Borderline in a linear city: Urban living brings borderline personality disorder to crisis through neuroplasticity—an urgent call to action
Year: 2025
Type: article
Abstract: Since its identification in the late 1930s by the American psychiatrist and psychoanalysis Adolph Stem (Stem, 1938), there has been a steeper increase in borderline personality disorder (BPD) only over the past few years (Min et al., 2023). BPD is found in around 1.7% of the general population but in 15-28% of patients in psychiatric clinics or hospitals and in a large proportion of individuals seeking help for psychological problems as reported in general health facilities (Gunderson et al., 2018). BPD is one of the most complex disorders to date characterized by sudden shifts in identity, interpersonal relationships, impulsive behaviour, periodic intense anger, the feeling of emptiness, dissociative symptoms, and sometimes suicidal thoughts or behaviours (Leichsenring et al., 2023). BPD results in severely poor outcomes from low occupational and educational attainment to disturbed and unsustainable relationships (Bohus et al., 2021). BPD can be genetic, but the risk of developing BPD can also be environmental, which this article shows that it may not only be due to an unhealthy social environment as commonly perceived, but also due to the physical environment to a great extent.The critical problem is that BPD is often untreatable, which urges a critical exploration of the silent physical environment variables triggering BPD and pushing it to a critical risky crisis. Leichsenring et al. (2024) have recently explained that up to 96% of patients with BPD seek treatment receive at least one psychotropic drug (Bridler et al., 2015), and 19% of BPD patients report taking four or more psychotropic drugs (Zanarini et al., 2015). No class of psychoactive medications has been proven to be consistently effective, and no medication has been proven for that (Gartlehner et al., 2021). Leichsenring et al. (2024) further explained that pharmacotherapy is not recommended for the treatment of any core symptom of BPD but only addresses discrete and severe depression, anxiety or psychotic symptoms for the shortest possible time and in crises. The complexity of the BPD symptoms and of effective psychoactive medication raises a critical need to understand this complexity at the brain level, specifically since the human brain is neuroplastic and continuously adapts to its environment. This is in line with the current research efforts where today neuroscience is interested in understanding the connection between the physical environment and mental health (Kühn & Gallinat, 2024) and exploring how the physical environment promotes sustainable adaptive neuroplasticity for mental health (Khalil, 2024a). However, to date, researchers only focus on the social environment to understand the gene-environment influences on BPD (Carpenter et al., 2013;Distel et al., 2010;Wilson et al., 2021), but a plethora of evidence, presented shortly in this paper, suggests that the physical environment, particularly urbanism, can be the silent trigger and chronic worsener for BPD patients or subjects with genetic predisposition. By the early 20th century, when BPD was formally identified, cities, particularly in the United States and England, were undergoing rapid expansion. This may make it unsurprising that the evidence presented in this article explains the adverse effects of urban living on triggering BPD and driving it to a crisis. This article adopts a novel perspective to prevent triggering BPD in populations with genetic predisposition, facilitate treatment of current BPD patients, reduce suicide, and also show how can the physical environment benefit the general population who may not be as vulnerable as BPD patients or genetically predisposed individuals. However, it will inevitably benefit from the insights presented in this paper.A comprehensive search for existing reviews was conducted using the Scopus database with no specific timeframe ranges or subject area limits. Firstly, the search was conducted using the keywords (("borderline personality disorder") AND (amygdala OR hippocampus OR cortex)). This is because, in many people with BPD, those three brain regions (amygdala, hippocampus, orbitofrontal cortex) are either smaller than expected or have unusual activity levels. The amygdala is responsible for emotional regulation, the hippocampus for behavioural regulation and self-control, and the orbitofrontal cortex for planning and decision-making (United Kingdom National Health Service, 2022). The BPD symptoms introduced earlier are strongly associated with the functions of those affected brain regions. Secondly, due to the rising interest in promoting neurosustainability through the physical environment by focusing on the same three brain regions (amygdala, hippocampus, cortex) (Khalil, 2024a), further research was conducted using Scopus on the impact of both built environment and natural environment on the three identified brain regions to observe any potential association with the maladaptive plasticity outcomes observed in people with BPD in the first search through Scopus. The search primarily focuses on studies conducting brain scans, while supplementary studies using EEG are searched for and introduced when combined with MRI or relevant to enriching the discourse. The following sections discuss BPD in the brain, urbanicity and maladaptive plasticity outcomes related to maladaptive plasticity in people with BPD, nature-driven