As I’ve written in four previous blogs devoted to examining the barriers that block persons presumed to have major mental illnesses from living longer and more effective lives, it’s time to discard the disease/biological model that’s been used for the past 30 and more years to explain the causes and course of schizophrenia and all other major mental illnesses. First and foremost, the disease model is centered on treatment that relies predominately on psychoactive medications which, prescribed too-often in too-great quantities for too-long periods of time, put a premature end to too-many lives (c.f. # III for a full discussion of this issue).

Secondly, a biological or genetic cause for major mental illnesses has never been uncovered, and biology or genetics don’t determine the course of these illnesses. Rather, the recent WHO schizophrenia prevalence studies, as well as the long-term outcome studies conducted by Bleuler and Harding and colleagues over thirty years ago underline the importance of environmental factors, particularly the presence or absence of support systems, in influencing whether a person undergoes recovery or not. The key question, then, and the focus of this blog, is what new model, if any, do we put in its place?

My own struggle to uncover a conceptual and treatment frame for schizophrenia began when I was a rookie social worker on Maimonides Medical Center’s in-patient psychiatric unit in 1976. This was at the time when the work of Stack Sullivan, Fromm Reichmann and other proponents of “intensive psychotherapy” was being discredited as costly and ineffective; when the family therapists, e.g., Ackerman and Bowen, among others, were being hailed, then assailed, for examining family systems and family interaction as causative of schizophrenia; when there appeared to be no practical, i.e., therapeutic, application of Bateson’s “double bind” theory; when neuroleptic medications were being prescribed extensively to control psychotic symptoms and the disease model began to gain acendancy.

Ironically, this was also the time, the mid-70s, when Leonard Mosher and colleagues were opening the doors to Soteria in northern California, the scaled-down and relatively short-lived American version of R.D. Laing’s Philadelphia Association, where staff was trained “to be with” rather than “treat” residents as they cycled through the various stages of their psychoses. Over time, I’ve cycled back to agree with Laing, whom I’ve begun to re-read, that schizophrenia is an existential problem, a problem in living, regardless of the putative cause.

In my rookie year, I can clearly remember feeling overwhelmed by the upset and anxiety of an Orthodox Jewish family whose vivacious 16-year-old daughter had just been diagnosed with schizophrenia. I was unprepared to help them, so I turned to family therapy for the additional clinical training I needed and entered a three-year long internship program headed by Dr. Phil Guerin, Bowen’s widely published successor. When Bowen’s multi-generational approach to schizophrenia proved impractical to implement in the Community Mental Health Center where I was working, I fastened on the psychoeducational family therapists—Anderson, Hogarty and McFarlane—and began to adapt McFarlane’s multi-family model for use with the patients and families I was working with in our Day Hospital program. In fact, I wound up replicating McFarlane’s two-year long study for my doctoral dissertation with results similar to his, principally a marked reduction in study participants’ symptoms and psychiatric hospitalizations and their families’ levels of expressed emotion.

Interestingly, the psychoeducational approach is rooted in the disease model, which I embraced because it seemed to offer concrete treatment solutions. The key assumption in psychoeducation is that knowledge is power; that, if the presumed patient and her/his family “know” that the patient has a disease, incurable but treatable, not caused by environmental factors, i.e., not by any family interactions, but probably by factors beyond anyone’s control, viz., genetics and the patient’s biological vulnerability, then all family members will calm down, i.e., their individual and collective level of expressed emotion will be reduced.

Expressed emotion is the key concept here, and one that would remain valid even should the disease model be discarded. As defined by McFarlane, et al, and by Leff and colleagues, who did the pioneering work, “EE” is comprised of critical, intrusive comments directed by family members at their ill member, which the latter experiences as demeaning and invalidating. Leff demonstrated in his studies a direct correlation between “High EE” and psychiatric relapse and re-hospitalization. When “EE” was lowered, so, correspondingly, was relapse. In short, “EE”, although not causative, was the key environmental factor governing the patient’s course of illness. As per Watters, “high EE”, while not exclusive to the United States, is a distinct American cultural phenomenon, affecting the course of all the major mental illnesses, including schizophrenia and the affective disorders.

Given its ubiquity, it is probably experienced by persons with serious mental illnesses as emotional abuse, unintentional perhaps but nonetheless quite real. It should be noted that Watters, referring to the work of cross-cultural psychiatrists, has remarked that informing ill persons that they have an incurable disease serves to raise their anxiety rather than lower it.

Other fundamental and still-useful psychoeducational concepts include the following: “communication deviance” between family members and the presumed ill family member, originally introduced by Bateson, et al, as causative in schizophrenia, later revised by McFarlane and others as consequent to the major mental illness; and the salience of psychosocial treatment and its synergistic interaction with prescribed medications, rooted in the treatment/medication studies conducted by Hogarty, et al, in Pittsburgh in the early 70’s, which demonstrated that medication alone, i.e., without psychosocial treatment, did not prevent or even significantly forestall psychiatric relapse.

Our own psychosocial treatment was comprised of weekly multi-family therapy sessions, which included the indexed patients’ principal caretakers and the patients themselves, and weekly individual clinical case management sessions with the patients, our own unique contribution to the psychoeducational approach.

Finally, relapse in psychoeducation is conceived as a “stress diathesis” phenomenon, i.e., consequent to the ill person’s biological vulnerability to environmental or life stressors, exacerbated by abuse of intoxicants and medication non-compliance. Given what I’ve learned over the years, I would amend that conceptualization as follows: first, a person’s vulnerability to psychosis is consequent to that person’s inability, i.e., lack of adequate life skills, to address life stressors, whether rooted in a characterological vulnerability or simple lack of life experience. In the 1980s, we attempted to address this by teaching our study participants social skills, but met with little success because of our own lack of training in this area. Once I had been trained in DBT in the mid-90s, I began to teach the persons whom I treated in my private practice skills of emotion regulation with good results. Accordingly, I would recommend that persons vulnerable to psychosis be taught such skills today.

Secondly, abuse of intoxicants can indeed precipitate psychosis in vulnerable individuals, as can non-compliance with neuroleptic medications. Conversely, because of their iatrogenic nature, compliance with neuroleptics can and does lead to the premature deaths of those who take them. To take a page from Will Hall, the best treatment strategy to address all three problems is harm reduction. (Again, c.f. # III for a fuller discussion re. psychoactive medications and their adverse effects.)

Back to the $64 question, what will a post-disease model look like? What will its principal components be?

As you might have surmised, I always draw on my own experiences, on what I have firsthand knowledge of. I’m partial to environmental variables, not so much to explain etiology—frankly, I don’t believe isolating etiology is all that crucial here, since, as per Laing and Mosher, I view psychosis as a transitory life experience—but to determine course of illness and outcome. In sum, I like coupling the basic psychoeducation approach and the key concepts I identified above—I’m basically talking treatment approach here—to a set of environmental variables that can be used in lieu of the concept of biological vulnerability. I’m referring to the ACEs, the Adverse Childhood Experiences identified in a large study sample of 17,337 Kaiser Permanente patients in California.

The initial phase of the ACE study, when baseline data was gathered, was conducted between 1995-1997 as a collaboration between Kaiser Permanente and the Centers for Disease Control and Prevention. A longitudinal study, it will track the medical status of the baseline participants for an indefinite period of time. Its objective is to analyze the relationship between nine categories of childhood trauma and later health and behavioral outcomes. Specifically, each study participant, collectively considered representative of middle class Americans, was asked via a 10-part questionnaire whether he/she had grown up experiencing any of the following before the age 18:

THE ACEs