In spite of over a hundred years of research and many billions of dollars spent, we still have no clear evidence that schizophrenia and other related psychotic disorders are the result of a diseased brain. Considering the famous PET scan and MRI scan images of “schizophrenic” brains and the regular press releases of the latest discoveries of one particular abnormal brain feature or another, this statement is likely to come as a surprise to some, and disregarded as absurdity by others. And yet, anyone who takes a close look at the actual research will simply not be able to honestly say otherwise. And not only does the brain disease hypothesis remain unsubstantiated, it has been directly countered by very well established findings within the recovery research, it has demonstrated itself to be particularly harmful to those so diagnosed (often leading to a self-fulfilling prophecy), and is highly profitable to the pharmaceutical and psychiatric industries (which likely plays a major role in why it has remained so deeply entrenched in society for so many years, in spite of our inability to validate it).
Deconstructing the Myths of Madness
The claim I am making here clearly runs counter to the mainstream understanding of schizophrenia, but we find that it’s a relatively straightforward task to back up this claim. We simply need to take the time to extract the actual research findings from the unsubstantiated assumptions and propaganda that are so often used to back up the brain disease hypothesis. I’ll go through the largest of these here:
Hypothesis #1: Schizophrenia is caused by a biochemical imbalance within the brain
This theory originated from the observation that drugs which block the transmission of the neurotransmitter dopamine within the brain (so called “antipsychotics,” originally referred to as “major tranquilizers”) appear to reduce the symptoms of schizophrenia. The reasoning behind the origin of this hypothesis was, since schizophrenic symptoms are reduced when dopamine transmission is suppressed, then perhaps schizophrenia is caused by too excessive dopamine within the brain.
This hypothesis originally appeared quite plausible; however, it has since been seriously discredited:
- First, although it is known that an individual’s dopamine receptors (the type of receptors most affected by antipsychotic drugs) are completely blocked within hours of consuming a sufficient dose of an antipsychotic drug, the actual antipsychotic effects often do not become apparent for up to several weeks (even though a significant degree of apathy towards one’s psychotic experiences often does kick in quickly, as would be expected with any kind of tranquilizer; Bentall, 2004). If psychotic symptoms are the direct result of too much dopamine, then why don’t we see a more immediate abatement of these symptoms as soon as the dopamine levels have been effectively reduced?
- Second, with the introduction of PET and MRI scans, the dopamine hypothesis was apparently substantiated when it was recognized that many “schizophrenic” brains do indeed seem to be set up to transmit excessive dopamine. However, it was eventually realized that the vast majority of brains studied had been exposed to long-term antipsychotic drugs, and it’s since been established that the effects of these drugs alone may very well account for these anomalies (Burt, Creese & Snyder, 1977; Kornhuber et al., 1989; Mackay, 1982).
- Finally, even many of the proponents of this theory have been forced to acknowledge that we still have not found any clear biochemical imbalance that we can associate consistently with schizophrenia or any of the “mental illness” diagnoses, and that all we can really say for sure is that psychiatric drugs themselves (and virtually any psychoactive drug, for that matter) does lead to the development of a biochemical imbalance in one’s brain.
Hypothesis #2: Schizophrenia is caused by anomalous brain structures
This hypothesis essentially states that schizophrenia is a disease caused by something wrong with the actual structure of one’s brain, specifically with regard to the relative size of the cerebral cortex and/or other nearby regions of the brain. This hypothesis is generally supported by the actual findings of such anomalies of the brains of those so diagnosed. But again, upon closer scrutiny of the research, we find an empty hypothesis that quickly crumbles away:
- First, we have discovered that there are many different factors that can lead to these abnormalities, including: depression, alcoholism, early childhood trauma (Read, 2004), water retention, pregnancy (Woodruff & Lewis, 1996), advancing age, variations in educational achievement, social class, ethnicity, and head size (Bentall, 2004). It was also discovered that the sizes of these regions of the brain can fluctuate quite rapidly within even healthy individuals, leading to varying results even within the same individual (Bentall, 2004). And once again, what do you imagine we have found that is probably the most relevant factor causing such anomalies in the brain? You guessed it… the use of antipsychotic drugs themselves. And virtually all of the research that has discovered such brain anomalies in those diagnosed with schizophrenia did not account for this very important factor, meaning that once again, most of the brains studied had most likely been affected by the long-term use of antipsychotic drugs (Read, 2004; Siebert, 1999).
