Development and Psychopathology (2019), 31, 1143–1156

doi:10.1017/S0954579419000658

Special Issue Article

Borderline personality disorder and emotion dysregulation

Alexander L. Chapman
Department of Psychology, Simon Fraser University, Vancouver, BC, Canada

Abstract
Borderline personality disorder (BPD) is a severe and complex disorder characterized by instability across many life domains, including
interpersonal relations, behavior, and emotions. A core feature and contributor to BPD, emotion dysegulation (ED), consists of deficits
in the ability to regulate emotions in a manner that allows the individual to pursue important goals or behave effectively in various contexts.
Biosocial developmental models of BPD have emphasized a transaction of environmental conditions (e.g., invalidating environments and
adverse childhood experiences) with key genetically linked vulnerabilities (e.g., impulsivity and emotional vulnerability) in the development
of ED and BPD. Emerging evidence has begun to highlight the complex, heterotypic pathways to the development of BPD, with key heritable
vulnerability factors possibly interacting with aspects of the rearing environment to produce worsening ED and an adolescent trajectory con-
sisting of self-damaging behaviors and eventual BPD. Adults with BPD have shown evidence of a variety of cognitive, physiological, and
behavioral characteristics of ED. As the precursors to the development of ED and BPD have become clearer, prevention and treatment efforts
hold great promise for reducing the long-term suffering, functional impairment, and considerable societal costs associated with BPD.
Keywords: borderline personality disorder, development, emotion, emotion dysregulation
(Received 30 November 2018; accepted 24 March 2019)

Borderline personality disorder (BPD) is a severe and complex
disorder characterized by instability in interpersonal relations,
behavior, and emotions (American Psychiatric Association,
2013). Findings have suggested that the defining and associated
features of BPD are best characterized by a phenotype consisting
of emotion dysregulation (ED), relational dysfunction (often
referred to as relational disturbance or instability), and impulsiv-
ity (Gunderson, 2007; Links, Helsegrave, & van Reekum, 1999;
McCloskey et al., 2009). Among these features, ED, involving dif-
ficulty modulating emotional responding, appears particularly
central to many of the serious behavioral difficulties associated
with BPD, including nonsuicidal self-injury (NSSI), suicidal
behavior, and self-damaging impulsive behaviors (e.g., substance
use, risky sexual behavior, and recklessness). Therefore, under-
standing how ED develops and crystallizes into a core feature of
BPD should be considered a high priority.
A clearer understanding of the developmental processes con-
tributing to ED could illuminate possible targets for preventative
and efficient, targeted treatment interventions. Prevention, in
turn, has the potential to forestall the escalation of serious behav-
ioral problems, functional impairments, and heavy utilization of
health and mental health resources associated with BPD. Within
later adolescence and earlier adulthood, when BPD is established,
understanding the processes contributing to and maintaining ED
Author for Correspondence: Alexander L. Chapman, Department of Psychology,
Simon Fraser University, 8888 University Drive, Burnaby, BC, Canada V5A 1S6;
E-mail: chapman_lab@sfu.ca.
Cite this article: Chapman AL (2019). Borderline personality disorder and emotion
dysregulation. Development and Psychopathology 31, 1143–1156. https://doi.org/
10.1017/S0954579419000658
© Cambridge University Press 2019
could help facilitate the development of more efficient, targeted
treatments.
Over the past few decades, considerable progress has been
made in our understanding of the developmental processes con-
tributing to BPD and ED, as well as in the treatment of BPD
and related clinical problem areas among children, adolescents,
and adults. Consistent with a developmental psychopathology
perspective on the development of personality disorders
(Cicchetti, 2014), this review addresses theory and research on
the possible biopsychosocial process operating at various levels
of development to contribute to the development of ED and
BPD. Contemporary developmental psychopathology models of
BPD and ED have suggested that key underlying biologically
based, heritable vulnerabilities (e.g., trait impulsivity) manifest
in a variety of ways throughout development (e.g., attention-
deficit/hyperactivity disorder, early conduct, and mental health
problems) and confer vulnerability to key environmental risk fac-
tors (e.g., childhood maltreatment), which exacerbate the develop-
ment of ED and eventual BPD (e.g., see Beauchaine, Hinshaw, &
Bridge, 2019; Crowell, Beauchaine, & Linehan, 2009; Crowell,
Kaufman & Beauchaine, 2014).
BPD
Many of the defining features of BPD either include or are related to
ED. The symptoms of BPD, represented in both the DSM-V
(American Psychiatric Association, 2013) and the tenth edition of
the ICD-10 (World Health Organization, 2016), represent marked
instability in several life domains. According to the DSM-V, five of
nine criteria are required for the diagnosis; these criteria largely cap-
ture difficulties in relationships, impulsive and self-damaging
1144
behavior, identity and mood disturbance, and affective instability.
Similarly, in the ICD-10, BPD symptoms fall within the category
“emotionally unstable personality disorder” and include distur-
bances in emotions, cognition, relationships, and behavior. ED or
instability are central features of BPD within both diagnostic systems.
BPD is associated with considerable emotional suffering,
severe behavioral problems, heavy utilization of health and mental
health resources, and functional impairment. Approximately 70%
to 80% of people with BPD have a history of NSSI and/or suicide
attempts, and approximately 10% die by suicide (Black, Blum,
Pfohl, & Hale, 2004; Gunderson, 2001; Paris & Zweig-Frank,
2001; Skodol et al., 2002). The high prevalence of co-occurring
disorders further underscores the considerable suffering associ-
ated with BPD and complicates treatment (as clinicians must be
reasonably proficient in many area). The vast majority of patients
with BPD have at least one additional diagnosis (Fyer, Frances,
Sullivan, Hurt, & Clarkin, 1988; Zanarini et al., 1998). Studies
have suggested that up to two-thirds of patients with BPD have
substance use problems, over half have PTSD, and well over
half have a co-occurring anxiety disorder (up to 88% in one
study of inpatients; Zanarini et al., 1998; Zarini, Frankenburg,
Hennen, Reich, & Silk, 2004). Major depressive disorder is partic-
ularly common, affecting approximately 80% of people with BPD
(Lieb, Zanarini, Schmahl, Linehan, & Bohus 2004; Zanarini et al.,
1998, 2004). Consistent with this complex clinical picture and
high prevalence of self-damaging behaviors, people with BPD
heavily utilize emergency, inpatient, outpatient psychiatric, and
primary care services, costing an average of $12,000–$30,000
per patient per year (in USD; Comtois, Elwood, Holdcraft,
Smith, & Simpson, 2007; Linehan & Heard, 1999). The prevalence
of BPD (1.4% to 5.9%) also is comparable to or higher than that
of other costly disorders, such as schizophrenia and bipolar disor-
der (Lenzenweger, Lane, Loranger, & Kessler, 2007).
Although rates of remission and recovery (approximately 60%
at 16 years after hospital discharge; Zanarini, Frankenburg,
Reich, & Fitzmaurice, 2012) suggest a prognosis that is more hope-
ful than previously thought, substantial, and persistent functional
impairment persists among a majority of BPD patients (Biskin,
2015). A sizable proportion of BPD patients experience impair-
ments in social and occupational functioning requiring public
assistance, including psychiatric disability support and Social
Security disability income benefits (Bateman & Fonagy, 2003;
Bateman & Fonagy, 2008; Grant et al., 2008; Jørgensen et al.,
2009; Koons et al., 2006; Soloff & Chiappetta, 2017; Zanarini,
Jacoby, Frankenburg, Reich, & Fitzmaurice, 2009). In one longitu-
dinal study of patients with BPD, 69.4% fell within the range of
poor psychosocial functioning at baseline assessment, and this pro-
portion only reduced to 51.2% at the 8-year mark of the study
(Soloff & Chiappetta, 2017). In another study examining long-term
follow-up data following mentalization-based treatment, 54% of
patients remained within the range of poor psychosocial function-
ing 5 years following treatment, despite findings supporting the
possible efficacy of mentalization-based treatment (Bateman &
Fonagy, 2008). Given the likely role of ED in many of the behav-
ioral and functional difficulties associated with BPD, understand-
ing the developmental trajectory of ED will hopefully illuminate
ways to curtail persistent functional impairment and suffering.
