Journal of Abnormal Psychology Copyright 2004 by the American Psychological Association

2004, Vol. 113, No. 2, 302–314 0021-843X/04/$12.00 DOI: 10.1037/0021-843X.113.2.302

Neuropsychological Executive Functioning in Children at Elevated Risk for

Alcoholism: Findings in Early Adolescence

Joel T. Nigg Jennifer M. Glass and Maria M. Wong

Michigan State University University of Michigan

Edwin Poon Jennifer M. Jester

Michigan State University University of Michigan
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

Hiram E. Fitzgerald Leon I. Puttler, Kenneth M. Adams, and

This document is copyrighted by the American Psychological Association or one of its allied publishers.

Michigan State University Robert A. Zucker

University of Michigan

One component of individual risk for alcoholism may involve cognitive vulnerabilities prodromal to
alcoholism onset. This prospective study of 198 boys followed between 3 and 14 years of age evaluated
neurocognitive functioning across three groups who varied in familial risk for future alcoholism.
Measures of intelligence, reward–response, and a battery of neuropsychological executive and cognitive
inhibitory measures were used. Executive functioning weaknesses were greater in families with alco-
holism but no antisocial comorbidity. IQ and reward–response weaknesses were associated with familial
antisocial alcoholism. Executive function effects were clearest for response inhibition, response speed,
and symbol-digit modalities. Results suggest that executive deficits are not part of the highest risk,
antisocial pathway to alcoholism but that some executive function weaknesses may contribute to a
secondary risk pathway.

Alcohol use disorders represent a major public health problem
that afflicts adults as well as nearly a quarter of youths in late
adolescence (Johnston, O’Malley, & Bachman, 1996; Tarter,
Kirisci, & Mezzich, 1997). Neuropsychological problems are as-
sociated with severe and chronic alcoholism (Giancola & Moss,
1998; Tarter, 1975; Victor, Adams, & Collins, 1971), even in the
absence of neurological findings (Parsons & Leber, 1981; Tuck &
Jackson, 1991). However, beyond the known neuropsychological
effects of alcoholism, a persisting question over the last decade has
been whether subtle neuropsychological problems precede prob-
lem alcohol use and contribute to its onset (Corral, Holguin, &
Cadaveira, 1999; Deckel, Bauer, & Hesselbrock, 1995; Finn, Ma-
zas, Justus, & Steinmetz, 2002; Peterson, Finn, & Pihl, 1992;
Joel T. Nigg, Edwin Poon, and Hiram E. Fitzgerald, Department of
Psychology, Michigan State University; Jennifer M. Glass, Maria M.
Wong, Jennifer M. Jester, Leon I. Puttler, Kenneth M. Adams, and Robert
A. Zucker, Psychiatry and Addiction Research Center, University of
Michigan.
This work was supported by National Institute on Alcohol Abuse and
Alcoholism grants RO1 AA12217 to Robert A. Zucker and Joel T. Nigg,
and R37 AA07065 to Robert A. Zucker and Hiram E. Fitzgerald. We are
also deeply indebted to Susan Refior, Family Study Director of Field
Operations, for her commitment and skill in maintaining this study’s
viability over such a long time. We are likewise grateful to participating
families for their willingness to engage with us in what is an essentially
altruistic activity over so many years.
Correspondence concerning this article should be addressed to Joel T.
Nigg, Department of Psychology, 153 Snyder Hall, Michigan State Uni-
versity, East Lansing, MI 48824. E-mail: nigg@msu.edu
Tarter, 1991; Tarter et al., 1999). This is a crucial question for
understanding etiology. Developmental models of alcoholism
point to an activating environment impinging on within-individual
vulnerabilities (Loukas, Krull, Chassin, & Carle, 2000; Tarter &
Vanyukov, 1997), of which neuropsychological vulnerabilities
may be a portion.
To answer this question effectively, it is necessary to examine
children at risk (West & Prinz, 1987) prior to onset of problem
alcohol use. The most common and practical high risk group has
been children of alcoholic parents, who are two to five times as
likely to develop alcoholism in adulthood (Goodwin, 1979; Russel,
1990). However, most studies using this sampling strategy have
examined adults or late adolescents who may have already begun
problem alcohol use, often with mixed results, leaving open the
question of whether executive function weakness preceded prob-
lem alcohol use (Deckel et al., 1995; Drejer, Theilgaard, Teasdale,
Schulsinger, & Goodwin, 1985; Gillen & Hesselbrock, 1992). Finn
et al. (2002) found that young adults with early-onset alcoholism
had behavioral inhibition weakness compared with those without
early-onset alcoholism. Other studies looked at nonalcoholic adults
with and without a family history of alcoholism (e.g., Alterman,
Bridges, & Tarter, 1986; Peterson et al., 1992; Shuckit, Butters,
Lyn, & Irwin, 1987; for a review, see Nixon & Tivis, 1997). Yet
many studies again have had negative results and/or had small
samples. Moreover, it is not clear that cognitive risk should be
transmitted to nonalcoholic children of alcoholics. Thus, exami-
nation of children at risk prior to alcohol use onset is needed.
Various cognitive problems may precede alcohol use (Giancola
& Tarter, 1999; Pihl, Peterson, & Finn, 1990) including verbal
ability (Sher, Walitzer, Wood, & Brent, 1991), lower IQ (observed

