Schizophrenia: a Brain Disease or not?-part 2

Hypothesis No.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, water retention, pregnancy, advancing age, variations in educational achievement, social class, ethnicity, and head size. 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. 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.

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]”‌; 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.


Hypothesis No.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 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 maybe 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; another study found that 46% of women hospitalized for psychosis had been victims of incest; 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; 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. 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.

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”‌, 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”‌. Similarly, the American Psychiatric Association also confidently proclaims that “schizophrenia is a chronic brain disorder”‌, but then they acknowledge on the very same page that “scientists do not yet know which factors produce the illness”‌, and that “the origin of schizophrenia has not been identified”‌. 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”‌. 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 and the World Health Organization. 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.

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.

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 dodevelop 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.

Printed from: