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Description

Read any one case study from Chapter 13 (Personality Disorders) in

DSM-5 in Action

and research the specific personality disorder.

Create a 10-15-slide PowerPoint presentation about your selected case study and include the following:

Include the following in your presentation:

A brief description of the selected case study

Explanation and rationale for the Personality Disorder Diagnosis using the latest version of the

DSM

as a reference.

Information on the course of treatment for the disorder.

Identification of which cluster (A, B, or C) this personality disorder belongs to and an explanation of your rationale.

Information on the prognosis and prevalence of the disorder.

A minimum of five scholarly references including your textbook and the latest version of the

DSM

. Be sure to only use current and scholarly references for this assignment.

Detailed speaker notes that represent what you would say if giving the presentation in person.

While APA style is not required for the body of this assignment, solid academic writing is expected, and documentation of sources should be presented using APA formatting guidelines.

This assignment uses a rubric. Please review the rubric prior to beginning the assignment to become familiar with the expectations for successful completion.

1. Read Chapter 11 in DSM-5 in Action. Read pages 507-521 in DSM-5 in Action.
Dziegielewski, S. F. (2014). DSM-5 in action (3rd ed.). John Wiley & Sons.
2. Read pages 31-86 and 156-160 in the DSM-5.
Diagnostic and statistical manual of mental disorders: DSM-5 (5th ed.). (2013). American
Psychiatric Publishing.
3. Read “Erikson’s General and Adult Developmental Revisions of Freudian Thought: ‘Outward,
Forward, Upward,'” by Hoare, from the Journal of Adult Development (2005).
https://lopes.idm.oclc.org/login?url=http://search.ebscohost.com/login.aspx?direct=true&db=a
9h&AN=17023694&site=ehost-live&scope=site
4. Read “The Past Achievements and Future Promises of Developmental Psychopathology: The
Coming of Age of a Discipline”, by Cicchetti & Toth, from the Journal of Child Psychology &
Psychiatry (2009).
https://lopes.idm.oclc.org/login?url=http://search.ebscohost.com.lopes.idm.oclc.org/login.aspx
?direct=true&db=a9h&AN=36294841&site=ehost-live&scope=site
5. Review the “Child and Adolescent Mental Health” section of the National Institute of Mental
Health website.
http://www.nimh.nih.gov/health/topics/child-and-adolescent-mental-health/index.shtml
6. Read “Responding to the Crisis in Children’s Mental Health: Potential Roles for the Counseling
Profession” by Mellin, E. A. from the Journal of Counseling & Development, (2009).
https://lopes.idm.oclc.org/login?url=https://search.ebscohost.com/login.aspx?direct=true&db=
a9h&AN=44678195&site=ehost-live&scope=sit
7. Read “The Concept of Development in Developmental Psychopathology” by Sroufe, from Child
Development (2009).
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a9h&AN=71689214&site=ehost-live&scope=site
8. Read ” A Developmental Psychopathology Perspective on Adolescence” by Cicchetti & Rogosch,
from Journal of Consulting and Clinical Psychology (2002).
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pdh&AN=2002-10464-002&site=ehost-live&scope=site
9. Read “Annual Research Review: Current Limitations and Future Directions in MRI Studies of
Child- and Adult-Onset Developmental Psychopathologies” by Horga, Kaur, & Peterson, from
Journal of Child Psychology & Psychiatry (2014).
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9h&AN=97233083&site=ehost-live&scope=site
10. Read “Focusing on the Positive: A Review of the Role of Child Positive Affect in Developmental
Psychopathology,” by Davis, & Suveg, from Clinical Child and Family Psychology Review (2014).
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9h&AN=95877741&site=ehost-live&scope=site
11. Read “Developmental Level and Psychopathology: Comparing Children With Developmental
Delays to Chronological and Mental Age Matched Controls” by Caplan, Neece, & Baker, from
Research in Developmental Disabilities (2015). https://www-sciencedirectcom.lopes.idm.oclc.org/science/article/pii/S0891422214004594?via%3Dihub
12. Read “Can Psychopathology at Age 7 Be Predicted from Clinical Observation at One Year?
Evidence from the ALSPAC Cohort” by Allely, Doolin, Gillberg Gillberg, Puckering, Smillie, &
Wilson, from Research in Developmental Disabilities (2012). https://www-sciencedirectcom.lopes.idm.oclc.org/science/article/pii/S089142221200176X?via%3Dihub
13. Read the “Developmental Milestones” section of the Centers for Disease Control and Prevention
website. http://www.cdc.gov/ncbddd/actearly/milestones/index.html
14. Read “Interdisciplinary Critical Inquiry: Teaching About the Social Construction of Madness” by
Connor-Greene, from Teaching of Psychology (2006).
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9h&AN=19493697&site=ehost-live&scope=site
15. Read “Biological Conceptualizations of Mental Disorders Among Affected Individuals: A Review
of Correlates and Consequences” by Lebowitz, from Clinical Psychology: Science and Practice
(2014).
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9h&AN=95052985&site=ehost-live&scope=site
16. Read “Diagnosis – The Limiting Focus of Taxonomy,” by Sturmberg and Martin, from Journal of
Evaluation in Clinical Practice (2016).
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a9h&AN=113901834&site=ehost-live&scope=site
Personality Disorders: Theory, Research, and Treatment
2013, Vol. 4, No. 3, 270 –283
© 2012 American Psychological Association
1949-2715/13/$12.00 DOI: 10.1037/a0026255
TARGET ARTICLE
Behavior Genetics of Personality Disorders:
Informing Classification and Conceptualization in DSM-5
Susan C. South and Nathaniel J. DeYoung
This document is copyrighted by the American Psychological Association or one of its allied publishers.
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
Purdue University
Personality pathology is currently captured in the Diagnostic and Statistical Manual through 10
categorical personality disorder (PD) diagnoses grouped into three descriptive clusters. This classification
system has been criticized by many for using discrete categories and arbitrary thresholds when making
clinical decisions. To address these critiques, the DSM-5 Personality and Personality Disorders Work
Group has put forth a proposal that significantly alters the structure and content of the DSM–IV PD
section. If this DSM-5 Work Group has conducted its own systematic review of the empirical literature,
this review has not been released or made widely available. As such, it is up to the psychology
community at large to determine how well the suggested changes align with findings from extant PD
research. The current article joins this effort by addressing the contribution of behavior genetic findings
to the revision process for classification of PDs in DSM-5. First, we provide a brief review of the history
of PD classification in the DSM. Next, we present an overview and rationale for each of the five major
suggested changes to PD diagnoses. For each suggested change, we outline the available evidence from
behavior genetics and interpretations of these findings. Finally, we offer a summary of considerations for
PD classification as the DSM-5 moves forward. Review of the behavior genetics literature suggests that
several features of the DSM-5 proposal, including the elimination of 4 PDs, merging clinical disorders
and PDs on a single axis, and the implementation of a trait rating system, require significantly greater
explication before a product is finalized.
Keywords: behavior genetics, personality disorders, classification, DSM-5
understand the genetic and environmental influences on a phenotype, and the role of causal factors is inevitably tied to issues of
classification and conceptualization of pathology (Kendler, 2006).
There is a continuous, reciprocal synergy between behavior genetics research and the process of classification. Empirical findings
from behavior genetics inform how disorders are conceptualized
and classified, and this in turn influences how disorders will be
studied in future behavior genetics research. Thus, the behavior
genetics literature is perfectly poised to help shape and inform the
upcoming DSM-5 PD revisions. Using behavior genetics findings
to understand the connections in etiological processes between the
PDs will bring us closer to a classification system built on how
nature is truly structured.
Since the original DSM-5 proposal by the Personality and Personality Disorders Work Group was posted online in February
2010, several negative critiques have emerged about the suggested
changes (Pilkonis, Hallquist, Morse, & Stepp, 2011; Shedler et al.,
2010; Widiger, 2011). A “significant reformulation” of the original
proposal was posted in June 2011 “in response to comments
received and to critiques in the published literature” (see “Changes
to the Reformulation of Personality Disorders for DSM-5” para. 1
at http://www.dsm5.org/proposedrevision/pages/personalitydisorders.aspx); however, a review of the behavior genetics literature
indicates that some aspects of the proposed revisions are at odds
with behavior genetics findings. A key strength of the DSM–IV
process and ultimate product was that revisions were based on
While personality is clearly linked to various forms of psychopathology (cf. South, Eaton, & Krueger, 2010), it is primarily
incorporated in the formal diagnostic nomenclature as 10 personality disorders (PDs) on Axis II of the Diagnostic and Statistical
Manual of Mental Disorders (DSM–IV–TR; American Psychiatric
Association, 2000). These disorders are defined according to specific criterion sets, require an identifiable impairment to meet a
