Substance Use Disorders and Cluster BPersonality Disorders: Physiological, Cognitive,

and Environmental Correlates in aCollege Sample

Jeanette Taylor, Ph.D.

Department of Psychology, Florida State University, Tallahassee, Florida, USA

Abstract: Substance use disorders (SUDs) and Cluster B personality disorders (PDs)

are both marked by impulsivity and poor behavioral control and may result in part

from shared neurobiological or executive cognitive functioning deficits. To examine

the potential utility of such models in explaining variance in SUDs and PDs at the

lower end of symptom expression and impairment, 123 (73 female) volunteer college

students were administered 2 measures of executive cognitive functioning; a task

assessing autonomic reactivity to aversive noise blasts; a life events and a peer

substance use measure; and structured clinical interviews to assess symptoms of

substance abuse/dependence and antisocial, borderline, histrionic, and narcissistic

PDs. As expected, symptoms of SUDs and PDs were significantly positively

correlated. Antisocial PD, alcohol and cannabis use disorder symptoms were

significantly positively related to proportion of friends who use alcohol and drugs

regularly and drug use among romantic partners. Number of negative life events was

positively related to PD symptoms and to alcohol use disorder symptoms. Executive

cognitive functioning was not related to SUD and PD symptoms in the expected

direction. Findings suggest that, among higher functioning young adults, environ-

mental factors may be particularly relevant to our understanding of SUDs and cer-

tain PDs.

Keywords: Substance use disorder, personality disorder, skin conductance, life events

The author thanks Leonardo Bobadilla and Mark Reeves for their help with data

collection.

Address correspondence to Jeanette Taylor, Ph.D., Department of Psychology,

Florida State University, Tallahassee, FL 32306-1270, USA; E-mail: taylor@psy.

fsu.edu

The American Journal of Drug and Alcohol Abuse, 31:515–535, 2005

Copyright D Taylor & Francis Inc.

ISSN: 0095-2990 print / 1097-9891 online

DOI: 10.1081/ADA-200068107

Order reprints of this article at www.copyright.rightslink.com

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INTRODUCTION

Substance abuse and dependence are common mental health disorders that

typically onset in young adulthood (1). Alcohol use problems are found in

10–25% of young adults (2, 3), and risk for heavy drinking and drug use that

may lead to substance use disorders (SUDs) is particularly high among young

adults (4). Costs associated with alcohol and drug abuse in the United States

(lost earnings, medical consequences, special services, accidents, etc.) are

estimated at $110–170 million annually (5), which underlines the importance

of SUDs as a mental health issue and as a focus of research.

SUDs are often comorbid with each other and with other mental

disorders, including personality disorders (PDs) (6), which are defined by

patterns of maladaptive responses related to one’s perceptions, cognitions,

emotional range/reactivity, or impulse control. Like SUDs, PDs are relatively

common and are found at high rates among young adults (7), In clinical

populations, comorbidity is especially high between SUDs and Cluster B

PDs, which are marked by erratic, dramatic behavior and includes antisocial

(ASPD), borderline (BPD), histrionic (HPD), and narcissistic (NPD). Cluster

B PDs are found at a high rate (>50%) among patients with various SUDs

(8, 9), and the association is strongest for ASPD and BPD. Around 30–50%

of patients with BPD have a SUD (10), and the link between ASPD and SUDs

is well documented with a widely used typology of alcoholism using ASPD

as a defining feature (11, 12). Onset of ASPD typically precedes onset of drug

dependence (13), indicating that ASPD may pose a risk for development of a

SUD. The association of SUDs to ASPD extends beyond clinical populations

to both college (14) and epidemiological ones (15).

Numerous explanatory models for SUDs and various Cluster B PDs have

been put forth, but few have focused on comorbidity. One model for the

comorbidity posits that high levels of the temperament factor novelty seeking

increases the likelihood of expressing features of both SUDs and Cluster B

PDs (16). Similar to this idea is that a common externalizing factor mediated

by genes contributes to the joint expression of SUDs and certain Cluster B

PDs (e.g., antisocial) (17). Gray’s (18) appetitive/aversive motivational

system has been offered as a factor in the expression of impulsivity and

behavioral inhibition, areas of dysfunction associated with SUDs and Cluster

B PDs. According to Fowles (19, 20), variation in the strength of Gray’s

(18, 21) behavioral inhibition system (BIS) and behavioral activation system

(BAS) may be reflected in physiological reactivity and in expressed

psychopathology. Gray (21) suggested that the neural structure of the BIS

includes inputs to the prefrontal cortex, the area of the brain associated

with executive cognitive functioning; the neural structure of the BAS is

thought to relate to the dopaminergic ‘‘reward circuit’’ (the circuit associated

with SUDs).

