Editing Borderline personality disorder (section)

==Causes==<!-- This section needs its sub-headers redone and re-imagined. -->

The [[etiology]], or causes, of BPD is multifaceted, with no consensus on a singular cause.<ref name="mayo">{{cite web|url=http://www.mayoclinic.com/health/borderline-personality-disorder/DS00442/DSECTION=3|title=Borderline personality disorder|publisher=Mayo Clinic|access-date=15 May 2008|url-status=live|archive-url=https://web.archive.org/web/20080430112844/http://www.mayoclinic.com/health/borderline-personality-disorder/DS00442/DSECTION%3D3|archive-date=30 April 2008}}</ref> BPD may share a connection with [[post-traumatic stress disorder]] (PTSD), having both a traumatic substrate.<ref name="BPD & PTSD">{{cite journal|vauthors=Gunderson JG, Sabo AN|title=The phenomenological and conceptual interface between borderline personality disorder and PTSD|journal=The American Journal of Psychiatry|volume=150|issue=1|pages=19–27|date=January 1993|pmid=8417576|doi=10.1176/ajp.150.1.19}}</ref> While childhood trauma is a recognized contributing factor, the roles of congenital brain abnormalities, genetics, [[neurobiology]], and non-traumatic environmental factors remain subjects of ongoing investigation.<ref name="mayo" /><ref>{{cite journal|vauthors=Zanarini MC, Frankenburg FR|year=1997|title=Pathways to the development of borderline personality disorder|journal=Journal of Personality Disorders|volume=11|issue=1|pages=93–104|doi=10.1521/pedi.1997.11.1.93|pmid=9113824|s2cid=20669909}}</ref>

===Genetics and heritability===
Compared to other major psychiatric conditions, the exploration of genetic underpinnings in BPD remains novel.<ref name="pmid29032046">{{cite journal|vauthors=Bassir Nia A, Eveleth MC, Gabbay JM, Hassan YJ, Zhang B, Perez-Rodriguez MM|title=Past, present, and future of genetic research in borderline personality disorder|journal=Current Opinion in Psychology|volume=21|pages=60–68|date=June 2018|pmid=29032046|pmc=5847441|doi=10.1016/j.copsyc.2017.09.002}}</ref> Estimates suggest the [[heritability]] of BPD ranges from 37% to 69%,<ref name="Her2014">{{cite journal|vauthors=Gunderson JG, Zanarini MC, Choi-Kain LW, Mitchell KS, Jang KL, Hudson JI|date=August 2011|title=Family Study of Borderline Personality Disorder and Its Sectors of Psychopathology|journal=JAMA: The Journal of the American Medical Association|volume=68|issue=7|pages=753–762|doi=10.1001/archgenpsychiatry.2011.65|pmid=3150490|pmc=3150490}}</ref> indicating that [[human genetic variation]]s account for a substantial portion of the risk for BPD within the population. [[Twin study|Twin studies]], which often form the basis of these estimates, may overestimate the perceived influence of genetics due to the shared environment of twins, potentially skewing results.<ref>{{cite journal|vauthors=Torgersen S|title=Genetics of patients with borderline personality disorder|journal=The Psychiatric Clinics of North America|volume=23|issue=1|pages=1–9|date=March 2000|pmid=10729927|doi=10.1016/S0193-953X(05)70139-8}}</ref>

Certain studies propose that personality disorders are significantly shaped by genetics, more so than many [[Axis I disorders]], such as depression and eating disorders, and even surpassing the genetic impact on broad [[personality traits]].<ref name="TS" >{{cite journal|vauthors=Torgersen S, Lygren S, Oien PA, Skre I, Onstad S, Edvardsen J, Tambs K, Kringlen E|title=A twin study of personality disorders|journal=Comprehensive Psychiatry|volume=41|issue=6|pages=416–425|year=2000|pmid=11086146|doi=10.1053/comp.2000.16560}}</ref> A twin study found that BPD ranks as the third most heritable among ten surveyed personality disorders.<ref name="TS"  />

Research involving twin and sibling studies has shown a genetic component to traits associated with BPD, such as impulsive aggression; with the genetic contribution to behavior from [[serotonin]]-related genes appearing to be modest.<ref name="neurotrauma">{{cite journal|vauthors=Goodman M, New A, Siever L|title=Trauma, genes, and the neurobiology of personality disorders|journal=Annals of the New York Academy of Sciences|volume=1032|issue=1|pages=104–116|date=December 2004|pmid=15677398|doi=10.1196/annals.1314.008|bibcode=2004NYASA1032..104G|s2cid=26270818}}</ref>