Emotion Regulation and Dysregulation
Understanding the specific characteristics and development of ED
in BPD requires a broader framework in which to conceptualize
A. L. Chapman
emotion regulation and dysregulation. Definitions of emotion
tend to emphasize that emotions (a) have several components,
including cognitive, physiological, and behavioral features; (b)
evolved over millennia to motivate adaptive behavior and facilitate
social cohesion in a manner that maximized survival; and (c) gen-
erally arise in motivationally relevant contexts, such as contexts
that are relevant to an individual’s goals (e.g., the goal of survival,
connecting with others, maintaining social standing, and so
forth; Gross, 2014; Lazarus, 1991; Mauss, Levenson, McCarter,
Wilhelm, & Gross, 2005; Scherer, Schorr, & Johnstone, 2001).
When a friend cancels plans, for example, an individual with
BPD who is particularly sensitive to rejection or abandonment
might respond with intense fear, consisting of physiological
changes (e.g., alterations to heart rate and hormonal, neurotrans-
mitter, and sympathetic nervous system responding), appraisals
of the situation as disastrous or threatening (e.g., “He hates
me.” “He doesn’t want to be my friend.”), and actions functioning
to prevent perceived negative outcomes (e.g., texting or calling
the friend repeatedly, seeking reassurance). The situation may be
especially relevant to the individual’s goals if he is afraid to be
alone, highly values the relationship, or historically has experi-
enced severe rejection or abandonment.
Emotion regulation entails alterations to these different aspects
of the multicomponent emotion system, involving changes in the
form, frequency, experience, or expression of emotions
(Beauchaine, 2015; Gross, 1998, 2014; Thompson, 1994).
Emotion regulation also can occur at various stages of the emo-
tion generative process. The process model of emotion regulation
(Gross, 1998), for example, indicates which types of emotion reg-
ulation processes occur at different points in the sequence of
events related to an emotional response. The individual could
engage in situation selection by deciding not to put himself in a
position where a friend might cancel plans by avoiding the friend
or mitigating the situation by asking if they can reschedule for the
next evening. If the situation arises, he could decide to modify his
attention by distracting from the situation or related emotions and
focusing on other activities (e.g., binge watching a favorite show)
or focusing on less emotionally evocative aspects of the situation
(e.g., by paying attention when the friend says he wants to get
together net week). He could also engage in cognitive reappraisal
(e.g., “He doesn’t hate me; he’s just busy. I have a great opportu-
nity to catch up on my show.”). Later in the chain of events, he
might use response modulation strategies (e.g., diaphragmatic
breathing or progressive muscle relaxation) to dampen the phys-
iological arousal associated with fear of abandonment. He also
might modify his emotional expressive behavior by changing
his facial expression or body language. Other options are to
avoid reaching out repeatedly or asking for reassurance and
engaging in behavior that is less compatible with or opposite to
fears of loneliness (e.g., “opposite action”; Linehan, 1993b, 2015).
An extended version of this process model (Gross, 2014;
Sheppes, Suri, & Gross, 2015) encapsulates the sequence of emo-
tion regulation into three key processes: (a) identification, involv-
ing the recognition and identification of an emotional response;
(b) selection, involving the selection of a strategy to regulate emo-
tions; and (c) implementation, involving the implementation of an
emotion regulation strategy. Within each stage, emotion regula-
tion problems can be characterized as aberrations in the percep-
tion or valuation (cost-benefit analysis) of emotional events,
experiences, or potential regulation strategies. Emotion regulation
difficulties could also come in the form of problems with the
selection or implementation of regulation strategies.
Development and Psychopathology 1145

Some researchers have operationalized ED in terms of the Biosocial Developmental Theories of BPD
characteristics of emotional responding (e.g., overly intense or
Among theories of the development of BPD, Linehan’s (1993a)
prolonged responses), whereas others have defined ED primarily
biosocial theory most strongly emphasizes ED. In her early treat-
in terms of deficits in the ability to use explicit emotion regulation
ment development efforts, Linehan (1993a) discovered that a sub-
strategies. Beauchaine (2015), for example, has distinguished
stantial proportion of highly suicidal patients met criteria for
emotion regulation from dysregulation, defining ED as the pres-
BPD. Many of the hallmark interpersonal, emotional, and behav-
ence of emotional responses that are too prolonged, intense,
ioral problems accompanying BPD presented during treatment,
labile, or situationally inappropriate, or maladaptive behaviors
making it difficult to proceed with standard cognitive or behavio-
related to emotional states. Within this framework, evidence for
ral interventions, which largely focused on changing thoughts and
ED would consist of measures of the intensity, duration, or
behavior and building skills. Patients with BPD (who frequently
changeability of emotional responses in particular contexts. The
had a history of pervasive invalidation or maltreatment) often
client who feels intensely distraught for the whole evening after
experienced the change-oriented focus of cognitive–behavioral
a friend has canceled plans would be considered emotionally dys-
therapy as invalidating, became emotionally dysregulated, and
regulated by virtue of maladaptively intense and prolonged emo-
withdrew; became critical or hostile toward the therapist; or
tional responding. Other indications of ED might include the
dropped out. To address these problems, Linehan (1993a) system-
client repeatedly texting the friend or repeatedly seeking reassur-
atically incorporated into this emerging treatment the balance and
ance, expressing hostility or anger, or self-injuring. Gratz and
synthesis of acceptance and change-oriented therapeutic styles
Roemer (2004), in contrast, have framed ED as difficulty with
and strategies within a dialectical theoretical framework. She
the use of key, explicit emotion regulation tasks or behaviors.
also used existing theory and research on BPD to assemble a
Within this model, ED consists of difficulties in one or more of
working model, the biosocial theory, to better understand the
the following areas: emotional awareness and clarity, the ability
development and maintenance of BPD. Along with dialectical
to accept emotional experiences and inhibit impulsive behavior,
and behavioral theory, the biosocial theory became the basis for
and the capacity to regulate emotions. Similarly, another concep-
a comprehensive cognitive–behavioral treatment approach
tualization of ED, advanced in the context of dialectical behavior
(Linehan, 1993a, 1993b, 2015) emphasizing the role of ED in
therapy (DBT), is “the inability, even when one’s best efforts are
the development and maintenance of BPD.
applied, to change in a desired way emotional cues, experiences,
Within the biosocial theory, the transaction of a biologically
actions, verbal responses, and/or nonverbal expressions under
based vulnerability to emotions (emotion vulnerability) with an
normative conditions” (Linehan, Bohus, & Lynch, 2007, p. 583).
invalidating rearing environment contributes to the development
Similar to Beauchaine’s (2015) definition, this conceptualization
of ED. Emotion vulnerability consists of a combination of a low
emphasizes the importance of goals (i.e., “in a desired way”),
threshold for emotional elicitation (emotional sensitivity), intense
and similar to Gratz and Roemer (2004), emphasis is placed on
emotional responses (emotional reactivity), and a prolonged
particular emotion regulation capacities or skills.
return to baseline emotional responding (slow return to baseline).