diagnosis, and are presumed to be distinct from each other and
from Axis I disorders. With the upcoming publication of the
DSM-5, members of the American Psychiatric Association’s
(APA) Personality and Personality Disorders Work Group, with
input from the scientific and research community, must decide
what changes should be made to the PD diagnoses that will, “on
the basis of convincing evidence. . .improve upon the performance
of their predecessor” (Kendler, 2009, p. 1940).
The current article focuses on how PDs may be revised in the
upcoming DSM-5 from the viewpoint of what behavior genetics
can add to this endeavor. The goal of behavior genetics is to
This article was published Online January 23, 2012.
Susan C. South and Nathaniel J. DeYoung, Department of Psychological
Sciences, Purdue University.
Correspondence concerning this article should be addressed to Susan C.
South, 703 Third Street, West Lafayette, IN 47907. E-mail:
ssouth@purdue.edu
270
This document is copyrighted by the American Psychological Association or one of its allied publishers.
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
BEHAVIOR GENETICS OF PERSONALITY DISORDERS
thorough reviews of the empirical literature (American Psychiatric
Association, 1994; Widiger, 2011); because these types of reviews
are not yet available for the DSM-5 process, the current article
provides readers with an empirical review of the proposal with
regard to behavior genetics.
To fully understand the weight and significance of the suggested
changes, it is necessary to review how the DSM–IV PD section
came about. The current article briefly reviews the history of PDs
in the DSM. Then, we outline the suggested changes to PDs as
proposed by the DSM-5 PD Work Group. In addition to the four
major changes recommended by this Work Group, we also address
the suggestion to eliminate Axis II completely as proposed by a
DSM-5 Diagnostic Spectra Study Group. The majority of this
article evaluates how these five key changes to PD classification
align with evidence from behavior genetics findings. We focus on
quantitative genetic findings, as opposed to molecular genetics
analyses, because the search for measured genes for PDs is relatively small and focused on only a few disorders (e.g., borderline
PD; Tadı́c et al., 2008; Tadı́c et al., 2009). We conclude by,
discussing considerations for PD conceptualization in DSM-5 as
the process continues to move forward.
PD Classification in the DSM
Prior to DSM–III, PDs were defined according to narrative
paragraphs that provided a two-to-five sentence general description and clinical conceptualization for each disorder (American
Psychiatric Association, 1952, 1968). If a person fit the description, that person could be diagnosed with the disorder regardless of
the impact of symptoms on daily life. Clinicians were tasked with
using best-guess judgment to decide how closely an individual
matched the description from the DSM. The PD descriptions were
a-theoretical in nature and have continued to be so in every
subsequent edition. The general definition for a PD, however, did
suggest a psychosocial origin to this class of disorders, with an
emphasis on deeply ingrained behavioral problems and developmental dysfunction.
Beginning with DSM–III, classification for PDs took a major
leap forward. PDs were moved to Axis II and explicit criteria were
specified for each PD (American Psychiatric Association, 1980). A
categorical model continued to be used for diagnosing PDs, but the
distinction between normal and abnormal personality traits appeared for the first time (Spitzer, Williams, & Skodol, 1980). By
requiring that maladaptive personality traits lead to significant
impairments in daily life in order for a PD diagnosis to be assigned, the DSM allowed clinicians to assess the severity of the
symptoms in a more dimensional manner (Endler & Kocovski,
2002). PD criteria have been revised since DSM–III, but the basic
classification scheme remains the same: a person must surpass a
certain number of identified personality symptoms that define a
specific PD in order to meet the necessary conditions for a diagnosis. This means that all people who endorse anywhere from none
to one less criterion than the required threshold exist in the same
diagnostic “space” (i.e., nondisordered) with no differentiation.
The proposed revisions to the PD classification system for
DSM-5 are a combination of new and old suggestions that may
ultimately satisfy no one. The DSM-5 proposals do heed the call
for an emphasis on dimensions by implementing ratings of 25
personality trait facets from five domains (American Psychiatric
271
Association, 2011). Instead of completely replacing the current 10
PDs with dimensional personality trait ratings, six of the current
PD categories will be retained as “types” and diagnosed according
to a combination of impairments in personality functioning (Criterion A) and pathological personality traits (Criterion B). The
DSM-5 website also includes a “Cross-Walk” that allows translation of all DSM–IV PDs to a DSM-5 PD type (including Personality Disorder Trait Specified [PDTS], which replaces Personality
Disorder⫺Not Otherwise Specified [PD-NOS]). This may be a
compromise between proposals to move all DSM–IV PDs to
DSM-5 (Skodol, 2011), and alternate suggestions to move the
DSM–IV PD categories to an Appendix in DSM-5 as “legacy
constructs” (Krueger & Eaton, 2010).
There is a long-standing argument over how to classify psychopathology (e.g., Bergner, 1997), given the lack of either clear
theory or known pathophysiology that links the etiology of different disorders. Much like the classification of most Axis I clinical
disorders, PD classification is based largely on phenomenology,
that is, shared descriptive characteristics and clinical course. There
is general dissatisfaction with the DSM’s reliance on surface
attributes and similarity of symptoms to form the basis of a
classificatory system (Hyman, 2007; Kupfer, First, & Regier,
2002; McHugh, 2005). However, debate continues as to whether
DSM-5 should strive, with this epistemic iteration, to come closer
to how nature is truly structured (Kendler, 2009), or whether
understanding shared etiology and pathophysiology should come
second to appropriately defining clinical syndromes (Jablensky,
2009). By appropriately identifying the phenotype, we can hope to
better understand its etiology and achieve both aims within the
same diagnostic system.
The question then becomes one of how to accomplish these
goals. There are many potential validating criteria for a disorder
(e.g., shared neural substrates, biomarkers, temperament, impact
on social adjustment, prognostic significance, response to treatment), but the current review focuses on one— genetic and environmental influences as estimated by behavioral genetic methodologies. Because family and genetic factors have long been one of
the key indicators for the construct validity of a disorder (Robins
& Guze, 1970), findings from behavior genetics should play a role
in the DSM-5 revision process. Quantitative behavior genetics, the
focus of the current review, is silent as to which genes are associated with psychopathology; the real advantage of this method of
inquiry lies in the ability to estimate the magnitude of genetic
influences on different phenotypes and how those influences overlap. This ultimately reveals the true boundaries among personality,
PDs, and clinical disorders, bringing us that much closer to a
nosological system based in nature.
Behavior genetic findings are not referenced on the DSM-5 web
page (American Psychiatric Association, 2011). The Work Group
includes a leading expert on behavior genetics—John Livesley
(Livesley, 2005; Livesley & Jang, 2008) —and his presence on the
Work Group ensures that these findings most likely play a part in
the discussions. While it is impossible to ascertain any single
member’s role and contribution to a work group, he is not listed as
a coauthor in a recent publication outlining the description and
rationale for the proposed DSM-5 changes (Skodol et al., 2011b).
Indeed, from every possible outlet for dissemination, including the
DSM-5 website, publicly available minutes from Work Group
meetings, or other peer-reviewed publications from Work Group
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This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
272
SOUTH AND DEYOUNG
members, the only indication that behavior genetics played a part
in the decision-making process is a few sentences in one publication (Skodol et al., 2011a) that is now out of date with recent
revisions to the website. Much of the explanatory material providing rationale for the suggested changes (American Psychiatric
Association, 2011; Skodol et al., 2011a; Skodol et al., 2011b)
appears to focus on analysis of comorbidity and impairment,
particularly with regard to disorders that were included in the
Collaborative Longitudinal Personality Disorders Study (CLPS;
Skodol et al., 2005). This work contains important considerations
for the revision process, yet, it appears that the Work Group has
focused primarily on phenotypic research instead of the findings
from family and genetic research. There are limitations to behavior
genetics studies, as with any method; often, there are only a small
number of studies for any particular disorder, and they have
limited generalizability in terms of sample ages, sex, and assessment methods. We would not suggest that behavior genetics be the
sole or even primary method by which to make decisions about
classification; however, it is not clear how much, if any, weight the
DSM PD Work Group has given to findings from behavior genetics work. As a result, the changes suggested by the Work Group
