Journal of Personality Disorders, 32(2), 148-167, 2018

© 2018 The Guilford Press

COMPETING THEORIES OF BPD
GUNDERSON ET AL.

COMPETING THEORIES OF BORDERLINE

PERSONALITY DISORDER
John G. Gunderson, MD, Alan Fruzzetti, PhD, Brandon Unruh, MD,
and Lois Choi-Kain, MD

The authors review four theories that propose different conceptualizations

of borderline personality disorder’s (BPD) core psychopathology: excess
aggression, emotional dysregulation, failed mentalization, and interpersonal
hypersensitivity. The theories are compared in their ability to explain BPD’s
coaggregation of four usually distinct sectors of psychopathology, their
high overlap with other disorders, their ability to distinguish BPD from
other disorders, their integration of heritability, and their clinical applica-
bility. The aims of this review are to increase awareness of these theories,
to stimulate improved theories, and to foster testable hypotheses so that
research can advance our knowledge about BPD’s core.

At present there are multiple theories about what comprises the core of bor-
derline personality disorder (BPD) psychopathology, each with distinctive
features and each with an associated model of treatment. We will examine
the distinctions between four major theories of BPD and assess their relative
merits (Table 1). These four theories were selected because each defines an
organizing core for BPD, all have associated and widely recognized models
for psychotherapy, and each model is taught by an active, influential, and
committed faculty. Moreover, each theory has a significant body of research
that supports its claims (Fonagy, Luyten, & Bateman, 2015b; Gunderson &
Lyons-Ruth, 2008; Kernberg, Yeomans, Clarkin, & Levy, 2008; Kring &
Sloan, 2010).
This review uses five standards for evaluating BPD’s theories. In the ab-
sence of standards for such comparison, these were chosen because of their
clinical relevance and significance and because of their feasibility for compar-
ison. The first standard considers their ability to explain the coaggregation of
BPD’s four component sectors: interpersonal, affective, behavioral, and self/
cognitive. The second standard addresses BPD’s high rates of comorbidity
with other disorders—how well does each theory account for these over-
laps? The third standard is whether a theory distinguishes BPD from other

From McLean Hospital, Belmont, Massachusetts (J. G. G., A. F., B. U., L. C.-K.); and Harvard Medical
School, Boston, Massachusetts (J. G. G., B. U., L. C.-K.).
Address correspondence to John G. Gunderson, McLean Hospital, Department of Psychiatry, Harvard
Medical School, 115 Mill St., Belmont, MA 02478. E-mail: jgunderson@mclean.harvard.edu

148
COMPETING THEORIES OF BPD 149

TABLE 1. Four Theories of Borderline Personality Disorder

Theory
1 Excessive Aggression
2 Emotional Dysregulation
3 Failed Mentalization
4 Interpersonal
Hypersensitivity
Main source Summary
Kernberg (1967) In this theory of BPD, aggression is considered a basic
human instinct; excessive aggression can be either
genetically determined or due to excessive frustra-
tions during childhood. In either event, this excessive
aggression alternates between inappropriate and
offensive expression and being defensively suppressed
and split off (“disowned”), in which case it gets di-
rected at the self (“bad” self) or projected onto others
(“bad” other, “good” self).
Linehan (1993) This theory identifies a deficient capacity to regulate
emotion. This deficiency is thought to be a neuro-
biological disposition that is evident in excessively
intense and prolonged emotions. This deficit becomes
manifest only when the preborderline child’s experi-
ences are not validated. The dysregulated emotions
trigger the borderline patient’s behavioral and inter-
personal problems.
Fonagy and Luyten (1999) Failed Mentalization refers to an inability to identify
mental states (e.g., attitudes or feelings) in oneself
(akin to mindfulness or introspection) or in others
(akin to empathy) and to recognize how these mental
states are influenced by each other. This psychological
handicap begins early in development due to parental
failures to help children accurately and verbally
identify their feelings or those they evoke.
Gunderson (2008) In this theory, hypersensitivity and excessive reactivity
to interpersonal cues are a genetic disposition. The
preborderline child will find even modest slights and
frustrations very stressful. The BPD person reacts to
perceived failures of support from others by feeling
either that this is cruelly unfair (“bad other”) or that
he or she is inherently bad (“bad self”). Being alone is
intolerable, triggering either dissociative or paranoid
experiences or desperately impulsive acts that force
others to become involved.

mental illnesses. The fourth standard is how well each theory incorporates
knowledge about BPD’s heritability. The fifth standard concerns their clinical
usefulness, that is, their clarity, understandability, and clinical applications.
These standards are efforts to reflect each theory’s content validity (Stan-
dards 1–4), predictive validity (Standard 3), discriminant and convergent
validity (Standard 2), and treatment validity (Standard 5). The potential bias
within each of these standards will be considered and their overall limita-
tions will be discussed.
The methodology used for preparing this review rests heavily on knowl-
edge and critical analysis of the relevant literature. This grounding has been
combined with clinical experience, notably using the therapies based on these
four theories, and with the perspectives gained from the authors’ experience
teaching or writing about these theories.*

* Because of the lead author’s investment in the theory of interpersonal hypersensitivity, coauthors in-
clude experts with a primary commitment to other theories, that is, Alan Fruzzetti and emotional dysregu-
lation, Brandon Unruh and failed mentalization.
150 GUNDERSON ET AL.

TABLE 2. Four Sectors of Psychopathology of Borderline Personality Disorder

Sector DSM Traits Summary
Affective Anger BPD is characterized by excessively intense
and poorly controlled emotions. This is evident
in emotional instability and recurring states of
anxiety, depression, and anger
Affective instability
Emptiness
Interpersonal Intense, unstable relationships BPD is characterized by intense, unstable relation-
ships, fears of separation and rejection, and long-
ings for an exclusive partner combined with fears
of being abandoned.
Abandonment fears
Needy, fearful attachments
Behavioral Self-harm/suicidality BPD is characterized by impulsive behaviors that
are often self-destructive, either intentionally or
unintentionally (unconsciously).
Impulsivity (e.g., substance abuse,
promiscuity)
Self/Cognitive Self-image instability and distortions The BPD person’s sense of self is unstable and often
distorted. This can be evident by feelings of being
unreal (derealization) or that the world is unreal
(depersonalization), or by quasi-psychotic episodes
of distrust
Dissociation and brief paranoid episodes
Note. From Gunderson et al. (2011), Archives of General Psychiatry, 68, 753–762.

STANDARD 1: HOW WELL DOES EACH THEORY OF BPD’S CORE

EXPLAIN BPD’S FOUR SECTORS OF PSYCHOPATHOLOGY?

Multiple factor analytic studies have found four component sectors of BPD
psychopathology (Becker, McGlashan, & Grilo, 2006; Clarkin, Hull, &
Hurt, 1993; Hurt, 1984; Moor, Distel, Trull, & Boomsma, 2009; Sanislow,
Grilo, & McGlashan, 2000; Sanislow et al., 2009, 2002; Taylor & Reeves,
2007) (see Table 2). Each of these sectors represents a broad phenotype that is
found in multiple non-BPD disorders. A good theory for BPD should thus be
able to explain the presence of all four of these. Genetic evidence for a latent
organizing factor that accounts for the coaggregation of these four sectors
(Distel et al., 2010; Gunderson et al., 2011; Kendler et al., 2011) demands
that a good theory for BPD can explain why these phenotypes coaggregate.
The Excessive Aggression theory posits that alternation between the mal-
adaptive expression (excessive anger against an unfair other) and suppres-
sion (excessive anger toward self) of aggression constitutes a basic conflict
within the BPD personality (identified as a “splitting” defense). This theory
places the core of BPD within the self/cognitive sector (see Table 3). This split
around aggression explains impulsive acts, a disturbed and distorted sense of
self, and self-damaging behaviors. Paranoid experiences are conceptualized
as defensive projections of disowned hostility onto others. Lapses in reality
sense or testing (e.g., dissociation) are seen as psychological defenses against
“intolerable” realities. Thus, this theory identifies latent factors that organize
COMPETING THEORIES OF BPD 151

TABLE 3. Standard 2: Do Theories Explain the Four Sectors of BPD Psychopathology?