For the purposes of the present paper, I conceptualize ED
The invalidating environment consists of the indiscriminate rejec-
broadly as a deficit in the implicit (e.g., through physiological
tion of the child’s communication of internal experiences (emo-
homeostatic mechanisms) or explicit (e.g., through effortful emo-
tions, thoughts, and sensations), intermittent reinforcement of
tion regulation) regulation of the emotion system that hampers
emotional escalation (e.g., inconsistent provision of attention
the individual’s ability to engage in effective goal- or value-
and support that is sometimes contingent on extreme emotional
oriented behavior. Persons with BPD, therefore, may evidence ED
expression), and the oversimplification of the ease of problem
through indicators of heightened or prolonged emotional respond-
solving. The biosocial model is a transactional model, whereby
ing, if such responding impedes value- or goal-directed action or
the child’s emotional temperament influences the invalidating
contributes to suffering. Other indicators of ED would include def-
environment, and vice versa. High emotionality elicits invalida-
icits in the skills needed to select or implement effective emotion
tion, and invalidation exacerbates high emotionality and does
regulation strategies (i.e., deficits in explicit emotion regulation).
not provide the type of emotional socialization needed to develop
The distinction between an overly intense or prolonged emo-
core emotion regulation capacities. Over time, the individual
tional responding and an individual’s capacity to effectively regu-
develops ED, and various behavioral problems characteristic of
late emotions has important developmental implications and is
BPD emerge (e.g., NSSI, suicide attempts, substance use, and
likely to continue to be a subject of debate. One model is that
harmful impulsive behaviors) and are negatively reinforced and
ED in BPD is essentially a behavioral skill deficit fostered by
maintained by the reduction of intolerable emotional arousal
the invalidating overlaid on an emotionally vulnerable tempera-
and/or changes in the social environment. Within this framework,
ment (as suggested by Linehan’s original theory; Linehan,
many of the serious, harmful behaviors (e.g., NSSI, suicidal behav-
1993a). Alternatively, the situation may be more complex, with
ior, reckless impulsivity, drug and alcohol use, etc.) associated
ED consisting of both characteristics of emotional responding
with BPD occur in response to or function to reduce ED
and a deficit in the capacities needed to regulate emotions (as sug-
(Linehan, 1993a). For example, NSSI and other problem behav-
gested by Beauchaine, 2015; Crowell et al., 2009, 2014). In both
iors characteristic of BPD often result in negative or positive rein-
cases, developmental processes and interventions that encourage
forcement through the up- or downregulation of emotions
the development of emotion regulation capacities or skills
(Brown, Comtois, & Linehan, 2002; Chapman, Gratz, & Brown,
would be important. With the more complex model, however, it
2006; Kleindienst et al., 2008; Linehan, 1993a; Nock &
would also be important to examine how various psychosocial
Prinstein, 2004). These behaviors also further contribute to dis-
and biological processes shape how emotional response character-
ruptions in functioning, relationships, and so forth.
istics (e.g., high reactivity and sensitivity, or slow return to base-
At the time of the publication of Linehan’s (1993a) biosocial
line), rather than simply coping or emotion regulation behaviors,
theory, the literature on emotions and emotion regulation in
develop over time.
1146
BPD was scant. Even the broader literature on emotions and emo-
tion regulation was in its infancy until the early 1990s (Gross,
1998, 2014; Thompson, 1994). Much of the developmental liter-
ature on psychopathology focused on syndromes of disinhibition
(Patterson & Newman, 1993), such as attention-deficit/hyperac-
tivity disorder (ADHD), and the developmental factors influenc-
ing the progression from child conduct problems to adult
antisocial personality disorder (e.g., coercive behavioral processes;
Patterson, DeBaryshe, & Ramsey, 1989). The biosocial theory was,
therefore, based primarily on clinical observations, findings on the
enduring effects of childhood maltreatment, and existing emotion
and behavioral science. Since then, the literature on the develop-
ment of psychopathology more broadly, and BPD and ED more
specifically, has proliferated, providing an expanded picture of
the potential factors contributing to ED in BPD.
Crowell et al.’s (2009) biosocial developmental model of BPD
Crowell et al. (2009, 2014) have proposed an expanded biosocial
developmental model of BPD, incorporating developments in
research on developmental psychopathology as well as biological
and psychosocial factors associated with BPD. Compared with
Linehan’s (1993a) biosocial theory, which proposes that emotion
vulnerability is the key biologically based vulnerability factor,
Crowell et al. (2009, 2014) more strongly emphasize the role of
trait impulsivity, a heritable genetic predisposition that confers
vulnerability to various childhood behavioral disorders (e.g.,
oppositional defiant disorder and ADHD). Crowell et al. (2009,
2014; see also Beauchaine, Hinshaw, et al., 2019) propose that
trait impulsivity moderates the effects of invalidating or adverse
rearing contexts, such that those with high trait impulsivity are
particularly vulnerable to developing ED and related behavioral
problems (e.g., NSSI and suicide attempts) in these contexts.
Instead of necessarily serving as a biologically based vulnerability
factor, within Crowell et al.’s (2009, 2014) model, emotion vulner-
ability and dysregulation develop in the context of the invalidating
rearing environment, primarily through coercive conflict-
escalation processes, the intermittent reinforcement of emotional
lability, abuse, neglect, and other adverse circumstances.
This expanded biosocial developmental model has five key
tenets, some of which have garnered additional support since
the model was articulated about 10 years ago. First, as mentioned,
trait impulsivity is a key biologically based and heritable vulnera-
bility factor for the development of BPD and other externalizing
behavioral problems sometimes referred to as syndromes of disin-
hibition (e.g., oppositional defiant disorder, ADHD, conduct dis-
order, eventual adult antisocial personality disorder, etc.). Second,
adverse, invalidating environmental contexts shape the develop-
ment of emotional vulnerability (referred to as “emotional labil-
ity”), which can be considered both biologically based and
highly susceptible to environmental influence. Third, trait impul-
sivity continues to interact with environmental risk factors to
exacerbate ED and disrupt normative social and emotional devel-
opment. Among youth who are higher in impulsivity, various
environmental risks may have a more potent effect on their devel-
opment of behavioral, social, and emotional difficulties, compared
with those who are lower in trait impulsivity. Fourth, in adoles-
cence, at-risk individuals begin to engage in maladaptive coping
and problematic behaviors that pose risk for BPD, further disrupt
the development of emotion regulation capacities, and carry their
own negative interpersonal and intrapersonal consequences. In
particular, NSSI and suicide attempts are considered key
A. L. Chapman
precursors to the development of adult BPD. These and other
behaviors commonly associated with BPD (e.g., drug and alcohol
use, reckless, and self-damaging behavior) become entrenched
due to repeated reinforcement in the form of emotion regulation
and/or changes in the social environment. Fifth, in adolescence,
the presence of ED more generally and NSSI and suicidal behavior
more specifically continue to contribute to risk for the develop-
ment of adult BPD.
The Development of ED in BPD
As described by Crowell et al. (2014), the development of BPD
more broadly and ED more specifically, likely follows a complex,
heterotypic trajectory (Belsky et al., 2012). Key heritable factors
(e.g., trait impulsivity and possibly neuroticism) appear to elevate
the risk of a range of childhood emotional and behavioral prob-
lems and may contribute to vulnerability to the adverse environ-
mental circumstances that foster the development of ED. Key
signs of worsening ED often emerge in adolescence, where under-
lying dispositional factors (such as impulsivity) may increase vul-
nerability to alterations in the development of the social cognitive
capacities needed to effectively regulate emotions. During this
period, worsening ED and related interpersonal and behavioral
problems, along with various peer and other environmental influ-
ences fostering maladaptive coping (e.g., through peer and possi-
bly parental modeling processes and influences), elevate the risk
of NSSI and suicidal behavior, which further contribute to the
development of BPD. In adulthood, where BPD tends to show
more temporal stability (compared with adolescence and child-
hood), findings have shown evidence of a variety of biological,
cognitive, and behavioral characteristics of ED that reflect some
of these earlier developmental processes.
Key genetic and heritable vulnerability factors
Heritable factors may play an important role in the development
of BPD and ED, predisposing individuals to be vulnerable to the
effects of adverse environments in childhood and adolescence. In
turn, environmental risk factors may influence the expression of
particular genetic and biological propensities (e.g., see Amad,
Ramoz, Thomas, Jardri, & Gorwood, 2014, regarding a “plastic-
ity” theory). As mentioned, Crowell et al. (2009, 2014) have sug-
gested that impulsive children are particularly likely to develop
behavioral and emotional difficulties in adverse or invalidating
environments. Heritable factors also may operate in a transac-
tional manner, whereby the heritable trait and its manifestations
influence and are exacerbated by environmental factors. Highly
impulsive children may be particularly difficult to parent, present-
ing behavioral challenges through inattentiveness, hyperactivity,
noncompliance, and so forth. Parents who share with their chil-
dren a propensity toward impulsivity may be prone to use coer-
cive tactics to control their children’s behavior as well as to
erratically and intermittently reinforce emotional escalation.