and their decisions on how to implement these changes are, in part,
at odds with the current scientific literature.
Proposed Revisions to the PD Diagnoses
in DSM-5
Plans for the next edition of the DSM have been underway for
more than a decade, and the Personality and Personality Disorders
Work Group has been meeting since 2007. The proposed revisions
suggest that the upcoming DSM-5 will mark a dramatic shift in
how PDs are conceptualized and classified (American Psychiatric
Association, 2011). As of this writing, the APA’s DSM-5 website
outlines the following changes to PD classification and diagnosis:
a) reducing the 10 PD diagnoses to six PD types; b) replacing the
79 DSM–IV PD criteria with 25 personality trait facets (from five
higher-order trait domains: negative affect, detachment, antagonism, disinhibition, and psychoticism), with each of the PD types
defined by different combinations of these traits; c) assessing five
severity levels of personality functioning based on impairment in
core self- and interpersonal capacities; d) new criteria for the
general PD diagnosis based on a combination of core deficits and
specified pathological traits; and e) the “Proposed DSM-5 Organizational Structure and Disorder Names” indicates that Axis II
will be eliminated and clinical disorders and PDs will be included
on the same Axis.
The suggested changes to the assessment and diagnosis of PD
have undergone significant reformulation from the original proposal, first posted on the DSM-5 website in February 2010 and
outlined in a recent peer-reviewed publication (Skodol et al.,
2011b). The assessment sequence has been streamlined, one additional PD (narcissistic) is now retained from the DSM–IV, and the
trait system has been revised downward from the original proposal
of 37 facets under 6 domains. It is still unclear, however, as to how
far the Work Group will move from the categorical model of
DSM–IV to a dimensional model in DSM-5. The Work Group
explicitly states on the APA DSM-5 website that it is shifting to a
“hybrid dimensional-categorical model.” The decision to move to
a dimensional system follows a push for dimensional conceptual-
izations of mental disorders in general (Widiger & Mullins-Sweatt,
2007) and PDs in particular (Widiger, Livesley, & Clark, 2009). A
version of the word “dimension” appears in the Skodol et al.
(2011b) article 33 times, and even though no section of the article
was explicitly devoted to this topic, the authors provided substantial empirical evidence as to the appropriateness of shifting to a
dimensional model in regard to PDs (Skodol et al., 2011b). The
implementation, though, is not done in a unified fashion. Patients
will be assessed on a Levels of Personality Functioning Scale from
0 (healthy functioning) to 4 (extreme impairment) regarding their
level of disturbance in self (i.e., identity and self-direction) and
interpersonal (i.e., empathy, intimacy) functioning. Further, the PD
criteria from DSM–IV (a mix of affective, cognitive, behavioral,
and interpersonal deficits) will be replaced by a combination of
pathological personality facets from five higher-order domains.
The Work Group states in a Brief Rationale that the full DSM Task
Force requested that the trait model be implemented in a “hybrid
fashion,” and that “the PD diagnosis proposed for DSM-5 that
implements the model in its full form is Personality Disorder Trait
Specified” (American Psychiatric Association, 2011). The current
proposal thus allows for seven possible PD “diagnoses” (six
DSM–IV PDs plus the new PDTS).
Certainly, arguments in favor of dimensional conceptualizations
of personality pathology (Arntz et al., 2009; Eaton, Krueger,
South, Simms, & Clark, 2010; Rothschild, Cleland, Haslam, &
Zimmerman, 2003; Haslam, 2003; Trull & Durrett, 2005; Widiger,
Livesley, & Clark, 2009) are in line with how behavior genetics
research tends to view psychopathology in general and personality
pathology in particular. Biometric modeling generally assumes
multiple gene systems, or quantitative trait loci, underlying complex behavioral phenotypes (Plomin, DeFries, McClearn, &
McGuffin, 2008). In theory, the risk alleles for personality pathology are distributed throughout the population, with some people
having very few, some have a moderate amount, and some having
many, thus creating a dimension of risk (but see Keller & Miller,
2006, for alternative genetic models of disease). One model of
psychopathology, the liability-threshold model, posits that at the
extreme end of this liability continuum is a point at which the
disorder is obviously manifested and a person is said to have
crossed a threshold (Falconer, 1965). This is in contrast to spectrum models of psychopathology, in which there are only quantitative differences between people, depending on where they lie on
the dimension, but one’s position on the spectrum does not result
in any qualitative differences.
Most behavior genetic modeling of DSM-defined PD concepts
assumes a dimensional, spectrum model of disorder. As such,
researchers often use symptom count variables (i.e., total number
of symptoms met), instead of yes⫺no dichotomous diagnoses, as
the input variable in biometric modeling. Liability-threshold models can use either continuous or categorical data as input, but again
assume a continuous underlying distribution. In contrast, the
DeFries-Fulker extremes analysis (DeFries & Fulker, 1985, 1988)
directly tests whether a continuum underlying the phenotype exists. While the DeFries-Fulker extremes method has never been
directly applied to PDs, it has been used to examine other types of
psychopathology (e.g., attention-deficit hyperactivity disorder;
Levy, Hay, McStephen, Wood, & Waldman, 1997). In general,
results with other syndromes support continuums of liability rather
than discrete disorders that have identifiable cutoffs. There is little
BEHAVIOR GENETICS OF PERSONALITY DISORDERS
reason to believe that different results would be found with PDs,
although this is an obvious gap in the literature and clearly a
starting place for future research into the dimensionality of PD
constructs. If the Work Group moved closer to a fully dimensional
reconceptualization of personality pathology, then findings from
behavior genetic studies conducted to date would firmly support
this.
This document is copyrighted by the American Psychological Association or one of its allied publishers.
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
The Six Proposed PD Types
In the proposed revisions for DSM-5, six of the 10 DSM–IV PD
diagnoses will be retained as “personality disorder types”: antisocial (dyssocial), avoidant, borderline, obsessive– compulsive, narcissistic, and schizotypal. The DSM–IV convention of clustering
the disorders (e.g., Cluster A encompasses the paranoid, schizoid,
and schiotypal disorders) will be abandoned completely. The Work
Group states that each PD type will be defined “by criteria based
on typical impairments in personality functioning and pathological
personality traits in one or more trait domains” (American Psychiatric Association, 2011). Initially, the Work Group had proposed
that the DSM-5 PD types would be formulated such that clinicians
would rate patients on a) how well they matched a narrative
description of the PD type and b) how well their personality traits
matched the traits associated with the specific type (Skodol et al.,
2011a; 2011b). The most recent revisions have eliminated the
narrative descriptions of each “prototype,” and instead delineated
specific trait facets that would be required to diagnose each of the
six PD types. A trait assessment measure has been developed to
accompany the new trait system (available as supplementary material, Krueger et al. in press, or from Work Group member R.
Krueger), but it is not clear how clinicians will decide if a person
“meets” each of the traits that define a disorder. The DSM-5 PD
website recognizes this difficulty by stating that, “scoring of the
individual criteria and scoring algorithms for the specific disorders
are currently under development.” Once this is available, the
discussion about whether this type of trait rating system improves
on the DSM–IV system of meeting a specific number of objective
“yes⫺no” criteria can commence. Until then, the behavior genetics
literature can inform the decision to include 6 PD types.
The rationale for retention of these six PD types is based on a
large research base, higher prevalence rates, associated dysfunction and quality of life, and clinical utility (American Psychiatric
Association, 2011; Skodol et al., 2011a). The specific rationales
for each disorder are no longer available online. In the only
peer-reviewed publication from the Work Group members that
explains the number and specification of proposed DSM-5 types,
which is now out of date in that it recommended deletion of
narcissistic PD, the authors state “Space limitations preclude a
complete justification for the five PDs retained” (Skodol et al.,
2011a, p. 138, emphasis added). The Work Group reports that the
PDs proposed for removal “can be largely modeled using fewer
traits, often from a single, specific trait domain,” but the support
for this statement is not provided (Skodol et al., 2011a, p. 139). In
addition, the Work Group appears to have reversed its position on
narcissistic PD because it is now included as a PD type in the most
recent proposal on the website.
Current DSM–IV PDs that will not be kept as PD types in the
DSM-5 will be described as dimensions of personality pathology.
The Work Group reported that the results of its own literature
273
reviews “support conceptualizing them as one or more dimensions
of personality psychopathology rather than as types” (Skodol et al.,