Skin conductance reactivity reflects autonomic nervous system arousal

that (like executive cognitive functioning) appears to be regulated by the

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frontal cortex (22, 23), the area associated with the BIS (18). According to

Fowles (20), a weak BIS and a strong BAS contribute to the expression of

SUDs and ASPD and this idea has been supported through findings of

autonomic hypo-reactivity among men at risk for alcoholism (24), adolescent

boys with SUDs (25, 26), young adult men and women with SUDs (27), and

people with psychopathy (28)—a construct related to ASPD. This model

could be extended to other Cluster B PDs to help explain their high

comorbidity with SUDs. For example, impulsivity and poor behavioral

control are prominent features of BPD and thus, the highly reactive BAS and

underactive BIS that lead to excessive substance use also may lead to

behaviors that characterize people with BPD. Consistent with this idea,

autonomic hyporeactivity has been observed in women with BPD (29).

Deficits in executive cognitive functioning can manifest as impaired

judgment, poor planning, and impulsivity: problems associated with SUDs

and Cluster B PDs. Executive cognitive functions are controlled by the frontal

cortex, which shows marked development in adolescence and early adulthood

(30)—the period in which SUDs and PDs typically onset—and are related to

motivation and learning (31)—domains associated with BIS/BAS functioning.

Given the idea that BIS/BAS strength could provide a liability toward SUDs

and Cluster B PDs, poorer executive functioning would likely enhance that

liability and perhaps contribute to other aspects of the disorder (e.g.,

impairment). Deficits in executive cognitive functioning have been linked to

SUDs (32–35) BPD (36–38), and ASPD (39); also see Ref. (40). However,

negative findings also exist for SUDs (41), BPD (42), and ASPD (34, 43).

Behavior stemming from motivation and learning (related to BIS/BAS

functioning) and from executive cognitive processes occur within the context

of the environment, which may further enhance the risk for SUDs and Cluster

B PDs, both individually and jointly. For example, poor judgment resulting

from executive cognitive functioning deficits may lead to excessive

substance use despite negative consequences and also to affiliation with a

deviant social group that enhances and reinforces the substance use problem

(or perhaps even introduces the person to substance use). Consistent with this

idea, peer deviance (drug use and/or antisocial behavior) has been robustly

associated with both substance use (44–49) and substance abuse (50–52) at

least among adolescents. Further, relationship between peer attributes and

substance abuse may be mediated by behavioral control (51).

Peer alcohol use continues to be a salient correlate of alcohol use into

early adulthood (53, 54). However, peer substance use has not been ade-

quately examined in relation to SUDs beyond adolescence or to Cluster B

PDs at any age and, therefore, it is not clear whether substance using peers

are an important contributor to SUDs in young adulthood or even a

significant correlate of associated disorders such as Cluster B PDs. The latter

may be an important link in that certain PDs (e.g., antisocial) may increase

the likelihood of an association with substance using peers that in turn

increases the risk for SUDs.

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Stressful life events are another salient environmental factor that has

been linked to SUDs (55). Kendler (56) proposed a gene-environment

correlation such that genetic factors associated with the liability toward SUDs

also contribute to behaviors that make certain negative life events more

likely. Cluster B PDs are also associated with higher rates of negative life

events (57), but it is not clear if this relationship is independent of the one

between life events and SUDs. It is conceivable that people with Cluster B

PDs have chaotic lives as a result of their personality which in turn leads to

negative life events and an increased use of alcohol and drugs (perhaps as a

coping behavior).

The BIS/BAS model provides a neurobiological/motivational framework

for SUDs, ASPD, and BPD, and perhaps their comorbidity. The literature

suggests that an executive functioning deficit may be part of the cognitive

framework for these same disorders. Finally, the literature suggests at least 2

important environmental factors—negative life events and deviant peers—in the

environmental framework for SUDs and perhaps also Cluster B PDs. Both ASPD

and BPD have received vastly greater research attention than NPD and HPD

leaving their comorbidity to SUDs more of a mystery. Moreover, previous

research has not adequately examined nonclinical samples. Such investigations

are needed to test the appropriateness of etiological models in explaining

variance in SUDs and Cluster B PDs across the presentation spectrum.

The present study examined individual differences in symptoms of SUDs

and all 4 Cluster B PDs as they relate to individual differences in executive

cognitive functioning, autonomic reactivity, peer substance use, and negative

life events in early adulthood. Data were collected from a volunteer sample of

college students who, as a demographic group, are at risk for heavy substance

use and SUDs (3, 4) as well as PDs (1, 7). Importantly, college students who

are heavy substance users are unlikely to seek treatment even when their

substance use leads to problems (4). Thus, the present study examined

correlates of SUDs and Cluster B PDs in people who may not be seeking

treatment for these problems but who are at risk to experience them.

