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.

ISEPP's Jim Gottstein won another Alaska Supreme Court case on January 29th.   Appellant H.R.was subjected to an involuntary psychiatric evaluation based solely on the testimony presented by her condominium association, which she had accused of financial improprieties.  The statute authorizing the court to grant an ex parté (no notice) order to have someone picked up by the police and taken to a psych hospital for evaluation requires a screening investigation that included interviewing the person if possible.  The Alaska Supreme Court reversed the order of involuntary psychiatric evaluation because the court did not try to interview H.R.    See, the Opinion. Three cheers for Jim!

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.

ISEPP's Jonathan Leo pulls the curtain back and allows us to see what's really happening. In his article The Search for Schizophrenia Genes, he provides an excellent explanation of why genetic research into mental disorders is a failed project.

One of ISEPP's members, David Rose, wrote this poem to express his frustration in connecting with someone to explain his journey in Vietnam.

The Fear In My Doctor's Eyes

I have seen the fear in their eyes
When they first realize
What I did during the war
And my issues we have yet to explore

One of my docs even backed away
I'm over my head, as if to say
So he referred me to another doc
I'm tossed around like a dirty old sock

I was referred to an in-patient facility
Do I really have that much instability
I wasn't admitted in though
They said I needed more time to grow

I was actually rejected
For the reason I should have been selected
That's like going to the doctor for a vaccine
And he says you're too sick to be seen

I wish I knew what my docs are thinking
When they stare at me without blinking
My PTSD must be rather severe
When they look at me with such fear

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!

During the last two weeks of October, Al Galves and Joe Tarantolo (the former ISEPP Executive Director and Chairperson of the Board, respectively) visited several Congressional offices on Capitol Hill, to express ISEPP’s grave concern about HR 2646. This bill was reintroduced in June by Representative Tim Murphy (R-Pennsylvania) in the Energy and Commerce Committee. It is ostensibly a reaction to the spate of violent incidents that have caught the public’s eye over the past few years. A 2014 Energy and Commerce Committee investigation concluded, “…those with untreated severe (or, used interchangeably, “serious”) mental illness (SMI) are at an elevated risk of exhibiting violent behavior….” The Committee referenced only one, quite dated, study to support this contention. In addition to being 25 years old, the study also conflates labels of “mental illness” with the actual factors that increase risk of violence (Swanson, J., Holzer, C., Ganju, V., & Jono, R. (1990). Violence and Psychiatric Disorder in the Community: Evidence from the Epidemiologic Catchment Area Surveys, Hospital and Community Psychiatry, 41(7), 761 -770).

Nevertheless, Al and Joe were very impressed with the members of the Energy and Commerce Committee staff. Both the Republican and Democratic staffers had spent enough time with people who oppose the bill to have a deep and comprehensive understanding of its problems. They suggested Al and Joe meet with Representative Murphy's staff and to write a letter to the Chairman and Ranking Member of the Committee. While they were unable to meet with Murphy's staff, they did draft a letter in record time (as is typically needed for Congressional action) and sent it to the Committee. The letter was signed by Al, Joe, Dominick Riccio (current Board Chair) and Chuck Ruby (current Executive Director).

During the Committee hearing, Ranking Member Pallone twice mentioned ISEPP by name as one of several organization, including the ACLU, who have concerns about the bill. That makes us think Al and Joe’s visit to the Hill made a difference. Let's hope we made enough of a impact to keep this bill from being passed by Congress.

A better bill to replace HR 2646 should have provisions that support and expand non-medical model approaches such as Vermont’s Soteria house, which has been recently opened in Burlington. Also, New York could expand the open dialogue approach that is now being used by the Parachute Project in New York City. The bill could even fund private non-profits like Melwood in the greater metropolitan DC area. For over a year now, Melwood (with the help of ISEPP’s Mary Vieten) has been running a unique, non-medical model, program that helps military and veterans suffering from war trauma.

The text of ISEPP’s letter reads:

Dear Chairman Upton and Ranking Member Pallone:

We write to you as practitioners in mental health, and advocates for safe, humane, and life-enhancing treatment for people diagnosed with mental disorders. Our organization, the International Society for Ethical Psychology and Psychiatry (ISEPP), is made up of professional mental health clinicians, scholars, educators, peer-advocates, and “psychiatric survivors.” This is the term we use to designate those who have been hurt by the current, broken, mental health system. We applaud Congress’ intense interest in addressing this brokenness, and we thank Representative Tim Murphy’s efforts to bring this issue to the forefront of Congress’ attention.

We have serious problems, however, with many of the H.R. 2646 provisions:

(1) We oppose, both as mental health practitioners and citizens vested in civil liberties, provisions that restrict civil rights. It is mandatory that criminal behavior be distinguished from eccentric behavior and bizarre speech. In a word, it is not against the law to be “crazy.” It is against the law to behave illegally. We realize, of course, that the two often are mixed, that criminals can also be mentally ill. The alleged criminal is entitled to due process. The mentally ill person, criminal or not, needs treatment.

