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Your emotional state has powerful control over your body — and Kim Bullock, MD, knows just how strong that hold can be. The Stanford psychiatrist works with patients who experience seizures that aren’t generated from the electrical brain storms of epilepsy, but instead are driven by their own psychological turmoil.
From neurology to psychiatry: Bullock probes mysterious seizures
January 9th, 2012 in Psychology & Psychiatry
Your emotional state has powerful control over your body — and Kim Bullock, MD, knows just how strong that hold can be. The Stanford psychiatrist works with patients who experience seizures that aren’t generated from the electrical brain storms of epilepsy, but instead are driven by their own psychological turmoil.
As a medical student in the early 1990s in Washington, D.C., Bullock volunteered to help the mentally ill homeless population. “It was the best education of my life,” she said. “I saw how much suffering they experienced and yet how much support and community they also provided each other.” But it wasn’t until she was about to interview for a neurology residency at Stanford in 1995 that she realized her true passion was psychiatry.
“When I was in medical school I really thought I was going to be a neurologist, but in the middle of my interviews, I changed my mind,” she said. She realized she wouldn’t be able to interact with the sort of people she was fascinated with in D.C. or use the wisdom she had gained in those years if she went into neurology. So she quickly changed her application at the last minute and interviewed for a position in psychiatry. “It just felt like the right thing to do and things fell into place,” she said. “That must be evidence of the unconscious, that at the last minute I changed my mind. Another part of me knew the right direction.”
Bullock, now a clinical associate professor of psychiatry, also had deeper, personal motivations for wanting to study psychiatric disease. She grew up in the Bay Area in a family troubled by addictions. “I didn’t understand why my own family would behave in certain ways and would make such foolish choices, and that made me curious about mental illness,” said Bullock. “I wanted to understand it and have some keys for possibly fixing this kind of behavior.”
Bullock now studies another type of involuntary behavior called psychogenic non-epileptic seizures. The condition resembles epilepsy, but is not accompanied by the electrical brain wave abnormalities measured in epileptic patients. Instead, the seizures are an involuntary response to physical, emotional or social distress. The mysterious nature of these seizures and their “orphan” position between neurology and psychiatry appealed to Bullock.
The problem can manifest itself in convulsions, loss of consciousness or paralysis of a limb. It’s a disabling affliction, and patients, the majority of whom are female, are often unable to work or even drive. Although these seizures affect as many as one in 100,000 people — a rate as high as multiple sclerosis — there’s a lack of awareness in the public and the medical community, little knowledge of the physical pathways that cause them, and no standardized treatment.
Bullock had her first significant exposure to the disorder as a psychiatry resident at Stanford Hospital, where she assisted with several studies led by John Barry, MD, a professor of psychiatry and behavioral sciences. Bullock and Barry looked at the frequency of past trauma among people with psychogenic non-epileptic seizures and whether group therapy could be an effective treatment.
But as her career was taking off, Bullock grappled with a tough question. Could she take time off from her psychiatry residency to have kids? The answer, it turned out, was yes. In fact, she took two breaks from her residency to raise her two now-teenage children. “It was kind of scary because you assume most programs won’t let you back in,” said Bullock, but she added that if you ask for things, they often work out. Now, back in the clinic, Bullock continues to look for ways to treat psychogenic seizures.
Patients diagnosed with psychogenic non-epileptic seizures often receive incorrect diagnoses and treatment, said Bullock. It takes an average of seven years before patients are properly diagnosed. Typically, Bullock said, people suffering from the psychogenic seizures are first sent to neurologists who specialize in epileptic seizures. About one third of patients in epilepsy monitoring units at Stanford and hospitals across the country will eventually be diagnosed with non-epileptic seizures, but some patients take ineffective epilepsy medication for years.
Many of these patients have problems with their emotions, which can be either too extreme or too blunted. “Some patients are so shut down they don’t display emotions, are unaware of them, or have emotions all over the map that they can’t control,” said Bullock, “so we teach them skills for handling both problems.” Basic interpersonal skills such as how to appropriately ask for things or say no to requests can also be difficult for these patients, who face obstacles due to their disability, gender or other personal circumstances.
Often, psychogenic seizure patients feel they have no voice. “For example, a woman in an unhappy marriage may display these symptoms as a way to indicate that something is wrong,” said Bullock. “It can be as if their true feelings are expressed through their bodies instead of through their emotions,” she said. “In a sense the body is speaking for them.”
