Borderline personality disorder

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Question Description

1.In this part of the comprehensive project, students will select a research question of their choosing. It is best to find one that interests you, however, it is also permissible to simply be creative. The research questions should be unique, not simply a retesting of a known hypothesis or result that already exists in the field.

2.Students will submit a 3 page explanation of what the research question is along with a formal hypothesis. Students should be able to articulate why they chose this particular topic.

3. APA style

4. Great grammar and punctuation.

5. APA references page

I think we have to write why this is something I would like to do.

(why)-> recently I became closer to borderline personality disorder while my best friend was just diagnosed. So that s why.

SO, I found two nice article about Borderline personality disorder, now. My question is that.

https://patch.com/california/carlsbad/bp--how-moth...

you can also go and see other resources.

IT's ok if you will pick up some hypothesis based on that articles, I was thinking about trauma (MOTHER VS CHILD), but there is already research showing that that Borderline mother is easly to pass down border. Line. Pers. Disor. What about healthy mothers, how that is happening that children from NON borderline Mother have Borderline personality disorder. How the trauma occur, in what stage exacly, etc. I also think right now, what kind of laving cause borderline (main factor for borderline is that they are scare to being abandoned.

What do you think>??

If there is anything you come up with after reading articles let me know, so I can accept it and than you can write this for me,

I need help.

