by William Schultz, Doctoral Student

Lena Dunham, a well-known actress, recently received attention and praise because of a collection of Instagram photos she publicly posted, which highlighted her emotional and psychological challenges (subsequently referred to as “mental illnesses”; although I think this and other medical terms are misleading, I’ll use them in this post just for clarity sake) and the medications she uses in response to those challenges. Her central message was that there should be “no shame” surrounding mental illnesses or the use of medications.[1] By “shame”, Dunham was referring to the stigma surrounding mental illnesses, which is pervasive and has a variety of negative effects, such as increasing distress and discouraging individuals from seeking help.[2] Due to the widespread, negative effects of stigma, mental health patients, mental health advocacy organizations, mental health professionals, researchers, celebrities, and politicians have communicated their commitment to ending stigma through psychoeducational campaigns.

For example, actress Glenn Close co-founded an organization called “Bring Change 2 Mind” whose purpose is to “end stigma and discrimination surrounding mental illness” through education. The method for combatting stigma endorsed by Dunham and Close appears to rely on explaining mental illnesses as brain diseases. For instance, the “facts” section of the Bring Change 2 Mind website states that “The fact is, a mental illness is a disorder of the brain – your body’s most important organ – and one in four adults experience mental illness in a given year, including depression, bipolar disorder, schizophrenia, and PTSD.”[3]

By asserting that mental illnesses are brain disorders, this approach highlights supposed brain defects as causes of mental illnesses. This, in turn, challenges the stigmatizing belief that mental illnesses are the result of some sort of moral failure or character weakness. The reasoning goes: You wouldn’t blame someone for being diagnosed with a physical disease to which they didn’t contribute. So why would you blame someone for their mental illness, since mental illnesses are really brain disorders to which they didn’t contribute?

This approach to stigma has been identified in research. For example, Corrigan et al. summarized the perspective described above when they wrote, “Moral models yield attributions that mental illness is onset controllable and persons with mental illness are to blame for their symptoms. Biological models are more consistent with attributions that mental illness is uncontrollable at onset.”[4] In other words, moral models suggest that individuals can control the development of their mental illness while biological models suggest they cannot. This is in line with Bring Change 2 Mind’s claim that “Like most diseases of the body…Mental illnesses are no one’s fault.”[5]

It seems to me that identifying and challenging stigma are excellent goals and I praise individuals and groups, like those mentioned above, for their efforts. However, I’m also concerned because I believe there are at least three important problems with this approach.

The first problem is the assertion that mental illnesses are “brain disorders” contradicts the scientific data and some important philosophic considerations underlying that data. To begin, consider what Thomas Insel, until recently the head of the National Institute for Mental Health, wrote near the end of 2015: “The problem is that even though there have been thousands of studies looking for biological markers of mental health problems such as depression or schizophrenia, none has proven clinically actionable. And, in truth, little has been replicable even in a research setting.”[6] Insel’s comments aren’t out of the ordinary. Congruent statements have been made by many mental health experts.[7] In sum: scientific research has not identified reliable biological pathologies causing mental illnesses. And it’s a plausible argument that if we’ve not identified biological pathologies, it’s a stretch to call mental illnesses “brain disorders” or “brain diseases.”

Perhaps it’s true that researchers may someday identify biological pathologies. Even if they don’t, at the least mental illnesses still involve or are mediated by the brain.[8] And as neuroscience continues to progress, it’s likely that more and more precise correlations between mental illnesses and brain structure and function will be discovered. But even these discoveries wouldn’t immediately justify understanding mental illnesses as brain disorders because a change in the brain is not synonymous with a brain disorder. Let me explain:

All mental phenomenon and behaviors are mediated by the brain. That is, everything changes our brain, from our developmental environment to stressful life events, falling in love, studying for an exam, meditating, and participating in psychotherapy.[9] So even if researchers reliably identified brain differences in individuals who experience, for example chronic anxiety, this does not lead to the conclusion that a disordered brain is causing the anxiety. It merely identifies that the brain changes in response to experiences. To illustrate this point, consider a study in which researchers identified that when individuals diagnosed with social anxiety are administered cognitive-behavioral psychotherapy, their distressful symptoms diminished and their brains changed.[10] Crucially, the mechanism involved in changing the brain was not primarily biological but psychological. In other words, it was not an individual’s disordered brain that was causing their symptoms, but their unhelpful beliefs and behaviors related to social situations.

An objection I’ve often heard to this sort of example is that even though the mechanism of change may be psychological, the change still occurs fundamentally at the biological level. This objection opens up a large discussion which I’ve explored elsewhere and can easily lead us off track (if it hasn’t already). [11] But before returning to discussing stigma, I’ll try to briefly explain an important aspect of my reply to this type of reductionist objection:

If fundamentality is what we are after, then mental illnesses aren’t “really” brain disorders but, instead, patterns of quarks (or quantum fields or whatever else physics identifies) interacting in particular ways. In fact, from this type of reductionist perspective, sciences such as “chemistry” and “biology” aren’t real: they’re useful fictions -- epistemological tools with pragmatic explanatory powers that scientists use until our understanding of physics becomes powerful enough to achieve our explanatory goals. So if we want to be scientific about mental illness, then we need to rely not on neuroscientists, psychiatrists, psychologists, and those who’ve experienced mental illness, but on physicists.

I hope you’ll agree with me that this sort of thinking doesn’t make a lot of sense. At the least, I think it’s important to note that many biological oriented researchers agree that this perspective isn’t comprehensive or functional. For example, Kendler argued “It is possible to study scientific questions from perspectives that are both too basic and too abstract” and this is why he thought it important to reject looking for “big, simple neuropathological explanations for psychiatric disorders” and instead accept that in “ways we can observe but not yet fully understand, subjective, first-person mental phenomena have causal efficacy in the world.”[12] In short: psychosocial factors are crucial to understanding the development of mental illnesses and approaches which emphasize only biological features, such as claiming that mental illnesses are brain disorders, overstate the current evidence and are deeply misguided.

Now that we’ve gotten muddy in that philosophical swamp…I want to return to the subject of combatting stigma and my two other concerns about approaches that emphasize brain deficits. My next concern is straight-forward: a significant body of evidence suggests that emphasizing bio-pathological etiologies of mental illness does not reduce stigma. For instance, Angermeyer et al. used a population-based study design to investigate “the question whether promulgating biogenetic explanations may help reduce the stigma attached to mental illness and, therefore, should be included into anti-stigma messages.” [13] They found that biogenetic explanations are linked to increased stigmatizing attitudes and, as a result, should be avoided in anti-stigma campaigns.

Their findings aren’t unusual. In fact, they’re typical. Similar outcomes are found in numerous studies and meta-analyses.[14] Even recent experimental studies suggest that biogenetic etiologies of mental illnesses increase perceived differentness – such as increased perceived incompetence and unpredictability – and do not reduce stigma as well as explanations which emphasize that mental illnesses may not be discrete diseases.[15]

When I first examined this evidence, I was perplexed. I wondered: if biological etiologies emphasize that individuals are not responsible for their mental illnesses – their genetics, brains, and/or chemical imbalances are – then why do biological etiologies not decrease, and often increase, stigma? Well, in short, the research strongly suggests that the reason is that stigma is not only comprised of responsibility. Schomerus et al. emphasized that while biological etiologies of mental illness are often associated with reduced levels of perceived responsibility and blame, these reduced levels can be “outweighed by the adverse effects mediated by perceived differentness and dangerousness, respectively” and similar findings are common.[16] These increased levels of perceived differentness and dangerousness can contribute to the negative effects of stigma that organizations like Bring Change 2 Mind are attempting to challenge. Thus, it seems to me that there’s good reason to rethink this strategy.

Finally, my third concern surrounding emphasizing brain deficits is that this way of thinking can have significant negative impacts on clinical outcomes. Within the past decade, a new area of research has explored the relationship between an individual’s beliefs regarding the etiology of mental illnesses and her or his treatment preferences and prognostic expectations. The research has consistently found that the greater an individual endorses a biological etiology of mental illness, the greater her or his prognostic pessimism. That is, they expect that their symptoms will persist at greater levels for longer periods of time. The proposed mechanism of this finding is that the greater an individual endorses biological etiologies, the greater she or he endorses “essentialist” views of her or himself – the view that an individual’s emotional and psychological states are largely determined by biological factors and that psychological and social factors are largely or completely impotent.[17] This prognostic pessimism is important because a clients’ expectancies to improve are an important contributor to their improvement – individuals who expect to do better, do better.[18] Thus, factors which contribute to individuals expecting to do worse – such as biological etiologies – can contribute to individuals doing worse.

