“Schizophrenia Breakthrough” – Or a Case of Ignoring the Most Important Evidence?

Ron Unger, LCSW
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Last week, the headlines blared: “Schizophrenia breakthrough as genetic study reveals link to brain changes!”  We heard that our best hope for treating “schizophrenia” is to understand it at a genetic level, and that this new breakthrough would get us really started on that mission, as it showed how a genetic variation could lead to the more intense pruning of brain connections, which is often seen in those diagnosed with schizophrenia.  “For the first time, the origin of schizophrenia is no longer a complete black box,” said one (while admitting that “it’s still early days”).  The acting director of the National Institute of Mental Health (NIMH) described the study as “a crucial turning point in the fight against mental illness.”

But is all this hype justified?

A “back story” to this article is that the NIMH has a long history of bias toward biological approaches to understanding mental and emotional difficulties, with an accompanying tendency to ignore even the most obvious evidence that these difficulties often relate to problems in living experienced by people.  For example, even though numerous studies confirm that adverse childhood experiences make a later diagnosis of schizophrenia much more likely (more so than do any particular genes), the NIMH, on a website about the possible causes of schizophrenia, claims it’s “unknown” what kind of psychosocial factors might contribute to putting people at risk.

But it really isn’t a mystery.  To people like NYU professor Brian Koehler who have been following both the biological and the psycho-social research for decades, it’s clear that the real story is that the biological differences we often see in people diagnosed with disorders like “schizophrenia” are often the result of stressful life events, not something that requires specific genes (even though it may be true that some genetic variations increase vulnerability to some limited degree.) He presented his theory recently in a presentation at NYU on “Social Factors in Schizophrenia” which (thanks to MIA) you can watch here:

Brian Koehler on “Social Factors in Schizophrenia,” February 30, 2016 at New York University. Filmed by Mad in America.

Below (with his permission) I am quoting a recent email from Brian Koehler, where he shared some of what we would be hearing from the media if the media were being given the whole story.  (His writing will make more sense to you if you understand that microglia are the type of brain cells active in the synaptic pruning that was being discussed, though only in reference to possible genetic causes, in the articles about the recent “breakthrough”…..)

In the late 1970s & early 1980s, as a result of some biochemical research I was conducting and my work in psychotherapy with people on an inpatient unit of a NYC hospital, I became very interested in the pervasive effects of chronic and significant anxiety on our brain and body. I partly made it my life’s work to study and demonstrate that the neuroscience of what we call “schizophrenia” (a highly problematic term) is in actuality, and often in many persons, the neuroscience of severe, chronic stress/anxiety/fear. I am grateful for the opportunity to be educated on the neuroscience of psychosis and stress at such places as the Nathan Klein Institute of Psychiatric Research (NKI), which is managed by the NYS Office of Mental Health and maintains a strong academic collaboration with New York University.

I quickly observed in the persons I was working with on inpatient and outpatient settings, that the content of what we call “delusions” and voices, are re-traumatizing to the person experiencing them. Not only may they be attempts at “cure” or “restitution” (as Freud thought), but they may create significant distress for many persons experiencing them, especially if they feel not in control of aversive threats, accusations, danger situations such as social exclusion, etc. Psychological and social traumas, I quickly learned in the 1970s and 1980s, were prevalent in the histories of many of the persons I was working with. Surviving survival of various social and psychological traumas also played a role in the neurobiological and immunological changes we were observing (even in persons who had not yet started taking antipsychotics, which we now know can cause neural atrophy, mostly subtle, but atrophy nevertheless). In the 1990s, I learned of transgenerational transmission of traumas (specifically, the transmission through epigenetic channels of inducible defences against threats to survival) first in plants, then insects and then in mammals. Since 1990 I have checked on every single finding in the neuroscience of “schizophrenia” and have cross-checked with the emerging literature (thanks to sMRIs, fMRIs, PET, etc.) on the neuroscience of chronic stress. To this day, I still have not found one single specific neuroscience finding in “schizophrenia.” The findings are mostly non-specific (I am leaving the door open, in the name of science, for specific findings). When one is emotionally and intellectually invested in a particular belief, it is important to look even more intensively at the evidence that disconfirms one’s belief and to strive for intellectual and emotional honesty. I admire the current Dalai Lama for when he was asked if science definitely disproved reincarnation, what would he believe? He said, he would give up his belief in reincarnation!