(2) We realize as practitioners that it is very often necessary to engage family members, friends, and associates of the identified patient. As good clinicians we should always be open to listening to what they have to tell us about the patient. But it is also crucial that we respect any of the patient’s expressed instructions not to divulge very private matters. It remains clinical judgment when to seek out help or give counsel if a patient is incapacitated or in a dangerous predicament. HIPAA regulations do not need revision. There is adequate leeway now allowing appropriate interchange between therapists and family. There need be no significant change in HIPAA’s regulations. Therefore, we oppose Section 401 of H.R. 2646.

Section 401 sets a dangerous precedent by making diagnosis-specific exception to the privacy rule. In one fell swoop, the mentally ill no longer have the same privileges of any other sick person being treated by professional caregivers. Do not make treatment odious to the mental patient by depriving him of legitimate privacy.

(3) Assisted Outpatient Treatment (AOT) laws as prescribed by H.R. 2646 are a very slippery slope. These laws are heavily geared toward forcing psychotropic medication, usually the neuroleptic (also called anti-psychotic) drugs. Although as practitioners we realize there is a place for offering these drugs to distressed individuals, they should only be prescribed with adequate informed consent. Given their profound adverse reaction profile (severe neurological damage, brain shrinkage, cognitive decline, metabolic abnormalities, decreased life expectancy, deadening of emotionality) it cannot be considered an irrational decision to reject their use. The argument that the mentally ill cannot make that decision is vastly overstated. As clinicians we have rarely had patients who can’t say, “yes, that helps” or “no, that feels terrible.” For these reasons we oppose rescinding funding from states that have not passed AOT laws.

(4) As practitioners and advocates for the mentally ill we have grave concerns about H.R. 2646 weakening standards that justify in-patient commitment.

(5) AOT programs are heavily invested in the use of drugging patients as a first line of treatment. Although drugging may be indicated in selected patients, the weight of the evidence is that drugs are at best short-term solutions. In a penetrating study published in 2007 by Martin Harrow and Thomas Jobe, they found in their 15-year follow-up “A larger percent of schizophrenic patients not on anti-psychotics showed periods of recovery and better global functioning (p< .001).” (“Factors Involved in Outcome and Recovery in Schizophrenic Patients Not on Anti-psychotic Medications: A 15-Year Follow-Up Study,” Journal of Nervous and Mental Disease, Volume 195, page 406, 2007).

A landmark study in Michigan demonstrated that skilled therapists had substantially better long-term results using no drugs. Notably, drugs had better results only in the first few months. (see Karon, B and VandenBos, GR (1994) Psychotherapy of Schizophrenia ,Treatment of Choice. Northvale, NJ: Jason Aronson).

A recent study featured on the front page of the New York Times (“New Approach Advised to Treat Schizophrenia” October 20, 2015) reported an approach used in Finland and imported to the US called “Open Dialogue” which uses intensive family therapy and social interventions with minimal anti-psychotic medication. The Open Dialogue approach fared significantly better than the usual high dose drug approach. A pilot program in New York called the “Parachute Mental Health Program” offers both respite centers for the mentally ill and mobile treatment teams that go to the home of the identified patient. Preliminary data suggest these programs prevent hospitalization and therefore potentially give more bang for the mental health system buck. Hospitalizations are extremely expensive and disruptive. Investment in these alternative approaches merits Congressional support.

(6)We oppose the provisions of H.R. 2646 which constrict the work of the patient protection and advocacy agencies which protect the rights of disabled persons.

(7)As practitioners and patient advocates we oppose provisions of H.R.2646 which defund and weaken the recovery oriented approaches that have been promoted by the Substance Abuse and Mental Health Systems Administration (SAMHSA). There is ample evidence that these non medical approaches are not only effective but also less costly than the typical AOT’s. We believe it is important to maximize the voices of mental health consumers. And that is what SAMHSA programs provide.

(8) Any legislation must approach the arena of mental health treatment with great humility. There are myriad theories and ideologies. Resources supplied to the States by the Federal government must be given with strings attached, viz., “show us the evidence” that your approach(es) is/are effective, safe, humane, and life-enhancing.

Joanne Cacciatore has what many would find to be an unbearable calling: to help counsel parents through their grief after the death of a child. As a professor of social work at Arizona State University, the Sedona resident and mother of four grown kids — and one stillborn — is a top expert in the field of child loss and traumatic grief; her vast body of research ranges from maternal depression after stillbirth to fathers’ grief after infant loss and parental bereavement in Native American cultures. She’s founder of the support-giving MISS Foundation, as well as the Center for Loss and Trauma. But as a therapist, Cacciatore, 50, has a more basic if hard-to-fathom focus — to support and guide moms and dads through their darkest days. Recently, ahead of National Pregnancy and Infant Loss Awareness Month, she sat down with Yahoo Parenting to discuss the importance of facing a topic that pretty much everyone wants to avoid.

Read her interview here.

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.