PsychRights Wins Again!



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!


Breaking News: The Cause of Schizophrenia Finally Discovered?

2/3/2016        In the News 14 Comments

Scanning of a human brain by X-raysby 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 made7, 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 outcomes21, 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.


  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.

Looking Behind the Curtain of Genetic Research

1/12/2016        ISEPP In Action 0 Comments

JonathanISEPP'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.

The Fear in My Doctor’s Eyes

12/18/2015        ISEPP In Action 3 Comments

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


Fictional Memoir – Ron Leifer

12/2/2015        ISEPP In Action 1 Comment


ISEPP's Ron Leifer, M.D., is announcing the publication of his new book, The Search for Sin Semilla: A Fictional Memoir. His book is about a psychiatrist who helps an involuntary patient escape from a mental hospital from whom he learns the true meaning of his profession.
Anyone interested can obtain a copy by writing to Ron at: Ron Leifer, 92 West Hill School Rd., Richard, NY 13835. Include a check for $20 and your return address.

More Opposition to the Murphy Bill

11/23/2015        In the News 1 Comment

US Capitol Building, Washington DC, USA

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!

Fighting the Murphy Bill

11/9/2015        ISEPP In Action 2 Comments

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.

ISEPP In Yahoo Interview

10/22/2015        ISEPP In Action 0 Comments

tumblr_inline_nwhi49yg9g1s3412d_1280Joanne 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.

ISEPP Leadership Changes

10/18/2015        In the News 0 Comments

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.

ChuckRubyChuck 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.

DominicRiccioReplacing 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.

JoanneJoan 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-Neal-Vieten-179x300Mary 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.

nhunterNoel 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 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.

NAMI Increases Stigma

10/11/2015        In the News 0 Comments

miaw-bannerby William Schultz, Doctoral Student, Minnesota School of Professional Psychology

The first full week of October (October 4th – 10th) 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).


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 Psychology3, 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 Psychiatry199(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 Psychology28(1), 91-102.

Corrigan, P. W., & Watson, A. C. (2004). At issue: Stop the stigma: call mental illness a brain disease. Schizophrenia Bulletin30(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 Psychiatry12(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 Review33(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 Practice42(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 Medicine42(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 Therapy56, 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 one7(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 Review33(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 Practice21(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 Services63(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

National Alliance on Mental Illness. (2015b). Fact sheet library. Retrieved from

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 Disorders174, 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 Medicine44(02), 303-314.

Schultz, W. E. R. (2015) Binge eating and genetics. Retrieved from

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 Disorders168, 224-228.