Review
Psychopathology Received: September 13, 2017
DOI: 10.1159/000486602
Personality Disorder and Alcohol Use
Disorder: An Overview
Giles Newton-Howes a James Foulds b
a Department
of Psychological Medicine, University of Otago, Wellington, New Zealand; b Department of
Psychological Medicine, University of Otago, Christchurch, New Zealand
Keywords
Personality disorder · Alcohol use disorder · Diagnosis ·
Outcomes
Abstract
Background: Clinically, personality disorder (PD) commonly
coexists with alcohol use disorder (AUD), although within
mainstream mental health services both of these mental dis-
orders are routinely overlooked. Despite a rich literature ex-
amining the interactions between AUD and personality
functioning, personality traits, and PD, there remains con-
flicting evidence as to the degree of association and impact
of one on the other. Methods: A narrative review and a syn-
thesis of the literature were done. Results: The lifetime prev-
alence of AUD approaches 50% in some PD populations. The
rates of PD in AUD populations are less clear but likely simi-
lar. Personality influences outcomes in AUD regardless of
whether a categorical personality diagnosis or dimensional
trait domain approach is taken. There are, however, no good
data to inform clinicians on the impact of AUD on the out-
comes of PD. Understanding the extent of this impact is
complicated by the multiple tools used for diagnosis (of both
PD and AUD) and the statistical methods used. Overall, cau-
tion is required in interpreting the data due to the quality of
the current literature; however, comorbidity between the
© 2018 S. Karger AG, Basel
E-Mail karger@karger.com
www.karger.com/psp
Accepted after revision: December 26, 2017
Published online: February 21, 2018
two disorders is likely significant and the impact of PD on
AUD outcomes is sufficient to require consideration. Conclu-
sions: From a research perspective, better agreement on
both diagnoses and outcomes is urgently needed to im-
prove the overall quality of the evidence. Clinically, despite
the limitations in the literature, it is unacceptable for PD ser-
vices to ignore AUD and for AUD services not to screen for
PD. Both are likely to have an impact on health and function-
ing and should be considered in routine reviews. A better
conceptualization of the putative mechanisms of this inter-
action, as well as an understanding of the neurobiology and
reasons for the impact on treatment outcomes, will help to
move the field forward. © 2018 S. Karger AG, Basel
In this special issue of Psychopathology, the editor’s
lens is focused on functioning and health. Not only are
these obvious candidate outcomes for clinicians but they
also represent recovery-oriented goals [1], a current focus
in the public policy of many jurisdictions [2]. This per-
spective is of particular importance to those treating pa-
tients with personality disorder (PD) and alcohol use dis-
order (AUD), both of which are often lifelong conditions
associated with high levels of impairment [3, 4]. AUD and
PD pose similar challenges for clinicians. Both conditions
commonly coexist with mental state disorders [5–7]; they
Dr. Giles Newton-Howes
Department of Psychological Medicine
23b Mein Street
Newtown, Wellington 6242 (New Zealand)
E-Mail Giles.newton-howes @ otago.ac.nz
are easily overlooked (or at least underdiagnosed) in
treatment settings [8–10]; and they influence treatment
outcomes in other mental state disorders, usually for the
worse [11].
PD is no longer a diagnosis of exclusion [12], but re-
search into comorbidity with PD remains immature.
Addictive behaviors, including the broad gamut of alco-
hol use problems (hereafter labeled as alcoholism), have
the advantage of a longer psychological lineage than is
the case for PD, more highly developed specialist clinical
services, and historically better research funding. How-
ever, the outcomes remain problematic; some countries
report an increasing per capita alcohol consumption and
AUD prevalence despite considerable investments in ba-
sic science research, prevention, and treatment initia-
tives [13].
There are several reports on concurrent personality
and addiction treatments in the scientific literature. These
treatments range from specific individual interventions
delivered by specialists [14] to broad based screening
from nonclinical generalists [15]. The landmark alcohol
treatment study Project MATCH reported a transient su-
periority of 12-step facilitation for participants with co-
existing antisocial PD (ASPD), but this effect was not sus-
tained [16]. However, the overall evidence remains poor
for treatments in patients with AUD which specifically
consider their personality or PD. Most of the literature
focuses on PD as a unitary construct (either present or
not), borderline PD (BPD) or personality traits, such as
those of the “big five” [17], as opposed to a focus on per-
sonality functioning or other personality constructs. Ex-
isting evidence has not yet routinely crossed the transla-
tional chasm into clinical practice.