So, given my concerns, where does this leave us? Unfortunately, with no quick and easy solution. Corrigan, Druss, and Perlick noted that “Advocates need to learn from the complex research on stigma change to implement programs that improve care seeking while not exacerbating other forms of discrimination.”[19] That’s not easy because mental illness and stigma are large, often complicated, subjects. At the least, though, I think it’s important to recognize that there are alternatives to biological etiologies of mental illnesses – such as psychosocial approaches -- which are congruent with the scientific evidence and may avoid promoting stigmatizing attitudes. That is, individuals who experience mental illness may be responding to harmful environments and/or lack the knowledge/resources to manage their lives in more adaptive ways. This perspective doesn’t reduce mental illnesses to brain disorders and it doesn’t imply that we should blame individuals for their mental illnesses. It seems to me that this is an approach worth considering.

[1] Holmes, L. (2016). Lena Dunham shuts down mental illness stereotypes in new photos. Retrieved from http://www.huffingtonpost.com/entry/lena-dunham-mental-illness-instagram_us_56a259b7e4b0d8cc1099cf59

[2] Corrigan, P. W., Druss, B. G., & Perlick, D. A. (2014). The impact of mental illness stigma on seeking and participating in mental health care. Psychological Science in the Public Interest, 15(2), 37-70.

[3] Bring Change 2 Mind (2016). The facts. Retrieved from http://bringchange2mind.org/learn/the-facts/

[4] Corrigan, P. W., River, L. P., Lundin, R. K., Wasowski, K. U., Campion, J., Mathisen, J., Goldstein, H., Bergman, M., Gagnon, C., & Kubiak, M. A. (2000). Stigmatizing attributions about mental illness. Journal of Community Psychology, 28(1), 91-102.

[5] Bring Change 2 Mind (2016). The facts. Retrieved from http://bringchange2mind.org/learn/the-facts/

[6] Insel, T. (2015). A different way of thinking. New Scientist, 227(3035), 5.

[7] Deacon, B. J. (2013). The biomedical model of mental disorder: A critical analysis of its validity, utility, and effects on psychotherapy research. Clinical Psychology Review, 33(7), 846-861; Fuchs, T. (2012). Are Mental Illnesses Diseases of the Brain?. Critical Neuroscience: A Handbook of the Social and Cultural Contexts of Neuroscience, 331-344; Graham, G. (2013). The Disordered Mind: An Introduction to Philosophy of Mind and Mental Illness. New York, NY: Routledge; Miller, G. A. (2010). Mistreating psychology in the decades of the brain. Perspectives on Psychological Science, 5(6), 716-743.

[8] Fuchs, T. (2011). The brain--A mediating organ. Journal of Consciousness Studies, 18(7-8), 196-221.

[9] Hunter, N., & Schultz, W. (2016). Brain scan research. Ethical Human Psychology and Psychiatry, 18(1), In press.

[10] Månsson, K. N., Salami, A., Frick, A., Carlbring, P., Andersson, G., Furmark, T., & Boraxbekk, C. J. (2016). Neuroplasticity in response to cognitive behavior therapy for social anxiety disorder. Translational Psychiatry, 6, e727, 1-8.

[11] Schultz, W. (2015). Neuroessentialism: Theoretical and clinical considerations. Journal of Humanistic Psychology, published online before print on December 3, 2015, doi:10.1177/0022167815617296.

[12] Kendler, K. S. (2005). Toward a philosophical structure for psychiatry. The American Journal of Psychiatry, 162(3), 433-440.

[13] Angermeyer, M. C., Millier, A., Kouki, M., Refaï, T., Schomerus, G., & Toumi, M. (2014). Biogenetic explanations and emotional reactions to people with schizophrenia and major depressive disorder. Psychiatry Research, 220(1), 702-704.

[14] Kvaale, E. P., Gottdiener, W. H., & Haslam, N. (2013). Biogenetic explanations and stigma: A meta-analytic review of associations among laypeople. Social Science & Medicine, 96, 95-103; Schomerus, G., Matschinger, H., & Angermeyer, M. C. (2014). Causal beliefs of the public and social acceptance of persons with mental illness: a comparative analysis of schizophrenia, depression and alcohol dependence. Psychological Medicine, 44(02), 303-314; Speerforck, S., Schomerus, G., Pruess, S., & Angermeyer, M. C. (2014). Different biogenetic causal explanations and attitudes towards persons with major depression, schizophrenia and alcohol dependence: Is the concept of a chemical imbalance beneficial?. Journal of Affective Disorders, 168, 224-228.

[15] Wiesjahn, M., Jung, E., Kremser, J. D., Rief, W., & Lincoln, T. M. (2016). The potential of continuum versus biogenetic beliefs in reducing stigmatization against persons with schizophrenia: An experimental study. Journal of Behavior Therapy and Experimental Psychiatry, 50, 231-237.

[16] Schomerus, G., Matschinger, H., & Angermeyer, M. C. (2014). Causal beliefs of the public and social acceptance of persons with mental illness: a comparative analysis of schizophrenia, depression and alcohol dependence. Psychological Medicine, 44(02), 303-314.

[17] Schultz, W. (2015). Neuroessentialism: Theoretical and clinical considerations. Journal of Humanistic Psychology, published online before print on December 3, 2015, doi:10.1177/0022167815617296.

[18] Constantino, M. J., Ametrano, R. M., & Greenberg, R. P. (2012). Clinician interventions and participant characteristics that foster adaptive patient expectations for psychotherapy and psychotherapeutic change. Psychotherapy, 49, 557-569.

[19] Corrigan, P. W., Druss, B. G., & Perlick, D. A. (2014). The impact of mental illness stigma on seeking and participating in mental health care. Psychological Science in the Public Interest, 15(2), 37-70.

by Chuck Ruby, Ph.D.

“ADHD” is not a condition or disorder. It is a descriptive label given to people who are not interested enough in a particular topic that an authority figure says they should be. It is a moral judgement about what one ought to be interested in, how much, and when should that person be interested in it.

Yet, a recent article in the Washington Post entitled "ADHD in kids: What many parents and teachers don’t understand but need to know", like many others, continues to claim it is a “brain-based medical disorder”, a “neuro-behavioral disorder”, and “a type of mind, genetically transmitted”. These phrases are misleading and give the impression that ADHD is truly a neurological ailment, when in fact, there is no evidence of such an ailment. There is no research that shows the brains of people labeled ADHD are defective or in any other way pathological. Any “deficits” asserted by researchers are actually differences, not deficits. One would expect a child who has a history of paying attention very well to have a different looking brain than one who doesn’t. That’s what the brain does. It changes in structure and activity depending on how it is used over time. Those changes are not deficits. Further, the great majority of research fails to address the effect that the ADHD treatment of choice, stimulant drugs, have on the brain, making it difficult to determine what brain differences are true deficits created by long-term use of stimulant drugs.

It has been increasingly difficult over the years for psychiatry to explain why a child diagnosed with ADHD can sit for hours in rapt attention to a video game, when he is supposed to have a neurological deficit of attention. Instead of concluding from this that ADHD is actually a matter of the child’s willingness (not ability) to pay attention, this article demonstrates the typical response to that quandary. Linguistic gymnastics are used to re-describe ADHD, not as a neurological deficit per se, but as “wandering attention”, “inconsistency of attention”, or some other phrase that suggests a deficit of brain functioning, but without saying so directly. The concept of “self-regulation” has also been invoked as another linguistic fence-sitting tactic. Self-regulation merely means a person’s desire to bring behavior in line with societal expectations. But again, the idea is that there is a deficit of self-regulation, a contention which the evidence doesn’t support. So while no neurological deficit can be found, the believers in ADHD continue to suggest there is a deficit of attentional, disinhibition, or self-regulation capacity.

The announcement of the Mayo Clinic’s study, which found that girls diagnosed with ADHD have a “two-fold risk” of becoming obese, is also grossly misleading. Not only does it gives the impression that ADHD causes obesity, it also implies ADHD is a real and alarming disorder. In truth, the study simply shows a correlation between the behaviors that get one diagnosed with ADHD and weight control problems. This is something my grandmother would have known. The ADHD behaviors include a general failure to abide by societal expectations regarding self-regulation. It is logical to then assume those people who do not self-regulate according to societal expectations are likely to have similar failures of self-regulation in other areas of life, including eating behaviors. I cringe at the possibility of another study that compares ADHD kids who are prescribed stimulant drugs to “treat” the ADHD with those who are not. It would not be surprising in such a study to see that those not treated with stimulants were more obese than those treated. The conclusion? Treating ADHD reduces obesity. In fact, such a result would be what is expected for someone taking stimulant drugs - they lower appetite and induce weight loss.

