Scientists discover a brain process that explains why some fear-related memories may not be accessible to traumatized patients. TraumaAndDissociation, CC by 2.0
While some victims of trauma too easily remember what causes their pain, other victims suffer tremendous anxiety for no apparent reason whenever they’re in some innocuous-seeming place — a room in their grandparents’ house, for example. Some mysterious event clearly happened there, yet no memory exists. In a new study (conducted on mice), scientists discovered a brain process that explains why some fear-related memories may not be available.
“Distinct neurobiological mechanisms can explain why some trauma victims go on to remember and re-experience their trauma, whereas [other victims] develop dissociative amnesia (an inability to consciously access a stored memory),” Dr. Jelena Radulovic, principal investigator and a professor at Northwestern University Feinberg School of Medicine, toldMedical Daily in an email.
Scientists have long understood that there’s more than one pathway through the brain to the storage closet of memory. Now, Radulovic and her colleagues track a unique trail directly related to trauma. In fact, the microRNA-GABA pathway they describe in their new study may also indicate how susceptible each of us is to developing amnesia after a traumatic event.
They discovered this pathway by exploring a special phenomenon of learning.
What Influences Memory?
Learning is a state-dependent process, which means that when we learn something new in a particular situation or state of consciousness, we’re able to remember it best when we place ourselves back in the original circumstance or state of mind. Students, then, who learn information in one room will get higher scores if they are tested in the same room. Not only place, but time of day as well as common drugs also influence memory abilities. If students learn something while drinking coffee, for instance, they will remember it best when they return to their original caffeinated state.
Based on this phenomenon, various researchers have used drugs to try and access hidden memories. But while some pharmaceuticals may return the brain to the state of consciousness that occurred during encoding — the first step in memory storage — they haven’t done well in excavating traumatic memories. A drug targeting different processes in the brain, then, would be necessary for fear-based recall.
So, Radulovic and her colleagues focused on two amino acids in the brain: glutamate and GABA. These work in tandem to control levels of excitation and inhibition in the brain, and, under normal conditions, remain balanced. Hyper-arousal, however, which occurs when we are terrified, causes glutamate to surge.
Glutamate, is known as the excitable amino acid; it’s also the primary chemical that helps store memories across distributed brain networks. GABA, on the other hand, is calming and partly works by blocking glutamate and its excitable actions. Synaptic GABA receptors, in particular, will balance glutamate receptors in the presence of stress. Yet, extra-synaptic GABA receptors also exist. These work independently, responding to levels of a variety of neurochemicals, including sex hormones and micro RNAs.
Between the drugs amobarbital and diazepam, only amobarbital, which binds to all GABA receptors is able to stimulate memory recall — diazepam is ineffective, due to the fact it only binds to synaptic GABA receptors. Knowing this, Radulovic and her colleagues hypothesized the ability to remember stressful experiences might be mediated by the extra-synaptic GABA receptors.
For its experiment, the research team injected the mice with gaboxadol, a drug that stimulates extra-synaptic GABA receptors. Next, they placed the mice in a box and gave them an electric shock. When the mice returned to the same box the next day, they moved about freely and without fear. Clearly, the rodents did not remember the electric shock.
Then, the scientists injected the mice with the drug once again and returned them to the box. This time, the rodents froze in anticipation of another shock.
Rerouting Painful Memories
When extra-synaptic GABA receptors were activated by a drug, the researchers said, the brain used completely different molecular pathways and neuronal circuits to store the memory. The brain rerouted the memory so that it couldn’t be accessed. The researchers say their findings imply that in response to trauma, some people will not activate the glutamate system but instead the extra-synaptic GABA system.
This system is regulated by a small microRNA: miR-33. Some patients with psychiatric illnesses have different levels of miR-33 compared to healthy individuals.
The power of any memory lies, to a large extent, in the amount of processors within the cells creating a pathway through the brain, explained Dr. Vladimir Jovasevic, lead study author and a former postdoc in Radulovic’s lab.
“The role of microRNAs is to fine-tune the amount of the processors, so they can function at optimal level,” said Jovasevic, and “miR-33 sets the optimal amount of processors involved in state-dependent learning.” But when levels of miR-33 change, this “results in an increased predisposition to psychiatric disorders caused by improper processing of state-dependent memories.”
Evidence from the new study, Radulovic and Jovasevic said, may lead to new treatments for patients with psychiatric disorders who cannot recover unless they gain conscious access to the memory of what caused their trauma.
Source: Jovasevic V, Corcoran KA, Leaderbrand K, et al. GABAergic mechanisms regulated by miR-33 encode state-dependent fear. Nature Neuroscience. 2015.
In my mid-20s, at the beginning of my training as a clinical psychologist, I was placed on a psychiatric day treatment ward in one of the poorer parts of Boston. One day, the experienced therapist with whom I led a men’s group was sick, and I was called on to do the group by myself. A ball of nerves, I decided to ask the men about their ancestry (with the helpful presence of a globe in the room) rather than risk silence. I briefly spoke of my Russian and Eastern European great-grandparents to set the tone and then spoke with each man in turn. After a few minutes of this exercise, there was a pause. A fellow from across the room looked at me and said softly, “You think you’re better than us, don’t you? You think this could never happen to you.”
I was stunned. Somehow I stammered a denial, but of course he was right. Perhaps I didn’t think I was better than them, but I certainly thought I was different from them. Like most of us in Western societies, I had grown up believing that psychiatric disorders were illnesses—diseases like any other—and there had been nothing in my training until then to convince me otherwise.
But learning about trauma, dissociation, and attachment in the ensuing decades has changed my mind. And I am not the only one.
PARADIGMS IN CONFLICT
Over the past several decades, the study of schizophrenia and the study of the dissociative disorders have been dominated by opposing paradigms. For schizophrenia, the assumption of a genetic basis and biological causation has reigned supreme. Adverse childhood experiences are viewed as irrelevant at best and adult stressful or traumatic experiences as only “releasing” underlying disease mechanisms. Symptoms are considered meaningless—unrelated to a person’s life circumstances—and psychotherapeutic approaches, when used at all, are limited to supporting medical interventions. In diagnosing schizophrenia for clinical or research purposes, posttraumatic and dissociative disorders are rarely considered or ruled out; indeed, in adherents to this paradigm, posttraumatic disorders are frequently disdained, discredited, or simply ignored.
In contrast, the overriding paradigm for the study of dissociative disorders has focused almost exclusively on life events—traumatic or otherwise—that are assumed to be meaningfully related to the symptoms a person experiences. A wide range of psychotherapeutic approaches to treatment are supported and advocated, whereas most medical interventions are viewed as anathema. At the same time, many trauma-oriented clinicians and researchers think of schizophrenia only as something dissociative disorders are not—but are often confused with; schizophrenia’s validity as a biologically based entity is rarely questioned.
