I spoken about mentalization on this site before. Since I’ve lately been on a TED talk kick, mainly watching TED talks about neuroscience, I wanted to post this one from Rebecca Saxe which is called “How we read each other’s minds”. It is basically describing the process of mentalizing and how a certain part of the brain, the Right Temporo-Parietal Junction, is highly specialized for seeking to understand the motivations of others, the essence of mentalization. What is fascinating about this talk is her use of the pirate/cheese sandwich story with children of various ages. She demonstrates how the process of mentalization develops over time. I talked about another mentalization test (which is based on the same principles) in this post. I’d encourage all of my readers to watch this video. Although she doesn’t use the words mentalizing or mentalization, that is what she is describing. Additionally, I suppose that when someone with BPD experiences a “failure to mentalize”, that part of the brain is most likely dimmed.
Epigenetic inheritance of the negative impact of stressful events across generations
Depressive, impulsive and antisocial symptoms caused by severe chronic stress during childhood are transmitted epigenetically from one generation to the next. This has now been demonstrated by researchers at the University of Zurich and ETH Zurich.
Peter Rueegg
In human, chronic severe stress or traumatic experiences during childhood can lead to various psychological and mental disorders in adult life, such as borderline personality disorder and bipolar depression. A study carried out by a team under the supervision of the neuroscientist Isabelle Mansuy has used mice to demonstrate that such negative experiences can also have an impact on following generations. Mansuy holds a double professorship at the University of Zurich and ETH Zurich.
Stress during childhood, problems during adulthood
The scientists used mice as an experimental model, and exposed newborn pups to chronic and unpredictable maternal separation for two weeks. They also exposed the mother to additional unpredictable stress during the separation. This procedure was designed to induce extremely severe stress in the young mice, and is thought to simulate neglect and traumatic upbringing that children sometimes experience in uncaring, negligent or violent families. The young mice reacted so dramatically to the separation that they became depressive and impulsive as adult, and had social problems.
In particular, these animals were unable to deal appropriately with unfamiliar or adverse situations, and easily lost control of their behavior. For example, they lost their natural sense of caution when exploring new territories, and were no longer able to evaluate the potential risk of unfamiliar situations. They also reacted with apathy and despair in adverse conditions, and did not struggle for life in contrast to mice that grew up in normal conditions.
The traumatized mice retained these altered behaviours during their entire life and strikingly, «transmitted» these behaviours to their offspring. The researchers even provided evidence that transmission was across three generations, and that the offspring of that offspring was also affected.
Epigenetics determines behaviour
However, these behavioural changes are not attributable to mutations in the genetic make-up of the traumatized mice, since the genome is fixed and cannot be modified by stress. The researchers demonstrated that instead, stress interferes with the epigenome, in particular with the profile of methylation of certain genes in the brain and the sperm of male mice. This epigenetic plasticity is based on changes in chromatin structure, that alters the expression of the affected genes. In a way «Stress confuses the methylation machinery in the germline of the stressed pups, and the confusion persists and is transmitted», explains Isabelle Mansuy.
“Much of it comes from self-destructive behaviors that are used to stop the horrible pain of dysphoria; anxiety, rage, depression and despair. When an individual behaves out-of-control, in a manner that’s inconsistent with their beliefs or normal choices, terrible self-hate develops. Additionally many individuals had low self-esteem and related problems since childhood and are in an environment that causes self-hate to flourish.” – from the interview
Bon: I found an interview with Dr. Leland Heller about Borderline Personality Disorder. He does a good job explaining the pain associated with the disorder… Here are some excerpts. The entire interview can be read here.
Diagnosing Borderline Personality Disorder And Finding Treatment That Works
Dr Heller: Good evening, It’s great to be here. I have a way of explaining the Borderline Personality Disorder in layman’s terms that might be useful. It’s how I explain it to patients and their families.
Imagine you had a pet dog and it runs into the street and by accident it’s hit by a car. The dog’s leg is broken and it limps off into an alley to lick it’s wounds. A friend of yours sees the dog and comes over to help. The dog is now feeling trapped and cornered – a “wounded animal” – and misinterprets the friend’s attempts to help. The dog snaps at the friend’s hand who is trying to help. The BPD (Borderline Personality Disorder) is a malfunction in the brain’s trapped or “cornered” animal area. Under stress, a seizure develops in that area. That’s why under stress, while raging, a borderline will say to him or herself: “Why am I doing this” – yet be unable to stop it. It’s a seizure – nerve cells firing inappropriately and out of control.