Theory Emotional Interpersonal Behavioral Self/Cognitive
Excessive Aggression 2° - unintegrated 2° - projections and 2° - defensive acting 1° - unstable self
self/other percep- splitting of self out, avoidance initiates and
tions regulates BPD S/Sxs
Emotional Dysregulation 1° - inability to 2° - emotionality 2° - adaptations that NA re-self, 2°-
accept and regulate alienates others regulate emotions emotions disrupt
emotions triggers cognitions
BPD S/Sxs
Failed Mentalization 2° - inability to 1° - incapacity to 2° - activated 2° - self formed by
recognize or read self and others attachment interpersonal
communicate triggers BPD S/Sxs impairs judgment interactions (alien
emotional states; self formed by
emotions impair failures)
mentalizing
Interpersonal 2°- triggered by 1° - interpersonal 2° actions evoke 2° - self has significant
Hypersensitivity catastrophic context triggers others’ genetic determinants.
meanings assigned BPD S/Sxs involvement Like Excessive
to interpersonal Aggression retro-
events flected anger → bad/
evil self
Note. S/Sxs: signs and symptoms. NA: not applicable.

and explain all four sectors of BPD psychopathology. It establishes a tension

between a basic human instinct toward aggression (normal or excessive) and
prefrontal cortical failures to accept and adaptively express this instinct.
The Emotional Dysregulation theory claims that the symptoms of BPD
in both the behavioral (impulsivity, self-harm) and interpersonal (clinging,
hostilities) sectors are maladaptive ways of coping with unaccepted and of-
ten unrecognized feelings. BPD hostility, which is a “primary” emotion in the
Excessive Aggression theory, in this theory is a secondary reaction to exter-
nal stressors and/or a means to escape what are considered more distressing
primary emotions such as shame, sadness, and fear. Note that what is called
a defense—unconsciously triggered in response to internal conflicts—in the
Excessive Aggression theory is identified as maladaptive coping—a socially
learned strategy for managing the external environment or internal experi-
ence—in the Emotional Dysregulation theory. This theory places the emo-
tional sector at BPD’s core (see Table 3). This theory’s conclusion that inter-
personal symptoms are not the primary phenomena in BPD (i.e., maladaptive
ways of coping with unwanted or unacceptable emotions) is notable. The
interpersonal sector is central to most theories of personality. Moreover, Fru-
zzetti, Shenk, & Hoffman (2005) noted that insofar as invalidation, an inter-
personal transaction, is essential for BPD’s development, the theory needs to
amplify this. Bender and Skodol (2007) add to this that insofar as the experi-
ence of invalidation causes the preborderline child to doubt or ignore his or
her perceptions, it becomes difficult to escape the concept of a self. Articles in
which Linehan is a coauthor recognize the need for modifying the theory to
include self and to expand its developmental perspective (Bohus, & Neacsiu,
2014; Crowell, Beauchaine, & Linehan, 2009). Still, other than reference to
how a child can resist or misunderstand validation and that invalidation has
harmful effects on one’s self, Linehan has not fully integrated these perspec-
152 GUNDERSON ET AL.

tives very satisfactorily into her theory (Linehan, 2015). The result is that for
a theory of personality, Emotional Dysregulation gives inadequate attention
to transactional origins of BPD and to the self sector of BPD and, unlike
other theories, consigns a secondary role to the interpersonal sector.
Just as importantly, by being relatively ahistorical (other than noting the
role of current or past invalidation, it is nondevelopmental), this theory does
not reflect those brain activities that allow for a self, that is, those activities
that organize and interpret each person’s world in ways that reflect past ex-
periences and that initiate responses consistent with one’s past.
Failed Mentalization theory conceptualizes an interpersonally acquired
psychological handicap that is central to interpersonal relatedness (see Table
3). This handicap explains BPD’s interpersonal symptoms as products of the
preborderline child not having had his or her mental states (e.g., emotions,
attitudes, intentions) attended to, labeled correctly, and accepted by caretak-
ers. The resulting unrealistic, extreme, or unbalanced perceptions of self or
others are thought to cause BPD’s behavioral and emotional problems. Be-
cause the mentalization concept is inextricably tied to self-awareness and to
misattributions of others, it implicitly absorbs the same self–other dynamic
interplay that characterizes the Excessive Aggression theory, and easily ac-
commodates the self/cognitive sector. As with the Emotional Dysregulation
theory, emotions are assigned particular importance as triggers for lapsed
mentalization, and aggression/anger in BPD is considered secondary to en-
vironmental frustrations, not a primary motivating force. Of note, by as-
signing anger/aggression this secondary role, both the Emotional Dysregula-
tion and Failed Mentalization theories adopt the self psychology school of
thought developed by Kohut and others in the 1970s, and applied to BPD by
Adler and Buie (1979).
According to the Interpersonal Hypersensitivity theory, people with
BPD are at baseline anxious and/or depressed; these individuals give way to
anger when they perceive an impending separation or rejection. Then angry
devaluation (bad other) and/or self-harm and suicidality (bad self) occur.
Thus, like in the Excessive Aggression theory, the management of anger is
important, but, unlike in the Excessive Aggression theory, anger is not neces-
sarily excessive or instinctive and is not considered core. What is excessive is
the catastrophic significance, that is, the sense of abandonment and hatred,
assigned to the impending separation or rejection. When the person with
BPD feels alone, dissociation (self or world as unreal) or brief paranoid ex-
periences (self as endangered) occur. Fears of rejection or abandonment, or
the actual experience of being alone, prompt desperate impulsive behaviors
such as substance abuse or promiscuity. Thus, in this theory all BPD symp-
toms are understood to be directly related to the person with BPD’s immedi-
ate interpersonal context. While both the Interpersonal Hypersensitivity and
Failed Mentalization theories describe the same attachment paradox, that
is, an intense need for closeness and attention and an equally intense fear of
rejection or abandonment, in the Interpersonal Hypersensitivity theory, this
type of attachment is secondary to this genetically determined hypersensitiv-
ity’s effect on triggering maladaptive parental responses, not as an attach-
ment that is created primarily by parental failures.
COMPETING THEORIES OF BPD 153

In summary, controversy remains over what constitutes the primary

(core) sector of BPD. The Excessive Aggression theory places it within the
self/cognitive sector; the Emotional Dysregulation theory places it within the
emotion sector; the Failed Mentalization and Interpersonal Hypersensitivity
theories both place it within the interpersonal sector. Each theory can then
explain the symptoms of BPD’s other sectors as secondary, with one notable
exception: Emotional Dysregulation theory does not recognize the self sector.

STANDARD 2: HOW WELL DOES EACH THEORY EXPLAIN BPD

COMORBIDITIES?

