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An Opioid Deficit in Borderline Personality Disorder: Self-Cutting, Substance Abuse,

By Spucky, Aug 26, 2010 | | |
  1. Spucky
    An Opioid Deficit in Borderline Personality Disorder: Self-Cutting, Substance Abuse, and Social Dysfunction

    Borderline personality disorder is far more common than has been previously recognized, with a prevalence rate as high as 5.9% in the general population (1). The disorder has high morbidity and mortality: these patients have higher rates of suicide and poor functioning and utilize more mental health resources than most patients with axis I diagnoses (2). Psychotherapeutic treatments for borderline personality disorder typically show partial efficacy, and while patients may respond to medications in a circumscribed and often transient manner, there are currently no pharmacologic treatments for borderline personality disorder approved by the Food and Drug Administration. Patients are, therefore, left without the benefit of reliable and effective therapies. Furthermore, pharmacotherapeutic and neurobiological research that might inform treatment in borderline personality disorder has made less progress than one would hope, especially considering the seriousness and pervasiveness of the disorder.

    The article in the current issue by Prossin and colleagues (3) holds promise for helping to move the field forward. They present evidence that patients with borderline personality disorder suffer from a definitive abnormality in opioid activity. While there has been a great deal of interest in the opioid system in borderline personality disorder (4), until this study, the role of opioids in borderline personality disorder was largely theoretical with little empirical support. The few pieces of evidence—reviewed by Stanley and Siever (4)—include 1) decreased endogenous opioids, especially beta-endorphins and met-enkephalins, in self-injurers with cluster B personality disorders (predominantly borderline personality disorder) compared to individuals without self-injury (5); and 2) a reported association between a μ-opioid gene polymorphism and borderline personality disorder. Prossin and colleagues, however, are the first to measure μ-opioid receptor binding directly in the brains of living patients with borderline personality disorder.

    They used a μ-opioid ligand, [11C]carfentanil, to examine binding in the cerebral cortex of patients with borderline personality disorder during induction of neutral and sad sustained emotional states. The participants were female patients with borderline personality disorder and matched healthy comparison subjects. During the neutral state, the patients showed more μ-opioid binding in regions of the prefrontal cortex, in the reward center (accumbens), and in the amygdala, while the comparison subjects showed more μ-opioid binding in the thalamus. μ-Opioid binding in the prefrontal cortex during the neutral mood correlated negatively with neuroticism in borderline personality disorder. During induced sadness, neurotransmission mediated by μ-opioid receptors was greater in the patients than in the comparison subjects. An important feature of the study is that it experimentally manipulated the subjects’ emotional state, since opioid ligand binding is likely to be state dependent. The authors interpreted the greater baseline μ-opioid receptor availability in borderline personality disorder as perhaps reflecting a deficit in endogenous circulating opioids. The results also seems to suggest that enhancement of endogenous opioid availability during sad mood is greater in patients with borderlinepersonality disorder than in healthy subjects, which might reflect a compensatory response and is consistent with lower levels of endogenous opioids in self-injurers (5).

    Opioid-Deficit Model
    How might abnormal opioid activity help to explain the symptoms and etiology of borderline personality disorder? For decades, researchers have theorized that at least one behavior common in borderline personality disorder—self-cutting—relates to abnormalities in opioid activity. It has long been noted that patients with borderline personality disorder report that they engage in self-cutting not as a suicidal act but, rather, as a means to relieve psychic pain. Many patients report that they do not feel physical pain at the moment when they cut themselves; instead, cutting engenders feelings of relief or well-being. One view of cutting in borderline personality disorder is that it represents a method of endogenous opioid generation. In this view, patients learn to cut themselves, thereby releasing opioids, which reward their behavior. This, coupled with evidence that patients with borderline personality disorder who do not cut themselves are less symptomatic than those who do, led to efforts to treat borderline personality disorder with opiate antagonists by eliminating the positive feedback from cutting. While we know of no large-scale randomized, controlled trial, pilot studies on the efficacy of opiate antagonists showed mixed results (reviewed in reference 4) and overall showed that while opiate antagonists may slightly decrease cutting behavior, they do not improve the intrapsychic distress that leads to the cutting (6). This lack of diminished distress is consistent with the model of opioid deficiency.

