The Less Than Jolly Heretic, 4th Edition [preview 3]

Chapter Three: Psychiatry is a Sham

 

Having attended the local clinic for an interview with the Israeli psychiatrist I was briefly placed under (as they changed my psychiatrist yet again soon after), some time into Spring 2022, I was able to temporarily quit taking those blasted ‘meds’ – I say ‘temporarily’ as the later months of the trial, leading up to my April 2025 day of sentencing in court undid any progress I had made in clawing back bodily sovereignty, given that I was sectioned boldly in July 2024 and not allowed out at all, despite no signs of psychosis four days into my stay, unless I signed their treatment order at the end of six hideous weeks of increasingly impotent verbal self-defence – albeit first having to invoke the first principle of The Nuremberg Code on her (which she promised she would look up on her smartphone later). This principle states unequivocally that: 

The voluntary consent of the human subject is absolutely essential. This means that the person involved should have legal capacity to give consent; should be so situated as to be able to exercise free power of choice, without the intervention of any element of force, fraud, deceit, duress, overreaching, or other ulterior form of constraint or coercion; and should have sufficient knowledge and comprehension of the elements of the subject matter involved as to enable him to make an understanding and enlightened decision. This latter element requires that before the acceptance of an affirmative decision by the experimental subject there should be made known to him the nature, duration, and purpose of the experiment; the method and means by which it is to be conducted; all inconveniences and hazards reasonably to be expected; and the effects upon his health or person which may possibly come from his participation in the experiment. The duty and responsibility for ascertaining the quality of the consent rests upon each individual who initiates, directs, or engages in the experiment. It is a personal duty and responsibility which may not be delegated to another with impunity.

She pleaded fervently with me, and scolded me, and launched into a sales pitch for the efficacy of Big Pharma brain-poisons, then pleaded some more whilst reminding me of her authority and professional expertise, then counselled me on how ill I had been back in late December (prodding tyres with twigs, punching corrupt officials, and, most importantly, disagreeing with the government presumably being the height of insanity – my earlier, genuine madness in the face of despair not mentioned by her, as if her memory was short and each new episode had overridden the previous), and how much she cared about me and was worried for my health (though there were then no visible signs of madness), then simultaneously scolded and pleaded a little longer until eventually relenting after approximately 45 minutes and dismissing me from the room with a very sharp glance, closing her folder of notes with a snap, pressing the button to release the bolts of the secure door, and informing me that I would still be kept on their system, and that, in the event of any sign of future illness, it would be very likely that she would thoroughly review this decision on her part to allow me (presumably!) to retain free informed choice over bodily sovereignty in the face of a vast, full-spectrum dominance machine of genocidal, pseudo-medical, anti-European, Police State liberal egalitarian anarcho-tyranny, stretching from under 6368.164 generous miles from the centre of the earth’s core (if one includes some potential modern military installations, which will have to remain unnamed) to more than a few metres outside the thermosphere, with the only pushback opportunity presenting, very occasionally, as the equivalent of a single looser (serrated) flange nut.

I had wanted to explain more of my position to her, as she took a keen interest in noting down that, in her words, I had “political opinions”. If anything, I hate politics. Activists and mobs infuriate me. What is it with these people, making every philosophical or scientific societal analysis into a matter of politics or ideology as if there was no difference? Yes, I know quite a bit about politics. Still, I prefer talking about significant, vital – civilisational scale – problems in our culture and our race to hearing about the toing and froing of various politicians and dignitaries, and the endless armchair spiel of journalists and disc jockeys, and the talking heads of nightly podcasts or TV panel programs, and current affairs broadcasting is as asinine as it is never-ending. I don’t care about this or that president or political faction or what any little group is up to, seeing them as all the same. I don’t vote, and I don’t campaign or hold any memberships. I’m certainly not an activist.

It was probably not worth her while being made aware of these minor considerations as she was pretty content cradled in her current mental predicament. Besides, I knew I would be considered totally mad by conventional internal mandate. My speech idioms, turns of phrase, and especially my lexicon and referential allusions don't do me any favours with these people. That, coupled with my frequent gesticulations, a rapid rate of speech, and a quiet, muffled, often stuttered delivery hampered by missing teeth, has led to much communication breakdown and an inability on their parts to interpret my thoughts, much as they're lazy enough to fill in the blanks in understanding with their ranked assumptions, evidently pushed for time.

I also wanted to inform her that biomedical psychiatry is a sham. Despite their enthusiasm for destroying contrary lives and making too much money, psychiatrists have never found any physiological pathology behind mental disorders. No genes for mental illness have ever been found, and not for the lack of a near century's determined and well-funded, heavily promoted research. No neurological lab test can determine who is mentally ill. There is no genuine proof of chemical imbalances. They claim all the time that they're making terrific progress and are just on the cusp of working it out and that they will be there ‘any generation now, shortly, probably within a decade,’ but genuinely, this is a fallacious claim and it's all pseudoscience, albeit damningly extensive, firmly entrenched, with enormous societal power.

I had quietly asked the psychiatrist whether neuroleptic drugs themselves can stimulate episodic psychosis or brain damage on account of brain shrinkage and the long-term alteration of brain chemistry, let alone what the other severe impacts of side effects would be. I knew the answer to my question already. I have quite a lot of formal research literature on the matter, including PDF copies of the original research papers of the studies themselves.