The latest findings in the neuroscience of psychosis have included the role of microglia and neuroinflammatory processes. (e.g., “Microglial activation and the onset of psychosis” by Tyrone Cannon, published in the American Journal of Psychiatry, January 2016). Microglial cells, are glial cells (which are at least as plentiful as neurons in the brain, of which there are close to 100 billion with trillions of connections with other neurons-the connectome) are innate immune cells of the brain. They have a role in the regulation of the extracellular milieu and they participate in neuronal regeneration. They respond quickly to injury and produce a wide variety of pro-inflammatory molecules, neurotrophic factors, and neurotransmitters. Microglial cells can be activated by several factors including systemic infection, physical trauma, oxygen and energy depletion, and some neurodegenerative disorders.

Stress definitely activates the microglia-and this has been known for quite some time. I am no longer surprised when persons researching “schizophrenia” present their findings without checking the research on such important factors as social adversities and chronic stress. I strongly believe that in many, if not most, persons with a diagnosis of “schizophrenia” the neuroscience findings could never fully be understood without reference to the whole person living in a particular sociocultural context, both of which are impacted by social adversities across the generations (e.g., the individual and social traumas of one’s parents, grandparents, social group, etc.). Not so easy to study with only neuroimaging, genome wide association scans, microarrays, etc!!

I have included only a few recent research studies documenting the effects of stress on microglia from such journals as Molecular Psychiatry, Stress, etc.

Brian Koehler PhD

Stress 2015 Jan;18(1):96-106. doi: 10.3109/10253890.2014.995085. Epub 2015 Jan 8.
Microglia activation regulates GluR1 phosphorylation in chronic unpredictable stress-induced cognitive dysfunction.
Liu M, Li J, Dai P, Zhao F, Zheng G, Jing J, Wang J, Luo W, Chen J.

Abstract
Chronic stress is considered to be a major risk factor in the development of psychopathological syndromes in humans. Cognitive impairments and long-term potentiation (LTP) impairments are increasingly recognized as major components of depression, anxiety disorders and other stress-related chronic psychological illnesses. It seems timely to systematically study the potentially underlying neurobiological mechanisms of altered cognitive and synaptic plasticity in the course of chronic stress. In the present study, a rat model of chronic unpredictable stress (CUS) induced a cognitive impairment in spatial memory in the Morris water maze (MWM) test and a hippocampal LTP impairment. CUS also induced hippocampal microglial activation and attenuated phosphorylation of glutamate receptor 1 (GluR1 or GluA1). Moreover, chronic treatment with the selective microglial activation blocker, minocycline (120?mg/kg per day), beginning 3?d before CUS treatment and continuing through the behavioral testing period, prevented the CUS-induced impairments of spatial memory and LTP induction. Additional studies showed that minocycline-induced inhibition of microglia activation was associated with increased phosphorylation of GluR1. These results suggest that hippocampal microglial activation modulates the level of GluR1 phosphorylation and might play a causal role in CUS-induced cognitive and LTP disturbances.

CNS Neurol Disord Drug Targets. 2015;14(3):304-8.
Commentary: the effects of psychological stress on microglial cells in the brain.
Yuan TF, Hou G, Zhao Y, Arias-Carrión O.

Abstract
Psychological stress leads to activation and proliferation of microglial cells in different brain regions. These effects are mediated by inflammatory cytokines, as well as stress hormones including glucocorticoids and norepinephrine. Eliminating microglia from the nervous system or blocking their activation prevented the stress-induced impairments on brain cognitive functions. We conclude that microglial cells are important meditators underlying anti-depression therapies.

Molecular Psychiatry 2014 Jun;19(6):699-709. doi: 10.1038/mp.2013.155. Epub 2013 Dec 17.
Dynamic microglial alterations underlie stress-induced depressive-like behavior and suppressed neurogenesis.
Kreisel T, Frank MG, Licht T, Reshef R, Ben-Menachem-Zidon O, Baratta MV, Maier SF, Yirmiya R.

Abstract
The limited success in understanding the pathophysiology of major depression may result from excessive focus on the dysfunctioning of neurons, as compared with other types of brain cells. Therefore, we examined the role of dynamic alterations in microglia activation status in the development of chronic unpredictable stress (CUS)-induced depressive-like condition in rodents. We report that following an initial period (2-3 days) of stress-induced microglial proliferation and activation, some microglia underwent apoptosis, leading to reductions in their numbers within the hippocampus, but not in other brain regions, following 5 weeks of CUS exposure. At that time, microglia displayed reduced expression of activation markers as well as dystrophic morphology. Blockade of the initial stress-induced microglial activation by minocycline or by transgenic interleukin-1 receptor antagonist overexpression rescued the subsequent microglial apoptosis and decline, as well as the CUS-induced depressive-like behavior and suppressed neurogenesis. Similarly, the antidepressant drug imipramine blocked the initial stress-induced microglial activation as well as the CUS-induced microglial decline and depressive-like behavior. Treatment of CUS-exposed mice with either endotoxin, macrophage colony-stimulating factor or granulocyte-macrophage colony-stimulating factor, all of which stimulated hippocampal microglial proliferation, partially or completely reversed the depressive-like behavior and dramatically increased hippocampal neurogenesis, whereas treatment with imipramine or minocycline had minimal or no anti-depressive effects, respectively, in these mice. These findings provide direct causal evidence that disturbances in microglial functioning has an etiological role in chronic stress-induced depression, suggesting that microglia stimulators could serve as fast-acting anti-depressants in some forms of depressive and stress-related conditions.