Historically, the co-occurrence of four different sectors of psychopathology

in the BPD syndrome has led to conceptualizations of BPD as an atypical
form of some other parent condition: Schizophrenia overlaps with BPD in the
cognitive sector, while both major depressive and bipolar disorders overlap
with BPD in the emotion sector. BPD’s interpersonal and impulse symptoms
are shared with the so-called dramatic cluster (antisocial, narcissistic, and
histrionic) of personality disorders. Appreciating that our classification sys-
tem has failed to identify clear boundaries around any psychiatric disorder,
there is nonetheless reason to expect that high levels of comorbidity reflect
overlaps in underlying psychopathology. A good theory of BPD should be
able to account for such near neighbors. This standard examines a theory’s
sensitivity, that is, its ability to include and explain the disorders with which
BPD co-occurs (see Table 4).
The Excessive Aggression theory offers a good explanation for BPD’s
high rates of comorbidity with other disorders. The theory was, after all,
originally expected to characterize and explain the broad range of nonpsy-
chotic but severe mental disorders under the rubric of borderline personal-
ity organization (Kernberg, 1967). Major depressive disorder (MDD) and
posttraumatic stress disorder (PTSD) can be seen as products of retroflected
hostility, while externally directed hostility can explain antisocial personality
disorder (ASPD) and narcissistic personality disorder (NPD). Both bulimia
and substance abuse can be caused by vacillations between expressed aggres-
sion (defiance) and retroflected aggression (self-harm). Excessive Aggression
can explain existential anxiety as the result of living in a dangerous world.
It does not easily account for panic disorder or other anxiety disorders: The
primitive defenses that dominate BPD in this theory would be expected to
ward off such severe anxiety states.
The Emotional Dysregulation theory is best in explaining behavioral
disorders such as substance abuse, bulimia, and ASPD. These are maladap-
tive behavioral means by which to escape unwanted feelings. Notably, the
broader concept of poor distress tolerance often used to explain such im-
pulsive behavior is narrowed here because the triggering stress is always
considered to be evoked emotions (Leyro, Zvolensky, & Bernstein, 2010).
Similarly, PTSD and dissociative disorders involve an escape from painful
feelings. Emotional Dysregulation does not deal so well with other comor-
bidities. Severe depression is considered an unwanted emotional response
154 GUNDERSON ET AL.

TABLE 4. Do Theories Explain BPD’s Comorbidities?

Other PDs
Theory MDD Bipolar D Subst Ab Panic D PTSD Bulimia ASPD NPD AVPD
(50%) (15%) (35%) (50%) (30%) (15%) (25%) (15%) (?)
Excessive Aggressiona ++ + + – – + ++ + +
Emotional Dysregulationb ± – + – + + + + ++
Failed Mentalizationc + + + + ++ ? ++ ++ –
Interpersonal Hypersensitivityd ++ + + ++ ++ + – ++ –
Note. Percentages are the prevalence rates in patients with BPD. MDD = major depressive disorder; Bipolar D =
bipolar disorder; Subst Ab = substance abuse; Panic D = panic disorder; PTSD = posttraumatic stress disorder; ASPD =
antisocial personality disorder; NPD = narcissistic personality disorder; AVPD = avoidant personality disorder. aExces-
sive Aggression: MDD – retroflected and/or unintegrated aggression; convictions of badness/evil; Bipolar D – consistent
with independence; Subst Ab – either hostile defiance or self-harm; PTSD – self-punishment; Bulimia – unintegrated
split of acceptance (eat)/rejection (expel); ASPD – uninhibited and maladaptively expressed aggression; NPD – exces-
sive aggression when idealized self is threatened; Panic D – not good for Panic D as symptom of conflict, OK with Ax
as symptom of perceived danger. bEmotional Dysregulation: Subst Ab, Bulimia, AVPD – behavioral means of avoiding/
controlling painful emotions; PTSD – maladaptive coping with unacceptable (? intolerable) feelings of shame and fear;
MDD – a dysregulated emotion; recognizes shame, but doesn’t address either self-esteem or anger; Bipolar D – not
good; should be closely related, but isn’t; Panic D – not good; a dysregulated emotion to be avoided; ASPD and NPD –
not good; doesn’t include self-concept. cFailed Mentalization: MDD – due to hypomentalizing; Bipolar D – consistent
with independence; Subst Ab – defensive (self-medicating) response to uncertainty and inchoate feelings; Panic D –
existential state of fearfulness; PTSD – trauma disrupts mentalization capability; Bulimia – body image, impulsivity re-
flect failed mentalization; ASPD and NPD – failures of both empathy and introspection. dInterpersonal Hypersensitiv-
ity: MDD – retroflected anger → badness/evil plus realistic concerns about failures in work/love; Bipolar D – consistent
with independence; Subst Ab – disinhibiting effects allow otherwise shameful pursuit of relationships; Panic D – acute
fear of rejection, response to aloneness; PTSD – temperamentally hypersensitive to stress; Bulimia – unintegrated split
of acceptance/rejection; NPD – reflects sensitivity to slights, criticisms, or perceived rejection; ASPD – not good; ASPD
callousness inconsistent with BPD rejection sensitivity.

with negative cognitions that reflects failed regulation. Still, this theory lacks
the developmental explanatory power of MDD’s major psychological expla-
nations (i.e., retroflected anger or low self-esteem). Similarly, panic disorder
is considered another painful emotional state with negative cognitions to be
regulated, but neither its origins nor its psychology are inherent in the theory.
Emotional Dysregulation theory also does not do well with explaining other
personality disorders because of its disregard for the concept of self and its
psychology. It has particular problems with explaining NPD and ASPD be-
cause its concept of BPD does not incorporate aggressive personality traits
such as cruelty and exploitativeness, let alone grandiosity or disdain. In this
theory, these are states of “emotion mind.” Moreover, and this is notable,
the Emotional Dysregulation theory predicts high overlap and interaction
with bipolar disorder, a prediction that is disconfirmed by existing evidence
(Gunderson et al., 2014). This is notable because the theory that BPD is
based on emotional dysregulation has fueled the persistent proposition that
BPD is a bipolar spectrum disorder.
The Failed Mentalization theory is best at explaining comorbidities with
other personality disorders such as ASPD and NPD with their discernible
failures of self-appraisal, introspection, and empathy. These are attachment
strategies that guard (defend) against becoming vulnerable or hurt. Disor-
ders that entail histories of past trauma, most notably PTSD, are also read-
ily affiliated with BPD according to this theory by virtue of the destructive
consequences trauma has on mentalization capabilities (Allen, 2013; Fonagy,
COMPETING THEORIES OF BPD 155

2002). Insofar as co-occurring depression (or MDD) is secondary to “hypo-

mentalizing” (as opposed to BPD’s hypermentalizing), and insofar as bipolar
disorder is an autonomous disorder whose psychology is unrelated to men-
talization, their independence is reconcilable (Bateman & Fonagy, 2015).
The Interpersonal Hypersensitivity theory accepts Excessive Aggression
theory’s explanation of MDD, adding only that the retroflected aggression
need not be either driven by instinct or a defensive response to projected an-
ger, and that BPD’s depressive moods are triggered by adverse interpersonal
events. It proposes that hypersensitivity enhances the likelihood of PTSD
resulting from adverse interpersonal events and that panic disorders and dis-
sociation are responses to feeling alone. This theory is consistent with Failed
Mentalization in seeing ASPD as a callous response within individuals who
become defensively distrustful and dismissive to avoid the pain that caring
about others can otherwise cause. Both theories would also consider that the
distrust and dismissiveness found in ASPD may be due to failures in early
caregiving.
In summary, both the Excessive Aggression and Failed Mentalization
theories offer broad explanatory concepts that readily include most of BPD’s
major comorbidities. The Interpersonal Hypersensitivity theory, borrowing
concepts from both Excessive Aggression and Failed Mentalization, also
comfortably incorporates the comorbidities. Some major problems occur
with the Emotional Dysregulation theory. Because it does not include the
concept of self and because of its reluctance to emphasize the interpersonal
sector, it does not map onto other personality disorders. Its theory is also
inconsistent with BPD’s independence from bipolar disorder.

STANDARD 3: HOW SPECIFIC IS EACH THEORY’S PROPOSED

CORE TO DSM BPD?

