Family members of those with borderline personality disorder (BPD) show similarities in their brains and personalities


Family members of those with borderline personality disorder (BPD) show similarities in their brains and personalities—and even interpret some facial expressions similarly, according to a series of studies by researchers at the University of Toronto.

“One of the more urgent questions I hear when I speak with family groups is whether the disorder can be passed down from parents to their children,” says Anthony C. Ruocco, professor, interim graduate chair and director of clinical training in U of T Scarborough’s department of psychological clinical science.

“We are among the first researchers to study how factors in addition to symptoms and personality traits might run in families with BPD.”

BPD is a personality disorder categorized in part by impulsivity and difficulty with emotional regulation. Studies into BPD tend to focus on those with the disorder, but Ruocco wanted to identify which social and biological factors, beyond a BPD diagnosis, run in families. He says these characteristics might offer clues into what causes the disorder to develop and what can prevent it.

Diagnoses other than BPD observed in relatives

Ruocco found symptoms of BPD persist in families beyond those who are actually diagnosed with the disorder. For example, relatives show the same bias toward sad facial expressions, a pattern of weakness and strength in self-regulatory skills and distinct brain activation patterns during impulse control.

Ruocco conducted his research in the Clinical Neurosciences Laboratory, where he acts as director. He compared 103 people with BPD, 73 first-degree biological relatives (parents, siblings and children) and 99 people with no history of psychiatric illness. Participants completed a range of tests, including interviews, questionnaires, emotion perception tests, problem-solving tasks and brain scans. Those findings informed four papers published between 2019 and 2021.

He found that both those with BPD and their relatives showed higher levels of depression and substance use disorders. Relatives also received similar psychiatric diagnoses and showed more personality traits associated with emotional dysregulation and impulsivity.

“Even though you don’t see the full BPD diagnosis commonly in first-degree relatives, even having a few of the symptoms can be quite impairing,” he says. “This research really brings into focus some of the mental health challenges that many relatives of people with BPD experience.”

Families see fear in sad faces

Families of someone with BPD are prone to interpersonal conflicts—and Ruocco wondered whether facial expressions play a role. Several parents told him they try to show no emotion when their child with BPD is upset, yet often receive the response, “Why are you mad at me?”

It’s well documented that people with BPD interpret facial expressions differently than those without the disorder, but Ruocco found their relatives do, too. When shown a sad expression, people with BPD and their relatives took longer to decode the emotion, and both were more likely to interpret it as fearful.

“This pattern could suggest a heightened sensitivity to signals of threat in families with BPD, which could lead to arguments between family members, for example,” he says. “It’s important to understand what we can do to better align social-emotional communication to improve family functioning.”

Strengths and weaknesses found in impulse control

Another part of the study looked at impulse control via brain imaging. Researchers measured oxygen levels in the frontal part of the brain when participants were shown images and told to withhold responses for certain pictures.

People with BPD activated their prefrontal cortex less than the control group with no psychiatric diagnoses, but relatives showed greater brain activity than both. This pattern could mean relatives use more brain resources to control impulses, or they use similar resources differently to regulate themselves.

Ruocco calls impulsivity “potentially the most dangerous symptom of BPD.” Reckless driving, binge eating, excessive spending and substance abuse are all examples of impulsivity. It’s also associated with self-harm and suicide.

Ruocco’s most recent paper examined which cognitive abilities are associated with impulsivity and BPD. These abilities are known as executive functions, which are the complex thinking skills used to identify goals and plan the steps to reach them.

People with BPD tend to struggle more with executive functions, and researchers expected relatives to show similar difficulties. But relatives who had no psychiatric illness showed both strengths and weaknesses. These relatives had stronger impulse control and abstract thinking abilities, though they also had less efficient problem-solving skills. This aligns with stories Ruocco heard from parents.

“People who have a child with BPD sometimes say to me, “We need to be able to better regulate ourselves to help regulate our child,’” he says. “These findings also might highlight the strengths in self-regulation that could protect the relatives of people with BPD from developing a psychiatric illness themselves.”