David: And the cause of Borderline Personality Disorder?
Dr Heller: The BPD has many causes including head trauma and brain infections, but it appears that emotional hurts literally damage the brain. Most likely the brain’s support cells – the 90% of brain cells called “glial cells” – are damaged by traumas, causing the person to overreact to stress once puberty strikes. During puberty the brain’s limbic system goes into “overdrive” and adolescents are at their highest risk of seizures in their lifetime. “Sticks and stones may break my bones…but names cause brain damage.” So does incest, abuse, severe trauma, head injuries, attention deficit disorder, and other causes.
David: From my understanding, one of the biggest difficulties facing individuals who have BPD is maintaining stable relationships. This is a great cause of consternation for those people who are on the other side of the relationship. What causes this?
Dr Heller: There are a number of problems. The three most significant are 1) inappropriate mood swings; 2) misinterpretation of motives; and 3) remembering those misinterpreted motives as real. Oftentimes self-fulfilling prophecies occur, and self-hate eventually leads to a significant other coming to the same conclusion – that the individual isn’t worth being with.
…
janet: Would you please tell us more about the self-hate characteristic and how that damages the BPD or his/her relationships?
Dr Heller: Much of it comes from self-destructive behaviors that are used to stop the horrible pain of dysphoria; anxiety, rage, depression and despair. When an individual behaves out-of-control, in a manner that’s inconsistent with their beliefs or normal choices, terrible self-hate develops. Additionally many individuals had low self-esteem and related problems since childhood and are in an environment that causes self-hate to flourish.
crazy32810: How is self-injury related to BPD?
Dr Heller: We all injure ourselves to stop noxious neurological sensations. Interestingly we do it in a linear manner, ripping the skin. A common noxious neurological sensation is the toxins released with an insect bite. BPD dysphoria is about as bad as it gets. The pain is horrible. Many individuals have broken major bones and declared the pain of the fracture was nowhere as severe as dysphoria. When an individual with the BPD discovers that self-mutilation, or other techniques of self injury, work to temporarily stop the pain of dysphoria – they’ll do what it takes to stop it. This is no different than the individual with a fracture wants pain medication. I broke my shoulder last December and I tried to deal with it without taking narcotics. I was foolish and wrong. The pain was so bad it needed to be treated medically. Once individuals with the BPD have their chronic symptoms stabilized, and have safe medication options that work for dysphoria, the self-destructive patterns are no longer needed to stop their pain.
Neurobiology Informs Successful Psychotherapy for BPD
Mark Moran
A common feature of all psychotherapies for borderline personality disorder is activation of the prefrontal cortex through reappraisal of painful affect states generated by a hyperactive amygdala.
Neurobiological research can help psychotherapists tailor talking therapies to the individual characteristics of patients with borderline personality disorder (BPD).
That’s what Glen Gabbard, M.D., told psychiatrists at this year’s APA annual meeting in Honolulu in an address titled, “Neurobiologically Informed Psychotherapy of Borderline Personality Disorder.”
A prominent psychoanalyst and psychodynamic therapist, Gabbard said he believes the theoretical constructs of psychoanalysis—drives and conflicts—find expression in, and can be interpreted within, a patient’s individual neurobiology. “You can see psychoanalytic meaning at the same time you are looking at biology,” he said. “This was the dream of Freud, to build bridges between psychoanalytic concepts and a neurobiological science of the brain.”
He is the Brown Foundation Professor of Psychoanalysis and professor and director of the Baylor Psychiatry Clinic.
In the case of BPD, Gabbard stressed the role of hyper-reactivity of the amygdala, and a corresponding inactivity of the prefrontal cortex, as well as emerging evidence that patients with BPD have an opioid deficiency. These neurobiological characteristics account for the emotional dysregulation and impulsivity common in BPD (see Key Points Concerning Neurobiology and Psychotherapy for BPD).