    Thus, a promising way of construing cutting behavior in borderline personality disorder is to consider that these patients may have a preexisting deficit in endogenous opioids. According to this view, patients are self-medicating by cutting themselves, attempting to attenuate severe intrapsychic distress that healthy individuals—without such a deficit—would not be experiencing. This is consistent with the observation that opiate antagonists might decrease cutting behavior by rendering ineffective the patient’s attempts to treat his or her pain (thereby decreasing the frequency of cutting) but would not relieve the underlying intrapsychic distress. A deficit in opioids is also consistent with the high rate of opiate abuse in borderline personality disorder, as patients may be compensating for a deficit in endogenous opioids. Not only is there is a high rate of opiate abuse in borderline personality disorder, but there is also a high rate of borderline personality disorder among patients seeking substance abuse treatment; for instance, 44.1% of individuals seeking buprenorphine treatment have borderline personality disorder (7). Clinically, it has been noted that individuals with borderline personality disorder who are taking opiates report feeling euthymic rather than euphoric, while withdrawal is associated with sustained dysphoria.

    An opioid-deficit theory of borderline personality disorder might explain far more than the self-injurious behavior of these patients. For example, their extraordinary difficulties in social behavior may also be linked to a preexisting deficit in endogenous opioids. The endogenous opioid system not only regulates pain but also has an important role in social behavior. This system, through μ-opioid receptors, has long been implicated in regulation of emotional and stress responses. Reductions in its function have been associated with attachment behavior deficits and anxiety-like responses in animal models. In many species, the soothing and comforting that infants receive from maternal grooming and touching is mediated through the opioid system (8). In human beings, opioids are involved in normal and pathological emotion regulation (9) in addition to their more traditional role in modulating the sensory and affective dimensions of pain (10). In short, there is reason to think that endogenous opioids facilitate normal social function in healthy individuals.

    If the proposed model is accurate, then a deficit in endogenous opioids might go some way toward explaining not only cutting behavior and substance abuse in borderline personality disorder but also the almost ubiquitous social dysfunction observed inthis condition. Gunderson has argued for a greater focus on interpersonal dysfunction in understanding borderline personality disorder, stating that the relational style characteristic of the disorder “offers the best discriminators for the diagnosis” of borderline personality disorder (11). Mood shifts and self-destructive behaviors in borderline personality disorder seem to arise specifically in response to interpersonal triggers (12). Furthermore, the domains of intrapsychic pain and interpersonal dysfunction in borderline personality disorder are closely linked.

    Clinical Implications
    The findings of Prossin and colleagues have both broad and specific clinical implications. Broadly, they lend support to a model of an opioid deficit in borderline personality disorder that may be “hard wired” (consistent with the high heritability of borderline personality disorder). This view could provide a heuristic model to help patients and clinicians understand the social disruption in borderline personality disorder. The satisfaction that normally accompanies closeness to other people both in early attachment and throughout life may elude patients with borderline personality disorder. If these individuals do not have sufficient endogenous opioids, then the continual craving for relationships and heightened reaction to their loss is understandable. Such a model could provide a better understanding and improve management of disappointment in relationships for patients. It might also destigmatize the disorder; the difficulty in forming a therapeutic alliance, for example, could be reconstrued as the result of an opioid deficit. Furthermore, it provides support for targeting the μ-opioid receptor as a novel molecular target for pharmacotherapy in borderline personality disorder.

