Is Schizophrenia a Valid Disease?

Joy Bose
8 min readAug 7, 2022

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Photo by Sander Sammy on Unsplash

Schizophrenia is a mental disorder characterized by two or more of the following symptoms during a one-month period as per DSM-5 (American Psychiatric Association, 2013): two or more symptoms among hallucinations, delusions, disorganized speech, disorganized or catatonic behavior, and negative symptoms, and which are not attributable to any other condition.

Schizophrenia was first identified by the German psychologist Emil Kraepelin in the 19th century as ‘dementia praecox’, an incurable and progressively deteriorating disease. It affects a significant percentage of the population, across different countries, and results in a significant cost to both affected individuals as well as the wider society, including mental health costs, a reduced Quality of Life (Narvaez et al., 2008) and the number of Quality Adjusted Life Years or QALYs lost (Carr et al., 2006).

Moncrieff and Middleton (2015) among others criticize the validity of schizophrenia from a critical psychiatry perspective. Their criticism includes the lack of defects in structure and function of the brain that is specific to schizophrenia, as well as the lack of behavioral traits that are specific to it. In doing so, they echo the view by Szasz (1960) which criticizes the classification of schizophrenia and all mental illnesses in general as diseases.

Statz pointed out that mental illnesses are metaphorical rather than actual diseases, since they are only thoughts and feelings that society considers undesirable and want to control, rather than having a proper biological basis.

However, schizophrenia does have objective symptoms such as those defined in nosology-based classification systems such as Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and International Classification of Diseases (ICD-11).

Why schizophrenia may not be a valid disease

Moncrieff and Middleton cite papers by Bentall (1990) and Bleuler (1911) which define the symptoms of schizophrenia in a generic way. They make the claim that it is better to use a generic label such as “psychosis” instead of schizophrenia, since the disease model of schizophrenia is not supported by evidence and no specific biological disorder has been demonstrated that is specific to schizophrenia. For example, it has been found in MRI scans (Woods et al., 1996) that schizophrenia sufferers have a lower brain size, especially in the frontal lobes, however this could be explained as side effects of antipsychotic drugs used to treat schizophrenia (Moncrieff & Leo, 2010). Also, such studies typically lack proper differentiation of treatment and control subjects by intelligence quotient (IQ) in the studies, and hence may not constitute a valid argument, given the schizophrenia sufferers may have lower IQ.

There is additional empirical evidence to support the points made by Moncrieff and Middleton and that go against the disease model of schizophrenia. The etiology of schizophrenia is still unknown, although it has something to do with dopamine and serotonin neurotransmitters and environmental factors and triggers such as stress. There are similarities between the symptoms of schizophrenia and those of other conditions such as bipolar disorder, schizoaffective disorder and major depression, which also sometimes experience delusions and hallucinations (Goghari & Harrow, 2016). The experiments conducted between 1969–72 by Rosenhan and colleagues (Rosenhan, 1973) further demonstrate how false diagnosis in schizophrenia is common and support the theory of mental illness as a social construct. In the experiment, eight sane people gained admission to twelve mental hospitals by faking symptoms of hearing voices and acting normal otherwise, but after a few weeks seven of them were diagnosed with schizophrenia before being discharged as being in remission.

Evidence against the claim that Schizophrenia is not a valid disease

There is a huge amount of evidence that goes against the claims that schizophrenia is not a valid disease. For one, there are better and more precise definitions of schizophrenia available in the DSM-5 handbook and ICD-11, that improve the reliability and to a certain extent validity of the diagnosis among different practitioners. DSM-5 proposes a diagnosis of schizophrenia based on at least one of the core symptoms (delusions, hallucinations and disorganized speech) and at least two out of the total symptoms including negative symptoms such as impaired levels of functioning. ICD-11 classifies schizophrenia on the basis of symptoms similar to DSM-5 and additionally contains separate diagnosis for different cases of schizophrenia including the first episode, multiple episodes, continuous and partial remission, along with cultural, developmental and gender related features. Keeley and Gaebel (2018) propose symptom rating scales to be used in ICD-11 for schizophrenia including positive, negative, depressive, cognitive and psychomotor symptoms, that provide a holistic basis taking into account the different varieties of the illness.