Other patients don’t know how to regulate their emotions, so “when they get really mad they have seizures and their bodies just go offline,” said Bullock. Still others need to address deeply buried effects of childhood trauma to end the debilitating seizures.
“Our hypothesis is that there’s something in the limbic system that is dysregulated,” Bullock said. The limbic system comprises the functionally and anatomically connected brain structures that regulate responses like emotion and behavior. There may be a biological vulnerability and a stressful environment that come together in a perfect storm, creating mental turbulence.
Figuring out the exact physical cause of the disease will be difficult because of such heterogeneity. Continue reading From neurology to psychiatry →
Q-factor analysis of adolescents who have attempted suicide may shed light on personality subtypes of attempters.
Personality Type Might Help Identify Teens at Suicide Risk
Leslie Sinclair
Q-factor analysis of adolescents who have attempted suicide may shed light on personality subtypes of attempters.
Studies of adolescents who have attempted suicide usually focus on identifying how they differ from their nonsuicidal peers. Researchers at Emory University, however, have begun to identify how adolescents who attempt suicide differ from one another.
Their work adds to previous studies that have reported personality subtypes within samples of adult suicide attempters and completers. “Overall, assessing adolescents’ risk of suicide attempt should include not only a list of risk factors but also a deeper understanding and consideration of personality,” wrote lead author Dorthie Cross, a doctoral student in the Department of Psychology at emory University, and her colleagues in the October Journal of Nervous and Mental Disease.
The researchers used a Q-factor analysis to identify subtypes based on the Shedler-Westen Assessment Procedure-II for Adolescents (SWAP-II-A), a 200-item measure of personality pathology administered by clinicians that was codeveloped by Drew Westen, one of the authors of the new study.
“Q-factor analysis is also called inverted factor analysis because it aggregates patients rather than variables, identifying people with similar profiles across a set of items instead of items with similar content across cases,” the researchers noted. “the goal of Q-factor analysis in this study is to identify groups of adolescent attempters with shared personality characteristics that distinguish them from other adolescents who have attempted suicide,” they explained.
The researchers recruited 950 psychiatrists and psychologists with at least three years’ postlicensure experience from membership rosters of the American Academy of Child and Adolescent Psychiatry and the American Psychological Association. Participating clinicians were asked to provide data on a single randomly selected adolescent patient currently in treatment of “enduring maladaptive patterns of thought, feeling, motivation, or behavior—that is, personality.” they were asked to select a patient without a particular diagnosis, yielding 267 patients with a history of suicide attempt. Publications detailing the sampling procedure and the rationale for using clinicians as informants in basic science research, also coauthored by westen and published in the American Journal of Psychiatry, were referenced.
Q-factor analysis of the 267 patients with a history of suicide attempt resulted in six subtypes: externalizing, internalizing, emotionally dysregulated, high functioning, narcissistic, and immature. Continue reading Personality Type Might Help Identify Teens at Suicide Risk →
An article from pain.org regarding BPD, emotional lability and Opiate Abuse:
The medical borderline: personality characteristics that promote increased risk of opioid misuse
Geralyn Datz, Melissa Bonnell, Toni Merkey, Todd Sitzman
Forrest General Hospital, Hattiesburg, MS, USA,
University of Southern Mississippi, Hattiesburg, MS, USA, Advanced Pain Therapy, PLLC, Hattiesburg, MS, USA
Purpose
 Opiate Abuse Undiagnosed or untreated psychiatric comorbidities may contribute to medication misuse. In particular, personality disorders may place patients at risk for medical nonadherence, via negative coping styles. Patients with Borderline Personality Disorder (BPD) utilize medical services more frequently than those without BPD and are less likely to adhere to medical regimens. Patients with borderline traits have greater incidences of risky behavior, including abuse of prescription medications. We examined a large outpatient sample of chronic pain patients being screened for appropriateness of long-term opioid therapy in order to determine correlations between high-risk behaviors and personality type.
Method
Participants were 96 patients who were assessed in an outpatient pain management program. Participants were administered the Millon Behavioral Medicine Diagnostic (MBMD), which measures psychosocial assets and liabilities that affect treatment response, and the Screener and Opioid Assessment for Patients with Pain – Revised (SOAPP-R), which is a measure designed to predict aberrant medication-related behavior. Hierarchical regression analysis was used to evaluate which psychiatric indicators of the MBMD would predict total SOAPP-R score. Each analysis adjusted for age, gender, duration of pain, and number of pain sites.
