indicative of abuse are best conceived of as a mental disorder per se.
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Continued efforts to refine the conceptualization and diagnosis of alcohol use disorder are
clearly warranted (cf. Babor, 2007; Martin et al., 2008; Midanik, Greenfield, & Bond, 2007).

Limitations and Suggestions for Research


Limitations of the present study should be noted. First, the sample for the research was a
predominantly White college population with some under-representation of males, and
generalization to other populations should be tested. There was slightly greater attrition for
heavier drinkers, as is typical in longitudinal studies of alcohol and other drug use (Wills,
Walker, & Resko, 2005). Second, the participants were studied in one developmental stage,
and the theoretical model used here could be evaluated at earlier and later ages. Third, the
follow-up period was relatively short and more extended designs with additional time points
suitable for examining trajectories of use and abuse would be beneficial.

In summary, the results showed that alcohol abuse and dependence are correlated constructs
with unique antecedents beyond a large shared association with alcohol consumption. The
significant role of affective factors in the model suggests further attention to the interrelation
of affect and other risk factors for drinking, both in between-person studies and in within-
person analyses (Neal & Carey, 2007; Simons & Carey, 2006; Simons et al., 2005b). Further
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research is suggested to explore the cognitive as well as affective concomitants of alcohol


problems, through understanding the explicit and implicit cognitive processes that underlie
drinking motivations and decisions, and the role of controlled vs. automatic processes in
compulsive behaviors (Baker et al., 2004; Gibbons, Gerrard, Reimer, & Pomery, 2006; Stacy
& Wiers, 2006; Wiers et al., 2007).

Moderating effects of poor control on both affective lability and consumption relationships are
congruent with a proposed mechanism of decreased deliberative cognitive processing
strengthening the associations between these predictors and use-related problems. Studies to
integrate cognitive concepts with measures of personality and self-regulation may also help to
understand linkages of these areas and implications for alcohol abuse and other addictive
behaviors (Cervone, Orom, Artistico, Shadel, & Kassel, 2007; Sussman et al., 2004). Finally,
in view of the significant role of social aspects in college alcohol use, detailed research on how
drinking is embedded in social networks can help to better understand the role of normative
and social factors in drinking behavior (Valente, Gallaher, & Mouttapa, 2004). Research on
alcohol consumption and problems can benefit from testing theoretical models that reflect the
multidimensional nature of alcohol problems and the multiple processes involved in their
development, presentation, and course.
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Acknowledgments
This research was supported in part by National Institute on Alcohol Abuse and Alcoholism Grants AA014573 to
Jeffrey S. Simons and K02AA15574 to Kate B. Carey.

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Figure 1.
Heuristic model depicting primary hypotheses. Dashed lines are moderation effects.
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Figure 2.
Structural model for the full alcohol use sample (N = 2084). All values are standardized
coefficients. Gender is coded 1 = Men, 0 = Women. *p < .05, †p < .01, §p < .001. Error variances
between paired T1 and T2 indicators were allowed to covary. Nonsignificant paths from family
history, lability, poor control, and use utility to T2 consumption, poor control to T2 dependence,
lability to T1 abuse are omitted for clarity but are included in model estimation.
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Figure 3.
Structural model for the multigroup analysis (N = 2084). All values are unstandardized
coefficients. Gender is coded 1 = Men, 0 = Female. *p < .05, †p < .01, §p < .001. Error variances
between paired T1 and T2 indicators were allowed to covary. Path coefficients that were
significantly different across groups are depicted with the high poor control group above, and
the low poor control group below the horizontal lines. Nonsignificant paths from lability, use
utility, and family history to T2 consumption, and gender to T1 abuse are omitted in the figure
for clarity but are included in model estimation.
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Table 1
Descriptive Statistics for the Sample of Drinkers
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M SD Skew Range

Alcohol use utility 1 −0.50 0.68 0.44 −2 - 2


Alcohol use utility 2 −0.50 0.74 0.45 −2 – 2
Alcohol use utility 3 −0.47 0.74 0.39 −2 – 2
Alcohol use utility 4 −0.47 0.75 0.46 −2 – 2
Alcohol use utility 5 −0.47 0.73 0.44 −2 – 2
Social norms 1 4.47 1.16 −1.49 0–6
Social norms 2 5.68 2.31 −0.32 1-9
Social norms 3 6.14 2.25 −0.64 1-9
Family history 0.21 0.33 1.88 0-2
Lability (anx./dep.) 8.75 3.62 0.86 5 – 20
Lability (dep./ela.) 16.70 5.34 0.28 8 – 32
Lability (anger) 7.98 3.25 1.25 5 – 20
Eysenck – I7 items 2.68 2.13 0.42 0–7
Impatience 5.95 2.13 0.81 3 – 15
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Distractability 15.18 4.86 0.34 6 – 30


Weekly drinks (T1) 14.77 14.25 1.87 0 - 100
Alcohol freq. (T1) 3.06 1.38 −0.51 0-8
Drinks/DD (T1) 3.98 2.71 0.81 0 -10
DSM-Abuse (T1) 0.80 0.96 1.08 0-4
DSM-Dep. (T1) 0.88 1.28 1.70 0–7
Weekly drinks (T2) 14.27 13.33 2.09 0 - 121
Alcohol freq. (T2) 3.25 1.20 −0.30 1-8
Drinks/DD (T2) 3.84 2.36 1.02 0 - 10
DSM-Abuse (T2) 0.84 0.99 1.04 0-4
DSM-Dep. (T2) 0.81 1.25 1.91 0–7

Note. T1 N’s 2043 – 2084, T2 N’s 1659 – 1664, 64% women. Anx. = anxiety, dep = depression, ela. = elation. See measures section for description
of Social norms 1-3. DD = drinking day. DSM-Dep. = DSM dependence checklist, DSM-Abuse= DSM Abuse checklist.
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Table 2
Correlations among Latent Constructs in the Sample of Drinkers

1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
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1. Alcohol Use Utility 1.00


2. Social Norms .43 1.00
3. Affective Lability .03ns .02ns 1.00
4. Poor Control .21 .16 .61 1.00
5. T1 Consumption .52 .64 .00ns .22 1.00
6. T2 Consumption .46 .57 .01ns .18 .82 1.00
7. T1 Abuse .40 .60 .19 .45 .86 .70 1.00
8. T2 Abuse .38 .55 .18 .39 .75 .82 .69 1.00
9. T1 Dependence .33 .49 .29 .42 .71 .58 .87 .74 1.00
10. T2 Dependence .25 .36 .32 .38 .52 .68 .65 .85 .71 1.00

Note. N = 2084. ns = not significant. All other correlations significant at p < .001.

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Table 3
Standardized Indirect and Total Effects in Predicting T2 Alcohol Consumption, Abuse, and Dependence

T2 Consumption T2 abuse T2 Dependence


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Indirect Total Indirect Total Indirect Total

1. Gender .13† .31† .14† .09* .11† .06

2. Alcohol use utility .12† .16† .13† .15† .10† .12†

3. Social norms .33† .42† .35† .40† .28† .32†

4. Family history .04* .05 .04* .05* .03* .04*

5. Affective lability −.08 −.04 −.08 −.03 −.07 .26†

6. Poor control .11* .10* .12* .31† .10* .12

Note: N = 2084. Gender is coded 0 = Female, 1 = Male. Indirect effects are all of the indirect effects via T1 alcohol consumption. Bias-corrected bootstrapped confidence intervals were used to determine the
significance of effects (MacKinnon, Lockwood, & Williams, 2004). Superscripts denote significant effects based on
*
= 95% confidence interval or

= 99% confidence interval.

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