Curr Immunol Rev. 2010 Aug 1; 6(3): 195–204.
Responses of glial cells to stress and glucocorticoids
Jauregui-Huerta, Y. Ruvalcaba-Delgadillo, R. Gonzalez-Castañeda, J. Garcia-Estrada, O. Gonzalez-Perez,1and S. Luquin

Microglial cells are the innate immune cells of the brain. Like astrocytes, they have a role in the regulation of the extracellular milieu and they participate in neuronal regeneration. Like other immune cells, they respond quickly to injury and produce a wide variety of pro-inflammatory molecules, neurotrophic factors, and neurotransmitters. Microglial cells can be activated by several factors including systemic infection, physical trauma, oxygen and energy depletion, and some neurodegenerative disorders.

Psychological stress and glucocorticoids have long been shown to suppress immune responses. Thus, GCs could be expected to exert immunosuppressive actions on brain resident microglia. Consistent with this immunosuppressive hypothesis, in vitro studies have shown that treatment of microglia with GCs decreases the ability of these cells to proliferate, to produce proinflammatory cytokines, and to produce toxic radicals. These anti-inflammatory actions were confirmed in a spinal cord injury model treated with methylprednisolone. However, recent in vivo studies suggested that stress and GCs can enhance immune function within the brain. Restraint stress combined with water immersion, for example, induces massive microglial activation in the rodent brain. In addition, brief tail-shock, immobilization, and social isolation stress increase the expression of interleukin-1?(IL-1?) in the rat brain. Moreover, four sessions of restraint stress were capable of increasing the proliferation of microglia, apparently due to corticosterone-induced, NMDA receptor activation. This proinflammatory evidence has lead to the suggestion that stress-induced microglial activation may be involved in the progression of neurodegenerative disorders.

In conclusion, maybe the real “breakthrough” we should be working for, would be to get the NIMH and eventually the media to become interested in a “person in context” view of mental distress and mental disorders, so that biological facts will not be taken out of context, and we can orient our institutions both toward doing more prevention of distress and disorder in the first place, and more appropriate interventions once problems have occurred!

For another, more detailed look at this same subject, I recommend the article by ISPS member Noel Hunter, Breaking News! The “Cause” of “Schizophrenia” Finally “Discovered”!(?)

19 COMMENTS

  1. Bruce Koehler:
    We need to “talk”…. I can confirm about 99% of what you’re saying here, from my own lived experience.
    PLEASE get in touch with me. I live in the abject poverty of SSDI & SSI, and I am a slow typist, with unreliable phone service. Email & snail mail work best. I’m also ready, willing and able to meet in person, here in Keene, N.H. What I say to you goes for any colleague whom you might have faith in.
    I can’t do it without you, and you won’t do it as fast or well without me. Yeah, kinda arrogant and delusional-sounding. That doesn’t negate the sincerity or genuine-ness of my words….
    And, I don’t know whether I wish I did, or am glad I don’t – have YOUR level of formal education!
    Breggin’s “Toxic Psychiatry”, which I read first in late 1980’s – early 1990’s, was the first paving stone in MY “Yellow Brick Road”!…. Let’s give the World its’ “Wizard of Oz” moment. Those still suffering from iatrogenic neurolepsis cry out for our careful haste….
    (c)2016, Tom Clancy, Jr., *NON-fiction
    ps: Yes, some consideration must be made, for the infrastructure & manufacturing capacity of Pharma, and the same for the College / University / Academae bureaucracy. But we can safely flush both the DSM, and the pseudo-science of psychiatry VERY FAST. How? Simple. Make that *ALL* either “Neurology”, or “Family Medicine” A Nurse Practioner can do the Rx, working with an M.D…..
    Hey, I’ve been thinking about this for a LONG time!…..
    P.O. Box 1860, Keene, N.H., 03431
    email available from Emmeline Mead! ~thanks, my friends

  2. “reveals link to brain changes”

    That phrase “link to” or “linked to” What does that mean “linked to”

    “People are more at risk of schizophrenia if they inherit genes that lead to excessive loss of healthy brain synapses during adolescence, a major US study suggests.”