2011b, p. 12). It would be beneficial for the field if these literature
reviews were identified or made available on the DSM-5 website
for general consumption. One of the major limitations is that four
of the DSM–IV PDs proposed to be retained in the DSM-5 were
included in the CLPS (Skodol et al., 2005). Because only four of
the 10 DSM–IV PDs were evaluated in the CLPS, they have a
comparatively larger research base than the PDs suggested for
removal (although, see Widiger, 2011, and Miller, Widiger, &
Campbell, 2010, for arguments about the research literature base
for narcissism). This may lead those four PDs to have an appearance of being more useful and clinically relevant in comparison to
the others.
One published article by the Work Group discusses the quantitative genetic findings on PDs (Skodol et al., 2011a). Rather than
thoroughly reviewing the behavior genetic evidence for or against
retention of each of the 10 DSM–IV PDs, the authors point to
selected findings to buttress their arguments for a few of the PDs
(e.g., small genetic effects have been found for histrionic PD in
some studies). If a PD needed to demonstrate at least moderate
genetic influences in order to be included in DSM-5, then all of the
DSM–IV PDs would be retained. The proportion of variance in a
phenotype (like a PD) that is due to genetic influences is referred
to as heritability; commensurate variance estimates for shared and
nonshared environmental influences make up the sum total of
phenotypic variance in a trait, with error falling into the nonshared
component. Across several studies, biometric modeling of twin
data demonstrates significant genetic influence (i.e., heritability)
on variation in DSM PDs, although estimates differ in magnitude
across studies. Torgersen et al. (2000), using data from structured
diagnostic interviews for the DSM–III–R PDs in a national Norwegian sample of adult twins, reported heritability estimates from
28% (paranoid, avoidant) to 77% (narcissistic, obsessive–
compulsive). A twin study using parental ratings of DSM–IV PD
criteria in a sample of children and adolescents found relatively
high heritability estimates: from .50 (paranoid) to .81 (dependent,
schizotypal), with a median heritability of .75 (Coolidge, Thede, &
Jang, 2001). A recent study used an unselected community sample
of twins recruited from the Norwegian Institute of Public Health
Twin Panel (NIPHTP), assessed with a structured interview for
DSM–IV PDs, and found lower heritability estimates, ranging from
21% (paranoid) to 38% (antisocial) (Kendler et al., 2006a;
Reichborn-Kjennerud et al., 2007a; Torgersen et al., 2008).
While specific estimates might differ, the important point is that
all of the PDs seem to have some biological basis. Thus, there is
family or genetic evidence (one of the key defining features of a
disorder; Robins & Guze, 1970) for all of the DSM–IV PDs,
including ones that would be eliminated in DSM-5. Heritability
estimates certainly differ, both across disorders within a sample
and for the same disorder across different samples. This is not
surprising, given that heritability estimates are population estimates, and thus dependent on the specific aspects (e.g., age, race,
culture) of the sample. Even if it were possible for the field to
agree on a heritability “threshold” to demarcate the disorders
worthy of retention as genetically crisp concepts, there is no true
consistency across studies as to which disorders have the highest
heritability estimates. Obsessive– compulsive personality disorder
(OCPD), for instance, had one of the highest heritability estimates
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SOUTH AND DEYOUNG
of the PDs, .77, in two studies (Coolidge et al., 2001; Torgersen et
al., 2000), but the lowest heritability of the three Cluster C disorders (.27) in a third study (Reichborn-Kjennerud et al., 2007a).
Evidence of at least moderate heritability alone, of course, would
not be enough to conclude that a constellation of symptoms represents a true disorder. It is possible that the significant heritability
estimates found for the DSM PDs reflect genetically influenced
personality traits that underlie the syndrome (a point we return to
below), or even a genetic predisposition to more basic cognitive
and affective processes (e.g., emotional dysfunction in borderline
PD; Linehan & Koerner, 1993).
The magnitude of environmental influences is relatively uninformative here as well, because the majority of the remaining
variance in all PDs is due to nonshared environmental factors that
are unique to each twin. This may be an underestimate of the
shared environment, given the large sample sizes needed to detect
these effects in twin studies (Martin, Eaves, Kearsey, & Davies,
1978). It has also been posited that influences of what is commonly
thought of as shared family environment may actually fall under
unique environmental influences, as two siblings’ experiences of
the same family characteristic might be quite different (i.e., two
siblings might have quite different relationships with their mother).
The one exception to low estimates of shared environment is
antisocial PD; when broadly defined according to various measures of antisocial behavior, it appears to demonstrate substantial
shared environmental effects (Rhee & Waldman, 2002).
Multivariate behavior genetics studies are perhaps more informative for classification purposes than estimates of heritability and
environmental variance for individual PDs. These multivariate
studies can start to untangle the etiology of covariances among
different disorders. For instance, evidence as to which PDs within
each DSM–IV cluster are the most genetically robust could inform
the Work Group’s decision on which PD types to retain in the
(cluster-free) DSM-5. In the NIPHTP community twin sample,
schizotypal PD had the strongest loading on the genetic and
environmental factors and appeared to be the strongest marker of
the genetic and nonshared environmental liability to Cluster A
pathology (Kendler et al., 2006a). Among Cluster B disorders, one
genetic factor influenced all four disorders, but a second genetic
and nonshared environmental factor was also needed to account
for influence on antisocial and borderline PDs (Torgersen et al.,
2008). Finally, a common factor accounted for 83 and 48% of the
variance in avoidant and dependent PDs, respectively, but most of
the genetic influence on OCPD was disorder-specific (ReichbornKjennerud et al., 2007a). The fact that OCPD appears to be
etiologically distinct from avoidant and dependent PDs is evidence
in support of the planned disbanding of Cluster C.
Findings regarding the clusters must be interpreted in light of
more recent work on the multivariate structure of all 10 DSM PDs.
Again using the NIPHTP sample, Kendler et al. (2008) found three
genetic factors that did not directly correspond to the DSM cluster
structure. The first genetic factor included loadings on paranoid,
histrionic, borderline, narcissistic, dependent, and obsessive–
compulsive PDs; the second had loadings on borderline and antisocial PDs; and the third had loadings on schizoid and avoidant
PDs. These three genetic factors captured only a modest proportion
of the total genetic variance, with six of the 10 PDs demonstrating
substantial disorder-specific genetic effects. In contrast, the three
unique environmental factors corresponded well to the DSM clus-
ter structure, although as with genetic influences, all disorders
(with the exception of schizotypal) demonstrated substantial
disorder-specific unique environmental influences. The authors
concluded that the three genetic factors reflect a) a broad tendency
toward personality pathology or negative emotionality, b) genetic
risk for a factor of “impulsive aggression”, and c) a factor of low
extraversion or inhibition. Further, they posited that the pattern of
findings for genetic and environmental influences have implications for the comorbidities commonly found among PDs. That is,
antisocial and borderline PDs may be highly comorbid because
they share the same genetic influences. Other Cluster B PDs may
be comorbid because the same environmental influences (i.e.,
those not shared in common with other family members) lead to a
“final common pathway” of Cluster B-type pathology.
Thus, when the covariance of all 10 DSM PDs is considered
together, understanding of shared etiology is somewhat different
than when the clusters are considered separately. Again, there may
be general genes for personality per se, and these genes show
pleiotropic effects such that they can lead to many different ultimate phenotypic manifestations (Livesley, 2005). This may explain why genetic influences across the PDs are generally of a
similar magnitude and why the dysfunction associated with any
PD is generally along one of two dimensions, disturbed identity or
inability to get along well with others (Krueger, Skodol, Livesley,
Shrout, & Huang, 2007). Environmental influences, then, have a
guiding hand in how these common genetic influences translate
into phenotypic trait descriptions of a person’s behavior. It is
important to note that all of the studies reviewed above utilized
continuous measures of PDs, that is, a criterion count, and included
many individuals who were below threshold. While research
strongly suggests that PDs are best represented dimensionally
rather than as clearly demarcated “types” (see Eaton, Krueger,
South, Simms, & Clark, 2010), it is possible that different results
would have been obtained using diagnostic information that incorporated indices of severity and impairment.
Ultimately, what can be concluded about the number of proposed PDs to be included in DSM-5, from the perspective of
