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I had moved away from this topic and on to some other research and writing, but then I watched a film about R.D. Laing, ” Mad to Be Normal”, about the time period from 1965-1970, when Laing operated Kingsley House in London, and it drew me right back into the alternative programs of treatment for people with schizophrenia.

I returned to a few of Laing’s books and Joe Berke’s “I Haven’t Had to Go Mad Here” (1979), as well as John Weir Perry’s “The Far Side of Madness”(1974). Laing, Berke, and Perry subscribed to the view that societal reaction to individuals with psychotic symptoms (or even other emotional/interpersonal disturbances) has typically been to employ various means of control and treatments to transform or even obliterate (electric shock, tranquilizers, etc.) troublesome symptoms. They ask, “troublesome to whom?” According to Laing, Berke, and Perry, it has been “troublesome” to family members, friends, work mates, and the psychiatric profession has been enlisted to “normalize” behavior – sometimes by whatever means possible. In addition, I listened to the recording of my 1993 interview with Joe Berke, which I mentioned in an earlier post about Berke’s book with Mary Barnes, ” Two Accounts of a Journey Through Madness”.

My interest here is in the epistemology of what is considered “mental illness” and how a particular cultural and institutional construction determines approaches to treatments and aspects of marginalization. From Foucault’s notion of discipline and punish (with particular reference to prisons and mental institutions) to Mary Douglas’s ( in her “Purity and Danger”) notion of things out of order being perceived as polluting, people with schizophrenia have historically been warehoused, heavily medicated, and/or otherwise marginalized from any mainstream society. Laing, Berke, and Perry, as well as the relational psychotherapists, Harry Stack Sullivan, Otto Will, and Frieda Fromm-Reichman, approached people with schizophrenia as regular human beings with different behavioral challenges, for whom the need to be able to have genuine communication with others is essential to their healing prognosis. Though Laing’s Kingley Hall and Berke’s Arbours Centre did not use medications, except when a resident was a danger to themselves or others, the development of several anti-psychotic drugs in recent years, has provided options of combination treatments – as explained in my earlier posts. Nevertheless, the temptation to medicate and not provide appropriate psychotherapy for people who have schizophrenia continues to be a significant weakness of contemporary psychiatry.

When I visited one of the Arbours Centre residences in 1993 and talked with several of the guests (residents with schizophrenia), I learned that they had dramatic stories of the contrast between their previous institutional experiences and the structure/non-structure and atmosphere of an Arbours House. The guests experienced what they called a “drug holiday” while at Arbours. They experienced respect. They experienced a balance between structure and freedom. They experienced supportive companionship. They experienced empathic healers who treated them as human beings who had needs for attachment, love, and communication with others.

There is enough current research on the part genetics may play in the etiology of schizophrenia to assume that genetics needs to be a part of a systems understanding of schizophrenia. From a purely genetics stance, Siddhartha Mukherjee includes a section on schizophrenia in his book, “The Gene: An Intimate History” (2017). He States:

“Like many other genetic diseases, schizophrenia also comes in two forms – familial and sporadic. In some families with schizophrenia, the disorder courses through multiple generations. Occasionally some families with schizophrenia also have bipolar disorder. In sporadic or de novo schizophrenia, in contrast, the illness arises as a bolt from the blue: a young man from a family with no prior history might suddenly experience the cognitive collapse, often with little or no warning. Geneticists tried to make sense of these patterns, but could not draw a model of the disorder” (p.442).

Again, from a purely genetic stance, Mukherjee works to navigate through the schizophrenic genetic puzzles: “In some families, perhaps, there are fewer gene variants, but with more potent effects – thereby explaining the recurrence of the disorder across generations. In other families, the genes may have weaker effects and require deeper modifiers and triggers – thereby explaining the infrequent inheritance. In yet other families, a single, highly penetrant gene is accidentally mutated in sperm or egg cells before conception, leading to the observed cases of sporadic schizophrenia” (p.446).