    Always that word “suggests” verb (used with object)

    1. to mention or introduce (an idea, proposition, plan, etc.) for consideration or possible action: The architect suggested that the building be restored.
    2. to propose (a person or thing) as suitable or possible for some purpose:
    We suggested him for president.
    3. (of things) to prompt the consideration, making, doing, etc., of:
    The glove suggests that she was at the scene of the crime.
    4. to bring before a person’s mind indirectly or without plain expression:
    I didn’t tell him to leave, I only suggested it.
    5. to call (something) up in the mind through association or natural connection of ideas:The music suggests a still night.

    I think that word suggests may be linked to deception.

    Why not words and phrases like “caused by” or “resulting from” instead of suggests, may and linked to ?

  3. Thanks Ron for sharing some of the conversation from the ISPS listserv on here. It’s valuable for people to see that many professionals do not agree with the reductionist biological perspective on “schizophrenia”, and are upset that these narrow-minded researchers continue to ignore social and environmental causes of psychosis.

    On another note, Brian Koehler looks like he has not had a haircut in a long time 🙂 But he is giving a good description of the history of ISPS and its views on psychosis.

    • Just for the heck of it I am going to repost this again so that more readers not familiar with the psychological viewpoints on psychosis can access some of the links below –

      —————-

      Here again is my critique of the McCarroll C-4A study: ———

      Here are adapted excerpts from a letter I sent to four of the principal authors behind this research: ————–

      Dear Professors Stevens, McCarroll, Barondes, and Lander,

      I’m a member of the organization ISPS (the International Society for Psychological and Social Approaches to Schizophrenia, http://www.isps.org) and also a person who was once diagnosed with schizophrenia but fully recovered.

      I am emailing you because I wanted to give you a window into our group’s discussion of this research. I thought you would find it interesting and perhaps useful. Below, I have put a long comment from our listserv that I placed there today. I expect you may find it disturbing and challenging to read (and I apologize, do not take my critique personally; it is possible that Benedict Carey oversimplified or miscommunicated some of your findings) – but I encourage you to read through it because it may broaden your perspective about schizophrenia in an eye-opening way.

      Lastly, I’d like to also share with you some of our research into psychosocial approaches for psychotic states and schizophrenia. Some of the best psychosocial approaches to “schizophrenia” have been able to return about 80% of first episode-psychotic schizophrenic youth to full engagement with work and relationships, usually with no or minimal remaining psychotic symptoms. The recent RAISE, EASA, and PREP trials actually adopted significant aspects of the models we pioneered. However, this work, particularly the Open Dialogue approach and the 388 program, is little known in the United States due to the dominance of the biological model. Here’s a look:

      The Open Dialogue Approach to Schizophrenia:

      http://www.taosinstitute.net/Websites/taos/Images/ResourcesManuscripts/seikkula-OpenDialoguesWithGoodAndPoorOutcomes.pdf

      http://psychrights.org/Research/Digest/Effective/fiveyarocpsychotherapyresearch.pdf

      The 388 Program, A New Perspective for Treating Schizophrenics

      https://www.youtube.com/watch?v=mmqT-4W4Cvg Individual Psychotherapy for Schizophrenia, Lewis Madrona’s Approach

      http://www.transpersonalstudies.org/ImagesRepository/ijts/Downloads/IJTS_33-1-07_pp_57-76_Mehl-Madrona_et_al_2014_Results_of_a_Transpersonal_Narrative_and_Phenomenological_Psychotherapy_for_Psychosis.pdf

      Gottdiener’s Meta-analysis of Psychotherapy for Schizophrenia

      http://psychrights.org/Research/Digest/Effective/BGSchizophreniaMeta-Analysis.htm

      ———————————— (My own comment on ISPS listserv)

      I would like to offer a detailed critique of the Benedict Carey article reporting progress in discovering the “Cause of Schizophrenia” of January 27

      (http://mobile.nytimes.com/2016/01/28/health/schizophrenia-cause-synaptic-pruning-brain-psychiatry.html?hp&action=click&pgtype=Homepage&clickSource=story-heading&module=second-column-region%c2%aeion=top-news&WT.nav=top-news&referer=&_r=0)

      I took some time this morning to cut out quotes from the article and offer my responses. These are my opinions:

      “(Scientists have) taken a significant step toward understanding the cause of schizophrenia”

      Response: I cannot say it better than Brian K: “There is no entity called “schizophrenia.” It is a syndrome and heterogeneous. The New York Times article “Scientists Home in on Cause of Schizophrenia,” is misleading in its title. It is not a single category (nature is not “carved at her joints” and our genomes did not evolve to reify DSM categories), nor is there one “cause.” The research is correlational not causal.”