evidence collected to date on etiological coherence and/or distinctiveness? OCPD appears to stand on its own as a disorder, with
substantial disorder-specific genetic influences and minimal
shared genetic influences. Borderline PD and antisocial PD seem
to form a strong genetic factor, possibly based on antagonism and
impulsivity. Schizotypal PD, like OCPD, shares little in common
genetically with other PDs within its cluster; however, schizoid
PD, which is not proposed for inclusion in DSM-5 as a type, has
comparable heritability estimates to schizotypal. It also formed a
genetically robust factor with avoidant PD, which is proposed for
inclusion. The strongest arguments for schizotypal PD may in fact
come from its links with psychotic disorders; indeed, the genetic
factor linking schizoid and avoidant may speak more to common
personality trait dimensions underlying these disorders. The bulk
of the evidence from the behavior genetics literature, however,
provides no compelling reason to eliminate four of the DSM–IV
PDs; instead, the evidence appears to call for elimination of the
cluster system and a restructuring of the disorders, in tandem with
a revision of how Axis I disorders are organized (see Elimination
of Axis II, below).
BEHAVIOR GENETICS OF PERSONALITY DISORDERS
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Assessment of Personality Trait Domains
The PD Work Group has proposed that patients be evaluated on
five broad, higher-order, personality trait domains: negative affect,
detachment, antagonism, disinhibition, and psychoticism. Each of
these higher-order domains can be broken down into a number of
lower-order trait facets. For example, antagonism would be assessed by rating individuals on facets of manipulativeness, deceitfulness, grandiosity, attention seeking, callousness, and hostility.
Each patient, whether meeting the criteria for one of the six PD
types or not, will have a systematic, detailed, and accessible
description of their personality functioning. This approach is akin
to Five Factor Model (FFM) profiles that have been delineated for
the current 10 DSM–IV PDs (Samuel & Widiger, 2008), because it
adopts the idea that broad personality types can be described using
lower-order facets in a dimensional model as a way to assess the
differing levels and types of pathology.
As rationale for the change, the Work Group points to several
potential benefits of a dimensional model of personality trait
domains that have been summarized by others (e.g., Clark, 2007;
Krueger et al., 2011a; Widiger et al., 2009; Widiger & Trull,
2007). In brief, the new assessment procedure would eliminate the
problems of comorbidity, overuse of the PD-NOS diagnosis,
within-disorder heterogeneity, diagnostic instability, and weak
convergent and discriminant validity of PDs. As the Work Group
notes, the DSM–IV PD definition is already inherently trait based,
but the traits as delineated in the PD diagnoses do not truly
represent multivariate pathological personality space (Skodol et
al., 2011b).
The Work Group clearly states that they want to incorporate a
personality domain model that can describe every patient—
whether or not they meet criteria for a PD diagnosis. The Work
Group’s starting point is four (bipolar) domains of personality that
at their maladaptive end are associated with PD features. In the
Brief Rational for the proposed trait system, the Work Group states
that there are no existing personality measures that encompass all
of the maladaptive personality variation. The FFM of personality,
for instance, is operationalized in assessment measures that do not
capture the maladaptive end of personality pathology (Haigler &
Widiger, 2001; Krueger & Eaton, 2010). This is a major concern,
given that the Work Group states that it is “proposing a model, first
and foremost, of personality pathology” (Skodol et al., 2011b, p.
16, emphasis added). The Work Group also argued that comprehensive coverage of all PD concepts required the inclusion of a
fifth domain that would include cognitive⫺perceptual distortions
and eccentric behavior. Thus, the Work Group and its consultants
moved forward with designing a new trait system that is designed
to capture the pathological end of four higher-order domains from
the FFM, a fifth domain of psychoticism, and lower-order facets
within these domains (Krueger et al., 2011a; Krueger et al., in
press). The strength of this effort is that an instrument designed to
assess this trait system is in the public domain, (i.e., included as
supplementary material to an in-press publication, Krueger et al.,
in press), or available from a Work Group member (Robert
Krueger); other members of the Work Group may be working on
a measure of adaptive personality traits (Skodol et al., 2011b, p.
16), but less has been made publicly available about this measure.
Given that the PD Work Group focused on finding the maladaptive variants of normal personality trait domains, research on the
275
genetic structure of normal and abnormal personality was reviewed. Overall, this work has been conducted separately, although there is some biometric modeling of normal and pathological personality trait measures within the same sample. Biometric
modeling of normal personality has relied heavily on the NEO
Personality Inventory⫺Revised (NEO-PI-R), the most popular
measure of the FFM. Heritability estimates of the five higher-order
domains are around 50% (for a review, see Bouchard & Loehlin,
2001). The 30 lower-order facet scales of the NEO-PI-R also show
moderate heritability, generally between 30 and 50% (Jang, McCrae, Angleitner, Riemann, & Livesley, 1998). There is also
significant heritability of the residual variance in the specific facets
when the common variance is partialed out; that is, when the
common variance of the five higher-order domains is regressed
out, the residual scores for each of the facets demonstrate measurable heritability. Jang et al. (1998) found facet-residual heritabilities ranging from 11–37%, although estimates were closer to
40 –50% when correcting for unreliability. Another recent study
also found substantial genetic influences on facet-specific trait
variance (Kandler, Riemann, Spinath, & Angleitner, 2010). This
would suggest both general genes that contribute to the coherence
of higher-order normal personality domains and specific genetic
influences on more fine-grained, lower-order personality facets. In
a multivariate biometric modeling study, researchers found that the
lower-order NEO-PI-R facets did not load cleanly onto five genetic factors (i.e., one for each of the FFM domains), but instead
required two genetic and two nonshared environmental factors,
suggesting that higher-order domains “do not exist as veridical
psychological entities per se, but rather they exist as useful heuristic devices” (Jang, Livesley, Angleitner, Riemann, & Vernon,
2002, p. 99). A more recent study, however, concluded that there
were five, genetically robust domains that paralleled the FFM
higher-order traits (Yamagata et al., 2006).
Most biometric modeling of pathological personality traits has
relied on the Dimensional Assessment of Personality Pathology
(DAPP; Livesley & Jackson, 2001). The four higher-order personality domains of the DAPP— emotional dysregulation (lability),
dissocial behavior (antagonism), inhibitedness (interpersonal unresponsiveness), and compulsivity—are also moderately heritable;
53, 50, 52, and 38%, respectively (Jang, Livesley, Vernon, &
Jackson, 1996). Total genetic influences on the 18 lower-order
DAPP traits varied from 0% (conduct problems) to 64% (narcissism), although most heritability estimates were in the 40 –50%
range (Livesley, Jang, Jackson, & Vernon, 1993). Nonshared environmental estimates were substantial across the traits. The only
DAPP scales that showed any evidence of the shared environment
were conduct problems and submissiveness; interestingly, the only
NEO-PI-R facets to demonstrate moderate effects of the shared
environment were feelings (Openness), modesty (Agreeableness),
order (Conscientiousness), self-discipline (Conscientiousness),
and deliberation (Conscientiousness; Jang, Livesley, & Vernon,
1996). Livesley, Jang, and Vernon (1998) examined whether the
genetic and environmental structure of the DAPP lower-order
personality domains mapped onto the phenotypic factor structure.
They found four factors that were highly congruent with results
from the phenotypic factor analysis. Thus, the trait structure of the
DAPP, and to some extent the FFM, does come close to carving
nature at her joints. This stands in contrast to other models of
personality. Ando et al. (2004), for instance, found that there was
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276
SOUTH AND DEYOUNG
little correspondence between the phenotypic and genetic structure
of the Temperament and Character Inventory (Cloninger, Svrakic,
& Przybeck, 1993), challenging Cloninger’s model of the distinction between temperament and character.
What the studies above fail to tell us is the amount of overlap
between normal and abnormal personality. If the goal of the
DSM-5 is to capture the maladaptive ends of the bipolar domains
of the personality spectrum, then there should be etiological coherence across normal and abnormal personality trait models. A
key strength of biometric modeling is the ability to determine
whether there is genetic and environmental overlap between normal and maladaptive personality traits. In multivariate biometric
models, this degree of overlap is indexed with a genetic (rG) or
environmental (rC or rE) correlation, which ranges from ⫺1 to ⫹
1 and indicates how much of the (for instance) genetic influences
on one variable overlap with the genetic influences on another
variable.
