It is commonly said that schizophrenia is biologically caused. This blog is going to discuss why it is not. It is also said that “schizophrenic” brains are different than normal brains. However, there are three important issues with this idea that are frequently ignored. Many people diagnosed with schizophrenia have no symptoms in common with each other (APA, 2000). This means that researchers could be studying people who have little in common with each other. Second, if we do find that “schizophrenic” brains are different, does that automatically mean that we have found the cause? When we are going through the loss of a loved one, our brains are acting differently than usual. Is this sadness caused by our altered brain functioning or by the loss itself? This logical flaw completely ignores external events, and it seems that many researchers forget that the brain is designed to respond to the environment (Read et al., 2013). The third issue ignored is that one of the external events that can change people’s brain chemistry is antipsychotic medication (Burt, 1977; Chouinard, 1978, 1982, 1991; Ho, 2011; Muller, 1978; Porceddu, 1985).
The term “chemical imbalance” is used by biological psychiatry to explain a vast array of mental health issues, including schizophrenia. This theory was not based on any direct evidence of dopamine over activity. The first drugs that were used to treat schizophrenia in the 1950’s were originally used for sedation before surgery, and it was not understood why they worked for treating schizophrenia (Swazey 1974, Symposium Proceedings 1955). It was only later discovered that these drugs blocked the dopamine receptor, D2 (Creese 1976). Psychiatry quickly jumped on this and said that if these drugs cure schizophrenia, and these drugs block dopamine receptors, then the cause of schizophrenia must be over stimulation of the dopamine receptors (New York Times, 1979, Read et al., 2013).
However, by that time it had been discovered that the drugs not only caused a block in the dopamine system, but also initiated a response in the brain to compensate for the blockage (Burt, 1977; Chouinard, 1991; Muller, 1978; Porceddu, 1985). “So, over-activity in the dopamine system can be caused by the drugs that are supposedly treating the illness, which is supposed to be caused by over-activity of the dopamine system!”(Read et al., 2013). For this reason, it is essential that studies investigating whether schizophrenia is caused by increased dopamine activity must use participants who have not received antipsychotic drugs. Several reviewers of the evidence at that time confirmed that “no consistent differences between drug-free schizophrenics and normals have been found in terms of dopamine levels” (Bowers 1974; Haracz 1982; Jackson 1986).
After it had been proven that the levels of dopamine in schizophrenics who had never been medicated were normal, another approach was to find differences in the dopamine receptors. However, dopamine receptors have been shown to be increased by antipsychotics (Burt, 1977; Chouinard, 1991; Muller, 1978; Porceddu, 1985), and multiple post-mortem studies show no increases in dopamine receptors in those with schizophrenia who were not treated with antipsychotics (Hietala, 1994; Kornhuber, 1989). The 2009 edition of the popular Comprehensive Textbook of Psychiatry acknowledges that: “Increases in D2 receptors is a consistent finding…but these findings have been largely attributed to a medication effect” (Saddock et al., 2009). Biological psychiatry’s continued failure to prove its lead hypothesis has resulted in investigating other neurotransmitters. As one reviewer noted this search has been no more productive than with dopamine (Dean, 2000). For example, serotonin is another neurotransmitter that is “blocked” by antipsychotic medication, but several studies have found no evidence of serotonin abnormalities in those with schizophrenia (Dean, 2000). The psychiatric textbook The Neuroscience of Clinical Psychiatry, claims that people with schizophrenia have changes in the neurotransmitter GABA, but makes no mention if this research was based on those treated with antipsychotics versus those who were not (Higgins & George, 2013).
Despite the lack of evidence, the chemical imbalance theory remains very popular today (Higgins & George, 2013; nami.org; mentalhealthamerica.net). The reason for this is that without it, biological psychiatry could no longer justify its use of antipsychotics, and instead would have to admit that they are simply mind numbing medications that may relieve some symptoms but do not cure anything (New York Times 2008, Ho, 2011) while also having an effect that induces psychosis itself and worsens symptoms in the long term (Chouinard, 1978, 1982, 1991; Muller, 1978; Samaha, 2007). The increase in dopamine receptors makes the brain “supersensitive” to dopamine, which is a neurotransmitter that has been known to mediate psychosis. Thus, if the person ever stops taking their medication, the previously blocked dopamine is now unblocked on a brain that is now very sensitive to dopamine through extra dopamine receptors, potentially leading to psychosis (Chourinard, 1978). Also, long-term use of antipsychotics eventually leads to permanent dopamine dysfunction, which can cause tardive dyskinesia or tardive psychosis. Doctors would then need higher doses of antipsychotics to dampen those symptoms. “The most efficacious treatment is the causative agent itself, the neuroleptic” (Chouinard, 1982). In order for it to be said that antipsychotics are curing a chemical imbalance, it would first have to be proven that there is an imbalance in the first place which I have shown has not been done. Instead, what has been done is proving that antipsychotics themselves cause a chemical imbalance in the brain (Burt, 1977; Chourinard,1978, 1982, 1991; Muller, 1978; Porceddu, 1985; Samaha, 2007).