Consider how these two paradigms deal with auditory verbal hallucinations. To persons adhering to the dominant biological paradigm (or “medical model”), voices are psychotic symptoms to be treated with medications or coped with using distraction techniques. As Colin Ross (2008Ross, C. A.2008. “Dissociative schizophrenia”. In Psychosis, trauma and dissociation: Emerging perspectives on severe psychopathology, Edited by: Moskowitz, A., Schäfer, I. and Dorahy, M. J.281–294. London, , England: Wiley.[Google Scholar]) put it, from this perspective the notion of talking with someone’s voices would be as absurd as “asking a patient’s knee a question” (p. 284). In contrast, in a trauma/dissociation paradigm, voices are split-off parts of the personality that are ignored at one’s own peril—acknowledging and engaging these disowned parts, though often challenging, is typically advocated. The schizophrenia field views voices as biologically generated indications of a brain disorder, whereas the dissociation field views them as psychological indications of unresolved trauma or loss. Two more disparate perspectives cannot be imagined. Currently, these fields eye each other with considerable suspicion and, to a large extent, do not speak the same language or experience the world in the same way.
EUGEN BLEULER: THE MARRIAGE OF DISSOCIATION AND SCHIZOPHRENIA
But it was not always this way. When Eugen Bleuler published his Dementia Praecox oder Gruppe der Schizophrenien (Dementia Praecox or the Group of Schizophrenias) 100 years ago, the construct of schizophrenia was infused with dissociative concepts (Moskowitz, 2008Moskowitz, A.2008. “Association and dissociation in the historical concept of schizophrenia”. In Psychosis, trauma and dissociation: Emerging perspectives on severe psychopathology, Edited by: Moskowitz, A., Schäfer, I. and Dorahy, M. J.35–49. London, , England: Wiley.[Google Scholar]; Moskowitz & Heim, 2011Moskowitz, A. and Heim, G.in press. “Affect, dissociation, psychosis: Essential components of the historical concept of schizophrenia”. In Psychosis and emotion: The role of emotions in understanding psychosis, therapy and recovery, Edited by: Gumley, A., Gilham, A., Taylor, K. and Schwannauer, M.London, , England: Routledge.[Google Scholar]). While insisting on an organic basis for the disorder, Bleuler recognized the symptoms his patients described as meaningfully related to their life experiences and used hypnotherapy and psychotherapy in his clinical work. He justified changing the name of the disorder largely on the basis that the “splitting” of the “different psychic functions” was central to its pathology (Bleuler, 1911/1950Bleuler, E.1950. Dementia praecox or the group of schizophrenias, Edited by: Zinkin, J.New York, NY: International Universities Press. Original work published 1911[Google Scholar], p. 8). Bleuler’s 1911Moskowitz, A. and Heim, G.2011. Eugen Bleuler’s Dementia praecox or the group of schizophrenias (1911): A centenary appreciation and reconsideration. Schizophrenia Bulletin, 37(3): 471–479.[Google Scholar]“definition” of schizophrenia reads almost as a calling card for dissociative disorders:
If the disease is marked, the personality loses its unity; at different times different psychic complexes seem to represent the personality … one set of complexes dominates the personality for a time, while other groups of ideas or drives are “split off” and seem either partly or completely impotent. (p. 9)
The profoundly dissociative nature of Bleuler’s concept of schizophrenia has been ignored for many decades but should be apparent to any unbiased reader, as has been recognized by Colin Ross (2004Ross, C. A.2004. Schizophrenia: Innovations in diagnosis and treatment, New York, NY: Haworth Press.[Google Scholar]) and myself (Moskowitz, 2008Moskowitz, A.2008. “Association and dissociation in the historical concept of schizophrenia”. In Psychosis, trauma and dissociation: Emerging perspectives on severe psychopathology, Edited by: Moskowitz, A., Schäfer, I. and Dorahy, M. J.35–49. London, , England: Wiley.[Google Scholar]; Moskowitz & Heim, in press).
However, Bleuler’s ideas about schizophrenia have little currency in today’s nosological world; all but the name has been jettisoned, and even that has been retained with considerable squeamishness—requiring constant vigilance against its interpretation as “split personality.” Instead, the architects of our current diagnostic system harked back to Bleuler’s predecessor, Emil Kraepelin, for inspiration.
EMIL KRAEPELIN, TAXONOMIES, AND GENERAL PARESIS
Despite Kraepelin’s experimental psychology pedigree (he studied with Wilhelm Wundt early in his career), his ideas on Dementia Praecox were far less informed by psychology than those of Bleuler (who used Jung’s word association experiments to aid his understanding), and he saw concepts of dissociation as irrelevant to diagnostic conceptualization. Rather, Kraepelin’s approach to parsing mental disorders was strongly influenced by biological classifications, such as Linnæus’s taxonomy of plants and the system developed by his own esteemed older brother, the biologist Karl Kraepelin (Weber & Engstrom, 1997Weber, M. M. and Engstrom, E. J.1997. Kraepelin’s “diagnostic cards”: The confluence of clinical research and preconceived categories. History of Psychiatry, 8: 375–385.[Google Scholar]). In addition, the model on which Kraepelin based his concept of Dementia Praecox was General Paresis of the Insane—sometimes called Dementia Paralytica. General Paresis was a terminal condition that combined psychotic symptoms with paralysis and ultimately death and was widespread in Europe during the early part of the 19th century. The triumphant linking of its symptoms with a brain disorder caused by late-stage syphilitic infections in the mid-19th century clearly provided Kraepelin with a template or paradigm—a “model disease entity”—for mental disorders in general and dementia praecox in particular (Jablensky, 1995Jablensky, A.1995. Kraepelin’s legacy: Paradigm or pitfall for modern psychiatry?. European Archives of Psychiatry and Clinical Neuroscience, 245: 186–188.[Google Scholar], p. 186).
THE NEO-KRAEPELINIAN PARADIGM OF MENTAL DISORDERS
The example of General Paresis, mental disorders were brain disorders but that any classification of psychopathology was best pursued through identifying brain pathology, not only drove Kraepelin’s typology but also still underpins that of the current diagnostic systems influenced by his thinking—the Diagnostic and Statistical Manual of Mental Disorders(3rd ed. [DSM–III]), the International Classification of Diseases–9, and their related progeny (Jablensky, 2007Jablensky, A.2007. Living in a Kraepelinian world: Kraepelin’s impact on modern psychiatry. History of Psychiatry, 18: 381–388.[Google Scholar]). For the past three or four decades, the classification of mental disorders has been dominated by this approach, which came out of a group of primarily American psychiatrists self-identified as neo-Kraepelinian (frequently referred to as a movement or even a revolution).