Further evidence supporting the disease model of schizophrenia include biological, molecular and genetic markers. Clementz et al., (2016) collected biological evidence from a set of psychotic subjects and analysed their data from MRI and EEG scans and brain responses on a number of standard tasks using machine learning techniques, showing that subjects with schizophrenia had higher scores on the Schizo-Bipolar scale compared to bipolar and schizoaffective disorders, as well as differences in the amount and spread of grey matter in the brain. Ripke et al., (2014) performed similar studies from a genetic perspective and identified 108 independently associated genetic loci that function as markers of schizophrenia and can be potentially used to flag susceptibility to schizophrenia based on genetic factors alone. The dopamine hypothesis of schizophrenia states that dopamine neurotransmitters disturbances in the mesolimbic pathway and prefrontal cortex of the brain could be a cause of the positive symptoms of schizophrenia. Another hypothesis is the correlation of schizophrenia with underactivity of the mesocortical pathway. Other evidence suggests correlation with molecular pathways focusing on mRNA changes, based on transcriptome profiling (Horváth & Mirnics, 2015).

All the above evidence show that significant biological, environmental and genetic markers may exist for schizophrenia, which are distinct from markers related to other illnesses with shared symptoms. Therefore, it may not be correct to state that there are no biological or other markers specific to schizophrenia.

How an alternative system for diagnosis of schizophrenia could look like

An alternative system for diagnosis of schizophrenia could provide a unified view incorporating and combining recent evidence from biological, genetic and other markers, understand schizophrenia as part of a broader spectrum as well as incorporate social and environmental factors that identify the risk of a person developing schizophrenia in later life.

Considering schizophrenia as part of the broader psychotic disorder spectrum, rather than an isolated diagnosis, has been proposed by Guloksuz and Os (2018). They place schizophrenia on a continuum of psychotic disorders, varying from normal to abnormal functioning across different dimensions, as opposed to an all or nothing diagnosis. This could be one way of looking at an alternative system, and address the criticism by Moncrieff and Middleton that there is little to distinguish schizophrenia from other disorders with some common symptoms.

Another way of thinking of an alternative system could be to consider developmental factors. Insel (2010) proposed a way to look at schizophrenia as a neurodevelopmental disorder whose early signs may emerge in one’s childhood, which matures in adolescence and develops throughout one’s life, as opposed to a static diagnosis at a given point. Prevention of schizophrenia can be updated to incorporate these aspects. For example, children at risk of developing schizophrenia can be identified and treated early. Similarly, care of schizophrenic subjects can be modified as per the stage of development of schizophrenia with the passage of time. Such a system would address the shortcomings resulting from an all or nothing diagnosis of schizophrenia, and one that does not adapt with the subject’s age.

The social environmental risk factors for schizophrenia and their neurological basis have been analysed by Akdeniz et al. (2014). They consider factors such as ethnic minority status, socioeconomic and social status, and perceived discrimination in addition to genetic and other factors. By incorporating these, we may be able to devise a strategy that can identify risks in subjects as per their social circumstances and act accordingly at an early stage, so that the later development of schizophrenia can be prevented. This system would incorporate often overlooked factors related to the environment and socioeconomic status of the subject, which are also important factors in the diagnosis and development.

Finally, the Hierarchical Taxonomy of Psychopathology (HiTOP) model, proposed by Kotov et al. (2018) proposes a new way to classify disorders that addresses some of the criticisms by Moncrieff and Middleton and other critical psychiatrists. They propose a hierarchical approach to classify psychiatric disorders that groups individual symptoms of various disorders into traits, syndromes and finally psychopathology spectra. The system promises to be more clinically informative, and hence improve the validity of diagnosis, compared to commonly used systems such as DSM and ICD. Research Domain Criteria (RDoC) is another framework that incorporates related illnesses together, grouping them on the basis of neurobiological and other similarities.

Conclusion

There are valid criticisms of the disease model of schizophrenia, but these do not take into account more recent evidence from biological, genetic and molecular markers of schizophrenia.