302
 EXECUTIVE FUNCTIONS AND RISK FOR ALCOHOLISM
in our own sample at earlier time points; Noll, Zucker, Fitzgerald,
& Curtis, 1992; Poon, Ellis, Fitzgerald, & Zucker, 2000; Puttler,
Zucker, Fitzgerald, & Bingham, 1998), and possibly spatial abil-
ities (e.g., the ability to mentally rotate shapes; Schandler, Thomas,
& Cohen, 1995). However, perhaps the domain most discussed as
a potential precursor is executive functions, which refers to the
ability to regulate cognition or response in relation to goals rather
than immediate stimuli and to temporally organize behavior; it
includes such abilities as working memory and response
suppression.
Clarification of the role of executive functioning in the risk
pathway is needed for several reasons. Executive function prob-
lems have been suggested as one core element in child risk
(Giancola & Tarter, 1999), are pertinent to the externalizing be-
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This document is copyrighted by the American Psychological Association or one of its allied publishers.
havioral risk for alcoholism (Barkley, 1997; Nigg, 2001), and are
readily linked conceptually to behaviors that involve self-
regulation, including alcohol use problems. Thus, one expects poor
executive functions to be correlated with impulsive or stimulus-
driven behavior, inability to resist short-term gratification or re-
ward, and weakened ability to make planned decisions that keep a
long-term goal in mind. To the extent that alcoholism is influenced
by impulsive responding, failure to override immediate but risky
incentives, and poor organization of one’s life activities, executive
functioning might then be expected to influence this pathway.
However, this is an empirical question. In short, whereas risk in the
domain of intelligence (IQ) is well established (Poon et al., 2000),
the role of executive functions as a risk factor remains debatable
because of a dearth of studies of suitable child samples.
Executive Functions
Executive functions still suffer from conceptual underspecifica-
tion (Lyon & Krasnegor, 1996; Pennington, 1997), but tractable
models are emerging (Pennington & Ozonoff, 1996; Posner &
DiGirolamo, 1998). Executive function tasks represent multiple-
component operations (Miyake, Friedman, Emerson, Witzki, &
Howerter, 2000) that may be related to distinct parallel thalamo–
cortical– basal ganglia neural loops (Fuster, 1997; Middleton &
Strick, 2001; Nigg, 2000; Stuss & Knight, 2002). Component
processes identified in traditional, clinical neuropsychological
tasks include set shifting, interference control, inhibition, planning,
and working memory (Pennington, 1997; Pennington & Ozonoff,
1996). Traditional or molar clinical executive function tasks (e.g.,
the Wisconsin Card Sort [Heaton, et al., 1993], Stroop [MacLeod,
1991], Trailmaking [Reitan & Wolfson, 1992], and Word Fluency
[Thurstone & Thurstone, 1949]) were developed for their ability to
identify brain damage in adults (Lezak, 1995) rather than to isolate
component operations, though they differ meaningfully in the
functions they emphasize (Pennington, 1997).
Chronometric tasks borrowed from cognitive psychology are
often designed to try to isolate specific component operations and
so may be referred to as molecular tasks (Nigg, 2000, 2001). This
literature suggests a related set of components such as conflict
detection, sustaining working memory via control of mental inter-
ference, inhibition of competing responses, and regulation of re-
sponse via alertness or allocation of effort (Botvinick, Braver,
Barch, Carter, & Cohen, 2001; E. K. Miller, 2000; Posner &
DiGirolamo, 1998). Efforts to evaluate performance on such cog-
nitive tasks can increase the interpretive and functional reach of an
executive battery. In all, it is important to examine a range of tasks
303
that cover multiple domains and constructs related to executive
control.
Few studies of nonadult children of alcoholics have examined
executive measures. Tarter, Jacob, and Bremer (1989) found weak-
nesses in children of alcoholic fathers (ages 8 –17) on visual
attention. Ozkaragoz and Noble (1995) found that 10- to 14-year-
old sons of familial alcoholics were weak on verbal, motor, and
attentional components of the Halstead-Reitan (Reitan & Wolfson,
1992) battery but did not probe executive functions per se. Corrall
et al. (1999) found no differences on the Wisconsin Card Sort Test
between children aged 7–15 years from families of high- and
low-density alcoholism and control individuals. In a follow up on
a small subgroup, Corrall, Holguin, and Cadaveira (2003) found
differences between children in high-density families and controls
on the WCST at ages 11–17 years, but 30% of that sample had
started drinking. Bauer and Hesselbrock (1999) found no differ-
ences on a Stroop test between 15- to 20-year-old children of
fathers with alcohol or substance dependence and controls, but the
age range implies that drinking had already started in a substantial
percentage.
Harden and Pihl (1995) administered an extensive battery to a
small sample (N ⫽ 28), comparing 10- to 14-year-old boys from
multigenerational families with alcoholism to controls. Harden and
Pihl found weaker performance in the high-risk group on the
Wisconsin Card Sort Test, written word fluency, self-ordered
pointing, and spatial conditioned–associative learning tests but not
on paired associate learning, matching familiar figures, or abstract
self-ordered pointing. Giancola, Martin, Tarter, Pelham, and Moss
(1996) and Giancola and Parker (2001) created a composite exec-
utive function score (Porteus Mazes, a continuous performance
task, a delay of gratification task, and block design). It was not
correlated with drug use in their longitudinal study of boys at risk
for drug use (Giancola & Parker, 2001; r ⫽ .02) or with family
history status in 10- to 12-year-old boys (Giancola et al., 1996).
Overall, very mixed results across the few studies of children have
led to uncertainty about the status of executive functioning in
alcoholism risk (Harden & Pihl, 1995), with most studies using
either small sample size or a narrow battery of executive measures
and many involving substantial age variation in their samples.
Executive Functions and Risk for Alcoholism in Early
Adolescence
From a developmental perspective, if executive functions con-
tribute to alcoholism, studying executive processes in early ado-
lescents (rather than younger children) at risk for alcoholism
makes sense for several reasons. First, executive control continues
to mature throughout adolescence (Haung-Pollock, Carr, & Nigg,
2002), consistent with the ongoing development of frontal cortex
into adolescence (Krasnegor, Lyon, & Goldman-Rakic, 1997).
Thus, early adolescence is a sensitive period for the evaluation of
individual differences in processes related to anterior cortical–
subcortical networks development. Second, early adolescents are
on the threshold of risk for beginning problematic alcohol use
(Grunbaum et al., 2002; Johnston, O’Malley, & Bachman, 1996).
As a result, within the context of an ongoing developmental study
of the epigenesis of risk, late childhood– early adolescence is a
period where children are old enough to have a strong probability
of highlighting risk variations but young enough so that any
detected differences could not be attributed to prolonged alcohol
 304 NIGG ET AL.

use. Crucially, this age span thus enables relatively short-term
longitudinal evaluation of the predictive use of any cognitive
vulnerability identified. At a practical level, children at this age are
able to tolerate the relatively lengthy and difficult battery required
to evaluate a full range of executive function measures.
Risk Subtypes
It has become increasingly apparent that the alcoholism pheno-
type is heterogeneous (Babor & Dolinsky, 1988; Zucker, 1994),
which may be one reason that results in studies to date have been
mixed. If risk is concentrated more in one subtype than another,
the sampling frame of the study would weight the odds more or
less toward the detection of differences to the extent that it favored
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families would be at elevated risk for later AUD outcome. Men were
initially identified through a network covering all courts in a four county-
wide area. All men with drunk-driving convictions involving a blood
alcohol concentration of at least 0.15% (if first conviction; or at least
0.12% if a previous drinking-related legal problem had occurred) were
potential study candidates. In addition, the men were required (a) to make
a Feighner diagnosis for probable or definite alcoholism (Feighner et al.,
1972), (b) to have at least one son between 3 and 5 years of age, and (c)
to be living with the child and his biological mother at the time of
enrollment. Mother’s AUD status was free to vary. Last, (d) presence of
child fetal alcohol syndrome was exclusionary (n ⫽ 146 court-referred
fathers).
A contrast/control group of families who resided in the same neighbor-
hoods as the alcoholic families but who had no substance abuse history was
also recruited using door-to-door canvassing (n ⫽ 95). In addition, an

intermediate risk group (n ⫽ 61) was provided by recruiting all families

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or excluded the relevant risk subtype. Furthermore, Zucker and