- A second serious challenge to the validity of the abnormal brain structure hypothesis came when it was recognized that the majority of those diagnosed with schizophrenia do not show any obvious brain abnormality at all. Lewine found that “there is no brain abnormality in schizophrenia that characterizes more than 20-33% of any given sample. The brains of the majority of individuals with schizophrenia are normal as far as researchers can tell at present [emphasis added]” (Lewine, 1998, p. 499); and this in spite of the fact that most of these participants were likely exposed to other brain changing factors such as trauma and/or antipsychotic medications. Conversely, it is common to find healthy individuals who have no schizophrenic symptoms at all and yet have brain abnormalities similar to those sometimes found in schizophrenics (Siebert, 1999).
Hypothesis #3: Schizophrenia is a Genetic Disorder
This hypothesis is in close alignment with the two brain disease hypotheses (above) and suggests that this brain disease is transmitted genetically. But again we find some serious problems with the assumptions that have given rise to this hypothesis:
- This hypothesis is based on a small handful of twin and adoption studies (Joseph, 2004) conducted many decades ago which, even when we ignore the many serious methodological flaws with these studies, the only conclusion that can actually be drawn from them is that there may be a hereditary component in one’s susceptibility to developing psychosis. However, this is not any different than the findings that there may be a hereditary component in intelligence, shyness, and other psychological characteristics that clearly are not indicative of any kind of physiological disease. In other words, it’s an illogical leap to assume that a hereditary predisposition for a psychological trait or experience must imply biological disease. Yes, there does seem to be some evidence that some of us may be born with a temperament or other psychological characteristics which make us more vulnerable to experiencing psychosis at some point in our life; but no, this evidence does not lend any validity to the hypothesis that schizophrenia is a genetically transmitted biological disease.
- Another important area of research discrediting the “genetic disease” hypothesis is the far more substantial research showing high correlations with environmental (non-hereditary) factors and the development of psychosis/schizophrenia. For example, one study looked at 524 child guidance clinic attendees over 30 years and discovered that 35% of those later diagnosed with schizophrenia had been removed from their homes due to neglect, a percentage twice as high as that for any other diagnostic category (Robins, 1974); another study found that 46% of women hospitalized for psychosis had been victims of incest (Beck & van der Kolk, 1987); another study of child inpatients found that 77% of those who had been sexually abused were diagnosed psychotic compared to only 10% of those who had not been so abused (Livingston, 1987); and yet another study found that 83% of men and women who were diagnosed with schizophrenia had suffered significant childhood sexual abuse, childhood physical abuse, and/or emotional neglect (Honig, Romme, Ensink, Escher, Pennings, & de Vries, 1998). Bertram Karon, researcher and acclaimed psychosis psychotherapist, has found evidence of a high correlation between the experience of intense feelings of loneliness and terror within childhood and the later onset of schizophrenia, a finding that is clearly closely related to the findings of these other studies (Karon, 2003).
