See here for a recent study by ISEPP’s Joanne Cacciatore on the effects of poverty and parental education on the experience of bereaved mothers. Her study is the first to investigate poverty, education, and parental bereavement while examining the relative risk of other variables as informed by the literature. The findings reveal that poverty was the strongest predictor of psychological distress when compared to others factors which have traditionally been considered significant in parental bereavement. Bereaved parents living in poverty may be less likely to seek support and have fewer available resources.
by Chuck Ruby, Ph.D.
Investigators from the French Land Transport Accident Investigation Bureau (French acronym BEA), which has been investigating the March 2015 Germanwings crash, have recently recommended that world aviation agencies require mental health workers report pilots whose mental heath condition "could threaten public safety". This is an alarming mistake. See the NBC story here: http://www.nbcnews.com/storyline/german-plane-crash/germanwings-crash-bea-investigators-urge-new-rules-about-reporting-mental-n537416.
One of the most robust findings of research is that mental health professionals are not good at predicting others' future violence or harmful actions. There are clear risk factors that increase a person's likelihood of doing so, but they do not enable us to predict whether the behavior will occur. The best we can do is manage those risk factors in order to reduce the chances. Complying with BEA's recommendations and putting mental health workers in the position of making predictions, will result in a huge false alarm problem, destroying people's lives in the process, and ironically causing those who would benefit the most from help with emotional problems avoiding such help.
Many occupations require employee background evaluations in order to determine continued psychological suitability and readiness for the job. In addition to airline pilots, other examples are law enforcement officers, employees working in national security programs, and nuclear power plant workers. The employers in these settings have a reasonable interest in knowing their employees can be trusted. And employers can understandably err on the side of caution by denying employment when possible problems exist. But requiring a psychological evaluation for a suitability determination and requiring mental health workers to report people to the authorities are two different things.
A mental health worker, most likely some type of counselor in this situation, has a fiduciary obligation to the person being helped. The relationship between the counselor and the client is paramount, and the confidential nature of the relationship is at the core of this trust. Requiring the counselor to report people who "could threaten public safety" places the counselor in an ethical double bind. If the counselor reports, she or he damages the relationship and harms the person. If the counselor fails to report and the person commits some act, the counselor becomes the target of legal and ethical censure.
Attempting to determine who "could threaten public safety" is impossible. This could actually mean anyone. How many times have uncharacteristic acts of violence been committed by people who never showed any warning? It would be easy to predict future harm when a client makes a statement about intent to harm a specific person(s), but how often does that actually happen? Hardly ever. Besides, there are already laws and guidelines in place that require counselors to warn of such clear cases.
But other than these clear cases, where does the counselor draw the line? How much of a risk is needed prior to warning? How do we quantify that? Must we use standardized instruments to assess the level of risk? How valid and reliable are those instruments? The answer is: not very. With behavior that happens infrequently among the population, any assessment of risk will necessarily have very high false positive results or false alarms. This is just a matter of statistics. Violent behavior is no exception. For instance, the FBI reported a .4% base rate of violent crime in 2013, and this includes all types of violence, not just murders and assaults (see https://www.fbi.gov/about-us/cjis/ucr/crime-in-the-u.s/2013/crime-in-the-u.s.-2013/tables/1tabledatadecoverviewpdf/table_1_crime_in_the_united_states_by_volume_and_rate_per_100000_inhabitants_1994-2013.xls). With such a low base rate occurrence, even the most accurate assessment instrument is doomed to result in extremely high false alarms. In other words, the great majority of those identified as potentially dangerous and reported by counselors to aviation authorities, will never commit a dangerous act. But being reported as at risk for such behavior can ruin their lives and damage the value of professional help.
The slope is slippery. For what other occupations will this kind of big brother monitoring apply? Should counselors be required to report police officers? Teachers? Bus drivers? Investment bankers? Physicians? Who would report the counselors?
