Theories of Schizophrenia: Can They Work in Harmony?

In this article, I use illustrations taken from the website of Bryan Charnley, an artist who suffered with schizophrenia and very tragically took his own life soon after these self-portraits were completed. Each painting was created as an experiment to come “face-to-face” with his illness. I felt it would be appropriate to use them here as they demonstrate, far better than can be done with words, what schizophrenic symptoms can feel like.

Psychiatrist Eugen Bleuler first coined the term ‘schizophrenia’, originating from the Greek “schizo” meaning to tear or split, and “phren” meaning intellect. This could explain the common contemporary myth about the illness involving a split personality. In reality, schizophrenia comprises a range of distressing symptoms including delusions, hallucinations, incoherent thoughts and speech, catatonic behaviour, affective flattening, alogia and avolition. The varied nature of the illness makes it challenging to diagnose using a single modality. However, it is one of the most debilitating of mental illnesses, with more than 24 million sufferers worldwide, which compels scientists in a variety of fields to continue in their search. Psychological and biological accounts present quite distinct determinist perspectives, unless combined within the ‘diathesis-stress’ model – a more holistic explanation that is now the leading approach in providing aetiology for the illness.

Bryan Charnley: Self-Portrait (1991) “My mind seemed to be thought broadcasting very severely and it was beyond my will to do anything about it. I summed this up by painting my brain as an enormous mouth, acting independently of me… I feel I am always divided against my self by myself… the nail in the mouth expresses my social ineptitude and an inability to socialise which makes me a target…”

A genetic susceptibility for psychotic symptoms is problematic to trace back to a particular genetic locus or even a small amount of genes. Therefore, a range of methods provide evidence for the involvement of numerous specific genes and rare mutations within them. Findings strongly indicate a heritable aspect to the disease, such as the fact that those with a first-degree relative with schizophrenia are ten times more likely to develop symptoms than those without. Moreover, twin studies reveal an overall heritability estimate of 80%. These discoveries highlight schizophrenia to be one of the most heritable of mental disorders. However, it can be difficult for researchers to discriminate between findings that are due to one’s environment as opposed to genetic makeup. To overcome this issue, adoption studies have been conducted using adoptees with and without schizophrenic family members. One early study found that 16.6% of adopted children with schizophrenic mothers developed the illness while none did within the control group. These findings were supported by a more recent study, where adopted children with psychotic symptoms had a 21.4% chance of having biological relatives with schizophrenia, compared to 5.4% in those who did not.

The leading biochemical theory of schizophrenia is the dopamine hypothesis, which maintains that symptoms like hallucinations, thought disorder and behavioural problems are significantly correlated to excess activity of the neurotransmitter dopamine. Antipsychotic drugs such as phenothiazines act on symptoms of psychosis by blocking the brain’s dopamine receptor sites, lowering dopamine activity. While these drugs attenuate many symptoms of schizophrenia, they have side effects such as tremors similar to those shown in Parkinson’s Disease, which is known to be caused in part by low dopamine levels. This effect is interestingly reversed when Parkinson’s patients are administered L-dopa – a drug that raises dopamine levels – resulting in the display of psychotic symptoms. Post-mortem studies have also revealed increased levels of dopamine and a considerably greater number of dopamine receptors in the brains of deceased schizophrenia patients.

Cognitive theories of schizophrenia centre on attributional and interpretational biases regarding anomalous experiences. For instance, auditory hallucinations are typically experienced by around 10 to 15% of healthy individuals, but may be interpreted in a way that makes them believe they are becoming insane, or that they ought to listen to and adhere to what the voices say in order to avoid negative consequences. Such biases are associated with deficits in cognitive functioning, again linked to excess dopamine activity, resulting in a slow decline in abilities such as early stages of sensory information processing. As a result, some sufferers experience affective flattening – a symptom rendering them socially isolated with a lack of emotions – meaning schizophrenic patients who have developed paranoid beliefs are not in the presence of others who can disconfirm their ideas, leading to a spiralling self-fulfilling prophecy.