A study conducted by Trull et al. in the Netherlands, which included 711 sibling pairs and 561 parents, aimed to identify [[genetic marker]]s associated with BPD.<ref name="Possible Genetic Causes">{{cite web|url=https://www.sciencedaily.com/releases/2008/12/081216114100.htm|title=Possible Genetic Causes of Borderline Personality Disorder Identified|publisher=sciencedaily.com|date=20 December 2008|url-status=live|archive-url=https://web.archive.org/web/20140501161311/https://www.sciencedaily.com/releases/2008/12/081216114100.htm|archive-date=1 May 2014}}</ref> This research identified a linkage to genetic markers on [[chromosome 9]] as relevant to BPD characteristics,<ref name="Possible Genetic Causes" /> underscoring a significant genetic contribution to the [[Variability (statistics)|variability]] observed in BPD features.<ref name="Possible Genetic Causes" /> Prior findings from this group indicated that 42% of BPD feature variability could be attributed to genetics, with the remaining 58% owing to environmental factors.<ref name="Possible Genetic Causes" />

Among specific genetic variants under scrutiny {{as of|2012|lc=y}}, the [[DRD4 7-repeat polymorphism]] (of the [[Dopamine receptor D4|dopamine receptor D<sub>4</sub>]]) located on [[chromosome 11]] has been linked to disorganized attachment, and in conjunction with the 10/10-repeat genotype of the [[dopamine transporter]] (DAT), it has been associated with issues with [[inhibitory control]], both of which are characteristic of BPD.<ref name="Brain Structure and Function">{{cite journal|vauthors=O'Neill A, Frodl T|title=Brain structure and function in borderline personality disorder|journal=Brain Structure & Function|volume=217|issue=4|pages=767–782|date=October 2012|pmid=22252376|doi=10.1007/s00429-012-0379-4|s2cid=17970001}}</ref> Additionally, potential links to [[chromosome 5]] are being explored, further emphasizing the complex genetic landscape influencing BPD development and manifestation.<ref>{{cite journal|vauthors=Lubke GH, Laurin C, Amin N, Hottenga JJ, Willemsen G, van Grootheest G, Abdellaoui A, Karssen LC, Oostra BA, van Duijn CM, Penninx BW, Boomsma DI|title=Genome-wide analyses of borderline personality features|journal=Molecular Psychiatry|volume=19|issue=8|pages=923–929|date=August 2014|pmid=23979607|pmc=3872258|doi=10.1038/mp.2013.109}}</ref><ref>{{Cite journal|last1=Bassir Nia|first1=Anahita|last2=Eveleth|first2=Matthew C.|last3=Gabbay|first3=Jonathan M.|last4=Hassan|first4=Yonis J.|last5=Zhang|first5=Bosi|last6=Perez-Rodriguez|first6=M. Mercedes|year=2018|title=Past, present, and future of genetic research in borderline personality disorder|journal=Current Opinion in Psychology|volume=21|pages=60–68|doi=10.1016/j.copsyc.2017.09.002|issn=2352-2518|pmc=5847441|pmid=29032046}}</ref>