As the neo-Kraepelinians set about revising the psychiatric diagnostic system in the 1970s, and reached their goal with the 1980 publication of the DSM–III, they were ostensibly creating an atheoretical system with improved reliability over its precursors. But in reality, they were clearly motivated by the belief that these conditions were medical disorders like any other; indeed, in a publication from that time, two prominent researchers spoke of “coveting” for schizophrenia the solid genetic grounding of “pellagra, paresis, tuberculosis, polio, and PKU [phenylketonuria]” (Gottesman & Shields, 1973Gottesman, I. I. and Shields, J.1973. Genetic theorizing and schizophrenia. British Journal of Psychiatry, 122: 15–30.[Google Scholar], p. 15).
A fundamental task for the neo-Kraepelinians was to shore up the distinction between schizophrenia and manic depression, a distinction that had been blurred by Bleuler’s broad category. They accomplished this primarily by strongly emphasizing specific psychotic symptoms in the diagnostic criteria for schizophrenia (particular auditory hallucinations and delusions proposed by Kurt Schneider—so-called first rank symptoms) and by undermining the validity of the schizoaffective disorder category in a number of ways (Moskowitz & Heim, in press-a). The Kraepelinian dichotomy of schizophrenia and bipolar disorder has been explicitly seen as providing the foundation for a biologically based nosology; indeed, challenges to the clear differentiation of schizophrenia and bipolar disorder are often viewed as undermining the validity of the entire diagnostic system (Kendell, 1987Kendell, R. E.1987. Diagnosis and classification of functional psychoses. British Medical Bulletin, 43: 499–513.[Google Scholar]). In addition, the neo-Kraepelinians have articulated a number of more general assumptions, including (a) that mental disorders are discrete from one another and from “normality” and (b) that advances in understanding mental disorders will come primarily from focusing on neurobiology (Klerman, 1978Klerman, G. L.1978. “The evolution of a scientific nosology”. In Schizophrenia: science and practice, Edited by: Shersow, J. C.91–121. Cambridge, MA: Harvard University Press.[Google Scholar]). This level of domination over research and practice (for example, DSM–IV diagnoses are required for insurance payments and frequently for journal article acceptance) clearly constitutes what Thomas Kuhn termed a scientific paradigm.
PARADIGMS AND SCIENTIFIC REVOLUTIONS
According to Kuhn (1970Kuhn, T. S.1970. The structure of scientific revolutions, 2nd, Chicago, IL: University of Chicago Press.[Google Scholar]), in The Structure of Scientific Revolutions, the idea that science advances in a linear fashion with knowledge continually accruing so that “reality” or “truth” is more and more closely approximated over time is a myth. Rather, he argued, a field advances under the influence of a dominant paradigm, meaning both a particular past scientific achievement held up as a model or exemplar (as in the case of General Paresis and psychopathology) and the generally accepted beliefs and attitudes of a particular scientific community. A paradigm exerts an organizing influence on a field and guides research, determining to a large extent what types of research questions are considered legitimate and what sorts of answers are considered acceptable.
Kuhn (1970Kuhn, T. S.1970. The structure of scientific revolutions, 2nd, Chicago, IL: University of Chicago Press.[Google Scholar]) argued that paradigms change and a scientific revolution ensues when three conditions are met: (a) a period of crisis develops in which the paradigm fails to adequately answer questions considered fundamental; (b) serious “anomalies” occur in which phenomena not clearly compatible with the paradigm are observed; and, importantly (c) a suitable alternative paradigm that explains many of the previous findings and at least some of the observed anomalies comes to light. Kuhn saw scientific revolutions as taking time to resolve; he argued that changing such strongly held beliefs involved a process of persuasion and fundamental reorganization not unlike that of religious conversion: “Conversions will occur a few at a time until, after the last holdouts have died, the whole profession will again be practicing under a single, but now different paradigm” (Kuhn, 1970Kuhn, T. S.1970. The structure of scientific revolutions, 2nd, Chicago, IL: University of Chicago Press.[Google Scholar], p. 152).
Since the publication of the DSM–III in 1980, the ascendance of the neo-Kraepelinianparadigm in the psychiatric world has been paramount. It has driven our view of schizophrenia and marginalized acceptance of the dissociative disorders and posttraumatic stress disorder (PTSD). However, this paradigm is now under threat from many quarters—from within its ranks as well as from outside—and there is good reason to view it as a paradigm in crisis.
FAILURES OF THE NEO-KRAEPELINIAN PARADIGM
Evidence for fundamental tenets of the neo-Kraepelinian paradigm—that there are clear genetic or biological bases for schizophrenia and other mental disorders and that mental disorders are discrete from one another and from normal experiences—have not been supported.
Comorbidity of diagnoses, incompatible with viewing diagnoses as discrete categories, is rampant in the DSM–IV system and typically viewed as a major problem. Psychotic symptoms are now recognized as common to many disorders other than schizophrenia, and their presence in a significant portion of the community with no diagnosed mental disorder firmly suggests that the line between “normality” and “pathology” is not hard and fast (Van Os, Linscott, Myin-Germeys, Delespaul, & Krabbendam, 2008Van Os, J., Linscott, R. J., Myin-Germeys, I., Delespaul, P. and Krabbendam, L.2008. A systematic review and meta-analysis of the psychosis continuum: Evidence for a psychosis proneness—persistence—impairment model of psychotic disorder. Psychological Medicine, 39: 179–195.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]). In addition, evidence for the validity of schizoaffective disorder, a fundamental challenge to the Kraepelinian dichotomy, has accumulated over the years. The demonstrated existence of persons with prominent schizophrenic and affective symptoms undermines the core distinction between schizophrenia and bipolar disorder and provides an argument for viewing even severe psychopathology as a dimension or series of dimensions instead of as categories. Finally, the abject failure of genetic-based research to find any strong link with schizophrenia or bipolar disorder provides a further anomaly for the neo-Kraepelinianparadigm to explain or attempt to ignore (if anything, the genetic evidence points to a “shared neurobiology across the two disorders,” Thaker, 2008Thaker, G.2008. Psychosis endophenotypes in schizophrenia and bipolar disorder. Schizophrenia Bulletin, 34: 720–721.[Google Scholar], p. 720).