Toby Watson, Psy.D., recently submitted an ISEPP challenge to an FDA proposed rule to reclassify ECT so it can be used in "treating severe major depressive episode in patients 18 years of age and older who are treatment resistant or require a rapid response." You can read his challenge here.
Lena Dunham, a well-known actress, recently received attention and praise because of a collection of Instagram photos she publicly posted, which highlighted her emotional and psychological challenges (subsequently referred to as “mental illnesses”; although I think this and other medical terms are misleading, I’ll use them in this post just for clarity sake) and the medications she uses in response to those challenges. Her central message was that there should be “no shame” surrounding mental illnesses or the use of medications. By “shame”, Dunham was referring to the stigma surrounding mental illnesses, which is pervasive and has a variety of negative effects, such as increasing distress and discouraging individuals from seeking help. Due to the widespread, negative effects of stigma, mental health patients, mental health advocacy organizations, mental health professionals, researchers, celebrities, and politicians have communicated their commitment to ending stigma through psychoeducational campaigns.
For example, actress Glenn Close co-founded an organization called “Bring Change 2 Mind” whose purpose is to “end stigma and discrimination surrounding mental illness” through education. The method for combatting stigma endorsed by Dunham and Close appears to rely on explaining mental illnesses as brain diseases. For instance, the “facts” section of the Bring Change 2 Mind website states that “The fact is, a mental illness is a disorder of the brain – your body’s most important organ – and one in four adults experience mental illness in a given year, including depression, bipolar disorder, schizophrenia, and PTSD.”
By asserting that mental illnesses are brain disorders, this approach highlights supposed brain defects as causes of mental illnesses. This, in turn, challenges the stigmatizing belief that mental illnesses are the result of some sort of moral failure or character weakness. The reasoning goes: You wouldn’t blame someone for being diagnosed with a physical disease to which they didn’t contribute. So why would you blame someone for their mental illness, since mental illnesses are really brain disorders to which they didn’t contribute?
This approach to stigma has been identified in research. For example, Corrigan et al. summarized the perspective described above when they wrote, “Moral models yield attributions that mental illness is onset controllable and persons with mental illness are to blame for their symptoms. Biological models are more consistent with attributions that mental illness is uncontrollable at onset.” In other words, moral models suggest that individuals can control the development of their mental illness while biological models suggest they cannot. This is in line with Bring Change 2 Mind’s claim that “Like most diseases of the body…Mental illnesses are no one’s fault.”
It seems to me that identifying and challenging stigma are excellent goals and I praise individuals and groups, like those mentioned above, for their efforts. However, I’m also concerned because I believe there are at least three important problems with this approach.
The first problem is the assertion that mental illnesses are “brain disorders” contradicts the scientific data and some important philosophic considerations underlying that data. To begin, consider what Thomas Insel, until recently the head of the National Institute for Mental Health, wrote near the end of 2015: “The problem is that even though there have been thousands of studies looking for biological markers of mental health problems such as depression or schizophrenia, none has proven clinically actionable. And, in truth, little has been replicable even in a research setting.” Insel’s comments aren’t out of the ordinary. Congruent statements have been made by many mental health experts. In sum: scientific research has not identified reliable biological pathologies causing mental illnesses. And it’s a plausible argument that if we’ve not identified biological pathologies, it’s a stretch to call mental illnesses “brain disorders” or “brain diseases.”
Perhaps it’s true that researchers may someday identify biological pathologies. Even if they don’t, at the least mental illnesses still involve or are mediated by the brain. And as neuroscience continues to progress, it’s likely that more and more precise correlations between mental illnesses and brain structure and function will be discovered. But even these discoveries wouldn’t immediately justify understanding mental illnesses as brain disorders because a change in the brain is not synonymous with a brain disorder. Let me explain:
All mental phenomenon and behaviors are mediated by the brain. That is, everything changes our brain, from our developmental environment to stressful life events, falling in love, studying for an exam, meditating, and participating in psychotherapy. So even if researchers reliably identified brain differences in individuals who experience, for example chronic anxiety, this does not lead to the conclusion that a disordered brain is causing the anxiety. It merely identifies that the brain changes in response to experiences. To illustrate this point, consider a study in which researchers identified that when individuals diagnosed with social anxiety are administered cognitive-behavioral psychotherapy, their distressful symptoms diminished and their brains changed. Crucially, the mechanism involved in changing the brain was not primarily biological but psychological. In other words, it was not an individual’s disordered brain that was causing their symptoms, but their unhelpful beliefs and behaviors related to social situations.