Results
Hierarchical regression analysis was used to evaluate which psychiatric indicators of the MBMD would predict total SOAPP-R score. Each analysis adjusted for age, gender, duration of pain, and number of pain sites. Model 1 included demographic variables, duration of pain, and number of pain sites, F(5,91)=5.81, P<.001. Overall, the model explained 24.2% of the variance in SOAPP-R scores. Results indicated that age and number of pain sites significantly predicted SOAPP-R score. Model 2 added the psychiatric indicators of the MBMD. Overall, Model 2 explained 42.7% of the variance in SOAPP-R scores, F(5,91)=6.42, P<.001. Number of pain sites and emotional lability significantly predicted SOAPP-R score over other psychiatric indicators.
Conclusions
Identifying “at-risk” patients for opioid misuse has significant importance in today’s climate of increased scrutiny towards pain medications. These findings suggest personality assessment serves as an effective adjunct to risk stratification. Personality factors such as emotional lability and traits of borderline personality may increase opioid misuse potential. Clinical interview, history taking, and psychological assessment are valid ways pain specialists can assess personality. Prescribing strategies such as prescreening, close monitoring, limit setting, inclusion of psychological support can mitigate risk. Personality traits are key factors that may contribute to aberrant behavior and are of importance to prescribers of opioid regimens.
An article about the opioid system and the neurobiology of borderline personality disorder.
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.”
The NIAAA study begins to spread out and spur on new views of the findings regarding BPD. Here is a study about Major Depressive Disorder and BPD.
Can Epidemiology Translate Into Understanding Major Depression With Borderline Personality Disorder?
Myrna M. Weissman, Ph.D.
Epidemiologic surveys have mapped the terrain of psychiatric disorders. Personality disorders have bedeviled the clinician’s practice. Rarely have these two been rearranged in a meaningful clinical dialogue. Using the largest psychiatric epidemiologic survey ever, the National Epidemiologic Survey on Alcoholism and Related Conditions, and among the few to venture into axis II disorders, Skodol et al. (1), in this issue of the Journal, give a community-based national view of a common clinical question: What is the effect of specific personality disorder comorbidity on the course of major depression?
The original sample included over 40,000 adults, and 2,422 met criteria for DSM-IV current major depressive disorder. Three years later, 1,996 of the original currently depressed subjects were available for reinterviewing, which makes both a respectable sample size and response rate for generalizability. However, some caution is needed, since the sample was over-represented with Caucasian, college-educated, and married respondents. Fifteen percent of participants had persistent major depressive disorder, and 7.3% of those who remitted had a recurrence over the follow-up period. These figures are within the range of longitudinal studies of patients with major depressive disorder (2). While the presence of any personality disorder elevated the risk for persistence of major depressive disorder, when all axis I and II disorders, age of onset of major depressive disorder, number of previous episodes, family history, treatment, and duration of illness were controlled, borderline personality disorder remained the most robust predictor of major depressive disorder persistence. Neither personality disorders nor other clinical variables predicted recurrence of major depressive disorder. Thus, an epidemiologic survey yielded a practical jewel. The finding, undoubtedly, does not surprise the clinician but is now confirmed nationally. As the authors conclude, borderline personality disorder should be assessed in all depressed patients and considered in prognosis and addressed in treatment.
One can raise a number of methodologic issues about this study, including the use of lay interviewers or the instrument for assessing axis II disorders. The diagnostic interview, the Alcohol Use Disorder and Associated Disabilities Interview Schedule, DSM-IV version (3), was developed for this survey. The personality disorders included were adapted from items in the Structured Clinical Interview for DSM-IV Personality Disorders. The test-retest and internal consistency results reported for all personality disorders are fair to good, not great. However, the agreement with clinician interviews for borderline personality disorder (kappa=0.71) is about as good as it gets (4). The only other national survey to venture into assessing all axis II disorders was the National Comorbidity Survey Replication (5), which used the International Personality Disorder Examination. The investigators carried out a clinical reappraisal in a sample of 214 subjects using clinically trained interviewers to follow up screened, positive subjects and reported excellent predictions of classification. They also noted that the International Personality Disorder Examination is commonly regarded as a conservative diagnostic assessment of axis II disorders. The community rate they generated for any personality disorder in the United States was 11%, and in the World Health Organization World Mental Health Surveys (6), involving 13 countries, the rate was 6.1%. These rates seem to be lower than those reported in the National Epidemiologic Survey on Alcoholism and Related Conditions, but different presentations make it difficult to directly compare rates between studies. No articles from the National Epidemiologic Survey on Alcoholism and Related Conditions reporting overall rates of axis II disorders could be found. Unfortunately, given the findings in the Skodol et al. article, not all personality disorders were included in the first wave of the survey, and borderline personality disorder was added in the second wave. Both of these landmark studies used state-of-the-art measures. While they are imperfect, these are the best available. It is too bad they could not share the same methods.
