Consumption: Addendum 3

Further Quotations on Psychiatry

Note: so much good literature has already been composed on this topic that I feel unable to add to that. Thus I shall merely be quoting from better researchers. I have included a bibliography of excellent reading material on this wide, vital issue at the end of this document.

I have written this entire book whilst under the recent influence – since July 2024 – of 400mg of monthly Aripiprazole injections (the highest available dosage), taken against my will via a Community Treatment Order, for refusing their ‘meds’. Aripiprazole (‘Abilify’) is a 2002 atypical antipsychotic used to drug those diagnosed with schizophrenic disorders.

Thus, due to its brain-disabling component, I feel unable to continue without jeopardizing my literary cogency, already under some significant strain throughout the writing process. I have done the best I can so far, given the conditions, although I’m sure my writing has suffered due to this ‘chemical cosh’. I apologise in advance for any spelling errors or grammatical inconsistencies in my work. I do all my own proofreading, and in general I’m exhausted by all this! Please email me if you spot any.

After all, as stated in Rethinking Madness: Towards a Paradigm Shift In Our Understanding of Psychosis, by Paris Williams, Chapter 5, “research has found that antipsychotics typically cause a significant level of cognitive impairment, especially regarding the capacity to learn, retain information, and perform executive functions such as problem solving and planning¹”

1. Hagen et al., 2010; Keefe, Bollini, & Silva, 1999.

Devastatingly, for someone such as myself writing a book on long-repressed painful emotions, Williams goes on to state in Chapter 5 that “It has long been recognised that antipsychotics cause emotional deadening [resulting] in a lack of joy and sense of meaning in life¹. … [T]he authors conclude that “by far the most common and disturbing side-effect was a chronic sense of ‘numbness’ and/or lack of emotion, associated particularly with the use of antipsychotics². These participants described the antipsychotics as resulting in “not feeling anything,” “feeling isolated,” “being completely numb,” and feeling like “a complete, drooling zombie”³.

1. Breggin, 2008a.

2. Hagen et al., 2010, p. 50.

3. Ibid.

Indeed, also in Chapter 5, Williams highlights that “[Guy] Chouinard and his research team¹ were among the first to suggest… that antipsychotics affect the brain in ways that make the individual more vulnerable to psychosis. Chouinard posited that the brain attempts to compensate for the effects of these drugs by increasing the number of dopamine receptors, which subsequently increases the individual’s susceptibility to psychosis (a condition often referred to as tardive psychosis or supersensitivity psychosis – psychosis caused as a direct result of using the drugs), a hypothesis that still holds weight today². A closely related hypothesis has been generated and validated with the invention of the MRI. It was discovered that antipsychotic drug use (both of the older typicals and the newer atypicals) causes atrophy of the cerebral cortex and enlargement of the basal ganglia³, changes which have been demonstrated to increase the severity of both positive and negative psychotic symptoms⁴… the evidence has been surprisingly robust in demonstrating that the long-term use of antipsychotics significantly increases the likelihood of developing a chronic psychotic disorder.”

1. Chouinard et al., 1978.

2. Whitaker, 2010.

3. Chakos et al., 1994; Gur et al., 1998; Madsen, Keiding, Karle, Esbjerg, & Hemmingsen, 1998.

4. Gur et al., 1998.

I am afraid that, as of writing this book, my story remains an unfinished one, as I have yet to be provided with the trauma-based psychotherapy I have been begging the NHS for in nigh-on every meeting with them for over 6 years. As with all other sufferers, they were content only to force me onto their damnable medications, and then to effectively wash their hands of me, the entire long context to my illness ignored, and never spoken on, for over 23 years of fruitless and demeaning engagement. Still, I wish other patients the best of luck in this regard. Hopefully, as this issue becomes more widely understood and discussed in the public domain, they will be provided with genuine therapeutic help, and their outcomes will thus prove more positive than I suspect my own will be.

After all, again in Chapter 5 of Rethinking Madness, Williams reminds us that “Recent research has revealed that “people with serious mental illness (SMI), die on average 25 years earlier than the general population”¹. The authors of this research have concluded that a number of the risk factors leading to this extraordinary shortening of one’s lifespan – particularly obesity and diabetes – may be directly attributed to the use of antipsychotic drugs.”

