Understanding living systems must recognize that such systems do not operate one variable at a time. Groups of variables work together to produce a result. All the research studies which report results for only one or two variables in a living system are misleading.
When one looks at statistical results for studies of living systems, one sees that correlations between variables are statistically significant but moderate to weak in strength. This is pretty consistent from system to system. This observation influences how you think about the system. That is one aspect of systems thinking. One is forced to think about how the variables work together to influence any other single variable in the system.
Schizophrenia has 20 or more significant precursors, and they pretty much all are also connected to each other moderately. This is a system of loosely coupled variables. Thinking about such a system is different from thinking about a system which has only one or two variables predicting other important variables.
Precursors of Schizophrenia
Family system vulnerabilities-stressors
Parental communication deviance(CD)
Parental expressed emotion(EE)
Family acknowledgement
Adverse Childhood Experiences(ACE)
Low family and parental level of differentiation
Intense parent-child symbiosis
Family projection process
Grandparent death near birth
Early parent death near birth
Emotional shock wave reaction
Intense and chronic family system anxiety Individual child vulnerability
Individual child vulnerabilities
Genetics and family history of schizophrenia and schizophrenia spectrum disorders
Abnormal eye tracking
Movement disorders
Fish neurointegrative abnormalities
Pregnancy and/or birth difficulties
Sociological variables
Low Socioeconomic Status(SES)
Community violence and/or poverty
Low community economic opportunities
Consider one example. Genetics of the family is important in schizophrenia, but it is only partially correlated with the development of schizophrenia. It has to work together with other partial correlates in order to decisively predict the development of schizophrenia. This is illustrated by adding a few other partial predictors. For example, genetics, SES(socioeconomic status), parent-child intense symbiosis, ACE( adverse childhood experiences), an extended family system intense chronic anxiety. Each one of those is a partial predictor of the development of schizophrenia. However, put together the five variables and you can get a pretty powerful influence on the development of schizophrenia.
These observations are generally true for predicting other important variables in any living system, not just schizophrenia.
Look at the long list of precursors of schizophrenia. Each one individually is only a partial predictor. Put together any group of precursors and one starts to get much stronger predictions. I will review several of these precursors to flesh out what I mean by partial predictor.
The concept of a partial predictor can be illustrated with the genetics of schizophrenia. People glibly talk about schizophrenia being a genetic disease, as if having the genes or a family history of schizophrenia is a complete 100% predictor of schizophrenia. It’s not. Genetics is an important partial predictor of the development of schizophrenia. The prevalence of schizophrenia in the general population is about 1%. The extreme example that best illustrates the point are studies of pairs of adult identical twins, one of whom has been diagnosed with schizophrenia. The other twin would have almost the same genome as the schizophrenic twin, a near 100% association.
The actual numbers tell us that the other twin has a 30-45% chance of being schizophrenic, pretty strong but not 100%. So, genetics is a partial predictor of schizophrenia. A moderately strong partial predictor but nevertheless partial.
Similarly, all the other precursors of schizophrenia are partial predictors of the development of schizophrenia.
Another example of a partial predictor. ACE, adverse childhood experiences. ACE is very statistically significant in its association with the development of serious symptoms, the correlation with schizophrenia is about 0.30-0.34, a decidedly partial predictor.
Concretely, we know from that correlation that there are many exceptions to the association. Many people can have difficult childhood families represented by a high ACE score but not develop serious symptoms. A partial predictor. This also means that there are many with serious adult symptoms who did not have the childhood family environment of a high ACE score; their ACE score was low.
Parental expressed emotion(EE) and parental communication deviance(CD) are two more partial predictors of the development of schizophrenia. EE is a combination of harsh criticism of the child by a parent and parental over involvement. Communication deviance is the use of odd communication such that the listener is not able to share a focus of attention with the speaker. These have more impact on a vulnerable child. They are well summarized by Goldstein 1987. They both are partial predictors; meaning they can be present without the child developing schizophrenia, or schizophrenia can develop even when the two are not present. Partial predictors, weak to moderate correlation of the two behaviors with later development of schizophrenia.
Another important partial predictor is the SES of the child’s family. Low SES is a chronic stressor in the family’s life. This chronic stress would exacerbate the impact of other risk factors. SES is a partial predictor of moderate strength. It is not a slam dunk predictor. Many low SES families do not produce schizophrenia, and many high SES families have a child who turns out to develop schizophrenia.
Parent-child symbiosis is one precursor for which there is little or no quantitative evidence. Intense parent-child symbiosis was claimed to be an important influence on the development of psychopathology by psychoanalytic theorists. Bowen included it as one influence on the development of schizophrenia. I include it because so many clinicians claimed to see it as a factor in development of schizophrenia. In addition, its blurring of two selfs into one is consistent with the confused cognition seen in those who develop schizophrenia.
Parent-child symbiosis is a part of normal development of the child. It only becomes a problem when the child does not develop more autonomy at the times in development when one would expect to see it. Intense symbiosis appears to be a kind of folie-a-deux, two people with one self not easily distinguished as two.
It appears that this is another partial predictor, since intense symbiosis is observed in the childhoods of some who develop serious symptoms other than schizophrenia. I assume that the intense parent-child symbiosis, like the other precursors, appears to have a moderate association with later schizophrenia, and would be loosely connected with the other precursors. This is all theory-driven speculation on my part, given the lack of research data.
Conclusion
One takeaway from all this is that when one needs to predict the occurrence of a variable in a living system, one may need to identify precursors of the variable and then figure out how to use a group of the precursors working together to predict the occurrence of another variable in the system.