I propose that a purely genetic explanation of the etiology of schizophrenia is insufficient, but that some aspect of what Mukherjee suggests likely plays a role – in combination with other factors. I would add the diathesis-stress model, which is a psychological theory that attempts to explain a disorder or its trajectory, as a result of an interaction between a predisposition vulnerability and stress caused by life experiences. A diathesis can take the form of genetic, psychological, biological, or situational factors. This is also, what Christine C. Gispen-de Wind and Lucres MC Jansen explain in their article, “The Stress-Vulnerability Hypothesis in Psychotic Disorders: Focus on the Stress Response Systems” (2002):

“The vulnerability-stress model is an intriguing concept to look into the etiology of psychotic disorders, and in particular, into the ‘nature-nurture’ principle. That stress affects a vulnerable nature may be obvious, but its mechanism is not well understood, and many questions remain to be answered, let alone how to define ‘vulnerability'”. Their article covers the biologic stress response systems, the autonomic nervous system (ANS), the hypothalamic pituitary adrenal (HPA) system, and the immune system and highlights the plasticity of the HPA system as the mediator of adaptation.

An aspect of vulnerability might also include impairments in sensory gating. Sensory gating is the ability of the central nervous system to adapt to sensory stimuli upon their repeated presentation. It is commonly impaired in schizophrenia patients, and may relate to the inability to concentrate, and to the overload of attended stimuli and a reduced ability to suppress processing of irrelevant and uninformative sensory input.

It is possible that six of the Galvin family children had varying degrees of predispositional vulnerability for possible schizophrenia and combined with familial and other social stresses, schizophrenic symptoms became manifest, while such vulnerabilities were either not at all a factor or were minimal enough that the other six children did not succumb to schizophrenia. Since genetics alone cannot explain the expression of schizophrenia in the Galvin family, I believe the diathesis-stress model is likely and the stresses within the family seem quite obvious. Perhaps the dynamics of early interpersonal relationships between the Galvin parents and their first two boys played a role in the environmental stresses. This would uphold at least some of the interpretations of the Interpersonal Psychiatrists, such as Freida Fromm- Reichmann, Harry Stack Sullivan, and Otto Will. The older two boys who did have symptoms of schizophrenia had then affected the other most vulnerable siblings. There were ongoing serious battles between and among some of the boys, and as illness impacted all family members – those with schizophrenia and those without, the pressure on the non-schizophrenic parents became increasingly challenging. Their need to keep as much of this a secret as possible must also have had an effect on those most affected with symptoms.

Since we know there is no known cure for schizophrenia and that medications alone may have as many deleterious affects as ameliorating ones, I suggest as part of a systems approach to treatment for schizophrenia, combining therapeutic work on communications and relationships, along with the best available symptom management medication (this will change over time and will need to be calibrated to each specific person). Bateson’s papers on schizophrenia in “Steps to an Ecology of Mind”(1972) suggest the ways that people with schizophrenia communicate and characterize the types of double binds created by parents as possible clues to understanding and treating patients. While the Interpersonal Psychotherapists subscribed to an early mother-infant relationship contributing to schizophrenia, they approached the treatment of people who were seriously ill much as psychotherapists might approach helping non-psychotic people with their personal relationships.

It is well known that Freud did not believe that psychoanalysis was appropriate with people suffering from psychosis, yet Freida Fromm-Reichmann, in “Psychoanalysis and Psychotherapy” (1960) said that Freud did not close off the possibility: “He (Freud) expressed the hope for future modifications of psychoanalytic techniques which would make it possible to do intensive psychoanalytically oriented psychotherapy with schizophrenics” (p.176). And this is what she and other Interpersonal Psychotherapists believed they were able to do at Chestnut Lodge, Austen Riggs, and other psychiatric hospitals which treated people with schizophrenia.

Elyn Saks, in her memoir (reviewed in an earlier post), made a convincing argument for combining psychoanalytic treatment along with medication for her to manage her ongoing struggles with schizophrenia, even while she has developed a very successful life and career. She did not write about the specific psychoanalytic approach she has been involved with, but it may be somewhat similar to what Christopher Bollas discloses in his book, “When the Sun Bursts: The Enigma of Schizophrenia”(2015). Bollas has practiced psychoanalysis with people suffering from schizophrenic for well over thirty years. Based on his experience, he writes about how to approach de-coding the language of someone with schizophrenia. His position has been, along with that of Bateson and the Interpersonal Psychotherapists, that there is a logic to the language of schizophrenia, and that the schizophrenic patient wants someone, such as a clinician, to recognize this and be able to communicate with them. Most people with schizophrenia have been institutionalized or otherwise isolated, with no one to communicate with them. Bollas has this to say about his understanding of the condition of people with schizophrenia:

“We shall never know whether schizophrenia is the outcome of phylogenetic, genetic, intra-uterine, early infantile, infant-mother, linguistic, sex shock, family, or accident-in-the-real causes. Clearly it is yet another form of being human.