    1. Grant BF, Chou SP, Goldstein RB, Huang B, Stinson FS, Saha TD, Smith SM, Dawson DA, Pulay AJ, Pickering RP, Ruan WJ: Prevalence, correlates, disability, and comorbidity of DSM-IV borderline personality disorder: results from the Wave 2 National Epidemiologic Survey on Alcohol and Related Conditions. J Clin Psychiatry 2008; 69:533–545
    2. Zanarini MC, Frankenburg FR, Khera GS, Bleichmar J: Treatment histories of borderline inpatients. Compr Psychiatry 2001; 42:144–150
    3. Prossin AR, Love TM, Koeppe RA, Zubieta J-K, Silk KR: Dysregulation of regional endogenous opioid function in borderline personality disorder. Am J Psychiatry 2010; 167:925–933
    4. Stanley B, Siever LJ: The interpersonal dimension of borderline personality disorder: toward a neuropeptide model. Am J Psychiatry 2010; 167:24–39
    5. Stanley B, Sher L, Wilson S, Ekman R, Huang YY, Mann JJ: Non-suicidal self-injurious behavior, endogenous opioids and monoamine neurotransmitters. J Affect Disord 2010; 124:134–140
    6. Schmahl C, Meinzer M, Zeuch A, Fichter M, Cebulla M, Kleindienst N, Ludascher P, Steil R, Bohus M: Pain sensitivity is reduced in borderline personality disorder, but not in posttraumatic stress disorder and bulimia nervosa. World J Biol Psychiatry 2010; 11(2, part 2):364–371
    7. Sansone RA, Whitecar P, Wiederman MW: The prevalence of borderline personality among buprenorphine patients. Int J Psychiatry Med 2008; 38:217–226
    8. Panksepp J, Herman BH, Vilberg T, Bishop P, DeEskinazi FG: Endogenous opioids and social behavior. Neurosci Biobehav Rev 1980; 4:473–487
    9. Kennedy SE, Koeppe RA, Young EA, Zubieta JK: Dysregulation of endogenous opioid emotion regulation circuitry in major depression in women. Arch Gen Psychiatry 2006; 63:1199–1208
    10. Zubieta JK, Smith YR, Bueller JA, Xu Y, Kilbourn MR, Jewett DM, Meyer CR, Koeppe RA, Stohler CS: Regional mu opioid receptor regulation of sensory and affective dimensions of pain. Science 2001; 293:311–315
    11. Gunderson JG: Disturbed relationships as a phenotype for borderline personality disorder (commentary). Am J Psychiatry 2007; 164:1637–1640
    12. Brodsky BS, Groves SA, Oquendo MA, Mann JJ, Stanley B: Interpersonal precipitants and suicide attempts in borderline personality disorder. Suicide Life Threat Behav 2006; 36:313–322

    source: http://ajp.psychiatryonline.org/cgi/reprint/167/8/882


  1. littleonion
    Re: An Opioid Deficit in Borderline Personality Disorder: Self-Cutting, Substance Abu

    This is an excellent article.
    Swim is sure she is not the only swimmer that can relate to a lot of that is mentioned, especially as it surmises that BPD may be directly affecting as many as 5.9% of the general population!

    An opioid deficit does certainly make A LOT of sense, and it almost feels, whilst reading the article that a few things suddenly fit together!

    Whilst swim appreciates this is only the beginning of finally finding some answers regarding BPD (and suitable treatment), it does seem that this research offers a glimmer of hope to borderlines, not only in providing reasoning for development of the disorder i.e, evidence that the causes are not purely environmental, but also that the quest for decent treatments may be taken more seriously by the medical establishment. (any borderline can tell you how they are treated differently by medics) An organic cause surely may be treated more simply.

    Perhaps an opioid antagonist will one day be a standard treatment for Borderline Personality Disorder along with other meds and therapies.

    Thanks for posting Spucky. :thumbsup:
  2. Spucky
    AW: An Opioid Deficit in Borderline Personality Disorder: Self-Cutting, Substance Abu

    I think it is amazing how much of the common Medical Opinion has changed,
    when you said 20 years ago "there is not enough of endogenous Opiate in my system"
    People would have send you directly to a Asylum for "mentally challenged People"!