On the other hand, there is scope to revise the definition of schizophrenia to be more holistic and considering the social and developmental aspects and placing it in the continuum of psychotic disorders. New models of classification of psychotic disorders, such as HiTOP, also look promising in addressing the criticisms in classification and diagnosis of schizophrenia.

References

Akdeniz, C., Tost, H., & Meyer-Lindenberg, A. (2014). The neurobiology of social environmental risk for schizophrenia: an evolving research field. Social psychiatry and psychiatric epidemiology, 49(4), 507–517.

American Psychiatric Association. (2013). DSM 5 diagnostic and statistical manual of mental disorders. DSM 5 Diagnostic and statistical manual of mental disorders.

Bentall, R. P. (1990). The syndromes and symptoms of psychosis. Reconstructing Schizophrenia, 23–60.

Bleuler, E. (1911). Dementia praecox oder Gruppe der Schizophrenien (Vol. 4). Deuticke.

Carr, V. J., Lewin, T. J., & Neil, A. L. (2006). What is the value of treating schizophrenia?. The Australian and New Zealand journal of psychiatry, 40(11–12), 963–971.

Clementz, B. A., Sweeney, J. A., Hamm, J. P., Ivleva, E. I., Ethridge, L. E., Pearlson, G. D., Keshavan, M. S., & Tamminga, C. A. (2016). Identification of Distinct Psychosis Biotypes Using Brain-Based Biomarkers. The American journal of psychiatry, 173(4), 373–384.

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Goghari, V. M., & Harrow, M. (2016). Twenty year multi-follow-up of different types of hallucinations in schizophrenia, schizoaffective disorder, bipolar disorder, and depression. Schizophrenia research, 176(2–3), 371–377.

Guloksuz, S., & van Os, J. (2018). The slow death of the concept of schizophrenia and the painful birth of the psychosis spectrum. Psychological medicine, 48(2), 229–244.

Horváth, S., & Mirnics, K. (2015). Schizophrenia as a disorder of molecular pathways. Biological psychiatry, 77(1), 22–28.

Insel T. R. (2010). Rethinking schizophrenia. Nature, 468(7321), 187–193.

Ripke, S., Neale, B. M., Corvin, A., Walters, J. T., Farh, K. H., Holmans, P. A., & Milanova, V. (2014). Biological insights from 108 schizophrenia-associated genetic loci. Nature, 511(7510), 421.

Keeley, J. W., & Gaebel, W. (2018). Symptom rating scales for schizophrenia and other primary psychotic disorders in ICD-11. Epidemiology and psychiatric sciences, 27(3), 219–224.

Kotov, R., Krueger, R. F., & Watson, D. (2018). A paradigm shift in psychiatric classification: the Hierarchical Taxonomy Of Psychopathology (HiTOP). World Psychiatry, 17(1), 24.

Moncrieff, J., & Leo, J. (2010). A systematic review of the effects of antipsychotic drugs on brain volume. Psychological medicine, 40(9), 1409–1422.

Moncrieff, J., & Middleton, H. (2015). Schizophrenia: a critical psychiatry perspective. Current Opinion in Psychiatry, 28(3), 264–268.

Narvaez, J. M., Twamley, E. W., McKibbin, C. L., Heaton, R. K., & Patterson, T. L. (2008). Subjective and objective quality of life in schizophrenia. Schizophrenia research, 98(1–3), 201–208.

Rosenhan D. L. (1973). On being sane in insane places. Science (New York, N.Y.), 179(4070), 250–258.

Szasz, T. S. (1960). The myth of mental illness. American psychologist, 15(2), 113.

Woods, B. T., Yurgelun-Todd, D., Goldstein, J. M., Seidman, L. J., & Tsuang, M. T. (1996). MRI brain abnormalities in chronic schizophrenia: one process or more?. Biological Psychiatry, 40(7), 585–596.

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Joy Bose
Joy Bose

Written by Joy Bose

Working as a software developer in machine learning projects. Interested in the intersection between technology, machine learning, society and well being.

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