with an alcohol abuse– dependence diagnosis who were found during the
colleagues, in a series of reviews (Fitzgerald, Mun, Zucker, Puttler,
community canvass. Although original recruitment used the Feighner et al.
& Wong, 2002; Zucker, Chermack, & Curran, 2000; Zucker, (1972) criteria, in later years all parents were rediagnosed using the alcohol
Fitzgerald, & Moses, 1995) and empirical papers (Poon et al., abuse– dependence criteria of the Diagnostic and Statistical Manual of
2000; Puttler et al., 1998; Zucker, Ellis, Bingham, Fitzgerald, & Mental Disorders (fourth edition; DSM-IV; American Psychiatric Associ-
Sanford, 1996), have assembled a large body of evidence indicat- ation, 1994), which occasionally produced reclassification of risk-group
ing that virtually all of the potentially confounding factors de- membership. In addition, at later data waves, all siblings within ⫹/– 8 years
scribed above may be subsumed under a very powerful subtyping of the primary male target child were also recruited, but not all of these
schema that has been dominant within the adult alcoholism liter- participants have yet gone through the neurocognitive assessment protocol.
ature for a generation: the distinction between alcoholism comor- In the literature, some experts advocate separating data by gender because
of potentially different precursors, determinants, and outcomes in relation
bid with antisocial personality disorder (ASPD) and alcoholism
to alcoholism risk (Pihl et al., 1990). Because the study design provided
without this comorbidity (Babor, 1996; Hesselbrock et al., 1984;
initial data on substantially more boys than girls, this report focuses only
Zucker et al., 1994). The power of this differentiating framework on the boys who completed the neuropsychological protocol. To preserve
is that it discriminates among families with and without an assort- independence of observations, this study only involves 1 boy per family.
ment of alcoholism among the parents, denser versus lesser family- We plan to report on girl siblings when that sample is large enough to
history-positive, greater versus lesser family conflict, lower versus warrant it. A more detailed description of study procedures, recruitment
higher family socioeconomic status (SES), as well as differences in strategies, and eligibility criteria can be found in Zucker et al. (1996;
IQ and achievement, with the antisocial subtype consistently Zucker et al., 2000). Full family assessments involving both parents and
showing poorer functioning in these areas (Jansen, Fitzgerald, participating children occurred at 3-year intervals, starting at baseline
Ham, & Zucker, 1995; Jester, Zucker, Wong, & Fitzgerald, 2000; (Wave 1). Figure 1 summarizes the recruitment flow into the study,
showing the process by which the participants in the current report were
Puttler et al., 1998; Zucker et al., 1996). Equally important, ASPD
obtained.
has the strongest comorbid association to alcohol use disorders of
all the psychiatric disorders (12:1 among men and 30:1 among
women; Helzer, Burnam, & McEvoy, 1991; Helzer & Pryzbeck,
1988; Kessler et al., 1997; Morganstern, Langenbucher, Labouvie,
& Miller, l997). Therefore, in the present study we rely on this
framework as the basis of a core hypothesis: namely, that neuro-
cognitive risk among children of alcoholics (COAs) versus con-
trols will be distinct among those with and without parental anti-
sociality. Virtually no prior studies of young children at risk have
used the antisocial versus nonantisocial alcoholism-family-risk
designation, so it remains unclear whether executive function risk,
if any, will covary with antisociality and IQ risk, or represent a
potentially distinct cognitive risk pathway.