The major issue now is not a debate about the methods of personality disorder assessment but about the future of personality disorders. The DSM-5 committee is working on the next version of psychiatric classification (7). In parallel, the National Institute of Mental Health is working on moving diagnosis away from clinical presentations to understanding of syndromes based on pathophysiology in a new project called Research Domain Criteria (8). These efforts will certainly effect how personality disorders are described, classified, or reimbursed in the future.
DSM-5 raises issues about the categorical conceptualization of personality disorders because of the high concurrence among disorders, both within and across axes, and the difficulty in differentiating normal from pathological. How dimensions will solve the problem of a lack of understanding of the pathophysiology underlying the disorders is unclear. Some cutoff along the dimension will need to be established for clinical practice.
The Skodol et al. study, based on an epidemiologic survey, may add light to the issue or, at least, generate a hypothesis about diagnosis that can be translated into a more experimental approach. Borderline personality disorder, defined categorically, and not the other axis II disorders explained the persistence of major depressive disorder over 3 years. Other axis I disorders may map out to different axis II disorders. The National Epidemiologic Survey on Alcoholism and Related Conditions, because of its large sample, could be mined for these clues about the relationship between specific axis I and II disorders.
The Research Domain Criteria project, in the long run, may offer more enlightenment for personality disorders if its goals can be achieved. The primary focus is on neural circuitry, with levels of analysis progressing from measures of circuitry function to clinically relevant variation or downward to the genetic and molecular cellular function (8). In the final analysis, the new molecular and neurobiological parameters will need to predict prognosis or treatment response. They will need to do as well as borderline personality disorder in predicting major depressive disorder persistence. If the Research Domain Criteria approach is successful, more than prediction of prognosis might be achieved, including a deeper understanding of the biological mechanism underlying the joined symptoms.
The epidemiologic finding that borderline personality disorder contributes to poor prognosis of major depressive disorder might be viewed as a hypothesis that can be translated into methods in the neurosciences to understand the mechanism behind this association. The features of borderline personality disorder, particularly the pervasive instability of the regulation of emotions and impulse control, would seem ripe for the Research Domain Criteria approach. When these symptoms occur in conjunction with major depressive disorder, a different syndrome may be present. Further experimental work may test how the symptoms of borderline personality disorder contribute to the prognosis of major depressive disorder. But what about the persistence of borderline personality disorder without major depressive disorder? Can the epidemiologic data provide any clues? In the meantime, the clinician treating major depressive disorder would be wise to assess for borderline personality disorder, even as currently defined.
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Overcoming Borderline Personality Disorder by Valerie Porr is perhaps the most up-to-date and complete book for family members of people with BPD published to date. When I read the book, I couldn’t help but think that Ms. Porr had the therapists and mental health professional more in mind than the family members. It appears as though she is trying to dispel many myths about BPD that exist not only in the family environment but also in the mental health community. This book is steeped in scientific research, including research involving the biological under-pinnings of BPD. It includes many skills for family members from both DBT and mentalization based therapy (MBT). Clearly Ms. Porr is highly respected by the clinical community since many of the leading experts in research and practice in BPD treatment have written blurbs for this book. The book is quite dense and a must read for family members of those with BPD. Yet it might not be the best book to start with because of the complexity of the scientific research, the psychoeducational aspects and the technical details about the various therapies for those with BPD. Still, I highly recommend Overcoming Borderline Personality Disorder.
 Genetics in Borderline Personality Disorder 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.
An article that mentions BPD in the context of oxytocin….
Could ‘Love Hormone’ Oxytocin Cure Our Ills?