Key Points Concerning Neurobiology and Psychotherapy for BPD
There are common therapeutic elements in all of the psychotherapies for BPD, most notably activation of the prefrontal cortex to bring “thinking” to bear on unbearable affects produced by amygdala hypersensitivity.
An opioid deficit appears to be prominent in BPD. Patients with BPD
○ have difficulty deriving satisfaction from intimate relationships,
○ often say they experience emotional pain as physical pain,
○ often resort to cutting themselves for release of endogenous opioids,
○ show a high rate of opioid abuse.
Neurobiological research can help clinicians tailor psychotherapies to the needs of individual patients. Some evidence has emerged indicating that BPD patients with dissociative symptoms may not respond as well to dialectical behavior therapy as other patients, suggesting that other treatments may be needed for this subgroup.
“What’s exciting to me is that the neurobiological research gives us an opportunity to get more specific about tailoring psychotherapies to specific borderline patients,” Gabbard said. “There is a spectrum to BPD, and one of the principles we learn in medical school is to adjust the treatment to the patient, not the patient to the treatment.
“Our psychotherapeutic theories are often like churches or belief systems, and the more we can get science involved in knowing how to tailor therapies to the individual’s neurobiology, the more we are a science rather than a religion.”
He noted, as an example, that recent research indicates that BPD patients with dissociative symptoms may not respond as well to dialectical behavior therapy, suggesting that this subgroup of patients may need to be treated with a different approach.
Gabbard said the psychotherapies that have been proven effective in the treatment of BPD probably all “speak” to common neurobiological processes, but one especially prominent feature is the activation of the prefrontal cortex through active reappraisal of emotions generated by an overactive amygdala. “A feature common to all of the therapies is the emphasis on self-reflection and mindfulness in which one is trying to look inward and manage painful affect states,” he said. “If you are actively reappraising, that appears to cause activation of the prefrontal cortex, which then modulates the amygdala” (Psychiatric News, April 1).
And he added that patients will often experience emotional pain in a physical way that is unbearable. Research by Prossin and colleagues published in the American Journal of Psychiatry in May 2010 implicates an opioid deficiency in BPD, possibly accounting for the high rate of opioid abuse among patients, as well as the high number of borderline patients among those who seek out opioids from physicians and hospitals or from illicit sources. And it is likely that the phenomenon of “self-cutting,” so common in borderline patients, is related to the release of endogenous opioids that accompanies cutting.
“Opioids are involved in emotion regulation and social functioning, so it makes conceptual sense that deficits in endogenous opioids could be related to the ubiquitous dysfunction in social and interpersonal relationships,” he said.
Also intriguing is the fact that patients with BPD report feeling euthymic—as opposed to euphoric—when using opioids, suggesting the neurobiologically determined difficulty they may have experiencing pleasure.
“This means satisfaction in intimacy is going to be challenging and is linked to the insecure attachment that patients experience over and over,” Gabbard said. “So when we see these people having difficulty forming a therapeutic alliance, it is so important that therapists not think of them as ‘difficult’ or ‘bad’ patients, but as people who are struggling with a biological deficit they are trying to overcome in order to link up with someone in a way they may never have experienced.”
Simon Baron-Cohen has been giving interviews about his new book The Science of Evil: On Empathy and the Origins of Cruelty in which he discusses “mind-blindness” in autism and the lack of empathy in other disorders, including BPD. Here is the text of the interview he gave to Time magazine. I have added emphasis on the part that I find most “telling” about BPD. I have to disagree though that people with BPD have zero empathy. They can behave that way at times, but people with BPD can exhibit a lot of empathy and compassion when their motivation is not IAAHF, pain avoidance or threat reaction. When their emotions become reflective, rather than reflexive, the empathy come through.
Mind Reading: Psychologist Simon Baron-Cohen on Empathy and the Science of Evil
By MAIA SZALAVITZ Monday, May 30, 2011
Cambridge psychology professor and leading autism expert Simon Baron-Cohen is best known for studying the theory that a key problem in autistic disorders is “mind blindness,” difficulty understanding the thoughts, feelings and intentions of others. He’s also known for positing the “extreme male brain” concept of autism, which suggests that exposure to high levels of testosterone in the womb can cause the brain to focus on systematic knowledge and patterns more than on emotions and connection with others. (Oh, and yes, he’s also the cousin of British comedian Sacha “Borat” Baron Cohen.)