Method
Participants
Participants were boys from 198 families who had completed the Wave
4 executive function battery as part of an ongoing, prospective, multiwave
study that is tracking a community sample of families with high levels of
alcohol use disorder (AUD), along with a community contrast sample of
families drawn from the same neighborhoods who do not have the high
substance abuse profile (Zucker & Fitzgerald, 1991; Zucker et al., 2000).
In the initial sample, of which these boys were a part, parental alcoholism,
ascertained through the father, assured that offspring in the high-risk Figure 1. Summary of the study recruitment flow.
 EXECUTIVE FUNCTIONS AND RISK FOR ALCOHOLISM
In this study we report on cognitive data from preschool (Wave 1 IQ and
self-control), middle childhood (Waves 2 and 3 IQ and achievement), and
early adolescence (Wave 4 IQ, achievement, and executive measures; child
ages ⫽ 12–15 years). This restricted the original sample of 302 to 198
families, for whom executive measures at Wave 4 (when the first compre-
hensive neuropsychological assessment was done) were available. This
subsample included 91 (62% of Wave 1) children from court-recruited
alcoholic families, 38 (62% of Wave 1) from community-recruited fami-
lies, and 69 (73% of Wave 1) from control families, who were then
stratified according to AUD–antisocial risk type as described below.
Note that the percentage recruited at the Wave 4 way point steadily
increases from court alcoholic to community alcoholic to controls. This
might initially appear to be a differential across-wave retention bias;
however the phenomenon is directly attributable to the Wave 1 recruitment
process and the fact that the neurocognitive protocol was started after the
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regular Wave 4 assessment protocol had started. At Wave 1, court alco-
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holics were recruited first. Community alcoholic and control families
followed because the design specified an age and neighborhood match
between court alcoholics and their contrast families. This required the
recruitment team to recruit until a suitable control family was located, such
that court alcoholic families were always recruited and seen prior to control
families at each wave. At Wave 4, the neurocognitive protocol was started
after the regular Wave 4 assessment process had started. Therefore, a lesser
proportion of the first recruited group (the court alcoholic families) was
available, followed by increasing proportions of the latter two groups.
Even so, to evaluate quantitatively the degree to which the subsample
available at Wave 4 could be generalized to the original sample, we
compared those participants included and excluded on available cognitive
and behavioral measures. The two groups did not differ in composite child
IQ (averaged over the first 3 waves, p ⫽ .90) or composite total behavior
problems as rated by mothers ( p ⫽ .90) or teachers ( p ⫽ .83). They also
did not differ in SES (p ⫽ .66) even though a higher proportion of
nonalcoholic controls was involved in the Wave 4 than in the Wave 1 data
( p ⫽ .04). Among the alcoholic families (father lifetime alcoholism at
Time 1), SES also did not differ between those included and those not
included in the present report ( p ⫽ .86); the same was true among the
nonalcoholic families ( p ⫽ 90).
Measures
Health history. Developed by the Rutgers Longitudinal Study (Car-
penter & Lester, 1980), this self-administered questionnaire assessed per-
sonal health and illness in 15 areas. The mother’s form contained questions
about prenatal health and early development that were used to obtain
information on mother’s drinking during pregnancy for use in covariance
analysis.
Parental AUD. Parental AUD at Wave 1 and Wave 4 was assessed by
the Diagnostic Interview Schedule, Version III (DIS; Robins, Helzer,
Croughan, & Ratcliff, 1980), the Short Michigan Alcohol Screening Test
(SMAST; Selzer, Vinokur, & van Rooijen, 1975), and the Drinking and
Drug History Questionnaire (DDHQ; Zucker, Fitzgerald, & Noll, 1990).
On the basis of information collected by all three instruments, a diagnosis
of AUD (lifetime as well as past 3 years) was made at Wave 1 and Wave
4 by a trained clinician using DSM-IV criteria. The availability of three
sources of information collected over three different sessions separated in
some instances by as much as several months served as an across-method
corroboration/validity check on respondent replies. Given the volume of
material collected as well as the spacing between sessions, it is unlikely
respondents would recall their specific replies. In cases of discrepant
information, the data represented by the majority of information sources
were used in establishing the diagnosis. Interrater reliability for diagnosis
was excellent (␬ ⫽ .81). We also separately coded DSM-III-R (third
edition, revised; American Psychiatric Association, 1987) level of severity,
with interrater r ⫽ .85.
Parent ASPD. Parent ASPD was assessed by the Wave 1 Diagnostic
Interview Schedule and the Antisocial Behavior Inventory (ASB; Zucker,
305
Noll, Ham, Fitzgerald, & Sullivan, 1994; Zucker et al., 1996). Information
on the ASB was used to supplement the DIS data in establishing a
diagnosis. The ASB is a 46-item questionnaire that assesses the frequency
of aggressive and antisocial activities in both childhood (e.g., lying to
parents, being suspended from school for fighting) and adulthood (e.g.,
being fired for absenteeism, defaulting on a debt, resisting arrest). ASPD is
an Axis II personality disorder that requires a long course over childhood
and adulthood to meet criteria. It is always a lifetime diagnosis and was
treated that way here in light of evidence for the long-term stability of this
syndrome (Caspi, Elder, & Bem, 1987; Krueger, Caspi, Moffitt, & Silva,
1998).
Alcoholism subtype groups. AUD and ASPD diagnoses were used to
establish the three risk groups. The primary classification was based on the
father’s diagnosis, although in no case was a nonantisocial alcoholic father
coupled to an antisocial alcoholic mother. The three families where the
father was antisocial but not alcoholic were excluded from these analyses.
This association has been elsewhere documented to be an antitype, that is,
an association whose frequency is significantly rarer than would be ex-
pected from base rate (von Eye, 1990; Zucker et al., 1996). The three
groups were therefore community control (n ⫽ 74; these were the 69
controls noted earlier, plus 5 of the community-recruited alcoholic families
that had moved to control on rediagnosis when DSM-IV criteria were
applied later), alcoholism only (AUD, n ⫽ 89), and AUD ⫹ ASPD (n ⫽
35). A child was put in the alcoholism-only risk group if either parent had
ever had a DSM-IV diagnosis of dependence or if both parents had current
diagnoses of abuse. A child was put in the AUD ⫹ ASPD group if they met
the alcoholism-group criteria and the father or both father and mother had
ASPD.
Child behavioral adjustment. We obtained measures of child behav-
ioral adjustment to evaluate their possible contribution to any findings.
Among the primary domains thought to be associated with long-term risk
are inattention, hyperactivity, conduct problems, and aggression (Zucker et
al., 1995). At Wave 4, mothers and teachers rated children’s adjustment
using the Child Behavior Checklist (Achenbach, 1991a) and the Teacher
Report Form (Achenbach, 1991b). These scales provide standardized
scores that can be related to a representative normative database on
empirically derived problem scales with adequate psychometric properties.
Child academic impairment. Academic functioning was assessed with
the Wide Range Achievement Test—Revised (WRAT–R; Jastak &
Wilkinson, 1984) Reading, Spelling, and Arithmetic subtests in elementary
and early adolescent years, for descriptive purposes.
Child drinking and drug use. Twenty children reported alcohol use in
the last 6 months; of those, only 5 reported more than four drinks in the past
month (all in the higher risk, alcoholic family groups). An additional 26
reported ever trying marijuana or other drugs, primarily children from the
risk groups ( p ⬍ .01). A composite risk score of drug and alcohol use was
unrelated to executive function measures. We opted not to covary these
experimental uses because of the overall light amount of use, viewed as not
interpretable as an influence on results.
Early Cognitive Functioning
Our group previously reported on IQ differences in preschool (Fitzgerald
et al., 1993; Noll et al., 1992) and elementary school (Poon et al., 2000;
Puttler et al., 1998) children. Those data along with Wave 4 IQ scores are
included here to compare and contrast patterns of effect versus executive
functions in the two risk groups. Because all Wave 1 families had not yet
been recruited when those earlier analyses were conducted, the present
report also includes more children on the Wave 1 and Wave 2–3 measures
than in the prior reports.
Wave 1 (preschool). At Wave 1, children completed two cognitive
tasks that are included in the current article. Intellectual development was
assessed with the Stanford-Binet (Terman & Merrill, 1973), Form L–M,
which provided an estimated full-scale IQ. To assess regulatory control in
relation to management of reward incentive, children completed the Delay
of Gratification Task (Funder, Block, & Block, 1983; for a prior report on
 306 NIGG ET AL.
this task on a subset of the present sample, see Fitzgerald et al., 1993).
Subsequent to the IQ testing, the child was thanked for participating and
told she or he could have a present. As the gift-wrapped present is being
shown, the examiner apologizes and says there is one more task to be
completed. The toy is set aside but within view and reach of the child. The
child is then shown a complex task (Wechsler Intelligence Scale for
Children—Revised [WISC–R] block design, Problem 11; Wechsler, 1974)
and told that the design must be completed prior to opening the present.
The task involves a maximum of 5.5 min of delay (4 min for task