Published December 06, 2010 | LiveScience
In recent years, we’ve been bombarded with studies about the hormone oxytocin – researchers have demonstrated it increases trust and helps aid in social bonding. It has even garnered a reputation as the “love hormone.” But what good is it for? Despite all these findings, the hormone’s medical use remains limited to obstetrics – it is used to induce labor and aid in breastfeeding.
But researchers are now trying to apply these findings, and are investigating oxytocin as a treatment for psychiatric illnesses. They say its unique ability to adjust our wiring could remedy symptoms of schizophrenia, post-traumatic stress disorder (PTSD) and anxiety, and improve social abilities among those with autism.
A number of oxytocin studies have even reached the stage of clinical trials – which test the effectiveness and safety of a substance before it can become an approved drug – with promising findings.
“The idea of augmenting … the way we connect to and with each other, would just be so helpful for so many people,” said Dr. Kai MacDonald, an adjunct professor of psychiatry at the University of California, San Diego, who has studied oxytocin as a treatment for schizophrenia.
However, the results so far, while hopeful, have not been “earthshaking,” MacDonald said.
There are hurdles to such research. Because oxytocin is a large molecule, it doesn’t cross from the bloodstream into the brain very easily. It is also rapidly degraded in both the stomach and the blood.
Also, researchers don’t know how big doses need to be, or how frequently it should be given to have a meaningful impact, MacDonald told MyHealthNewsDaily. Figuring out such dosing can be difficult.
Still, “if we could do it with any degree of precision, that would be a lovely therapeutic venue,” MacDonald said.
What is oxytocin?
Oxytocin is a hormone released by the pituitary gland that affects both the body and the brain. In the human body, it facilitates contractions of the uterus during labor and helps release milk during breastfeeding.
The hormone affects social interactions in a number of mammals, from mice and moles to dogs and monkeys, MacDonald said. For example, studies have shown that mice given oxytocin will huddle together, and monkeys given the hormone will spend longer grooming each other.
A barrage of studies over the last decade has indicated it has social effects on people as well.
One study found a nasal spray of oxytocin – a frequently used way to deliver the hormone, because it provides a direct route to the brain – made people more trusting. Participants were more willing to hand over money in an experimental game than those not given the spray.
Other researchers gave men oxytocin and found they more frequently looked to the eye region when shown pictures of human faces. People look to the eyes to read another’s emotional state and trustworthiness, MacDonald said. [Related: 11 Interesting Effects of Oxytocin]
It’s not clear that people who take oxytocin feel any different, MacDonald said. It may be that it acts subtly to change behavior or how we process social information, he said.
Though you can buy the hormone on websites that sell what they claim is an oxytocin nasal spray, whether it actually works is a different story. The claims need scientific scrutiny, a process still in its infancy, MacDonald said.
Under investigation
Oxytocin has not been approved to treat any psychiatric disorder, but evidence that it may be effective is building.
A small study published Oct. 1 in the journal Biological Psychiatry found that patients with schizophrenia who took oxytocin for three weeks along with their regular antipsychotic medication improved in their symptoms and hallucinated less than those who took a placebo with their antipsychotic.
While there were only 15 patients and the findings are preliminary, the results suggest oxytocin could treat patients with schizophrenia whose symptoms are not fully alleviated by their antipsychotics, said study researcher David Feifel, also of UCSD.
“The field of treating schizophrenia is kind of at an impasse,” Feifel told MyHealthNewsDaily. “All our drugs that we have to date work through the same mechanisms as they did when antipsychotic drugs were first discovered 50 years ago,” he said. “We are in desperate need of novel mechanisms that will improve symptoms through a different pathway, and oxytocin clearly is a novel mechanism.”
Considering oxytocin’s social effects, it makes sense to hypothesize it could treat autism, a condition characterized by having trouble interacting with others. And researchers have shown people with autism naturally have lower levels of oxytocin than those without autism.
A study published in 2007 in Biological Psychiatry found people with autism given oxytocin were able to determine the emotional tone of speech more consistently than those given a placebo.
Studies on other disorders have shown more mixed results. A paper published last year in the journal Psychoneuroendocrinology involving patients with social anxiety disorder found that oxytocin improved participants’ self-image when they gave a speech. However, after five weeks of treatment, which also included teaching the patients to confront their social fears, those given oxytocin did no better than patients given the placebo.
Oxytocin is also being tested in clinical trials as a treatment for depression, borderline personality disorder and alcohol withdrawal.