    But more and more Bio-Chemical Discoverys are made and accepted,
    this is imo. a/ the good sign!
  3. Niandra
    Re: An Opioid Deficit in Borderline Personality Disorder: Self-Cutting, Substance Abu

    This is really interesting.
    My pet insect has borderline personality disorder and her symptoms are getting quite bad lately, so she was thinking of doing some kratom every now and then, and this article makes this idea more interesting and kind-of-reasonable, since that plant has opiate antagonists.
  4. psyche
    Re: An Opioid Deficit in Borderline Personality Disorder: Self-Cutting, Substance Abu

    No, it has opiate agonists. It activates the reward system and induces pleasure, opiate antagonists disable the pleasurable response to endoprhins released by cutting onesself, and to other opiate agonists.
  5. imyourlittlebare
    Re: An Opioid Deficit in Borderline Personality Disorder: Self-Cutting, Substance Abu

    I would look at this article with a certain level of skepticism.

    I wish I had more time but here is the major concerns I have with the theory behind this article

    1. There are similar hypotheses for autism but also that autism is the by-product of too much endogenous opioids and has led to the use of naltrexone in ASPD with neither being successful in any meaningful capacity (Abnormal Psychology, Butcher, Mineka, Hooley).

    2. Similar ideas with PTSD have been suggested. However, both the use of opioids and opioid antagonists were not useful in the treatment of PTSD. This would be similar as BPD has been suggested to occur in a high proportion of individuals who were raped or who suffered trauma (Wilson, Friedman, & Lindy; Treating Psychological Trauma & PTSD). In addition, both those with PTSD and BPD are susceptable to dissociation which was a major reason why these theories were developed. However, PTSD has not been successfully treated with either class of drugs.

    3. These alterations in binding can also be explained by a number of factors that would precede or mediate the activity of the opioid system. Those include the following

    a. Altered activity in the orbitolateral prefrontal cortex
    b. Altered activity in the anterior cingulate (which has been the focus of depression. In 2009, Society for Neuroscience discussed that the successful treatment of depression is less dependent on the type of drug and more on long term changes in this region. Therefore, stimulation in this region was shown to be more effective than buprenorphine treatment AND/OR stimulation to nucleus accumbens). This pathway, decribed by Mayburg (or Mayberg) discusses how activity is linked to changes observed in depression including altered reward pathways. Without directly altering the reward pathway, altering activity in ACC led to changes in these reward regions indirectly as the mechanisms of depression had more to do with this region than an actual deficit in reward.

    c. Trauma induced changes in the brain: Some areas may have altered opioid receptor activity but what about pain-pathways more involved? Periaquiductal grey is involved in pain sensations. There are other factors involved in the development of meaningful relationships including vasopressin and oxytocin which mediate opioid activity (Psychopharmacology: Grilly, 2006).

    d. Unfortunately, I do not like their wording on why people with BPD abuse opiates. Minorities are more likely to abuse drugs. Males are more likely to abuse drugs than women. Criminals are more likely to abuse drugs than non-criminals. Those with anti-social personality disorder are more likely to abuse drugs. All abuse opiates too. Those with PTSD abuse opiates but more likely to abuse alcohol (Wilson, Friedman, Lindy).

    1. The simpler explanation is this. Opiates are reinforcing. Thats why they are abused. You cannot have a control group of those with BPD who have not engaged in some form of self-injurous behaviors which a person gains tolerance to. Also negative affect causes alterations in opioid activity. Anger, outbursts, sensitivity to rejection, and other factors influence this as well. If a person with BPD is angry and believing that their partner/friend is going to leave, the biological response may be similar to an animal seeing a predictor. That is, more activity of endogenous opioid system in the periaqueductal grey in response to what is going to happen. Partialling out the effects of these other variables is impossible since this is a pervasive, long-term personality disorder.