This is not to say that psychiatry has ignored the inter-
action between addiction and personality. Indeed, as ear-
ly as DSM-I [18] alcoholism was defined as a form of so-
ciopathic personality disturbance – in other words, a PD.
Although this idea is no longer widely supported [19],
personality structure remains relevant to the genesis of
addictive behaviors. Indeed, as discussed later in this re-
view, some aspects of personality structure – notably an-
tisocial behavior and high novelty seeking – are strongly
predictive of future substance disorders. The drift away
from the concept of alcoholism as a form of PD may have
led to the impact of each condition on the other being
underemphasized, both in the literature and in clinical
practice.
Recent reviews in this area have focused largely on
BPD [20, 21], summarizing the impact of 4 therapies that
have been developed for this “dual diagnosis.” Our aims
2 Psychopathology
DOI: 10.1159/000486602
are broader, taking an overview of the impact of PD in
AUD and the impact of AUD in PD. We consider diag-
nosis, epidemiology, and impact.
Diagnostic Considerations
An important question in both the addiction and per-
sonality fields is whether a categorical or dimensional
paradigm better models the condition under investiga-
tion. Dimensional approaches are generally more valid
representations of nature, and current statistical methods
provide a reliable and plausible approach to modeling
personality along a continuum [22, 23]. However, dimen-
sional approaches are arguably less clinically useful: the
choice of cut points to delineate variations of normal
from clinical disorders is often expedient. This debate is
current in the personality field [24]. In contrast, there has
already been a more dimensional approach to substance
use disorders in the DSM-5, with the previous categorical
terms “abuse” and “dependence” being replaced by a uni-
tary construct occurring along a continuum of severity
[25]. Without clear markers for cut points in a dimen-
sional system, as is the case in the personality field, the
improved validity of this approach is diminished but with
a potential loss of utility [26].
There is little dispute that the current categorical sys-
tem for personality is unfit for purpose [27], but what is
not clear is the best approach to replace it. In the DSM-5
categorical PD diagnoses remain, despite publications
from the DSM-5 Work Group for Personality and Per-
sonality Disorders suggesting that an alternative should
be put in place [28, 29]. This more dimensional approach
does, however, exist in section III of the Diagnostic and
Statistical Manual [30]. Much of the literature from the
World Health Organization working group for PD diag-
nosis for the ICD-11 suggests a significant departure from
that found in the DSM-5, with a unitary, severity-based
system proposed to replace distinct categories [31, 32]. If
nothing else this highlights the continuing controversial
nature of personality taxonomy.
Within the addictions field, diagnosis has evolved with
each iteration of the DSM [33]. Societal views on alcohol-
ism have also shifted substantially in the past 100 years
[34]. The ascent of the temperance movement in the ear-
ly 20th century was accompanied by concerns about the
morally degenerative effects of alcohol. Over the course
of the 20th century there has been a gradual shift away
from this stance and towards the disease concept of alco-
holism promoted by Jellinek [35]. Although the classifi-
Newton-Howes/Foulds
cation of substance use disorders in the DSM-5 [30] re-
mains atheoretical, the diagnostic criteria are increasing-
ly aligned with underlying biological dimensions of
addictive behavior such as neuroadaptation, salience,
dyscontrol, and compulsivity [33], reflecting advances in
the understanding of the neurobiology of addiction [36].
The abandonment of the former diagnostic categories
“abuse” and “dependence” also represents an acknowl-
edgement that addictive behaviors occur on a continuum
of severity; that is, there is no “zone of rarity” [26] be-
tween normal and pathological behaviors. Given the shift
towards empirically supported dimensional diagnostic
systems describing both PD and AUD, what does this im-
ply regarding their cooccurrence? Comorbidity is much
easier to define using categorical rather than dimensional
constructs, and there is a risk that the role of comorbidity
becomes obscured with the evolution in diagnostic sys-
tems towards more dimensional paradigms.