completion and an additional 90 s of delay). The session is ended prior to
the maximum period when the child takes the gift. The score is the number
of seconds the child waits before taking the present, after the task is
assigned. Higher scores reflect more well-developed delay of gratification.
Waves 2–3 (elementary school). At Wave 2, cognitive assessment data
were missing for approximately a third of the sample because of funding
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restrictions. Those missing-by-design data were obtained at the Wave 3
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assessment for those cases. We therefore combined Wave 2 and Wave 3
data into an elementary school-age assessment. Measures completed were
as follows. To assess intellectual development, the WISC–R (Wechsler,
1974) Full Scale, Verbal, and Performance IQ subscales were derived from
the full 12 subtests (Poon et al., 2000). We focus on the Full Scale IQ in
the present analyses because it is the most reliable score and is a composite
of verbal IQ (VIQ) and performance IQ (PIQ).
Wave 4 (early adolescence). The WISC–R was readministered
at Wave 4.
Wave 4 Executive Neuropsychological Function
At Wave 4, executive functions were assessed with eight tests chosen to
focus on different aspects of executive control during visits in the family’s
home or on campus. The rationale for each measure was as follows.
Set shifting and working memory. To obtain a complex measure of
executive functioning that required both working memory and set shifting,
we administered a computerized version of the Wisconsin Card Sorting
Test (Heaton et al., 1993). The test is associated with activation in dorso-
lateral prefrontal cortex (Weinberger, Berman, Gold, & Goldberg, 1994)
perhaps because of its requirement to protect working memory (Botvinick
et al., 2001) and is impaired in patients with prefrontal brain injury
(reviewed by Lezak, 1995). After 10 correct decisions, the rule was
changed without the participant’s knowledge. The number of perseveration
errors (i.e., decisions that were based on a previous category) and the
number of categories completed were correlated at r ⫽ –.70 and were
therefore viewed as redundant. Following prior reports (e.g., Harden &
Pihl, 1995) we report on the perseverative errors score herein.
Response suppression. Executive behavioral inhibition requires the
suppression of a prepotent motor response (Logan, 1994; Nigg, 2001). This
function entails activation of areas in prefrontal cortex, particularly the
right inferior frontal gyrus (Aron et al., 2003) and associated regions in the
striatum, particularly the caudate (Casey et al., 1997). It was evaluated with
the Stopping Task (Logan & Cowan, 1984), which is drawn from the
cognitive science literature. During this two-alternative choice reaction-
time (RT) task, participants saw an “X” or an “O” on a computer screen
and responded rapidly with one of two keys. On some trials a tone sounded
shortly after the X or O was displayed, indicating that participants were to
withhold their response. After two practice blocks of 32 trials each, four
blocks of 64 trials were administered. We averaged the final three blocks
unless data quality checks suggested otherwise (see Nigg, 2000, and
comment on outliers below). The most reliable estimates of stop signal RT
are obtained with a response-RT tracking methodology (Band, van der
Molen, & Logan, 2003). In this procedure, the delay between the visual
stimulus and the warning tone is varied to maintain 50% success rate at
withholding the response. A quantitative model of RT processes enables
calculation of each participant’s speed of stopping or inhibiting a response
(the stop RT) by subtracting average stop signal delay from average RT
(Logan & Cowan, 1984; Logan, Schachar, & Tannock, 1997). This stop
signal RT estimate serves as the index of executive inhibitory control.
Response regulation. Response regulation can involve alertness, acti-
vation, or effort. Weakness is indexed as relating to slower and more
variable output speed on fast, effortful tasks (Posner & Peterson, 1990;
Sergeant, van der Meere, & Oosterlaan, 1999). In the Symbol-Digit Mo-
dalities Test (Smith, 1991), several symbols are associated with digits. The
participant was shown the symbols and required to give the correct digit
associated with that symbol. The participant was to respond as rapidly as
possible. Thus, the task required rapid cognitive processing of routine
information paired with a rapid response. Both an oral measure and a
written measure were obtained. For the current analyses, the sum of the
oral and written scores was the dependent measure. On the stopping task,
go RT (response speed on trials with no stop tone) and variability of go RT
were viewed as indexes of alertness or effort. Symbol digit and go RT–
variability may be distinct, because whereas symbol digit requires rapid
motor output but little computational effort, go RT and variability require
little motor control but rapid decision making.
Verbal fluency. Fluency was defined as the ability to rapidly generate
verbal associations to a particular concept. This paradigm was operation-
alized with verbal production by Thurstone and Thurstone (1949). It
appears to activate a range of language areas neurally, but left dorsolateral
prefrontal cortex appears to be especially important to controlling the word
search (Frith, Friston, Liddle, & Frackowiak, 1991; Perret, 1974). In this
task, the Controlled Oral Word Association Task (COWAT), participants
were to generate as many words beginning with various letters as they
could in 1 min (Benton & Hamsher, 1978). Three letters were given (C, F,
and L). The dependent measure was the total number of valid words
generated.
Interference control. Interference control refers to the ability to mon-
itor response conflict and suppress a competing response to carry out a
primary response. It entails activation of anterior cingulate and dorsolateral
prefrontal cortex (Cabeza & Nyberg, 1997). Interference control was
operationalized with the Stroop Color–Word Interference Test (Golden,
1978). The Stroop test is a widely used clinical and cognitive measure
(MacLeod, 1991). The paper-and-pencil version of the task was adminis-
tered, with 45 s per trial. Interference control was calculated by subtracting
color–word naming total from color-naming total.
Visual working memory–planning. The term planning is used here to
describe the ability to manipulate complex visual information in working
memory. It was operationalized with the Tower of Hanoi procedure
(Lezak, 1995). Performance on tasks of this nature is associated with
frontal neural injury (Goel & Grafman, 1995) and we speculate that the
task activates spatial working memory modules in right prefrontal cortex as
described in the cognitive neuroscience literature (Courtney, Petit, Maisog,
Ungerleider, & Haxby, 1998). In this test, participants were to move
different-sized rings on a three-peg board from one peg to another, fol-
lowing specific rules, including not placing a smaller ring on top of a larger
one, and moving only one ring at a time. Three rings were used. The
outcome variable was number of moves before correctly solving the
problem.
Data Reduction
Interrelations among the neuropsychological variables. From the neu-
ropsychological tests we obtained eight scores to examine. Although the
preceding provides the conceptual logic for obtaining these measures, their
intercorrelations, displayed in Table 1, reflect imperfect fidelity to such
conceptual organization, and subsequent exploratory and confirmatory
factor analyses did not clarify the picture further. We therefore opted to
report variables individually in light of their unclear factor structure and to
maximize comparability with other past and future studies.
Missing data. As with all longitudinal data sets, data were sometimes
missing because of changes in study procedure (addition of more measures
when funding was obtained), participants missing a data-collection wave,
participant fatigue, or computer malfunction. No correlations were signif-
icant between amount of missingness and any dependent measure (ranging
in absolute value from r ⫽.02 to r ⫽ .10). We therefore imputed missing
 EXECUTIVE FUNCTIONS AND RISK FOR ALCOHOLISM
Table 1
Correlations Among Executive Function Measures in Early Adolescence
Variable 1 2
1. Go reaction time (RT) —
2. Response variability .53** —
3. Stop signal RT ⫺.03 .43**
4. Symbol digit ⫺.10 ⫺.27**
5. Verbal fluency ⫺.03 ⫺.16*
6. WCST perseverations ⫺.07 ⫺.01
7. Tower of Hanoi .01 .04
8. Stroop interference .05 ⫺.06
Note. WCST ⫽ Wisonsin Card Sort Test (Heaton et al., 1993).
* p ⬍ .05. ** p ⬍ .01. All significance values are two-tailed; all significant correlations are in expected
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directions.
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data using the estimation maximization (EM) algorithm, which is one form
of maximum likelihood estimation. These methods preserve similar pa-
rameter estimates to the raw data and are viewed as superior to alternatives
such as listwise deletion of cases or estimating missing data points via
regression (Shafer & Graham, 2002). Missing data were estimated for all
behavioral rating scales, the IQ measures, and the eight executive function
scores. Overall, we estimated of a total of 9.7% of data points (10.6% of the
cognitive variables, and 12.7 % of the executive neuropsychological data)
for the participant number of 198 reported earlier. As expected, the change
in equation parameters for analysis of variance (ANOVA) models after
imputation was minimal, with a median change of F ⫽ – 0.12.
Outliers. Following recent recommendations in the methodological
literature (Wilcox, Keselman, & Kowalchuk, 1998), one extreme outlier
score (z ⬎ 4.0) was truncated to 0.5 SD beyond the next most extreme
score (only needed for WCST perseverative errors, n ⫽ 1; ⬍ 1%). For the
stopping task, data were excluded if accuracy of response was less than