    2. While the M-PACI and MACI (Millon, Theodore) personality inventories are useful in detecting personality traits that may lead to the development of BPD, the disorder has a low base-rate and many other factors involved including personality vulnerablities. Therefore, one could not do a great study unless they conducted longitudinal studies on a number of girls. But those with BPD are more likely to come from screwed up families so longitudinal work would be difficult. They might look at a group of those with BPD who have not engaged in cutting behaviors for years and have been "significantly" helped looked at for continued alterations.

    3. The simpler explanation is that cutting is one of many methods used to self-injure. It may be the disorder with a high proportion of cutting but it also is highlighted by other pseudo-suicidal acts.

    I applaud the research's attempt to look at this from another perspective. But I think the reason why opiates are abused is much simpler. If those with BPD exclusively abused opiates, I would think differently. But they also abuse benzodiazepines, barbiturates, amphetamines, etc. with each drug having its own unique effect.

    The interplay between behavior and neurophysiology is too difficult to decipher as trauma is often involved in the development of BPD and the disorder is characterized as "A deeply ingrained and maladaptive pattern of behavior of a specified kind, typically manifest by the time one reaches adolescence and causing long-term difficulties in personal relationships or in functioning in society". To make biological deductions about a personality disorder is difficult because of their behaviors, their interactions, their affect/poor emotional regulation, etc. all affect their biology and/or trauma alter biology.

    I applaud the effort of this researcher to deduce with the evidence they have. But this rationale has been used before for other disorders and cannot be substantiated in this disorder between the complex interplay of biology, emotions, cognitions, behaviors, interpersonal, and intrapersonal factors.
  6. Niandra
    Re: An Opioid Deficit in Borderline Personality Disorder: Self-Cutting, Substance Abu

    Yes, sorry, I wanted to say agonists. My pet insects has made a contorted reasoning, so I have to explain it better.

    She's a self injurer and at periods the problem gets really severe, but on overall she can be quite in control of that. The biggest troubles she's currently having are more on the side of daily functioning (trivial things like cleaning the house, get to work, cook a meal etc) and interpersonal relationships.

    So, she'd like to relieve the psychological distress and pain to get more eurythmic when things are getting too worse (rather than stop cutting which is something not urgent now since she's SI-free from 5 weeks and she's doing pretty well at avoiding it), in order to manage to focus on strategies to overcome the relationship problems.

    Besides the mechanism you've explained, this article states that the reason why people suffering from borderline personality disorder experience amplified emotional distress and pain may be due to an opioid deficit in their brain, thus the statistical data on their frequent recoursing to opioid drugs, which by the way seems to make them more high functioning than euphoric. This is just what my pet insect would like to achieve every now and then, when her life is too messed up and she needs to get more eurythmic to rearrange it and start again, and focus on keeping relationships intact and decenlty healthy.

    She reckons that the reasoning may sound twisted, but she's really looking for something that would ease the psychological pain for a certain window of time, in order to let her function better on other aspects, arrange plans and schedules to live a decent life. If the data proposed are some way true, then kratom should balance her brain a little bit, and she could take it when she's at the bottom.
  7. imyourlittlebare
    Re: An Opioid Deficit in Borderline Personality Disorder: Self-Cutting, Substance Abu

    There is no single cause of BPD. There are several risks factors that, when present, increase the chances of a person developing BPD. As I stated before, this article highlights how this is merely a theory and unfortunately, the theoretical evidence does not support the conclusions.