The irony in this article is that although it markets ADHD as a real brain disorder, it inadvertently pulls back the psychiatric curtain a little so we can see what is really going on behind it. That is, it points out that ADHD is a label given to people who are not willing to fall in line with the status quo and who are interested elsewhere. Their creativity, vision, and inquisitiveness can lead to wonderful ideas and inventions. Perhaps there is a cost to such independence of thought, but that independence of thought is not a sign of brain deficit.

by Noel Hunter, M.A., M.S., Doctoral Student

On January 27, 2016, a study¹ was published online in the prestigious journal Nature that touted the possibility of discovering some potential biological origins of an "illness" called "schizophrenia" (See note at the end). Subsequently, headlines across the world beamed excited proclamations of the latest breakthrough to occur in psychiatric research. Here is just a small sample of what the major media outlets were purporting:

"New study helps explain cause of schizophrenia" - CNN

"Researchers say they're now closer than ever to understanding the science behind schizophrenia" - The New York Times

"Scientists open the 'black box' of schizophrenia with dramatic genetic finding" - The Washington Post

"Genetic study provides first-ever insight into biological origin of schizophrenia" - The Broad Institute of MIT and Harvard

"Schizophrenia breakthrough as genetic study reveals link to brain changes" - The Guardian

Clearly some amazing discoveries must have emerged from this groundbreaking study! The sound bites have certainly led a very large population to come to believe so. The problem is, there is nothing profound about this study at all and, in fact, it is one of the least profound studies to emerge in the last few years on the topic of "schizophrenia". The information that has been disseminated to audiences across the globe, no doubt with the assistance of a rhetorically biased news release and included highlights, is distorted, it asserts exaggerated claims based on reductionistic conclusions, and it ignores the robust support that has accumulated that undermines the genetic disease model of "mental illness" and the categorical understanding of experiences falling under the umbrella term "schizophrenia".

While these news reports discuss the "dramatic" "first-ever insights" and the assumed fact that scientists do not have a clue what causes "schizophrenia", the accumulating evidence indicating an almost irrefutable causal relationship between childhood adversity and most experiences labelled psychotic gets completely disregarded. This is despite the fact that childhood adversity can actually explain the very biological "discoveries" being promoted in the first place. Additionally, many of the biological correlates associated with the category of schizophrenia are also found in persons not diagnosed as such, whether they meet criteria for another disorder or none at all, and are more generally associated with chronic stress and trauma than any discovered disease process. How can this "breakthrough" study go viral across the globe without any consideration of context or the broader literature base explaining the causal pathways of "schizophrenia"? How does this study actually fit in to greater research base?

What are the study findings?

Genetic associations with "schizophrenia"

The authors' premise for conducting the study was an association previously found between variations of the genes of the major histocompatibility complex (MHC) locus and a diagnosis of schizophrenia at the population level. What does this mean in English? It means that there was a very tiny statistical likelihood that variations of genes associated with the immune system were more prevalent in a group of individuals determined to fall into a category called schizophrenia as compared to another group not diagnosed as such. In this particular study, Sekar et al. discovered that, specifically, part of this association was explained by an increased expression of the C4 protein. This particular protein in humans is involved in a process called synaptic pruning. As stated in the New York Times article, an increase in the C4 protein is estimated to be associated with a .25 (one quarter) percent increase in the risk of meeting criteria for a diagnosis of schizophrenia in the general population.

Reduced synapses and synaptic pruning as possible causal mechanisms for schizophrenia

The theory that synaptic pruning may be defective in individuals diagnosed with schizophrenia, and therefore may explain why it tends to emerge in late adolescence, was first purported over 30 years ago by Feinberg². Synaptic pruning refers to a process that occurs in early childhood (around ages two to four) and again in late adolescence (around the ages of 15 to 18) wherein "excess" neural synapses, or connections, are eliminated in the brain. There is some evidence that individuals who are diagnosed with schizophrenia tend to have reduced neural connections in the brain. The Feinberg hypothesis asserts that this may be explained by a faulty process that occurs during this synaptic pruning in adolescence that is likely genetic in origin.

Due to lack of evidence at that time, this hypothesis was largely ignored, until it was revisited³ 10 years later during the "decade of the brain". It was believed that a specific errant process of synaptic pruning may underlie schizophrenia wherein there is an excessive elimination of neural connections, specifically in the prefrontal cortex. This means that there is less activity in the area of the brain associated with decision making, problem-solving, rational thought, and attention. The prefrontal cortex has been shown fairly frequently to have decreased activity and decreased neural connections in individuals experiencing so-called psychotic phenomena.

The Feinberg hypothesis of excessive synaptic pruning emerging from some illness process is still an unproven hypothesis, but is indirectly supported by the evidence demonstrating the deceased connections and activities in the prefrontal cortex of some individuals diagnosed with schizophrenia. The Sekar et al. study was based upon trying to help explain how, if this hypothesis is true, the process might be explained. The study did not prove this hypothesis, nor did it develop the hypothesis; it simply gave some evidence of how this process might be explained at a biological level if it is, in actuality, true. The study also did not "help explain [the] cause of schizophrenia", as purported by CNN; it simply provided some possible evidence of a biological correlate that exists in a small number of individuals diagnosed with schizophrenia that may underlie a hypothesized process that may exist in some individuals diagnosed with schizophrenia. This is breaking "dramatic" news?

The bigger picture

Taken at face value, if there is, in fact, a greater number of C4 protein and variations of the genes in the MHC locus in some individuals diagnosed with schizophrenia than in the general population, and this explains a hypothesized excessive pruning process that occurs in adolescence, then what might really be going on? Remember, this study (and most others like it) have found a biological correlate associated with a small number of individuals fitting into a particular category called schizophrenia. This does not necessarily mean that there is a causal relationship or that an actual illness process is occurring. As I write this, my brain is demonstrating many biological correlates in activity, including an increased stress response. As you read this, your brain is demonstrating a very different biological correlate that may or may not also have an associated stress response. Just because there is a difference in brain biology, and just because there is an associated stress response, this does not mean that an illness is in place, nor does it prove that either of us is "mentally ill".

Looking at the broader scientific literature, it is clear that there are certain biological correlates associated with a diagnosis of schizophrenia at the group level. But, this does not tell us much of anything beyond the fact that the brain and body are demonstrating a different physiology than those who are not in such extreme distress. This is to be expected. However, these associations are also evident in other major DSM-defined diagnostic categories, including posttraumatic stress disorder. Most problems that get labelled as mental illness emerge in adolescence as well, and synaptic pruning has been suggested as one major reason for this across diagnostic categories⁶. In other words, what we seem to be looking at are physiological and neurological responses to difficult life experiences that are correlated with varying manifestations of distress, emotional pain, and socially unacceptable behaviors.

How does all of this relate to the Sekar et al. study?

The immune system

The immune system, inflammation, and schizophrenia

Recall that the genetic variations found in this study, and previous studies, to be minutely associated with schizophrenia are those genes that are also associated with the immune system. C4 proteins, those found to be increased for those with "schizophrenia" in the Sekar et al. study, work within the immune system, in part, by responding with inflammation in order to protect the body. In general, when the immune system responds to a perceived injury or infection, inflammation is the result. Abnormalities in C4 are associated with various autoimmune diseases, such as lupus, kidney diseases, and even alcoholic liver disease (they did not, as far as I can tell, account for the potential confound of alcoholism, by the way).

Interestingly, an unbalanced immune response and a slight inflammatory process of the central nervous system have been associated with individuals diagnosed with schizophrenia⁴. Because of the discovery of a higher than normal immune cell activity in the brains of those diagnosed with, or considered at risk of, schizophrenia, it has been suggested that early anti-inflammatory treatments might prove an invaluable treatment intervention⁵. So, the idea that the immune system may be faulty in some individuals diagnosed with schizophrenia is not surprising. Nor is it surprising that genes associated with immune system may demonstrate some variation in individuals diagnosed with schizophrenia. However, this does not mean that C4 abnormalities or inflammatory responses cause some disease called schizophrenia. It may be that some individuals experiencing a psychotic reaction are suffering the direct results of an autoimmune reaction targeting the neuronal structure of the brain. This is the case with encephalitis. Of course, we call this disease of inflammation in the brain encephalitis not schizophrenia. It is understood that they are at least two entirely different problems.