1. National Association of State Mental Health Program Directors, 2006, p. 5.

If not death, it seems I can look forward to the acknowledgement that “A host of other serious physical problems have been associated with antipsychotic treatment, including diabetes, obesity, agranulocytosis (the potentially fatal loss of white blood cells), neuroleptic malignant syndrome (a life threatening neurological disorder), blindness, seizures, arrhythmia, fatal blood clots, heat stroke, swollen breasts, leaking breasts, sexual dysfunction, and debilitating skin rashes.¹”

1. Arana, 2000; Joukamaa, et al., 2006, Waddington, Youssef, & Kinsella, 1998.

For an overview of the dangers of psychiatric drugs consult Chapter 4 of Psychological Interventions for Psychosis: Towards a Paradigm Shift, edited by Juan Antonio Díaz-Garrido, Raquel Zúñiga, Horus Lafitte and Eric Morris, and published in 2023 by Springer. The book is available online at https://doi.org/10.1007/978-3-031-27003-1.

A further selection of pertinent quotations continues below:

“Psychiatrists are not being consciously dishonest when they claim that schizophrenia is a physical disease much like cancer or diabetes. Their ideological commitments are such that they are simply incapable of seeing any facts that would undermine the medical model.”

John Modrow, How to Become a Schizophrenic, Chapter 6, The Anatomy of a Dogma, pp. 311-312

“…they simply cannot question the validity of the medical model without in effect committing suicide; for once the protective ideological veil of the medical model is torn away, they will be revealed as total incompetents incapable of managing such mental disorders as schizophrenia in even a halfway enlightened or effective or humane way.”

John Modrow, How to Become a Schizophrenic, Chapter 6, The Anatomy of a Dogma, p. 311.

“Although psychiatrists are perceived as medical specialists, nowadays with fewer and fewer exceptions, their training is virtually identical to that of an ordinary general practitioner. What specialized training psychiatrists do receive is limited largely to diagnosing the various mental disorders so that the proper drug can be prescribed.”

John Modrow, How to Become a Schizophrenic, Chapter 6, The Anatomy of a Dogma, p. 311.

 “In fact, as far as increasing their ability to understand and empathise with the patient is concerned, medicine is the very worst subject that the psychiatrist could possibly study. In medical school the psychiatrist is taught to dehumanize the patient: to regard the patient as nothing more than a complex physiochemical machine.”

John Modrow, How to Become a Schizophrenic, Chapter 6, The Anatomy of a Dogma, pp. 311-312.

“Most psychiatrists have no knowledge at all of the actual social and psychological causes of schizophrenia and other mental disorders for the very simple reason that they firmly believe that such causes do not exist. What little training most psychiatrists have in psychology is limited to some very superficial instruction in the obsolete theories of Sigmund Freud.”

John Modrow, How to Become a Schizophrenic, Chapter 6, The Anatomy of a Dogma, pp. 312.

“In view of their lack of any useful training and lack of any insight that their training is totally useless, it is hardly surprising that psychiatrists generally do more harm than good.”

John Modrow, How to Become a Schizophrenic, Chapter 6, The Anatomy of a Dogma, p. 312.

“[P]sychiatrists and their corporate masters are not the only ones who benefit from the medical model. The medical model is also a great benefit and source of comfort to the schizophrenic’s parents for it absolves them of all responsibility for causing their child’s mental breakdown. What a relief it is for these parents to be able to believe their son or daughter’s problems stem solely from a physical disease – an illness for which no one is responsible! Consequently, as soon as the child is diagnosed as schizophrenic, the parents usually conclude that all the family’s problems can be localized exclusively within the patient. They are sane, he or she is sick, and the doctor will take care of everything.”

John Modrow, How to Become a Schizophrenic, Chapter 6, The Anatomy of a Dogma, p. 318.

“the threat to clinical psychology and psychiatry is very real and rational; it is doubtful that either profession, especially psychiatry, could survive in its current form if people’s context and life experiences were made central ... it is imperative to be aware of what is at stake. If psychology’s and psychiatry’s neglect of social context is simply seen as an oversight to be corrected by the provision of evidence, rather than a highly strategic and complex defence mechanism, then we may be very unprepared for the strength and, I have to say, at times aggressiveness of resistance to any attempt to insert context as cause into discussions of emotional or behavioural problems.”

Mary Boyle, De-Medicalizing Misery, Chapter 3, Making the World Go Away, p. 40.