An objection I’ve often heard to this sort of example is that even though the mechanism of change may be psychological, the change still occurs fundamentally at the biological level. This objection opens up a large discussion which I’ve explored elsewhere and can easily lead us off track (if it hasn’t already).  But before returning to discussing stigma, I’ll try to briefly explain an important aspect of my reply to this type of reductionist objection:
If fundamentality is what we are after, then mental illnesses aren’t “really” brain disorders but, instead, patterns of quarks (or quantum fields or whatever else physics identifies) interacting in particular ways. In fact, from this type of reductionist perspective, sciences such as “chemistry” and “biology” aren’t real: they’re useful fictions -- epistemological tools with pragmatic explanatory powers that scientists use until our understanding of physics becomes powerful enough to achieve our explanatory goals. So if we want to be scientific about mental illness, then we need to rely not on neuroscientists, psychiatrists, psychologists, and those who’ve experienced mental illness, but on physicists.
I hope you’ll agree with me that this sort of thinking doesn’t make a lot of sense. At the least, I think it’s important to note that many biological oriented researchers agree that this perspective isn’t comprehensive or functional. For example, Kendler argued “It is possible to study scientific questions from perspectives that are both too basic and too abstract” and this is why he thought it important to reject looking for “big, simple neuropathological explanations for psychiatric disorders” and instead accept that in “ways we can observe but not yet fully understand, subjective, first-person mental phenomena have causal efficacy in the world.” In short: psychosocial factors are crucial to understanding the development of mental illnesses and approaches which emphasize only biological features, such as claiming that mental illnesses are brain disorders, overstate the current evidence and are deeply misguided.
Now that we’ve gotten muddy in that philosophical swamp…I want to return to the subject of combatting stigma and my two other concerns about approaches that emphasize brain deficits. My next concern is straight-forward: a significant body of evidence suggests that emphasizing bio-pathological etiologies of mental illness does not reduce stigma. For instance, Angermeyer et al. used a population-based study design to investigate “the question whether promulgating biogenetic explanations may help reduce the stigma attached to mental illness and, therefore, should be included into anti-stigma messages.”  They found that biogenetic explanations are linked to increased stigmatizing attitudes and, as a result, should be avoided in anti-stigma campaigns.
Their findings aren’t unusual. In fact, they’re typical. Similar outcomes are found in numerous studies and meta-analyses. Even recent experimental studies suggest that biogenetic etiologies of mental illnesses increase perceived differentness – such as increased perceived incompetence and unpredictability – and do not reduce stigma as well as explanations which emphasize that mental illnesses may not be discrete diseases.
When I first examined this evidence, I was perplexed. I wondered: if biological etiologies emphasize that individuals are not responsible for their mental illnesses – their genetics, brains, and/or chemical imbalances are – then why do biological etiologies not decrease, and often increase, stigma? Well, in short, the research strongly suggests that the reason is that stigma is not only comprised of responsibility. Schomerus et al. emphasized that while biological etiologies of mental illness are often associated with reduced levels of perceived responsibility and blame, these reduced levels can be “outweighed by the adverse effects mediated by perceived differentness and dangerousness, respectively” and similar findings are common. These increased levels of perceived differentness and dangerousness can contribute to the negative effects of stigma that organizations like Bring Change 2 Mind are attempting to challenge. Thus, it seems to me that there’s good reason to rethink this strategy.