Distel et al. (2009) reported additive genetic correlations between borderline personality traits and four of the FFM domains
(all but Openness) ranging from .56 (Conscientiousness) to .95
(Neuroticism), dominant genetic correlations ranging from ⫺.07
(Agreeableness) to .34 (Neuroticism), and unique environmental
correlations ranging from .22 (Extraversion) to .59 (Neuroticism).
Thus, there was a large amount of genetic overlap between BPD
and the FFM domains, while the amount of unique environmental
overlap was lower. Another way to index degree of overlap is to
determine how much of the phenotypic correlation between two
variables can be explained by genetic influences. In the same
study, genetic influences explained between 47 and 57% of the
correlation between BPD and each of the FFM traits, while unique
environmental effects explained 39 – 42% of the correlation.
Markon, Krueger, Bouchard, and Gottesman (2002) also found
strong genetic overlap between normal and pathological personality scales, including a) negative affect and various maladaptive
trait scales and b) disinhibition and antisocial behavior. Jang and
Livesley (1999) reported moderate-to-large genetic overlap between scores on the DAPP and a measure of the FFM, particularly
for the FFM trait of neuroticism. Indeed, some of the genetic
correlations between FFM domains and DAPP lower-order scales
were higher than the phenotypic correlations. Certainly, it is possible that measures of both the normal and pathological personality
traits would contain error; if uncorrelated, this measurement error
would reduce the nonshared environmental correlations (e.g., between FFM domains and pathological traits) and artificially inflate
the genetic correlations (Markon, Krueger, Bouchard, & Gottesman, 2002).
Pathological personality traits as measured by various instruments, however, appear to show etiological overlap with normal
personality traits, particularly the FFM domains. Both normal and
abnormal personality traits show significant and substantial unique
genetic and environmental components. This certainly makes conceptual sense. There are most likely several fundamental, genetically influenced temperament domains that, in enriched or neutral
environmental conditions, lead to relatively normal levels of personality functioning or, in impoverished conditions (or in combination with certain other genes), lead to pathological personality
traits and/or other forms of psychopathology. As Jang and Livesley
(1999) astutely noted more than 10 years ago, multivariate biometric modeling at the facet or item level would help to clarify the
similarities and differences between normal and abnormal personality traits; more than 10 years after the authors made this recommendation, this work has still not been done.
Can behavior genetics tell us anything about which personality
traits should be included in a comprehensive model aimed at
“describing the personality characteristics of all patients, whether
they have a personality disorder or not” (American Psychiatric
Association, 2011)? In general, behavioral genetic research largely
supports the proposed DSM-5 trait domains as they currently stand.
Phenotypic factor analysis of normal and abnormal trait models,
behavior genetic modeling of pathological trait models, and behavior genetic modeling of DSM–IV PD traits are converging on a
four-factor model of negative emotionality/neuroticism/emotional
dysregulation, detachment/inhibition/social withdrawal, dissocial
behavior, and compulsivity. This model is similar, but not identical, to the proposal on the DSM website; these models are, however, much more similar than the original trait system proposed by
the DSM-5 PD Work Group, which included 37 facets under six
domains. That original model was at odds with findings from the
behavior genetics literature (e.g., it split the domains of antagonism and disinhibition, which seem to coalesce in behavior genetic
modeling).
In the newest, five domain system, four of the domains (Emotional Dysregulation, Detachment, Antagonism, Disinhibition) resemble the four higher-order factors that are consistently found in
structural models of normal and abnormal personality traits. The
Work Group rationale explicitly states that the FFM domain of
Openness, which “shows essentially no relationship . . . to
DSM–IV PDSs”, was dropped in favor of a Psychoticism domain
in an attempt to capture psychotic experiences and dissociation
(American Psychiatric Association, 2011). Some argue that these
types of experiences are not well-represented in FFM inventories
(Watson, Clark, & Chmielewski, 2008), although there are several
factor analytic studies that find cognitive-perceptual aberrations
and/or schizotypal symptoms load with an openness factor (see
Widiger, 2011, for a recent review). Unfortunately, as noted above,
all twin studies of pathological personality traits have relied on the
DAPP, which does not have good coverage of the types of cognitive⫺perceptual aberrations that would be captured with Psychoticism. It will be particularly important to utilize twin samples
to examine the genetic and environmental influences on, and
multivariate etiological structure of, the new proposed trait model
for DSM-5.
Levels of Personality Functioning and New Definition
of PD
In this section, we discuss the Work Group’s proposals for
assessing levels of personality functioning and the new definition
and general criteria for PD, because they are strongly related.
Under the current DSM-5 proposal, all patients can be described
using the dimensional trait rating system; it is the presence of
impairment in personality functioning that leads to a PD diagnosis
per se. It is suggested that a first step in any DSM-5 PD assessment
is the measurement of personality functioning, defined by amount
of impairment in either self or interpersonal functioning. The Work
Group’s rationale is that severity is often the strongest predictor of
future functioning, and the self and other domains repeatedly arise
as representing the core deficits in any PD (American Psychiatric
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BEHAVIOR GENETICS OF PERSONALITY DISORDERS
Association, 2011). Deficits in these two areas represent the new
Criterion A of the general criteria of a PD. Individuals will be rated
on a five-point scale ranging from 0 (healthy functioning) to 4
(extreme impairment) in the areas of Identity and Self-Direction
(Self domains) and Empathy and Intimacy (Interpersonal domains). The Levels of Personality Functioning Scale describes
each of the four areas at each severity level so that clinicians can
decide which level most closely characterizes a patient’s functioning.
The general criteria for PD have been modified to fit with the
proposed revisions to personality functioning and trait dimensions.
Criterion A requires significant impairments in self or interpersonal functioning, as described above. Criterion B requires one or
more pathological personality trait domains or facets. The final
three criteria require that the impairments in personality functioning are: relatively stable across time and situations; not a culturally
or developmentally normative personality feature; and not solely
due to the psychological effects of a substance or general medical
condition. This iteration of the general PD definition reflects the
efforts of the Work Group to streamline and simplify the system
that was originally proposed (see Skodol et al., 2011a; Skodol et
al., 2011b).
While the Work Group is moving toward a dimensional conceptualization of personality pathology, they are still incorporating
the ability to make a diagnosis by means of meeting impairment in
one of the two specified domains. The Work Group cites Wakefield (1992, 2008) in support of their position that, even though
pathological personality traits are dimensional in nature, “an extreme position on a trait dimension is a necessary but not sufficient
condition to diagnose a PD (American Psychiatric Association,
2011).” As the Work Group notes, difficulties with sense of self
and chronic interpersonal dysfunction represent problems that are
frequently described in relevant clinical literature (Benjamin,
1996; Rutter, 1987). Assessment of the two areas is intended to
distinguish between extreme traits and a disorder by looking for
the pervasive disorganization in personality structure that is present in PDs. Theoretically, this definition of PD accomplishes that
goal. The majority of the empirical support for these domains is
still in press and is not yet available on the APA website.
There has been a growing call for the type of PD definition on
which the Work Group ultimately settled. This is noted in the
burgeoning literature surrounding this issue (Clark, 2007; Gutiérrez et al., 2008; Krueger et al., 2007; Mullins-Sweatt & Widiger,
2010), including a special issue in World Psychiatry. Separating
the assessment of pathological personality traits from dysfunction
or disability would acknowledge a distinction between personality
disorder and normal range personality functioning. That is, while
most of us have personalities that differ in range and variability of
different personality traits, only about 10 –15% of the population
(Grant, Stinson, Dawson, Chou, & Ruan, 2005) will experience
personal distress, occupational difficulties, or other forms of dysfunction as a result of their personalities. Many have speculated on
the major categories of dysfunction associated with PDs, and most
revolve around aspects of interpersonal functioning (work, romantic relationships) and self-concept (knowing oneself) (Gutiérrez et
al., 2008; Krueger et al., 2007; Verheul et al., 2008)— or as one
study put it, “to love and to work” (Parker et al., 2004). The PD