“Within the biomedical context, insight means that the person accepts that they are ill and that the cause of their distress is biomedical in origin. This most usually means that ‘help’ is in the form of reliance on, and compliance with, long-term use of psychotropic  medications and other interventions that professionals deem to be useful for the person’s rehabilitation including mandatory, ongoing psychiatric intervention. People will be encouraged to reduce their expectations for the future to take account of their illness. Recovery is – in the traditional approach – inexplicably tied to the person’s acceptance of their experiences as being biomedical in origin. Relapse frequently occurs, as the underlying issues that precipitated the initial crisis have not been addressed. As well as this the person now has additional problems including hopelessness, loss, stigma, social exclusion and the toxic effects of medications and associated problems of lethargy, weight gain, sexual dysfunction and secondary health problems to contend with. Many former patients have described to me the terrifying experience of forced hospitalization and sedation, which have further traumatized them and engendered profound feelings of shame, despair and alienation… as a society we are investing time and money in creating chronic, revolving-door patients through the self-prophesizing medical model. The long-term financial cost of repeat inpatient admissions, visits from assertive outreach and crisis resolution teams, a care coordinator, social worker, medication, healthcare for secondary problems caused by the long term use of neuroleptics, disability-living allowance, housing and council tax benefit and free bus passes cost billions of pounds annually. In 2007 mental healthcare in England cost £22.5 billion pounds with an additional £26.1 billion in lost earnings (see McCrone et al., 2008). Of course the biggest cost is the appalling personal cost to individuals. People face a lifetime of chronic ‘illness’, passivity and dependency, condemned to lives dulled by drugs and blighted by stigma, and offered no opportunity to make sense of their experiences.”

Jacqui Dillon, De-Medicalizing Misery, Chapter 11, The Personal is The Political, pp. 153-154.

“every week in the UK, intelligent people are expected to accept discredited diagnoses for fear of being labelled as ‘lacking in insight’ and having treatment forced on them. Every week thousands of people are coerced into taking medication that they don’t want and which frequently does more harm than good. Every week, people are incarcerated against their will, sectioned under the mental health act, ‘for their own good’. The Human Rights Act is exempt for those who are of ‘unsound mind’… as Mary Boyle has said:

The claim that there exists a biologically based diagnosable disorder called schizophrenia has been the focus of intense and persistent criticism and been shown to be scientifically bankrupt. The label also appears to justify drugs as a major intervention as a vast and very unsuccessful research programme searching for biological and genetic causes. But schizophrenia is much more than a label. Behind it lies the medical model – the claim that emotional distress and problem behaviour are pathological symptoms of illness or disorder rather than meaningful responses to serious problems and adversity in people’s lives and relationships.”

Jacqui Dillon, De-Medicalizing Misery, Chapter 11, The Personal is The Political, p. 156.

“the [vulnerability-stress] hypothesis (quickly promoted to the state of a ‘model’) has, with its close relative the biopsychosocial model, become an extraordinarily useful and effective strategy for downplaying the impact of life experiences on emotional distress. One of the advantages of this strategy is that … it actually acknowledges a causal role for the environment (stress) thus averting criticism that this aspect is being ignored. But as soon as context or life experiences are invoked, they are negated by the implication that negative experiences are not inherently stressful but are made so by pre-existing vulnerability so that only ‘the vulnerable’ are adversely affected – ‘normal’ people would be able to cope. Part of the power of this strategy lies in the inventiveness of its proponents in generating supposed vulnerabilities and in the non-specific nature of these attributes, for example that the faulty brain ‘overreacts’ to the environment. Such suggestions cover virtually any eventuality. Indeed, it is difficult not to be struck by the efforts made by the proponents of the vulnerability-stress hypothesis to preserve the primacy of biology and to downplay even the most aversive environments… without the slightest theoretical or empirical justification ... In a more oblique argument, Fowler et al., (2006) seems to suggest that childhood sexual abuse may assert some of its harmful effects via a genetic or constitutional inability to contextually integrate information. It is perhaps only a matter of time before it is claimed that some ‘vulnerable’ people are over-sensitive to sexual abuse.”

Mary Boyle, De-Medicalizing Misery, Chapter 3, Making the World Go Away, pp. 31-32.