All of this is taking its toll on the medical model. As the neo-Kraepelinian edifice begins to crumble, adherents resort to stronger and stronger biological language, as though words such as neuropsychiatry and endophenotypes have the power to restore its once shining façade. The emphasis on endophenotypes is particularly telling, as this concept involves exploring putative underlying biological variables that may have only an indirectrelationship to the signs and symptoms of mental disorders. For example, a recent large-scale twin and family study focused on apparent genetic impairments in memory and intelligence as conveying liability for schizophrenia (Toulopoulou et al., 2010Toulopoulou, T., Goldberg, T. E., Mesa, I. R., Picchioni, M., Rijsdijk, F., Stahl, D.and … Murray, R. M.2010. Impaired intellect and memory: A missing link between genetic risk and schizophrenia?. Archives of General Psychiatry, 67: 905–913.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]). The strong emphasis on endophenotypes, arising from a failure to find clear connections between genetic makeup and psychiatric diagnoses or symptoms, suggests that the neo-Kraepelinianstalwarts have beaten a strategic retreat; at the same time that psychological approaches to treating and understanding psychiatric symptoms, including delusions and hallucinations, have made great strides, the dominant paradigm has given up the traditional territory of mental disorders—the signs and symptoms that people suffer from and that treatments target.
So, the neo-Kraepelinian, categorical, medically based diagnostic system clearly seems to be in a state of crisis. But, as Kuhn has noted, a discipline such as psychopathology will not loosen its grip on a paradigm unless a suitable alternative is available to take its place. What is the evidence that one is appearing?
THE EMERGING TRAUMA/DISSOCIATION PARADIGM
In recent years, evidence has accumulated that traumatizing events are strongly linked to psychopathology in general and psychotic symptoms in particular. Kenneth Kendler, a prominent psychiatric geneticist, concluded from a carefully designed large-scale twin study that childhood sexual abuse was “causally related” to the development of psychiatric and substance abuse disorders (Kendler et al., 2000Kendler, K. S., Bulik, C. M., Silberg, J., Hettema, J. M., Myers, J. and Prescott, C. A.2000. Childhood sexual abuse and adult psychiatric and substance use disorders in women: An epidemiological and cotwin control analysis. Archives of General Psychiatry, 57: 953–959.[Crossref], [PubMed], [Web of Science ®], [Google Scholar], p. 953). In a subsequent commentary, he noted that the more than threefold increase in major depression attributable to severe sexual abuse was “much greater” than the odds ratios associated with any gene putatively linked to schizophrenia or bipolar disorder (Kendler, 2006Kendler, K. S.2006. Reflections on the relationship between psychiatric genetics and psychiatric nosology. American Journal of Psychiatry, 163: 1138–1146.[Crossref], [PubMed], [Web of Science ®], [Google Scholar], p. 1140); he soberly concluded, “The project to ground our messy psychiatric categories in genes … may be in fundamental trouble” (Kendler, 2006Kendler, K. S.2006. Reflections on the relationship between psychiatric genetics and psychiatric nosology. American Journal of Psychiatry, 163: 1138–1146.[Crossref], [PubMed], [Web of Science ®], [Google Scholar], p. 1145). Psychotic symptoms in particular appear to be strongly linked to trauma, both adult trauma (particularly when associated with PTSD; e.g., Scott, Chant, Andrews, Martin, & McGrath, 2007Scott, J., Chant, D., Andrews, G., Martin, G. and McGrath, J.2007. Association between trauma exposure and delusional experiences in a large community-based sample. British Journal of Psychiatry, 190: 339–343.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]) and childhood interpersonal traumas (including in longitudinal studies such as Arseneault et al., 2011Arseneault, L., Cannon, M., Fisher, H. L., Polanczyk, G., Moffitt, T. E. and Caspi, A.2011. Childhood trauma and children’s emerging psychotic symptoms: A genetically sensitive longitudinal cohort study. American Journal of Psychiatry, 168: 65–72.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]). These studies are becoming increasingly well designed, typically controlling for many potentially confounding variables, even apparently genetic ones. Furthermore, psychological trauma has been strongly linked to the development of delusions and hallucinations (Moskowitz, Read, Farrelly, Rudegeair, & Williams, 2009Moskowitz, A., Read, J., Farrelly, S., Rudegeair, T. and Williams, O.2009. “Are psychotic symptoms traumatic in origin and dissociative in kind?”. In Dissociation and the dissociative disorders: DSM–V and beyond, Edited by: Dell, P. and ’Neil, J. O. 521–533. New York, NY: Routledge.[Google Scholar]), and dissociation has been found to consistently and powerfully predict auditory hallucinations (but not delusions) in a range of populations (Moskowitz & Corstens, 2007Moskowitz, A. and Corstens, D.2007. “Auditory hallucinations: Psychotic symptom or dissociative experience?”. In Trauma and serious mental illness, Edited by: Gold, S. N. and Elhai, J. D.35–63. Binghamton, NY: Haworth Press.[Google Scholar]; several recently published studies have supported this relationship). Finally, brain changes long assumed to indicate a core genetic or biological neurodevelopmental disturbance in schizophrenia have been linked with chronic stressful or traumatic childhood experiences (Read, Perry, Moskowitz, & Connolly, 2001Read, J., Perry, B., Moskowitz, A. and Connolly, J.2001. The contribution of early traumatic events to schizophrenia in some patients: A traumagenic neurodevelopmental model. Psychiatry: Interpersonal and Biological Processes, 64: 319–345.[Taylor & Francis Online], [Web of Science ®], [Google Scholar]; Teicher et al., 2003Teicher, M. H., Andersen, S. L., Polcari, A., Anderson, C. M., Navalta, C. P. and Kim, D. M.2003. The neurobiological consequences of early stress and childhood maltreatment. Neuroscience and Biobehavioral Reviews, 27: 33–44.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]). And these trauma-based brain changes are entirely consistent with emerging evolutionary-based explanations for psychotic symptoms (Grace, 2010Grace, A. A.2010. Ventral hippocampus, interneurons, and schizophrenia: A new understanding of the pathophysiology of schizophrenia and its implications for treatment and prevention. Current Directions in Psychological Science, 19: 232–237.[Google Scholar]; Moskowitz, 2004Moskowitz, A.2004. “Scared stiff”: Catatonia as an evolutionary-based fear response. Psychological Review, 111: 984–1002.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]).
IS THERE A SCIENTIFIC REVOLUTION IN THE HOUSE?