Invalidation, abuse, or neglect, along with parental modeling of
maladaptive behaviors (e.g., poor impulse control and emotional
lability) may further exacerbate the child’s existing propensities
toward heightened emotionality and impulsivity. Heritable factors
may also influence alterations in the development of social cogni-
tive capacities needed to regulate emotions. Some have suggested,
for example, that impulsivity plays a key role in the development
of neuropsychological deficits in executive functioning that
Development and Psychopathology
influence later conduct problems (Caspi, Henry, McGee, Moffit,
& Silva, 1995).
Findings from several studies have suggested an important role
of heritable factors in the propensity to develop BPD and ED.
First-degree relatives of individuals with BPD are several times
more likely to have BPD than the general population (Baron,
Gruen, Asnis, & Lord, 1985; Links, Steiner, & Huxley, 1988;
Zanarini, Gunderson, Marino, Schwartz, & Frankenburg, 1988),
and twin studies have suggested moderate heritability for BPD
(.40 to around .70). Torgersen et al. (2000), for example, found
a heritability for BPD of .69 among 221 twin pairs assessed for
the presence of personality disorders. Another study of 5,000
twins in the Netherlands, Belgium, and Australia found consistent
heritability estimates of .42 using a self-report measure of BPD
features (Distel et al., 2008). Another study, focused on
Norwegian twins, found evidence that BPD features are best
accounted for by a model including a moderately heritable over-
arching latent “BPD” factor (Reichborn-Kjennerud et al., 2013),
with heritable and unique environmental factors accounting for
55% and 45% of this factor, respectively. Within this model,
two subfactors included an interpersonal factor, which had low
heritability (2.2%), and an affective instability factor, with herita-
bility of 29.3%. In addition, the BPD impulsivity criterion, con-
sisting of self-inflicted injuries and impulsive, self-damaging
behaviors, received the majority of its genetic influence (which
was 44.6%) from what the authors referred to as “criterion-
specific” factors not accounted for by the heritable influences
related to the overall BPD factor. These findings support the exis-
tence of a highly heritable impulsivity dimension. In contrast,
unique environmental factors seem to account for the majority
of the variability in the interpersonal and affective symptoms of
BPD. Together, these findings provide at least indirect support
for the notion that impulsivity is a key heritable risk factor for
BPD, and that aspects of the rearing environment substantially
influence the development of ED and interpersonal dysfunction.
Studies also have examined potential heritable vulnerabilities
to BPD within the framework of normal personality theory,
largely anchored in the Five-Factor Model (FFM) of personality,
consisting of openness, conscientiousness, extraversion, agreeable-
ness, and neuroticism. Distel et al. (2009), for example, examined
FFM traits in relation to BPD in a large study of twins from the
Netherlands, Belgium, and Australia. The overall heritability esti-
mate for BPD was .45, and findings indicated that all of the
genetic variance in BPD was shared by FFM traits. Among asso-
ciations of FFM traits with BPD, neuroticism had the strongest
association, accounting for 45% of the variability in BPD traits,
and the additive genetic correlation of BPD with neuroticism
was the highest among the FFM traits (r = .95). It is interesting
to note that nearly one-third of the variance in unique environ-
mental effects on BPD was not shared with the FFM traits. The
authors concluded that heritable vulnerabilities conferred by
high neuroticism and low conscientiousness and agreeableness
might make people vulnerable to some of the unique environ-
mental factors that play a role in the development of BPD.
These findings, in conjunction with findings on the heritability
and association of trait impulsivity with BPD and possible precur-
sors to BPD, suggest that heritable vulnerability to BPD and ED
may consist of a combination of trait impulsivity and neuroticism.
Findings have indicated that both neuroticism and impulsivity are
at least moderately heritable. One study examining heritability for
different forms of impulsivity found heritability of 45%–50% for
impulsivity assessed by trait measures and 28%–55% for
1147
behavioral indicators of impulsivity (e.g., delay discounting, risk
taking, and behavioral disinhibition; Bevilacqua & Goldman,
2013). Similarly, findings on the heritability of the FFM traits
have generally indicated significant and moderate heritability esti-
mates for neuroticism (ranging from 15% to 50%; Power & Pluess,
2015; Vukasović & Bratko, 2015). Children with high trait impul-
sivity and neuroticism may be particularly vulnerable to the types
of environmental influences that shape the development of ED
and eventual BPD. Further, the high co-occurrence of mood
and anxiety disorders with BPD suggests a heterotypic model in
that neuroticism may manifest in different ways at various stages
of development, culminating (with the right mix of experiences)
in disorders characterized by anxiety and mood disturbance.
Therefore, it seems likely that, when it comes to underlying her-
itable vulnerabilities and their manifestations throughout devel-
opment, BPD straddles the internalizing and externalizing
dimensions.
Adverse rearing environments
Adverse childhood environments have received considerable
attention as key environmental factors that influence the develop-
ment of BPD and ED (Calkins & Hill, 2007; Eisenberg et al.
1999). The literature on childhood maltreatment in relation to
BPD is substantial, so I will highlight a few key findings here.
Adults with BPD tend to report high rates of childhood adversity,
suggesting an important role for trauma or abuse, at least in some
cases. Rates of reported past childhood sexual abuse among per-
sons with BPD are high (Zanarini et al., 2002). Findings also have
suggested that persons with BPD report a higher prevalence of
childhood sexual (Paris, Zweig-Frank, & Guzder, 1994; Yen
et al., 2002) and physical abuse (Paris et al., 1994) than those
with other personality disorders. A chart-review study found a
prevalence of past sexual abuse of 50% among inpatient adoles-
cents with BPD (Westen, Ludolph, Misle, Ruffins, & Block,
1990). Given these findings, some have speculated that BPD rep-
resents complex PTSD, suggesting that past trauma drives the ED
characteristic of BPD (Cloitre, Garvert, Weiss, Carlson, & Bryant,
2014; Ford & Courtois, 2014; Trippany, Helm, & Simpson, 2006;
van der Kolk, Pelcovitz, Roth, & Mandel, 1996). Other researchers
have suggested that past abuse or trauma are neither necessary
nor sufficient for a BPD diagnosis (Zanarini et al., 1997).
Although it appears that childhood adversity is unusually com-
mon in BPD, up to 50% of adults with BPD do not report child-
hood sexual abuse, and up to 54% do not meet criteria for PTSD
(Lieb et al., 2004). It is likely, therefore, that trauma and severe
childhood adversity plays an important role for some people,
and that characteristics of childhood environments likely transact
with biological and other factors in complex ways to influence the
development of ED and BPD (Chapman, Hope, & Turner, in
press; Crowell et al., 2009, 2014).
Some research has examined the types of childhood maltreat-
ment that might be particularly associated with BPD. One study,
for example, examined BPD features among maltreated and non-
maltreated children (Hecht, Cicchetti, Rogosch, & Crick, 2014).
Findings indicated that greater chronicity of maltreatment was
associated with more severe BPD features. Further, the number
of developmental periods in which maltreatment occurred pre-
dicted whether individuals fell within a high-risk for the BPD
group (those with high scores on three or more categories of
symptoms; Hecht et al., 2014). Maltreatment status was associated
with higher scores on all categories of BPD features, suggesting
1148
that maltreatment may not uniquely influence the development of
particular types of symptoms, such as emotional instability or
ED-related features.
Some findings also have suggested that ED may play an impor-
tant mediating role in the association between childhood experi-
ences and the later development of BPD. In a study examining
the influence of mothers’ personality disorder symptoms on
child psychopathology, Kaufman, Puzia, Mead, Crowell, and
Beauchaine (2017) found that children’s difficulty regulating
emotions partially mediated the association of a composite of
maternal BPD/antisocial personality disorder symptoms on inter-
nalizing and externalizing symptoms a year later. In another study
examining the association of childhood parental emotion social-
ization (reported retrospectively) with ED and self-harm among
college students, emotional invalidation (specifically, punishment
and neglect) predicted self-harm, and difficulty evaluating emo-
tions (an aspect of difficulties with emotion regulation) mediated
the relationship between these parental responses and self-harm
(Buckholdt, Parra, & Jobe-Shields, 2009). Another study exam-
ined the association of reports of childhood parental emotion
socialization and trauma with current BPD features among college
students, finding that difficulties regulating emotions mediated
the association of emotion socialization and parental psychologi-
cal control (but not childhood trauma) with BPD features (Hope
& Chapman, in press). Some of this literature on parenting,
trauma, abuse, and other childhood experiences is limited by its
focus on adult reports of childhood experiences, and lack of
examination of interactions of heritable and environmental
factors.