“The basic premise of traditional CBT [Cognitive Behavioural Therapy] is that dysfunctional assumptions about self and the world develop as a result of negative childhood experiences. These ‘schemata’ are then reactivated by later critical incidents (such as failing an exam, a relationship breakdown) mediated by negative automatic thoughts of which the person may not be aware. These cognitive patterns are said to produce negative affective states such as depression and anxiety. Here, the potentially damaging effects of adverse environments are directly acknowledged but placed firmly out of reach and out of sight in the past, in the person’s early experience; its main role is to create a person who now thinks dysfunctionally, irrationally or idiosyncratically about a seemingly benign or only averagely difficult present. But it is dangerously easy to ‘forget’ these past events and focus only on the cognitive present, which CBT explicitly does. Indeed, it is increasingly common to refer to cognitive accounts as theories of problem maintenance so that questions about early adverse experiences may no longer even be asked, far less answered. This safety strategy, most popularly exemplified by cognitive theory and therapy, therefore obscures the potential impact of context in two distinct ways. The first is by theoretically placing experiences experienced as being very negative (for example, abuse, neglect, or bullying) in the distant past so that their remoteness, and the fact that they cannot now be changed, appear to justify lack of close attention to them. The second is by constructing the present as a series of triggers or critical incidents which by implication are not sufficient in themselves to produce serious emotional distress. This construction is greatly facilitated by the use in textbooks of triggers which are, if not exactly mundane, then relatively common such as being ignored by an acquaintance, failing an exam or being rejected following a job interview … the theory underlying traditional CBT can thus be seen as a sophisticated version of the vulnerability-stress hypothesis – and this is no doubt part of its popularity … neutral or ‘technical’ language such as expressed emotion, low social support, stress, life events, and so on to refer to highly negative life experiences … are then further sanitized by being converted to numbers stripped not only of factual description but also of all personal meaning. The result is that what has actually happened to people is rarely spelled out, making it much easier for others to assume that the experiences of those who receive psychiatric diagnoses cannot be that negative or important in causing distress in comparison to putative biological or psychological defects.”

Mary Boyle, De-Medicalizing Misery, Chapter 3, Making the World Go Away, pp. 32-33.

“Almost all psychiatric drug research is done on the normal brains of animals, usually rats. … We have no techniques for measuring the actual levels of neurotransmitters in the synapses between the cells. Thus all the talk about biochemical imbalances is pure guesswork More important, what’s actually being studied is the disruption of normal processes by the intrusion of foreign substances. The research in no way bolsters the idea that psychiatric drugs correct imbalances. Rather, it shows that psychiatric drugs create imbalances. … In reality we are disrupting its function.”

Peter R. Breggin, Your Drug May Be Your Problem, Introduction, p. 25.

“Because they impair normal brain function, such drugs only add to any existing brain malfunction. When psychiatric drugs are given to patients who do have known brain dysfunctions such as head injury … psychiatric drugs add to their brain dysfunction, frequently causing further mental deterioration. Experienced clinicians who work with brain-injured patients, for example, avoid prescribing brain-altering chemicals to them. … No psychiatric drug has ever been tailored to a known biochemical derangement. At the same time, no biochemical imbalances have ever been documented with certainty in association with any psychiatric diagnosis. The hunt goes on for these elusive imbalances, but their existence is pure speculation, inspired by those who advocate drugs.”

Peter R. Breggin, Your Drug May Be Your Problem, Chapter 2, The Limits of Psychiatric Drugs, pp. 53-54.

“Despite a hugely successful promotional campaign by drug companies and biological psychiatry, the effectiveness of most or all psychiatric drugs remains difficult to demonstrate. The drugs often prove no more effective than sugar pills, or placebos (see: Fisher and Greenberg (1997, 1989) and Antonuccio et al, (1999), and Breggin (1997a, 1998a)) – and to accomplish even these limited positive results, the clinical trials and data that they generate typically have to be statistically manipulated. Furthermore, no psychiatric drugs have consistently demonstrated effectiveness in studies lasting more than a few weeks or months (see also: Chapter 3, pp. 65-68).”

Peter R. Breggin, Your Drug May Be Your Problem, Chapter 2, The Limits of Psychiatric Drugs, p. 55.

“Considering what we have learned about neuropharmacology, it is indeed amazing how little biochemical theories of mental disorders have changed over the last half century. … Shortly after dopamine was recognised as a separate  neurotransmitter in the 1960s it assumed the central role in almost all theoretical speculation about the etiology of [schizophrenia]. Judging from the latest antipsychotic drugs being marketed, dopamine is still thought to play a major role in schizophrenia. Is this conservatism the result of having been fortunate in getting the theories essentially right at the outset? No, but it reflects two facts: First, a theory that is wrong is considered preferable to admitting our ignorance. Second, the tendency of pharmaceutical companies to develop drugs that are similar to those being successfully marketed seemingly provides support for existing theories without ever really testing them.”