The failures of the current dominant medically based neo-Kraepelinian paradigm, coupled with the successes of an alternative paradigm focusing on adverse life experiences (including attachment disturbances) and dissociation, could herald the approach of a scientific revolution. Evidence that this may be occurring includes the increased willingness of prominent medical journals such as the American Journal of Psychiatry and Archives of General Psychiatry to publish studies supportive of this view (e.g., Arseneault et al., 2011Arseneault, L., Cannon, M., Fisher, H. L., Polanczyk, G., Moffitt, T. E. and Caspi, A.2011. Childhood trauma and children’s emerging psychotic symptoms: A genetically sensitive longitudinal cohort study. American Journal of Psychiatry, 168: 65–72.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]; Kendler et al., 2000Kendler, K. S., Bulik, C. M., Silberg, J., Hettema, J. M., Myers, J. and Prescott, C. A.2000. Childhood sexual abuse and adult psychiatric and substance use disorders in women: An epidemiological and cotwin control analysis. Archives of General Psychiatry, 57: 953–959.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]; Scott et al., 2007Scott, J., Chant, D., Andrews, G., Martin, G. and McGrath, J.2007. Association between trauma exposure and delusional experiences in a large community-based sample. British Journal of Psychiatry, 190: 339–343.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]). As more and more psychiatrists are shifting paradigms, it must be recognized that many medically trained individuals within the trauma and dissociative disorders field have long championed this perspective (of course, there are psychologists and other non-physicians who continue to firmly embrace the “medical model” as well, but these paradigms to a large extent do map onto disciplinary distinctions and tensions).
Should a new paradigm emerge, it will be a genuine biopsychosocial one, recognizing that genetics plays a role in psychopathology, likely in providing vulnerability to certain broad forms of mental disorders or to mental disorders in general. It will also recognize that life experiences from gestation on play a major role not only in the expression of psychiatric symptoms but also in the expression of the genes that underlie vulnerability to mental disorders. This new paradigm must also recognize some form of dimension or dimensions across apparently different types of mental disorders (evaporating the comorbidity “problem”) and between pathology and so-called normality. It will require recognition of the extent and severity of childhood trauma, a reality that has long faced considerable resistance from adherents to the medical model. Finally, the presence of dissociative conditions, with the corollary that such individuals are radically different at different times, must be taken into account not only clinically but also in the design of research—something to which the current paradigm has been blind.
The DSM–5 committees appear to have some awareness of these challenges. Dimensional perspectives are being considered for personality disorders and possibly as an axis alongside other categories. What is striking is that the schizophrenia committee is recommending the elimination of the (currently pathognomic) first rank symptoms (voices conversing or commenting, delusions involving intrusions or withdrawals of thoughts or behavior), belatedly recognizing that they have “no unique diagnostic specificity” for schizophrenia (American Psychiatric Association, 2011American Psychiatric Association. (2011). Schizophrenia.http://www.dsm5.org/ProposedRevisions/Pages/proposedrevision.aspx?rid=411# (http://www.dsm5.org/ProposedRevisions/Pages/proposedrevision.aspx?rid=411#)[Google Scholar]). This is obviously welcome news (an early indication of a paradigm shift?), as the association of these clearly dissociative symptoms with schizophrenia has led to substantial misdiagnosis of dissociative identity disorder patients. But it also reminds us of the enigma that practically every attempt to define schizophrenia, from Bleuler to the present day, has invariably called forth dissociative identity disorder. That the paradigmatic biological disorder can be so easily confused with the paradigmatic environmental disorder should already be shaking the rafters of this house (but of course, as the dominant paradigm does not recognize dissociative identity disorder, it does not recognize this enigma!). The explanation for this puzzle should help us to understand the nature of schizophrenia—until then, we can firmly state that whatever schizophrenia is, it is not psychotic symptoms and certainly not auditory hallucinations. Unfortunately, the DSM–5 schizophrenia committee has not gone this far and continues to emphasize psychotic symptoms, even as the head of that committee, William Carpenter, warns against this approach (“Psychotic experience is to the diagnosis of mental illness as fever is to the diagnosis of infection—important, but non-decisive in differential diagnosis,” Fischer & Carpenter, 2009Fischer, B. A. and Carpenter, W. T.2009. Will the Kraepelinian dichotomy survive DSM–V?. Neuropsychopharmacology, 34: 2081–2087.[Crossref], [PubMed], [Web of Science ®], [Google Scholar], p. 2081).
If a new paradigm does emerge, we can be sure that Kraepelin’s paradigmatic disease entity—General Paresis of the Insane—will be replaced. Perhaps it may not be possible to find a new exemplar for mental disorders in general, but PTSD would seem a worthwhile candidate for at least some of them—those clearly linked to trauma and characterized by dissociation (as, for example, has been proposed by Van der Hart, Nijenhuis, & Steele, 2006Van der Hart, O., Nijenhuis, E. and Steele, K.2006. The haunted self: Structural dissociation and the treatment of chronic traumatization, New York, NY: Norton.[Google Scholar], in their structural dissociation model). And the possibility that schizophrenia, or at least some form of psychotic disorder, could fit this model should not be rejected outright. Even Bleuler, the progenitor of schizophrenia, despite his commitment to an organic etiology, seemed to recognize this. A growing appreciation of this possibility could, quite literally, trigger a scientific revolution in our view of mental disorders altogether.
The stronger the affects, the less pronounced the dissociative tendencies need to be in order to produce the emotional desolation. Thus, in many cases of severe disease, we find that only quite ordinary everyday conflicts of life have caused the marked mental impairment; but in milder cases, the acute episodes may have been released by powerful affects. And not infrequently, after a careful analysis, we had to pose the question whether we are not merely dealing with the effect of a particularly powerful psychological trauma on a very sensitive person, rather than with a disease in the narrow sense of the word. (Bleuler, 1911/1950Bleuler, E.1950. Dementia praecox or the group of schizophrenias, Edited by: Zinkin, J.New York, NY: International Universities Press. Original work published 1911[Google Scholar], p. 300; Sünje Matthiesen, translation)
Lost connections by Johann Hari is simply the best book I’ve ever read. It asks all the right questions and it also provides many possible answers. I hope this will be a book that ultimately will change our society and the way we think about mental illness. Working as a psychologist myself, it felt like somebody finally provided solutions that will work in therapy and possibly change.
From the New York Times bestselling author of Chasing the Scream: The First and Last Days of the War on Drugs, a startling challenge to our thinking about depression and anxiety.
Award-winning journalist Johann Hari suffered from depression since he was a child and started taking antidepressants when he was a teenager. He was told—like his entire generation—that his problem was caused by a chemical imbalance in his brain. As an adult, trained in the social sciences, he began to investigate this question—and he learned that almost everything we have been told about depression and anxiety is wrong.Across the world, Hari discovered social scientists who were uncovering the real causes—and they are mostly not in our brains, but in the way we live today. Hari’s journey took him from the people living in the tunnels beneath Las Vegas, to an Amish community in Indiana, to an uprising in Berlin—all showing in vivid and dramatic detail these new insights. They lead to solutions radically different from the ones we have been offered up until now.