It is also entirely possible (and not even considered in these studies) that behaviors and experiences associated with the diagnosis of schizophrenia are interconnected with an immune response that are all, or partially, resulting from some other source. In fact, the increased response of the C4 genetic proteins and other variations found may be entirely the result of emotional breakdown rather than the cause. Genes are not determinants of most human behavior or experience. Genes are affected by the environment and may get "turned on" by events within the environment, such as pollution, viruses, psychological trauma, and other acquired experiences. The statement by Sekar et al. that "schizophrenia is a heritable brain illness" is a rhetorical declaration that has not been proven, and there are numerous refutations of the research upon which such assertions have been made^{7, 8}. This is an important point to make because genetic variation does NOT equate with genetic (or inherited) disease. And, brain differences do NOT equate with brain disease. Genetic and brain variations can easily arise from environmental events; first, however, one needs to set aside the assumption that "schizophrenia" is a genetic disease and examine the evidence as a whole.

The immune system, trauma, and autoimmune problems

When the immune system becomes faulty, especially over time, tissue damage may ensue. Autoimmune diseases, such as rheumatoid arthritis, are actually inflammatory disorders that occur when an organ, tissue, or internal system is damaged by the immune response. C-reactive protein (CRP) is a biomarker of inflammation that is also involved in the regulation of the complement system⁹, which includes the C4 protein measured by Sekar et al. In 2007, Danese et al.¹⁰ published a study demonstrating that childhood adversity is associated with increased CRP levels in adults 20 years after the experience of trauma. In fact, childhood trauma has been found to be independently associated with autoimmune diseases (including rheumatoid arthritis¹¹ and chronic fatigue syndrome¹²) later in life, in part through the process of inflammatory and neuroendocrine responses.

There may be some value in considering the Sekar et al. findings in terms of some forms of psychosis being the result of an autoimmune disorder resulting from childhood trauma. The relationships of childhood adversity and "schizophrenia", and the problems in ignoring this relationship, will be discussed shortly, but the point to be made here is that no such possibilities were raised. Rather, there was some discussion about "schizophrenia" being an autoimmune disorder caused by a genetic abnormality, despite the fact that not ALL people diagnosed with this disorder demonstrate an inflammatory response, not ALL demonstrate predictable physiological differences of any kind, and that genetics (or more correctly, epigenetics) may simply be a mediating factor wherein something in the environment (i.e., childhood adversity) may actually be the cause.

Synaptic Pruning

Synaptic pruning, as stated previously, is a normal process that occurs in all humans during two different periods of life: early childhood and adolescence. There is large variation in the amount of pruning that occurs, particularly across genders⁶. The process basically consists of eliminating connections in the brain that are redundant or unused. So, if one is isolated, depressed, and uncared for, areas of the brain associated with empathy, socialization, and executive functioning are likely to be eliminated. Although surely there is some function of genetic determinism in the selection of synapses to eliminate, this is not proven and the environment and one's lifestyle appear to be much more prudent factors in this regard.

The Feinberg hypothesis, which is the basis upon which the Sekar et al. study and their conclusions are based, purports that "schizophrenia" results from an excess of synaptic pruning in the prefrontal cortex. Yet, it has been found that stress and trauma, especially when experienced during adolescence, can result in decreased synaptic density in the prefrontal cortex and these changes can endure into adulthood¹³. In other words, one cannot differentiate if decreased synapses in the prefrontal cortex are the result of trauma and childhood adversity or if they are the result of some theoretical disease process called "schizophrenia".

Trauma and Psychosis

Recently, another study was published regarding "schizophrenia" that did not go viral through the media, but, some (i.e., me) might argue, should have. Anjnakina et al.¹⁴ built on several other recent studies to demonstrate specificity of childhood adversity and psychotic experiences as an adult. A robust association was found between childhood adversity, most notably childhood sexual abuse, and delusions and hallucinations. In a previous study, Bentall et al.¹⁵ found that bullying had a specific relationship with paranoia. Perhaps most importantly to the Sekar et al. study is the finding that being taken into custody (i.e., foster care, juvenile justice) as a child was associated directly and robustly with an "excited" dimension of psychosis, characterized by hostility, lack of impulse control and uncooperativeness. This builds on previous research demonstrating that children who experience abuse that comes to the attention of social services are more likely to behave in antisocial and impulsive ways¹⁶. These traits are often associated with decreased activity in the prefrontal cortex.

In a very different tone than that of "schizophrenia is a destructive, inherited brain disease", Anjnakina et al. state at the top of their article "The relationship between childhood adversity and psychotic disorder is well documented". Indeed, this is true. There is not enough room here to begin to do the vast amount of literature justice, but I will provide just a few key resources. Read et al.¹⁷ concluded in 2005 that child abuse is a causal factor in "schizophrenia". Read et al.¹⁸, after identifying similarities in the brains of traumatized children and adults who were diagnosed with schizophrenia, demonstrated the neurodevelopmental pathways through which childhood adversity may cause psychosis. In 2004, Janssen et al.¹⁹ established a strong dose-response relationship between childhood abuse and psychosis after following 4045 individuals from the general population for two years. Bentall et al.¹⁵ also found a dose-response relationship between childhood abuse and psychosis (meaning that the greater number of adverse experiences and/or the higher the severity, the greater the risk), wherein those who had a high-severity of childhood abuse were 48.4 times more likely to develop psychosis as an adult. When specificity and dose-response relationships are demonstrated, a causal relationship is strongly probable. In fact, Bentall et al.¹⁵ stated that "experiencing multiple childhood traumas appears to give approximately the same risk of developing psychosis as smoking does for developing lung cancer". And, lastly, in the same month as the Sekar study was released (January 2016), so to was a nationwide cohort study out of Denmark and Sweden²⁰ which found that experiencing the death of a first-degree relative before 18 years of age, especially from suicide or accident, resulted in a 39% increased risk of schizophrenia.

Yet, the media screams from the proverbial rooftops the "dramatic" findings that a genetic variant has shown there to be an estimated increase of .25% in the risk of "schizophrenia"? How does this happen? I can surmise many reasons, including corporate and guild interests and financial resources, but at the end of the day no one likes to hear about the bad things that exist in the world. Sadly, as a result, those who are unfortunate enough to live with oppression, social isolation, poverty, institutionalization, and/or child abuse find that when they turn for help, their traumatic experiences are rendered meaningless, their response to the trauma is reduced to a "brain disease" that was probably risen from some defective genes in the first place, and "help" consists of further traumatization and isolation and promises of a better life through a pill. This is, at this point, unjustifiable.

To sum up

It may seem after reading this that the Sekar et al. study has, indeed, given us some useful findings in understanding the pathophysiological mechanisms behind the psychotic experience for some people. This would be correct as far as academic gratification is concerned. Inflammation is at the root of most modern diseases, and dietary changes, exercise, and psychotherapy have proven invaluable in treating such conditions. It is a positive step forward to consider the healing effects of anti-inflammatory changes in diet and lifestyle.

The conclusions and recommended possible clinical responses suggested by Sekar et al, however, are dangerously reminiscent of some Orwellian terror. Shall we really entertain the idea that it might be useful to mess around with the brain as it develops and changes over time through invasive chemical or other biological interventions? Does anybody have a clue what Frankenstein result may come out of such actions? Are we supposed to start genetically manipulating people because of a barely noticeable increased risk of a category of disease that is not even valid or reliable in the first place? There is a strong association of "mental illness" and creativity; are we to rid the world of innovation and creation? This may reek of hyperbole, but if there is even a small chance of such outcomes is it worth it? Have we not learned from previous experience that just because those in power say something is so, or even that it is helpful, that this means it's true?

We keep hearing about how wonderful modern Western mental healthcare is…if that were the case why did the World Health Organization find that countries who did not adopt our paradigm of "care" (i.e., "undeveloped" countries) had better outcomes^{21, 22} only to find that 30 years later, after adoption of that very paradigm, outcomes are no better than they are here? If our treatment paradigm was so "advanced", then why have disability rates and rates of illness continued to climb year after year, even as non-mental illnesses have decreased?²³

What if, instead, we tried to decrease poverty, inequality, racism, and child abuse? What if that? What if we paid heed to more humane interventions that allow for the variety of human experience (for instance, the Hearing Voices Network, Soteria, Open Dialogue, etc. ) and helped people to feel less isolated, more secure, and empowered to find meaning in life, as those who have personal experience with such experiences have asked for? What if we listened to those who have been there instead of telling them what they should or should not find helpful? What if we considered the whole person instead of reducing them to cells in a brain? These would be silly suggestions for someone facing a genetic brain disease. But, for someone experiencing the natural result of overwhelming life experiences, perhaps they are not. Will the media pay attention to this before it's too late?

Note: The category of "schizophrenia" has been determined to lack validity and reliability as a diagnostic category and does not have any predictive value, and this is agreed upon even by the most preeminent experts in mental health research. In order to argue the points as they have been put forth in the media, and as they exist in the research, this subject was not argued here for purposes of brevity.