Historically, diagnostic criteria dating to the early
1970s [37] have emphasized the importance of determin-
ing whether a mental disorder is primary, or rather sec-
ondary, to another disorder. This is particularly relevant
for AUD and mood disorders, where heavy drinking is
often accompanied by a mood disturbance which resolves
as the drinking ceases [25]. Perhaps surprisingly, there is
no such tradition of categorizing AUD as primary or sec-
ondary to PD, or vice versa, yet plausible arguments could
be made for this approach. Diagnosing PD in the context
of long-term heavy alcohol consumption is problematic,
suggesting that “secondary PD” might be a useful con-
struct in this setting. This would highlight the likelihood
that effective treatment for AUD might produce substan-
tial improvement in personality functioning in some cas-
es, even if a PD may still be present. Similarly, a concept
of “secondary AUD” among patients with primary per-
sonality dysfunction would identify the possibility of the
use of alcohol as a mechanism to manage the cumulative
problems associated with severe PD. These problems are
myriad, i.e., affective dysregulation, impulsivity, inter-
personal distress, alexithymia, anankastia, suicidality,
and continual social dysfunction to name a few. For these
patients, therapy aimed at understanding and managing
personality might lead to secondary reductions in alcohol
use as more adaptive skills are acquired.
Of course, in reality matters are seldom straightfor-
ward and a one-way causal path from one disorder to the
other is inevitably an oversimplification. Nonetheless,
what this discussion highlights is the importance of clear
longitudinal data for patients presenting with an appar-
ent AUD and PD, including the collateral history. While
PD and AUD
imperfect and prone to bias, formulating a picture of tem-
poral relationships between drinking and personality
functioning is a cornerstone of treating this challenging
group. Some have hypothesized that PD is better consid-
ered a diathesis [38–40] or cause of recurrence [41] as op-
posed to a separate disorder. Irrespectively of how the
problems of personality or alcoholism are conceptual-
ized, a coherent nosological approach [42] and formula-
tion provide a clear clinical pathway forward from which
the literature can be applied.
The Prevalence of AUD in PD and PD in AUD
With these diagnostic limitations in mind, estimating
the prevalence of one condition in the presence of the oth-
er provides a measure of how relevant comorbidity is like-
ly to be among groups of patients with either condition. If
substantial comorbidity exists, this also suggests that the
two conditions share common causal risk factors, psycho-
pathology, or biological markers. Those with comorbidity
are also likely to be an important subgroup for prognosis
or treatment response. Comorbidity is, unfortunately, the
“norm” in psychiatric diagnosis [43, 44]. It clouds clinical
taxonomic systems and complicates research. Nonethe-
less, accurate prevalence rates can guide both clinical
thinking and the research agenda within a particular field,
in this case the overlap between PD and AUD.
In order to examine this question, we undertook a sys-
tematic review and meta-regression of all studies that ex-
amined the prevalence of AUD in the presence of PD. The
methodology of this search has been published elsewhere
[45]. These findings are currently under review (unpubl.
data). The overall prevalence of lifetime AUD, defined
categorically and of any sort, in patients with AUD was
nearly 60%. The lifetime prevalence of AUD was highest
for those with ASPD, at 77%, while over half of the pa-
tients with BPD had a lifetime AUD. Among the 16 stud-
ies included in our analysis, there were 8 different instru-
ments used to develop a diagnosis of PD and the between-
study heterogeneity was high (I2 = 74.7%). Smaller studies
reported higher but less reliable AUD prevalence figures.
After excluding those studies in a sensitivity analysis, ap-
proximately half of all of the PD patients in the remaining
studies had experienced an AUD. This suggests that very
significant comorbidity exists when examining a PD pop-
ulation.
The prevalence of PD among people with AUD is high
in both clinical and population samples, although the re-
ported prevalence figures have varied widely, i.e., from 5
Psychopathology 3
DOI: 10.1159/000486602
[46] to 86% [47]. These have yet to be systematically ana-
lyzed and reported. The largest study to examine the
prevalence of PD in a clinical population was a retrospec-
tive study of discharges “against medical advice” among
58,995 attendees of veteran medical settings in the USA.
In that study, the prevalence of cluster A, B, and C PD was
14, 18.1, and 11.1%, respectively, among those with AUD.