===Psychosocial factors===
[[Empirical studies]] have established a strong [[correlation]] between [[adverse childhood experiences]] such as [[child abuse]], particularly [[child sexual abuse]], and the onset of BPD later in life.<ref>{{cite journal|vauthors=Cohen P|date=September 2008|title=Child Development and Personality Disorder|url=http://ereserve.library.utah.edu/Annual/PSY/6330/Crowell/child.pdf|journal=[[The Psychiatric Clinics of North America]]|volume=31|issue=3|pages=477–493, vii|doi=10.1016/j.psc.2008.03.005|pmid=18638647|archive-url=https://web.archive.org/web/20240531104923/http://ereserve.library.utah.edu/Annual/PSY/6330/Crowell/child.pdf|archive-date=2024-05-31|access-date=2025-01-08}}</ref><ref name="Herman91">{{cite book|url=https://archive.org/details/traumarecovery00herm_0|title=Trauma and recovery|vauthors=Herman JL|publisher=Basic Books|year=1992|isbn=978-0-465-08730-3|location=New York}}</ref><ref name="AxisOne/AxisTwo" /> Reports from individuals diagnosed with BPD frequently include narratives of extensive abuse and neglect during early childhood, though [[causality]] remains a subject of ongoing investigation.<ref>{{cite journal|vauthors=Ball JS, Links PS|date=February 2009|title=Borderline personality disorder and childhood trauma: evidence for a causal relationship|url=https://link.springer.com/article/10.1007/s11920-009-0010-4|journal=[[Current Psychiatry Reports]]|volume=11|issue=1|pages=63–68|doi=10.1007/s11920-009-0010-4|pmid=19187711|s2cid=20566309|url-access=subscription}}</ref> These individuals are significantly more prone to recount experiences of verbal, emotional, physical, or sexual abuse by caregivers,<ref>{{cite news|url=http://www.mayoclinic.org/diseases-conditions/borderline-personality-disorder/basics/risk-factors/con-20023204|title=Borderline personality disorder: Understanding this challenging mental illness|work=Mayo Clinic|access-date=5 September 2017|url-status=live|archive-url=https://web.archive.org/web/20170830054834/http://www.mayoclinic.org/diseases-conditions/borderline-personality-disorder/basics/risk-factors/con-20023204|archive-date=30 August 2017}}</ref> alongside a notable frequency of [[incest]] and loss of caregivers in early childhood.<ref name="failchild">{{cite journal|vauthors=Zanarini MC, Frankenburg FR, Reich DB, Marino MF, Lewis RE, Williams AA, Khera GS|year=2000|title=Biparental failure in the childhood experiences of borderline patients|url=https://guilfordjournals.com/doi/abs/10.1521/pedi.2000.14.3.264|journal=[[Journal of Personality Disorders]]|volume=14|issue=3|pages=264–273|doi=10.1521/pedi.2000.14.3.264|pmid=11019749|url-access=subscription}}</ref>

Moreover, there have been consistent accounts of caregivers [[Emotional validation|invalidating]] the individuals' emotions and thoughts, neglecting physical care, failing to provide the necessary protection, and exhibiting emotional withdrawal and inconsistency.<ref name="failchild" /> Specifically, female individuals with BPD reporting past neglect or abuse by caregivers have a heightened likelihood of encountering sexual abuse from individuals outside their immediate family circle.<ref name="failchild" /> Research also indicates that neurodevelopment variations such as [[autism]] spectrum traits, [[ADHD]], or [[highly sensitive people]] (HSP) may increase vulnerability to trauma and subsequent borderline personality organization.<ref>{{Cite journal|last1=Matthies|first1=Swantje D|last2=Philipsen|first2=Alexandra|year=2014|title=Common ground in Attention Deficit Hyperactivity Disorder (ADHD) and Borderline Personality Disorder (BPD)–review of recent findings|journal=Borderline Personality Disorder and Emotion Dysregulation|language=en|volume=1|issue=1|pages=3|doi=10.1186/2051-6673-1-3|issn=2051-6673|pmc=4739390|doi-access=free|pmid=26843958 }}</ref>

The enduring impact of chronic maltreatment and difficulties in forming [[secure attachment]]s during childhood has been hypothesized to potentially contribute to the development of BPD.<ref name="Dozier-1999">{{cite book|title=Handbook of attachment|vauthors=Dozier M, Stovall-McClough KC, Albus KE|publisher=[[Guilford Press]]|year=1999|veditors=Cassidy J, Shaver PR|location=New York|pages=497–519|chapter=Attachment and psychopathology in adulthood}}</ref> [[Marsha Linehan]]'s biosocial developmental theory posits that BPD arises from the interaction between a child's inherent emotional vulnerability and an invalidating environment – an environment characterized by the neglect, ridicule, dismissal, or discouragement of a child's emotions and needs.<ref>{{Cite journal|vauthors=Crowell SE, Beauchaine TP, Linehan MM|date=May 2009|title=A Biosocial Developmental Model of Borderline Personality: Elaborating and Extending Linehan's Theory|journal=[[Psychological Bulletin]]|volume=135|issue=3|pages=495–510|doi=10.1037/a0015616|pmc=2696274|pmid=19379027}}</ref>