70% or probability of stopping was outside the range of .20 –.80 (indicating
failure to comply with the task or use of other strategies not intended in the
task). This resulted in exclusion of 11% of scores for the stopping task
(absent scores were then imputed and included in the total missing amount
given above).
Covariates. If executive weaknesses are observed, alternate explana-
tions should be considered. We sought by sampling method (above) to rule
out direct neurological injury that was due to maternal drinking during
pregnancy; a covariance check revealed no effect of maternal drinking
during pregnancy on results. We report correlations of executive measures
with children’s conduct problems and hyperactivity (Giancola & Mezzich,
2000; Finn et al., 2002) as a context for interpreting effects. In addition, we
examined whether any cognitive risk was associated with early parental
alcoholism independently of recent parent alcohol problems. The latter
would suggest that cognitive vulnerability is a familial marker of risk in the
child. On the other hand, an association primarily with current parental
drinking could be regarded as either a more persistent form of alcoholism
(and simultaneously a marker of child cognitive risk) or simply as an
indication that cognitive findings reflect current disruption in parental
functioning. Because lower SES is very much a part of the antisocial risk
subgroup profile (as described), partialing SES was deemed inappropriate
(G. M. Miller & Chapman, 2001; Zucker et al., 1996). Child age did not
correlate significantly with group status or any executive scores and so was
not covaried. We checked independence of executive and IQ effects in
multivariate logistic regression models.
Analysis. We emphasize patterns of effect using multivariate analysis
of variance (MANOVA), with univariate effects described. For each model
we report the effect-size statistic partial eta-squared (␩2), interpreted like r2
(Cohen, 1988). According to Cohen, a small effect size is ␩2 ⫽ .01
(roughly d ⫽ .20), medium is ␩2 ⫽ .06 (⬃d ⫽ .50), and large is ␩2 ⫽ .14
(⬃d ⫽ .80).
307
3 4 5 6 7 8
—
⫺.27** —
⫺.25** .26** —
⫺.01 ⫺.28** ⫺.20** —
⫺.04 ⫺.07 .08 .08 —
⫺.16* .35** .13* ⫺.11 ⫺.05 —
Results
Overview of Samples
Although families came from similar neighborhoods and census
tracts, as expected the groups differed in SES, F(2, 195) ⫽ 9.11,
p ⬍ .001, because of lower SES in the AUD ⫹ ASPD group than
either the control ( p ⬍ .001) or the AUD group ( p ⫽ .005). Boys’
age did not differ across groups (control, AUD, and ADU ⫹ ASP
mean years ⫽ 13.68, 13.63, and 13.62, respectively, p ⫽ ns).
Compared with the community control group, by one-tailed test,
boys in the AUD group exhibited slightly worse teacher-rated
attention problems (␩2 ⫽ .027, p ⫽ .047) and aggression (␩2 ⫽
.022, p ⫽ .05), whereas boys in the AUD ⫹ ASPD group had
markedly worse teacher-rated attention problems (␩2 ⫽ .074, p ⫽
.006), and aggression (␩2 ⫽ .065, p ⫽ .009). These effects were
replicated in maternal report for the boys in the antisocial families
but not for the boys in the alcoholic families. Thus, clear exter-
nalizing behavioral problems were more characteristic of the
AUD ⫹ ASPD group than the AUD group. Groups generally did
not differ significantly on academic performance, except that boys
in the AUD ⫹ ASPD group had weaker math scores than the
control group in early adolescence ( p ⬍ .01).
To evaluate whether our two-domain, pairwise comparison ap-
proach was justified, we conducted a preliminary three-group
MANOVA with all hypothesized cognitive measures (Full Scale
IQ at all time points, Delay of Gratification, and the executive
functions scores). This omnibus test revealed meaningful variation
among the groups, justifying further decomposition, F(24, 368) ⫽
1.85, Wilks’s ␭ ⫽ .796, ␩2 ⫽ .108, p ⫽ .01. Following our
conceptual logic, we therefore analyzed IQ and Delay of Gratifi-
cation as one risk domain and executive functions as another risk
domain, in a pairwise, two-group analytic strategy, anticipating
different results in the two risk domains.
IQ and Delay of Gratification
Two-group MANOVA models (Full Scale IQ at all time points,
Delay of Gratification at Time 1) served to evaluate patterns of
effect for (a) control versus AUD and (b) control versus AUD ⫹
ASPD. For the first model, no omnibus group effects were ob-
served, F(4, 158) ⫽ 1.16, Wilks’s ␭ ⫽ .971, ␩2 ⫽ .029, p ⫽ .33.
The second model, however, revealed an effect three times as large
and significant, F(4, 104) ⫽ 3.15, Wilks’s ␭ ⫽ .892, ␩2 ⫽ .108,
 308
p ⫽ .017. Thus, risk effects were detectable for the AUD ⫹ ASPD
group but not the AUD group versus controls, consistent with
expectations in the literature. However, when the two risk groups
were compared with one another in a MANOVA, they did not
differ, F(4, 119) ⫽ 1.12, Wilks’s ␭ ⫽ .964, ␩2 ⫽ .036, p ⫽ .35.
Table 2 gives the univariate effects from the first two models,
showing the differential results. Boys in AUD ⫹ ASPD families
had consistent cognitive risk versus controls, with lower Full Scale
IQ at all time points and weaker delay of gratification (also worse
in the AUD ⫹ ASPD group than the AUD group, p ⫽ .048).
Executive Functioning in Early Adolescence
Again following our pairwise strategy, we conducted omnibus
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two-group MANOVAs of executive measures, with univariate data
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summarized in Table 3. The first model revealed large differences
between the control and AUD groups, F(8, 154) ⫽ 2.81, ␩2 ⫽ ⫽
.127, p ⫽ .006. Univariate effects were apparent on four of eight
measures (all related to output speed, control, or response suppres-
sion). In contrast, the second model did not reveal overall differ-
ences between the control and AUD ⫹ ASPD groups, F(8, 100) ⫽
1.45, Wilks’s ␭ ⫽ .896, ␩2 ⫽ .104, p ⫽ .185, although the effect
size was only a little less than for the first model (.127 vs. .104).
Only one of the univariate effects was significant. However, when
the two risk groups were compared directly by MANOVA, group
differences were present, F(8, 115) ⫽ 2.17, Wilks’s ␭ ⫽ .869,
␩2 ⫽ .131, p ⫽ .035. The two risk groups (comparisons not
shown) differed in stop signal RT ( p ⫽ .027; worse in the AUD
group) and in Stroop interference (worse in the AUD ⫹ ASPD
group) but neither group differed from controls on the latter
measure, rendering it less notable.
Correlates, Covariates, and Cross-Domain Multivariate
Checks on Results
To provide context for further interpreting the effects observed,
we checked correlates and covariates. Covarying Wave 4 maternal
Table 2
Preschool Delay of Gratification and Preschool, Childhood, and Early Adolescent IQ Scores in
Control and Risk Groups and Pairwise Effect Sizes
Variable Control: A
Preschool
Delay of gratification (s) 71.4 (32.7)
Full-scale IQ 106.2 (14.1)
Childhood
Full-scale IQ 108.6 (14.4)
Early adolescence
Full-scale IQ 108.8 (13.4)
Note. Standard deviations are in parentheses. Data are derived from the multivariate analysis of variance
models reported in the text. The final two columns present the effect size statistic partial eta-squared (␩2). It is
interpreted similarly to R2. According to Cohen (1988), a small effect is ␩2 ⫽ .01 (roughly equal to d ⫽ .20);
a medium effect is ␩2 ⫽ .06 (equivalent to d ⫽ .50), and a large effect is ␩2 ⫽ .14 (equivalent to d ⫽ .80). All
comparisons are two-tailed. B vs. A ⫽ AUD vs. control; C vs. A ⫽ AUD ⫹ ASPD vs. control; AUD ⫽ alcohol
use disorder; ASPD ⫽ antisocial personality disorder.
* p ⬍ .05. ** p ⬍ .01.
NIGG ET AL.
and paternal parent alcoholism status did not alter results for the
boys in AUD families (two-group effect with covariates: stop
signal RT, p ⫽ .032; go RT, p ⫽ .013; RT variability, p ⫽ .025;
symbol digit, p ⫽ .012), but weakened the effect of go RT in the
AUD ⫹ ASPD boys ( p ⫽ .12). To provide interpretive context,
Table 4 provides key correlates of the cognitive scores. As can be
seen, several measures were related to both SES and behavioral
adjustment. With only one time point of executive measures, we
did not evaluate directional effects. Behavioral problems may
mediate cognitive effects on risk, or vice versa.
Table 4 also shows the correlations among early IQ and Delay
and later executive measures. We sought a further analysis to
determine whether the IQ, Delay, and executive function effects
we had observed might be unique versus overlapping in explaining
risk group effects and to further evaluate whether it was plausible
to argue that there might be some distinction in cognitive risk
pathways for children coming from these two types of risk fami-
lies. We therefore constructed three multivariate binary logistic
regression models, comparing (a) control with AUD, (b) control
with AUD ⫹ ASPD, and (c) AUD with AUD ⫹ ASPD.
We constructed models following logic recommended by Hos-
mer and Lemeshow (2000). Cognitive predictors were included in
the model if they met the inclusion criteria of being related to one
of the group effects at p ⬍ .10 in the univariate comparisons. The
variables thus selected were the four significant executive mea-
sures (Table 2; we excluded Stroop interference because its effect
was in the wrong direction, so that it did not add to risk charac-
terization), Time 1 Delay of Gratification, and IQ. To minimize
collinearity, we created a composite Full Scale IQ score across all
time points. These six variables were entered in each model.
Backward elimination (based on chi-square, or Wald, with p ⫽ .10
for entry and p ⫽ .15 for removal) was then applied to arrive at the
most parsimonious model.
Final results for each model are displayed in Table 5. These
models, all of which provided acceptable fit and significant om-
nibus chi-square effects, indicated some distinction in cognitive
Two-group
comparisons’ effect
size (partial ␩2)
AUD: B AUD ⫹ ASPD: C B vs. A C vs. A
66.4 (36.5) 51.8 (37.2) .005 .068**
102.4 (13.5) 99.3 (11.7) .019 .056*
104.9 (12.3) 102.9 (11.6) .022 .051*
104.8 (13.3) 102.8 (9.0) .019 .037*
 EXECUTIVE FUNCTIONS AND RISK FOR ALCOHOLISM 309