However, we do know something about how schizophrenics perceive reality, how they think, how they behave, and how they relate. We know a great deal about why they resist many forms of treatment, but we also know how, why, and when they seem prepared to work with a clinician.

Whatever the genesis of schizophrenia, the first distinct outcome is a split in the self in which one part functions in an ordinary manner and another part develops a radically different way of perceiving, thinking, and relating”(p.181).

Bollas summarizes my own position regarding the importance of psychotherapy along with medication in the treatment of schizophrenia:

“Although medications may prove valuable in the course of psychotherapy, nothing helps schizophrenics more than a single one-on-one commitment by a fellow human being who has taken the time and endured the training to know how to read them, be with them, understand them, and talk to them.”(p.187).

I hope that my systems approach to the etiology and treatment of schizophrenia is helpful for those touched in one way or another by this devastating illness. I will revisit this topic as any new and relevant information becomes available.

Is there a way to think about the etiology, the de-coding/unwrapping and possible treatment options of schizophrenia which avoids the single model approach? Considering the multiple memoirs from insiders (patients and therapists) and theoretical and medical approaches I have already reported, and considering the fact that we have not yet “solved” the schizophrenia “dilemma”, how might we pull together bits and pieces of data into some understandable systemic whole? In my previous post I referred to Harrington’s statement that a group of researchers in 2008, who identified and critically assessed all known facts about schizophrenia concluded that the facts did not, as a group, lead logically to any coherent explanation of schizophrenia. She also said that these same researchers in 2011 claimed that the field seemed to be operating like the fabled six blind Indian men groping different parts of an elephant and coming up with different conclusions. “In fact they admitted, in the current state of knowledge, one could not rule out the possibility: ‘that there may be no elephant, more than one elephant, or many different animals in the room'” (p.182). I will propose a possible way through this dilemma.

Why am I interested in schizophrenia? While studying psychology in undergraduate school , I worked as a counselor at The Lawrence School for emotionally disturbed children in VanNuys, California (1959-1961), and as a volunteer on the children’s ward at the Camarillo State Hospital in Camarillo, California. The Lawrence School was one of the first of its kind in the U.S. Our objective was to take children in early elementary school grades and prepare them to be mainstreamed after the sixth grade. If they were too disturbed and /or organically impaired, so that the prognosis was not positive, we could not take them and the only option for them usually was a state hospital. We did not typically place diagnostic labels of these children, but many were likely on the autism spectrum, with several other disturbances, some with possible symptoms of schizophrenia. While it is not thought that schizophrenia shows up before adolescence, there may have been pre-psychotic symptoms with some of our children. While working in the children’s ward at the Camarillo State hospital, I had access to the records of the children I worked with. Most were given a diagnostic label of “Schizophrenia Reaction, Childhood Type”. I believe that this was because psychiatrists at that time knew almost nothing about how schizophrenia might affect children. Since most children had obvious psychotic symptoms or were extremely autistic, the label was used as a “holding place” until more was known. Meanwhile, these children were essentially being “housed” in an institution because their families could not manage them. Treatment options were minimal. I don’t remember if the children were medicated as were the adults at the hospital. I do remember that I was fascinated with trying to communicate with the most disturbed children. One boy had become a Bumble Bee and would buzz the ward non-stop. The staff ignored him. I decided to buzz alongside him to see if he would notice and perhaps talk to me. He definitely noticed, but he never talked. This at least hinted to me that he was aware of what was happening around him, while he was living as a bee.

Many years later, while I was in graduate school, I was studying with Gregory Bateson and using some his ideas for my dissertation. I became intrigued with his development of the “double bind theory”, which came out of the research with families with schizophrenia that he, Don Jackson, Jay Haley, and John Weakland, had done from 1952-1954 through Stanford University. I have posted earlier on the double bind theory. Bateson’s idea about this actually goes well beyond the research with families, but it was the family dynamics around mental illness which provided observable material for this theory. While this research was very influential for the family therapy and family systems movement, the emphasis on the etiology of schizophrenia resting with family dynamics and particularly on the influence of the mother, caused ongoing backlash from families with schizophrenia in their midst. It is true that the interpersonal psychotherapy psychiatrists also identified the mother as a primary agent within a family unit, but their interpretation was based more on developmental psychology and the early mother-child relationship. The Bateson group noticed the roles played by each member of a family grouping, and in families where a father was mostly absent and ineffective, the burden for raising children fell mostly on the mother. This was certainly true of the Galvin family in Colorado Springs. What I learned from revisiting the papers that Bateson published about schizophrenia in “Steps to an Ecology of Mind”(1972) is that he considered the possibility of genetics influencing the occurrence of schizophrenia within families, though this genetic influence will still need environmental or interpersonal influence as well. In posing the dilemma between genetics and environment, Bateson asks if simply noting which family member becomes hospitalized with schizophrenia will tell us that they have a particular gene for schizophrenia:

“We cannot simply assume that the hospitalized members carry a gene for schizophrenia and that others do not. Rather, we have to expect that several genes or constellations of genes will alter patterns and potentialities in the learning process, and that certain of the resultant patterns, when confronted by appropriate forms of environmental stress, will lead to overt schizophrenia” (p.259). This statement and Bateson’s next one ( part of his 1959 lecture delivered at the Institute for Psychosomatic and Psychiatric Research and Training in Chicago), presages current thinking about the relationship between genetics and environment in the etiology of schizophrenia: “In the most general terms, any learning, be it the absorption of one bit of information or a basic change in the character structure of the whole organisms, from the point of view of genetics, the acquisition of an ‘acquired characteristic.’ It is a change in the phenotype, of which that phenotype was capable thanks to a whole chain of physiologic and embryologic processes which lead back to the genotype”(p.259).

My interest in schizophrenia comes from my work with emotionally disturbed children and from the family systems research and from the mystery of the etiology and treatment approaches.

I propose a systems approach to understanding schizophrenia, which includes genetics and biochemistry, vulnerability markers or endophenotypes, impairments in sensory gating, early parental-child relationships, family dynamics, and communication theory. I will explain the connections among these variables in my next post…

I am revisiting my previous material about schizophrenia because there are two new books which raise some important issues and current research regarding this mental illness. “Mind Fixers: Psychiatry’s Troubled Search for the Biology of Mental Illness” (2019) by Anne Harrington covers some material I have covered in previous posts and she also moves further into the current state of biological psychiatry with separate sections on Depression, Bi-Polar Disorder, and Schizophrenia. I will focus specifically on this latter section for this post. “Hidden Valley Road: Inside the Mind of an American Family”(2020) by Robert Kolker investigates the case of the Galvin family from Colorado Springs who had twelve children, six of them diagnosed with schizophrenia. Kolker traces the history of various psychiatric/psychotherapeutic approaches to understanding and treating schizophrenia, particularly with the Galvin family children.

Neither Robert Kolker or Anne Harrington are clinicians or former patients, therefore they are not what I have referred to as “insiders”. Kolker is a journalist, and Harrington is a professor of the history of science.

While Kolker spends a good deal of his reportage on the lives of the individuals in the family and I believe this appeals to a wide readership he brushes over highlights of the history of theories, interpretations, treatments, and research regarding schizophrenia, he ends up spending the last half of his book reporting on the unfolding advances in genetic research. He is careful not to assume anything conclusive (since there is nothing conclusive), but he essentially discards family dynamics as a possible significant ingredient in the outcomes of what happened in the Galvin family. The mother, Mimi, obviously created double-binds, and both parents covered up the illnesses of their children with distractions, denials, and secrets. Both parents failed to protect their young girls from the predatory behavior of Jim (the second oldest brother). One son committed murder-suicide. I believe there was more denial than Kolker reports. The direct and indirect trauma was ongoing and insidious throughout the lives of all children. So with or without so-called markers for a genetic predispossession, the family dynamics played a role in the various outcomes – those with established diagnoses of schizophrenia and obvious symptoms – and those without.

In fairness to Harrington, her book is primarily about biological psychiatry and not psychotherapy or psychoanalysis, so my comments about how she lightly touches base with psychoanalysis and family therapy and then presumes them to be fairly dealt with may expect too much. Yet, the epistemology of linearity in the historian’s chronological treatment diminishes a more nuanced and complete understanding of how both psychoanalysis and family therapy contributed to and continue to contribute to a dynamic picture of the complicated disease we still refer to as schizophrenia. Psychoanalysis and family therapy are dealt with almost as straw men to be put in place as historical failures in treating schizophrenia.

