An Overview of Competing Theories of Schizophrenia
Copyright 2009, K.M. Vekquin
This article gives a chronological overview of various competing theories of the psychosis known as 'schizophrenia'. Most theories of schizophrenia maintain that there is a genetic basis, either entirely, or partially, for the etiology of the psychosis. However, there is no true evidence of a genetic etiology of schizophrenia. The chronology of theories ends with the relatively recently developed 'traumagenic neurodevelopmental model' which the author finds to be the most plausible theory of schizophrenia.
The typical day of the average psychiatrist involves prescribing and monitoring medication to persons with psychoses, such as schizophrenia. "Schizophrenia is a serious mental disorder that afflicts approximately 1 percent of the world's population. The cost of schizophrenia to society exceeds the cost of all cancers" (Carlson, 2010, p. 556). For psychiatrists, schizophrenia is not merely a mental disorder, but is a lucrative industry. It appears that as long as psychiatry is only minimally successful in treating schizophrenia, it is guaranteed to be a stable source of profit. One psychiatrist notes of the industry in which he makes a living: "[T]he real crux for the theory and practice of psychiatry is the multifarious and picturesque group of psychotic conditions referred to as schizophrenias. This is a rather heterogeneous group with a common denominator that seems to be our basic ignorance about the nature and etiology of the psychological states involved" (Grof, 1985, p. 304).
One of the reasons why psychiatrists don't understand schizophrenia is because they don't genuinely listen to their patients; instead, they simply look for a cluster of symptoms in order to assign a diagnosis and prescribe medication. Thereafter, psychiatrists simply monitor their patients' medication without ever analyzing the symbolic value of the symptoms. Some of these men say that schizophrenia is a brain disease because they have no interest in getting 'too close' to schizophrenia, since the its phenomenological state "includes intense feelings of terror and rage" (Breeding, 2008).
The peculiar set of symptoms called 'schizophrenia' has been part of human society for thousands of years, has remained basically unchanged through time, is the same in all cultures, primitive or industrialized, and is still found in only a minuscule percentage of the population of any given nation or tribe. "The major symptoms of schizophrenia are universal, and clinicians have developed criteria for reliably diagnosing the disorder in people of a wide variety of cultures" (Carlson, 2010, p. 556). For a millennium between The Holy Roman Empire and the Enlightenment, schizophrenia was generally thought of as the result of 'possession' by 'evil demons', which required exorcism, conducted by Roman Catholic priests with special training.
Today, instead of being exorcised, the demons of schizophrenics are sedated by heavy tranquilizers that cause neurological damage to the body, often permanently. In primitive tribal nations, what is called 'schizophrenia' by industrialized nations, is considered to be a sign of the potential to become a shaman (Walsh, 2007).
The Age of Geneticism
During the last 40 years of the 18th century, since no physical evidence of disease had been found in the brains or bodies of people with Ômadness', it was clinicians, not physicians, who began questioning patients about their personal history, postulating that life experiences may be the cause of madness. The physicians, in opposition to the clinicians, who had much more political power and social influence than the clinicians, declared that all madness must be the result of physical disease. This brought on the age of geneticism, which we are still in today, and it still has not reached its peak. In all ages, there are always parallel oppositional forces that hold much less power over society's beliefs and practices than the dominant paradigm. By the end of the 18th century, physicians had successfully censored the views of clinicians who had derived their explanations of the etiology of madness by listening to the life stories of their patients. It was during this crucial period that geneticism became the preferred model to explain behavioral deviancy, promoted by the dominant school of thought, and since then, thousands of bodies and brains have been cut open in search of physical evidence of disease in people who have great difficulty in controlling their thoughts and emotions (Foucault, 1973).
Indeed, Scientists have been cutting open the brains of schizophrenics for more than 200 years, yet still have not found any evidence that schizophrenia, nor any other type of emotional disorder, is a physical disease. There is no evidence of degeneration of brain tissue in schizophrenics (Carlson, 2010) except in the case of those who have taken psychiatric medication for several years, since medication causes the loss of brain tissue (Breggin, 2009). Michel Foucault explains why psychiatry has taken genetics to be the explanation for all emotional disorders:
"The study of heredity, or the attribution of the origin of the abnormal condition to heredity, constitutes the 'metasomatization' required by the whole theoretical construction [of psychiatry]. This metasomatization and the study of heredity offer in turn a number of advantages to psychiatric technology. First of all, it allows an indefinite causal permissiveness characterized by the fact that anything can be the cause of anything. The theory of psychiatric heredity establishes that not only can a certain type of illness cause an illness of the same type in descendants, but also that with equal probability it can give rise to any other kind of illness of any type whatsoever. [...] The causal permissiveness of heredity makes it possible to establish the most fantastic or, anyway, the most supple heredity networks. Finding a deviant element at any point in the hereditary network will be sufficient to explain the emergence of a condition in an individual descendant" (Foucault, 1999, p. 313-314).