The previous standard examined how well BPD’s theories can explain its
major comorbidities—its overlap with other disorders. This third standard
looks instead at each theory’s specificity for BPD: Does the theory define a
core unique to BPD, or could the proposed core apply to other disorders as
well? In this discussion, it is important to bear in mind that although the
Diagnostic and Statistical Manual of Mental Disorders (DSM) definition of
BPD has been the diagnostic standard for 40 years, it is unfair to assume
that specificity of a theory to the DSM definition of BPD is a strength. Of
particular significance here is the significant scientific support accorded to
redefining this disorder using traits. Whether and how these theories would
fit with such a redefinition invites consideration. As we learn more about
this disorder, the DSM definition will surely evolve. Current theories frame
hypotheses about BPD that may prove as useful or more useful in advancing
our understanding of BPD and redefining this disorder than does their fit
with the DSM definition.
Excessive Aggression theory was derived by Otto Kernberg from psy-
choanalytic theory, specifically from the object relations theory pioneered
by Melanie Klein (Kernberg, 1967). This theory emphasizes the vicissitudes
156 GUNDERSON ET AL.

of an aggressive instinct thought to be universal. It is concerned with intra-

psychic traits, specifically with defenses, reality testing, and identity. Based
on the severity and “primitiveness” of a person’s functioning in these three
domains, humans were divided into those with psychotic, borderline, or
neurotic levels of personality organization. This theory is concerned only
secondarily with observable and descriptive characterizations. Those who
meet the DSM criteria for BPD are a subgroup of the broader class of people
within those having the borderline level of personality organization. This
DSM-based subgroup was both a particularly symptomatic exemplar of this
level of personality organization, but also the subgroup who were particu-
larly common in psychiatric and especially psychotherapeutic settings. As a
consequence, they had dominated the psychoanalytic literature before and
after the DSM construct.
Emotional Dysregulation theory was derived from observations of pa-
tients who self-harmed viewed through Marsha Linehan’s theoretical lens of
a “radical behaviorist.” Linehan’s initial interest was in helping people who
self-harmed and attempted suicide to learn skills to regulate their emotions
and thereby control this behavior. After observing her patients’ resistance
to her lessons, she incorporated the Buddhist lesson of mindfulness (aware-
ness of self, other, and the physical world) and the practice of validation
(actively accepting the patient’s experience and perspective). Her patients
then became willing to use the skills needed to stop self-harming. Linehan
thereby connected her observation that self-harm functions to avoid other-
wise dysregulated painful feelings with others’ failures to validate emotions.
Only after she developed this theory and its associated therapy did she learn
that her clients’ self-harm and suicidality were symptoms of a psychiatric
disorder, that is, BPD. It was in this context that she was intensively exposed
to the psychoanalytic concept of borderline personality organization and the
theory of excessive aggression during a 6-month sabbatical spent in the same
hospital in which Kernberg directed his treatment program. So the emotional
dysregulation theory started with a narrow focus, and the subsequent as-
sociation with BPD broadened its application. Emotional dysregulation has
subsequently been recognized as a central characteristic of many psychiatric
disorders (Kring & Sloan, 2010; Linehan, 2015).
The Failed Mentalization theory was derived from Peter Fonagy’s ex-
amination of mother–child interactions while conducting research on the
development of insecure attachments. Thus, the theory of Failed Mentaliza-
tion—like those of Excessive Aggression and Emotional Dysregulation—was
not based on observations of adult BPD patients. Like the Emotional Dys-
regulation theory, Failed Mentalization was applied to BPD only after the
theory had been developed. Mentalization was increasingly recognized as
a psychological function believed to exist more or less in everyone. Con-
sistent with these expansions, Fonagy and Bateman are now advocating a
dimensional approach to personality classification in which mentalization is
centrally represented. What became confusing is what or whether BPD had
specific mentalization failures. The theory now posits that it is the instability
of the mentalization capacity that is specific to BPD (Fonagy et al., 2015b).
If the “activated attachment system” prompts emotions that cause BPD’s
COMPETING THEORIES OF BPD 157

failed mentalization, this model overlaps with the Emotional Dysregulation

theory. However, if, as seems more likely, an “activated attachment system”
is a result of a sensitivity to adverse interpersonal events, the theory overlaps
with the Interpersonal Hypersensitivity theory. Improvements in mentaliza-
tion became increasingly implicated as the mechanism for change in all effec-
tive psychotherapies (Allen, Fonagy, & Bateman, 2008).
The Interpersonal Hypersensitivity theory began with observations of
individuals who meet the DSM criteria for BPD in diverse clinical settings,
from hospital wards to the psychoanalytic couch (Gunderson, 1984). Thus,
the theory was built to fit with DSM-defined BPD from the beginning of its
development. It emphasizes the threat of rejection and feelings of aloneness,
both of which are considered in this theory to cause BPD’s symptoms to
emerge. The early theory was influenced by Kernberg’s object-relations per-
spective and by the emphasis that Adler and Buie (1979) gave to intolerance
of aloneness.
In summary, three of BPD’s theories originated from observations of
non-BPD populations by observers who were immersed in preexisting theo-
retical models. Excessive Aggression arose from psychoanalytic theory, Emo-
tional Dysregulation from behaviorism plus emotion theories, and Failed
Mentalization from attachment theory. Their proposed cores fit with what
was independently identified as BPD, but they were never intended to be
specific for this disorder. As such, the Excessive Aggression theory was in-
tended to cover a much broader portion of psychologically impaired adults,
the Emotional Dysregulation theory was intended to cover a much narrower
group of self-harming and suicidal adults, and the Failed Mentalization the-
ory was originally intended to describe a psychological incapacity resulting
from the interactions that lead to insecure attachments. Mentalization theory
has now defined a narrower, more DSM-BPD specific form of mentalization
that identifies the fragility of this capacity in response to either emotions or
interpersonal reactivity.

STANDARD 4: HOW WELL DOES EACH THEORY INTEGRATE

BPD’S GENETIC CAUSATION?

Genetic causes for BPD were largely ignored until the first significant twin
study estimated its heritability at 69% about 17 years ago (Torgersen et
al., 2000). Subsequent research has lowered this estimate, but convincingly
confirms that BPD’s heritability accounts for more than half the variance in
whether BPD develops (Distel et al., 2010; Gunderson et al., 2011; Kendler
et al., 2011). As noted earlier, this research has also confirmed an underlying
unifying common pathway genetic model. This research now requires theo-
ries about BPD’s core to account for the major role played by genes and to
propose what the nature of the unifying genetic disposition is.
The aggression central to the Excessive Aggression theory may be either
genetically determined (an extreme variation of the aggressive instinct shared
by all humans) or develop as a consequence of excessive frustration. In either
event, the resulting development of BPD is related to “primitive” (meaning
158 GUNDERSON ET AL.