References:

1. Sekar, A., Bialas, A. R., de Rivera, H., Davis, A., Hammond, T. R., Kamitaki, N.,…& McCarroll, S. A. (2016). Schizophrenia risk from complex variation of complement component 4. Nature. doi:10.1038/nature16549
2. Feinberg, I. (1983). Schizophrenia: Caused by a fault in programmed synaptic elimination during adolescence? Journal of Psychiatric Research, 17(4), 319-334.
3. Keshavan, M. S., Anderson, S., Pettergrew, J. W. (1994). Is schizophrenia due to excessive synaptic pruning in the prefrontal cortex? The Feinberg hypothesis revisited. Journal of Psychiatric Research, 28(3), 239-265.
4. Muller, N., Myint, A. M., Schwarz, M. J. (2012). Inflammation in schizophrenia. Advances in Protein Chemistry and Structural Biology, 88, 49-68.
5. Bloomfield, P. S., Selvaraj, S., Veronese, M., Rizzo, G., Bertoldo, A., Owen, D. R.,…& Howes, O. D. (2015). Microglial activity in people at ultra high risk of psychosis and in schizophrenia: An [11C]PBR28 PET brain imaging study. The American Journal of Psychiatry, 173(1), 44-52.
6. Paus, T., Keshavan, M., Giedd, J. N. (2008). Why do many psychiatric disorders emerge during adolescence? Nature Reviews: Neuroscience, 9, 947-957.
7. Joseph, J. (2015). The trouble with twin studies: A reassessment of twin research in the social and behavioral sciences. New York: Routledge.
8. Ross, C. A., & Pam, A. (1995). Pseudoscience in biological psychiatry: Blaming the body. New York: John Wiley & Sons.
9. Pepys, M. B., & Hirschfield, G. M. (2003). C-reactive protein: A critical update. Journal of Clinical Investigation,111, 1805-1812.
10. Danese, A., Pariante, C. M., Caspie, A., Taylor, A., & Poulton, R. (2007). Childhood maltreatment predicts adult inflammation in a life-course study. Proceedings of the National Academy of Sciences, 104, 1319-1324.
11. Dube, S. R., Fairweather, D., Pearson, W. S., Felitti, V. J., Anda, R. F., & Croft, J. B. (2009). Cumulative childhood stress and autoimmune diseases in adults. Psychosomatic Medicine, 71(2), 243-250.
12. Heim, C., Nater, U. M., Maloney, E., Boneva R., Jones, J. F., & Reeves, W. C. (2009). Childhood trauma and risk for chronic fatigue syndrome. Archives of General Psychiatry, 66(1), 72-80.
13. Leussis, M. P., Lawson, K., Stone, K., & Andersen, S. L. (2007). The enduring effects of an adolescent social stressor on synaptic density, Part II: Poststress reversal of synaptic loss in the cortex by Adinazolam and MK-801. Synapse, 62, 185-192.
14. Ajnakina, O., Trotta, A., Oakley-Hannibal, E., Di Forti, M., Stilo, S. A., Kolliakou, A.,…& Pariante, C. (2016). Impact of childhood adversities on specific symptom dimensions in first-episode psychosis. Psychological Medicine, 46(2), 317-326.
15. Bentall, R., Wickham, S., Shevlin, M., & Varese, F. (2012). Do specific early-life adversities lead to specific symptoms of psychosis? A study. Schizophrenia Bulletin, 38, 734-740.
16. Cohen, P., Brown, J., & Smaile, E. (2001). Child abuse and neglect and the development of mental disorders in the general population. Development and Psychopathology, 13, 981-999.
17. Read, J., van Os, J., Morrison, A. P., & Ross, C. A. (2005). Childhood trauma, psychosis, and schizophrenia: A literature review with theoretical and clinical implications. Acta Psychiatrica Scandinavica, 112, 330-350.
18. Read, J., Fosse, R., Moskowitz, A., & Perry, B. (2014). The traumagenic neurodevelopmental model of psychosis revisited. Neuropsychiatry, 4(1), 65-79.
19. Janssen, I., Krabbendam, L., Bak, M., Hanssen, M., Vollebergh, W., de Graaf, R., & van Os, J. (2004). Childhood abuse as a risk factor for psychotic experiences. Acta Psychiatrica Scandinavica, 109, 38-45.
20. Liang, H., Olsen, J., Yuan, W., Cnattingus, S., Vestergaard, M., Obel, C., Gissler, M., & Li, J. (2016). Early life bereavement and schizophrenia: A nationwide cohort study in Denmark and Sweden. Medicine, 3. Doi: 10.1097/MD. 0000000000002434.
21. de Girolamo, G. (1996). WHO studies on schizophrenia. The Psychotherapy Patient, 9, 213-231.
22. Jablensky, A., & Sartorius, N. (2008). What did the WHO studies really find? Schizophrenia Bulletin, 34(2), 253-255.
23. Viola, S., & Moncrieff, J. (2016). Claims for sickness and disability benefits owing to mental disorders in the UK: Trends from 1995 to 2014. BJPsych Open, 2, 18-24. Doi: 10.1192/bjpo.bp.115.002246.

by Chuck Ruby, Ph.D.

See the Huffington Post article written by Leah Harris here. She thoroughly explains the problems of the proposed legislation H.R. 2646 and is one of a growing number of grass roots advocates, survivors of the mental health system, and professionals who are speaking up about the dangers of the "Murphy Bill".

The Murphy Bill would essentially criminalize people who have been diagnosed with a mental illness. Keep in mind that two former NIMH Directors and the Chair of the DSM-IV Task Force have publicly admitted that mental illness diagnoses are invalid and unreliable. Then how can this legislation adequately identify people who will be subjected to its provisions?

The bill also conflates, and continues to confuse the public, about  the real causes of violence. H.R. 2646 is a descendant of earlier failed legislation that was proposed on the heals of horrific mass shootings. It was ostensibly to get at the reasons these shootings occur. But it does nothing more than seek a scapegoat to take the blame for these violent incidents, while it ignores the real issues involved in the very real problem of violence in our society.

In the process it proposes inhumane solutions that will erode personal freedom, privacy, and dignity. One of its main proposals is that of "Assisted Outpatient Treatment", or better known as forced treatment. If the bill is passed, untold thousands of people who are diagnosed with the unreliable and invalid mental illness labels will be subjected to state-ordered drugging and other forms of forced treatment. Anyone who complains or does not comply can be incarcerated involuntarily. Further, the bill threatens the right to privacy of one's most personal and sensitive information, and forces providers to share such information with family members in order to ensure "compliance". Besides its obvious threat to humane treatment, such forced treatment programs have been shown to be ineffective.

The Murphy Bill would be a scourge on humanity. Join us in fighting against it!

On October 11, 2015 the ISEPP Board of Directors held elections for the following leadership positions of Executive Director, Chairperson of the Board, and new Board members.

Chuck Ruby, Ph.D., was unanimously elected to assume the position of Executive Director effective immediately. Chuck joined ISEPP (ICSPP) about 10 years ago and since 2013, had held the position of Chairperson of the Board. He is the Director and General Manager of the Pinnacle Center for Mental Health and Human Relations, a group private practice in southern Maryland. He is also a member of Psychologists for Social Responsibility, a nonprofit volunteer organization seeking to apply psychological knowledge and expertise to promote peace, social justice, and human rights.

Replacing Chuck as Chairperson of the Board is Dominick Riccio, Ph.D. Dominick held the position of Executive Director from 2002 to 2008, and from 2013 to 2015. He has been with ISEPP (ICSPP) for many years. He is a clinical psychologist and psychoanalyst in private practice in New York City. He has been a supervisor and training analyst at various psychoanalytic institutes.  He is past co-founder and clinical director of Encounter, Inc., a prototype drug rehabilitation for teenagers. He has previously served as both president and vice-president of the Association for Modern Psychoanalysis, as well as founder and executive director of the Institute for the Treatment and Research of Psychosomatic Disorder.

Three new Board members were also elected.

Joan Cacciatore, Ph.D., has worked with people who are affected by traumatic death, particularly the death of a child, for nearly 20 years. She uses non-traditional, mindfulness-based approaches such as trauma focused psychoeducation, fully present narration, emotion-focused imaginal dialogue, symbols-metaphor-and-rituals, bibliotherapy, ecotherapy, meditation, yoga, and shinrin-yoku. She is also a professor & researcher at Arizona State University and the founder of the MISS Foundation, an international nonprofit organization with 75 chapters around the world aiding parents whose children have died or are dying.