Inadequate Research Methodology
Science is based on discovering correlations by isolating variables, but when it comes to studying human cognition or behavior, it is impossible to isolate all variables, thus correlations made are often false. Only when a certain gene is on and 100% of the time a certain physical disease is also present, can a strong correlation be made, but this is extremely rare, and so far, only degenerative physical diseases have been found to be correlated to certain genes. Schizophrenia "is not caused by a degenerative process, as are Parkinson's disease, Huntington's disease, and Alzheimer's disease, in which neurons continue to die over a period of years" (Carlton, 2010, p. 565).
Scientists who operate under the paradigm of geneticism fervently hold onto their belief that all psychiatric problems are genetic in origin, by using the null hypothesis theory as their method of research, which can be used to Ôprove' almost anything. The way that it works basically is that they begin with a hypothesis, and try to disprove it, and if they are unable to disprove it, (perhaps because they did not design a good study) they assume that it must be true. This results in making claims of truth based on no actual real evidence, such as this one: "One of the strongest pieces of evidence that schizophrenia is a biological disorder is that it appears to be heritable" (Carlson, 2010, p. 557). For these researchers, adoption and twin studies Ôprove' to them that schizophrenia is a heritable trait because there is a 10% higher incidence of schizophrenia running in families than in the general population. In mental disorders, a 10% prevalence rate seems to be good enough for them to claim they have proof of heritability, yet in diseases such as Parkinson's and Huntington's there is a 100% genetic correlation. Moreover, all of the twin and adoption studies that are used as proof that schizophrenia is a genetic trait, were conducted using the null hypothesis method of research. Though it is an invalid method of conducting scientific research it is still in constant use in the field of psychiatry. Various researchers, including Don Jackson, Theodore Lidz, and Lewontin, have criticized the twin and adoption studies as rendering bogus results (Joseph, 2006). Peter Breggin explains: "The frequently cited Scandinavian genetic studies [...] actually confirm an environmental factor while disproving a genetic one. Such conclusions may seem incredible to readers who have been bombarded with psychiatric propaganda" (Breggin, 2009). Another thing to consider is that if schizophrenia really is a disease caused by a genetic defect,
geneticists should be able to explain why it remains at a constant affliction rate even though the majority of schizophrenics do not produce children.
After decades of a fruitless search for genes that cause emotional disorders, some scientists have begun a new trend in research, which they call Ômeta-analysis', and it appears to be a desperate maneuver. The meta-analyses of genetic research that claim to have identified the gene responsible for schizophrenia are misleading, because they actually only show linkages to chromosomal regions rather than actual genes, and only one of the eight linkages claimed has ever been replicated in a subsequent study. A meta-analysis that makes a claim on truth is not to be taken seriously, because "it only means the null hypothesis has not been disproved in that particular study" (Joseph, 2006, p. 234). Scientists who are critical of the field of psychiatry are concerned about the growing trend: "Sometimes meta-analyses are used to distort information and make it appear in a more favourable light, [...] [T]his trend of using meta-analysis to resurrect largely negative genetic linkage studies disturbing. It appears to be nothing more than a manipulation of data to obtain a desired result" (Joseph, 2006, p. 238).
In every decade since the 1950s, a new hypothesis to explain schizophrenia has been introduced by various clinicians and researchers all over the world, yet in the US none of the new models have gained even a fraction of the notoriety that the genetic and epigenetic models maintain. One historian of psychiatry observes:
Theories professing to reveal the roots of psychosis include organic, genetic, neurobiological, biochemical, cultural, socioeconomic, psychosocial, behavioral, cognitive, and psychodynamic models -- to mention just a few of the multifarious factions. Of these, the most ascendant and widely accepted explanation for psychotic conditions such as schizophrenia or bipolar disorder [...] is the biochemical model, which presumes that there is an inherited, biochemical abnormality in the brains of certain people predisposing them to psychosis. [...] But to blithely attribute such a vitally intense, dynamic, and dramatic phenomenon as psychosis solely to imbalanced neurotransmission or maladaptive behavior (as do many modern clinicians) is a gross oversimplification of a highly complex, multidetermined syndrome. (Diamond, 1996, p. 125)
The Dopamine Imbalance Hypothesis
The Ôdopamine imbalance hypothesis' suggests that schizophrenia is caused by hyperactivity of nerve synapses between dopaminergic neurons of the ventral tegmental area and neurons in the nucleus accumbens and amygdala, along with increased secretion of dopamine in the nucleus accumbens (Carlson, 2010) and some researchers also suggest that there is an over-abundance of dopamine receptor sites in the hippocampus of the schizophrenic. These claims have been made by observing the behavioral effects of psychiatric medication, not by laboratory evidence (Joseph, 2006). "These critical pharmacological observations suggest, but do not establish, the existence of a dysregulation of DA [dopamine] transmission in schizophrenia" (Hirsch & Weinberger, 2003, p. 366). Thousands of scientists, for more than four decades, have been searching for evidence to substantiate the dopamine hypothesis, yet there is still none (Talkowski, Bamne, et al., 2007). Because the hypothesis has not been disproved, yet has still not been proven, pharmaceutical companies pretend that its true because it promotes the use of (very expensive) medication as the main treatment for schizophrenia.