reality-altering) conflicts about integrating the aggression into the self. Curi-
ously, despite having pioneered the plausibility of a genetic basis for BPD,
this is the only theory that does not concede a deficit to be the core of BPD:
Whatever its genetic sources might be, they are secondary.
The Emotional Dysregulation theory emphasizes a self-regulatory bio-
social deficit. In this theory, excessive emotionality is the core of BPD. This
excessive emotionality is thought to be based in the limbic system (Line-
han, 1993), but the core problem with its regulation is thought to be based
in the prefrontal cortex and is therefore a “top-down” problem (Herpertz
& Bertsch, 2015). Perhaps because this theory was developed before BPD’s
heritability was established, the theory has not explicitly adopted a genetic
explanation for excessive emotionality or the problems in its regulation.
The Failed Mentalization theory proposes a handicap in mentalization
as the core of BPD. This handicap was observed while conducting research
on child attachment, yet attachment patterns in childhood have little to
no heritability (Bokhorst et al., 2003). As such, this theory was not well-
grounded in biology or genetics. Rather, it began as the most mentalistic
theory (i.e., it involves prefrontal functions of self-awareness, language, so-
cial learning, and interpretation). Recognizing this, Fonagy has made efforts
to integrate genetics by proposing that BPD involves a genetic predisposi-
tion to hypermentalize (excessive and inaccurate attributions). This, in turn,
he proposes, is a result of a genetically determined persistence or excess of
epistemic vigilance (distrust in the believability of others; Fonagy, Luyten, &
Allison, 2015a). This shift introduces the picture of a pre-BPD child who is
suspicious—sees the world as dangerous. This is not dissimilar to the picture
painted by the Excessive Aggression theory, except that the suspicion is ge-
netically determined in the Failed Mentalization theory rather than projected
as in the Excessive Aggression theory. Alternative—or perhaps complemen-
tary—sources for BPD’s genetic disposition are being suggested that arise
from widely distributed genetic dispositions. One of them is a “P” factor
common to all personality disorders (Sharp et al., 2013). Fonagy adds to
this a second, equally broad disposition, an under endowment of a geneti-
cally based resilience “R” factor. From these various propositions about the
nature of BPD’s genetic disposition, BPD itself emerges as a particular form
of phenotypic expression that is environmentally determined. The proposal
that BPD arises from such broad genetic disposition(s) that lack specificity
for this syndrome is similar to the role for genes proposed for excessive ag-
gression.
The theory of Interpersonal Hypersensitivity moved from its descrip-
tion of how BPD symptoms are sensitive to interpersonal context into a
more substantive model only after BPD’s transmission was discovered. This
knowledge led to a theory in which BPD’s genetic disposition is considered
the disorder’s core. This proposal reflected a retreat from the theory’s prior
reliance on the attachment paradigm because attachment lacked heritability
and was unstable over development. This theory gives BPD’s interpersonal
behaviors a genetic basis rather than seeing them as secondary to acquired
handicaps in psychological or social functioning as proposed in the other
three theories. Here interpersonal hypersensitivity is seen as a cause of, rath-
COMPETING THEORIES OF BPD 159

er than as a result of, dysfunctional parenting. This theory suggests that such
hypersensitivity may originate in the midbrain and that it disrupts the devel-
opment of organizational and reality-assessment functions of the prefrontal
cortex: It is a “bottom up” explanation (Herpertz & Bertsch, 2015).
In summary, the theories are highly diverse in their efforts to integrate
BPD’s genetic disposition. Although both excessive emotionality and exces-
sive aggression might logically be considered as promising candidates for
BPD’s genetic disposition, this perspective has not been adopted by the theo-
ries. The Excessive Anger, Emotional Dysregulation, and Failed Mentaliza-
tion theories all identify top-down cortical failures of organization, percep-
tion, or regulation as BPD’s core. Of these, only the Failed Mentalization
theory has undertaken efforts to incorporate BPD’s genetics, but the nature
of what comprises this genetic determination remains unresolved. The Ex-
cessive Aggression theory stands alone in seeing a conflictual, rather than
deficit, core for BPD. The Interpersonal Hypersensitivity theory stands alone
in seeing BPD’s core as genetic.

STANDARD 5: HOW WELL DOES EACH THEORY GUIDE CLINICAL

INTERVENTIONS?

This standard addresses the theories’ relative clinical usefulness. This in-
cludes their understandability and learnability, and also how well each theo-
ry guides treatments in different settings and with different modalities. This
discussion will highlight distinctions, but readers should appreciate that the
clinical approaches from these disparate theories have many common fea-
tures (Bateman, 2012; Clarkin, Levy, Lenzenweger, & Kernberg, 2007; Gab-
bard, 2007; Gunderson, 2011; Weinberg, Ronningstam, Goldblatt, Schech-
ter, & Maltsberger, 2010).
Because of its origins within psychoanalytic theory, and notably the ar-
cane concepts of object relations, the Excessive Aggression theory is difficult
for nonpsychoanalytic clinicians to understand. Because the aggression so
central to this theory is dismissed and unacknowledged by patients with BPD,
it also requires the most inference by clinicians. The clinical applications are
truly theory driven. The technical neutrality or interpretations of aggressive
motives that this theory requires by therapists are inherently counterintui-
tive to their supportive instincts, especially when these interventions elicit
anger from patients. Its concepts of projective identification and splitting
model how patients with BPD assign disowned aspects of themselves onto
the clinician. From its start, this theory has alerted clinicians to the risks of
their responding harmfully. Excessive Aggression’s derivative psychotherapy,
transference-focused psychotherapy (TFP), has primarily interested psycho-
analysts or psychoanalytically trained clinicians. Therapy aligned with this
theory requires highly disciplined specialists. TFP is a twice-weekly individ-
ual psychotherapy. In contrast to the unchanging quality of its Excessive Ag-
gression theory, TFP has undergone many iterations in the process of becom-
ing manualized (Clarkin, Yeomans, & Kernberg, 2006). These revisions have
sustained technical neutrality and the absence of overt support by therapists,
160 GUNDERSON ET AL.

but TFP has become more structured and more cautious about interpreta-
tions (Caligor, Diamond, Yeomans, & Kernberg, 2009). This model of ther-
apy retains great loyalty by those who have been schooled in it, but, as that
generation ages, it is being less taught and it remains inherently the most dif-
ficult to learn. Ironically, this most psychoanalytically based theory has not
received wide endorsement by the psychoanalytic community, which resists
the idea of operationalized therapies and of measurable indices of outcome.
Because Emotional Dysregulation theory is based on observables, it re-
quires the least inference and is the least difficult to understand. However,
for this same reason, the theory has less broadly applicable explanatory prin-
ciples. Emotional Dysregulation’s derivative treatment, dialectical behavioral
therapy (DBT), while structurally a group and individual therapy, has also
been applied to family therapy and has found valued applications at different
levels of care. Still, even basic DBT is labor intensive (~5 hours/week) and
requires extensive training. The total package, that is, individual appoint-
ments plus group sessions with 24/7 coverage, is burdensome on treaters and
often exceeds available resources. Both DBT’s intensiveness and Linehan’s
historical reluctance to support “impure” practices have limited the use of
this therapy. Recent evidence that DBT can be effective using skills groups
without the individual component and without 24/7 coverage suggests that
DBT’s applications can expand considerably (Linehan et al., 2015). This ap-
plication has not, however, been represented or endorsed by the latest ver-
sion of the DBT manual (Linehan, 2015).
The theory of Failed Mentalization, like the theory of Excessive Aggres-
sion, is not easily understood. The concept of mentalization is inherently
complicated (Choi-Kain & Gunderson, 2008). It has three components: self-
awareness (akin to mindfulness or introspection), other-awareness (akin to
empathy), and awareness of how one’s own mental state and those of others
influence each other. Making accurate clinical judgments about the skill with
which a person—including one’s self—performs these functions requires mo-
tivation and persistence. The central clinical application of Failed Mentaliza-
tion is mentalization-based therapy (MBT), which, like DBT, consists of both
individual and group modalities. MBT has proven effective in both long-stay
day hospital and outpatient settings and has been adapted for an increasingly
wide range of clinical settings and non-BPD patients (Bateman & Fonagy,
2012). MBT’s emphasis on mental states and interpersonal interactions, and
the therapist’s nonauthoritarian stance of “not-knowing,” make this model
of therapy poorly suited for patients who require an authoritative stance and
unexamined limits in settings such as emergency rooms or hospitals where
quick and unilateral decisions are required. Notably, derivatives of MBT are
being applied in many schools of psychotherapy training (Bateman & Fona-
gy, 2012). Fonagy’s introduction of the epistemology paradigm has brought
with it some conflict with MBT’s attachment paradigm. The latter highlights
the significance of one-to-one interaction with caretakers (most applicable to
COMPETING THEORIES OF BPD 161