Even the strongest proponents of the brain disease hypothesis acknowledge that it has not yet been validated
The National Institute of Mental Health, on its Schizophrenia home page, proclaims confidently that “schizophrenia is a chronic, severe, and disabling brain disorder” (NIMH, 2010a, Para. 1), a statement you find on nearly every major page or publication they have put out on the topic; and yet if you spend a little more time looking through their literature, you will find that they admit that “the causes of schizophrenia are still unknown” (NIMH, 2010b, Para. 1). Similarly, the American Psychiatric Association also confidently proclaims that “schizophrenia is a chronic brain disorder” (APA, 2010, Para. 1), but then they acknowledge on the very same page that “scientists do not yet know which factors produce the illness” (APA, 2010, Para. 10), and that “the origin of schizophrenia has not been identified” (APA, 2010, Para. 1). The strong bias towards the brain disease theory is clearly evident in the literature of these and other similar organizations, and yet the message comes through loud and clear that we still do not know the cause of schizophrenia. Even the U.S. Surgeon General began his report on the etiology of schizophrenia with the words, “The cause of schizophrenia has not yet been determined” (Satcher, 1999, Para. 1). It would appear, then, that it is simply not appropriate to claim with such confidence that schizophrenia is the result of a brain disorder.
If schizophrenia really is a brain disease, then how do we account for the relatively high rates of full recovery from it?
The recovery research is extremely robust: Many people experience full and lasting recovery after having been diagnosed with schizophrenia. We see this evidence in the vast majority of the longitudinal recovery studies (See Chapter 4 in my book, Rethinking Madness, for a complete list of all major longitudinal studies), including those conducted by the National Institute of Mental Health (Harrow & Jobe, 2007; Harrow, Jobe, & Faull, 2012) and the World Health Organization (Hopper et al., 2007). There is evidence of spontaneous recovery in between 5% and 71% of cases, depending upon the country of origin and other factors, and even as high as 82% with certain psychosocial interventions (Mosher, 1999; Seikkula, Aaltonen, Alakare, Haarakangas, Keränen & Lehtinen, 2006). It is illuminating to compare the high recovery rate for schizophrenia with the recovery rate for well-established diseases of the brain such as Parkinson’s, Alzheimer’s, or multiple sclerosis: There is no well documented evidence of even a single individual making a full recovery from any of these well-established diseases of the brain (Siebert, 1999).
The mainstream paradigm of care may actually be creating a self-fulfilling prophecy of brain disease
A tragic result of the entrenched belief that schizophrenia is caused by a disease of the brain is that, whether or not schizophrenia is ever determined to be a disease of the brain, our mainstream paradigm of care is actually ensuring that enormous numbers of people actually do develop such a disease (see the figure; I will also discuss this in more detail in a future blog).
So what does cause schizophrenia?
So, if schizophrenia is not caused by a disease of the brain, then the obvious question that arises is, “Well, then what does cause it?” This is an extremely important yet somewhat complex question, which I address in great detail in my book, Rethinking Madness, and which I will try to capture in a nutshell (or perhaps several nutshells) in future blog postings within this series.
A much more thorough discussion of this topic and other topics related to psychotic disorders and recovery can be found in the book, Rethinking Madness: Towards a Paradigm Shift in Our Understanding and Treatment of Psychosis.
For more information about Rethinking Madness, go to: www.RethinkingMadness.com
To purchase a copy from Amazon, go to: http://www.amazon.com/Rethinking-Madness-Understanding-Treatment-Psychosis/dp/0984986707
American Psychiatric Association [APA]. (2010). Schizophrenia. Retrieved from The American Psychiatric Association Healthy Minds, Healthy Lives website: http://www.healthyminds.org/Main-Topic/Schizophrenia.aspx
Beck, J., and van der Kolk, B. (1987). Reports of childhood incest and current behavior of chronically hospitalized psychotic women. American Journal of Psychiatry, 29, 789-794.