The double-bind hypothesis suggests that schizophrenic symptoms result from a pattern of contradictory, hostile and blameful treatment from family members. For instance, families with high expressed emotion (EE) tend to place blame on the sufferer for their circumstances, and express this through shouting rather than talking through. Prior to these findings, it was advised that schizophrenic patients should go home to their families from their institution, however it has now been established that the median relapse rate in a high-EE environment is 48% compared to 21% in a low-EE environment, and that interventions to control EE in families is a more effective approach to improving symptoms. This assumption is associated with the diathesis-stress hypothesis, which intends to merge biological and psychological approaches. For instance, an individual who is genetically liable to schizophrenia may not develop symptoms of psychosis until they encounter certain life stressors that can transpire during early development, in dysfunctional family relationships or in adolescence.

The above approaches are similar in their use of empirical methods, problems with defining cause and effect and investigation into family influences. They also coincide in their discussion of the influence of dopamine, which in turn affects cognitions and the attribution of symptoms to external factors. However, they differ in that the biological approach looks at inherent traits such as genetics and biochemical composition and uses pharmacological treatments, whereas the psychological approach focuses on upbringing and cognitive processes, and family therapeutic or cognitive behavioural treatments. Overall, they work in harmony within the diathesis-stress approach, which claims a genetic predisposition to schizophrenia will only result in symptoms when activated by life stressors.

If you would like to know more about schizophrenia and learn about treatments available, there are many websites to refer to and helplines and services to contact. I have listed some below:


American Psychiatric Association. (2003). Diagnostic and Statistical Manual of Mental Disorders:: DSM-5. ManMag.

Anderson, C. M., Reiss, D. J., & Hogarty, G. E. (1986). Schizophrenia and the family: A practitioner's guide to psychoeducation and management. Guilford Press.

Andreasen, N. C. (1982). Negative symptoms in schizophrenia: definition and reliability. Archives of General Psychiatry39(7), 784-788.

Andreasen, N. C., Flashman, L., Flaum, M., Arndt, S., Swayze, V., O'Leary, D. S., ... & Yuh, W. T. (1994). Regional brain abnormalities in schizophrenia measured with magnetic resonance imaging. Jama272(22), 1763-1769.

Angrist, B., Lee, H.K. & Gershon, S. (1974). Antagonism of amphetamine-induced symptomatology by a neuroleptic. American Journal of Psychiatry, 131(7), 817- 819.

Baker, C. A., & Morrison, A. P. (1998). Cognitive processes in auditory hallucinations: attributional biases and metacognition. Psychological Medicine,28(05), 1199-1208.

Bateson, G. (1978). The double-bind theory – misunderstood? Psychiatric News, April, 40.

Berry, N., Jobanputra, V., & Pal, H. (2003). Molecular genetics of schizophrenia: a critical review. Journal of Psychiatry and Neuroscience28(6), 415–429.

Bleuler, Eugen Dementia praecox or the group of schizophrenias. Oxford, England: International Universities Press Dementia praecox or the group of schizophrenias. (1950). 548 pp.

Cardno, A.G. & Gottesman, I.I. (2000). Twin studies of schizophrenia: From bowand-arrow concordances to star wars Mx and functional genomics. American Journal of Medical Genetics, 97, 12–17.

Davey, Graham C. (2008) Psychopathology: Research, Assessment and Treatment in Clinical Psychology, 235-255 John Wiley & Sons.

Davis, J.O. & Phelps, J.A. (1995). Twins with schizophrenia: Genes or germs. Schizophrenia Bulletin, 21(1), 13–18

Davis, K. L., & Kahn, R. S. (1991). Dopamine in schizophrenia: a review and reconceptualization. The American journal of psychiatry148(11), 1474.

Dickerson, F. B., Tenhula, W. N., & Green-Paden, L. D. (2005). The token economy for schizophrenia: review of the literature and recommendations for future research. Schizophrenia Research75(2), 405-416.

Freeman, D., Garety, P. A., Kuipers, E., Fowler, D., & Bebbington, P. E. (2002). A cognitive model of persecutory delusions. British Journal of Clinical Psychology41(4), 331-347.

Gejman, P.V., Sanders, A.R. & Kendler, K.S. (2011). Genetics of schizophrenia: New findings and challenges. Annual Review of Genomics and Human Genetics, 12, 121–144.

Gottesman, I.I., McGuffin, P. & Farmer, A.E. (1987). Clinical genetics as clues to the real genetics of schizophrenia (a decade of modest gains while playing for time). Schizophrenia, 13(1), 23-47.

Gottesman, I.I. & Bertelsen, A. (1989). Confirming unexpressed genotypes for schizophrenia: Risks in the offspring of Fischer’s Danish identical and fraternal discordant twins. Archives of General Psychiatry, 46(10), 867–872.

