After Hundred years of research and spending billions of dollars, researchers 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).
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). 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.
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.
#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.
#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 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; 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.
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, 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.