      “insight into the biology behind any common psychiatric disorders”

      This phrase presumes that psychiatric disorders are valid, reliable medical classifications. This is false: Mary Boyle, Richard Bentall, Jeffrey Poland, Paula Caplan, Stuart Kirk, and others have argued convincingly that these labels do not represent discrete entities that can be reliably identified by different outside observers. Therefore the “scientific” research on them is not truly scientific.

      “drugs… blunt some of (schizophrenia’s) symptoms but do not touch the underlying cause.”

      This mistakenly assumes there is one” cause of “schizophrenia” or psychotic states. But the research from the Adverse Childhood Experiences study, from John Read, etc. strongly implies that there are many complex causes that can lead to psychotic states (“schizophrenia”) in different combinations. For example, incest, child abuse, social isolation, illicit drug use, lack of sleep, all could lead to psychotic states of different kinds that get labeled “schizophrenia.”

      “why the disorder often begins in adolescence of young adulthood” – This is because psychosis is probably not primarily an illness caused by biology, but primarily a social-psychological-experiential reaction to the world that is expressed in biology. The biggest risk period for vulnerable people is when they are in their teens or 20s when their parenting/social support is not adequate for the task of moving into adulthood and becoming independent. If they are overwhelmed by this transition, psychosis may result.

      “provided researchers with their first handle on schizophrenia”

      Again this mistakenly assumes that there is one reliable discrete entity called schizophrenia, that can be caught, like a fly in amber. But this is an illusion…

      “That risk (of developing “schizophrenia”, another misleading description) is tied to a natural process called synaptic pruning, in which the brain sheds weak or redundant neurons as it matures…People who carry genes that accelerate or intensify that pruning are at higher risk of developing schizophrenia than those who do not, the new study suggests.”

      I will quote Brian K’s wise words at length again:

      “The increased expression of the complement C4A gene may be associated with other processes. First, it is important to rule out confounds like antipsychotic use. APs have effects on our immune system. There are dopamine receptors on immune cells. The MHC (major histocompatibility complex), referred to in the article is involved in cell-mediated immunity-MHC proteins bind viral or bacterial coat proteins, take the peptides to the cell surface where they can be killed by cytotoxic lymphocytes (which stops the cell from being a host to viral replication). There is a great deal of research being done on the role of neuroinflammatory processes (e.g., microglia) in psychosis, depression, etc.

      Second, one must search for other correlations. In regard to the latter, Bronikowski et al (2002) found that inflammatory and stress response genes were most affected by physical inactivity and age. Twenty one inflammatory response genes were upregulated (increased) by age in a sedentary group, including complement C4 (which is invloved in immune function). I wonder if loneliness (and other chronic stressors) also can play a role, since it has significant effects on immune function. The NY Times article neglected to refer to the myriad of social factors demonstrated to play a role in the diagnosis, onset, course and outcome of “schizophrenia,” e.g., urban birth/living, migration, social defeat/social isolation, expressed emotion and communication deviance, childhood maltreatment, etc.”

      I think it is particularly important to note that this article said absolutely nothing about childhood abuse and social isolation as causes of receiving a schizophrenia diagnosis. The ACE Research and John Read’s research implies that these factors are often much more important than any genetic contribution. Understanding these factors does not have to mean blaming the parents or the individual. Further, I wonder whether these researchers are using a model that is truly epigenetic and interactional, i.e. appreciating how much genes are modified by environment/experience after birth. Again, in this context the monolithic construct of schizophrenia is outdated and due for abolition.

      “any step forward is not only rare and unusual, it’s just one step in a journey of a thousand miles” to improved treatments.”

      This implies a narrative of gradual progress at improving treatments (and presumably outcomes) for people labeled schizophrenia. But that is a false narrative. The latest meta-analysis from Jaaskelainen (2013) clearly shows that outcomes for people labeled schizophrenic have been gradually worsening in recent decades, for both symptomatic and functional outcomes. Thus the continued biological and genetic research is not enabling a gradual movement forward to improved treatments. The narrative of psychiatry and schizophrenia is not one of progress and improvement, but one of increasing failure and chronicity.

      “Some researchers had suspected that the pruning must somehow go awry in people with schizophrenia, because previous studies showed that their prefrontal areas tended to have a diminished number of neural connections, compared with those of unaffected people.”