Just as Chasing the Scream transformed the global debate about addiction, with over twenty million views for his TED talk and the animation based on it, Lost Connections will lead us to a very different debate about depression and anxiety—one that shows how, together, we can change
When I was 15, I took the bus from Stavanger to Bergen after saying goodbye to my boyfriend. The last thing I wanted, was to talk with anyone. I struggled to keep my tears back and wanted to have time to think about everything we did and he said (like a typical teenager). But to my horror, an old woman sat next to me and I knew immediately that she was a talker. Little did I know that this would be one of the very conversations I remember from that year. We talked about everything, and soon started on a philosophical journey together. I told her about my boyfriend, and how hard it was to live so far apart from him (over 10 hours with a car or bus). She responded by saying how healthy it is to meet people who live in a different place than where you grew up. Because they probably see the world a little bit different than you, and that means you might end up learning something new.
This woman was so wise, and I learnt something new too: By opening up to all kinds off people, even strangers, you might change the way you think and see the world. I was reminded of this event when I listened to “an organized mind” by Daniel Levitin in my car. He described a study where the researchers asked people if they thought they would prefer sitting alone or talk with a stranger on the bus. They were quite sure about what they would like the most, but it seems like we don`t always know how much we crave connections with others. The study is described below, and I hope you enjoy it as much as me. Maybe the next time you`r filled with dread, hoping that somebody won`t disturb you on a bus, plane or train, you might look at the commute as an opportunity instead of fear.
Talking to the stranger in seat 4B on a cross-country flight is often considered one of the torments of air travel, to be avoided at all costs. But new research suggests people are deeply wrong about the misery of striking up conversations on public transit.
Contrary to expectations, people are happier after a conversation with a stranger, the study revealed.
“At least in some cases, people don’t seem to be social enough for their own well-being,” said study researcher Nicholas Epley, a professor of behavioral science at the University of Chicago Booth School of Business. “They think that sitting in solitude will be more pleasant than engaging in conversation, when, in fact, the opposite is true.” [7 Thoughts That Are Bad For You]
Talking to strangers
Epley, author of the book “Mindwise: How We Understand What Others Think, Feel, Believe and Want” (Knopf, 2014), studies social connection. Humans are social animals, he said, to the extent that having more and stronger friends and family connections is linked with a healthier life.
But in waiting rooms, trains, planes and other public spots, people fail to show their social stripes, Epley told Live Science. During his own commute in Chicago, he sees “highly social animals getting on the train every morning and being remarkably anti-social … They might as well be sitting next to a rock.”
Perhaps people know that interacting with a stranger is likely to be less pleasant than sitting in silence, so they choose the latter, Epley said.
Or maybe, just maybe, everybody is wrong about talking to strangers. Maybe it’s actually fun.
To find out which is true, Epley and his colleagues recruited real-life commuters at Chicago train stations. They also conducted a series of experiments with bus riders. In some of these experiments, they simply asked people to imagine striking up a conversation on the bus or train. Would it be pleasant? Would they feel happy afterward?
By and large, people said “no,” it wouldn’t be pleasant, and that such an interaction wouldn’t result in a happiness boost. In addition, people guessed, on average, that fewer than half of strangers would be interested in chatting. They expected to be rebuffed.
In other experiments, the researchers actually asked the commuters to go through with the conversations. At random, some participants were assigned to start a conversation. Others were asked to sit silently, and a third group was told to go about their normal commute routine (which involved silence for some and speaking to a friend for others). The participants were given sealed surveys to complete and mail in after their commute.
The results? People had a more pleasant time when they talked to a stranger versus when they stayed silent. Incredibly, the findings held even when the researchers controlled for personality traits, like extraversion and introversion.
Does the finding that talking to strangers makes people happier make you more likely to strike up conversations in public more often?
No way. You couldn’t pay me enough.
Maybe. I can see the upsides.
Definitely. I’d like to meet new people.
No – but only because I already chat with strangers.
“Everyone seems happier and has a more pleasant interaction when they connect versus sit in isolation,” Epley said.
Perhaps even more surprising, their conversation partners seemed to welcome the connection, too.
“Nobody was rejected in any of our studies, as far as I can tell,” Epley said. “Everybody who tried to talk to somebody was able to.”
In another study, the researchers set up participants in a waiting room, so they could test the happiness of both the conversation starter and their target. Again, everyone was happier after chatting — even the person who hadn’t started the conversation. Pairs of strangers deep in conversation also reported that the wait seemed shorter.
Nerve cells communicate through short, fleeting pulses of electrical activity. Yet some memories stored in the brain can persist for decades. Research into how the nervous system bridges these two radically different time scales has been going on for decades, and a number of different ideas have picked up some experimental support.
For instance, based on their past activity, nerve cells can dictate which partners they make contact with or increase or decrease the strength of those connections—in essence, rewiring the brain as it develops and processes experiences. In addition, individual cells can make long-term changes in the genes that are active, locking specific behaviors in place. In a paper released by Nature Neuroscience, scientists have looked at the changes in gene expression associated with memories of positive associations and found that they are held in place by chemical modifications of the cells’ DNA.
These chemical modifications fall under the broad (and somewhat poorly defined) category of epigenetic changes. Genetic changes involve alterations of the DNA sequence itself. Epigenetic changes, in contrast, alter how that DNA is processed within cells. They can be inherited as the cell divides and matures and, in rare cases, they’re passed on to the next generation. In some cases, epigenetic changes simply involve how the DNA is packaged inside a cell, which controls how accessible it is to the enzymes that transcribe it for use in making proteins. But in other cases, the DNA itself is chemically modified. That changes how various proteins interact with it.
The most common of these chemical modifications is called methylation, where a single carbon atom is attached at a specific location on one of the DNA bases. A number of studies suggest that methylation changes accompany the formation of long-term memories, so the researchers decided to test this in a well characterized experimental system that dates back to Pavlov: teaching a mouse to associate a sound with having a sugary treat appear in its cage. (Controls included playing the tone in a way that it wasn’t associated with treats and simply providing the tone.)
It only takes mice three tries before they start sniffing around the locations where the treat appears, and by five iterations, the behavior is pretty much locked-in. Past work in other systems has identified areas of the brain that are involved in this process, as well as some of the genes that are required. So, the authors started looking at how these changes came about when the association between the tone and a treat was being formed.
The researchers were able to confirm that the genes identified in past studies were involved in the formation of associative memories, and changes in the gene activity were detectable by the third trial just as behavior started to change. They were also able to detect significant changes in the DNA methylation that occurred at the same time, although only at a specific subset of the areas known to be methylated in that area of the chromosome. They were even able to show that the enzymes responsible for modifying the DNA appeared at these sites at around the time of the third trial.
All of that indicates that methylation changes are associated with the learning process, but it doesn’t get at the issue of cause and effect. So, the team injected a chemical that blocks DNA methylation into the area of the brain that’s involved with this form of associative memory, and they found that it would leave existing memories intact while blocking the formation of new ones. The effect was also specific to injections in this area of the brain. Injecting the drug into a different area, one that is involved in forming the associations involved in addiction, did not affect this particular form of memory.