Eliot S. Valenstein, Blaming The Brain, Chapter 4, A Closer Look at the Evidence, pp. 95-96

“The explanations of how psychotherapeutic drugs help to alleviate mental disorders rarely go beyond stating what chemical changes the drugs induce. The psychiatric literature rarely addresses how or why an excess or deficiency in serotonin or dopamine activity explains any particular mental disorder. There are few serious attempts to bridge the huge gap between neurochemistry and the psychological phenomena that must ultimately be explained. Unquestionably, our knowledge of how drugs interact with brain chemistry has increased enormously, but … we have made little real progress in answering these questions, yet the chemical theories of mental disorders are widely promoted as though they are firmly established scientific facts.”

Eliot S. Valenstein, Blaming The Brain, Chapter 4, A Closer Look at the Evidence, p. 96.

“…a more critical examination of the total evidence available reveals that it is far from established that a dopamine impairment underlies schizophrenia. While it is often said that schizophrenics have been found to have an abnormally high number of dopamine receptors, the evidence for this statement is not at all compelling. Even in those studies that found more dopamine receptors in schizophrenics compared to normal, the difference was only on average and did not apply to many schizophrenics. Furthermore, most researchers have not been able to find any evidence of dopamine abnormality in schizophrenics. A multinational research effort involving patients and researchers from Germany, the United Kingdom, and Austria concluded that any difference found in D2 (or any other dopamine) receptors in the brains of schizophrenic[s] is “entirely iatrogenic,” meaning that any difference found was totally caused by prior treatment with antipsychotic  drugs¹. In another report, Arvid Carlsson, one of the foremost contributors to the field of psychopharmacology in general, and to our understanding of dopamine mechanism in particular, concluded that there is:

no good evidence for any perturbation of the dopamine function in schizophrenia. An increase of dopamine D2 receptors in the brains of schizophrenic patients analysed postmortem has been reported, and one study with PET [Positron Emission Tomography] scan data showed the same thing, but the data from the Karolinska Institute by Farde and Sedvall show absolutely no difference at all².

Other (PET) studies fail to find high numbers of any dopamine receptors in schizophrenics³. Thus there is far from any agreement that most schizophrenics have an excess of dopamine receptors other than that caused by antipsychotic drug treatment. … it is not even in those schizophrenics who do seem to have [a] high number of dopamine receptors, unrelated to drug treatment, whether the dopamine abnormality was the cause or the effect of the disorder.”

Eliot S. Valenstein, Blaming The Brain, Chapter 4, A Closer Look at the Evidence, p. 113.

1. J. Kornhuber, P. Riederer, G. P. Reynolds, H. Beckman, K. Jellinger, and E. Gabriel 3H-Spiperone binding sites in postmortem brains from schizophrenic patients: Relationship to neuroleptic drug treatment, abnormal movements, and positive symptoms, J. Neural Transm., 1989, 75, 1-10.

2. A. Carlsson, Early psychopharmacology and the rise of modern brain research. Journal of Psychopharmacology, 1990, 4, 120-26 (information cited on p. 123). The PET studies were done by injecting living schizophrenic patients with radioactive drugs that bind to dopamine receptors. The PET brain scanner can detect the amount of radioactivity bound to different brain regions.

3. It is not reasonable to consider a finding that applies to less than one third of schizophrenics as a cause of the disorder. A. Breier, et al: Evidence from a novel positron emission tomography method, Proc. Natl. Acad. Sci., 1997, 94, 2569-74. See also M. Laruelle, et al., Proc. Natl. Acad. Sci., 1996, 93, 9235-40.

“The [Diagnostic and Statistical Manual] exerts an enormous influence … and its terminology is used in courts, social agencies, prisons, schools, and elsewhere. DSM-IV has been criticised for its proliferation of mental disorders and the variety of behaviour traits that are listed as mental disorders. Thus in a New York Times op-ed article, “Is Bad Writing a Mental Disorder?” Stuart Kirk and Herb Kutchins, both professors of social work in California, argued:

Since there are no biological tests for the vast majority of mental disorders, the psychiatric association has tremendous leeway in what it chooses to classify or not classify as illness. Unfortunately, there are few actions or traits that the association does not consider to be possible symptoms of some disorder.

Insomnia, worrying, restlessness, getting drunk, seeking approval, reacting to criticism, feeling sad and bearing grudges are all considered possible signs of a psychiatric illness. Where the association draws the line between mental illness and well-being arbitrarily determines how much “mental illness” there will be in the population.