===Brain and neurobiologic factors===<!-- Structural brain changes
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Research employing [[structural neuroimaging]] techniques, such as [[voxel-based morphometry]], has reported variations in individuals diagnosed with BPD in specific [[brain regions]] that have been associated with the [[psychopathology]] of BPD. Reductions in volume enclosed have been observed in the [[hippocampus]], [[orbitofrontal cortex]], [[anterior cingulate cortex]], and [[amygdala]], among others, which are crucial for [[emotional self-regulation]] and [[stress management]].<ref name="Brain Structure and Function" /><!-- Biochemical alterations
 --><!-- Alterations in glucose metabolism and brain oxygenation
 --><!-- Neurometabolites
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In addition to structural imaging, a subset of studies utilizing [[magnetic resonance spectroscopy]] has investigated the neurometabolic profile within these affected regions. These investigations have focused on the concentrations of various neurometabolites, including [[N-acetylaspartate|''N''-acetylaspartate]], [[creatine]], compounds related to [[glutamate]], and compounds containing [[choline]]. These studies aim to show the biochemical alterations that may underlie the symptomatology observed in BPD.<ref name="Brain Structure and Function" />

==== Neurological patterns ====
Research has shown changes in two [[brain circuits]] implicated in the emotional dysregulation characteristic of BPD: firstly, an escalation in activity within brain circuits associated with experiencing severe emotional pain, and secondly, a decreased activation within circuits tasked with the regulation or suppression of these intense emotions. These dysfunctional activations predominantly occur within the [[limbic system]], though individual variances necessitate further neuroimaging research to explore these patterns in detail.<ref name="Ruocco, Anthony C.; Amirthavasagam, Sathya, Choi-Kain, Lois W.; McMain, Shelley F. 2013 153–160">{{cite journal|vauthors=Ruocco AC, Amirthavasagam S, Choi-Kain LW, McMain SF|title=Neural correlates of negative emotionality in borderline personality disorder: an activation-likelihood-estimation meta-analysis|journal=Biological Psychiatry|volume=73|issue=2|pages=153–160|date=January 2013|pmid=22906520|doi=10.1016/j.biopsych.2012.07.014|s2cid=8381799}}</ref><!-- Seems this was inserted by someone related to study possibly for self-gain? -->

Contrary to earlier findings, individuals with BPD exhibit decreased amygdala activation in response to heightened negative emotional stimuli compared to control groups. John Krystal, the editor of ''[[Biological Psychiatry (journal)|Biological Psychiatry]]'', commented on these findings, suggesting they contribute to understanding the innate neurological predisposition of individuals with BPD to lead emotionally turbulent lives, which are not inherently negative or unproductive.<ref name="Ruocco, Anthony C.; Amirthavasagam, Sathya, Choi-Kain, Lois W.; McMain, Shelley F. 2013 153–160" /> This emotional volatility is consistently linked to disparities in several brain regions, emphasizing the neurobiological underpinnings of BPD.<ref name="Koenigsberg">{{cite journal|vauthors=Koenigsberg HW, Siever LJ, Lee H, Pizzarello S, New AS, Goodman M, Cheng H, Flory J, Prohovnik I|title=Neural correlates of emotion processing in borderline personality disorder|journal=Psychiatry Research|volume=172|issue=3|pages=192–199|date=June 2009|pmid=19394205|pmc=4153735|doi=10.1016/j.pscychresns.2008.07.010|quote=BPD patients demonstrated greater differences in activation than controls, when viewing negative pictures compared with rest, in the amygdala, fusiform gyrus, primary visual areas, superior temporal gyrus (STG), and premotor areas, while healthy controls showed greater differences than BPD patients in the insula, middle temporal gyrus and dorsolateral prefrontal cortex.}}</ref>

===Mediating and moderating factors<!-- These 'factors' are all causes anyway? Why not be part of causes, why their own 'mediating and moderating factors'? -->===

====Executive function and social rejection sensitivity<!-- Should likely be under Brain function -->====
High sensitivity to [[social rejection]] is linked to more severe symptoms of BPD, with [[executive function]] playing a mediating role.<ref name="Executive_function">{{cite journal|vauthors=Ayduk O, Zayas V, Downey G, Cole AB, Shoda Y, Mischel W|author-link6=Walter Mischel|title=Rejection Sensitivity and Executive Control: Joint predictors of Borderline Personality features|journal=Journal of Research in Personality|volume=42|issue=1|pages=151–168|date=February 2008|pmid=18496604|pmc=2390893|doi=10.1016/j.jrp.2007.04.002}}</ref> Executive function—encompassing [[planning]], [[working memory]], [[attentional control]], and [[problem-solving]]—moderates how rejection sensitivity influences BPD symptoms. Studies demonstrate that individuals with lower executive function exhibit a stronger correlation between rejection sensitivity and BPD symptoms.<ref name="Executive_function"/> Conversely, higher executive function may mitigate the impact of rejection sensitivity, potentially offering protection against BPD symptoms.<ref name="Executive_function"/>