individual therapy), whereas the former focuses on learning from all sources
(more applicable to groups) that is independent of attachment.
The theory of Interpersonal Hypersensitivity is explicitly intended to be
understandable to nonspecialist clinicians with a wide range of experience
and motivation. Its related therapy, good psychiatric management (GPM),
is a once-weekly individual session that is as much case management as it is
psychotherapy. Because this therapy pioneered and emphasizes psychoedu-
cation, includes medications, and emphasizes BPD’s genetic determinants, it
is more comfortably anchored within the medical model than are the other
theories. Because it is not intensive, but pragmatic and supportive, it is easily
provided by nonpsychiatrists and can be applied in all clinical settings (see
Choi-Kain & Gunderson, 2018). The GPM approach is less ambitious in
seeking to cause psychological changes from within-office insights or skill ac-
quisition than are the extended therapies developed from the other theories.
Change depends less on the closeness or empathy in the therapy relationship.
It depends more on the patient’s finding GPM’s psychoeducation and advice
helpful; these establish the epistemic trust that begets compliance that gets
with the model’s support for patients getting back into the world. In the psy-
choanalytic perspective, GPM clinicians prompt an idealized transference,
then knowingly use it. It is a treatment model well suited for ERs, hospitals,
and all outpatient settings where nonintensive treatments are provided.
In summary, Excessive Aggression is a theory that is difficult to under-
stand, and its clinical application is both the most difficult to learn and the
most restricted (it applies only to individual psychotherapy). It alone claims
to make structural changes in the BPD patient’s personality. Both the Emo-
tional Dysregulation and Failed Mentalization theories are implemented via
groups as well as individual sessions. These theories have become widely
applied. Still, both require extensive training and are resource-intensive.
They select for clinicians who want to become BPD specialists. Their group
component might have particular cost–benefit advantages. The Interpersonal
Hypersensitivity theory offers a treatment model suitable for general clinical
use and that fits more comfortably within medical/psychiatric settings. This
model requires the least resources, but offers the least ambitious expectations
for directly effecting psychological change.

DISCUSSION

All of the theories in this review have enlightened our understanding of BPD
and fueled significant improvements in the care of individuals with BPD.
Still, it follows from the content of this review that all of these theories in-
clude inherently controversial viewpoints. We hope that identification of
these viewpoints will increase awareness and prompt improvements. Theory
builders can hear most from devoted acolytes who do not give critical feed-
back. To our knowledge, there has been limited dialogue or open debate
162 GUNDERSON ET AL.

between those who have developed these theories. As noted, sometimes there
have been failures to address each other’s contributions or those of relevant
prior theories. Having said this, the conclusions reached during this review
lead to the following suggestions as to how these theories might improve:
1. The Excessive Aggression theory is the standard-bearing theory that
dominated conceptualizations of BPD for more than 20 years and against
which the other theories have needed to measure themselves. Its theory
has not changed much. It has good sensitivity (Standard 2) and specific-
ity (Standard 3). This review suggests that the theory should identify the
excess of aggression as likely to be genetically determined, and having
accepted this, then accept this as a deficit that therapies only incomplete-
ly resolve. The persistence of BPD as wholly a conflict disorder in this
theory is hard to justify. This theory has an important role to play in the
understanding of BPD: The field should hope for the continued training
of TFP specialists who offer hope for the most profound psychological
changes.
2. The Emotional Dysregulation theory is the one that pervades most clini-
cal discussion. It is overdue for the theory to identify either excessive
emotionality or emotional regulation as its candidate for BPD’s genetic
disposition. The theory also needs to adopt the transactional and devel-
opmental implications of the central role assigned to invalidation and its
role in shaping beliefs about the self and, perhaps too, interpersonal re-
lationships. Such revisions would give due recognition of the interactive/
interpersonal sector of BPD and better establish this theory’s relevance
to personality. The field will benefit from broader use of the skills group
component divorced from the individual therapy and the excessively bur-
densome 24/7 availability.
3. The Failed Mentalization theory is very appealing because of its devel-
opmental origins. It is a theory that is actively undergoing change. This
theory needs to clarify when mentalization refers to a generic and stable
psychological function that all people have more or less and that all psy-
chotherapies need to address, and when it refers to a type of failed men-
talization for BPD that is a specific form of psychopathology. These are
not necessarily incompatible. To advance the claim that mentalization is
a core of BPD, further work is needed to integrate the admirable but still
confusing efforts to define BPD’s genetic disposition, and to clarify how
this genetic disposition leads to BPD’s particular type of failed mental-
ization. The theory would also benefit from further reconciliation of the
epistemology and attachment paradigms.
4. The Interpersonal Hypersensitivity theory risks being too tightly bound
by the existing description of DSM BPD. So much is still unknown. Its
emphasis on a genetic core runs the risk of encouraging a biologically re-
ductionist model of BPD that could diminish patients’ sense of agency or
their hopes for basic psychological changes. Nonetheless, it fills a needed
role by offering a treatment model usable by nonspecialists that helps
COMPETING THEORIES OF BPD 163

address the major public health problem that these patients represent. It
has also provocatively raised the question about whether interpersonal
relationships, a domain that has traditionally been assumed to be inter-
personally shaped, can and should be seen as heavily influenced by one’s
genes.

The distinctions and relative merits of these theories help explain why their
comparably effective therapies have differential appeal to clinicians and dif-
ferent BPD patients. The Excessive Aggression theory’s dark and imperi-
ous feel appeals to psychodynamically trained clinicians, philosophers, and
students of human nature. It appeals to patients who like its depth and its
promise for curative change. It requires patients be able to withstand the
frustrations inherent in a less supportive therapy. The Failed Mentalization
theory’s cool and lofty ambience appeals to intellectual and developmentally
based clinicians. It also appeals to intellectual and introspective patients.
The universality of mentalization encourages it to be comfortably relevant
to all interactions and everyday life situations. The Emotional Dysregulation
theory’s clarity and ahistorical perspective appeal to clear thinking, “does
it work?”, problem solvers, and, most notably, to cognitive-behaviorally
trained clinicians. It appeals to BPD patients by explicitly rendering them as
students (because of its didactics) and collaborators. They also welcome its
benign view of their nonaggressive character. The Interpersonal Hypersensi-
tivity theory appeals to pragmatists who are comfortable being authoritative.
It can frustrate patients who seek an intensive relationship with their thera-
pist or who find its emphasis on “getting a life,” that is, especially getting
work, distasteful.
The controversial role of aggression in BPD that was evident in this re-
view demands added attention. A body of evidence from ethology (e.g., Lo-
renz & Wilson, 1966; Morris, 1967; Storr, 1968; Wilson, 1978) supports
the existence and adaptive necessity of an aggressive instinct. Two of the
theories about BPD, Emotional Dysregulation and Failed Mentalization, do
not accept this perspective. Like the self psychology school of thought that
preceded them, they see the aggression of BPD as secondary to environmen-
tal frustration or stress or as defensive flights from other internal states of
mind. These theories discourage clinicians from perceiving people with BPD
as wanting to intentionally hurt or defeat or control others. As noted, attrib-
uting such intentions to BPD patients can be expected to elicit anger, but this
does not make them untrue. From a developmental perspective, accepting
such aggressive motivations could be identified in the Emotional Dysregula-
tion theory as the pre-BPD person’s willfully resisting validation or failing
to recognize it. In the Failed Mentalization theory, this could be identified
as the pre-BPD child’s distrust or dismissal of the caretaker’s efforts to mark
or accept the child’s feelings or other mental states. There is a wide range of
aggression in people, including those with BPD, and theories should incor-
porate this factor.
164 GUNDERSON ET AL.