    This comes from the Essential Family Guide to Borderline Personality Disorder (2008). and Stop Walking on Eggshells, 2nd edition

    1. Biological factors:
    Dysfunction in SEVERAL neurotransmitters, as well as activity in specific brain regions, CAN lead to problems such as impaired reasoning, impulsivity, and unstable emotions. However, not all people with these abnormalities develop said condition. For example, look at this study in Alzheimer disease. The “Nun Study” involved 678 volunteer nuns and they took a battery of tests over the course of the study. They provided biographical records and life stories to the researchers and finally to donate their brains for scientific study after their death. In several cases, pathology studies of brain tissue from the deceased nuns did not correlate with their performance on cognitive function tests. Sometimes the pathologist would score a brain as having signs of extremely advanced AD, only to learn later that the nun herself scored extremely well on all cognitive tests. Other times a brain would show only slight damage associated with AD, and the nun was characterized as exhibiting the signs of advanced cognitive decline and dementia. The single most important conclusion from the study is that Alzheimer disease is not straight forward.

    A condition like AD (alzheimer's dementia) is considered very biologically oriented. However, even in the presence of the tell-tale signs of the disorder (the presence of plaques and tangles in post-mortem examination). There is no one biological factor that is indicated in BPD, even in post-mortem studies of brain tissues or different imaging. While orbitofrontal cortex and anterior cingulate/connections to the amygdala or the emotional center of the brain are implicated, its not as conclusive as AD findings.

    2. Genes- there is no single specific gene for BPD. There are genes that increase risk for disorders that may be passed on by those people who have the disorder OR a related disorder such as bipolar disorder, depression, substance use disorders, and PTSD.

    While some speculate that BPD is the result of instability in specific neural pathways, the evidence is more suggestive that there is a complex interaction between biology and environment that leads to the development of this disorder (particularly since those with genes implicated in other disorders/brain alterations similar to BPD develop different symptoms.

    In addition, while biology and environment may increase the risk of developing the disorder, it is even more likely that after it is developed, behaviors/cognitive/environmental variables are key factors in the maintenance of the disorder (those with opioid dependency, once clean, do not engage in behaviors similar to those seen in BPD. It would be hypothesized that using an opiate antagonist in those without the disorder or opiate addicts may universally display symptoms of BPD. However, they do not).

    3. Environmental factors

    Factors such as abuse, neglect, childhood trauma are factors that do appear to trigger BPD in someone who is predisposed to the condition

    4. Summary

    Studies only reflect borderline personalities within the mental health systema nd who are suicidal and self-harming. They are not a true random sample of the entire population with BPD because the entire higher functioning population is EXCLUDED.

    Opiates are reinforcing. As I stated before, it would be more interesting if all BPD's exclusively abused drugs with actions on opiate receptors. However, they dont. In fact, there is even gender differences in the types of substances preferred with males preferring stimulants and women preferring alcohol and sedatives (neither group had a rate of opiate addiction higher than other groups).


    Self-cutting is a coping mechanism and a pseudo-suicidal act but there are many other forms of self-harm/pseudo-suicidal acts that are committed within this population. It could be that there are some problems with opioid system functioning but that would be further dysregulated/thrown into chaos with opiate use as this leads to more tolerance and since substance abuse is common within this sub-population, its not wise to think that the use of opiates would help the condition. In fact, it may hurt it as inhibitions are weakened and that could lead a person to act on their anger or suicidal inclinations more readily.

    If one wanted to "help" their opiate system, antidepressents do this. In fact, it is a mechanism of action that occurs slowly and may possibly underlie the therapeutic effect of the medication. Below is an excerpt from an unpublished manuscript (2009) describing this action.