Hanging onto their beloved dopamine imbalance theory despite the lack of evidence, pharmaceutical companies appropriated some new research on stress and brain dysfunction, and distorted it for the sake of profit. They claimed that people with emotional disturbances have genetic predispositions that make them weak to environmental stressors, and that this in turn causes a 'dopamine imbalance' in the brain. In the words of one researcher: "Subjects at increased risk for psychosis show continuous [...] sensitization to environmental stress [...] reflecting dopaminergic hyper-responsivity in response to environmental stimuli" (Myin-Germeys, Delespaul, van Os, 2005).
The epigenetic and diathesis-stress models
After decades of failing to find any genetic clues for the cause of schizophrenia, yet finding extensive evidence of a correlation between trauma and psychosis, scientists created the Ôepigenetic' and Ôstress-diathesis' models. Schizophrenic brains produce more stress hormones than normal brains under laboratory-induced stress (Elman, Adler, et al., 1998). This is taken to be a genetic defect rather than some other possible explanation, for example, perhaps schizophrenics are constantly in a heightened state of stress. No doubt, having schizophrenia is an extremely stressful experience. The epigenetic and diathesis-stress models are basically the same except that the epigenetic model posits trauma in infancy as the cause of brain disease while the diathesis-stress model posits stress at any time during infancy, childhood, and adolescence as the cause of brain disease (Walker & Diforio, 1997). These scientists claim that some people have a 'genetic predisposition' towards developing schizophrenia or bipolar disorder (or any other form of psychosis). A "genetic deficit creates [...] an oversensitivity to stress" (Read, Perry, et al., 2001, p. 319). This means that in some people, environmental conditions cause the defective gene(s) to change from a dormant to an active state, which in turn causes brain in the form of structural damage or degeneration. The stress-diathesis model relies on the use MRI brain scans to 'prove' brain abnormalities. Two researchers explain the flaw in using MRI scans to prove the existence of brain development abnormalities and lesions or degeneration: "[Q]uantitative measurements of cerebrospinal fluid spaces and tissue volumes on an MRI scan cannot establish that tissue has degenerated nor, for that matter, that the brain has developed abnormally. This can be done only at the cellular level. MRI measurements during life represent the volume of living structures, which can vary depending not only on changes in neuronal elements, but also on changes in vascularity, perfusion, extracellular constituents, etc." (Hirsch & Weinberger, 2003, p. 332).
Stress and Brain Damage
Stress causes alterations in brain structure and function, as well as neuronal death (Robert, 1993). Often, this is interpreted as brain damage, and some of it probably is. However, the brain is usually capable of healing when the source of stress is removed. Some studies have found an abnormally sized hippocampus in schizophrenics (Hanlon & Weisend, 2005). This is probably because the hippocampus is particularly vulnerable to damage by stress (Margarinos, 1997; McEwen, 2007). Some researchers claim that the damage or change of structure caused by stress is the cause of psychosis. However, not all people with stress-induced brain damage develop a psychosis, and the 'genetic predisposition' hypothesis is weak because no genetic link has ever been found for nondegenerative (i.e. psychiatric) diseases. Many of the symptoms of schizophrenia are caused by stress, not by brain disease. For example, hallucinations are sometimes caused by chronic stress, and they seem to be jumbled or random memory content taken out of context (Waters, Badcock, et al., 2006).
Psychiatric Medication and Brain Damage
Post-mortem studies have revealed the evidence of brain damage in patients who have taken psychiatric medication over a number of years or decades. Anti-psychotic medications damage the basal ganglia of the brain (Lang, Kopala, et al., 2001). In unsophisticated post-mortem studies of the brains of schizophrenics who were on psychiatric medication for several years, a correlation is claimed between the brains that are found to be slightly shrunken in size, and schizophrenia. No
mention is made in these studies of the fact that the brains under study were heavily drugged for many years up to the point of death (Baumann, Danos, Krell, et al., 1999). It is sloppy, low-level research to simply assume that the shrunkenness of the brain causes schizophrenia, rather than considering other possible correlations, especially since post-mortem studies of the brains of unmedicated schizophrenics show no sign of shrunkenness. Many studies have shown that psychiatric medication damages the brain yet this well-known fact is ignored by many researchers who are employed by pharmaceutical companies. Clearly, their research is far from neutral, which violates basic scientific standards in research protocol (Joseph, 2006; Breggin, 2009).