Baron-Cohen’s new book, The Science of Evil: On Empathy and the Origins of Cruelty, examines the role of empathy, the ability to understand and care about the emotions of others, not only in autism but in conditions like psychopathy in which lack of care for others leads to antisocial and destructive behavior.
What do you mean when you write about “zero negative” empathy?
Zero empathy refers to people at the extremely low end of the scale. They tend to be people with personality disorders, particularly antisocial personality disorder (ASPD). I focus quite a lot on psychopathy [the extreme form of ASPD] and also on two other personality disorders, borderline personality disorder and narcissistic personality disorder.
The ‘negative’ is meant to be shorthand for this being negative for the individual but also for the people around them. It’s meant to contrast with what I call ‘zero positive’ empathy, which effectively describes the autistic spectrum.
[Autistic people] struggle with empathy just like zero negatives but it seems to be for very different reasons. I’m arguing that their low empathy is a result of a particular cognitive style, which is attentive to details and patterns or rules, which in shorthand, I call systemizing.
If we think about the autism spectrum as involving a very strong drive to systemize, that can have very positive consequences for the individual and for society. The downside is that when you try to systemize certain parts of the world like people and emotions, those sorts of phenomena are less lawful and harder to systemize. That can lead to having low empathy, almost like a byproduct of strong systemizing.
How do you account for people who are both highly empathetic and highly systematic, such as some of those with Asperger’s who are actually oversensitive to the emotions of others?
I’ve certainly come across subgroups like that. There are people with Asperger’s whom I’ve met who certainly would be very upset to learn they’d hurt another person’s feelings. They often have very strong moral consciences and moral codes. They care about not hurting people. They may not always be aware [that they've said something rude or hurtful], but if it’s pointed out, they would want to do something about it.
I was reading an article called “Social cognition in borderline personality disorder: evidence for disturbed recognition of the emotions, thoughts, and intentions of others” and noticed a line in the article that said this: “Thus, in addition to high heritability of BPD (Torgersen et al., 2008), these results argue that environmental factors (e.g., trauma) contribute to disturbed social cognition in BPD. In summary, for the current study we expected PTSD to be a negative predictor of social cognition.” That intrigued me on two levels. One was the “high heritability” part, because often I see comments about BPD and how many people believe that it is mainly caused by childhood trauma (and/or invalidation). In WHINE I state this: As I said earlier, one of the causes of BPD is the “invalidating environment.” Now, it could be that it is not an actual “cause” (and that all the real causes of BPD are biological), but more a reinforcer of BPD. So, the second part of the article that intrigued me was the idea that “we expected PTSD to be a negative predictor of social cognition” – and the discussion and methodology of comorbid PTSD with BPD. What they found was that people with BPD (with or without comorbid PTSD) are less able to understand the intent, thoughts and motivations of social interactions in others – in other words, people with BPD can’t mentalize as well as controls. They also found that this lack of ability is more marked in people with BPD who also have comorbid PTSD. The fact that they mention comorbid PTSD at all is something of a revelation – or perhaps should be to us nons. Many people come to support lists and do research on the Internet and begin their “introduction” of their BPD person with a long list of childhood traumas that explains why the person has BPD. This current research would indicate that PTSD and BPD are clearly two separate disorders and that, while PTSD is a contributor to poorer functioning that BPD alone, BPD is in itself a highly inheritable disorder and biological in nature, yet “reinforced” or made more severe (especially in a social functioning sense) when PTSD is present.
Anyway, this research led me to another scientific study called “Familial Resemblance of Borderline Personality Disorder Features: Genetic or Cultural Transmission?” In which the researchers studied twins, siblings and parents of borderlines to determine the genetic underpinning of BPD or whether the environment and/or cultural influences could have more of an influence on the development of BPD. They found this: “In the present study an extended twin-family design was applied to self-report data of twins (N = 5,017) and their siblings (N = 1,266), parents (N = 3,064) and spouses (N = 939) from 4,015 families, to estimate the effects of additive and non-additive genetic and environmental factors, cultural transmission and non-random mating on individual differences in borderline personality features. Results showed that resemblance among biological relatives could completely be attributed to genetic effects.” and this: “There was no effect of cultural transmission from parents to offspring.”