Overall, the study adds another example to the growing list of cases where epigenetic changes seem to be involved in the process of locking memories into place. This doesn’t mean that the memories are permanent, as there are enzymes that can eliminate methylation as well. Still, it should help maintain the status of the memories for long periods of time—far longer than a brief burst of activity.
But it’s important to note that this sort of methylation is very context dependent: it’s specific to a subset of cells in a single area of the brain. Different methylation patterns—or even the same methylation pattern in a different set of cells—will probably encode something very different.
“There is perhaps no psychological skill more fundamental than resisting impulse. It is the root of all emotional self-control, since all emotions, by their very nature, led to one or another impulse to act.”Daniel Goleman
It soars through you like a wave. The impulse to do something you will regret later. The urge is so irresistible, that you feel there is no other way. You just have to do it. Have another drink, although it is way beyond bedtime. A cigarette after managing to not smoke for three days. The ice-cream dripping with chocolate sause that you kept in the fridge. Just in case you get visitors. We know these impulses so well, and despair when we cannot do anything to stop them. Walter Mischel found in his famous Marshmallow experiment, that children who managed to postpone having a marshmallow and get two later if they waited, had better results at school and success later in life. Unbelievable, isn`t it? That just one experiment like this, can predict what happens years later? For some this might even lead to a feeling of despair: Especially if you struggle time and time again with resisting those impulses. Is it really impossible to stop the urge when it threatens to take over? Sometimes it honestly is. When you are stressed, have too many things to think about, have no time to think through what you do during a day or feel tired, you might slip on some of your promises to yourself. Studies show that choosing and resisting alternatives, drains mental energy. In the evening you might be so exhausted that willpower simply vanishes. BUT: We can trick our gratification searching brain. First: Prepare for the fight. Do not keep what you are trying to avoid, around you. Don`t buy that chocolate bar. To avoid doing so when you are stressed, plan to go shopping when you are not hungry. Shop everything you need so you don`t need to pop into the store later. If you feel bad from not having your usual way of regulating those difficult emotions or cravings, find alternative positive activities. Talk to yourself a LOT: I am strong. I can do this. I am actually doing it already by trying to resist. Good work! And if you manage to resist the impulse, for just one or ten minutes, be sure to tell yourself what accomplishment it is. Because you have just rode on the wave instead of letting it sweep you away. Even without a surf-board. Because who actually learn how to resist impulses? If we haven`t had good role models, like many of us haven`t (especially today when everything happened two minutes ago), how could we have learnt to resist? Luckily, the marshmallow experiment showed that if the experimenter learnt the children how to resist impulses, for example by distracting them (having interesting toys in the room, asking them to close their eyes) they managed to do so in the future too. Every time you find creative ways to resist your urges, your willpower grows. It is hard work, and sometimes it feels like it`s all for nothing. But just think about how happy people who have really tried to change, often are. Why might that be? I think you already have the answer: Because it is immensely gratifying to doing what we know in our hearts are right.
But, we have to balance resistance with acceptance. Sometimes we push the brakes to often, leading to us stopping impulses that are healthy and bring life to us.
From the blog feed your soul: My concern, however, is the squashing of the other impulses, the ones that guide us to life-enhancing decisions. The impulse to express a truth even if it is unpopular. The impulse to say no, when social mores would have us say yes. The impulse to radically change a life that looks perfectly fine from the outside but feels like death on the inside. I am afraid that we will begin to live only in extremes, much like the stratification of our socioeconomic classes. We become like the addict, powerless over any whim or desire, or we become the ascetic who deems any impulse evil, and the control over our desires the mark of superiority.
Is it possible to live in the middle ground, where our impulses can go through a highly developed discernment filter and we honor all ways?
I love those thoughts from the blog. And in my opinion, it is possible to find that balance. But first we must learn the skills to stop impulses first, and then we must learn to let go. Finding the balance can`t be done if we lack the knowledge and experience necessary to either resist or let go. So if you want to resist more, can it harm to try?
An encounter at a party changed Gay Hendricks forever. A stranger asked him to imagine himself on his deathbed and to consider this question:
“Was your life a complete success?” If not, then “What would be the things you’d wish had happened that would have made it a success?” Hendricks said his deepest wish was for a loving, lasting relationship with a woman. The stranger said, “turn that wish into a goal, and put it in the present tense.” On the spot, Hendricks came up with this goal, “I enjoy a happy marriage with a woman I adore and who adores me. I enjoy a lifelong blossoming of passion and creativity with her.” This goal helped him create his marriage to Kathlyn, the date he’d taken to the party, and during the past 27 years they’ve become well-known relationship experts and co-authors of 9 books together. This short, focused book shows readers how to discover their own five wishes for a fulfilled life.
Five wishes is a wonderful book. Books CAN change lives, and this one did that for me. Today I sat down to think about what my five wishes are. I am still not completely sure what they should be, but I am starting to get an idea:
For the first time, it is empirically proven that cognition can be improved with brain training – according to Prof. Dr. Lindenberger, Director of the Max-Planck Institute for Human Development in Berlin.
Only one year ago, Lindenberger was part of an academic group who published “Ageing in Berlin”, featuring a memorandum clearly stating brain training to not improve trainers everyday abilities. Now, however, Lindenberger and colleagues have published a study encouraging the use of brain training to improve cognition.
The COGITO study is the largest and probably most convincing study in the field of brain training. 101 young adults aged 20-31 years and 103 persons aged 65-80 years trained for 1 hour every 2-3 days, for a total of 100 sessions. A single training session was comprised of 12 exercises: 6 for comprehension and speed (similar to “Flash Glance”); 3 for working memory (“Dual 1-Back”); and 3 for information recall (similar to “Memo Pair”). The brain training exercises were adjusted at the beginning of the study to suit the participant’s performance, as indicated by the pre-tests.
The study was designed to test how effective brain training is at improving general cognitive abilities, and to see if age influences these improvements. In addition, the researchers wanted to evaluate if progress in brain training is transferrable to every day life.
Significant improvements in cognition were observed – especially for working memory. We need working memory to plan, understand complex topics, solve problems, and learn new things. All participants, regardless of age or sex, showed improvements in working memory capacity following the training. The researchers suspect that training positively altered and strengthened the neuronal connections between the two frontal lobes of the brain, hence participant’s progress in brain training could be observed in other areas of life
Professor Dr. med. Falkenstein:
„Many people are capable of improving specific cognitive functions with targeted cognitive training. NeuroNation consists of simple but motivating exercises.“
World memory champion Dr. Karsten:
„I know of no other program which is so intense and effective. Only when you reach your limit, you can really improve!“
You can benefit from the latest advancements in science by using NeuroNation brain training. We know that you perform better if you track the progress you’re making. For this reason, we have built in features to help you clearly monitor your results – comparing today’s results to yesterdays and tomorrows.