Harrow, M., & Jobe, T. (2007). Factors involved in outcome and recovery in schizophrenia patients not on antipsychotic medications: A 15-year multifollow-up study. Journal of Nervous and Mental Disease, 195(5), 406-414. Retrieved from http://www.madinamerica.com/madinamerica.com/Schizophrenia_files/OutcomeFactors.pdf
Harrow, M., Jobe, T. H., & Faull, R. N. (2012). Do all schizophrenia patients need antipsychotic treatment continuously throughout their lifetime? A 20-year longitudinal study. Psychological Medicine, First View Articles, 1-11. doi: 10.1017/S0033291712000220
Honig, A., Romme, M., Ensink, B., Escher, S., Pennings, M., & de Vries, M. (1998). Auditory hallucinations: A comparison between patients and nonpatients. The Journal of Nervous and Mental Disease, 186, 646-651.
Hopper, K., Harrison, G., Janca, A., & Sartorius, N. (2007). Recovery from schizophrenia: An international perspective: A report from the WHO Collaborative Project, The International Study of schizophrenia. New York, NY: Oxford University Press.
Joseph, J. (2004). Schizophrenia and heredity: Why the emperor has no genes. In J. Read, L. R. Mosher, & R. P. Bentall (Eds.), Models of madness: Psychological, social and biological approaches to schizophrenia (pp. 67-83). New York, NY: Routledge.
Karon, B. P. (2003). The tragedy of schizophrenia without psychotherapy. Journal of the American Academy of Psychoanalysis, 31(1), 89-119. doi:10.1521/jaap.220.127.116.1131
Lewine, R. (1998). Epilogue. In M. F. Lenzenweger & R. H. Dworkin (Eds.), Origin and development of schizophrenia (pp. 493-503). Washington, DC: American Psychological Association.
Livingston, R. (1987). Sexually and physically abused children. The Journal of the American Academy of Child and Adolescent Psychiatry, 26: 413-415.
Mosher, L. R. (1999). Soteria and other alternatives to acute psychiatric hospitalization: A personal and professional review. The Journal of Nervous and Mental Disease, 187, 142-149.
National Institute of Mental Health [NIMH]. (2010a). Schizophrenia. Retrieved from http://www.nimh.nih.gov/health/publications/schizophrenia/complete-publication.shtml
National Institute of Mental Health [NIMH]. (2010b). How is schizophrenia treated. Retrieved from http://www.nimh.nih.gov/health/publications/schizophrenia/how-is-schizophrenia-treated.shtml
Read, J. (2004). Biological psychiatry’s lost cause. In J. Read, L. R. Mosher, & R. P. Bentall, (Eds.), Models of madness: Psychological, social and biological approaches to schizophrenia (pp. 57-65). New York: Routledge.
Robins, L. (1974). Deviant children grown up: A sociological and psychiatric study of sociopathic personality. Malabar, FL: R. E. Krieger Pub. Co.
Satcher, D. (1999). Etiology of schizophrenia. Retrieved, from http://www.surgeongeneral.gov/library/mentalhealth/chapter4/sec4_1.html
Seikkula, J., Aaltonen, J., Alakare, B., Haarakangas, K., Keränen, J., & Lehtinen, K. (2006). Five-year experience of first-episode nonaffective psychosis in open-dialogue approach: Treatment principles, follow-up outcomes, and two case studies. Psychotherapy Research, 16(2), 214-228. doi: 10.1080/10503300500268490.
Siebert, A. (1999). Brain disease hypothesis for schizophrenia disconfirmed by all evidence. Retrieved from http://psychrights.org/states/Alaska/CaseOne/180Day/Exhibits/Wnotbraindisease.pdf
Woodruff, P. W. R., & Lewis, S. (1996). Structural brain imaging in schizophrenia. In S. Lewis & N. Higgins (Eds.), Brain imaging in psychiatry. Oxford, UK: Blackwell.
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- Schizophrenia: Coping with Delusions and Hallucinations (psychologytoday.com)
- New Schizophrenia Drug Shows Promise (medicalnewstoday.com)
- Rare genetic disorder points to molecules that may play role in schizophrenia (medicalxpress.com)
- New research project funded by the Foundation for Excellence in Mental Health Care is in process: (madinamerica.com)