Mary Vieten, Ph.D., ABPP, is a psychologist and U.S. Navy Commander with the Select Reserves. She has a private practice in southern Maryland where she serves clients who are military, paramilitary, veterans, and civilians who are exposed to high risk environments like police work and combat situations. She encourages clients to pursue trauma recovery work outside the medical model and educates them on the dangers and ineffectiveness of psychiatric drug treatment. Mary is ISEPP's Director of Operation Speak Up, an effort to critique and challenge the government's medical model treatment of those who suffer from traumatic experiences. In furtherance of this, she recently partnered with Melwood, a non-profit organization devoted to assisting people with disabilities, to develop and run a free week-long retreat for veterans and active duty military using this non-medical model.

Noel Hunter, M.A., M.S., is a clinical psychology doctoral candidate set to graduate in May 2016. She has over 40 publications and presentations on the topic of trauma and psychosis, barriers to humanistic approaches to suffering, and the need for major systemic change in all areas of mental health. Recently, she completed her dissertation of first-person perspectives on what is helpful and harmful in the treatment of severe dissociative states. Noel is also on the Board of Directors for Hearing Voices Network-USA, was previously the "experts-by-experience" Chair for ISPS, and is a blogger at madinamerica.com. Her own personal experiences and her passion for social justice fuel her outspoken nature and drive for change. To keep it real, however, she spends much of her time performing improv comedy in NYC.

by William Schultz, Doctoral Student, Minnesota School of Professional Psychology

The first full week of October (October 4^th – 10^th) is “Mental Illness Awareness Week” (MIAW). The primary purposes of MIAW are to fight stigma, provide educational material to the public, and to push for better mental health care. The National Alliance on Mental Illness (NAMI) has energetically promoted MIAW. This isn’t surprising since NAMI’s goals are to fight stigma, raise awareness, and provide education about “mental illness” to mental health patients, the public, and policy makers (NAMI, 2015a). But NAMI’s efforts may, in fact, be making the matter worse.

No doubt the stated NAMI goals are important. Millions of individuals suffer from significant emotional and mental distress (often called mental illness or psychological disorders – terminology I dislike but will use for clarity in what follows). Lack of awareness, as well as stigma surrounding psychological disorders, contribute to these individuals not seeking the assistance of mental health professionals (Bharadwaj, Pai, & Suziedeltye, 2015). This is unfortunate because many forms of psychological disorders can be significantly diminished through treatment. For example, Khan, Faucett, Lichtenberg, Kirsch, and Brown (2012) conducted a meta-analysis of hundreds of studies. Their meta-analysis found that the depressive symptoms of patients who participated in psychotherapy decreased by about 50%. On the other hand, the depressive symptoms of patients on a waiting list only decreased by about 10%. This finding led Khan et al. (2012) to argue “engaging in treatment is critical to improvement” (p. 9).  

Since treatment is important, and reducing stigma is thought to increase treatment seeking, it’s not surprising that for some time mental health advocacy organizations have done their best to try to reduce stigma. But NAMI's misstep is to promote a biological etiology of psychological disorders (Corrigan & Watson, 2004). The underlying idea behind this approach is that there will be less blame associated with psychological disorders if patients and the public conceptualize psychological disorders as biological illnesses (Corrigan et al., 2000). For example, if biological etiologies of depression were embraced, the public may view someone experiencing depression as chemically-imbalanced or genetically predisposed instead of weak willed or lazy. It’s thought that stigma can be diminished by decreasing or removing the element of moral blame associated with being weak willed or lazy. 

NAMI has a long history of ostensibly fighting stigma by claiming that psychological disorders are a biological, medical illness like cancer or diabetes (Angermeyer, Holzinger, Carta, & Schomerus, 2011; Deacon, 2013; Kvaale, Haslam, & Gottdiener, 2013; Lebowitz & Ahn, 2012). For example, a study by University of Michigan researchers found that NAMI’s web site information about depression emphasized biological etiologies (Hansell et al., 2011). While depression treatment centers, universities, and government websites generally provided approximately proportional descriptions of biological and psychosocial causes of depression, NAMI’s website – like pharmaceutical company websites -- focused much more on biological causes. While treatment centers, universities, and governments provided balanced explanations or even explanations that emphasized psychosocial causes, “The NAMI Website, for example, showed a 9:1 ratio in biological to psychosocial content about depression” (Hansell et al., 2011, p. 387). This sort of finding probably goes a far way of explaining why the first treatment option listed for the majority of the mental health conditions on NAMI’s “Fact Sheet Library” is medication (NAMI, 2015b) – though Hansell et al. (2011) suggested that the emphasis on biological etiologies “may in part reflect NAMI’s close relationship with pharmaceutical companies” (p. 387). 

If an accurate reflection of reality, NAMIs approach seems coherent. That is, if emphasizing biological etiologies can diminish stigma and diminishing stigma can lead to improved treatment outcomes, then NAMI’s approach seems to have some plausibility. 

However, NAMI’s perspective on psychological disorders is troublesome for at least three reasons:

First, biological etiologies of psychological disorders do not necessarily decrease stigma. In fact, a large body of evidence suggests that biological etiologies of mental illness can increase stigma associated with many psychological disorders (Schomerus, Matschinger, & Angermeyer, 2014; Speerforck, Schomerus, Pruess, & Angermeyer, 2014). One prominent explanation for this finding is that although biological etiologies may diminish moral blame, they increase the perceived dangerousness and difference of those experiencing mental illness.  

Second, emphasizing biological etiologies implies that biological interventions (e.g., medications) are the preferred treatment (Deacon, 2013; Kemp, J. J., Lickel, J. J., & Deacon, 2014; Read, Cartwright, Gibson, Shiels, & Magliano, 2015). This is concerning because substantial evidence suggests that very often medications do not provide significantly superior treatment benefits for psychological disorders when compared to psychotherapy (Cuijpers, Sijbrandij, Koole, Andersson, Beekman, & Reynolds, 2013; Harrow, Jobe, & Faull, 2012; Khan et al., 2012) and medications have a long list of negative effects, some of them very serious (Andrews, Thomson, Amstadter, & Neale, 2012; Kirsch, 2014; Moncrieff, 2009; Moncrieff 2013).

Third, emphasizing biological etiologies can have significant clinical impacts. Individuals who endorse a primarily or exclusively biological etiology of psychological disorders have increased prognostic pessimism, probably because they’ve accepted an essentialist account of their identity which leads them to believe they have little ability to modify their subjective experience (Lebowitz, 2014; Schultz, 2016). Increased prognostic pessimism is an important clinical factor because individuals’ expectancies for improvement is a significant contributor to their actual improvement. Individuals who expect to do better, do better (Constantino, 2012). 

To sum up, MIAW has a great chance to educate the public about the prevalence, causes, and treatment options for psychological disorders. I hope this short piece shows that the perspective adopted by NAMI is not comprehensive and probably harmful to clients. 

But what about stigma? Well, as I wrote previously: “… a biological understanding of psychological disorders is not the only way to combat stigma. We can adopt a compassionate attitude toward those struggling with [psychological disorders] even if we don’t also accept the view that their [psychological disorders are] biologically determined. For example, individuals [with psychological disorders] may simply not know other ways to manage their emotions or they may be dealing with a variety of stressors which overwhelm their ability to cope in a more adaptive way. Neither of these views suggests that the proper attitude is to judge and chastise individuals…as being weak willed” (Schultz, 2015).

References

Andrews, P. W., Thomson Jr, J. A., Amstadter, A., & Neale, M. C. (2012). Primum Non Nocere: An Evolutionary Analysis of Whether Antidepressants Do More Harm than Good. Frontiers in Psychology, 3, 117.

Angermeyer, M. C., Holzinger, A., Carta, M. G., & Schomerus, G. (2011). Biogenetic explanations and public acceptance of mental illness: systematic review of population studies. The British Journal of Psychiatry, 199(5), 367-372.

Bharadwaj, P., Pai, M. M., & Suziedelyte, A. (2015). Mental Health Stigma (No. w21240). National Bureau of Economic Research.

Constantino, M. J. (2012). Believing is seeing: an evolving research program on patients' psychotherapy expectations. Psychotherapy Research, 22(2), 127-138.

Corrigan, P. W., River, L. P., Lundin, R. K., Wasowski, K. U., Campion, J., Mathisen, J., Goldstein, H., Bergman, M., Gagnon, C., & Kubiak, M. A. (2000). Stigmatizing attributions about mental illness. Journal of Community Psychology, 28(1), 91-102.

Corrigan, P. W., & Watson, A. C. (2004). At issue: Stop the stigma: call mental illness a brain disease. Schizophrenia Bulletin, 30(3), 477-479.