The Neurodevelopmental Model
In the 1980s, researchers who no longer found it feasible to deny the mountain of evidence that there is a very strong correlation between childhood trauma, especially sexual abuse, and psychosis, introduced the 'neurodevelopmental model', which posits that whether the gene that causes brain disease becomes active or not is determined mainly by the experience of trauma early in life, while the brain is still developing. One leading neurologist, convinced that the epigenetic theory is true, explains: "Disorders of personality [...] are essentially a product of early childhood abandonment and trauma, usually within the first few years. [...] Even schizophrenia, a decidedly genetic trait, often is precipitated by a life stress or illness. Trauma essentially plays a role in causing or triggering most if not all mental illness" (Scaer, 2005, p. 287). Though this model recognizes the role of trauma in the development of schizophrenia, it is still based in geneticism.
The Traumagenic Neurodevelopmental Model
In the 1990s, a very progressive model was introduced: the 'traumagenic neurodevelopmental' model which takes the concept of neurodevelopment one step further. This model begins with a critical observation: "Schizophrenia is considered to be one of the most biologically based of the mental disorders [...]. However, the methodological rigor of the evidence for this proposition is often described as less than adequate" (Read, Perry, et al., 2001, p. 319). In the words of some of the main researchers developing the new model: "Neurodevelopmental theories have gradually replaced neurodegenerative theories. The dysfunction identified in the brains of schizophrenics has now been shown to precede, rather than result from, schizophrenia. [...] Even in this area, however, researchers limit investigation of the causes of the neurodevelopmental dysfunction to genetics and perinatal events" (Read, Perry, et al., 2001, p. 323).
During the development of their model, these researchers completely rejected genes as the cause of emotional disturbance, and instead, posited purely environmental causes. They reasoned that chronic life stress in combination with several incidents of acute stress, or trauma, causes schizophrenia (Read, Agar, et al., 2003). This is reasonable, given that "[a]bundant evidence documents the high rate of trauma, especially interpersonal violence, in the lives of persons with severe mental illnesses" (Foy, 1998, P. 493). In 70% of 426 cases, the onset of schizophrenia was preceded by an experience of trauma as defined by the DSM-IV (Neria, Bromet, et al., 2002). It is difficult for researchers to detect trauma in schizophrenics because it requires a certain level of insight on the part of the interviewer to be able to recognize trauma within psychosis, and because "the symptomatic nature of schizophrenia [...] may interfere with the ability to reliably report PTSD symptoms" (Gearon, Bellack, & Tenhula, 2004). Another study found that between 51% to 97% of patients with schizophrenia had experienced a series of traumas over their lifetime preceding the onset of their psychosis (Resnick, Bond, & Mueser, 2003). Along with evidence of chronic trauma preceding psychosis, these researchers were also influenced by new, more sophisticated brain research, which found that neural networks are not 'hard-wired' in the brain, that the brain constantly restructures itself with every new experience, and that new neurons are constantly being born while others are constantly dying.
By the early 2000s, various researchers in New Zealand, Australia, Scandinavia, and Germany viewed the traumagenic neurodevelopmental model as the most scientifically rigorous and logically consistent (Read, van Os, et al., 2005). However, in the US, the genetic and epigenetic models, created in the 1950s, still dominate the practice of psychiatry, probably because the US is the most medicalized nation on earth.
Alternatives to Psychiatric Medication
There are various accounts of doctors in the past who have successfully treated schizophrenia with psychotherapy rather than medication, and in every case, therapy involved the whole body in a very intensive physical process, rather than just the mind, as is the conventional method of psychotherapy. The most well-known examples of successful treatment for psychoses without the use of medication include Wilhelm Reich, Ronald Laing, Alexander Lowen, Robert Zaslow, and Jack Rosberg (Diamond, 1996). Some doctors have found that if they listen very closely to their patients and treat them with respect, their patients may recover from psychosis without the use of medication (Siebert, 2000).
"The difference between support for someone who can benefit from a little individual counseling and an individual in an extreme state of mind is mostly a matter of degree and resource" (Breeding, 2008, p. 498). In essence, schizophrenics tend not to overcome their psychosis because they never get the highly skilled, intensive, long-term therapy that they need to move through such a deep disturbance. Very few therapists have the therapeutic skill to not only withstand, but to be a gentle guide through the journey of profound sorrow, grief, rage, and terror that results in transcendence of psychosis. For this, one would need a shaman!
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