Addressing some of these limitations, Belsky et al. (2012)
examined the potential role of environmental and heritable fac-
tors in the development of BPD in a longitudinal cohort study,
following twins (N = 1,116) from birth to age 12. Findings indi-
cated that maltreatment in childhood more strongly predicted
BPD features at 12 years among children with family histories
of psychiatric disorder. Findings from this study painted a com-
plex picture of the development of BPD and indicated that
some of the unique environmental influences accounting for a
proportion of the variance in BPD features (at least among
those with high levels of BPD features) may include high maternal
negative expressed emotion.
Some research on the neurobiological correlates of adverse
childhood experiences has suggested potential mechanisms
underlying a link between childhood adversity, ED, and BPD.
As discussed later, adults with BPD appear to be prone to poor
frontal regulation of the limbic system, whereby the connectivity
of prefrontal regions with the amygdala appears reduced in BPD
patients. Typically, increases in the activity of certain frontal areas
(e.g., the ventrolateral and medial prefrontal cortex in particular)
are associated with reductions in the activity of the amygdala
(Lieberman et al., 2007). Some findings, however, have suggested
that persons exposed to significant early life stress may show a
positive association of ventrolateral prefrontal and amygdala acti-
vation (Taylor, Eisenberger, Saxbe, Lehman, & Lieberman, 2006).
If the prefrontal cortex typically acts as the “brakes” on the amyg-
dala in normally developing individuals, the opposite may occur
among those exposed to adverse childhood events. Further, ani-
mal research has suggested that the prefrontal cortex is particu-
larly dense with cortisol receptors (Sanchez, Young, Plotsky, &
Insel, 2000), and that stress increases dopamine activity in the
prefrontal cortex (Roth, Tam, Ida, Yang, & Deutch, 1988) and
may disrupt the communication between the prefrontal cortex
A. L. Chapman
and other brain regions (Liston, McEwen, & Casey, 2009).
These findings indicate possible mechanisms for the lingering
effects of childhood adversity on the emotion regulation system
(Diamond, 2018). Studies examining brain structure and func-
tioning in BPD, therefore, should incorporate measures of child-
hood adversity and clinical control groups with PTSD or past
child abuse.
Emerging BPD and related behavioral problems in adolescence
Adolescence appears to be a particularly important period mark-
ing increased severity of ED and the emergence of some of the key
behavioral problem areas associated with BPD (e.g., NSSI and sui-
cide attempts). Increasingly complex social dynamics, academic
demands, conflicts between autonomy and dependence, among
other factors, likely test and shape emotion regulation capabilities
during adolescence (Ahmed, Bittencourt-Hewitt, & Sebastian,
2015; Casey et al., 2008). In an excellent review of the develop-
ment of neurocognitive foundations of emotion regulation,
Ahmed et al. have argued that the amygdala, various regions of
the prefrontal cortex, and the connectivity of prefrontal and lim-
bic regions all mature during adolescence (with some of these
regions continuing to develop into young adulthood) and are
directly relevant to the development of emotion regulation capac-
ities (Ahmed et al., 2015). This pattern of development is partic-
ularly relevant to ED and BPD.
Findings have indicated that some of the cognitive and social
cognitive capacities that facilitate emotion regulation show partic-
ularly steep development during adolescence (Blakemore &
Robbins, 2012; Shaw et al., 2008). Adults with BPD show deficits
in a variety of neurocognitive domains, some of which are partic-
ularly important for effective emotion regulation (e.g., attention,
cognitive flexibility, and planning; Ruocco, 2005; Unoka &
Richman, 2016). The onset of various internalizing and external-
izing behavioral problems in adolescence (Lancefield, Raudino,
Downs, & Laurens, 2016) could indicate difficulties in the devel-
opment of emotion regulation capacities, perhaps stemming from
earlier and ongoing transactions of a vulnerable temperament
with aspects of the rearing environment. In particular, the devel-
opment of certain types of behavioral problems, such as NSSI, sui-
cidal behavior, and substance use problems, might at least
indirectly indicate that ED is beginning to crystallize. Therefore,
it appears that (a) basic capacities and characteristics of brain
functioning necessary for emotion regulation develop differently
in those with BPD, and (b) such developmental differences
begin to become more apparent in adolescence.
Findings on the trajectory of BPD symptoms in childhood,
adolescence, and adulthood have further suggested continuity in
these symptoms and indicated that adolescence may be a key
period in which to identify and try to prevent the further devel-
opment of ED. A study of the association of childhood psychopa-
thology and the later development of BPD (the Pittsburgh Girls
Study; N = 1,233; Stepp, Burke, Hipwell, & Loeber, 2012) found
that childhood ADHD and oppositional defiant disorder symp-
toms predicted poor impulse control, problems with self-
regulation, and BPD symptoms in adolescence. These findings
support the biosocial developmental model’s (Crowell et al.,
2009, 2014) hypothesis that early impulse control problems are
key indicators of a developmental trajectory toward increasing
ED and BPD.
BPD symptoms in adolescence also predict later behavioral
problems in early adulthood. The Children in the Community
Development and Psychopathology
Study, for example, followed a diverse group of 800 children in
various areas of New York over a 20-year period, examining the
trajectory of adolescents experiencing symptoms of BPD
(Cohen, Crawford, Johnson, & Kasen, 2005). Some of the findings
suggested that childhood sexual abuse predicted BPD but not
other personality disorder symptoms in adolescence. BPD symp-
toms in early adolescence (mean age = 14) predicted BPD symp-
toms as well as lower academic and occupational attainment and
greater psychosocial impairment in early adulthood (mean age =
33; e.g., lower global assessment of functioning and lower role
function). Consistent with other research (Zanarini et al., 2004),
the Children in the Community Study found age-related declines
in some BPD symptoms (Winograd, Cohen, & Chen, 2008).
Some of these behavioral problems likely are influenced by and
influence the development of ED and BPD. Adolescents with
developing BPD symptoms, for example, may be particularly
prone to substance use problems. Substance use, in turn, may
have direct effects on brain development, further exacerbate psy-
chosocial stressors (e.g., impairing functioning and contributing
to academic problems and relationship discord), and worsen the
trajectory of BPD symptoms (Bornovalova et al., 2018; Zanarini
et al., 2004). A recent study of female twins investigated genetic
and environmental influences on the association of BPD features,
major depressive disorder, and alcohol use disorders (AUD;
Bornovalova et al., 2017). Following adolescents from age 14
through early adulthood (age 24), the findings of this study sug-
gested that genetic and unique environmental factors accounted
for the covariation of BPD with major depressive disorder and
AUD over time, and that AUD predicted lower decline in BPD
features. These findings suggest that at least some of the behavio-
ral problems co-occurring with BPD may worsen the BPD
symptom trajectory, possibly through their effects on brain devel-
opment and exacerbation of ED and contextual factors (e.g., inter-
personal problems and stress). Similarly, other longitudinal
research with adults has indicated that the presence of SUDs,
PTSD, and mood and anxiety disorders reduces the likelihood
of remission from BPD (Zanarini et al., 2004). Another recent
longitudinal study examined self-harm and suicidal behaviors as
predictors of the development of BPD 5 years later among adoles-
cent psychiatric inpatients (Homan, Sim, Fargo, & Twohig, 2017).
Findings suggested that only suicide threats uniquely predicted
BPD 5 years later (Homan et al., 2017). As one of the key func-
tions of emotions is to communicate, suicide threats may indicate
a combination of high ED and deficits in communication skills,
along with a learning history reinforcing emotional escalation.