Given the documented comorbidity among SUDs and Cluster B PDs,

symptoms of those disorders were expected to correlate positively. Electro-

dermal response modulation was expected to correlate negatively with SUD

symptoms [based on findings from Taylor (27) and Taylor et al. (26)]. As per

the reviewed literature, both SUD and Cluster B PD symptoms were expected

to correlate negatively with indices of executive cognitive functioning and

positively with number of negative life events. Previous findings from ado-

lescent samples led to the expectation that SUD symptoms would correlate

positively with substance use among friends and romantic partners. Symp-

toms of Cluster B PDs were also expected to correlate positively with

substance use among peers based on the idea that people with Cluster B PDs

may select friends with similar levels of behavioral undercontrol (manifested

as substance use). Finally, it was assumed that behavioral undercontrol and

impulsivity would be most pronounced in people comorbid for SUDs and

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PDs and result in more severe problems (e.g., more negative life events).

Consistent with this idea, people with comorbid SUD and Cluster B PD

diagnoses were expected to show poorer electrodermal response modulation,

poorer executive cognitive functioning, more negative life events, and more

friends and partners using alcohol and drugs than those with only a SUD and

controls (who were expected to differ from those with only a SUD).

METHOD

Participants

Participants were 123 (73 female) students attending a large southeastern

U.S. university. Persons aged 18 or older without a self-reported history of

head injury, neurological disorder, or hearing problems were recruited

through advertisement fliers for a paid ($25) study of psychological and

physiological functioning. The sample was primarily White (59.3%), African

American (16.3%), and Hispanic/Latino (13.8%) with a mean age of 20.8

(SD=4.15). Informed written consent was obtained from each participant and

the study was approved by the IRB.

Procedures and Measures

Data were collected from individuals during a 2.5-hour laboratory session;

measures are described below in the order in which they were administered.

Psychophysiological Measurement

Participants washed their hands with Ivory soap and rubbing alcohol was

swabbed on the medial phalanx of the middle and ring finger of each hand prior

to placement of silver-silver chloride (Ag-AgCl) electrodes that were filled

with commercially available SC electrode cream and attached using electrode

collars (8 mm diameter opening). The SC from the right and left hands were

recorded through two DC amps connected to separate 24-bit digitizing SC

couplers from Contact Precision Instruments (Cambridge, MA). The system

used constant 0.5-V electrode excitation as specified by Lykken and Venables

(58). Data were digitized online at 128 Hz. All physiological data were

acquired and scored with the PSYLAB 7 software program from Con-

tact Precision Instruments running on two interfaced IBM-compatible PCs.

Participants were seated alone in a darkened room equipped with a

microphone, a video camera for monitoring participation, and a computer

monitor for visual stimulus presentation.

Participants received experimenter communications and auditory stimuli

through stereo headphones. Participants were asked about irregularities in

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food, drug, nicotine, and caffeine intake prior to the study session.

Psychophysiological recording began with a 2-minute relaxation period

followed by a 90-second task in which participants received a single 2-second

unpredictable blast of 92 or 1101 dB white noise that served to orient them to

the aversive sound used in the Cooltest.

In the Cooltest, participants were given 6 presentations of a video clip of

a numberless, unmarked clock with a sweep second hand and a 2-second blast

of white noise. Participants were told that the noise would be unpredictable

on some trials and that on other trials there would be a red hash mark on the

clock face to make the noise predictable (during the instructions, participants

were shown a still image of the predictable clock with a red hash mark in a

position not used in the actual test). Participants were told that the type of

trial coming next would be indicated on the computer screen just before each

trial began and their task was to ‘‘stay cool’’ and not react to any of the

noises. Consistent with an earlier Cooltest study (26), trials 1, 4, and 6 were

predictable; trials 2, 3, and 5 were unpredictable and blast times were

invariant across subjects and occurred between the 18th and 50th s of each 1-

minute trial (each trial was associated with a particular, unrepeated blast

time). No stimuli were presented in the 5 seconds between trials.

The SCR amplitude for each of the Cooltest trials, defined as the

difference (in msiemens) between the SCL preceding the response and the

SCL at the peak of the response, was scored from each hand via automated

procedures or by people blind to the participant’s other data. Electrodermal

response modulation, reflecting the percent change in SCR when the blast is

predictable, was quantified as follows (using raw SCR data given the built-in

range correction):

100 � ðMean SCRUnpredictable � Mean SCRPredictableÞ=Mean SCRUnpredictable

A t-test showed no significant difference between scores across hands and,

therefore, the scores were averaged for a mean electrodermal response

modulation score that was used in analyses.