Work Group cites work by Morey et al. (2011), who used itemresponse theory to identify manifestations of impairment at differ-
277
ent levels of severity of personality functioning (of note, this study
was supported by a DSM-5 Research Group Data Analysis proposal grant). The identification of a global dimension of personality pathology begins to mark a “threshold” that differentiates
patients with PDs from patients with non-PDs. A potentially important study would be to examine the genetic and environmental
influences on this global index.
Unfortunately, behavior genetics cannot clarify this issue at this
time. As noted above, most behavior genetic modeling of PDs
assumes a dimensional model and utilizes continuous measures of
the DSM criteria. Thus, behavior genetics does offer much in the
way of understanding etiological coherence and overlap for normal
and pathological personality traits and clinical disorders. Dimensional proponents of PDs have long argued that the DSM–IV
categories were an artificial and incorrect way of “carving nature
at its joints.” In some respects, the DSM-5 proposals for PD
definition would be shifting from arbitrary categories to arbitrary
cutoffs of dysfunction. Because the diagnosis of a disorder is used
in part for clinical decisions and treatment planning (First et al.,
2004), it is inevitable that definitions will be practical categories
based partially on value-laden judgments (Zachar & Kendler,
2007). Continued improvement is possible, however, as long as
empirical evidence, logic, and best practices are considered when
making revision decisions.
Elimination of Axis II
It appears that the multiaxial system of classification will be
eliminated from DSM-5. At one point, the DSM-5 website listed
recommendations from a Work Group on Structural, CrossCutting, and General Classification Issues for DSM-5 to eliminate
Axis II and Axis III, instead combining all psychological and
medical conditions on one domain. As of June 2011, this Work
Group is no longer referred to on the website. Instead, the website
identifies a Diagnostic Spectra Study Group, chaired by Steven E.
Hyman, the former head of the National Institute of Mental Health
and cochair of the DSM-5 research planning conferences, with the
goal of “examining the ways in which the disorders in DSM-5
might be organized.” The website outlines a DSM-5 organizational
structure of 20 chapters, including PDs, which was “designed to
better reflect scientific advances in our understanding of psychiatric disorders, as well as to make diagnoses easier and more
clinician friendly.” The inclusion of a PD chapter in this structure,
plus the text on the website describing a “diagnostic class of
Personality Disorders” would seem to indicate that PDs will remain in DSM-5 as their own section. In addition to the PDs being
listed under a separate section on the DSM-5 website, however,
two of the individual PDs are also cross-listed under other diagnostic classes: schizotypal PD under “Schizophrenia Spectrum and
Other Psychotic Disorders” and dyssocial PD (Antisocial PD)
under “Disruptive, Impulse Control, and Conduct Disorders.” In a
recent study coauthored by Hyman, a proposal was put forth to
distribute the PD constructs throughout the other diagnostic classes
(Andrews et al., 2009). Another article coauthored by several
members of the PD Work Group also raises this possibility, as well
as the option of keeping a PD chapter “and also detailing the
content-related connections with other forms of psychopathology
throughout DSM-5” (Krueger et al., 2011b, p. 329).
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SOUTH AND DEYOUNG
It is hard to know exactly how the removal of the multiaxial
system would impact the assessment and diagnosis of PDs, especially given the lack of clarity over how PDs will be included in
the final organization of the DSM-5. The website does not go into
depth about the rationale for the change. Given how momentous
this change will be for the PD field, particularly if there is no
separate PD section, it is surprising that there is no discussion of
this on the PD Work Group page of the website. The only direct
sentence addressing the elimination of the multiaxial system,
which no longer appears on the website, stated that, “This change
would bring DSM-5 into greater harmony with the single-axis
approach used by the international community in the World Health
Organization’s (WHO) International Classification of Diseases
(ICD).” Because DSM-5 revisions are frequently touted as being
empirically derived, it is surprising that this proposed change did
not receive more attention or a full rational statement pointing to
the empirical benefits for substantial rearrangement of the current
system. Work from the field behavior genetics examining the
etiological links between PDs and Axis I disorders is strong and
growing, so behavior genetics findings may be particularly useful
and influential on this point.
There are examples of family studies demonstrating genetic
links between PDs and clinical disorders, particularly between
Cluster A PDs and the psychotic disorders (Kendler et al., 1993;
Onstad, Skre, Edvardsen, & Torgersen, 1991; Parnas et al., 1993;
Torgersen, Onstad, Skre, & Edvardsen, 1993). This is not surprising, given that the schizotypal PD diagnosis was initially developed to account for subsyndromal pathology found in relatives of
schizophrenic probands. While formally categorized as a PD in the
DSM, schizotypy is classified among the schizophrenias in ICD10, reflecting a conceptualization of the pathology as a less-severe
form of psychotic disorder (Meehl, 1990). Research consistently
shows genetic influences on dimensional measures of schizotypy
(Jang, Woodward, Lang, Honer, & Livesley, 2005; Lin et al.,
2007; Linney et al., 2003) and schizotypal PD (Kendler et al.,
2006a) as well as genetic overlap between schizotypal PD and
schizophrenia (e.g., Torgersen et al., 1993). Some have suggested
that schizotypal PD be moved to a “Psychoses” cluster within the
DSM (Carpenter et al., 2009), returning it to Meehl’s original
conceptualization as a endophenotype of schizophrenia (Meehl,
1990). Indeed, schizotypal PD is cross-listed under the “Schizophrenia Spectrum and Other Psychotic Disorders” class of disorders on the DSM-5 webpage.
However, the extant behavior genetic literature suggests that the
etiology of schizotypy or schizotypal personality is more complex.
While the different components of schizotypal personality are all
at least moderately heritable, they also have substantial disorderspecific genetic influences (Lin et al., 2007). Linney et al. (2003)
found that the positive and negative components of schizotypy are
relatively etiologically distinct. Further, the cognitive distortion
component of schizotypy appears to cross over both of these
dimensions, indicating that it may form the “core” of the disorder.
Jang et al. (2005) concluded that there was significant genetic
overlap between the personality-based features of schizotypy and
the features reflecting psychosis-proneness, while the environmental contributions to each were relatively distinct. More research is
needed that combines measures of schizophrenia, psychosisproneness, schizotypal PD, and related maladaptive personality
traits within the same multivariate behavior genetic model.
The formal biometric modeling of the links between Axis I
clinical disorders and Axis II personality disorders using twin
studies is growing, shedding new light on the genetic and environmental overlap between clinical disorders and PDs that would
seem to be natural targets of investigation. For instance, major
depression has demonstrated overlapping phenotypic similarity
and biological processes with borderline PD (Goodman, New,
Triebwasser, Collins, & Siever, 2010), and there is evidence of
shared familial risk factors (e.g., Zanarini, Barison, Frankenburg,
Reich, & Hudson, 2009). Reichborn-Kjennerud et al. (2010) recently conducted multivariate modeling of dimensional representations of DSM–IV PDs and major depression. They found genetic
overlap between depression and borderline PD (rg ⫽ .56), avoidant
PD (rg ⫽ .22), and paranoid PD (rg ⫽ .40). Notably, one genetic
factor accounted for the overlapping genetic influences on all four
disorders, suggesting that there is a shared liability to multiple
forms of personality pathology and major depression. The strong
genetic correlation between depression and borderline PD, in particular, is not surprising, given that there is substantial overlap
between the genetic liability for major depression and neuroticism
(Kendler, Gatz, Gardner, & Pedersen, 2006b). In another recent
study using the same sample, the authors reported a high degree of
genetic overlap between avoidant personality disorder and social
phobia (Reichborn-Kjennerud et al., 2007b). There was no effect
of the shared environment, while the nonshared environmental
influences on each disorder were specific to that disorder.
Even more promising would be the inclusion of personality
pathology in twin studies examining shared etiology of multiple
clinical disorders. Phenotypic research supports the cluster of
common mental disorders into two spectrums of internalizing
(anxiety and mood disorders) and externalizing (substance use
disorders, conduct and oppositional defiant disorders, antisocial
personality disorder) psychopathology (Krueger, 1999; Slade &
Watson, 2006; Vollebergh et al., 2001). Behavior genetic research
suggests that these higher-order clusters also share common genetic factors; there is now strong support for genetic factor models
of internalizing and externalizing behavior in child and adolescent
(Krueger et al., 2002; Singh & Waldman, 2010) and adult samples