Some studies have investigated whether some of the differences
in the volume of certain brain areas that have been observed
among adults with BPD are also observable among adolescents
at risk of BPD (e.g., those engaging in self-injury) or with an
early diagnosis of BPD. One study, for example, found that self-
injuring adolescent girls demonstrated reduced volume in the
insular cortex and right inferior frontal gyrus, compared with
non-self-injuring controls (Beauchaine, Sauder, Derbridget, &
Uyeji, 2019). Another investigation compared the volume of pre-
frontal and orbitofrontal gray matter among adolescents with
BPD versus psychiatric and nonpsychiatric controls (Brunner
et al., 2010). Findings indicated that adolescents with BPD
showed reduced volume in the dorsolateral frontal gyrus and
left orbitofrontal gyrus compared with nonpsychiatric controls,
but that there were no differences in the volume of these or
other regions between clinical controls and BPD participants
(Brunner et al., 2010). Takahashi et al. (2009) also examined
1149
insular cortex volume among adolescent participants with BPD
and healthy controls and found no differences in volume between
these groups. BPD participants, however, with a history of violent
behavior over the past 6 months demonstrated a smaller bilateral
insular volume, compared with BPD participants with no such
history (Takahashi et al., 2009). Taken together, these findings
suggest that some of the brain differences associated with BPD
may begin to emerge in a narrower fashion (differences in volume
in fewer areas compared with adulthood) in adolescence com-
pared with adulthood, that these brain differences may not be
unique to BPD, and that the association of violence and brain vol-
ume and functioning should be further explored. Violence may be
a more extreme indicator of high trait impulsivity and ED among
adolescents at risk for BPD.
Self-injury and suicidal behavior
Models of the development of ED, BPD, and related problems
(e.g., NSSI and suicidal behavior) have emphasized important
transitions and transactions occurring in adolescence. The devel-
opment of NSSI and suicidal behavior in early to middle adoles-
cence, in particular, has received particular attention. Beauchaine,
Hinshaw, et al. (2019) have proposed a similar model as the bio-
social developmental model of BPD to explain the development of
NSSI and suicidal behavior among adolescents. In particular, chil-
dren with impulsive temperaments are especially vulnerable to the
effects of maltreatment, and are likely to have interpersonal diffi-
culties and to be involved in peer contexts that support the devel-
opment of severely maladaptive coping behaviors in early
adolescence, such as NSSI (i.e., through modeling and contagion
effects; Derbidge & Beauchaine, 2014). NSSI emerges as an indi-
cator of worsening ED and a way to regulate ED. In support of
this model, findings from one study suggested that adolescents
with histories of recent NSSI or suicide attempts (at least one epi-
sode in the past 6 months) may be particularly reactive to mater-
nal behavior during discussions of conflictual topics (Crowell
et al., 2014). In this study, adolescents with NSSI or suicide
attempt histories demonstrated both behavioral and physiological
reactivity to mothers’ behavior, but depressed adolescents only
showed behavioral reactivity, suggesting a potentially unique bio-
logical vulnerability among self-injuring or suicidal adolescents.
Findings from other research have suggested that children with
ADHD are particularly vulnerable to developing self-inflected
injury if they have had a history of childhood maltreatment (see
Beauchaine, Hinshaw, et al., 2019, for a review; see also
Derbidge & Beauchaine, 2014; Guendelman, Owens, Galan,
Gard, & Hinshaw, 2015; Swanson, Owens, & Hinshaw, 2014).
Similarly, Miller and Prinstein (2019) have proposed that
abnormal development of the biological stress response system
influences the emergence of NSSI and suicidal behavior in adoles-
cence. Within this model, normative changes in the biological
stress response system, such as changes in the hypothalamic–pitu-
itary–adrenal axis and sympathetic and parasympathetic nervous
system reactivity, result in a period of enhanced sensitivity to
stressors among adolescents. This may be particularly the case
for interpersonal stressors, given the importance of peer relation-
ships in adolescence and evidence of increased sensitivity to social
rewards and punishments (Casey, Jones, & Hare, 2008) and pre-
frontal brain response to social evaluation (Sommerville, 2013).
Miller and Prinstein (2019) have suggested that abnormalities in
the development of the stress response system (e.g., reduced con-
nectivity of the prefrontal and limbic systems) may begin to
appear in adolescence and influence the development of NSSI
1150
and suicidal behavior. Some studies, accordingly, have found that
youth with suicide histories have demonstrated reduced amygdala
and PFC connectivity in response to emotional stimuli, a finding
that parallels some of the research on adult BPD (discussed later
in this review; Johnston et al., 2017). As mentioned earlier, struc-
tural brain differences associated with self-injury and BPD may
begin to emerge in adolescence as well, albeit in a narrower fash-
ion than among adults patients with BPD.
The Course of BPD
In this section, I briefly summarize some of the research on the
course of BPD and BPD symptoms. As many of the studies
have begun following participants with BPD at a mean age corre-
sponding to young adulthood, this research is probably best
viewed as a snapshot of how BPD progresses through young
adulthood. In addition, although there have been many studies
of the course of BPD, I will focus primarily on findings from
the McLean Study of Adult Development, a large study of BPD
inpatients, followed posthospitalization for several years
(Zanarini, Frankenburg, Hennen, & Silk, 2003). Findings from
this research have suggested a fairly hopeful prognosis for many
people with BPD, with findings from the 16-year point indicating
that 99% of patients achieved at least 2 years of remission from the
diagnosis of BPD, 60% of patients recovered, and 5% died by sui-
cide (Zanarini et al., 2012). Earlier studies based on this data set
examining patterns of symptom remission have indicated that the
dysregulated behavioral patterns that are likely related to ED tend
to subside over time, but that enduring emotional suffering in the
form of mood symptoms often persists. Some of the most persis-
tent symptoms, even among people who no longer meet diagnos-
tic criteria, included mood and emotional disturbances (Zanarini
et al., 2003). Although NSSI, suicidality, affective instability, and
serious interpersonal instability subsided relatively rapidly, emo-
tional symptoms such as chronic dysphoria and intense anger
tended to remit more slowly (Zanarini et al., 2007). Moreover,
general impulsivity and recklessness also tended to remit more
slowly over a 10-year period. This finding suggested that, while
the severe, emotion-driven behaviors such as NSSI and suicide
attempts appear to resolve fairly quickly (Zanarini et al., 2007),
more enduring tendencies toward impulsivity may persist and
appear in various forms, again consistent with heterotypic models
highlighting trait impulsivity as an enduring predisposition to
BPD (e.g., Crowell et al., 2009, 2014).
Characteristics of ED in Adults With BPD
With these findings on the developmental factors and periods in
mind, it is helpful to consider what characterizes ED among
adults with BPD. What is the net result of the potential genetic,
biological, and psychosocial factors operating at various points
in development? Findings across several studies over the past cou-
ple of decades have begun to clarify the nature of ED in BPD. The
summary below is based on the conceptualization of emotions as
systemic responses to motivationally relevant situations, consist-
ing of cognitive, physiological, and behavioral components. ED,
therefore, consists of aberrations in cognitive, physiological, or
behavioral responding that impede the individual’s ability to
achieve goals or engage in effective action in particular contexts.
I will focus here on cognitive, behavioral, and physiological factors
that are indicative of ED in BPD, rather than on the literature on
emotional responding in BPD, which has been reviewed a few
A. L. Chapman
times in the past several years (Carpenter & Trull, 2013; Dixon-
Gordon, Haliczer, & Conkey, in press; Rosenthal et al., 2008).
Cognitive aspects of ED
Cognitively, persons with BPD tend to have difficulty with emo-
tional clarity and awareness (Leible & Snell, 2004), identifying and
describing emotions (Wolff, Stiglmayr, Bretz, Lammers, &
Auckenthaler, 2007; Derks, Westerhof, & Bohlmeijer, 2016),
and a tendency toward less specific differentiation among negative
emotions and lower emotional granularity (i.e., the tendency to
represent emotions in a nonspecific manner; Suvak et al., 2011).