The association is so eager to create and label disorders that it has revised the manual three times in 15 years and has expanded it from 106 mental disorders in the first edition to more than 300 in the new one. … these disorders and the criteria them include the tragic, the strange and the ridiculous. … Consider code 315.2 which the manual says is marked by the poor use of grammar, or punctuation, sloppy paragraph organization, awful spelling and bad handwriting.” (The New York Times, 20th June 1994, p. A11.)

Eliot S. Valenstein, Blaming The Brain, Chapter 5, The Interpretation of the Evidence, pp. 159-160.

“Simply listing a seemingly endless number of behavioural defects and maladaptive behaviours as distinct “disorders”, without any knowledge of etiology may be a meaningless exercise. Alfred North Whitehead called this “the fallacy of misplaced concreteness,” which others have related to psychiatric diagnoses:

Nowhere is this more true than with mental, intellectual, or behavioural disorders. Contemporary psychiatry is going through a paroxysm of line drawing. It is attempting to divide all human behaviour into discrete categories of ‘illness’ decided by a consensus. … The schizophrenic label provides the best example of an arbitrary and fluid designation wreaking havoc in its effort to assume the authority of a ‘disease.’”( M. P. Durmont, the nonspecificity of mental illness, The American J. of Orthopsychiatry, 1984, 54, 326-34 (quotation from pp. 327-28))

Eliot S. Valenstein, Blaming The Brain, Chapter 5, The Interpretation of the Evidence, pp. 160-161.

“The ideology in psychiatry has very practical consequences in the real world. If you read on the National Institute of Mental Health website it is impossible to find exact numbers for how much of the research budget goes to research on the effectiveness of psychotherapy and social interventions but. … I’d guess that it is well under 5% for sure, likely under 1%. A large number of psychiatrists do very little direct clinical work with patients besides taking a symptoms history and writing prescriptions. This is the stereotypical 15- minute med check, which can sometimes be less than 15 minutes. … This kind of psychiatric practice only makes sense within a bioreductionist framework – even if the biological psychiatrist’s theoretical framework is biopsychosocial, his or her actual practice is almost entirely biological. … An over-investment in biology and medications dominates inpatient psychiatric treatment throughout the world. … The hospitals don’t employ therapists, they employ case managers … entirely focused on discharge planning, which means setting up post-discharge appointments. The case manager very rarely talks to a supervisor about the person’s psychology. It’s all symptoms and behaviour. The group therapy is minimal in terms of amount of time, is never delivered by psychiatrists, and involves mostly common sense advice from a staff member who has no training in group therapy, does not attend psychotherapy conferences, and does not read the psychotherapy literature. All of this sociology of the mental health care system is driven by a huge over-emphasis on biology and medication, and a huge under-emphasis on psychotherapy. … Calling the bioreductionist model of psychiatry the medical model of psychiatry is a trick. It means that if you are against the genetic disease model of psychiatry, you are against medicine and science. This relegates critics of biological psychiatry to the fringes of the uninformed, the unscientific and the quacks. It’s a very effective strategy that fools a lot of people.”

Colin A. Ross, The Genetics of Schizophrenia, What is the Medical Model?, p. 30

“There are no specific or consistent structural anomalies in the brains of people with schizophrenia. Abnormalities like increased ventricular volume occur in people with and without schizophrenia, and so do normal ventricular volumes. … There is no structural brain abnormality that is specific for schizophrenia, or that can be used to diagnose schizophrenia, according to DSM-5. … For schizophrenia to be a genetic brain disease, the risk genes for schizophrenia would have to be controlling what is going on in the synapses. But look at the arithmetic. If there are a quadrillion synapses and 200 risk genes for schizophrenia, then each gene is controlling 10 x 1014/2 x 102 = 4 x 1012 synapses, which is 5 trillion synapses per gene.  Even this is an underestimate of the number of synapses per risk gene, since not all the 200 risk genes are thought to be operating in any individual person with schizophrenia. This is like one traffic light controlling all the intersections on the planet. … It just isn’t possible. In addition consider the number of synapses that are created each second in the human brain. … It is impossible to construct a scientifically testable model of how 100 or so genes are controlling the creation of 1-10 million synapses per second. There is no possible way to track the creation of 1-10 million synapses per second. There is no way to demonstrate a causal link between the proteins coded for by 100 genes in the nuclei of the millions of neurons … and the activity at the synapses of those neurons. … Scientists had to drill down to the level of the synapses and measure levels of neurotransmitters, in order to diagnose mental disorders. What were the findings, according to DSM-5? Zero. Finally, scientists had to dig down to the level of the DNA. What have the findings been to date, according to DSM-5? Zero. According to DSM-5, no genetic test is of any use for diagnosing mental disorders. … Psychiatry should consider the possibility that biological research on mental disorders is based on a fatal flaw: biology is the wrong level of analysis. … Maybe biological psychiatry can’t find anything, after decades of effort and billions of dollars spent, because there is nothing to find.”