THAnks

IF not

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Cattane et al. BMC Psychiatry (2017) 17:221 DOI 10.1186/s12888-017-1383-2 DEBATE Open Access Borderline personality disorder and childhood trauma: exploring the affected biological systems and mechanisms Nadia Cattane1, Roberta Rossi2, Mariangela Lanfredi2 and Annamaria Cattaneo1,3,4* Abstract Background: According to several studies, the onset of the Borderline Personality Disorder (BPD) depends on the combination between genetic and environmental factors (GxE), in particular between biological vulnerabilities and the exposure to traumatic experiences during childhood. We have searched for studies reporting possible alterations in several biological processes and brain morphological features in relation to childhood trauma experiences and to BPD. We have also looked for epigenetic mechanisms as they could be mediators of the effects of childhood trauma in BPD vulnerability. Discussion: We prove the role of alterations in Hypothalamic-Pituitary-Adrenal (HPA) axis, in neurotrasmission, in the endogenous opioid system and in neuroplasticity in the childhood trauma-associated vulnerability to develop BPD; we also confirm the presence of morphological changes in several BPD brain areas and in particular in those involved in stress response. Summary: Not so many studies are available on epigenetic changes in BPD patients, although these mechanisms are widely investigated in relation to stress-related disorders. A better comprehension of the biological and epigenetic mechanisms, affected by childhood trauma and altered in BPD patients, could allow to identify “at high risk” subjects and to prevent or minimize the development of the disease later in life. Keywords: Borderline personality disorder, Childhood trauma, HPA axis, Endogenous opioid system, Neurotransmission, Neuroplasticity, Neuroimaging studies, Epigenetic mechanisms Background Borderline Personality Disorder (BPD) is a pervasive pattern of emotional dysregulation, impulsiveness, unstable sense of identity and difficult interpersonal relationships [1]. The prevalence rates of BPD are between 0.2–1.8% in the general community, 15–25% among psychiatric inpatients and 10% of all psychiatric outpatients [2, 3]. Among the different aetiopathological theories that have been proposed over years, the most supported is the one proposed by Linehan in 1993 [4], which suggests that BPD can be the result of the interactions between * Correspondence: annamaria.cattaneo@kcl.ac.uk; acattaneo@fatebenefratelli.eu 1 Biological Psychiatry Unit, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, via Pilastroni 4, Brescia, Italy 3 Stress, Psychiatry and Immunology Laboratory, Department of Psychological Medicine, Institute of Psychiatry, King’s College London, 125 Coldharbour Lane, London SE5 9NU, UK Full list of author information is available at the end of the article biological and psychosocial factors [2], in particular between biologically based temperamental vulnerabilities and adverse and traumatic experiences during childhood. BPD is a disorder primarily characterized by emotion dysregulation and indeed, patients with BPD show heightened emotional sensitivity, inability to regulate intense emotional responses, and a slow return to emotional baseline. Linehan proposed also that the development of BPD occurs within an invalidating developmental context characterized by intolerance toward the expression of private emotional experiences during childhood [4]. As a consequence, children exposed to this adverse environment show inability to learn how to understand, label, regulate, or tolerate emotional responses and, conversely, they vacillate between emotional inhibition and extreme emotional lability. Recently, Hughes and colleagues [5] have proposed an integration to the aethiopathogenetic model of BPD, © The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Cattane et al. BMC Psychiatry (2017) 17:221 emphasizing the role played by a lack of social proximity or responsiveness from relevant caregivers in the development of BPD symptoms, which in turn impairs the individual’s emotion regulation. Affect regulation difficulties have been also proposed as key mediators in the relationship between childhood trauma and BPD [6]. Several studies have shown that a diagnosis of BPD is associated with child abuse and neglect more than any other personality disorders [7, 8], with a range between 30 and 90% in BPD patients [7, 9]. Adverse childhood experiences are also related to BPD symptom severity [9–11]. In support to this, Widom and collaborators [12] followed 500 children who had suffered physical and sexual abuse and neglect and 396 matched controls, and they observed that significantly more abused/neglected children met criteria for BPD in adulthood in comparison to controls. However, the presence of a risk factor, such as adverse childhood events, was not necessary or sufficient to explain the reason why some individuals developed BPD symptoms in adulthood, whereas others did not. In a recent study, Martin-Blanco and collaborators [10] have hypothesized that the interaction of childhood trauma and temperamental traits could be associated with the severity of BPD. In this regard, they have evaluated the self-reported history of trauma, the psychobiological temperamental traits and the severity of the BPD symptoms in a cohort of 130 BPD patients. Data showed a correlation only between childhood maltreatment and sociability and no other correlation was observed. Moreover, the interaction between high neuroticism-anxiety traits and the presence of severe emotional abuse was associated with the severity of the disorder. Symptom overlap has been reported between BPD diagnosis and other disorders including Post-Traumatic Stress Disorder (PTSD) and other axis I disorders [13]. Moreover, in recent decades, different nosographic descriptions have been suggested to characterize the different symptoms associated with trauma, like complex Post-Traumatic Stress Disorder (cPTSD) [14], also known as Disorders of Extreme Stress Not Otherwise Specified (DESNOS) [15], which describes a clinical syndrome following an experience of interpersonal traumatic victimization and shares many similarities with BPD, including pathological dissociation, somatizations, dysregulation of emotions, altered central self and relational schemas. The definition of cPTSD therefore refers to the experience of severe and/or prolonged traumatic situations, and does not