    " The endogenous opioid system, consisting of the three receptor subtypes mu, delta, and kappa, are involved in the function of the brain’s glutamatergic system. Opiate receptors within the neocortex regulate the release of glutamate through the mediation of 5-HT receptors (De Felipe, De Ceballos, Gil, & Fuentes, 1985; De Gandaria, Echevarria, Acebes, Silio, & Casis, 1998). Mu receptors inhibit serotogenic neurons which significantly reduces the release of glutamate in neocortex. Reductions in glutamate release reduce the risk of excitotoxicity within the CNS. Exogenous opiate exposure decreases glutamate released within the hippocampus (Guo, Xu, Li, Yang, Wu, & Pei, 2005) which is a contributing factor to altered anatomical and physiological activity of the hippocampus in those with depressive symptoms (Berton, & Nestler, 2006; Chen, Dowlatshahi, MacQueen, Wang, & Young, 2001). The opiate system regulates 5-HT-mediated glutamate release and is involved in SSRI and tricyclic anti-depressant drug activity.
    The opiate system is a key system involved in regulating HPA axis activity and changes within the neuroendocrine systems implicated in depression (Nikisch et al., 2005). Within the CNS, opiate receptors control the secretion of stress hormones released by the HPA axis (Pascoea et al., 2008). Mu receptor activity significantly decreases activity within the HPA axis (Pascoea et al., 2008). However, kappa opiate receptor activity causes increased HPA axis activity (Pascoea et al., 2008). The use of the exogenous mu receptor agonist fentanyl significantly reduces levels of adrenocorticotropic hormone ACTH and cortisol secretion within the HPA axis (Broadbear, Winger, & Woods, 2004). Since HPA axis activity is dependent on the regulatory effects of opiate receptor, this further suggests a link between opioid system functionality and depression (Henn & Vollymayr, 2003; Nestler & Carlezon, 2006). Ketamine has been shown to cause marked reductions in HPA axis activity comparable to the mu agonist fentanyl (Broadbear & Woods, 2006). Classical antidepressants cause marked reductions in HPA axis activity which correlate to the onset of their antidepressant action (Nickel et al., 2003; Nikisch et al., 2005) while other NMDA antagonists increase activity within the HPA axis (Pechnick & Poland, 2004) suggesting that, in part, some of the sustained and replicable antidepressant action of ketamine may be the result of altered HPA axis activity.
    Their appears to be a link between activity in the opioid system in the maintenance of antidepressant effects associated with classical antidepressant drug exposure (Singh, Jain, Naveen & Kulkarni, 2001) and the significant effect ketamine exerts on the opioid system (Reich, & Silvay, 2008). The use of opiate antagonists can block anti-depressant effects of chronically administered anti-depressant drugs in the FST (Singh, Jain, Naveen & Kulkarni, 2001; Torregrossa, Jutkiewicz, Mosberg, Balboni, Watson, & Woods, 2006). Furthermore, opiate antagonists can reverse the analgesic effects of chronic anti-depressant treatments (Singh, Jain, Naveen, & Kulkarni, 2001). Chronic tricyclic and SSRI administration is linked to analgesic effects and increased opiate receptor expression in the frontal portion of the brain and an increased level on endogenous opioids (De Gandaria, Echevarria, Acebes, Silio, & Casis, 1998; De Gandaria et al., 1999). In turn, NMDA receptor antagonists have been shown to have numerous modulatory effects on the opioid system of the brain (Meyer & Quenzer, 2005). "

    However, tolerance occurs with opiates but not antidepressants in this capacity. If the opiate system was truly involved, then antidepressants would universally work. However, it is much more complicated than one neurotransmitter system involved. There are intricate systems wide connections.

    This one article is not a green light for anyone to self-medicate using opiates for this disorder. It is a hypothesis that is being explored (albeit, not as widely accepted due to the findings of the literature regarding comparable disorders and this theory). If one were truly concerned about activity in opioid system activity, then antidepressants would take care of it without the risks or habit forming/tolerance inducing effects of opiates.

    This is particularly problematic because BPD is highlighted with black and white thinking. If one believes that this therapy is superior than another despite evidence to the contrary and due to the reinforcing effects of opiates clouding judgment, then one might become lost. Keep an open mind and research alternative theories on the disorder, not just ones that confirm that a drug with reinforcing effects is useful. Drugs with reinforcing value rarely are useful in the treatment of these types of disorders. While it may feel good, no therapeutic effect is achieved and learning how to better cope with issues can become harder if one relies simply on reinforcing drugs since the positive feelings those give are significantly more than those of even natural rewards (food, sex, etc). If natural rewards for change lose the reinforcing value, than it is more difficult to get unstuck and think straight (Read up on Thurstone and his theories in addition tothe book Science and Human Behavior by B.S. Skinner).