Cuijpers, P., Sijbrandij, M., Koole, S. L., Andersson, G., Beekman, A. T., & Reynolds, C. F. (2013). The efficacy of psychotherapy and pharmacotherapy in treating depressive and anxiety disorders: a meta‐analysis of direct comparisons. World Psychiatry, 12(2), 137-148.

Deacon, B. J. (2013). The biomedical model of mental disorder: A critical analysis of its validity, utility, and effects on psychotherapy research. Clinical Psychology Review, 33(7), 846-861.

Hansell, J., Bailin, A. P., Franke, K. A., Kraft, J. M., Wu, H. Y., Dolsen, M. R., Harley, V. S., & Kazi, N. F. (2011). Conceptually sound thinking about depression: An Internet survey and its implications. Professional Psychology: Research and Practice, 42(5), 382-390.

Harrow, M., Jobe, T. H., & Faull, R. N. (2012). Do all schizophrenia patients need antipsychotic treatment continuously throughout their lifetime? A 20-year longitudinal study. Psychological Medicine, 42(10), 2145-2155.

Kemp, J. J., Lickel, J. J., & Deacon, B. J. (2014). Effects of a chemical imbalance causal explanation on individuals' perceptions of their depressive symptoms. Behaviour Research and Therapy, 56, 47-52.

Khan, A., Faucett, J., Lichtenberg, P., Kirsch, I., & Brown, W. A. (2012). A systematic review of comparative efficacy of treatments and controls for depression. PloS one, 7(7), e41778.

Kvaale, E. P., Haslam, N., & Gottdiener, W. H. (2013). The ‘side effects’ of medicalization: A meta-analytic review of how biogenetic explanations affect stigma. Clinical Psychology Review, 33(6), 782-794.

Lebowitz, M. S. (2014). Biological conceptualizations of mental disorders among affected individuals: A review of correlates and consequences. Clinical Psychology: Science and Practice, 21(1), 67-83.

Lebowitz, M. S., & Ahn, W. K. (2012). Combining biomedical accounts of mental disorders with treatability information to reduce mental illness stigma. Psychiatric Services, 63(5), 496-499.

Moncrieff, J. (2008). The myth of the chemical cure: A critique of psychiatric drug treatment. New York, NY: Palgrave Macmillan.

Moncrieff, J. (2013). The bitterest pills: The troubling story of antipsychotic drugs. New York, NY: Palgrave Macmillan.

National Alliance on Mental Illness. (2015a). About NAMI. Retrieved from https://www.nami.org/About-NAMI

National Alliance on Mental Illness. (2015b). Fact sheet library. Retrieved from https://www.nami.org/Learn-More/Fact-Sheet-Library

Read, J., Cartwright, C., Gibson, K., Shiels, C., & Magliano, L. (2015). Beliefs of people taking antidepressants about the causes of their own depression. Journal of Affective Disorders, 174, 150-156.

Schomerus, G., Matschinger, H., & Angermeyer, M. C. (2014). Causal beliefs of the public and social acceptance of persons with mental illness: a comparative analysis of schizophrenia, depression and alcohol dependence. Psychological Medicine, 44(02), 303-314.

Schultz, W. E. R. (2015) Binge eating and genetics. Retrieved from https://www.madinamerica.com/2015/08/binge-eating-and-genetics/

Schultz, W. E. R. (2016). Neuroessentialism: Theoretical and clinical considerations. The Journal of Humanistic Psychology. Accepted for publication.

Speerforck, S., Schomerus, G., Pruess, S., & Angermeyer, M. C. (2014). Different biogenetic causal explanations and attitudes towards persons with major depression, schizophrenia and alcohol dependence: Is the concept of a chemical imbalance beneficial?. Journal of Affective Disorders, 168, 224-228.

by Rick Winking

We received word here at ISEPP that one of our favorite members had passed. Ben Hansen, alias Dr. Bonkers, ended his struggle with bladder cancer on September 14th. He was 60 years old and fought the good fight until the end, refusing any medication and dying pain free and peacefully at home with the help of Hospice of Michigan.

We all know that psychiatry is a joke. We know that scientifically, they don’t have a leg to stand on. It was Ben Hansen and his Bonkers Institute for Nearly Genuine Research that really helped put this in focus for us. He used past ads for medications from psychiatric journals to point out the absurdity of psychiatry's past. He used current ads and articles to show that nothing has really changed in the past 100 years…..old wine in new bottles or as they say in the military, “SSDD.”

I have been a student and critic of psychiatry for over twenty years and thought I knew a lot. Then along comes Dr. Bonkers. I found myself marveling at some of the stuff he dug up and thinking to myself “Wow! These guys have a history of this that is even crazier than I thought.”

Thorazine for Hiccups? With Partnership for a Drug Free America getting psychiatrists to look for drug abuse in their patients and help stop America’s drug problem? Drugs for deviant sexual behavior? Dr. Bonkers found all of this.

Noam Chomsky defined Anarchism as “A tendency in the history of human thought and action which seeks to identify coercive, authoritarian and hierarchic structures of all kinds and to challenge their legitimacy – and if they cannot justify their legitimacy, which is quite commonly the case, to work to undermine them and expand the scope of freedom.”

Using this definition, Ben was one of my all-time favorite anarchists. I would refer doubters to the Dr. Bonker’s web site and their response was usually one of “These ads and articles can’t be real!” …..and another hole was poked in the psychiatric Zeppelin. He did not live long enough to see the Zeppelin crash and burn but he most assuredly poked some major holes in it. I was informed that the site will stay up in the future. Let’s keep sending the doubters there.

 Let’s do it for Ben!

Chuck Ruby, Ph.D.

In these early hours after Chris Mercer’s mass shooting at the Oregon community college, it would be easy to blame the rampage on “mental illness”. As has happened all too often in the past, news reports zero in on whether the shooter suffered from this fictitious disease (for example, see http://www.cbsnews.com/news/mass-shootings-and-the-mental-health-connection/). Such unjustified analyses and reactions to these terrible events serves as nothing more than a distraction from the actual factors associated with violent behavior and prevents the development of viable policies to make our society safer (See ISEPP Public Statement: The Role of Mental Illness in Violent Behavior). But perhaps more problematic, it also sets up a false dichotomy that certain kinds of people commit these acts and the rest of us are not prone to such violence. It sends us on a crusade to find these defective souls, to brand them with mental illness diagnoses, and then to provide them with “treatment” to rid them of their infection. Screening tools used to identify these people are notoriously in error and result in huge false alarm predictions, meaning that the great majority of those identified would never have committed a violent act. So, thousands and thousands of people, including children, would be subjected to this flawed assessment and then herded into the traditional psychiatric corral and subjected to all its demeaning, dehumanizing, and debilitating harms. Ironically, it is this very process that can actually increase the chances that violent behavior will occur (See ISEPP White Paper: Psychiatric Drugs and Violence). In short, we continue to look for the demon within, rather than the actual causes of violence.

Noel Hunter, Doctoral Student

A recent article in the Washington Post, entitled “Her brain tormented her, and doctors could not understand why.” was a heart-wrenching story of a troubled young woman who suffered greatly in her final years before dying at the young age of 23 due to a reaction to a prescription drug. This story is a haunting example of the all-too-common tragic outcomes of people who suffer from extreme states of human distress. Unfortunately, the Post’s rhetorical tale, which is based on misinformation, extreme reductionism, and a distortion of research, only adds to the tragedy of Ms. Pam Tusiani.

The Post’s first error is in taking as fact the idea that extreme emotions, suicidal thoughts, and seemingly strange ideas and behaviors are “symptoms” of a medical, biological disease. The problem is exemplified in the statement: “What was once thought to be the result of child abuse or a manifestation of post-traumatic stress is now its own complex personality disorder. And it’s deadly”. This statement is somewhat incomprehensible considering that “personality disorder” is simply a label and nothing more. It doesn’t describe a “disease”; it describes a problem. 

At no point does the author express how or why a post-traumatic reaction suddenly was re-conceptualized as a “deadly” disease according to his resources (assuming he has any). In fact, research does continue to show that up to 92% of individuals labeled with borderline personality disorder (BPD) have experienced some kind of childhood abuse¹. In addition, they are more likely to have experienced sexual abuse, specifically, and they have a greater number of perpetrators than people labeled with other kinds of psychiatric diagnoses. Dismissing off-hand the post-traumatic nature of the problem called BPD is an egregious error and not based on the scientific research. Further, the biological evidence the author cites as proof of “disease” (i.e., problems in the amygdala and “fight or flight” reactions) are precisely those that occur in individuals who have experienced extreme, chronic stress and/or trauma such as child abuse. But it must be emphasized that these biological consequences do not cause BPD. They are natural human reactions to intense and chronic stress of any kind. Presenting them as evidence of disease is like saying concussions are evidence that playing football is a disease.