Finally, my third concern surrounding emphasizing brain deficits is that this way of thinking can have significant negative impacts on clinical outcomes. Within the past decade, a new area of research has explored the relationship between an individual’s beliefs regarding the etiology of mental illnesses and her or his treatment preferences and prognostic expectations. The research has consistently found that the greater an individual endorses a biological etiology of mental illness, the greater her or his prognostic pessimism. That is, they expect that their symptoms will persist at greater levels for longer periods of time. The proposed mechanism of this finding is that the greater an individual endorses biological etiologies, the greater she or he endorses “essentialist” views of her or himself – the view that an individual’s emotional and psychological states are largely determined by biological factors and that psychological and social factors are largely or completely impotent. This prognostic pessimism is important because a clients’ expectancies to improve are an important contributor to their improvement – individuals who expect to do better, do better. Thus, factors which contribute to individuals expecting to do worse – such as biological etiologies – can contribute to individuals doing worse.
So, given my concerns, where does this leave us? Unfortunately, with no quick and easy solution. Corrigan, Druss, and Perlick noted that “Advocates need to learn from the complex research on stigma change to implement programs that improve care seeking while not exacerbating other forms of discrimination.” That’s not easy because mental illness and stigma are large, often complicated, subjects. At the least, though, I think it’s important to recognize that there are alternatives to biological etiologies of mental illnesses – such as psychosocial approaches -- which are congruent with the scientific evidence and may avoid promoting stigmatizing attitudes. That is, individuals who experience mental illness may be responding to harmful environments and/or lack the knowledge/resources to manage their lives in more adaptive ways. This perspective doesn’t reduce mental illnesses to brain disorders and it doesn’t imply that we should blame individuals for their mental illnesses. It seems to me that this is an approach worth considering.
 Holmes, L. (2016). Lena Dunham shuts down mental illness stereotypes in new photos. Retrieved from http://www.huffingtonpost.com/entry/lena-dunham-mental-illness-instagram_us_56a259b7e4b0d8cc1099cf59
 Corrigan, P. W., Druss, B. G., & Perlick, D. A. (2014). The impact of mental illness stigma on seeking and participating in mental health care. Psychological Science in the Public Interest, 15(2), 37-70.
 Bring Change 2 Mind (2016). The facts. Retrieved from http://bringchange2mind.org/learn/the-facts/
 Corrigan, P. W., River, L. P., Lundin, R. K., Wasowski, K. U., Campion, J., Mathisen, J., Goldstein, H., Bergman, M., Gagnon, C., & Kubiak, M. A. (2000). Stigmatizing attributions about mental illness. Journal of Community Psychology, 28(1), 91-102.
 Insel, T. (2015). A different way of thinking. New Scientist, 227(3035), 5.
 Deacon, B. J. (2013). The biomedical model of mental disorder: A critical analysis of its validity, utility, and effects on psychotherapy research. Clinical Psychology Review, 33(7), 846-861; Fuchs, T. (2012). Are Mental Illnesses Diseases of the Brain?. Critical Neuroscience: A Handbook of the Social and Cultural Contexts of Neuroscience, 331-344; Graham, G. (2013). The Disordered Mind: An Introduction to Philosophy of Mind and Mental Illness. New York, NY: Routledge; Miller, G. A. (2010). Mistreating psychology in the decades of the brain. Perspectives on Psychological Science, 5(6), 716-743.
 Fuchs, T. (2011). The brain--A mediating organ. Journal of Consciousness Studies, 18(7-8), 196-221.
 Hunter, N., & Schultz, W. (2016). Brain scan research. Ethical Human Psychology and Psychiatry, 18(1), In press.
 Månsson, K. N., Salami, A., Frick, A., Carlbring, P., Andersson, G., Furmark, T., & Boraxbekk, C. J. (2016). Neuroplasticity in response to cognitive behavior therapy for social anxiety disorder. Translational Psychiatry, 6, e727, 1-8.
 Schultz, W. (2015). Neuroessentialism: Theoretical and clinical considerations. Journal of Humanistic Psychology, published online before print on December 3, 2015, doi:10.1177/0022167815617296.