      Again, this research is only correlational, not causal, and suffers severely from the lack of validity of the concept schizophrenia. The researchers also neglect the possibility that adverse environmental experience (e.g. loneliness, abuse) could be the primary (epigenetic) influence driving the process of accelerated pruning.

      “(this research) identifies the genes responsible (for accelerated pruning)”

      This research appears to be reductionistically viewing genes, in a pre-epigenetic way, as isolated actors which “do things” to people’s development. But genes do nothing without environmental input and interaction. So the possibility remains that the real link could be to the environmental experiences and interactions that are driving those genes to prune the neurons faster.

      “provides a showcase of biomedical investigation at its highest level.”

      Perhaps it would be more accurate to say that they are investigating a disease which has not been proven to exist as a discrete entity, and which may well have no one clear biomedical cause, in one way of understanding.

      “speculation that schizophrenia might be a kind of autoimmune condition, in which the body attacked its own cells.”

      It is incredible that this type of possibility is still seriously considered, in light of, 1) The lack of validity and reliability for labels such as schizophrenia, 2) The strong research that John Read has catalogued linking trauma to being diagnosed with schizophrenia. It speaks to the strong distorting influence that the drug companies’ money have on research and inadvertently on the minds of researchers.

      “C4-A could mean too much pruning — which would explain not only the thinner prefrontal layers in schizophrenia, but also the reason that the disorder most often shows itself in people’s teenage years or early twenties.”

      Like Brian, I am not purely or irrationally against genetic research. I think it’s possible that the overactive C4-A gene could confer a slightly increased risk for being overwhelmed by the stresses of life, all other factors being equal (in the statistical, aggregate sense). But that is very different from saying “this gene drives risk for schizophrenia.” Someone having an overactive version of this gene might never become psychotic due to other ameliorating factors. If I understand it right genes do not operate autonomously, but in concert with environmental influences which in turn can modify them throughout life. Further, it’s quite likely that this gene (and genes in general) might confer only a tiny percentage of the risk of “getting labeled with schizophrenia” (which is all it is, schizophrenia is not an illness someone has, but a label someone is given). Environmental-experiential factors may make up a far larger proportion of the risk of being so labeled, given the limitations of twin studies that Jay Joseph and Jonathan Leo have exposed (i.e. the notion that schizophrenia is 70 or 80% genetic is a myth; Brian Koehler is also working on a new model of this research).

      “Having such a variant, Dr. McCarroll estimates, would increase a person’s risk by about 25 percent over the 1 percent base rate of schizophrenia — that is, to 1.25 percent.”

      This is an admission of how small the influence of any one gene or group of genes is likely to be, and why genetic research into “schizophrenia” is unlikely to ever yield significantly improved outcomes, given the complexity involved in genetic-environmental interaction. Further, this sentence mistakenly assumes that there is a “1 percent base rate of schizophrenia”. But that is not a reliable average – “schizophrenia” is more common among poor people, certain ethnic groups, in inner cities, in certain developed countries, etc.

      “That is not nearly enough to justify testing in the general population,”

      Again, there would be little point to such testing because schizophrenia is not one coherent entity that can be reliably identified.

      “The researchers hope that the at-risk genetic profile, once it has been fleshed out more completely, will lead to the discovery of biomarkers that could help clarify a prognosis in these people.”

      This appears to me to be similar to the hopes of developing cold fusion or gold alchemy. The genetic environmental interaction that leads to individual psychotic states of greater or lesser severity is too complex to be reduced reliably to biomarkers, I think.

      “Developing a drug to slow or modulate pruning poses another kind of challenge.”

      Such a drug would probably not work because pruning must be subject to myriad internal and external genetic and environmental factors; I cannot imagine a pill that could precisely influence such a process, effectively reversing human pathological mind-body development from a biological level. Such a pill would almost have to be a “reverse time travel” pill or an “entire environment influence” pill that would do what human/environmental/biological curative influences together can do. Mind boggling.

      “But I’m not ready to call it a victory until we have something that can help patients.”

      I do not feel very optimistic about this, and would note that very effective social-psychological approaches that work such as Open Dialogue, 388, and intensive psychodynamic psychotherapy for schizophrenia already exist.