(Hettema, Neale, Myers, Prescott, & Kendler, 2006; South &
Krueger, 2008; Kendler, Prescott, Myers, & Neale, 2003). Antisocial PD is often included as part of the externalizing spectrum
(Hicks, Krueger, Iacono, McGue, & Patrick, 2004; Kendler et al.,
2003; Krueger et al., 2002; Slutske et al., 1998; Waldman &
Slutske, 2000), but the other nine DSM PDs have generally not
been included in these biometric factor models.
Only one study has conducted Joint biometric modeling of Axis
I and Axis II disorders. Kendler et al. (2011) used data from the
NIPHTP study to investigate the underlying genetic and environmental structure of 12 syndromal and subsyndromal common
DSM–IV Axis I disorders and dimensional representations of all 10
PDs. They found four correlated genetic factors: Axis I internalizing, Axis II internalizing, Axis I externalizing, and Axis II
externalizing. All four factors were intercorrelated, with the strongest relationships between the two internalizing factors (r ⫽ .49)
and the two externalizing factors (r ⫽ .38). Of note, paranoid PD
and dependent PD loaded on both of the Axis II genetic factors,
borderline PD loaded on both the Axis I and Axis II externalizing
factors, and antisocial PD loaded on the Axis I externalizing factor
only. Dysthymia and social phobia fit best on the Axis II internal-
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BEHAVIOR GENETICS OF PERSONALITY DISORDERS
izing cluster, suggesting that they share a stronger etiology with
PDs than other Axis I clinical disorders. The authors did acknowledge, however, that they could not formally test the number of
genetic and environmental factors that they extracted, a limitation
given the difficulty, particularly for PDs, of obtaining a goodfitting factor structure from explanatory factor analysis (see Huprich, Schmitt, Richard, Chelminski, & Zimmerman, 2010, for a
recent example). Even with this limitation, the authors concluded
that their findings provide tentative empirical support for maintaining a distinction between Axis I and Axis II pathology.
If current plans to eliminate the multiaxial system for DSM-5 are
implemented, it would be a significant change and a return to
pre-DSM–III. The addition of Axis II in the DSM–III had a large
impact on how many clinicians practiced (Coolidge & Segal,
1998). Because patients were to be evaluated on each axis, clinicians were prompted to assess every patient for a PD. The DSM-5
PD Work Group frequently states that every patient could potentially benefit from going through the (proposed) personality assessment sequence. Removing the current multiaxial format that
was specifically designed to compel clinicians to consider the
personality traits of each of their patients would seem to detract
from this stated goal of the PD Work Group. Given that the PDs
are the only disorders in the DSM that will have an official and
specific assessment sequence, it may be clinically useful to keep a
separation between the PDs and Axis I disorders. Lumping PDs
together with clinical disorders may further retard research interest
into PDs, as well as having the unintended consequence of diminishing the importance of clinical assessment of personality pathology. Certainly, the original justification for moving PDs to a
separate Axis in DSM–III— differences in course and stability—
have been challenged (Krueger, 2005). Findings from behavior
genetics, however, suggest that there may be an etiological basis
for separating disorders that are more acute, transient, and ego
dystonic from disorders that are chronic, stable, and ego-syntonic.
The distinction between internalizing and externalizing forms of
psychopathology, whether they are clinical or personality disorders, may largely reflect genetic variation, while both genes and
environmental influences seem to distinguish between Axis I and
Axis II disorders (Kendler et al., 2011).
PD Classification: Toward DSM-5
As the PD Work Group for DSM-5 moves closer to a finalized
product, they will have to make many decisions on which disorders
to retain, whether and how personality pathology can be captured
by personality domains, and whether PDs should continue to be
grouped according to phenomenology, or if there are structural
(e.g., internalizing, externalizing) groupings that have a basis in
shared etiology (e.g., genetic and environmental influences) that
should define different classes of disorders. The considerations
detailed below are intended to help in the continued reformulation
of PD assessment and diagnosis as the DSM-5 process moves
forward.
Considerations for DSM-5
First, there is a real concern that the concept of PD might find
itself revised out of the DSM-5. Under the current proposal, Axis
II and four DSM–IV PDs will be eliminated. It is possible that the
279
entire chapter on PDs may be eliminated in favor of moving all PD
types to different sections within the DSM. Andrews et al. (2009),
for example, argued for a new metastructure for the DSM that
would span both clinical and personality disorders. Based on
reviews of 11 risk and clinical “validators,” they suggested reorganizing current DSM diagnostic categories into five clusters:
emotional disorders, externalizing disorders, psychoses, neurocognitive disorders, and neurodevelopmental disorders (and a sixth
cluster for “other” disorders). In this scheme, Axis II would be
eliminated and only four of the DSM–IV PDs would be retained,
classified with the most appropriate cluster: schizotypal in the
psychosis cluster, borderline and avoidant in the emotional disorders cluster, and antisocial in the externalizing cluster. That may
seem too radical of a change to actually be approved for DSM-5,
but members of the DSM PD Work Group recently articulated a
similar meta-structure for DSM-5 in which disorders are organized
according to their underlying personality dimensions (Krueger et
al., 2011b).
A change of this magnitude would be a dramatic loss for PD
researchers, but more importantly would be unwarranted based on
the current state of the behavior genetics literature. For instance,
there is a relative dearth of evidence from phenotypic and behavior
genetic research about the links between certain personality traits
and clinical disorders (e.g., personality traits underlying psychosisspectrum disorders, Carpenter et al., 2009). And as noted above,
genetic and environmental influences distinguish clinical forms of
internalizing and externalizing psychopathology from more
personality-disordered forms (Kendler et al., 2011). A simple way
to maintain this distinction may be to keep a separate PD chapter
in the DSM-5, as currently proposed. If the PDs are incorporated
into clusters that share common risk and clinical characteristics, as
well as a common temperamental core (e.g., neuroticism for internalizing, Griffith et al., 2010), a distinction could be made
within each cluster between a clinical disorder and a PD. Certainly,
the behavior genetics literature supports more than one alternative
regarding the reorganization and restructuring of the DSM–IV PDs;
there is evidence, for instance, that antisocial PD is structurally
(Røysamb et al., 2011) and genetically (Meier, Slutske, Heath, &
Martin, 2011) related to Axis I externalizing disorders. Any one of
these interpretations could be equally valid, but the important point
here is that the overall behavior genetics literature does not support
the complete elimination of the PD concept.
Second, the existing behavior genetics literature does not support the elimination of four of the DSM–IV PDs. Findings from
behavior genetics would encourage retaining types for all 10 of the
DSM–IV PDs, as all of the PDs (including those suggested for
removal) appear to be capturing a core extreme pathology that is
based partly in genetics and which cannot be completely explained
by normal personality trait variation (e.g., Morey et al., 2007;
Samuel, Simms, Clark, Livesley, & Widiger, 2010). Removing
these PDs may discourage researchers from further examination of
what this core pathology represents. Continued refinement of any
of the PD constructs may lead to “purer” endophenotypes, constructs thought to lie in the intermediary between a phenotype and
a genotype (Gottesman & Gould, 2003). Endophenotypes can be
conceptualized as collections of core traits or temperaments, and
have been linked with cognitive, physiological, and neurobiological characteristics (Siever, 2005). PD endophenotypes may ulti-
SOUTH AND DEYOUNG
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280
mately demonstrate more cohesive etiological structures than the
current DSM disorders.
Third, more information is needed on implementation of the
proposed personality trait system. Specifically, data are needed
that support the current “cross-walk” translation of DSM–IV PD
concepts onto DSM-5 PD types. The newly revised trait system
appears to be more congruent with research, particularly from
behavior genetics findings, than the previous narrative prototype
model, which harkened back to DSM–II. The proposed traits can
be rated, either by clinicians or using a self-report questionnaire,
and subjected to empirical validation. A future in which PD
diagnoses are made by comparing a patient’s pattern of personality
traits to a profile of “disordered” personality, akin to an Minnesota
Multiphasic Personality Inventory code type, could be clinically
useful. However, determining which specific traits should be used
to define each PD would benefit from additional data collection.
Whether these considerations are entertained by the PD Work
group, the decision process as the DSM-5 moves forward is best
served through careful explication in peer reviewed journal articles
and on the DSM website.
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