Effective emotion regulation often requires and is facilitated by
clarity and awareness of an individual’s emotional state. Not
knowing what specific emotion one is feeling would make it dif-
ficult to select adaptive emotion regulation strategies. Persons
with BPD also may be especially prone to appraise certain situa-
tions or emotional experiences as excessively negative or intoler-
able or as having disastrous consequences. Linehan (1993a) has
suggested that some persons with BPD are phobic of emotions.
Clinically, persons with BPD often describe their emotions as
overwhelming, out of control, and intolerable.
Other cognitive characteristics of ED include difficulty regulat-
ing attention to emotionally evocative events. Linehan (1993a) has
proposed that persons with BPD may have difficulty disengaging
their attention from emotional material. Some research indicating
that people with BPD are particularly prone to rumination, for
example, suggests difficulty disengaging from emotional events
(Abela, Payne, & Moussaly, 2003; Smith, Grandin, Alloy, &
Abramson, 2006), and the cascade model of BPD posits that
NSSI is particularly likely when rumination has amplified nega-
tive emotional experiences to an intolerable level (Selby &
Joiner, 2009). Findings from some studies have suggested the
presence of an attentional bias toward negative and BPD-related
stimuli (words; Kaiser, Jacobs, Domes, & Arntz, 2017); this pos-
sible bias may amplify emotional responding and disrupt the abil-
ity of persons with BPD to disengage or distance themselves from
emotional events. The findings on attentional biases in BPD, how-
ever, are complex, sometimes inconsistent, and may depend on
the laboratory paradigms and stimuli used (Kaiser et al., 2017).
Physiological aspects of ED
Findings on physiological regulation of emotions in BPD paint a
fairly complex picture. Activity of the parasympathetic nervous
system, as indexed by respiratory sinus arrhythmia (RSA), has
been theorized to be an indication of emotion regulation
(Porges, 2001), with higher RSA indicating greater vagal influence
on heart rate variability. Research on parasympathetic reactivity in
BPD remains fairly limited. Some studies have found decreasing
RSA among BPD patients in response to emotionally evocative
films relative to nonpatient (Austin, Riniolo, & Porges, 2007) or
clinical controls (Fitzpatrick & Kuo, 2015). Another study did
not find differences in RSA activity among BPD participants in
response to a laboratory emotional stressor, compared with non-
clinical controls (Weinberg, Klonsky, & Hajcak, 2009).
Brain imaging research has examined the connectivity of activ-
ity in the prefrontal and limbic regions, as deficient inhibitory
influence of certain prefrontal areas on the amygdala could be
considered an aspect or mechanism of ED. Some findings have
indicated that participants with BPD show a combination of
heightened activation of the amygdala in response to emotional
Development and Psychopathology
stimuli (Donegan et al., 2003; Hazlett et al., 2012; particularly the
left amygdala) with lower activation of the dorsolateral prefrontal
cortex (Schulze, Schmahl, & Niedtfeld, 2016). In contrast, a meta
analysis of 11 studies comparing BPD patients to healthy controls
showed greater activation in the insula and posterior cingulate
cortex and lower activation in the amygdala, subgenual anterior
cingulate, and dorsolateral prefrontal cortex (Ruocco,
Amirthavasagam, Choi-Kain, & McMain, 2013). Extant findings,
therefore, are mixed with respect to brain-related characteristics of
ED in BPD. Further, the research generally has compared partic-
ipants with BPD to healthy controls in terms of responses to
unpleasant, emotionally evocative images; thus, more research is
needed to determine whether these patterns of brain activity are
specific to BPD or accounted for by elevated psychopathology,
or relevant to emotional reactions to other situations or stimuli.
Some evidence has suggested that differences in brain activity
during the implementation of certain emotion regulation strate-
gies may hamper the effectiveness of these strategies among
those with BPD. One study, for example, examined the effects
of cognitive reappraisal among patients with BPD and past
trauma, compared with healthy controls with and without past
trauma (Lang et al., 2012). Compared with non-trauma-exposed
healthy controls, those with BPD and past trauma showed less
activation in the prefrontal cortex during upregulation of emo-
tions and less activation of the anterior cingulate during downre-
gulation (Lang et al., 2012). These patterns of brain activity may
be due primarily to past trauma exposure, as there were no differ-
ences between trauma-exposed BPD participants and trauma-
exposed healthy controls without PTSD (Lang et al., 2012). In
another study, BPD patients and healthy controls viewed pictures
depicting social interactions and either used cognitive distancing
or simply viewed the pictures (Koenigsberg et al., 2010).
Findings indicated that, while healthy controls and BPD patients
similarly showed increased activation of the dorsolateral and ven-
trolateral prefrontal cortex and posterior cingulate when distanc-
ing, BPD patients showed less deactivation in the amygdala,
among other areas (Koenigsberg et al., 2010). Similarly, a recent
study compared the functional connectivity of various frontal
regions with the amygdala during an effortful emotion regulation
task (using emotional pictures), finding that BPD patients showed
weaker increases in functional connectivity compared with non-
patient controls, but not compared with clinical controls with
Cluster C personality disorders (Baczkowski et al., 2017). Taken
together, these findings suggest that brain functioning that nor-
mally facilitates emotion regulation may be impaired in BPD,
but it remains unclear whether these impairments are unique to
BPD.
In contrast, maladaptive emotion regulation strategies appear
to temporarily result in greater connectivity of the amygdala
and prefrontal regions (i.e., prefrontal inhibition of amygdala
activity) among BPD patients. In a study modeling the effects
of NSSI on brain functioning, Reitz et al. (2015) randomly
assigned self-injuring women with BPD (and healthy controls)
to an incision or sham condition following a stress induction.
The incision condition involved a shallow incision administered
by an experimenter with a sharp plastic device, designed as a lab-
oratory analogue for NSSI. Whereas healthy controls did not
demonstrate evidence of physiological stress-reduction or
increases in prefrontal connectivity in the incision condition,
women with BPD reported decreased aversive tension (distress),
decreased amygdala activation, and increased prefrontal connec-
tivity (to the superior frontal gyrus) in the incision versus the
1151
sham condition. Findings from other research examining the
effect of painful stimulation on brain activity among BPD patients
also have suggested that pain increases the functional connectivity
of prefrontal regions with the amygdala during emotional stress-
ors (Niedtfeld et al., 2012). Together with findings that adaptive
strategies such as cognitive reappraisal under-recruit prefrontal
regions associated with emotion regulation, these findings echo
what self-injuring patients with BPD often say about how letting
go of NSSI and learning more adaptive strategies is sometimes an
uphill battle.
Behavioral aspects of ED or heightened BPD features
Other studies have examined the behavioral aspects of emotion
regulation in BPD. BPD is associated with limited access to emo-
tion regulation strategies (Glenn & Klonsky, 2009; Salsman &
Linehan, 2012), and this would suggest that persons with BPD
might rely primarily on maladaptive strategies that produce
quick relief. Some findings, however, have suggested that rather
than simply relying on maladaptive emotion regulation strategies,
people with BPD may tend to engage in greater effort to their
emotions across both adaptive and maladaptive strategies
(Dixon-Gordon, Aldao, & De Los Reyes, 2015), with the possible
exception that they tend to use less acceptance as an emotion reg-
ulation strategy (Chapman, Dixon-Gordon, & Walters, 2013).
There also is some evidence that people with heightened BPD fea-
tures as well as those with a diagnosis of BPD might experience
and report fewer emotional benefits from acceptance versus sup-
pression and avoidance, both in the laboratory and in daily life
(Chapman, Rosenthal, Dixon-Gordon, Turner, & Kuppens,
2017). Compared with healthy controls, however, BPD patients
find certain adaptive emotion regulation strategies, such as cogni-
tive reappraisal and distraction, to be less effective (Sauer et al.,
2016). This could be due to lack of skillful use of the strategies,
lesser impact of the strategies on emotional distress (e.g., as sug-
gested by the research reviewed above on brain functioning in
relation to cognitive reappraisal), problems with the validity of
measures of emotion regulation strategies, or other factors.
Overall, though, this pattern of findings tentatively suggests that
persons with BPD may (a) put forth a fair amount of effort to reg-
ulate their emotions, and (b) find this effort largely unsuccessful.