neurosustainability for adaptive neural responses and potentially reduced symptoms, and last but not least, presenting final thoughts with potential implications and limitations at the urban, architectural and interior scales.The body of literature on the intersection of neuroscience with BPD is extensive, beginning in the early twenty-first century, but despite the strong identification of the key brain regions with maladaptive neuroplasticity, the main BPD problem remains unresolved, and more BPD patients are not responding to therapy.In the first decade of the millennium, several neurological studies emerged that were reviewed by multiple researchers who helped understand the neurological underpinnings of BPD. New & Siever (2002) discussed how impulsive aggression in BPD involves the lack of the prefrontal orbital cortex exerting an inhibitory control over aggressive behaviours in normal individuals. Teicher et al. (2002) show that severe early stress is one of the factors having the potential to alter brain development, potentially leading to attenuated development of the left neocortex, hippocampus and amygdala that all increase the risk of developing several mental health problems, including but not limited to BPD. Saper et al. (2002) reported that women patients with BPD have reduced hippocampal volume along with hypermetabolism in the premotor, prefrontal, and anterior cingulate cortex. Sala et al. (2004) showed in their review that BPD may suffer hippocampal atrophy as a result of stressors. McCloskey et al. (2005) also confirmed in their review that BPD is associated with a decrease in hippocampal volume. However, they also showed that BPD is associated with increased amygdala activation of general (though not personal) emotional stimuli, along with prefrontal hypermetabolism and functional dysregulation. Geuze et al. (2005) also confirmed in their review the relationship between BPD and reduced hippocampal volume. Brendel et al. (2005) have reviewed the evidence for dysfunction in certain frontolimbic regions that lead to a mechanistic model of symptom formation in BPD, proposing that future neuroimaging studies of BPD should encompass multilevel observations including not only the structural but also functional dynamics among others. On the contrary, Ivanovski & Malhi (2007) have shown that mindfulness-based therapeutic interventions were evidenced using fMRI and EEG studies to be effective in the treatment of multiple psychiatric conditions, including but not limited to BPD. New et al. (2008) followed up to show that the promising findings in BPD suggest that a diminished top-down control of affective responses is probably associated with the decreased responsiveness of midline regions of the prefrontal cortex that underlie the affective hyperresponsiveness in BPD. A meta-analysis confirmed the smaller volume found in both the right and left hippocampus and amygdala of BPD patients (Nunes et al., 2009). Zimmerman & Choi-Kain (2009) questioned whether the hypothalamic-pituitary-adrenal (HPA) axis functions normally in BPD because the activation of the HPA axis occurs to coordinate both behavioural and physiological responses to stress, showing through their review the possibility of developing an HPA-axis dysfunction in BPD.The last decade continued to build up on neuro evidence that existed by that time, beginning with a clearer synthesis (Dell'Osso et al., 2010), and confirming earlier findings (Hall et al., 2010) before further research started exploring the neural underpinnings in more detail. The beginning is with a review by Wingenfeld et al. (2010), who discussed that although stress seems to be associated with the development of BPD, the function of the HPA axis in BPD needed to be explored further, discussing it along with the hippocampus and amygdala and cortex patterns discussed previously. They hypothesised that BPD is characterized by a dysfunctional regulation of the HPA axis, disturbances of the serotonergic system, and the identified maladaptive patterns of the hippocampus, amygdala and cortex. A meta-analysis was published a couple of years later by Ruocco et al. (2012), aiming to evaluate whether the magnitude of the hippocampus and amygdala volume decreases and their associations with BPD, showing through 11 MRI-based studies that BPD patients showed an average of 11% and 13% decrease in the hippocampus and amygdala sizes, respectively, which is the minimum compared to earlier reports that it can even be up to 24% lower in the hippocampus volume and 20% in the amygdala volume (Schmahl et al., 2009). To explain before proceeding further, hippocampal volume and cell number reduced 20% -35% in patients with depression (Chen et al., 2020), which explains the depression symptoms in BPD. Another meta-analysis by de-Almeida et al. ( 2012) explained that the amygdalar volumes are reduced in patients with BPD, and this is confirmed in BPD patients without posttraumatic stress disorder (PTSD) but not in BPD patients with PTSD, concluding that comorbid PTSD cannot explain the reduced amygdalar volume in BPD patients. Besides the reduced hippocampal and amygdala volumes in patients with BPD, O' Neill & Frodl (2012) showed in their review an exaggerated amygdala activity in BPD patients when confronted with emotion-related stimuli. Mak & Lam (2013) showed in their review that EEG studies explain the right hemispheric deficit in high-order cortical inhibition in patients with BPD while confirming that the brain structures implicated in BPD are the hippocampus, dorsolateral