      As Noel said, it is sad to see that strong research on trauma, abuse, and social influences contributing to “schizophrenia” (below) is totally ignored while this research, which is actually very weak in its effect size and embryonic in its stage of development (if it ever progresses further), gets highlighted.

      https://www.researchgate.net/publication/282043036_Impact_of_childhood_adversities_on_specific_symptom_dimensions_in_first-episode_psychosis

      Furthermore, biological-genetic research continues to correlate with increasing rates of psychiatric disability:

      https://www.madinamerica.com/2016/01/what-disability-benefit-trends-tell-us-about-psychiatric-treatments-and-the-economy/

      Feel free to comment on any of these opinions. ——————–

  4. Hi Ron,
    I think “It’s a case of ignoring the most importance evidence…”

    I don’t believe in “reincarnation” but I believe in the Buddhist approach to mental distress, because I have personal experience of this approach working.

    There are probably lots of routes to longterm recovery, but only outside of the medical approach.

  5. Fiachra: This is a bit of sidetrack, but I believe in reincarnation as a possibility – not as a dogma. There is so much evidence for it that science currently ignores – it ignores only because it does not fit neatly with its ontological stance where a brain is needed to generate the mind.
    Many research studies (conducted by Dr. Ian Stevenson, Jim Tucker and many other researchers) have carefully investigated children who remember past lives. In these studies, children who present with memories of previous lives are extensively interviewed and if they give specific names or locations (cities, towns), the previous life individual is traced and verified using death certificates and autopsy records, etc. I think they currently have thousands of such cases (I have read books by these researchers).

    • Nancy99,

      I think you may be right, too. I know when my son was very young, he called water “agua,” the Spanish word for water. Despite not yet having had contact with Spanish speaking people. And my daughter was born the exact same day my aunt died, and she was always wise beyond her years. Her preschool teacher told me that when she spoke with my then four year old daughter, “it’s like I’m speaking to a forty year old woman.” It may be just a coincidence, but I think reincarnation is a possibility, too.

      • Thanks for sharing Someone Else. Dr. Jim Tucker’s books also have many interesting stories like that. I remember reading about a child who found things he had hidden in his previous life (when he was taken to the previous house), which no one else in his previous family knew about! Also, it seems some children report having existed in different realms (non-human) and he says that it is difficult ignore these statements in the context of other statements that the same child has made (on previous human births) that have been verified.
        I think near death experiences (NDEs) also strongly indicate that the mind is not mere electrical activity in the brain (as many scientists consider it to be).

        • Nancy99,

          I will admit, since I’ve had an electric-like “brain zap” problem, for the past 15 years, I do think electrical activity in the brain may be involved. Although, that’s not to say it’s all that’s involved, I don’t believe that. And I have had numerous people admit they could “feel the power,” surrounding me, at least when I was going through my drug withdrawal induced manic awakenings. So I have been searching for answers.

          My “brain zaps” were caused by an iatrogenic induced inappropriate antidepressant withdrawal, initially. But most people, at least that I’ve found online, don’t have this drug withdrawal induced issue continue forever. My current doctor is smart enough to confess he has no clue, but thought it was cool I could immediately get rid of a headache, by brain zapping it away.

          A lady in my church gave me a comparative religion document some years back, and I noticed the Mormons believe that electric-like emanations from the brain are how God communicates through people. And my medical records are filled with medical and religious “professionals” claiming “a man, Jesus” and “voices of God talk through her to other people.” I don’t know what to make of these comments, or the Mormon’s theory. But after I left my ex-religion, due to their betrayal of my family. A Mormon friend of mine, who knew nothing of my issues with my former religion, did show up on my door with a Book of Mormon and a bouquet of flowers.

          I too, was enamored with NDE books, when I was a teenager, and Nostredame’s ‘prophecies.’ And my awakening did imply Jesus did die for people’s sins 2000 years ago, thus allowing for all people to have a second or more chances, prior to His final judgement. I’m not certain what the truth is, but I know neither the medical community, nor any religion individually, has the answers either.

          So I’m quite certain those pretending to have all the answers need to stop pretending. And, as a society, we need to learn to live in a mutually respectful manner with all others within humanity, so we may continue to evolve collectively.

          • Someone Else,
            I am not denying electric activity in the brain! What I am saying is that we cannot point to electric activity and say “that’s the mind!” – this is because it is the mind itself that studies electrical activity in the brain – brains don’t talk. As I have stated earlier, it is the mind that thinks about the trees outside, about our body structures such as the digestive system, nervous system and even brain activity. So, the mind is a much more vast entity than mere electrical activity inside the head. If you read the article about the mind I posted sometime back, you might get an idea about the mind (link: http://sgo.sagepub.com/content/5/2/2158244015583860 ).
            Regarding NDEs, scientific studies have shown that patients recall descriptions of their resuscitation accurately – they recall what happened during the time their brain was clinically non-functional (when there was no electrical activity in the brain). It has been estimated that 25 million individuals worldwide have had a near death experience in the past fifty years, and these experiences have been reported throughout time in essentially all cultures, by not just religious individuals, but by atheists, agnostics as well as children who are commonly considered to be too young to have any real concept of death.
            Links for NDEs (scientific studies) : https://www.researchgate.net/publication/232463289_Near-Death_Experience_Out-of-Body_and_Out-of-Brain
            http://www.ncbi.nlm.nih.gov/pubmed/21988246