The emerging and diverging concepts of BPD’s genetic disposition also

deserve some added comment. Both the Excessive Aggression and Failed
Mentalization theories propose broadly distributed nonspecific genetic dis-
positions. This is consistent with a dimensional perspective on BPD psycho-
pathology in which “BPDness” is found more or less in many people. In con-
trast, the Interpersonal Hypersensitivity theory proposes a specific genetic
disposition that is consistent with the unitary common pathway concept and
is more consistent with a categorical concept of BPD psychopathology. It is
notable that such a categorical conceptualization seems inherently unlikely
given its failure to have been confirmed for any other major psychiatric dis-
order.
This review has significant limitations. Perhaps most notable is the limi-
tation set by the choice of standards for comparison. Many other standards
might have been used. Those selected were anchored in our own clinical
experience, knowledge, and values. The most notable absence is that the
relative empirical support for these theories deserves critical comparison.
This task warrants its own review. The most identifiable problem within the
existing standards is that they are anchored by the DSM definition of BPD. It
has not compared the fit between these theories and non-DSM classification
schemes. For advocates of the Excessive Aggression theory, a better classifi-
cation scheme would be one divided into psychotic, borderline, or neurotic
types of personality organization. For Emotional Dysregulation theory, a
preferred classification scheme would be based on behavioral and cognitive
adaptational patterns, perhaps even omitting the “personality” label from
the construct. For Failed Mentalization theory, a preferred classification
scheme might be a dimensional scheme in which mentalization is a central
trait. Of particular note is the failure to examine how the theories fit with
the proposed revision of the BPD construct based on the trait structure of
personality (American Psychiatric Association, 2013; Livesley & Jang, 2000;
Widiger, Livesley, & Clark, 2009). The most significant alternative diagnos-
tic scheme derives from the trait structure of personality. How these theories
would fit with such a redefinition is a question that deserves attention from
more knowledgeable sources. This significant task also warrants another re-
view. Still, the most important limitation of this review is that the choice of
standards for comparison and the critical examination of the theories neces-
sarily reflect biases within our own knowledge, values, and judgment.
Patients with BPD will remain notoriously difficult for clinicians to treat
for the foreseeable future. The 15%–20% of these psychiatric patients who
populate our hospitals and clinics will not allow themselves to be ignored.
Because of their prevalence and their clinical stressfulness, theories are par-
ticularly important. They provide a conceptual framework that organizes
clinicians’ understanding and gives them needed structure. This review will
have served its purpose if it diminishes faith-based loyalties to any theory, if
it encourages thought leaders to address their differences, and if it prompts
scientists to use these competing theories as hypotheses to be tested.
COMPETING THEORIES OF BPD 165
REFERENCES
Adler, G., & Buie, D. H., Jr. (1979). Aloneness and
borderline psychopathology: The possible
relevance of child development issues. In-
ternational Journal of Psychoanalysis, 60,
83–96.
Allen, J. G. (2013). Mentalizing in the develop-
ment and treatment of attachment trauma.
London, UK: Karnac Books.
Allen, J. G., Fonagy, P., & Bateman, A. (2008).
Mentalizing in clinical practice. Washing-
ton, DC: American Psychiatric Publishing.
American Psychiatric Association. (2013). Section
III: Alternative DSM-V model for personal-
ity disorders. In Diagnostic and statistical
manual of mental disorders (5th ed., pp.
761–781). Washington, DC: Author.
Bateman, A. W. (2012). Treating borderline per-
sonality disorder in clinical practice. Ameri-
can Journal of Psychiatry, 169, 560–563.
doi:10.1176/appi.ajp.2012.12030341
Bateman, A., & Fonagy, P. (2012). Handbook
of mentalizing in mental health practice.
Washington, DC: American Psychiatric
Publishing.
Bateman, A., & Fonagy, P. (2015). Borderline
personality disorder and mood disorders:
Mentalizing as a framework for integrated
treatment. Journal of Clinical Psychology,
71, 792–804.
Becker, D. F., McGlashan, T. H., & Grilo, C. M.
(2006). Exploratory factor analysis of
borderline personality disorder criteria in
hospitalized adolescents. Comprehensive
Psychiatry, 47, 99–105. doi:10.1016/j.
comppsych.2005.07.003
Bender, D. S., & Skodol, A. E. (2007). Border-
line personality as a self–other represen-
tational disturbance. Journal of Personal-
ity Disorders, 21, 500–517. doi:10.1521/
pedi.2007.21.5.500
Bohus, M., & Neacsiu, A. (2014). Dialectical be-
havior therapy: An intervention for emo-
tion dysregulation. In M. M. Linehan,
Handbook of emotion regulation (Vol. 2,
pp. 491–507). New York, NY: Guilford
Press.
Bokhorst, C. L., Bakermans-Kranenburg, M. J.,
Fearon, R. M., van IJzendoorn, M. H.,
Fonagy, P., & Schuengel, C. (2003). The
importance of shared environment in moth-
er–infant attachment security: A behav-
ioral genetic study. Child Development, 74,
1769–1782.
Caligor, E., Diamond, D., Yeomans, F. E., & Kern-
berg, O. F. (2009). The interpretive process
in the psychoanalytic psychotherapy of bor-
derline personality pathology. Journal of the
American Psychoanalytic Association, 57,
271–301. doi:10.1177/0003065109336183
Choi-Kain, L. W., & Gunderson, J. G. (2008).
Mentalization: Ontogeny, assessment, and
application in the treatment of borderline
personality disorder. American Journal of
Psychiatry, 165, 1127–1135.
Choi-Kain, L. W., & Gunderson, J. G. (2018). Ap-
plications of good psychiatric management.
Manuscript in preparation.
Clarkin, J. F., Hull, J. W., & Hurt, S. W. (1993).
Factor structure of borderline personality
disorder criteria. Journal of Personality
Disorders, 7, 137–143. doi:10.1521/
pedi.1993.7.2.137
Clarkin, J. F., Levy, K. N., Lenzenweger, M. F., &
Kernberg, O. F. (2007). Evaluating three
treatments for borderline personality disor-
der: A multiwave study. American Journal
of Psychiatry, 164, 922–928.
Clarkin, J. F., Yeomans, F. E., & Kernberg, O.
F. (2006). Psychotherapy for borderline
personality: Focusing on object relations.
Washington, DC: American Psychiatric
Publishing.
Crowell, S. E., Beauchaine, T. P., & Linehan, M.
M. (2009). A biosocial developmental mod-
el of borderline personality: Elaborating
and extending Linehan’s theory. Psycholog-
ical Bulletin, 135, 495–510. doi:10.1037/
a0015616
Distel, M. A., Willemsen, G., Ligthart, L., Der-
om, C. A., Martin, N. G., Neale, M. C., .
. . Boomsma, D. I. (2010). Genetic cova-
riance structure of the four main features
of borderline personality disorder. Journal
of Personality Disorders, 24, 427–444.