Colin A. Ross, The Genetics of Schizophrenia, The Number of Synapses in the Brain, pp. 50-52.

“The framework provided by Lilienfeld and others suggests that the twin method may belong in the pseudoscience category. Indeed, twin researchers’ defense of the EEA [Equal Environment Assumption] has done little if anything to dispel the idea that the greater environmental similarity experienced by identical twins explains their greater concordance for psychopathology  when compared to same-sex fraternal twins.”

Jay Joseph, The Missing Gene, Chapter 1, The Twin Method: Science of Pseudoscience?, p. 34.

“The psychiatric genetics field is now suffering the consequences of nearly 100 years of enormously flawed and biased research, carried out for the most part by people strongly devoted to the genetic position well before they carried out their studies. The “items on the bill” include … the reliance on highly questionable theoretical assumptions; changing the definition of particular mental disorders to ensure results in support of genetics; non-blinded diagnoses and zygosity determination; unwarranted assumptions about the reliability and validity of psychiatric diagnoses; arbitrary and biased methods of counting relatives; viewing statistically non-significant results as evidence in favor of genetics; failing to take potential environmental confounds seriously; ignoring, distorting, and dismissing important observations by critics; overlooking critical methodological flaws; ignoring, attempting to discredit, or twisting the results of studies whose results do not fit genetic predictions; conclusions drawn more from the researchers’ beliefs than from the data itself; the interpretation of family data as evidence in support of genetic influences on mental disorders; the conversion of hypotheses into “facts”; a reliance on secondary sources’ interpretation of previous research; the premature conclusion that previous kinship research proves that genes for mental disorders must exist; basing linkage results on models assuming a genetic transmission of the condition under study; the use of rhetoric as a means of covering up the unexpected and disappointing failure to find genes; and, finally, the transformation of years, if not decades, of fruitless gene finding efforts into evidence of the “complex genetic nature” of psychiatric disorders.

As we now see playing out before us, the sum total of these items amounts to a bill that reads: Genes for the major mental disorders are unlikely to exist.”

Jay Joseph, The Missing Gene, Chapter 11, Genotype or Genohype? The Fruitless Search for Genes in Psychiatry, pp. 262-263.

Evidence in Madness and Genetic Determinism: Is Mental Illness in Our Genes? by Patrick D. Hahn, also suggests that twin studies research is fundamentally flawed and that the evidence in favour of genetic influences is much weaker than mainstream sources report:

“any theoretical model is only as strong as its underlying assumptions. The fundamental assumption underlying twin studies, the equal environment assumption, is that MZ [monozygotic] and DZ [dizygotic] twin pairs share the same amount of environment similarity.

This assumption, which forms the bedrock of the entire field of twin studies, is demonstrably false,  a point made at least as far back as 1960 by psychiatrist Don Jackson in his review paper “A critique of the literature on the genetics of schizophrenia”¹. Since then a mountain of empirical studies have confirmed this point².”

Patrick D. Hahn, Madness and Genetic Determinism, Chapter 3, Franz Kallman and Twin Studies, p. 28.

1. Donald D Jackson, “A critique of the literature on the genetics of schizophrenia”, in The Etiology of Schizophrenia, ed. Donald D. Jackson, (New York Basic Books, 1960) 63-64.

2. Jay Joseph, “The Equal Environment Assumption of the Classical Twin Method: A Critical Analysis,” Journal of Mind and Behaviour, 19, no. 3 (Summer 1998): 323-358; Joseph, “’Schizophrenia’ and Heredity,” 72-89; Jay Joseph, Schizophrenia and Genetics, (Pennsauken: BookBaby 2017), chapter 4, Kindle.