Another takeaway is that in living systems, just looking for a single variable or two to predict the occurrence of an important variable is a priori doomed to failure. Open your eyes to the living system and look for variables working together to influence the occurrence of other variables.
References
Bentall, Richard, Wickham, Sophie, Shevlin, Mark, and Varese, Filippo. 2012. “Do Specific Early-Life Adversities Lead to Specific Symptoms of Psychosis? A Study from the 2007 Adult Psychiatric Morbidity Survey”. Schizophrenia Bulletin 38(4): 734-740.
Bowen, Murray. 1960. “A Family Concept of Schizophrenia.” In The Etiology of Schizophrenia Don D. Jackson, ed., 346-370. New York: Basic Books, Inc. doi:10.1037/10605-012.
Bowen, Murray. 1966. “The Use of Family Theory in Clinical Practice.” Comprehensive Psychiatry 7:345-374.
Bowen, Murray. 1976. “Family Reaction to Death.” In Family Therapy Philip Guerin, (ed.) 335-348. New York: Gardner Press.
Bowen, Murray. 1976. Family Therapy in Clinical Practice New York: Jason Aronson, Inc.
Garmezy, Norman PhD; Rodnick, Eliot PhD. 1959. “Premorbid adjustment and performance in schizophrenia: Implication for interpreting heterogeneity in schizophrenia”. The Journal of Nervous and Mental Disease, 129(5): 450-466.
Goldstein, Michael J. 1987. “The UCLA High-risk Project”.
Schizophrenia Bulletin, 13(3): 505-514.
Goldstein, M., E. Rodnick, J.E. Jones, S. McPherson, and K. West. 1978. Familial precursors of schizophrenia spectrum disorders. In The nature of schizophrenia: New approaches to research and treatment edited by L.Wynne, R. Cromwell, and S. Matthysse. New York: Wiley.
Herman, B.F. and J.E. Jones. 1976. Lack of acknowledgment in the Family Rorschachs of families with a child at risk for schizophrenia. Family Process,15:289-302.
Jones, J.E., E. Rodnick, M. Goldstein, S. McPherson, and K. West. 1977. Parental transactional style deviance as a possible indicator of risk for schizophrenia. Archives of General Psychiatry 34:71-74.
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Hi Jim Edd,
Congratulations on your well thought out and comprehensive article that outlines the partial possible contributors to schizophrenia. Do you plan to develop it further? I think you have filled out some of the factors like parental communication deviance in past writing. I will be interested to have the publishing information when you publish an article. As I mentioned previously, I have recently been interested in my own family’s genetic predisposition for schizophrenia, with two first cousins and a different first cousin’s child being diagnosed. I have, however, been most interested in the non-genetic family factors, and I can track those factors that led to schizophrenia in some family members but not to others, though I assume all on my mother’s side of the family have the genetics.
Jim Edd, One of the differences between Bowen family systems theory and other living systems theories is, I believe, the over-arching impact of the level of differentiation of self on all of the individual and multiple factors. It would be important to discuss that as part of your extensive and comprehensive research. What do you think?
Yes, Victoria.
Family and parental level of differentiation are on the list of precursors. I didn’t discuss differentiation; I wanted to discuss just a few precursors to focus on the perspective that statistically significant precursors all influence each other weakly to moderately. What you say about differentiation is true also about many of the other precursors. Differentiation is not the only one to have important influence on other variables.
I don’t think that differentiation is the only variable to have overarching influence. I do think that differentiation is the only precursor to be completely ignored by the majority of researchers and clinicians.
Thanks for your comment.
Fascinating and clear. I’d like to see it published in Family Systems or Family Systems Forum. It’s important to point out that such correlations are not simple. I also appreciate the acknowledgement that there is little or no quantitative data on the parent-child symbiosis as described by Bowen. I’ve been wondering how much impact would vary for concepts like DOS or the projection process? For example could a high projection level in a low DOS family produce widely different levels of symptoms in two kids who were identical in most ways? I suspect the answer is yes. Life ain’t simple.
May I share this with our faculty?
Sure, share it with anybody you want.
I’ll think about where I might want to submit. I’m thinking about nonBoen places. Thanks for reading and commenting.
Jim Edd,
This summary of your research on schizophrenia represents your comprehensive effort to identify variables that have been contributors to that diagnosis. I think those variables apply to other diagnoses as well. I think that the individual who is subject to intense pressures in the family and social environment is most vulnerable to symptoms. Being the target of the combination of the family projection process and many-against-one triangles looks to me like the most severe pressure.
How far do you think that goes to account for schizophrenia and other equally disabling symptoms? I agree with others in encouraging you to get this valuable work published.
Stephanie,
Yes, many things on the list would apply also to development of other symptoms. Family projection process is on my list of precursors, even though I haven’t run across any quantitative data that support it being on the list. Family projection process is, I believe, an important driver of development of symptoms but not schizophrenia specifically. The precursor list has other important influences on development.
In general, stressors in excess drive symptom development. I’m pretty sure one could develop a quantitive case for that.
In any case, I believe that, strong as it is, family projection process is not the only important influence on symptom development. For example, one might have a family mostly characterized by unrelenting spousal conflict. The child is not targeted but he is genetically vulnerable, has some of those odd movement disorders, the family is low SES in a physically dangerous community, has a moderately high ACE score without focus on the child. He would be probably very at risk for development of schizophrenia, even though he is not a target for family projection. However, his older unmanageable, delinquent brother is a target for family projection.
So, family projection is important when present, but even when present, there have to be other variables present, working together with family projection to be factors in the direction of development of schizophrenia.