Our new ‘MemoWork’ course specifically focuses on training your working memory, designed with the help of scientists from the Free University in Berlin. This intensive course includes personalized exercises tailored to your abilities, and requires 4- to 8-weeks of training to guide you to better cognition. The efficacy of the program has been extensively tested, and comes with a money-back guarantee – because we’re that confident you’ll like it! The course’s exercises have received much publicity for their effectiveness. We promise you’ll notice a difference!
I have two phobias: Trypohobia and blood phobia. What follows is a description of my first and most severe phobia.
Trypophobia is relatively unknown peculiar phenomenon that affects thousands of people. The term ‘trypophobia’ itself was only coined in 2005. It is not recognised as a phobia technically, but it does seem to be a uncontrolled reaction or response (typically fear, anxiety, revulsion and/or self-defense) of a kind of pattern of holes or bumps. It seems to affect all kinds of people young and old and across different cultural barriers which suggests it is not a culturally learned response. Often, a trypophobe will not know that anyone else suffers from the same experiences that they do.
For a long time I wondered why do certain patterns give me goosebumps? As long as I can remember since I was a kid I had this reaction, and there was very little information about it on the Internet that I could find. I wanted to add my knowledge on it.
What triggers it and what doesn’t?
The effect of a triggering image on any individual trypophobe can vary from no response to a severe reaction, but many trypophobes will agree that certain images are triggering. Generally speaking, any kind of cluster (of say at least 7) of holes or bumps (and in some cases, lesions) may cause discomfort. For me, asymmetric/non-uniform patterns are worse. Others have said that the texture of the holes (in the sense of touch) matters. Some repetitive patterns like honeycomb, clusters of bubbles on the surface of water, the texture of crumpets and the bumps in your skin on your knees when you kneel in carpet for too long can also be triggering.
You can do a Google search for “trypophobia” and many of the images that turn up will illustrate the concept.
To know more about triggers, we must explore why trypophobes have this reaction.
Why do trypophobes have this reaction?
There is not much research data on trypophobia to conclusively explain this reaction. From what I’ve read, and what I’ve experienced, my best guess is that certain kinds of clusters are similar in nature (visually) to some degenerative diseases, pox, infections/infestations, swarms, etc., which one would do well to avoid. You could bring some kind of evolutionary hypothesis into this, the revulsion and therefore aversion of anything that looks like this would be beneficial for survival.
For most, when the clusters/pattern is on something natural/biological such as skin, the reaction is worse. Perfectly symmetrical patterns like the holes in a cheese grater may not be triggering at all (like in my case) due to its visual uniformity (man-made appearance.) But again, different people are sensitive to different things.
As it is, trypophobes are not generally aware of any particular reason they have a reaction. It is like getting goosebumps when it gets cold; it is a reaction one cannot typically prevent.
I have done some small experimentation with this since I am affected by trypophobia, and it is very interesting to me (I’m sort of a scientist at heart.) In my case, the visual scale of holes makes a big difference. For example, looking at something from a certain distance may have no affect on me, but viewing it from further back may trigger a response. It doesn’t seem to depend so much on the “understood” scale (compared relative to other objects around it) as the visual scale – how many of the holes can be seen, how much detail, how big they are, the spaces in between them, etc.
What are the reactions to triggering images?
Reactions vary from person to person. Speaking only from my own experience, the first and most noticeable reaction I get is goosebumps. I always get goosebumps when I am triggered, and my hairs stand on end. It will continue until I am no longer triggered. I believe this is part of some kind of overall self-defense/self-preservation mechanism. At the same time, I feel anxious. I feel as though there is possibly some kind of danger. My mind starts analysing the image and for long exposure, it is all I can think about. Heart rate increases. It can have such a strong presence in the mind that it affects your ability to focus on a task. To that extreme level, it is a little bit debilitating.
The worst, though, is having the triggering images flash into your head. Continuously, more and more, until you start to feel panicky and feverish. In my opinion it is a very unpleasant experience to have a war with your mind, in trying “not” to think about something, which is slowly driving you crazy. After extended exposure, I got more sensitive to trypo triggers. I started to get reactions from simple everyday things like the shower head, bubbles of oil in the frying pan, and even the texture of toilet paper.
Others have said their reactions include things like anger (possibly aggression which can be linked to self-preservation), a desire to destroy the clusters, as well as wanting to cry (a natural reaction after being scared.) One thing that trypophobes all have in common is a very strong revulsion. Most will physically move further away (subconsciously) or look away from the image with disgust. Other common reactions include itching, skin crawling, and being sick to the stomach.
How can I get rid of it?
It takes a lot of mental solidarity to reduce your sensitivity to trypophobic triggers. I don’t believe you will be able to get rid of any reaction altogether, especially to the more severe triggers, but being able to control your reaction and curb the effect it has on you is a good start.
Firstly, I don’t recommend take the exposure/desensitizing route if you already experience any of the reactions above. Being exposed to a lot of triggers in a short amount of time can make you panicky. A lot of the images aren’t real and just created for shock value. Some people have said desensitizing works, and it can, depending on how you do it. Don’t go on a binge looking at triggers until you’re sick. If you’re out and about and see a trigger you can take the time to share your phobia with someone close to you. Being able to explain it and share it can turn it into a good experience and help condition you to associate less negativity with triggers.
Accept that you are not in control of the physical reaction your body has, and know that it is natural. Just like goosebumps, or getting hungry, these are natural feelings and it isn’t something to worry about. What you are in control of is how you deal with it.
If you need to, remind yourself that you are not in any danger.
Do not reinforce yourself into a corner of fear. The more you label trypophobia as something scary, the more it is scary, to you. It is uncomfortable and unpleasant, but do not encourage it by saying things like “This is going to give me nightmares,” and “I’m so afraid to click on this link.” Just forget those thoughts. Own it, don’t be a prisoner to it.
Finally, do not expose yourself more than you have to. I know there is a deathly curiosity that comes along with trypophobia. It takes a lot of willpower to pass up an opportunity to freak yourself out. But once you are able to say, “No, I don’t want to see that,” and go on to do other things, you will be one step closer to feeling more at ease.
By doing these, over time, your reactions to trypo images should decrease.
What are some of the worst triggers?
Here is a list of well-known trypophobia triggers. You will know immediately if you have trypophobia if you experience anxiety in response to these stimuli.
Lotus seed pod, lotus breast, lotus seeds photoshopped onto skin (there are many of these), etc.,
Surinam toad giving birth
Tafoni (rock formation)
The “frozen peas” image, most likely also photoshopped