Executive Cognitive Functioning Measures

The 64-card computerized research version of the Wisconsin Card Sorting

Test (WCST) (59, 60) and the Stroop test (61) were administered next. The

1A problem with the calibration of the white noise generator’s output inadvertently

caused a reduced noise of 92 dB to be delivered for all stimuli to the first 42

participants through the study. A t-test comparing the electrodermal response

modulation score of those who received all stimuli at 92 (n=36) versus 110 dB

(n=77) showed no significant difference, t (110)=�0.73, p=.47. Thus, data were not

excluded on participants who received the 92 dB noises.

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Stroop test yields an interference score reflecting the extent to which a

previously learned response (reading color names) interfered with ability to

inhibit the learned response (naming an ink color that is mismatched to the

target color word, e.g., ‘‘red’’ is printed in blue ink). The WCST requires the

sorting of cards by an unidentified preset criterion using trial and error with

only minimal feedback (i.e., ‘‘correct’’ or ‘‘incorrect’’ after each card is

sorted). The criterion changes after a preset number of successful responses.

The WCST produces t-scores for perseverative responses and errors (which

reflect the extent to which the examinee continued using a previously

successful strategy after the criterion changed), nonperseverative errors, and

total errors. Indices of executive cognitive functioning included these t-scores

from the WCST and interference score from the Stroop test.

Symptoms of Substance Use Disorders and Cluster B

Personality Disorders

Lifetime occurrence of symptoms of SUDs (alcohol, cannabis, sedatives,

stimulants, cocaine, opioids, hallucinogens, PCP, and ‘‘other’’ [inhalants,

steroids, non-prescription sleep or diet pills]) and other Axis I disorders was

assessed using the Structured Clinical Interview for DSM-IV, Non-patient

Edition [SCID-I/NP; Ref. (62)]. Symptoms of HPD, NPD, BPD, and ASPD

were assessed with the Structured Interview for DSM-IV Personality

Disorders (SIDP-IV) (63). Trained graduate students (who were blind to

the participant’s other study data) administered the interviews.

Symptoms of each disorder were assigned via consensus of at least 2

clinical graduate student interviewers examining all available clinical

information (including audio tapes of the interviews). Symptom data were

entered into a computer and a count of the symptoms met at threshold level

was generated for each diagnosis using a computer algorithm. This symptom

count was combined with the requisite other clinical criteria (e.g., duration)

to produce diagnoses via a computer algorithm. Diagnoses were generated at

the definite (all criteria met) and probable (all but one criteria met) certainty

levels to identify subthreshold diagnostic cases and avoid classifying them as

diagnostically clean. Symptom counts further captured the presence of

clinically significant problems at even subthreshold levels of diagnosis.

Reliability of diagnoses (probable or definite) using the consensus procedure

was good (kappas ranged from .61 to 1.0 for both the Cluster B PDs and the

SUDs). Similarly, reliability correlations for symptom counts were high

ranging from .84 to .96 for Cluster B PDs and .69 to 1.0 for SUDs.

An examination of the data indicated that alcohol and cannabis abuse and

dependence were the most common SUDs. As such, they were examined

separately from the remainder of the illicit drugs. Symptoms of abuse and

dependence were combined yielding counts of abuse/dependence symptoms

of alcohol, cannabis, and other (non-cannabis) illicit drugs.

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Life Events and Substance Use Among Friends and Partners

Self-reports to assess life events and substance use among peers were

created for this study. The life events measure included 20 events that were

rated on frequency of occurrence within the past 12 months (0, 1, 2, or 3

times or more coded 0 to 3, respectively) and how stressful the event was

on a scale from 0 (not at all) to 3 (very stressful) (for events occurring more

than once, the most stressful occurrence was rated). Twelve events were

rationally selected as negative (e.g., ‘‘Experienced a break-up in a sig-

nificant romantic relationship’’) and responses were summed within that

category. Internal consistency reliability was acceptable for number of

negative life events (alpha=.67). The stress ratings of the 12 negative life

events were averaged to produce an average level of stress associated with

negative life events.

An 8-item self-report was created to assess substance use among peers.

Participants indicated the number of friends they had (defined as people they

‘‘talk to or see regularly’’) on a scale from 0 (coded 0) to 10 or more (coded

5) within the past 12 months and the proportion of their friends (from 0=none

to 4=almost all) that drank alcohol, drank alcohol once a week or more, used

an illicit drug, and used an illicit drug once a week or more. Using those same

metrics, participants indicated the number of romantic partners they had

(defined as people they ‘‘had dated’’) within the past 12 months and the

proportion of partners who drank alcohol and used an illicit drug. Given that

the definition of romantic partner could easily include people the participant

did not know very long or very well, the validity of responses regarding

regular use of alcohol and drugs by partners was potentially low and was

therefore not assessed.