Despite the potential weakness of this methodological ap-
proach, that study is more than 10 times greater than any
other single study examining this question and examines
a clinical population using clinical parameters. Smaller
but more methodologically robust studies have found
prevalence rates closer to 50% [48–51], suggesting that
the prevalence of PD among people with AUD is substan-
tial.
The variation in prevalence figures between studies
highlights the need for this data to be systematically com-
bined. Meta-regression techniques would assist in identi-
fying the reasons for the heterogeneity observed, which,
in addition to true variation across populations, is likely
related to a lack of robust diagnostic approaches, ap-
proaches to prevalence data, and inconsistent reporting.
This data set is, however, considerably larger and more
complex, making such analysis demanding.
Potential Reasons for Comorbidity
The prevalence data clearly demonstrate a significant
overlap between PD and AUD. While these data cannot
identify the causal structure underlying this overlap, there
are at least 3 likely explanations. First, shared underlying
genetic or environmental factors may contribute to both
personality pathology and addiction. Second, there may
be causal pathways whereby early PD leads to AUD, or
vice versa. Finally, the two disorders may share sufficient-
ly similar psychopathological features that the taxonomic
system in use delineates two disorders when in fact they
are a single diagnostic entity. This final explanation ap-
pears improbable and therefore we will not consider it
further here.
The link between early personality and later PD is not
only implicit but well documented [52] and reviewed
[53]. This is not so clear for AUD, with evidence suggest-
ing that adolescent AUD diagnosis does not map strong-
ly to adult diagnosis [54, 55]. There is little literature map-
ping early alcohol use to later personality problems; how-
ever, the link between early extroversion and later alcohol
(and drug) use disorder has been identified [56] and ap-
pears particularly strong in men [57]. This is mirrored by
4 Psychopathology
DOI: 10.1159/000486602
the link between early novelty seeking and later AUD
[58]. Extroversion trait markers do not, however, lead to
later PD (with possibly the exception of ASPD) and may,
in fact, lead to better adult functioning.
Findings from twin studies suggest that much of the
vulnerability to mental disorders is explained by sets of
genetic factors which confer a generic risk for either in-
ternalizing or externalizing disorders [59]. Given the lack
of specificity of these genetic risk factors, it is unsurpris-
ing to find individuals expressing more than one pheno-
type, for example PD plus AUD. Similarly, the environ-
mental factors that are known to confer risk for PD and
AUD clearly overlap. Notably, childhood abuse is a po-
tent, likely causal risk factor for both PD and AUD [60].
Other early exposures including inadequate living condi-
tions or a lack of stable parental attachment figures are
likely to have diverse, nonspecific effects on outcomes in
adulthood, including an effect on addictive behaviors and
personality functioning. As with the genetic vulnerability
factors, the effect of these early life exposures on later out-
comes is nonspecific; many people with these early events
will not develop later PD or AUD, although they may de-
velop other internalizing or externalizing psychopatholo-
gies. This theory has face validity – it seems plausible that
a combination of heritable risk, adverse childhood expe-
riences and reinforcement would lead to adult behaviors
that are self-destructive and are found as a hallmark of
both PD and AUD. Heritability for AUD has been esti-
mated at ∼50% [61] and it is similarly high for PD [62–
65]. Potentially there is an underlying factor structure
that predisposes to varied psychopathologies [66] and
this would support a possible overlap in this heritability
[67].
PD and the Outcome of Treatment in AUD
Clinically, the goals in understanding the comorbid re-
lationship between PD and AUD are to predict the prog-
nosis, inform treatment options, and help tailor the ser-
vice delivery to specific groups. Large alcohol trials [68,
69] have proved disappointing in their ability to inform
personalized treatment approaches for AUD. Nonethe-
less, evidence of the role of personality in the treatment
of other disorders suggests that this area remains impor-
tant in AUD [70].
To this end, we conducted a systematic review of pub-
lished literature on the association between categorical
PD and treatment outcome for AUD [45]. At baseline
patients with PD tended to similar alcohol use character-
Newton-Howes/Foulds
istics as those of patients without PD. The notable differ-
ence occurred for ASPD, where an earlier onset and a
heavier use were reported. The review suggested that pa-
tients with PD were substantially less likely (OR 0.35) to
be retained in treatment than those without PD. Con-
versely, for those patients with PD who were retained in
treatment, alcohol outcomes, though mixed, were not
substantially different from those of patients without PD.