Table 3
Executive Function Scores in Control and Risk Groups in Early Adolescence and Pairwise Effect
Sizes

Two-group
comparisons’ effect
size (partial ␩2)

Variable Control: A AUD: B AUD ⫹ ASPD: C B vs. A C vs. A

Stop task: Go RT 729.4 (129.7) 797.6 (137.9) 791.9 (147.6) .061** .045*
Stop task variability 223.3 (62.9) 249.9 (61.7) 239.1 (75.8) .044** .012
Stop task: Stop RT 296.2 (93.9) 331.8 (106.1) 287.7 (75.8) .030* .002
Symbol digit 57.0 (11.1) 53.5 (11.2) 52.6 (10.3) .025* .035†
Verbal fluency 27.7 (8.7) 26.8 (7.7) 28.4 (8.1) .004 .001
WCST perseverations 13.0 (8.1) 11.6 (6.3) 12.8 (7.1) .009 .000
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Tower of Hanoi 11.9 (6.1) 11.3 (5.2) 13.6 (8.2) .003 .014
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Stroop Interference 28.0 (9.6) 25.0 (10.6) 29.5 (9.9) ⫺.021† .006

Note. Standard deviations are in parentheses. Data are derived from the multivariate analyses of variance
models reported in the text. The final two columns present the effect size statistic partial eta-squared (␩2); see
note to Table 2 for more explanation. RT ⫽ reaction time; B vs. A ⫽ AUD vs. control; C vs. A ⫽ AUD ⫹ ASPD
vs. control. Note that for Stroop Interference (color minus color word), higher scores indicate worse perfor-
mance.
* p ⬍ .05. ** p ⬍ .01. † p ⬍ .10 (all two-tailed).

risk pathways for the two groups versus controls. For control
versus AUD, the final model included stop signal RT (response
suppression) and go RT (output speed). For control versus AUD ⫹
ASPD, the final model included Full Scale IQ composite as the
only significant covariate. These models yielded different solu-
tions relative to the control group, yet did not tell us whether the
two risk groups differed from one another. The final model there-
fore compared AUD with AUD ⫹ ASPD; they were differentiated,
with the final model including Delay of Gratification ( p ⫽ .019)
and stop signal RT ( p ⫽ .015). For help in interpreting the odds
ratios, because the variables are on different scales from one
another, see the note to Table 5.
Discussion
Understanding endogenous precursors to alcoholism is one
crucial component to developing more effective prevention and
treatment. A key question has been whether children of alco-
holic parents, known to be at elevated risk for alcoholism later
in life (Dawson, Harford, & Grant, 1992), exhibit executive func-
tion vulnerabilities prior to onset of problem drinking behavior.
Efforts to associate risk status with neuropsychological perfor-
mance in adults have been inconclusive or negative (Nixon &
Tivis, 1997). The few studies of executive functioning in chil-
dren or early adolescents (prior to substantive problem drinking
onset) also yielded inconsistent results, perhaps because of small
sample sizes, varying definitions of risk, and varying selection
of measures. The present article provides one of the most com-
prehensive executive function batteries reported to date on a high-
risk sample of children and includes the first application to alcohol
risk samples of componential measures from the cognitive lit-
erature in an effort to further characterize any vulnerabilities. The
adolescent age of the children at the time of their neurocogni-
tive assessment was sufficiently young that drinking had barely
emerged (only 10% of children reported any alcohol use in the last

Table 4
Correlations of Early Adolescent Executive Function and IQ Scores With SES and Behavioral Ratings

Preschool Teacher-rated behaviors Maternal-rated behaviors

Childhood
DOG IQ-1 IQ-2 SES Inatt Ner/OA Aggress Inatt Delinq Aggress

Stop task: Go RT ⫺.14* ⫺.08 ⫺.09 ⫺.27** .17* .14* .16* ⫺.07 ⫺.07 ⫺.10
Stop task variability .21** ⫺.11 ⫺.11 ⫺.20** .19* .16* .19* .02 ⫺.06 .01
Stop task: Stop RT ⫺.15* ⫺.05 ⫺.14 ⫺.06 .14* .06 .14* .11 .04 ⫺.05
Symbol digit ⫺.29** .17** .37** .41** ⫺.34** ⫺.22** ⫺.18* ⫺.14* ⫺.21** ⫺.25**
COWAT .25** ⫺.04 .32** .11 ⫺.10 ⫺.0 .03 ⫺.14* ⫺.10 ⫺.15*
WCST perseverations ⫺.16* ⫺.16* ⫺.27** ⫺.12 .12 .02 .02 .08 .17** .06
Tower of Hanoi ⫺.05 ⫺.04 ⫺.07 ⫺.10 .04 .00 ⫺.04 .10 .03 .06
Stroop Interference ⫺.08 ⫺.22** ⫺.06 .07 ⫺.05 .05 .12 ⫺.09 ⫺.05 ⫺.10
FSIQ Time 4 .59** .19** .78** .35** ⫺.31** ⫺.20** ⫺.22** ⫺.30** ⫺.20** ⫺.13

Note. DOG ⫽ Delay of Gratification Task; IQ-1 ⫽ preschool Full-Scale IQ; IQ-2 ⫽ childhood Full-Scale IQ; COWAT ⫽ controlled Oral Word
Association Task; WCST ⫽ Wisconsin Card Sort Test; FSIQ ⫽ Full-Scale IQ. Inatt ⫽ inattention (includes items tapping activity level and impulsivity);
Ner/OA ⫽ nervous/overactive; Aggress ⫽ aggressive; SES ⫽ socioeconomic status; RT ⫽ reaction time.
* p ⬍ .05. ** p ⬍ .01, one-tailed correlations.
 310 NIGG ET AL.

Table 5
Binary Logistic Regression Models of Risk Group Effects: Results at Final Step

Variable Wald ␹2 df OR (Exp. B) 95% CI p

Model 1: Control vs. AUD 16.6 2 ⬍.001

Stop signal RT (SSRT) 5.57 1 1.004 1.001–1.008 .018
Go RT 10.06 1 1.004 1.002–1.007 .002
Hosmer–Lemeshow fit index ⫽
11.6 (df ⫽ 8), p ⫽ .17
Model 2: Control vs. AUD ⫹ ASPD 15.2 3 .002
Full-scale IQ 4.37 1 0.958 0.921–0.997 .037
Go RT 3.80 1 1.003 1.000–1.007 .051
Delay of gratification 2.99 1 0.989 0.977–1.001 .083
Hosmer–Lemeshow fit index ⫽
3.7 (df ⫽ 8), p ⫽ .88
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Model 3: AUD vs. AUD ⫹ ASPD 11.1 2 .004

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SSRT 5.90 1 0.993 0.988–0.999 .015

Delay of gratification 5.46 1 0.987 0.976–0.988 .019
Hosmer–Lemeshow fit index ⫽
13.8 (df ⫽ 8), p ⫽ .09

Note. The omnibus model chi-square is the first line of each model. The individual chi-squares are the result
of backward elimination procedure ( p ⫽ .10, entry; p ⫽ .15, removal). A nonsignificant Hosmer–Lemeshow
(2000) fit index indicates a good model fit. The variables are on different scales; odds ratios (OR) can be restated
as follows to make comparison easier. In Model 1, for every 100 ms of slower SSRT or go RT, the OR of being
in the AUD versus control group was 1.49. For Model 2, for every 10 points of lower IQ, the OR of being in
the AUD ⫹ ASPD versus control group was 1.54. For Model 3, for every 100-ms slower on SSRT, the OR of
being in the AUD ⫹ ASPD versus AUD group was 2.01. A minute of earlier response on delay of gratification
conferred an OR for the AUD ⫹ ASPD versus the AUD group of 2.18. CI ⫽ confidence interval; AUD ⫽
alcohol use disorder; ASPD ⫽ antisocial personality disorder.