 The primary cause of mental illness is also explained in Hahn’s Chapter 9 on Trauma and Psychosis, documenting the research findings of Dr John Read, the professor of Clinical Psychology at the University of East London, who reviewed the literature on the relationship between childhood maltreatment and psychotic symptoms, including eleven large-scale population studies in the United Kingdom, the Netherlands, Australia, the United States, and Germany, covering “numerous forms of childhood maltreatment, including sexual abuse, physical abuse, emotional abuse, violence in the home, running away from home, childhood institutionalization, serious neglect, and bullying,” and where, “Ten of the eleven studies found that there is a significant correlation between childhood maltreatment and psychosis, with odds ratios ranging for 1.5 (i.e. a 50 percent increase in risk) and up”.

Reflecting on the single outstanding study, by Josie Spataro et al.., that found the childhood sexual abuse was correlated with a 20 percent increase in manifestations of schizophrenia, albeit not a correlation rising to customarily accepted levels of significance, Read points out, in accordance with his findings in an earlier paper, that “perhaps the biggest source of bias was that the case subjects were drawn not from a population-wide survey but from official records of cases of abuse identified by the authorities” and that “the child victims most likely would have been removed from their homes and offered some kind of support or therapy”, concluding that “perhaps the lesson here is not that childhood sexual abuse has no aggravating effect on psychotic symptoms, but that reporting the abuse, being believed, and receiving help and support has a mitigating effect”.

As further stated by Patrick D. Hahn, “Nine of the eleven studies reviewed by Read and his colleagues looked for a dose-dependent relationship between childhood maltreatment and psychotic symptoms. All nine found it. One study found that those who had experienced five or more different types of childhood maltreatment were 200 times more likely to be diagnosed as psychotic than those who had not experienced any.” 

He goes on to say that “paranoia and delusions may also have their roots in childhood trauma. Paranoia stems from a state of hypervigilant awareness, which may well be essential to surviving an abusive situation, in which violence may be unleased on the child at any moment. Delusions are a cognitive attempt to make sense out of the paranoid emotional state.”

Hahn acknowledges that “since Read and his co-authors published their findings, at least thirteen narratives or systemic reviews (including eight meta-analyses) have been published on the correlation between adverse child experiences and psychosis… there is no longer any doubt: the correlation of schizophrenia and related disorders with trauma and other adverse childhood experiences is robust, reliable, and dose-dependent. It cuts across national boundaries, income brackets, and ethnic identities. It has been verified again and again in prospective cohort studies, population-based cross-sectional studies, and case-control studies.”

Useful Literature

Rethinking Madness, 2012, Paris Williams, Sky’s Edge Publishing.

Madness Explained, 2004, Richard Bentall, Penguin Books.

Psychosis, Trauma and Dissociation, Second Edition, 2019, Andrew Moskowitz, Wiley Blackwell.

The Gene Illusion, 2004, Jay Joseph, Algora Publishing.

The Missing Gene, 2006, Jay Joseph, Algora Publishing.

The Trouble with Twin Studies, 2015, Jay Joseph, Routledge.

Schizophrenia and Genetics, 2022, Jay Joseph, Routledge.

De-Medicalizing Misery, 2011, Mark Rapley, Palgrave Macmillan.

De-Medicalizing Misery II, 2014, Mark Rapley, Palgrave Macmillan.

Madness and Genetic Determinism, 2019, Patrick D. Hahn, Palgrave Macmillan.

The Trauma Model, 2007, Colin A. Ross, Manitou Communications, Inc.

The Genetics of Schizophrenia, 2020, Colin A. Ross, Manitou Communications, Inc.

The Assault on Truth, 1992, Jeffrey Masson, Fontana.

Against Therapy, 1989, Jeffrey Masson, Collins.

Deadly Medicines and Organized Crime, 2013, Peter C. Gøtzsche, Radcliffe Publishing.

Toxic Parents, 1991, Susan Forward, Bantam Books.

Banished Knowledge, 1991, Alice Miller, Anchor Books.

Breaking Down the Wall of Silence, Revised Edition, 1997, Alice Miller, Virago.

The History of Childhood, 2006, Lloyd deMause, Rowman & Littlefield.

Toxic Psychiatry, 2003, Peter Breggin, HarperCollins.

Interpretation of Schizophrenia, 1974, Silvano Arieti, Basic Books.

How to Become a Schizophrenic, Third Edition, 2003, John Modrow, iUniverse.

Blaming the Brain, 1998, Elliot S. Valenstein, The Free Press.

Soul Murder, 1973, Morton Schatzman, Allen Lane.

Sanity, Madness and the Family, 1970, R.D. Laing, Pelican Books.