    Meaningful, lasting change and increases in quality of life in individuals with BPD have been achieved using dialectal behavioral therapy because it challenges the core problems and emotional regulation issues of the disorder. It is hard work but meaningful and lasting change occurs. Again while I am happy the research is looking at the etiology of the disorder, their theory is very difficult to accept in the face of alternative evidence and problems with the study methodology.
  8. Niandra
    Re: An Opioid Deficit in Borderline Personality Disorder: Self-Cutting, Substance Abu

    Thank you for your entry, it is very informative.
    My pet insect and I perfectly know that BPD is a very complex disorder with a wide spectrum of possible causes and synergies, the fact is that my pet insect would love to start DBT therapy (which as you said is proved to be very effective) but she has no money to afford it at the moment, and life is really unbalanced at times that she thinks she needs some "chemical help". She took different psy-meds in the past when she was in treatment, but nothing gave satisfactory effects and she ended up drugging herself up with benzos because all that feeling apart and even more instable was driving her mad. She hasn't totally changed her opinion on trying some drugs, but if she's going to use them, she'll definitely take them "in another perspective".
  9. imyourlittlebare
    Re: An Opioid Deficit in Borderline Personality Disorder: Self-Cutting, Substance Abu

    If antidepressants affect the opiate system as they do (based on the discussion and evidence I provide from an unpublished manuscript with citations), then some relief based on this effect would have been expected. Unfortunately, I see all too often on this site the use of drugs create an unrealistic expectation of what therapy and psychotropics SHOULD do. The immediate relief reinforcing drugs induce causes a person to have an unrealistic ideal of what "normal" should feel like. Im not sure if this is a studied phenomenon, and you will be certain I will conduct a literature review on this when time is on my side.

    But unfortunately, many people self-medicate and this can cause problems for the therapist and the psychiatrist as those medications are not supposed to cause well-being. They are supposed to therapeutically reduce symptoms making things more manageable. Substance abuse (and the longer term problem of dependence) then becomes another obstacle that the person has to overcome before believing that something can help.

    One note I would like to put on this site is this. There is a distinct difference between social workers, psychologists with a master's degree, those with a Psy.D., those with a counseling Ph.D., and those with a Clinical Psychology Ph.D. Here is a guide to the differences in training, acceptance rates, and focuses although the guide was created for those interested in getting into the programs

    http://www.unc.edu/~mjp1970/Mitch's Grad School Advice.pdf

    Clinical Psychologists with a Ph.D. are the best trained out there. Getting into a Ph.D. is more difficult than getting into medical school or law school (APA, 2010; Sayette, Mayne, & Norcross, 2010).

    There are alternative ways to find help for this disorder and there are medications which help control the symptoms. One would expect that after finding a medication that controls the symptoms, they may feel different or not themselves. However, the true test of the medications efficacy is how interpersonal relationships hold up after the medication is taken for an extended period of time. Those that want changes in their life should expect that the drugs will change them and that is a sucky feeling that takes time. With fulfilling interpersonal relationships, perhaps a person would feel better overall and less empty. That is a hypothesis based on the evidence. However, here is a study that highlights this fact in regards to antidepressants


    I feel strongly on this and those that feel differently, I respect your opinion and am merely giving mine. My hope is that with the use of the internet, afforable and local help can be found. Although the focus of this site is the use of drugs, I feel obligated to post this due to the duty of this site in harm-reduction. While this typically means trying to reduce fatalities with drug use, I see it in a larger picture. To try and help the quality of life of people who are suffering by helping them better understand their options.

    While I have not tried this site, http://www.bpdcentral.com/ offers help in trying to find local support.

    Thank you for all your posts and respecting my opinions in regards to this article/topic.
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