Funded by the Canadian Institutes of Health Research, Ruocco hopes his work can help validate the experiences of people with BPD and their families and inspire new directions for treatment.

“As we better understand these familial factors, we can start to integrate these findings into the treatments for families with BPD.”

Borderline Personality Disorder (BPD) is a psychiatric disorder featured by intense fears of abandonment, difficulties in emotion regulation, feelings of emptiness, unstable interpersonal relationships, impulsivity, and heightened risk-taking behaviors, as well as high levels of interpersonal aggression. In addition, paranoid ideation and dissociative states may occur.

Many patients with BPD also show recurring self-injurious or suicidal behavior, although “self-cutting” is not specific to BPD (American Psychiatric Association, 2013). BPD is the most prevalent personality disorder with a reported lifetime prevalence of about 1.7 percent (Gunderson et al., 2018).

In clinical settings, BPD is even more frequent, with an 8.3-fold higher all-cause mortality compared to the general population (Kjær et al., 2018), rendering the condition as highly relevant for public health. Although controversially discussed, it seems that females are more frequently affected from BPD, at least in clinical settings, than males, with a ratio of about four to one (Paris et al., 2013).

Etiological models of BPD suggest that the development of “mistrustful inner working models” in relation to insecure attachment patterns predisposes to perceiving others as untrustworthy and rejecting (Fonagy et al., 2000; Agrawal et al., 2004). Causal factors in this development include emotional neglect and physical or sexual abuse, which occur in up to 80 percent of individuals with BPD (e.g., Zanarini et al., 1989; Hurlbert et al., 1992; Bandelow et al., 2005).

Indeed, according to Linehan’s theory, a developmental pathway leading to BPD begins with early vulnerability, initially expressed as impulsivity, based on which increased emotional sensitivity emerges (Crowell et al., 2009). As regards genetics, findings are more inconclusive, even though some studies show high heritability of BPD features (Amad et al., 2014). According to Linehan’s theory, BPD arises from a complex interplay between heritable biological vulnerability and an invalidating social environment (Linehan, 1993; Crowell et al., 2009).

Consistent with Linehan’s (1993) and attachment-related theories of BPD, evolutionarily grounded explanations have posited that some signs and symptoms associated with BPD can be seen as a pathological variant of adaptive responses to early environmental adversity (Chisholm, 1999; Chisholm et al., 2005; Brüne et al., 2010; Brüne, 2016).

This view is, in part, based on Life History Theory (Stearns, 1992), suggesting that individual differences in the allocation of resources to somatic growth or reproduction depend on an unconscious evaluation of future resource availability (Ellis et al., 2009).

Accordingly, if resources (which here includes emotional availability and trustworthiness of significant others) are predicted to be scarce, individuals may tend to adopt a “faster” life history strategy (LHS), i.e., investing more in reproductive activity than body maintenance and tissue repair (Ellis et al., 2009, 2011; Griskevicius et al., 2011), whereby early social stress in the form of abuse or neglect may “prepare” the individual at the neurobiological level to deal with future threat and malevolence (Teicher et al., 2016; Troisi, 2020). The distinction between “fast” and “slow” LHS is by no means dichotomous; the terms rather reflect the extremes on a continuum, with changes over the lifespan that critically depend on environmental cues (Stearns and Rodrigues, 2020).

On a psychological level, a “fast” LHS or “Pace-of-Life-Syndrome” (PoLS), which we here use interchangeably (Dammhahn et al., 2018) would also entail greater impulsivity, higher scores in neuroticism, lower empathy (or agreeableness), higher aggressiveness, less investment in own offspring, yet a tendency toward risky sexual behavior, and frequent disruptions of intimate relationships (Del Giudice, 2016) all of which are prominent characteristics of BPD (Brüne, 2016).