Other behavioral aspects of emotion dyregulation include
emotion-related disruptions in behavior and engagement in
mood-dependent actions. Consistent with clinical observations
and research suggesting that persons with BPD tend to engage
in maladaptive behaviors when they experience emotional distress
(e.g., NSSI), some laboratory research has suggested that
people with heightened BPD features or a diagnosis of BPD
might have difficulty inhibiting behavior or solving social
problems when they are emotionally distressed (Dixon-Gordon,
Chapman, Lovasz, & Walters, 2011). In addition, a recent study
also found that participants with BPD demonstrated a decreased
ability to learn from punishment following an emotional induc-
tion (Dixon-Gordon, Hackel, Tull, & Gratz, 2018). More research
is needed, however, to determine whether problematic behavioral
patterns in BPD are primarily mood dependent. Furthermore,
high rates of behaviors appearing to serve emotion regulation
functions (e.g., NSSI, suicide attempts, substance use, or harmful
forms of impulsivity), along with a strong association of BPD fea-
tures with avoidant coping, emotion suppression, and experiential
avoidance more broadly (Beblo et al., 2013; Chapman, Specht, &
Cellucci, 2005), could also be considered behavioral indicators of
1152
ED. Findings also have suggested that individuals with BPD have
difficulty tolerating distress in the service of goal-directed behav-
ior (Gratz, Frances, Sullivan, Hurt, & Clarkin, 2006), and dissoci-
ation in response to stress is a defining feature of BPD and has
been observed clinically and in laboratory and experience sam-
pling research (Ebner-Primer et al., 2005).
Conclusions
Although the developmental processes contributing to the devel-
opment of ED and BPD are complex, advances in research and
theory have begun to illuminate these processes. Influential theo-
ries of the development of BPD have strongly emphasized the role
of ED. Linehan’s (1993a) original biosocial theory proposed the
transaction of an emotionally vulnerable temperament and an
invalidating environment contributes to the development of ED
and BPD. More recent extensions of this model (Crowell et al.,
2009, 2014) have proposed that ED emerges from the interaction
between an impulsive temperament and an invalidating environ-
ment. Findings have suggested that trait impulsivity is a strong
candidate for a heritable vulnerability to BPD, and other findings
have also suggested a role for neuroticism. It seems likely that
both factors at play confer vulnerability to the adverse environ-
mental contexts that often contribute to the development of ED
and BPD. Broadly, an invalidating rearing environment may
play an important role in socializing the vulnerable child’s emo-
tion regulation tendencies, shaping increasing emotional lability
and dysregulation, culminating in the development of maladap-
tive coping behaviors that often begin to appear in adolescence
(e.g., NSSI, suicidal behavior, and substance use). In addition,
inadequate or delayed development of various social cognitive
capacities and adaptive stress response may further contribute
to ED and serious behavioral problems among adolescents.
These behavioral problems, in turn, contribute to and predict
the development of BPD. In adulthood, studies have highlighted
various key cognitive, behavioral, and physiological components
of ED, including possible differences in brain structure and func-
tioning that are likely rooted in earlier developmental processes.
One challenge moving forward in the research is to determine
where ED stops and BPD begins. Aspects of ED (emotional labil-
ity in particular) are built into the criteria for BPD. It is hard to
imagine the construct of BPD without ED. Is ED a causal, trans-
diagnostic contributor to the array of features and behaviors
observed among those with BPD, or is it best characterized as a
core feature of BPD? In addition, based on the notion that ED
consists of dysregulated emotional responding that interferes
with important, goal-oriented behavior, many of the problematic
behaviors occurring among those with BPD could be considered
at least indirect indicators of ED. Considered in this way, ED
could quickly devolve into a circular construct. The breadth and
reach of the construct of ED is both its major strength and limi-
tation, and this problem is not unique to BPD.
Invalidation has received considerable attention as an impor-
tant socialization factor contributing to ED and BPD, and more
research is needed to define and clarify the role of invalidation.
Invalidation can take many forms that do not involve trauma or
abuse, and recent reviews have suggested that studies thus far
have failed to adequately measure and capture the construct of
invalidation (Boucher et al., 2017; Musser, Zalewski, Stepp, &
Lewis, 2018). Further, it is very difficult to ascertain the specific
influence of parenting behaviors on the development of psycho-
pathology. There are many potential explanations for any
A. L. Chapman
association of parenting with negative outcomes, from shared
genetic factors, to proactive, evocative, and other person–environ-
ment transactions. More research is needed to refine and measure
the construct of invalidation, and more longitudinal research is
needed to determine when (e.g., what developmental period),
how, and for whom invalidation influences the development of
ED and BPD.
The emerging picture of the complex developmental processes
contributing to BPD and ED have important implications for pre-
vention and treatment. Beauchaine, Hinshaw, et al. (2019) have
outlined several key steps for the prevention and treatment of ado-
lescent NSSI and suicidal behavior, arguing in particular that pre-
vention should target the invalidating environment through
evidence-based parenting interventions, and that treatment
should address ED (which may be more influenced by environ-
mental factors and easier to address) rather than trait impulsivity
(which could be a fairly stable tendency). Beauchaine, HInshaw,
et al. (2019) have argued that we know enough about key precur-
sors and risk factors for NSSI and suicidal behavior that preven-
tative interventions or treatments should target these precursors
before the behaviors begin to emerge.
Furthermore, findings from recent research has supported this
approach. A recent randomized clinical trial examined an adapted
version of DBT (DBT-C; consisting of individual parent training
and skills training sessions with parents and their children, and
the availability of the therapist for phone coaching calls) for pre-
adolescent children (N = 43; Perepletchikova et al., 2017). The
focus was on children with disruptive mood dysregulation disor-
der (DMRD), as DMRD is a key indicator of the risk for future
childhood conduct problems and may indicate a trajectory toward
self-injury and BPD for some children. Findings indicated a much
lower dropout rate in DBT-C compared with treatment as usual,
as well as a higher rate of positive treatment response and a higher
remission rate for DMRD. It remains to be seen, however,
whether this type of treatment might curtail the later development
of NSSI, suicidal behavior, or BPD.
Theory and research suggest that, among adolescents, NSSI
should be a high-priority treatment target. NSSI likely emerges
earlier for most adolescents, compared with suicidal behavior,
and should be a key target for treatment. Prominent models,
for example, suggest that suicide attempts result from a combina-
tion of suicidal desire and the capability to enact lethal self-injury
(i.e., acquired capability; Joiner, 2005; Klonsky & May, 2015;
Witte, Gordon, Smith, & Van Orden, 2012). Within these models,
repeated NSSI increases an individual’s ability to enact suicide
plans (Hamza, Stewart, & Willoughby, 2012; May & Victor,
2018; Willoughby, Heffer, & Hamza, 2015). The integrated
model (Hamza et al., 2012), for example, proposes three potential
explanations for the NSSI–suicide attempt relation: (a) NSSI and
suicide are related by virtue of their shared relation with a third
variable (e.g., BPD); (b) NSSI is a “gateway” behavior that facili-
tates suicide attempts; and (c) based on Joiner’s (2005) interper-
sonal-psychological theory of suicide, NSSI is a painful/
provocative event that increases an individual’s capability to
enact suicidal behavior (i.e., acquired capability) by increasing
fearlessness of death and habituation to pain.
Along with preventative interventions targeting at-risk groups
before the emergence of NSSI, treatment addressing NSSI when it
emerges (and ideally beforehand) in adolescence would be
expected to have a major impact on eventual risk for suicide
and the development of problems characteristic of BPD.
Findings from two large studies of DBT for adolescents have
Development and Psychopathology
supported the efficacy of this treatment for reducing suicide
attempts, self-injury, suicidal ideation, and depression among self-
injuring adolescents (McCauley et al., 2018; Mehlum et al., 2014).
Further research is needed to determine if broader-scale preven-
tative interventions, such as emotion regulation training in
schools, might help to curb the development and exacerbation
of ED and future BPD among adolescents.
Financial support. Work on this chapter was supported by a Michael Smith
Foundation for Health Research Career Investigator Award and a Simon Fraser
University FASS Dean’s Research Grant.
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