How does oxytocin work?
One hypothesis is that oxytocin dampens the activity of the brain’s fear center, the amygdala, thereby easing stress and anxiety.
A decline in anxiety could “allow people to attend to the social cues maybe they normally would avoid,” said Jennifer Bartz, a professor of psychiatry at Mount Sinai School of Medicine in New York, who is conducting a clinical trial testing oxytocin as a therapy for autism. There is evidence people with autism experience anxiety in social situations, she said.
Because of oxytocin’s proposed blunting effects on the amygdala’s activity, scientists have also hypothesized it would help those with PTSD, which is a disorder of fear, said Miranda Olff, head of the Center for Psychological Trauma at the University of Amsterdam in the Netherlands. In PTSD, the brain “still gives the fear response as if people are back in that situation again,” she said.
Olff is testing oxytocin’s use in patients with PTSD in addition to standard therapies.
“Adding another biological component to this intervention might speed up recovery, or might increase the number of patients that respond to treatment at all,” Olff said.
And oxytocin’s trust effect could help those with schizophrenia, making them less paranoid, Feifel said.
Scientists don’t know how much oxytocin goes into the brain when it is administered as a spray, or whether it even gets there, Feifel said. There is no way to see the hormone in the brain. But the effects it produces – such as a reduction in hallucinations – would require brain changes, so researchers have reason to believe it reaches the brain, he said.
It’s also possible that an oxytocin dose simply triggers the brain to make more of it, MacDonald said.
Future research
While oxytocin’s effects so far have been subtle rather than drastic, it could still become an important therapy. MacDonald said that most studies have looked at effects on patients after only a single dose. If Prozac, the widely-prescribed antidepressant, were administered that way, its effects would seem more subtle as well, he said.
The side effects of oxytocin have so far been benign, MacDonald said. But while it’s something the body produces naturally, researchers don’t know whether upping the body’s natural amount, or giving it over long periods of time, could ultimately be harmful.
It also remains to be seen whether oxytocin affects men and women differently. It may present health risks to women because of its role in birth – inducing contractions of the uterus. Most studies to date have been conducted in men.
Besides mental disorders, researchers are investigating oxytocin’s potential benefit for a number of other ailments, including headaches, constipation and skin damage.
For those who think they might benefit from an oxytocin boost, MacDonald noted that you don’t need a spray to prompt the hormone’s production.
“Given that some of the things that are suspected of triggering oxytocin – massage, sex, touch, eye contact – given that those are uniformly likable, it’s hard not to recommend them,” he said.
Read more: http://www.foxnews.com/health/2010/12/06/love-hormone-oxytocin-cure-ills/#ixzz17XrvhZ6I
 How much do feelings of emptiness matter in BPD? Recently Rajkumar Kalapatapu, et al., released a report in which they hosted an Internet-based survey to ask people with BPD what they wanted to see in the next version of the DSM with respect to BPD. As many of you know, scores of people find BPD (Borderline Personality Disorder) stigmatizing and confusing, since the term “borderline” was adopted to indicate “on the border between neurosis and psychosis” (although some indicate that it refers to “borderline schizophrenia” – although no correlation between BPD and schizophrenia exists as far as I am aware) and “personality” often connotes a “character-flaw” or something that is immutable and incurable. The only part of the name that seem to be in agreement is “disorder” – although even that can be called into question given a spectrum emotional regulation, impulsivity and other factors that play a role in BPD. I mean, NAAA and Bridget Grant published an epidemiological study that showed a 5.9% lifetime occurrence of BPD. Is that possible? Or is there something else afoot here?
In the Internet survey/study, the researchers asked self-identified people with BPD their ideas on a name and criteria change for BPD. I was forwarded a copy of the study findings because ATSTP hosted a link to the study and encouraged our readers with BPD to fill it out. The most-mentioned alternative names for BPD included were (not surprisingly since the DBT community has been advocating some change like this for years) “emotion” (or emotional) and “regulation” (or dysregulation) with Emotional Regulation Disorder (or similar form) mentioned in 21.4% of the cases. Again, not surprising considering the idea has been in the DBT community for years. A total of 53.3% of accepted responses indicated that a name change is desired.