This compilation of psychological factors reflecting a “fast” PoLS is also compatible with empirical findings proposing a so-called “Super-K” factor subsuming the “Big Five” personality traits, positive affect, social support, aggression, education, pair-bonding, and physical and mental health. The term “Super-K” refers to the biological concept behind Life History Theory and concerns resource allocation to the timing of reproduction and somatic growth. It thus alludes to the continuum between slow and fast LHS (Richardson et al., 2017).

As regards BPD, several lines of research have corroborated the interpretation that BPD as a clinical syndrome largely echoes a fast PoLS, including studies into sociosexuality and mating (Alvergne et al., 2010; Brüne et al., 2017; Sansone et al., 2011), teenage pregnancy, and number of offspring (De Genna et al., 2012). Moreover, personality traits as well as temperament of people with BPD are compatible with the idea of a fast PoLS (Fossati et al., 2001; Láng, 2015; Del Giudice, 2012, 2016; Dammhahn et al., 2018).

Aside from psychological signs and symptoms associated with BPD, there is evidence to suggest that individuals with BPD are also at heightened risk of developing cardiovascular disease and stroke; in fact, the risk for cardiovascular disease and stroke seems to be even specific for BPD in comparison with other personality disorders (Moran et al., 2007), and largely independent of comorbid depression (Barber et al., 2020).

The risk for cardiovascular disease, in part, relates to elevated rates of overweight and obesity, as well as hypertension and diabetes mellitus among people diagnosed with BPD (Powers and Oltmanns, 2012).

However, it may also reside in the fact that BPD patients prematurely accumulate a higher “allostatic load” (AL) due to a dysregulated stress response (McEwen, 2000; Boyce and Ellis, 2005). Moreover, there is clear evidence to suggest that childhood adversity poses a risk for developing metabolic syndromes (Lee et al., 2014) and can exert life-long effects on stress responsivity (Boyce, 2014). Together, a larger AL could be a somatic consequence of a “fast” PoLS due to reduced investment in body maintenance and repair.

The concept of “allostatic load” entails that an over-burdened stress-coping system, foremost the hypothalamic-pituitary-adrenal axis, causes the body to accrue negative consequences of maladaptive stress responses in the form of somatic disease (McEwen, 2000). Typical somatic marker for allostatic load comprises morphological parameters, such as the waist-to-hip ratio and body mass index (BMI), and blood serum markers, such as C-reactive protein, the ratio of low-density to high density lipoprotein (LDL/HDL ratio), and glycated hemoglobin (HbA1c), as well as systolic and diastolic blood pressure (DBP; Seeman et al., 2001).

In line with Life History Theory, elevated markers for allostatic load in people pursuing a “fast” PoLS can be predicted on the basis of the “disposable soma” hypothesis (Kirkwood and Rose, 1991). The disposable soma hypothesis is similar to the “antagonistic pleiotropy” hypothesis, suggesting that investment in reproduction early in life may be related to earlier deterioration of body functions and senescence due to lower investment in maintenance and repair of tissue damage (Hammers et al., 2013).


In summary, current evidence seems to suggest that many features associated with BPD are consistent with characteristics of a fast PoLS (Brüne, 2016; Dammhahn et al., 2018). However, to the best of our knowledge, no study has directly examined LHS in BPD using specific scales designed for this purpose (Figueredo, 2007), measures of physical and mental health in relation to childhood adversity and stress exposure. From a clinical and public health perspective, such insights could be highly relevant in relation to early detection of risk factors for the development of emotionally instability and prevention of poor outcome of BPD.

Accordingly, we sought to explore the PoLS of a female cohort of BPD, how this relates to the exposure to early adversity, current stress perception, and physical health. Specifically, we (1) hypothesized that individuals with BPD would typically display features of a fast PoLS, relative to a control group not affected from the disorder (2) We also expected that a faster PoLS would be statistically predicted by childhood adversity as a causal factor driving this development, and (3) that the clinical group would display a higher allostatic load as an indicator of poor body maintenance and tissue repair.

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Source: University of Toronto


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