prefrontal cortex and anterior cingulate cortex. Later studies shifted towards comparing the neurological underpinnings of BPD to other disorders until a systematic and integrative review was published by Ruocco & Carcone (2016), who discussed future directions including but not limited to gene x environment interactions, urging to explore novel applications of neuroscience findings to treatment research. Winsper et al. (2016) showed through their systematic review some evidence for gene x environment interactions in childhood and adolescence as well. BPD patients with a risk of committing suicide are evidenced to heavily have dysfunction in the fronto-tepomral primarily of and volumes in the prefrontal cortex anterior and et al., showing the critical of maladaptive neuroplasticity of those specific brain regions on and among BPD were also confirmed by later reviews et al., & Since most reviews earlier findings and show more et al., et al., et al., et al., & et al., et al., & 2021), but the main problem remains date, since the key understanding of suicidal thoughts and behaviours among BPD in to of and volumes in the and other the physical environment has been an in research. By the time no more relevant research for BPD in that was research on the impact of the environment and on neuroplasticity has been a plethora of neuroscience evidence on how the urban environment heavily influences maladaptive plasticity brain plasticity is proven to activity the and amygdala with the of prefrontal orbitofrontal anterior cingulate cortex and dorsolateral prefrontal cortex along with functional between and prefrontal regions & the that on and drugs for a to the that a large population is not responding to for BPD et al., 2021), that the physical environment is the in the when it to BPD The sections explain how those insights on neuroplasticity explain that BPD patients are at risk in urban how natural and complexity can adaptive neuroplasticity for BPD patients, and the recommended to an of research on with BPD, showing that specific brain regions explain the complexity of BPD. This the physical environment variables associated with those brain regions and how the environment can a of adaptive or maladaptive the in regions showed right amygdala volumes compared to up in (Kühn et al., 2020), while et al. later that the of and not even urban was associated with amygdala several key studies can be on to that the urban environment can trigger emotional in BPD at multiple through chronic of the studies by et al. showed that living was associated with increased amygdala A compared of and showing that a in urban and natural in the amygdala activation the in a but it remains the in an urban environment, urging urban planning to more to urban to benefit mental health et al., 2022). 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(2024) showed that people who in increased in the right anterior cingulate cortex those studies the of to and for the of triggering BPD in people with genetic and of a adaptive neuroplasticity the of but most where and volumes can BPD to the risk of suicide, some variables are strongly evidenced to be associated with neuroplastic in both the and et al. (2024) show that to was associated with brain and the on presented by et al. that to in to the of is critical towards suicidal among patients with BPD on the earlier the synthesis of the neuroplasticity dynamics urban living and is to that the complexity of BPD from the complexity of adverse effects from hippocampal amygdala atrophy and reduced in the prefrontal and and this article explains BPD is medications and & 2010) when the complexity of neuroplasticity is BPD complex and that this complexity is by multiple variables in the physical environment, particularly urban for the explained and in article strongly that the physical environment is a triggering for BPD in patients with genetic and the should from childhood and to triggering BPD and adaptive early development of the brain regions associated with hippocampus and to the environment where those regions show dysfunction for a chronic to BPD symptoms and can lead to and that may to suicide in BPD. is not to treatment at the level, but the in BPD will the environment in the of on a or while drugs the depression and anxiety symptoms, will only to with the adverse effects by the urban environment. BPD cannot without efforts from health the American and on the one to urban urban and even interior on the other while BPD patients should have more the physical environment impact through and the adverse of urban living on BPD BPD from and which are among BPD et al., et al., et al., urging to the main which is how urban living is triggering BPD and driving it to a crisis. BPD patients and their or often with structural specific to BPD remains in health by factors in and including and and of a to et al., 2022). health has been for a few years to BPD as a severe mental health disorder at all a need for an to BPD et al., which this article not only strongly and with but also the with for and adaptive treatment through the discussed triggering interactions from genetic to behaviours BPD is The of BPD treatment et al., an to perspective health through the dynamics to current treatment with the current This article strongly the need for a more of BPD et al., urging an of the impact of and of is recommended to the of the factors BPD to physical factors as childhood and which are all but the of the physical environment to be are to the chronic impact of the physical environment