With this in mind, then, one must first wonder what “cure” all the medical doctors are looking for? Have they read the work of Bessel van der Kolk, M.D. or Marsha Linehan, Ph.D.? Have they read any of the extensive studies showing the effectiveness of trauma-focused therapy, dialectical behavior therapy, yoga, meditation, somatic therapies, and others? What is this biological cure so many are seeking? Perhaps they may start by increasing efforts to prevent and ameliorate child abuse.

Second, giving the benefit of the doubt that DSM-defined categories are true diseases that exist in nature separate from the subjectivity of the person making said diagnosis (which is a dubious assumption), the author discusses the case of a young woman diagnosed with BPD, yet goes on to state: “We barely understand a healthy brain, so how are we to understand one haunted by psychosis?” This statement is a glaring error in even the most rudimentary understanding of psychiatric problems, for one would be hard pressed to find a clinician who deemed BPD to be a characterized by psychosis. However, the author may be saved by the fact that DSM-diagnostic categories lack validity and reliability anyways (the Director of the National Institute of Mental Health said so in 2013) and there are, in fact, no distinct lines that can define any one person’s experience completely.

Another error in research reporting is the author’s claim that “The suicide rate is higher for people with BPD than for those with major depression and schizophrenia; about 4 to 9 percent kill themselves”. In fact, the commonly cited estimate for suicide in persons diagnosed with schizophrenia is 10% to 13%, with approximately two to five times that rate attempting suicide^{3, 4}. Additionally, approximately two thirds of all cases of suicide include the occurrence of “depression” ^{5, 6}. The overall message should be that people who suffer, and suffer deeply, are more likely to commit suicide. Why make erroneous comparisons that are not even backed up by resources?

Perhaps the greatest error within this article is the complete disregard for the long-standing iatrogenic effects her so-called “treatment” may have had.  The author’s own statement should have raised huge, waving red flags: “She was on a laundry list of medication”. Many of these that are listed, including Paxil, Prozac, and Zoloft, are known to create an increased risk of suicide, violence, and agitation, especially in young adults and adolescents. Even more importantly, a recent study showed that pharmacotherapy for BPD “is not supported by the current literature” and that “polypharmacy should be avoided whenever possible”, recommending psychotherapy is the first-line treatment for BPD⁷. Another disregarded potential exacerbating factor is the internalized stigma, shame, and helplessness that comes from being told one has a “brain disease” instead of having the source of her pain recognized and addressed. She was in and out of hospitals, an experience that has been shown to directly create post-traumatic phenomena in those with the most severe problems, such as psychosis⁸. Lastly, many of the drugs that Ms. Tusiani was on are also shown to create psychotic experiences. Yet, not once does the author acknowledge or explore these clearly evident possibilities. Even the fact that the young woman died as a direct result of taking the antidepressant Parnate does not lead to an investigation of how this “laundry list” of drugs might have affected her. Instead, the subject is put to rest by blaming it on the fact that the drug was prescribed in a treatment center that was providing unlicensed medical care. Would the outcome have been any better if the center had that license? 

The story of Ms. Tusiani and her fatal experiences with inner turmoil and ineffective treatments is one that should be heard by an audience much larger than that served by the Washington Post. However, her story also deserves to be told with the integrity and fortuitousness of a critical journalist unafraid to ask the important questions. The family of Ms. Tusiani is understandably angered and determined to ensure that others do not have to endure the misfortunes that became their daughter. Such prevention begins by looking at the evidence that stares us directly in the eyes.

References:

1. 1. Zanarini, M. C., Williams, A. A., Lewis, R. E., Reich, R. B., et al. (1997). Reported pathological childhood experiences associated with the development of borderline personality disorder. The American Journal of Psychiatry, 154, 1101-1106.
2. 2. Ogata, S. N., Silk, K. R., Goodrich, S., Lohr, N. E., Westen, D., & Hill, E. M. (1990). Childhood sexual and physical abuse in adult patients with borderline personality disorder. The American Journal of Psychiatry, 147(8), 1008-1012.
3. 3. Siris, S. (2001). Suicide and schizophrenia. Journal of Psychopharmacology, 15, 127-135.
4. 4. Caldwell, C. B., & Gottesman, I. I. (1990). Schizophrenics kill themselves too: A review of risk factors for suicide. Schizophrenia Bulletin, 16, 571-589.
5. 5. Conwell, Y., Duberstein, P. R., Cox, C., Herrmann, J. H., Forbes, N. T., & Caine, E. D. (1996). Relationships of age and axis I diagnoses in victims of completed suicide: A psychological autopsy study. American Journal of Psychiatry, 153, 1001-1008.
6. 6. Henriksson, M., Aro, H., Marttunen, M., Heikkinen, M., Isometsa, E., Kuoppasalmi, L., & Lonnqvist, J. (1993). Mental disorders and comorbidity in suicide. American Journal of Psychiatry, 150, 935-940.
7. 7. Francois, D., Roth, S. D., & Klingman, D. (2015). The efficacy of pharmacotherapy for borderline personality disorder: A review of the available randomized controlled trials. Psychiatric Annals, 45, 431-437.
8. 8. Berry, K., Ford, S., Jellicoe-Jones, L., & Haddock, G. (2013). PTSD symptoms associated with the experience of psychosis and hospitalization: A review of the literature. Clinical Psychology Review, 33, 526-538.

Chuck Ruby, Ph.D.

Dr. Thomas Insel, the head of the National Institute of Mental Health (NIMH), has announced he is stepping down after serving in the position for the past 13 years (see http://www.nytimes.com/2015/09/16/health/tom-insel-national-institute-of-mental-health-resign.html). Dr. Insel’s main impact was to reorient the focus of NIMH toward a biological approach to the understanding of mental disorders, especially the serious ones. During his tenure, NIMH’s budget has been about $1.5 billion annually, with the great majority of those dollars going to research on the biology of mental disorders.

Dr. Insel’s appointment to the NIMH, along with his shift in focus, came on the heels of George H. W. Bush’s Decade of the Brain in the 1990’s, that was promised to unlock the mysteries of psychiatric problems by uncovering the biology and genetics of disordered brain functioning. President Obama more recently boosted this focus in his Brain Initiative in 2013, although perhaps too late for Dr. Insel. Nevertheless, this shift in focus was touted as a more scientific approach to diagnosing and understanding brain disorder, bringing psychiatry in line with the other medical sciences like neurology and cardiology.

It was under Dr. Insel’s tutelage that NIMH initiated the Research Domain Criteria (RDoC) program, which is intended to replace the current psychiatric diagnostic system of the DSM series, by building a bottom up system of diagnoses based on brain scan and genetic technology showing dysfunctioning brain biology for each disorder. Dr. Insel launched this program after publicly announcing in 2013 that the prevailing DSM diagnostic scheme was seriously flawed (DSM continues to be used today!).

Despite all the billions and all the rhetoric about how we are almost to the point of unlocking the biological secrets of mental disorder, we still have no reliable or valid biological marker. All we have are pretty brain scan pictures and genetic data showing what we already knew: biology changes, depending on how the body is used. This is true for mental disorders as it is for any human activity, including thinking, imagining, running, singing, and crying. But even with all this research, not one biological marker has been discovered that would enable diagnostic decisions. One would wonder if this is the reason for Dr. Insel’s departure. Have the failed research attempts convinced him to throw in the towel?

Regardless of Dr. Insel’s motivation for leaving, NIMH is left with a problem. It has been assumed the reason they haven’t found the “Rosetta stone” of biological psychiatry is that their research is either underfunded, inadequate, or they just aren’t looking in the right direction. Frequent chants of “we’re almost there!” echo from their halls, but this claim is unjustified. No other scientific research endeavor would continue along such a long line of failed attempts, hoping for the tide to turn “soon”. Other areas of research would have long since abandoned such theories that are not supported by the evidence.

NIMH has overlooked the real reason for not finding the stone: mental disorders (even the “serious” ones) are not brain diseases. In all the decades of scientific research, there has been no reliable evidence that supports the theory of mental disorders as caused by bodily pathology. Therefore, there is neither a disease to diagnose, nor biological marker to find. So-called “mental disorders” or “mental illness” or “mental disease”, whatever interchangeable term is used, are natural human reactions to the vicissitudes of life. Trying to jam these square pegs into the round holes of medicine does nothing but harm people, strip them of their dignity and humanity, and funnel them into a psychiatric pipeline of disability and despair.

The billions poured into brain scan research has acted as a subterfuge. It is like a house built upon a very weak foundation. The house may look impressive, and sell at a high rate. But if its occupants insist on living in it without checking the condition of the foundation, it will soon crumble under its own weight and trap all inside.