  6. Thanks so much for sharing that! That was such an amazing integration of information – one could speculate how all sorts of factors might contribute to either increasing or decreasing how anxiety and stress affect the brain to more or less degrees – from childhood adversity or abuse, from all types of adversity, to nutrition, neurological suseptibility from toxins or genes, from accidents and head injuries, from having more developed sensibilities towards justice, adversity from peers, family crisis or dysfunction, from having more imagination, from hormonal changes etc, etc. etc….and makes it glaringly obvious how inadequate neuroleptic medication is as a solution.

  7. Thanks, Ron, interesting talk by Brian Koehler, too. I’m quite certain, in practice, “It’s a case of ignoring the most importance evidence…” Especially, when doctors judge a person, based solely upon lies and gossip from child abusers, while disbelieving everything the patient herself says. And when doctors are ignorant of the effects of their drugs. Such as when you give a non-psychotic person an antipsychotic, the neuroleptic drug can result in neuroleptic induced deficit syndrome, which is often misdiagnosed.

    https://www.madinamerica.com/2016/02/researchers-call-for-reappraisal-of-adverse-mental-effects-of-antipsychotics-nids/

    And, since psychiatric practitioners and mainstream doctors today claim ignorance of the fact today’s “bipolar” drug cocktail recommendations, like combining the antidepressants and antipsychotics or benzos, are actually a recipe for how to create “psychosis,” via anticholinergic toxidrome.

    https://en.wikipedia.org/wiki/Toxidrome

    I’m quite certain today’s psychiatrists’ practice of ignoring the client’s real problems, and pretending the adverse effects of their drugs are “lifelong, incurable, genetic mental illnesses,” rather than iatrogenesis, is likely the root cause of most so called “serious mental illness” today. Especially since 2/3’s of all so called “schizophrenics” today are child abuse or ACEs survivors, people who initially had real problems, not brain diseases.

    But it was confessed to me, by an ethical pastor, that the “dirty little secret of the two original educated professions” is that, it is the psychiatric practitioners historic, and obviously still today, role in society to cover up child abuse for the religions and easily recognized iatrogenesis for the incompetent doctors.

    Seems the cats out of the bag though, and this “dirty little secret” is likely known by most the child molesters now. I do so hope the psychiatrists some day get out of the business of profiteering off covering up child abuse. Thus aiding and abetting the child molesters in raping more children. Since this is technically illegal behavior, although the cops all know not to address child abuse issues, if one has been defamed with any of the DSM disorders.

    Only in a way too paternalistic, and sick, society would the child molestation profiteers be given total control, as they’ve obviously been given in the US today.

  8. You’d have less trouble with these issues if you realized schizophrenia is just a descriptive definition of a syndrome that occurs when any number of biological things are out of line. Of course you’re going to see all these claims that aren’t quite true, because their sample group is mixed, their symptoms caused by different things that only respond to the most appropriate treatment, not the most common treatment.
    I offer an example. Many years ago I had a friend who lived in a complex of duplex cabins, One day, while I was visiting him, we went to pay his rent at a small single unit occupied by the owner’s agent. The agent’s unit was dark and shadowy, a black-lit poster on one wall with an addition of a pair of glaring, staring eyes tacked on to it.
    The agent began to complain to my friend, who he knew was interested in social work, about feeling increasingly strange over a period of several weeks. Knowing my friend was a stoner (and I probably was), he offered to smoke a pipe with him and got out this elaborate thing made of plumbing fixtures, the bowl being soldered to the stem.
    I told the agent to throw the pipe away or give it to his worst enemy because he was giving himself lead poisoning from the solder.
    The next rent day, 30 days later, we went over there and the place was bright, the eyes were gone from the poster and the agent was cheerful.
    Now imagine the result had the agent gone to a mental health professional.

  9. ‘In conclusion, maybe the real “breakthrough” we should be working for, would be to get the NIMH and eventually the media to become interested in a “person in context” view of mental distress and mental disorders, so that biological facts will not be taken out of context, and we can orient our institutions both toward doing more prevention of distress and disorder in the first place, and more appropriate interventions once problems have occurred!’

    Oh god yes please. Sometime in my lifetime, hopefully.