on BPD patients they medication for the complex symptoms the it was found that and were not to consistently reduce the of BPD (Gartlehner et al., 2021). The presented in this article is that medication will consistently the adverse effects of the physical environment on the neuroplasticity of the amygdala volume and hippocampus and cortex of and combined it is that the BPD may have a sustainable benefit from treatment without taking the impact of the physical more than to with BPD patients more To date, and are the most by with BPD patients, and both are effective to a great et al., et al., 2023). focuses on the & while a therapeutic in the of suicidal thoughts and the of and in BPD et al., but as as the results a of those symptoms, living in an urban environment that to the and as explained due to the lack of and lack of cannot prevent those BPD patients may their or but their to their physical environment is chronic and is which neuroplasticity and the risk of than of BPD patients have been reported to while suicide are to be as as which is than in the general population et al., & urging to for to more as of the using either or health and are to existing BPD urban urban and interior are to by from triggering BPD and the symptoms for current BPD patients to an that can to are to be that their have neuroplasticity outcomes not only for BPD patients but also the general but BPD is more as explained in this that urban increased the around the et al., to be by complex et al., in to increase the of the hippocampus volume in to and the right hippocampus volume in to and also in the environment. urban with a of and is also promising for the hippocampus volume as by evidence et al., urging and planning to this & 2021). also the of from it was proven to be with and due to the of can increase the risk of BPD committing suicide in to the adverse planning should this et al., a key in the of urban planning and for BPD and treatment through the environment. that urban need to in and specifically but with a of through the of as as through the of and of is to reduce amygdala insights to the identified urban on et al., to the interest in and et al., to exploring health outcomes on & and to showing more of promoting in urban on and further the of et al., et al., from and in to as this is effective in the early development brain can with more can trigger or prevent BPD development through the neuroplasticity by the can prevent BPD triggering and facilitate treatment of existing BPD patients in several Firstly, with or can be but it also to adaptive and have been explored recently et al., et al., and et al., et al., 2021). Secondly, can to on of and and complexity et al. (2024) conducted a the impact of architectural on that to with of may result in decreased which as evidence to explain the for BPD due to having increased of stress and in to reduced of the et al., 2023). in to increase the of research shows that architectural promoting more physical activity through their can increase (Khalil, and that the by natural can the increase (Khalil, how can prevent BPD and reduce its symptoms is and to be in multiple as to were recently shown to increase the of depression, anxiety and compared to of the & how to prevent triggering and its symptoms, evidence can suggest at the interior as well. or individuals who their are to the of or that can lead to increased that to an increased risk of et al., which was explained earlier as critical for BPD This should also be to On the contrary, the of or compared to in interior can effects physiological stress through a in the right et al., of the also to but the outcomes of those may not be as risky as for BPD. will BPD patients, triggering BPD in genetically predisposed and the health of individuals. BPD patients and the with genetic are to increase time in natural as and until the of the the adverse neuroplasticity and main limitations at this Firstly, of the evidence is only expected to increase the BPD behavioural Secondly, the on the or without of BPD and its trigger has not only to be through a social environment but also to a physical environment from the beginning and but not least, while most presented evidence is explained using brain scans, EEG are et al., et al., 2020), a of that can be by BPD patients and individuals with genetic to be to risk and observe mental health need to with that the of urban This may the severe amygdala atrophy in BPD are to and from the while are to and interior should natural or of in interior and interior or using and in and and interior should and not with should around the are to more while are to the novel of for physical activity through structural of the are to increase complexity to increase the of right hippocampal and for the to the to around the and need to and urban should and and impact of the physical environment on BPD need not be or for as urban living through neuroscience evidence to be in relationship with BPD. urban living variables are proven in this to the adverse neuroplasticity outcomes for the hippocampus and cortex that the complexity of BPD and make it not only due to its complexity but because the physical environment not the crisis. the needed in this efforts are needed by and where the for borderline personality disorder at the of their
Source: Frontiers in Psychiatry
Author: Mohamed Hesham Khalil
Institution: University of Cambridge
Language: English
Subfield: Clinical Psychology
Field: Psychology
Domain: Social Sciences
Open Access status: gold
Estimated APC paid: $3,801
OpenAlex ID: W4406083712