Recently, in the ATSTP group, we have been discussing the idea that shame/honor-based cultures and whether that environment could be explanatory in some sense of the development of BPD. It appears (at least based on this 2009 study) that the development and transmission of BPD is NOT cultural. It is essentially genetic (mainly “additive”, meaning it is more than one gene involved) and the environment has an effect, yet cultural transmission was not apparent.
They do go on to say this: “Gene by environment interaction implies that genes determine the degree to which an individual is sensitive to an environment. In the presence of gene-environment interaction, individuals with a ‘sensitive’ genotype will be at greater risk of developing BPD if an undesirable environment is present, than individuals with an ‘insensitive’ genotype.” So, basically, although this interaction has not been fully studied, it appears that some sort of “sensitive” genotype is required to develop BPD.
Article on fMRI and BPD… I had the pleasure of meeting Dr. Montague last year. Intersting guy…
Brain imaging gives new insight into mental disorders
(Media-Newswire.com) – HOUSTON — ( August 25, 2010 ) — A new kind of psychiatry built on objective measures derived from functional magnetic resonance imaging ( or fMRI ) of the brain performed while patients play economic games could provide new insight into the diagnosis and, eventually, treatment of mental disorders, said researchers from Baylor College of Medicine in a review in the current issue of the journal Neuron.
New tools, new field
These new tools will not only help produce new brain “signatures” associated with disorders such as autism, schizophrenia and borderline personality, they will also help identify the nature of normal variation in human decision making and the brain, said Dr. P. Read Montague, professor of neuroscience and director of the Computational Psychiatry Unit at BCM, and Dr. Kenneth T. Kishida, a postdoctoral fellow in the area.
Montague is a pioneer in a discipline that uses powerful fMRI machines to measure how blood flows in the brain while individuals play economic games that always involve choice and sometimes require cooperation between participants – a growing paradigm that has come to be known as neuroeconomics. The areas of greatest blood flow reveal what parts of the brain are involved during the decision-making process.
The two, along with Dr. Brooks King-Casas, assistant professor of neuroscience at BCM, describe a number of studies involving people with and without mental disorders in a review of the beginning of a new field – computational psychiatry.
Identifying disorders, defining “normal”
In a crucial prior study, King-Casas and others at BCM identified a characteristic fMRI “signal” that distinguished borderline personality disorder – a disorder that is extremely hard to diagnose – from psychologically healthy controls.
Not only do Montague and his colleagues seek to build a more concrete or objective method of diagnosis for mental disorders, they also seek to determine the range of what is considered healthy or “normal”.
“What is the nature of normal variation in these games,” said Kishida. “Can this help us measure the difference between what is considered healthy and what is pathologic?”
Augmenting assessment
Currently, most psychiatric diagnoses are descriptive, based on a cluster of symptoms recognized by professionals and codified in a standard guide called the Diagnostic and Statistical Manual of Mental Disorders. ( It is now known as the DSM-IV, and the DSM-V is scheduled for release in three years. )
Montague said their aim is not to replace psychiatrists or psychologists but “to augment their way of assessing people.”
Once scientists identify the brain signals associated with a particular pathology and the areas or tissues involved, they can then start to look for the genes associated with those patterns, said Montague and Kishida. That will involve scanning the brains of thousands of people, both those who are healthy and those with known pathologies.
I believe that it has. Why? Well, there are a number of reasons that depression is a catch-all diagnosis. One certainly is the influence of the pharmaceutical industry given that billions of dollars are spent on anti-depressants each year. Also, doctors who are not mental health professionals (like GP’s) are prescribing anti-depressants if their patients are “depressed”.
Unfortunately, sometimes depression is not accurate. Many times when people say “I’m feeling depressed” they are really expressing that they are feeling emotional pain. Sometimes emotional pain is normal, sometimes a great deal of emotional pain is not normal and becomes problematic. When someone is feeling too much emotionally, it is not depression.