doi:10.1521/pedi.2010.24.4.427
Fonagy, P. (2002). Affect regulation, mentaliza-
tion, and the development of the self. New
York, NY: Other Press.
Fonagy, P., Luyten, P., & Allison, E. (2015a). Epis-
temic petrification and the restoration of
epistemic trust: A new conceptualization
of borderline personality disorder and its
psychosocial treatment. Journal of Person-
ality Disorders, 29, 575–609. doi:10.1521/
pedi.2015.29.5.575
Fonagy, P., Luyten, P., & Bateman, A. (2015b).
Translation: Mentalizing as treatment tar-
get in borderline personality disorder. Per-
sonality Disorders: Theory, Research, and
Treatment, 6, 380–392.
Fruzzetti, A. E., Shenk, C., & Hoffman, P. D.
(2005). Family interaction and the devel-
opment of borderline personality disor-
der: A transactional model. Development
166 GUNDERSON ET AL.
and Psychopathology, 17, 1007–1030.
doi:10.1017/s0954579405050479
Gabbard, G. O. (2007). Do all roads lead to Rome?
New findings on borderline personality dis-
order. American Journal of Psychiatry, 164,
853–855. doi:10.1176/ajp.2007.164.6.853
Gunderson, J. G. (1984). Borderline personality
disorder. Washington, DC: American Psy-
chiatric Press.
Gunderson, J. G. (2011). Borderline personality
disorder. New England Journal of
Medicine, 364, 2037–2042. doi:10.1056/
nejmcp1007358
Gunderson, J. G., & Lyons-Ruth, K. (2008). BPD’s
interpersonal hypersensitivity phenotype:
A gene-environment-developmental model.
Journal of Personality Disorders, 22, 22–
41. doi:10.1521/pedi.2008.22.1.22
Gunderson, J. G., Stout, R. L., Shea, M. T., Grilo,
C. M., Markowitz, J. C., Morey, L. C., .
. . Skodol, A. E. (2014). Interactions of
borderline personality disorder and mood
disorders over 10 years. Journal of Clini-
cal Psychiatry, 75, 829–834. doi:10.4088/
jcp.13m08972
Gunderson, J. G., Zanarini, M. C., Choi-Kain, L.
W., Mitchell, K. S., Jang, K. L., & Hudson,
J. I. (2011). Family study of borderline per-
sonality disorder and its sectors of psycho-
pathology. Archives of General Psychiatry,
68, 753–762. doi:10.1001/archgenpsychia-
try.2011.65
Herpertz, S. C., & Bertsch, K. (2015). A new per-
spective on the pathophysiology of border-
line personality disorder: A model of the
role of oxytocin. American Journal of Psy-
chiatry, 172, 840–851. doi:10.1176/appi.
ajp.2015.15020216
Hurt, S. (1984). Assessing borderline personality
disorder with self-report, clinical interview,
or semistructured interview. American
Journal of Psychiatry, 141, 1228–1231.
doi:10.1176/ajp.141.10.1228
Kendler, K. S., Aggen, S. H., Knudsen, G. P.,
Røysamb, E., Neale, M. C., & Reichborn-
Kjennerud, T. (2011). The structure of ge-
netic and environmental risk factors for
syndromal and subsyndromal common
DSM-IV Axis I and All Axis II disorders.
American Journal of Psychiatry, 168, 29–
39. doi:10.1176/appi.ajp.2010.10030340
Kernberg, O. (1967). Borderline personality or-
ganization. Journal of the American Psy-
choanalytic Association, 15, 641–685.
doi:10.1177/000306516701500309
Kernberg, O. F., Yeomans, F. E., Clarkin, J. F.,
& Levy, K. N. (2008). Transference fo-
cused psychotherapy: Overview and
update. International Journal of Psy-
choanalysis, 89, 601–620. doi:10.1111/
j.1745-8315.2008.00046.x
Kring, A. M., & Sloan, D. M. (2010). Emotion
regulation and psychopathology: A trans-
diagnostic approach to etiology and treat-
ment. New York, NY: Guilford Press.
Leyro, T. M., Zvolensky, M. J., & Bernstein, A.
(2010). Distress tolerance and psycho-
pathological symptoms and disorders: A
review of the empirical literature among
adults. Psychological Bulletin, 136, 576–
600. doi:10.1037/a0019712
Linehan, M. (1993). Cognitive-behavioral treat-
ment of borderline personality disorder.
New York, NY: Guilford Press.
Linehan, M. (2015). DBT skills training manual.
New York, NY: Guilford Press.
Linehan, M., Korslund, K., Harned, M., Gallop,
R., Lungu, A., Neacsiu, A., . . . Murray-
Gregory, A. (2015). Dialectical behavior
therapy for high suicide risk in individuals
with borderline personality disorder: A ran-
domized clinical trial and component analy-
sis. JAMA Psychiatry, 72, 475–482.
Livesley, W. J., & Jang, K. L. (2000). Toward an
empirically based classification of per-
sonality disorder. Journal of Personal-
ity Disorders, 14, 137–151. doi:10.1521/
pedi.2000.14.2.137
Lorenz, K., & Wilson, M. K. (1966). On aggres-
sion. New York, NY: Harcourt, Brace &
World.
Moor, M. H., Distel, M. A., Trull, T. J., & Booms-
ma, D. I. (2009). Assessment of borderline
personality features in population samples:
Is the Personality Assessment Inventory–
Borderline Features scale measurement in-
variant across sex and age? Psychological
Assessment, 21, 125–130. doi:10.1037/
a0014502
Morris, D. (1967). The naked ape. London, UK:
Corgi Books.
Sanislow, C. A., Grilo, C. M., & McGlashan, T.
H. (2000). Factor analysis of the DSM-III-
R borderline personality disorder criteria in
psychiatric inpatients. American Journal of
Psychiatry, 157, 1629–1633. doi:10.1176/
appi.ajp.157.10.1629
Sanislow, C. A., Little, T. D., Ansell, E. B., Grilo,
C. M., Daversa, M., Markowitz, J. C., . . .
McGlashan, T. H. (2009). Ten-year stability
and latent structure of the DSM-IV schizo-
typal, borderline, avoidant, and obsessive-
compulsive personality disorders. Journal
of Abnormal Psychology, 118, 507–519.
doi:10.1037/a0016478
Sanislow, C. A., Morey, L. C., Grilo, C. M.,
Gunderson, J. G., Shea, M. T., Skodol, A.
E., . . . McGlashan, T. H. (2002). Confirma-
tory factor analysis of DSM-IV borderline,
COMPETING THEORIES OF BPD 167
schizotypal, avoidant and obsessive-com-
pulsive personality disorders: Findings from
the Collaborative Longitudinal Personality
Disorders Study. Acta Psychiatrica Scandi-
navica, 105, 28–36. doi:10.1034/j.1600-
0447.2002.0_479.x
Sharp, C., Ha, C., Carbone, C., Kim, S., Perry, K.,
Williams, L., & Fonagy, P. (2013). Hyper-
mentalizing in adolescent inpatients: Treat-
ment effects and association with border-
line traits. Journal of Personality Disorders,
27, 3–18. doi:10.1521/pedi.2013.27.1.3
Storr, A. (1968). Human aggression. London, UK:
Allen Lane, The Penguin Press.
Taylor, J., & Reeves, M. (2007). Structure of bor-
derline personality disorder symptoms in
a nonclinical sample. Journal of Clinical
Psychology, 63, 805–816. doi:10.1002/
jclp.20398
Torgersen, S., Lygren, S., Øien, P. A., Skre, I.,
Onstad, S., Edvardsen, J., . . . Kringlen, E.
(2000). A twin study of personality disor-
ders. Comprehensive Psychiatry, 41, 416–
425. doi:10.1053/comp.2000.16560
Weinberg, I., Ronningstam, E., Goldblatt, M. J.,
Schechter, M., & Maltsberger, J. T. (2010).
Common factors in empirically supported
treatments of borderline personality disor-
der. Current Psychiatry Reports, 13, 60–68.
doi:10.1007/s11920-010-0167-x
Widiger, T. A., Livesley, W. J., & Clark, L. A.
(2009). An integrative dimensional classifi-
cation of personality disorder. Psychologi-
cal Assessment, 21, 243–255. doi:10.1037/
a0016606
Wilson, E. O. (1978). On human nature. Cam-
bridge, MA: Harvard University Press.