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  • 7/11/2012

Schizophrenia: a Brain Disease or not?

part 1


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). 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.




Other Links:

Understanding Schizophrenia

Causes & Effects of schizophrenia

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