merely identify the effects of devastating traumatic events (like violence or chronic maltreatment), which fall under the category of PTSD or Acute Stress Disorder. Indeed, exposure to particular types of traumatic experiences may result in far more insidious and crippling psychopathogenic disorders than Page 2 of 14 PTSD, compromising the sound development of attachment behavior related systems and of the ability to modulate emotions [16]. Recent research is currently trying to determine whether cPTSD and BPD diagnosis in comorbidity with PTSD are distinct or should both be considered and named as trauma-related disorders [17]. A recent review [18] has explored the mechanisms through which childhood trauma is related to the development of BPD in adulthood, and has discussed how interrelated factors (such as heritable personality traits, affect regulation and dissociation, trauma symptoms) could be mediators in the relationship between childhood trauma and BPD. Based on all these findings, in the following paragraphs we will discuss alterations in several neurobiological systems and in brain morphology that can be induced by exposure to early life adverse experiences and that are also associated with BPD (see Table 1). We will examine the impact of early stressful events on different biological systems and mechanisms, possibly identifying biomarkers that could be involved in BPD vulnerability. This might allow to identify at high risk BPD subjects earlier, and to develop intervention strategies and programs. Discussion Neurobiological mechanisms involved in BPD BPD and the hypothalamic-pituitary-adrenal axis The Hypothalamic-Pituitary-Adrenal (HPA) axis is one of the neuroendocrine systems which mediate the response of the body to stress. Although the stress response mechanism is meant to maintain stability or homeostasis, its long-term activation, as consequence of chronic stress exposure, may have deleterious effects on the body, increasing the risk for developing different kinds of illnesses, including stress-related psychiatric disorders. In stress conditions, corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) are released from the paraventricular nucleus (PVN) located in the hypothalamus. These peptides travel through the pituitary portal system and act synergistically to stimulate the release of the adrenocorticotropic hormone (ACTH) from the corticotroph cells. Then, ACTH is transported throughout the systemic circulation and binds to receptors in the adrenal cortex of the adrenal gland, resulting in the biosynthesis and release of cortisol [19]. Cortisol can affect multiple organs and biological processes, such as metabolism, growth, inflammation, cardiovascular function, cognition, and behavior [20, 21], by binding to specific receptors in the body and in several brain regions, as the hypothalamus, anterior pituitary and medial prefrontal cortex. The central and peripheral effects of cortisol are mediated by two intracellular glucocorticoid receptor subtypes: the high-affinity type I receptor or Cattane et al. BMC Psychiatry (2017) 17:221 Page 3 of 14 Table 1 Summary of the papers cited in the review and showing alterations in different biological systems in BPD Biological systems Authors Sample size Date of study Main Results HPA axis Southwick et al. [26] 37 subjects with PTSD comorbid with BPD; 18 subjects only with PTSD 2003 Higher 24 h urinary cortisol levels in patients with PTSD compared to patients with PTSD and comorbid BPD. Wingenfeld et al. [27] 21 female patients with BPD; 24 healthy female controls. 2007 Higher overnight urinary cortisol levels in BPD patients compared to controls. Very high cortisol levels were found only in BPD patients with a low number of PTSD symptoms. Rinne et al. [28] 39 BPD patients (24 with and 15 without sustained childhood abuse and comorbid PTSD (n = 12) or MDD (n = 11)); 11 control subjects 2002 Higher ACTH and cortisol levels in the blood of BPD females who had experienced childhood abuse during the DEX/CRH test. Carvalho Fernando et al. [29] 32 female BPD patients; 32 healthy female 2013 Acute cortisol levels decreased the reaction time to target stimuli in both BPD patients and controls. Martin-Blanco et al. [30] 481 subjects with BPD; 442 controls 2016 Case-control study focusing on 47 SNPs in 10 HPA axis genes. An association between polymorphic variants within the FKPB5 and the CRHR genes with the diagnosis of BPD was shown. Two FKBP5 SNPs were more frequently represented in patients with a history of childhood trauma. Wagner et al. [42] 159 BPD patients 2009 Association between stressful events and low impulsivity in BPD patients. 5-HTTLPR S-allele carriers showed higher impulsivity scores when exposed to stressful events than LL omozygotes. Wagner et al. [47] 112 female BPD patients 2010 COMT Val158Met SNP was associated with early life stressful events and impulsive aggression in female BPD patients Wagner et al. [48] 159 BPD patients 2010 The effect of COMT Val158Met SNP on the association between stressful life events and impulsivity was not confirmed. Tadic et al. [49] 161 Caucasian BPD patients; 156 healthy controls. 2009 The COMT Met158Met SNP was over-represented in BPD patients compared to controls. No differences in 5-HTTLPR genotype were found. An interaction between the COMT Met158 and the 5-HTTLPR s-allele was observed. Martin-Blanco et al. [50] 481 BPD subjects; 442 controls 2015 Genetic variants within COMT, DBH and SLC6A2 genes were associated with an enhanced risk to develop BPD 8 infant rhesus monkeys (4 males and 4 females) 1988 The endogenous opioid system mediates separate-induced vocalizations and influences the HPA axis activation in rhesus monkeys using the mother-infant separation paradigm. Prossin et al. [61] 18 un-medicated female BPD patients; 14 female controls 2010 BPD patients had greater regional μ-opioid availability at baseline in the left necleus accumbens, the hypothalamus and the right hippocampus/parahippocampus relative to controls, showing an endogenous opioid system activation. Driessen et al. [36] 21 female BPD patients; 21 female controls 2000 Volume reduction in the hippocampus and in the amygdala in BPD patients compared to controls. Schmahl et al. [38] 25 unmedicated female patients 2009 with BPD (10 with and 15 without comorbid PTSD); 25 female controls Hippocampal volume reduction in patients with BPD and comorbid PTSD as compared to controls. Neurotransmission Endogenous Opioid Kalin et al. [57] System Neuroimaging studies Cattane et al. BMC Psychiatry (2017) 17:221 Page 4 of 14 Table 1 Summary of the papers cited in the review and showing alterations in different biological systems in BPD (Continued) Epigenetics Neuroplasticity Kreisel et al. [70] 39 BPD patients; 39 controls 2014 Smaller hippocampal volume in BPD patients with a lifetime history than those without comorbid PTSD. Boen et al. [71] 18 women with BPD; 21 controls 2014 Two hippocampal structures (DG-CA4 and CA2–3 subfields) were significantly smaller in patients with BPD than controls. Kuhlmann et al. [73] 30 BPD patients; 33 controls 2013 Patients with BPD showed lower hippocampal volumes than controls, but higher volumes in the hypothalamus. Rodrigues et al. [63] 124 BPD patients; 147 controls 2011 Both the left and the right sides of the hippocampus were reduced in BPD patients with PTSD when compared to controls. Ruocco et al. [37] 205 BPD patients; 222 controls 2012 Bilateral volume reductions of the amygdala and hippocampus were not related to comorbid MDD, PTSD or substance use disorders. Martin-Blanco et al. [88] 281 subjects with BPD 2014 An association between NR3C1 methylation levels and childhood trauma was found in blood samples of BPD patients. Dammann et al. [89] 26 BPD patients; 11 controls 2011 An increase in the methylation levels of HTR2A,NR3C1,MAOA,MAOB and COMT was found in BPD patients as compared to controls. Perroud et al. [91] 346 BD, BPD, and ADHD patients 2016 Differential 5-HT3AR methylation levels were associated with the severity of childhood trauma, mainly found in BPD patients. Teschler et al. [93] 24 female BPD patients; 11 female controls 2013 Genome-wide methylation analyses revealed increased methylation levels of several genes (APBA2,APBA3,GATA4,KCNQ1,MCF2,NINJ2, TAAR5) in blood of BPD female patients and controls. Prados et al. [94] 96 BPD subjects suffering from a high level of child adversity; 93 subjects suffering from MDD and reporting a low rate of child maltreatment 2015 Several CpGs within or near genes involved in inflammation and in neuronal excitability were differentially methylated in BPD patients compared to MDD patients or in relation to the severity of childhood trauma. Teschler et al. [95] 24 female BPD patients; 11 female controls 2016 A significant aberrant methylation of rDNA and PRIMA1 was revealed for BPD patients using pyrosequencing. For the promoter of PRIMA1, the average methylation of six CpG sites was higher in BPD patients compared to controls. In contrast, the methylation levels of the rDNA promoter region and the 5′ETS were significantly lower in patients with BPD compared to controls. Koenigsberg et al. [109] 24 medication-free BPD patients; 18 healthy control subjects 2012 Decrease of PKC and BDNF protein levels in the blood of BPD patients. Tadic et al. [49] 161 Caucasian BPD patients; 156 healthy controls. 2009 Association between HTR1B A-161 variant and the functional BDNF 196A allele in BPD patients. Perroud et al. [90] 115 subjects with BPD; 52 controls 2013 Higher methylation levels in BDNF CpG exons I and IV in BPD patients than in controls. Higher BDNF protein levels in plasma of BPD patients than in controls. Thaler et al. [92] 64 women with bulimia nervosa and comorbid BPD; 32 controls 2014 Hypermethylation within BDNF promoter region sites in women with bulimia nervosa and with a history of BPD and/or trauma events. mineralcorticoid receptor (MR) and the low-affinity type receptor or glucocorticoid receptor (GR). It has been suggested that MRs have a high affinity for both cortisol and aldosterone; they bind cortisol when it is detectable at low concentrations. The GRs have a relatively low affinity for cortisol, but high affinity for dexamethasone (DEX) [22]; moreover, they bind cortisol at high concentration, reflecting what occurs in stress conditions. The HPA axis is regulated by an auto-regulatory mechanism mediated by cortisol itself, that is crucial in the maintenance of the homeostatic functions of the HPA axis. Indeed, when cortisol levels rise, as in Cattane et al. BMC Psychiatry (2017) 17:221 response to stress, the MRs are saturated and, consequently, cortisol binds the GRs, promoting a cascades of events that represent the main transduction signals of glucocorticoids in stress conditions. So far, the HPA axis activity has been widely investigated in the context of childhood trauma experiences and findings support alterations in HPA axis in subjects exposed to stress early in life. Indeed, several studies have reported alterations in the cortisol circadian rhythm and levels, indicating a deregulation of the HPA axis responsiveness, due to childhood trauma experiences, upon stress conditions [23–25]. Despite the large amount of data on the HPA axis functionality as consequence of exposure to stress early in life, only a few studies have investigated possible alterations of this axis in BPD patients. For example, higher urinary cortisol levels have been found in BPD patients compared to controls [26, 27]. Southwick and colleagues [26] found higher 24 h urinary cortisol levels in patients with PTSD compared to patients with PTSD and comorbid BPD, suggesting that these alterations might reflect differences in the severity of PTSD symptoms rather than factors related to BPD per se. Another study [27] explored overnight urinary free cortisol levels showing higher cortisol levels in BPD patients than in controls. A negative association between cortisol and PTSD symptoms was also observed. Moreover, when BPD patients were divided according to the presence of high or low number of PTSD symptoms, very high cortisol levels were found only in BPD patients with a low number of PTSD symptoms. Rinne and collaborators [28] found an exaggerated ACTH and cortisol response during the DEX/CRH test in the blood of BPD female subjects who had experienced childhood abuse. Carvalho Fernando and colleagues [29] investigated the effects of cortisol administration on response inhibition of emotional stimuli in patients with BPD compared to controls. They found that acute cortisol elevations decreased the reaction time to target stimuli in both BPD patients and controls, but they did not ...
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Tutor went the extra mile to help me with this essay. Citations were a bit shaky but I appreciated how well he handled APA styles and how ok he was to change them even though I didnt specify. Got a B+ which is believable and acceptable.

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