An example of Harrington not being a clinician is her bad habit of lumping people who suffer from a variety of mental illnesses that may not rise to the level of psychosis as “worried well” – a hackneyed reference which would not be used by either a clinician of a patient.

There is also a “cherry-picking ” problem. Harrington refers to Thomas McGlashan’s meta-analysis of case records from Chestnut Lodge, a psychiatric hospital near Washington, D.C. which cared for schizophrenic patients, “The Chestnut Lodge Follow-up Study: Long-term outcome of Schizophrenia and the Affective Disorders” (1984). She summarizes his conclusions with this “he reviewed the case records of some 446 patients and found that they showed, he said bluntly, that psychotherapy was ineffective for schizophrenia” and in McGlashan’s words, “‘ the data are in and the experiment failed'”(p.181). What does “failed” really mean? Yes, McGlashan was a clinician at Chestnut Lodge, and yes, he followed the psychotherapeutic approaches of Harry Stack Sullivan, Frieda Fromm- Reichmann, and Otto Will, generally known as Interpersonal Psychotherapy. His analysis of cases assumedly included those of these three clinicians, (each of whom had a period of directing the hospital), as well as other psychiatrists. I have not read his study, though I have read case material from Sullivan, Will, and Fromm-Reichmann. Without knowledge of the Interpersonal Psychotherapy treatment approach, an evaluation of “success” or “failure” seems a simplistic conclusion. Context is significant. To begin with, McGlashan had likely already been considering a medical-biochemical approach to treatment with schizophrenic patients and moving away from psychotherapy. He did shift into an enterprise of early medical intervention with pre-schizophrenic patients, which ultimately did not succeed. To be fair to the clinicians who devoted their careers to helping severely ill patients, the Interpersonal Psychotherapy practiced at Chestnut Lodge includes published accounts of their process as well as what they considered successes and failures with patients. While I might question some of the theoretical assumptions of Sullivan and Fromm-Reichmann, their shift away from some classical psychoanalytic positions and their humane treatment of all patients who they treated, deserve more intentional consideration.

Carlton Cornett, in “Being withPatients” (2017), writes about Harry Stack Sullivan and Otto Will, as well as Frieda Fromm-Reichmann and a few other clinicians who worked with schizophrenic patients and generally followed the approaches of Sullivan. He refers to Otto Will’s approach to treating patients, ” He noted that the more you come to know a patient, the less he will seem like a disease or disorder and will then take the form of an unhappy, despairing, and discouraged person confused by his relationships with others”(p.120)

Cornett summarizes his interpretation of Interpersonal Psychotherapy:

“Interpersonal psychotherapy is composed of a variety of elements that are treated as mutually exclusive: social learning theory, behaviorism, psychoanalysis, attachment and cognitive theory. I tend to favor the psychoanalytic aspects over others, but I know that all contribute significantly to the whole. How Interpersonal Psychotherapy primarily differs from psychoanalysis is its practical emphasis. It avoids the oft-disputed question of whether one’s technique is appropriately ‘analytic’ for the more important question of whether we are helpful” (p.160).

The case material from Sullivan, Will, and Fromm-Reichmann, indicates evidence of various successes in helping seriously disturbed patients overcome most of their symptoms, gain insight into their life challenges and relationships and manage their affairs outside of the hospital environment. The treatments did not include medication or any other experimental practices, such as electric shock. We now know that some combination of the most current medications, plus some form of psychotherapy, may be the most effective treatment at this time, but we also know that bio-psychiatry and pharmacological treatments alone have not provided answers for the sufferers of schizophrenia. Harrington includes in her chapter on schizophrenia sections on serotonin, dopamine, amphetamines, genes. she concludes with:

“In 2008 a group of researchers launched a multipart project designed to identify and critically assess all ‘facts’ currently established for schizophrenia. Each was graded on a 0-3 scale for reproducibility, relevance for understanding schizophrenia, and durability over time. Some turned out to be more robust than others, but none got full marks. More important, even the most robust individual facts pointed in a range of different directions; they did not, as group, lead logically to any coherent explanation of schizophrenia” (p.182).

I will continue my investigation into schizophrenia, to include a proposed systems approach to understanding and treating this challenging disease, in my next post.