There were a couple of things that I noticed in this survey data that actually piqued my interest. One was the most common symptom (based on the current DSM criteria) mentioned was emptiness (92.9%), not emotional instability. While unstable relationships was very high on the list, even higher was the “self image” aspects of BPD – emptiness and questions of identity. Personally, as someone who has for several years paid devotion to the “altar” of DBT, those aspects are not as noted within the clinical framework that is DBT. In fact, the idea of “systems-level” issues (emotional system, impulse control system) seems to be the most common way of approaching BPD, once you get out of the psychoanalytic backwater and into the CBT/DBT state of the art. Yet, these self-reporting people with BPD report emptiness and questions of identity as the most common symptoms (at 92.9% and 91.8% respectively) and relationship-based issues (fear of abandonment, unstable relationships) in a close second (each at 91.8%). I guess I am wondering then if a name change to “emotional regulation disorder”, while it is certain much less stigmatizing than BPD, would actually capture the crux of the issue? And what would instead? Frankly, I don’t really think the name matters all that much (if the stigma was expunged).
What further got me interested in this data was the biographical data. Of 646 included responses (1,186 were excluded), 88.5% of the population was female, 88.7% was Caucasian, the mean age was 36 (the median 35) and 45.2% of the respondents were single/never been married (with over 18% in the divorced or separated category). So what we have here is a group of white, 30-something women who are generally not married or not attached to another person – and almost half have NEVER been so attached, even though their biological clock is ticking (at 36). Plus, they feel empty and have unstable relationships and fear people will leave them. Granted, I am making assumptions based on this data and I am generalizing and “averaging the averages” at some level, but if this is the picture of a borderline person, it makes sense as to why she would be angry and fearful and shameful.
Recently, I started working with several men who want to get their BPD girlfriends back. And the picture of a thirty-something, white, never-before-married woman with BPD has arisen in several of these cases. That got me thinking about this person with BPD and how she must feel about her life. Here she is: empty, sad, distrusting, childless (when her friends probably have kids), unmarried (no one will truly love her), with a history of broken relationships thrown aside (if it doesn’t work out I’ll feel horrible, best to end it now). I rarely see a non-BPD man in a relationship with such a woman who actually thinks about how it must feel to be in her shoes. I think it would be quite beneficial to the men in the lives of these women with BPD to consider how it feels to be in that situation – empty, unmarried, childless, in your mid-30s, etc. I think if one were really to ponder and meditate on what that must feel like, the behavior might become less confusing and more compassion could flow into the relationship.
Only 23% of the British Population is not personality disordered?
Personality pathology recorded by severity: national survey
Min Yang, MD, MPH
Division of Psychiatry, School of Community Health Science, University of Nottingham, Nottingham
Jeremy Coid, MD, FRCPsych
Queen Mary College, London, Forensic Psychiatry Research Unit, St Bartholomew’s Hospital, London
Peter Tyrer, MD
Centre for Mental Health, Imperial College, London, UK
Correspondence: Correspondence: Professor Peter Tyrer, Centre for Mental Health, Imperial College, St Dunstan’s Road, London W6 8RP, UK. Email: p.tyrer@imperial.ac.uk
Declaration of interest
P.T. is the Chair of the World Psychiatric Association Section on Personality Disorders and the Chair of the World Health Organization Personality Disorder Working Group for the ICD–11 Classification. He is also Editor of the British Journal of Psychiatry but had no part in any decisions about this paper.
Background
Current classifications of personality disorders do not classify severity despite clinical practice favouring such descriptions.
Aims
To assess whether an existing measure of severity of personality disorder predicted clinical pathology and societal dysfunction in a community sample.
Method
UK national epidemiological study in which personality status was measured using the screening version of the Structured Clinical Interview for DSM–IV Personality Disorders (SCID–II) and reclassified to five levels using a modified severity index. Associations between levels of severity of personality pathology and social, demographic and clinical variables were measured.
Results
Of 8391 individuals interviewed and their personality status assessed, only a minority (n = 1933, 23%) had no personality pathology. The results supported the hypothesis. More severe personality pathology was associated incrementally with younger age, childhood institutional care, expulsion from school, contacts with the criminal justice system, economic inactivity, more Axis I pathology and greater service contact (primary care and secondary care, all P<0.001). Significant handicap was noted among people with even low levels of personality pathology. No differences contradicted the main hypothesis.
Conclusions
A simple reconstruction of the existing classification of personality disorder is a good predictor of social dysfunction and supports the development of severity measures as a critical requirement in both DSM–V and ICD–11 classifications.
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