Diagnostic Groups Used to Examine Comorbidity

Participants were placed into groups based on the presence of any SUD

diagnosis (abuse at the definite level or dependence at the probable or definite

level) and any Cluster B PD diagnosis (at the probable or definite level).

Participants without an SUD or Cluster B PD diagnosis (and no anxiety

disorder or depression) formed the control group (n=27; 17 female); 10

participants (7 female) with at least one SUD diagnosis (and no other

diagnosis) formed the SUD only group; and 18 participants (7 female) with at

least one SUD and at least one Cluster B PD diagnosis formed the comorbid

group. Diagnoses related to alcohol and cannabis made up the vast majority

of SUD diagnoses for the SUD only and comorbid groups and ASPD and

BPD made up the majority of PD diagnoses in the comorbid group.

Furthermore, adult antisocial behavior (ASPD without conduct disorder) was

included as a PD diagnosis based on research showing that people with ASPD

are similar to those with adult antisocial behavior on various correlates

(64, 65). Finally, there were not a sufficient number of cases to form a Cluster

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B PD only group, which precluded a test of the unique association of Cluster

B PDs with the various dependent variables.

Analyses

First, descriptive data on symptom counts and rates of diagnoses were

calculated for each disorder. Next, Pearson interclass correlations were

calculated between the symptom counts for SUDs and Cluster B PDs, and

the psychophysiological, cognitive, and environmental variables to index the

strength of the associations. Partial correlations were used to investigate the

impact of these variables on the association between symptoms of PDs and

SUDs. A Bonferroni correction for the total number of correlations to be

calculated would have been prohibitively conservative; therefore, a

Bonferroni correction was made for each disorder category. Alpha for the

4 Cluster B PDs was corrected (.05/4) yielding an alpha of .013 for

correlations with those disorders. Similarly, the alpha for correlations with

the three SUDs was set to .017. The maximum sample size for the

correlational analyses for PDs was 123, which yielded adequate power

(83%) to detect medium effects [d� .3 using conventions put forth by

Cohen (66)] at the corrected alpha of .013. Data were missing on some

measures (e.g., on electrodermal modulation score due to recording failures)

leaving a minimum of 107 cases for some of the correlations with PD

symptoms, which still left adequate power (76%) to detect medium-sized

correlations at the corrected alpha. The maximum sample size for the SUD

correlational analyses was 120 due to some missing interview information,

which yielded adequate power (85%) to detect medium effects (d� .3) at

the corrected alpha of .017. Missing data on the correlates led to a minimum

of 97 cases for some of the correlations with SUD symptoms, which still

left adequate power (75%) to detect medium-sized correlations at the cor-

rected alpha.

Finally, comorbidity between SUDs and Cluster B PDs was examined in

relation to executive cognitive functioning, physiological reactivity, life

events, and substance use among friends and romantic partners by comparing

scores on those variables among 3 diagnostic groups (control, SUD only, and

comorbid SUD-Cluster B PD). Groups were compared using one-way

ANOVA with post hoc Least Significant Difference follow-up tests. (The

sample was underpowered for tests of gender effects and thus no factorial

ANOVA models were tested.) A total of 55 participants were classified into

the 3 groups, which allowed detection of large effects [d� .45 using

conventions put forth by Cohen (66)] with adequate power (84%) at alpha set

to .05. Missing data for some dependent variables led to a minimum sample

of 48 for the group analysis, which still provided adequate power (77%) to

detect large effects. Power analyses were conducted using the G*Power

program (67).

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RESULTS

Table 1 presents the mean and standard deviation for raw symptom counts of

each disorder. As is often the case in nonclinical samples, the symptom count

distribution for each disorder was positively skewed and the data were

submitted to a log-transformation (log10 [x=1]) prior to analyses. Table 1

also presents rates of SUDs and Cluster B PDs, which were largely consistent

with general prevalence rates for those disorders (1–3). The rate of ASPD

was high and was not attributable to low diagnostic reliability. Instead, the

inclusion of probable cases of adult antisocial behavior (i.e., people meet-

ing just 2 ASPD criteria) may have contributed to the higher rate for

that disorder.

Table 2 presents interclass correlations among log-transformed symptom

counts of PDs and SUDs and psychophysiological and environmental

variables. As expected, correlations among the Cluster B PDs and among

SUDs were significant with the exception of HPD and NPD symptoms, which

did not correlate with SUD symptoms. As expected, electrodermal response

modulation showed a significant inverse relationship to drug use disorder

symptoms. Consistent with the report by Taylor (27) using this same sample,

symptoms of Cluster B PDs were not significantly associated with

electordermal response modulation. As expected, SUD, ASPD, and NPD

symptoms were significantly positively associated with peer substance use.

