“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, 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, pp. 32-32
“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. Mere exposure to evidence about context is therefore unlikely to be the whole answer as it will simply be neutralized in the ways I have described ... 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, 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, 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 and pathological symptoms of illness or disorder rather than meaningful responses to serious problems and adversity in people’s lives and relationships.”
Jacqui Dillion, De-Medicalizing Misery, p. 156
“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, 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, 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, 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, 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, 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 drugs.1 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 all.2
Other (PET) studies fail to find high numbers of any dopamine receptors in schizophrenics.3 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, 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 for 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.” 4
Eliot S. Valenstein, Blaming The Brain, pp. 159-160.
4. The New York Times, 20th June 1994, p. A11.
“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.’”5
Eliot S. Valenstein, Blaming The Brain, pp. 160-161
5. M. P. Durmont, the nonspecificity of mental illness, The American J. of Orthopsychiatry, 1984, 54, 326-34 (quotation from pp. 327-28).
“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, 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, pp. 50-52
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