year, and only 2.5% drank at even a moderate level of four or more
drinks in a month).
Overall, we conceptualized the relevant domains of cognitive
risk broadly in terms of intellectual ability (intelligence or IQ) and
executive functioning. These two meta-constructs each have ex-
tensive empirical and theoretical connections to risk for child and
adolescent behavior problems (Barkley, 1997; Nigg, 2000, 2001;
Sergeant et al., 1999) that are themselves elevated in children of
alcoholic parents (Kuperman, Schlosser, Lidrai, & Reich, 1999).
Yet the two domains are dissociable (Nigg & Huang-Pollock,
2003; Pennington & Ozonoff, 1996). The literature on child hy-
peractivity and child conduct problems points to possible difficul-
ties in the domain of behavioral inhibition (Pennington & Ozonoff,
1996) as well as poor output regulation (a classic pattern of slow
and variable response to fast tasks; Sergeant et al., 1999), but these
effects are clearest in relation to ADHD. In contrast, conduct
problems are related to lower IQ (Nigg & Huang-Pollock, 2003)
and so those effects might be expected in relation to an antisocial
risk pathway. Whether these domains would serve as two distinct
risk indicators (rather than being lumped together into a single,
cognitive vulnerability construct) was therefore of interest.
Consistent with that possibility, our results indicated that chil-
dren from families with AUD ⫹ ASPD in parents—the group at
highest risk of future alcoholism— generally did not differ from
community controls on executive functioning. Instead, that group
was characterized by relative weakness in intelligence and in
reward response, an effect that in aggregate was quite large.
Logistic regression models indicated that IQ was uniquely predic-
tive of their risk status versus controls. These results are consistent
with established findings in terms of IQ in relation to antisociality
and alcoholism risk but challenge the notion that executive func-
tion risk is an important contributor in this most severe risk group.
Indeed, an important possibility is that the risk factors in this group
are associated with risk for antisociality rather than alcoholism, a
conclusion also suggested by other recent work (McGue, Slutske,
& Iacono, 1999).
In contrast, the boys from nonantisocial AUD families had
relative weakness in executive functioning, an aggregate effect that
again was large in magnitude. The weakness in the children from
the AUD families was due to problems in response regulation and
suppression. Those domains were uniquely predictive of their risk
status versus controls whereas IQ was not. The two risk groups
were able to be partially distinguished in a MANOVA of executive
functions and in our focused multivariate logistic regression model
by significant differences in both Delay of Gratification (worse in
the AUD ⫹ ASPD group) and response suppression (worse in the
AUD group). At the same time, they did not differ on most
measures at the univariate level, and the effect size of their exec-
utive differences from controls were relatively similar in absolute
magnitude, so their cognitive risk status clearly overlaps substan-
tially as well. In all, these findings are largely consistent with the
few positive findings on at-risk children in the literature and help
to clarify previous findings.
First, results call into question the theory that the most at-risk
children (those with alcoholic plus antisocial parents) are charac-
terized by executive function weakness, although confirming that
they are characterized by relative weakness in IQ and possibly
reward functions or ability to delay gratification (Gillen & Hes-
selbrock, 1992). Instead, results raise the interesting possibility
that a second cognitive risk pathway involving specific relative
weakness in a subset of executive functions may exist but that this
pathway involves a nonantisocial risk pathway. Presumably, this
second risk pathway is less severe than the antisocial risk pathway.
Of course, the lack of main effects for executive functions in
 EXECUTIVE FUNCTIONS AND RISK FOR ALCOHOLISM
antisocial alcoholism risk does not rule out the possibility of
important moderator effects of executive functioning on other risk
variables, a possibility we will investigate in our longitudinal
follow-up of this sample (see Finn et al., 1999). Second, compar-
ison of our results with the few prior executive function studies of
children at risk is important. Like us, Harden and Pihl (1995)
found executive weakness on only a subset of measures in a
sample of at-risk children that probably did not include the highest
risk antisocial alcoholic families. However, they found group
differences on two tasks for which we failed to find effects: WCST
and Verbal Fluency. Their Verbal Fluency task was written and
thus demanded motor speed and skill; it may therefore be compa-
rable with our finding on symbol-digit rather than our findings on
the COWAT. Several studies of adults have identified weakness on
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This document is copyrighted by the American Psychological Association or one of its allied publishers.
the Porteus Mazes, a task that requires motor control and output
speed. The younger age of Harden and Pihl’s sample or differences
in control or risk-group definition may explain differences on the
WCST. Like us, Corral et al. (1999) failed to find group differ-
ences in children on the WCST. However, on follow up, the
high-risk group was weaker than controls on WCST (Corral et al.,
2003), which was attributed to late-appearing executive difficul-
ties. If so, we should see WCST effects when we follow up our
sample at an older age. Such differences suggest that further
attention to age, sampling, and specific executive domains will be
important.
Demonstration of consistent effects may require sizeable sam-
ples or multivariate strategies. Our multivariate effects were large,
but univariate effect sizes in at-risk samples are qualitatively
smaller than those in strictly psychopathological samples (our
largest univariate effect sizes were only medium in magnitude,
equal to d ⫽ .50, whereas d ⫽ .65–.80 is typical in externalizing
samples; Pennington & Ozonoff, 1996). Because only a subset of
the children in the at-risk groups will go on to develop psychopa-
thology, these groups differ from groups already exhibiting psy-
chopathology. Smaller effect sizes thus may be the norm.
Our executive measures could not be reduced into a common
factor. This underscores that executive functioning is not a unitary
construct but needs to be understood at the level of component
operations (Miyake et al., 2000). Several researchers have been
concerned about specific components of executive function that
may be relevant, such as working memory (Finn et al., 2002) or
cognitive efficiency (Nixon & Tivis, 1997). Our study was the first
to look at executive response suppression (inhibition) and one of
the few to measure response regulation in terms of both rapid
response speed and variability. Our data suggest that these do-
mains may be important as part of an alternate risk pathway but
probably do not contribute to the antisocial risk pathway, consis-
tent with the meta-analytic report by Pennington and Ozonoff
(1996).
We studied only boys herein. Results may not generalize to girls
(Giancola, Shaol, & Mezzich, 2001; Pihl et al., 1990). It is impor-
tant to recognize other limitations in these data. The executive
function data remain cross-sectional; our longitudinal follow up
will be an important next step as the children move into the age of
alcohol problem onset. Although we relied on MANOVAs for our
primary conclusions, specific univariate comparisons were uncor-
rected, so those univariate findings may be vulnerable to Type I
error. In addition, we did not examine formal psychiatric diagnoses
in the children, nor did we examine other psychopathology (e.g.,
depression, attention deficit hyperactivity disorder) in the parents
311
that could influence child neuropsychological performance. One
can also ask whether test motivation would affect results on the
challenging executive tests. Although such effects cannot be ruled
out (especially in light of slow RT findings), it seems unlikely that
motivation effects would lead to one group showing an executive
weakness and the other group an IQ weakness. It will be important
in future work to examine potential behavioral moderators of these
cognitive effects, which were correlated with behavior problems.
In conclusion, our data failed to support the hypothesis that the
highest risk youngsters (those from antisocial alcoholic families)
carry executive function risk for future alcoholism as a main effect.
Instead, results confirmed that the primary cognitive risk in that
group appears to lie in the verbal and intelligence domains and
possibly in reward–response dysfunction. The data also raise a new
possibility, which is that a second, probably less severe risk
pathway in children of alcoholic parents involves primarily exec-
utive function risk but not verbal, intelligence, or reward–response
dysfunction. The possibility of this dual-risk pathway will be a key
focus of follow-up efforts with this sample, to determine whether
both cognitive profiles lead to AUD.
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Received October 7, 2002
Revision received November 19, 2003
Accepted November 20, 2003 䡲