Grilly, D.M. (2002). Drugs and human behaviour (4th edn). Boston: Allyn & Bacon.

Harrop, C. & Trower, P. (2001). Why does schizophrenia develop at late adolescence? Clinical Psychology Review, 21, 241–266.

Heston, L.L. (1966). Psychiatric disorders in foster home reared children of schizophrenic mothers. British Journal of Psychiatry, 112(489), 819–825

Jablensky, A., Sartorius, N., Ernberg, G., Anker, M., Korten, A., Cooper, J. E., ... & Bertelsen, A. (1992). Schizophrenia: manifestations, incidence and course in different cultures A World Health Organization Ten-Country Study.Psychological medicine. Monograph supplement20, 1-97.

Kavanagh, D. J. (1992). Recent developments in expressed emotion and schizophrenia. The British Journal of Psychiatry160(5), 601-620.

Kety, S.S. (1988). Schizophrenic illness in the families of schizophrenic adoptees: Findings from the Danish national sample. Schizophrenia Bulletin, 14(2), 217– 222.

Kety, S.S., Wender, P.H., Jacobsen, B., Ingraham, L.J. et al. (1994). Mental illness in the biological and adoptive relatives of schizophrenic adoptees: Replication of the Copenhagen study in the rest of Denmark. Archives of General Psychiatry, 51(6), 442–455.

Lotharius, J., & Brundin, P. (2002). Pathogenesis of Parkinson's disease: dopamine, vesicles and α-synuclein. Nature Reviews Neuroscience3(12), 932-942.

Morrison, A. P. (2001). The interpretation of intrusions in psychosis: an integrative cognitive approach to hallucinations and delusions. Behavioural and Cognitive Psychotherapy29(03), 257-276.

Owen, M. J., Williams, N. M., & O'Donovan, M. C. (2004). The molecular genetics of schizophrenia: new findings promise new insights. Molecular psychiatry9(1), 14-27.

Schiffman, J., Abrahamson, A., Cannon, T., LaBrie, et al. (2001). Early rearing factors in schizophrenia. International Journal of Mental Health, 30, 3–16.

Schneider, F. & Deldin, P.J. (2001). Genetics and schizophrenia. In P.B. Sutker & H.E. Adams (Eds.) Comprehensive handbook of psychopathology (3rd edn). New York: Kluwer Academic/Plenum.

Seeman, P. & Kapur, S. (2001). The dopamine receptor basis of psychosis. In A. Brier, P.V. Tran, F. Bymaster & C. Tollerfson (Eds.) Current issues in the psychopharmacology of schizophrenia. Philadelphia: Lippincott Williams & Wilkins.

Segerbäck, D., Calleman, C. J., Schroeder, J. L., Costa, L. G., & Faustman, E. M. (1995). Formation of N-7-(2-carbamoyl-2-hydroxyethyl) guanine in DNA of the mouse and the rat following intraperitoneal administration of [14C] acrylamide. Carcinogenesis16(5), 1161-1165.

Sommer, I. E., Daalman, K., Rietkerk, T., Diederen, K. M., Bakker, S., Wijkstra, J., & Boks, M. P. (2010). Healthy individuals with auditory verbal hallucinations; who are they? Psychiatric assessments of a selected sample of 103 subjects.Schizophrenia Bulletin36(3), 633-641.

Tam, G. W., Redon, R., Carter, N. P., & Grant, S. G. (2009). The role of DNA copy number variation in schizophrenia. Biological psychiatry66(11), 1005-1012.

Waters, F., Allen, P., Aleman, A., Fernyhough, C., Woodward, T. S., Badcock, J. C., ... & Larøi, F. (2012). Auditory hallucinations in schizophrenia and nonschizophrenia populations: a review and integrated model of cognitive mechanisms. Schizophrenia Bulletin38(4), 683-693.

Walker, E. F., & Diforio, D. (1997). Schizophrenia: a neural diathesis-stress model. Psychological review104(4), 667.

Weakland, J. H. (1960). The 'Double-Bind' Hypothesis of Schizophrenia and Three-Party Interaction.

Basic Books. Oxford, England.

Weisman, A. G., Nuechterlein, K. H., Goldstein, M. J., & Snyder, K. S. (2000). Controllability perceptions and reactions to symptoms of schizophrenia: a within-family comparison of relatives with high and low expressed emotion.Journal of abnormal psychology109(1), 167.

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