In particular, PD was associated with modestly higher
numbers of drinks per drinking day and a higher percent-
age of drinking days during follow-up, but there was no
difference in the percentage days heavy drinking. There
was inconsistent evidence on the differences in time to
relapse between patients with or without PD, although
the findings for this outcome were inevitably clouded by
the issue of treatment dropout and therefore missing
data. Importantly, baseline characteristics suggest that
heavier drinking and an earlier onset of use among pa-
tients with ASPD may have impacted these findings. The
quality of evidence was very low according to GRADE
criteria [71], suggesting that one high-quality trial could
significantly alter these findings. Problems existed in
multiple domains including identification of popula-
tions, management of data, statistical approaches, and
follow-up. This requires caution when interpreting the
findings. A lack of consistency in the reporting of alcohol
outcomes also greatly impeded the ability to synthesize
findings across studies.
The Emerging Literature of the Impact of AUD on the
Outcome of PD
Interestingly, to date there has been no equivalent sys-
tematic review examining the impact of an AUD on the
outcome of PD treatment. Unlike other PD, treatment for
BPD is now well established, with an emphasis on psy-
chotherapy [72]. Expert consensus suggests that AUD is
likely to worsen the prognosis for BPD, as is the case for
many disorders. This is not, however, proven and it is
surprising this has not garnered more attention. Without
this evidence the impact of AUD on PD outcomes re-
mains unclear.
Despite this, clinically there is anecdotal evidence of
the negative effects of AUD on the treatment paradigms
for PD and to this end 3 treatments have been developed
to manage the impact of AUD (or substance use disorders
generally) in the treatment of PD. These include dialecti-
cal behavior therapy [73], dynamic deconstructive thera-
py [74], and dual focus schema therapy [14] and are PD-
PD and AUD
focused interventions that have been developed to treat
the combination of BPD and substance use disorders in
general. These approaches are developments from core
PD treatments, recognizing the need to address addiction
behaviors and cognitions while implicitly seeing these is-
sues as “secondary.” The reviews of Kienast et al. [20] and
Lee et al. [21] summarize the literature from the 10 stud-
ies to date. These show promise in symptom reductions
in both SUD and PD, although all the interventions are
trialed by the developers of the therapy – so-called “prod-
uct experts” [75] – with short-term follow-up and require
both replication and longer-term outcome reporting to
suggest that they are generalizable to standard clinical
practice. Only DDT has been specifically trailed in a ran-
domized fashion examining only AUD and PD, making
generalization of these findings difficult. Of note, the lat-
est of these trials was published in 2010, suggesting little
impetus for ongoing randomized control trial research in
this area at the current time.
Conclusions
The comorbidity between PD and AUD is substantial,
with upwards of 50% of people with PD experiencing an
AUD at some point in their life course, and a prevalence
of PD as high as 50% reported in some AUD samples.
This comorbidity likely relates to overlapping causal ge-
netic and early environmental risk factors and the effect
of some personality traits on the genesis of AUD. Among
patients with AUD, ASPD is associated with higher lev-
els of morbidity at baseline, while all forms of PD are as-
sociated with lower treatment retention for AUD. How-
ever, a pessimistic stance is not completely warranted
since patients with a PD who remain in treatment for
their AUD experience considerable benefit. Personality-
specific treatments for AUD have been investigated,
with some showing promise, but these data have not yet
been synthesized in meta-analyses and the evidence
from the trials to date lacks strength. From a service per-
spective there may be greater reward in focusing addic-
tion services on retaining patients with PD in existing
treatments as opposed to implementing new specialized
psychotherapies for patients with coexisting AUD and
PD. From a research perspective, further development
of promising therapy modalities for this group is imper-
ative. This will require larger trials of a longer duration
than those previously conducted. This would allow
translation of this promising research stream into clini-
cal practice.
Psychopathology 5
DOI: 10.1159/000486602
 In moving the field forward, a proliferation of small-
scale trials targeted at patients with comorbidity is un-
likely to be of benefit. Rather, a considered approach to
the implementation of a service provision that recognizes
the substantial comorbidity, and improvements in AUD
with retention, is needed. Developing a research base to
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