Partial correlations were used to investigate the influence of peer

substance use on the association between ASPD and SUD symptoms. The

correlation between ASPD and alcohol use disorder symptoms remained

significant and ranged in magnitude from .24 (when controlling for drug use

Table 1. Symptom count means (and standard deviations) and prevalence rate for

each disorder

Disorder N Mean (SD) % with Diagnosisa

Narcissistic personality disorder 123 0.43 (0.98) 3.3

Histrionic personality disorder 123 0.41 (0.90) 2.4

Borderline personality disorder 122 0.78 (1.25) 4.1

Antisocial personality disorderb 121 0.64 (1.17) 18.2

Alcohol abuse/dependencec 116 1.81 (2.53) 37.9

Cannabis abuse/dependencec 120 1.04 (2.04) 29.2

Non-cannabis illicit drug

abuse/dependencec120 1.00 (3.16) 14.2

aIncludes cases diagnosed at a probable or definite certainty level.bIncludes adult antisocial behavior in the mean and in the rate of diagnosis.cMean includes symptoms of abuse and dependence; rate of diagnosis reflect the

percent of the sample that met criteria for abuse at a definite level or dependence at a

probable or definite level.

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among friends) to .27 (when controlling for alcohol use among friends).

Similarly, the correlation between ASPD and cannabis use disorder

symptoms remained significant and ranged from .34 (when controlling for

drug use among friends) to .40 (when controlling for alcohol use among

friends). Finally, ASPD was significantly correlated with non-cannabis illicit

drug use disorder symptoms when controlling for drug use among friends

(r = .35). Narcissistic PD symptoms were significantly correlated with peer

drug use, which may have resulted from the association between NPD and

Table 2. Interclass correlations among symptom counts of personality disorders,

substance use disorders, substance use among friends and romantic partners, and

life events

NPD HPD BPD ASPD ALC CAN ILLIC

Histrionic personality

disorder (HPD)

.40

Borderline personality

disorder (BPD)

.42 .31

Antisocial personality

disorder (ASPD)

.25 .19 .38

Alcohol abuse/

dependence (ALC)

.18 � .01 .32 .35

Cannabis abuse/

dependence (CAN)

.15 .02 .33 .45 .46

Illicit drug abuse/

dependence (ILLIC)

.10 .07 .32 .43 .34 .35

Electrodermal response

modulation

.03 .21 .03 � .09 � .22 � .25 � .23

Number of friends .12 .05 � .06 .00 .26 .03 � .03

Friends drink alcohol .20 .11 .10 .25 .48 .35 .17

Friends drink 1� /week

or more

.17 .05 .10 .24 .58 .38 .19

Friends use drugs .30 .11 .19 .38 .40 .45 .34

Friends use drugs

1� /week or more

.28 .06 .15 .31 .45 .45 .20

Number of romantic

partners

.33 .21 .17 .12 .23 .11 � .03

Partners drink alcohol .10 � .07 .00 .15 .39 .15 .06

Partners use drugs .26 .06 .13 .34 .36 .44 .22

Number of negative

life events

.21 .24 .26 .30 .24 .19 � .01

Average stress for

negative events

� .02 .11 .23 � .12 � .05 � .04 .07

Note: ILLIC=non-cannabis illicit drug abuse/dependence. Drinking and drug use

variables for friends and partners refers to proportion of friends and partners who use

substances. Significant correlations ( p<.013 for personality disorders; p<.017 for

substance use disorders) are in bold type.

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ASPD (the latter of which was significantly correlated with peer drug use).

To test this, symptoms of NPD were correlated with the peer drug use

variables while controlling for ASPD symptoms and the correlations

remained significant at p < .05, indicating that people with NPD features

have higher proportions of friends and romantic partners who use drugs and

the association is not accounted for by antisocial or SUD symptomatology.

Finally, the correlations in Table 2 revealed that negative life events

were related as expected to most PDs and to alcohol use disorder symptoms.

When controlling for number of negative life events, the correlations between

alcohol use disorder symptoms and symptoms of BPD (r = .27) and ASPD

(r = .30) remained significant (p < .005).

Correlations between PD and SUD symptoms and executive cognitive

functioning variables were largely nonsignificant (most were <.10 in

magnitude) and, therefore, were not presented in detail. Total errors on the

WCST correlated significantly with symptoms of BPD (r = .23) and alcohol

use disorders (r = .24), which were also significantly associated with

nonperseverative errors (r = .27). These correlations were not in the expected

direction such that symptoms were associated with higher T-scores (i.e.,

better performance or fewer errors).

The results of the ANOVA analyses were consistent with the results of

the correlational analyses. As expected, diagnostic groups differed signifi-

cantly (p < .001) on number of negative life events, F (2, 53) = 7.52. Also

consistent with expectations, post hoc follow-up tests showed that the

comorbid group had significantly (p < .004) more negative life events than

both the controls and the SUD only group. On average, the comorbid group

reported nearly 7 negative life events within the past 12 months compared to

an average of about 2.7 for the SUD only and control groups. Groups did not

differ significantly on any of the executive cognitive functioning indices or

electrodermal modulation score.