 Kendler, K. S. (2005). Toward a philosophical structure for psychiatry. The American Journal of Psychiatry, 162(3), 433-440.
 Angermeyer, M. C., Millier, A., Kouki, M., Refaï, T., Schomerus, G., & Toumi, M. (2014). Biogenetic explanations and emotional reactions to people with schizophrenia and major depressive disorder. Psychiatry Research, 220(1), 702-704.
 Kvaale, E. P., Gottdiener, W. H., & Haslam, N. (2013). Biogenetic explanations and stigma: A meta-analytic review of associations among laypeople. Social Science & Medicine, 96, 95-103; Schomerus, G., Matschinger, H., & Angermeyer, M. C. (2014). Causal beliefs of the public and social acceptance of persons with mental illness: a comparative analysis of schizophrenia, depression and alcohol dependence. Psychological Medicine, 44(02), 303-314; Speerforck, S., Schomerus, G., Pruess, S., & Angermeyer, M. C. (2014). Different biogenetic causal explanations and attitudes towards persons with major depression, schizophrenia and alcohol dependence: Is the concept of a chemical imbalance beneficial?. Journal of Affective Disorders, 168, 224-228.
 Wiesjahn, M., Jung, E., Kremser, J. D., Rief, W., & Lincoln, T. M. (2016). The potential of continuum versus biogenetic beliefs in reducing stigmatization against persons with schizophrenia: An experimental study. Journal of Behavior Therapy and Experimental Psychiatry, 50, 231-237.
 Schomerus, G., Matschinger, H., & Angermeyer, M. C. (2014). Causal beliefs of the public and social acceptance of persons with mental illness: a comparative analysis of schizophrenia, depression and alcohol dependence. Psychological Medicine, 44(02), 303-314.
 Schultz, W. (2015). Neuroessentialism: Theoretical and clinical considerations. Journal of Humanistic Psychology, published online before print on December 3, 2015, doi:10.1177/0022167815617296.
 Constantino, M. J., Ametrano, R. M., & Greenberg, R. P. (2012). Clinician interventions and participant characteristics that foster adaptive patient expectations for psychotherapy and psychotherapeutic change. Psychotherapy, 49, 557-569.
 Corrigan, P. W., Druss, B. G., & Perlick, D. A. (2014). The impact of mental illness stigma on seeking and participating in mental health care. Psychological Science in the Public Interest, 15(2), 37-70.
“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!
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, 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.
- 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
- Feinberg, I. (1983). Schizophrenia: Caused by a fault in programmed synaptic elimination during adolescence? Journal of Psychiatric Research, 17(4), 319-334.
- 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.
- Muller, N., Myint, A. M., Schwarz, M. J. (2012). Inflammation in schizophrenia. Advances in Protein Chemistry and Structural Biology, 88, 49-68.
- 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.
- Paus, T., Keshavan, M., Giedd, J. N. (2008). Why do many psychiatric disorders emerge during adolescence? Nature Reviews: Neuroscience, 9, 947-957.
- Joseph, J. (2015). The trouble with twin studies: A reassessment of twin research in the social and behavioral sciences. New York: Routledge.
- Ross, C. A., & Pam, A. (1995). Pseudoscience in biological psychiatry: Blaming the body. New York: John Wiley & Sons.
- Pepys, M. B., & Hirschfield, G. M. (2003). C-reactive protein: A critical update. Journal of Clinical Investigation,111, 1805-1812.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- Read, J., Fosse, R., Moskowitz, A., & Perry, B. (2014). The traumagenic neurodevelopmental model of psychosis revisited. Neuropsychiatry, 4(1), 65-79.
- 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.
- 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.
- de Girolamo, G. (1996). WHO studies on schizophrenia. The Psychotherapy Patient, 9, 213-231.
- Jablensky, A., & Sartorius, N. (2008). What did the WHO studies really find? Schizophrenia Bulletin, 34(2), 253-255.
- 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.
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