Depression is usually a problem when someone is feeling a strong lack of emotions – causing a lack of interest in the usual activities (including sex) that once gave us pleasure. Although many configurations of “depression” exist (because it is a non-specific term nowadays), the configuration in which one lacks emotions is alexythimia, although if one lives without pleasure it’s called anhedonia. I suspect that most people, when they describe being “depressed” are really describing a combination of anhedonia (where they can’t enjoy anything anymore) and social anxiety.
As I said above, another configuration that is referred to as “depression” is when the emotional pain becomes too overwhelming. In this case the person is feeling too much and would possibly beg for anhedonia because, while the pleasure would not be present, at least the pain would go away. I think that BPD probably involves more of this kind of “depression” than other disorders. The constant emotional pain leads people to doing anything to stop it (thus, this site’s name), including substance abuse, sexual promiscuity, risk-taking, self-injury and other seemingly self-defeating behaviors.
How can this be explained? How can someone be in such emotional pain all the time? One explanation comes from the study of u-opiods in the brain. A recent study by Stanley and Siever showed that people with BPD have too few u-opiods (the precursor for natural pain-killing neuro-chemicals) AND have over-active u-opiod receptors. This combination provides a baseline of pain and, when opiods are added, the brain feasts on these pain-killing substances with the over-active receptors. This is why some people with BPD can ingest large quantities of pain killers to seemingly little effect (or less effect than those without the disorder). I have heard people with BPD say they only feel “normal” while taking pain killers.
So, the question here is two-fold: First, are anti-depressants an appropriate treatment for emotional pain that is not really “depression”? And secondly, if not, what is? Low-dose pain-killers?
Possible Genetic Causes Of Borderline Personality Disorder Identified
ScienceDaily (Dec. 20, 2008) — According to the National Institute of Mental Health, borderline personality disorder (BPD) is more common than schizophrenia or bipolar disorder and is estimated to affect 2 percent of the population. In a new study, a University of Missouri researcher and Dutch team of research collaborators found that genetic material on chromosome nine was linked to BPD features, a disorder characterized by pervasive instability in moods, interpersonal relationships, self-image and behavior, and can lead to suicidal behavior, substance abuse and failed relationships.
“The results of this study hopefully will bring researchers closer to determining the genetic causes of BPD and may have important implications for treatment programs in the future,” said Timothy Trull, professor of psychology in the MU College of Arts and Science. “Localizing and identifying the genes that influence the development of BPD will not only be important for scientific purposes, but will also have clinical implications.”
In an ongoing study of the health and lifestyles of families with twins in the Netherlands, Trull and colleagues examined 711 pairs of siblings and 561 parents to identify the location of genetic traits that influences the manifestation of BPD. The researchers conducted a genetic linkage analysis of the families and identified chromosomal regions that could contain genes that influence the development of BPD. Trull found the strongest evidence for a genetic influence on BPD features on chromosome nine.
In a previous study, Trull and research colleagues examined data from 5,496 twins in the Netherlands, Belgium and Australia to assess the extent of genetic influence on the manifestation of BPD features. The research team found that 42 percent of variation in BPD features was attributable to genetic influences and 58 percent was attributable to environmental influences, and this was consistent across the three countries. In addition, Trull and colleagues found that there was no significant difference in heritability rates between men and women, and that young adults displayed more BPD features then older adults.
“We were able to provide precise estimates of the genetic influence on BPD features, test for differences between the sexes, and determine if our estimates were consistent across three different countries,” Trull said. “Our results suggest that genetic factors play a major role in individual differences of borderline personality disorder features in Western society.”
A short article from About.com regarding an Article in Biological Psychiatry about moving BPD to Axis I:
Experts Argue That Borderline Personality Disorder Should Be Shifted to Axis I
Thursday October 16, 2008
In a recent paper published in Biological Psychiatry, Dr. Antonia New and her colleagues at the Mount Sinai School of Medicine and Bronx VA Medical Center argue the case for shifting borderline personality disorder (BPD) from Axis I to Axis II of the Diagnostic and Statistical Manual of Mental Disorders (DSM).In the most current, fourth edition of the DSM, BPD is diagnosed on Axis II, which is reserved for “longstanding disorders,” such as personality disorders. In their paper, Dr. New and her colleagues argue that research has not supported the distinction between BPD and Axis I disorders, and that moving BPD to Axis I will spur new research on this serious condition.
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