Figure 1 presents the mean proportion of friends and romantic partners

within the past 12 months who used alcohol and drugs. A significant group

effect was found for regular (once a week or more) use of alcohol, F (2,

52) = 3.48, p = .04, and illicit drugs, F (2, 50) = 5.35, p = .008, among friends.

A significant (p = .001) group effect was also found for drug use among

friends, F (2, 512) = 7.86, and romantic partners, F (2, 48) = 8.77. Differences

between groups were only partly consistent with expectations. As illustrated

in Figure 1, post hoc follow-up tests revealed that, as expected, the comorbid

group had significantly (p<.05) more friends and partners using substances

than controls. The SUD only group also differed significantly from controls

in the proportion of friends who regularly use alcohol (p <.03) and romantic

partners who use illicit drugs (p<.02). The difference between the SUD only

group and controls on the proportion of friends who use drugs and those who

use drugs regularly showed a trend toward significance (p<.08). However,

contrary to expectations, the comorbid group did not differ significantly from

the SUD only group in any of the post hoc tests. There was not a significant

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effect for group on number of friends or proportion of friends who drink

alcohol. A group effect was found for number of romantic partners, F (2,

54)= 4.59, p = .02, with the SUD only and comorbid groups evidencing

significantly (p< .04) more romantic partners than the control group.

DISCUSSION

Substance use disorders and Cluster B PDs may share neurobiological,

cognitive, and environmental risk factors that contribute to their individual

and joint manifestations. However, few studies have examined variables

tapping each of these domains in relation to SUDs and Cluster B PDs within

the same sample. The present study examined multivariable data in a young

adult sample to provide insights into factors that relate to SUDs and Cluster B

PDs individually and jointly and to shed light on whether various risk factors

are significantly associated with SUDs and PDs at the lower end of the

spectrums of severity and impairment. Certain environmental factors may be

particularly relevant to understanding SUDs, Cluster B PDs, and their

comorbidity in nonclinical populations.

Figure 1. Mean proportion of friends and romantic partners within the past 12

months who used alcohol and illicit drugs. The vertical line with cross bars

represents±1 SE. SUD = substance use disorder; PD = Cluster B personality disorder.

Descriptors for the scale values are given on the y-axis. Ratings were made only if the

participants indicated any friends or romantic partners within the past 12 months.

Control group n = 24–27; SUD only group n = 9–10; Co-morbid SUD-PD group

n = 17–18.

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The expected interrelations were found among symptoms of SUDs and

among symptoms of Cluster B PDs, indicating covariance of these problems

in nonclinical samples. These data from clinical interviews were consistent

with studies using self-reports that found significant comorbidity among

Cluster B PDs in nonclinical samples (68). Also as expected, symptoms of

Cluster B PDs and SUD were significantly related, but only with regard to

BPD and ASPD. Histrionic and NPD symptoms, while related to each other

and to the other PDs, were not related significantly to SUD symptoms in this

young adult college sample. Thus, consistent with research from clinical

samples, BPD and ASPD were the Cluster B disorders that were most

strongly related to SUDs. An important caveat to this conclusion is that BPD

and ASPD were more common in this sample and the restricted range of

symptoms of HPD and NPD may have attenuated their associations with the

other variables, including SUD symptoms.

The data were fairly consistent with previous work showing positive

associations between SUDs and number of negative life events experienced.

However, the association with negative life events was significant only for

alcohol use disorder symptoms in the present study. Also consistent with

previous work [e.g., Ekselius et al. (7)], symptoms of most Cluster B PDs

were significantly related to negative life events. Furthermore, the findings

from the group comparisons suggested that Cluster B PDs contributed

substantially to the likelihood of experiencing negative life events given that

the people with both an SUD and a comorbid Cluster B PD diagnosis reported

more than twice as many negative life events as those with only an SUD

diagnosis and those without a psychiatric diagnosis. Thus, the data suggest

that young adults with substance use problems and features of PDs marked by

impulsivity and erratic behavior are likely to experience higher numbers of

negative life events (e.g., having a serious fight with a close friend) than even

those with just substance use problems. The present data cannot address the

direction of causation and no single obvious causal pattern exists because

negative life events could conceivably be either a consequence of or a

contributor to a substance use problem or a maladaptive personality style.

The present data suggest that further study of life events as they relate to

SUDs and Cluster B PDs individually and jointly is warranted.