Another attempt by biological psychiatry is to say that larger ventricles in the brains of schizophrenics is the cause. I already highlighted above some of the issues with this logic, but for many biological psychiatrists this has been taken as incontestable evidence (Higgins & George, 2013). An early review showed that between 6% and 60% of those labeled schizophrenic have enlarged ventricles (Reveley, 1985; Copolov and Crook, 2000). However, we know that this finding is present in other disorders such as alcoholism (Pfefferbaum, 1998) and depression (Kempton, 2011), so this by no means can be used as a cause of schizophrenia. Trauma can also cause cerebral atrophy, ventricular enlargement, and dysfunction of the limbic system (Nemeroff, 2006, Teicher, 2006). Given the fact that a majority of people diagnosed with schizophrenia have been neglected or abused as children, this could easily account for the “evidence” that schizophrenia is a “brain disease” (Connor and Birchwood, 2012; Friedman, 2002; Outcalt and Lysaker, 2012).
Psychiatric medications also cause reduction in brain volume and increases in the ventricles (Dorph-Petersen et al., 2005; Gur, 1998; Ho, 2011; Radua et al., 2012; Weinmann and Aderhold, 2010). This was shown by the discovery that antipsychotics (typical and atypical) cause reduced brain volume in monkeys (Dorph-Petersen et al., 2005). Also, in 2008, it was shown in humans with one of the largest MRI studies to date published in the Archives of General Psychiatry which reported that “The more drugs you’ve been given, the more brain tissue you lose…The prefrontal cortex doesn’t get the input it needs and is being shut down by drugs. That reduces the psychotic symptoms. It also causes the prefrontal cortex to slowly atrophy” (New York Times, 2008, Ho, 2011). This study, which answers some of the most pressing problems in psychiatry, has been largely ignored. In addition to reduced gray matter in the brain, antipsychotic medication has also been linked to reduced white matter in the brain (Ho, 2011; Wang, 2013). Psychiatric textbooks (Higgins & George, 2013) and organizations like the National Institute of Mental Health (nimh.gov) continue to say that schizophrenia is a chronic brain disorder caused by enlarged ventricles, less gray matter, and less white matter in the brain. Of course, without citing any of the above studies showing that these are all caused by other things, especially antipsychotics.
There is not time here to explore some of the other psychological and social explanations for schizophrenia that have demonstrated correlations to higher rates, such as poverty (Wilkinson and Pickett, 2009), gender (Castle, 2000), living in cities (van Os et al., 2009), racism (Karlsen and Nazroo, 2002), and trauma (Shevlin et al., 2007a). Likewise, it can only be briefly noted that two WHO studies have shown that one of the greatest predictors of significantly poorer outcomes for schizophrenia is living in a developed country with continued access to antipsychotic medication (World Health Organization, 1973, 1979). These studies in addition to many others suggest that a one-size-fits-all, medication-based “treatment” of schizophrenia is neither substantiated nor effective, and in many cases makes people much worse (Bockoven, 1975; Bola, 2003; Bola et al., 2011; Carpenter, 1977; Chouinard, 1978, 1982, 1991; Epstein, 1962; Gardos and Cole, 1977; Gardos and Cole, 1978; Gur, 1998; Harding, 1987; Haro, 2011; Harrow, 2007; Hopper, 2000; Lepping et al., 2011; Madsen, 1998; Marshall and Rathborne, 2011; Mathews, 1979; May, 1981; Mosher, 1995; Muller, 1978; Prien, 1971; Rappaport, 1978; Samaha, 2007; Schooler, 1967; Seikkula, 2006; Stip, 2002). From this research, it is at best irresponsible and at worst negligent to be telling people in a fragile, impressionable state they have brain diseases when it is not proven that they do. The implications of this are that our mainstream biological understanding of schizophrenia is unfounded and that standard psychiatric treatment regimens based on unproven causal theories are largely unwarranted.
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