Consistent with research conducted largely in adolescent samples, the

present study found significant associations between symptoms of SUDs and

the substance use habits of friends and romantic partners in early adulthood

and extended earlier research findings to certain Cluster B PDs. Cannabis and

alcohol use disorder symptoms and ASPD symptoms were all significantly

associated with alcohol use among friends and drug use among friends and

romantic partners. Narcissistic PD symptoms also were significantly

associated with drug use among friends and romantic partners despite the

lack of association of narcissism with SUDs in this sample. Unlike with

negative life events, the comorbidity between SUDs and Cluster B PDs did

not relate to an increase in substance use among peers, suggesting that having

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an SUD increases the likelihood of hanging around with friends and getting

involved with romantic partners who use alcohol and/or illicit drugs in young

adulthood regardless of co-morbid Cluster B PD pathology. Again, the

present data do not address the direction of causation and various scenarios

are plausible including the possibility that SUDs lead to seeking friends and

romantic partners with similar levels of substance use or, alternatively,

substance use among friends and romantic partners increases one’s own use

thereby increasing the chances of developing an SUD. The nature of the

relationship between peer substance use and SUDs is an important area

for future study because of it has potential implications for intervention

and prevention.

Consistent with the notion that a weak BIS contributes to the liability

toward SUDs, symptoms of illicit drug use disorders (including cannabis)

were inversely related to electrodermal response modulation. However,

similar support was not found for Cluster B PD symptoms. Not surprisingly,

the present data were consistent with another report from this same sample

showing poor electrodermal response modulation to be associated with SUDs

and not Cluster B PDs (27). Thus, these findings do not represent independent

evidence for a potentially specific link between SUDs and electrodermal

response modulation, but are nonetheless consistent with that idea. The group

analyses failed to show a significant association between electrodermal

response modulation and SUD, suggesting a possible inconsistency with

earlier reports (26, 27). An examination of effect sizes revealed a large

difference (d=.69) between controls and the comorbid group and only small

differences (d=.23) between controls and the SUD only group and between

the SUD only and comorbid groups. Therefore, although other research

suggests that SUDs may be particularly strongly related to poor electrodermal

response modulation, more work is needed before ruling out the possibility

that Cluster B PDs are also related to this biological factor.

Negative findings from this study on the association between executive

cognitive functioning and SUDs may provide insights into the mixed picture

presented by the extant literature. The present study failed to find worse

performance on 2 widely used measures of executive cognitive functioning

among people with symptoms of SUDs and/or Cluster B PDs. Even the group

analyses, where participants met criteria for SUD and/or PD diagnoses, failed

to show an effect. In fact, the only significant findings indicated that college

students with more alcohol use disorder and/or BPD symptoms had better

performance on the WCST in terms of total errors and non-perseverative

errors compared to students with fewer such symptoms. The obvious caveat

to these negative findings is that the present sample was arguably high

functioning as evidenced by their enrollment in college and perhaps not

particularly severe in the SUD and PD pathology as evidenced by some

meeting diagnostic criteria at a probable certainty level. Thus, although

executive cognitive functioning deficits may be related to risk for SUD and

Cluster B PD, they may not characterize people with less severe

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presentations. The present study suggests the possibility that higher executive

cognitive functioning may help young adults who experience SUDs and BPD

features to avoid global impairment in occupational functioning (as

evidenced by their enrollment in college).

This study examined individual differences in SUD and Cluster B PDs as

they relate to empirically supported correlates that reflect neurobiological and

cognitive models for understanding these disorders and perhaps their

comorbidity. The findings suggested that young adults with SUD and ASPD

features are likely to experience more negative life events and to associate

with friends and romantic partners who drink and use illicit drugs, indicating

that environmental factors (not deficits in neurobiology and cognitive

functioning) may be particularly relevant to understanding SUDs and certain

PDs in higher functioning young adults. The findings from this study must be

taken within the context of several limitations. First, the sample did not

permit adequate test of gender effects, which may be particularly important in

understanding SUDs and Cluster B PDs (which differ in prevalence by

gender). Second, the present sample was clearly high functioning and there-

fore results cannot necessarily be generalized to other nonclinical popula-

tions. The use of a nonclinical sample also limited the range of psychiatric

symptoms and the number of people who fit into diagnostic groups but this

is a disadvantage of any nonclinical sample, not just those drawn from col-

lege populations.

The present study highlights the potential importance of environmental

variables in understanding phenomenology of SUDs and certain Cluster B

PDs, particularly at the less severe end of the spectrum of symptom ex-

pression and impairment. Although the etiology of SUDs and Cluster B PDs

may share a common underlying genetic liability (17), temperament (16), or

motivational structure (20), the environment may be crucial in determining

which disorder manifests. Future work is needed to understand what factors

pose risk for SUDs and Cluster B PDs individually and jointly to help answer

questions about their etiology and perhaps inform treatment.

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535Substance Use Disorder Correlates

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