A few that spring to mind from the modest hand-grabbed sample of 78 recent drug-harm papers (out of several thousand) stored on my computer would be the 2020 study by Tomi Bergström of the Department of Psychiatry in the Länsi-Pohja Hospital District in Kemi, Finland for Schizophrenia Bulletin Open that states, “The overall findings are in line with previous observational studies, in which long-term maintenance treatment—and thus higher exposure to antipsychotics—was associated with adverse outcomes,” and the 22nd June 2010 research in the British Medical Journal by Chris Parker, Carol Coupland and Julia Hippisley-Cox, titled “Antipsychotic drugs and risk of venous thromboembolism: nested case-control study”, which informs us that:

Venous thromboembolism is an important and preventable cause of morbidity and mortality. Up to a quarter of affected patients die within a week, and almost a third of survivors experience long term effects. Some research has indicated that antipsychotic drugs, some of which are also widely prescribed for nausea, vomiting, and vertigo, might be associated with an increased risk of venous thromboembolism.

The paper goes on to explain that, in other studies:

One case-control study found a sevenfold risk of venous thromboembolism among current users of antipsychotic drugs (Zornberg G, Jick H. “Antipsychotic drug use and risk of first-time idiopathic venous thromboembolism: a case-control study”. Lancet 2000;356:1219-23.), and another a 13-fold risk of death from pulmonary embolism (Parkin L, Skegg D, Herbison G, Paul C. “Psychotropic drugs and fatal pulmonary embolism”. Pharmacoepidemiol Drug Saf 2003;12:647-52.). ... A hospital based case-control study found a 3.5-fold risk associated with antipsychotics, with a lower risk for atypical drugs than for conventional drugs.(Lacut K, Le Gal G, Couturaud F, Cornily G, Leroyer C, Mottier D, et al. “Association between antipsychotic drugs, antidepressant drugs and venous thromboembolism”: results from the EDITH case-control study. Fundam Clin Pharmacol 2007;21:643-50.) ... A further cohort study focused on the atypical clozapine and found that current users had a fivefold risk of death from pulmonary embolism compared with past users (Walker A, Lanza L, Arellano F, Rothman K. “Mortality in current and former users of clozapine”. Epidemiology 1997;8:671-7.).

The authors state in their own results:

There were 25 532 eligible cases (15 975 with deep vein thrombosis and 9557 with pulmonary embolism) and 89 491 matched controls from a study population of 7 267 673. Individuals prescribed antipsychotic drugs in the previous 24 months had a 32% greater risk of venous thromboembolism than non-users, despite adjustment for potential risk factors ... Patients who had started a new drug in the previous three months had about twice the risk. ... The risk was greater for individuals prescribed atypical rather than conventional drugs ... It also tended to be greater for patients prescribed low rather than high potency drugs.

Thus the study concludes that: “There is an association between use of antipsychotic drugs and risk of venous thromboembolism in a large primary care population. The increased risk was more marked among new users and those prescribed atypical antipsychotic drugs.”

A further study of “Associations Between Venous Thromboembolism and Antipsychotics” conducted by Staffan Hägg from the Division of Clinical Pharmacology, Linköping University Hospital, Linköping, Sweden and Andrew Bate from the Uppsala Monitoring Centre, WHO Collaborating Centre for International Drug Monitoring, Uppsala, Sweden utilising the WHO Database of Adverse Drug Reactions (Drug Safety 2008; 31 (8); 685-694) found that “in the WHO ADR database, VTE was reported more often in combination with second-generation antipsychotic drugs and with the individual drugs olanzapine, sertindole, zuclopenthixol and clozapine than would he expected based on general reporting patterns in the dataset. ... In our study, the median age of the patients in the reported cases of VTE in users of olanzapine, sertindole or zuclopenthixol was between 37 and 52 years. The IC value was statistically significant for both olanzapine and clozapine in the younger (0-55 years) age group, but only for clozapine in the older age group (>55 years). Thus, young patients may also be at risk for this possible ADR.”

 The 1987 brief report by James B. Wade and Michael Alan Taylor in Biological Psychiatry titled “Tardive Dyskinesia and Cognitive Impairment” is also helpful to consult, where the results reveal:

A modest, but statistically significant, relationship between tardive dyskinesia and cognitive functioning in psychiatric patients, even after accounting for the effect of illness variables and motor speed. These findings are consistent with those of Famuyiwa et al. (1979), lending support to the hypothesis that tardive dyskinesia may represent the extent or severity of a chronic neuroleptic-induced neurotoxic process.

One could examine Peter C. Gøtzsche’s working preview of  Chapter 4 of the 2023 release Psychological Interventions for Psychosis: Towards a Paradigm Shift, edited by Juan Antonio Díaz-Garrido, Raquel Zúñiga, Horus Lafitte, and Eric Morris. Indeed, he estimates that just one neuroleptic drug, Olanzapine, has killed 200,000 patients up to 2007 (Gøtzsche, 2013).

We could consider the review article by J. Moncrieff of the Department of Mental Health Sciences, University College London, and J. Leo of the  Department of Anatomy, Lincoln Memorial University, Harrogate, TN, in Psychological Medicine, published by Cambridge University press in 2010, and titled “A systematic review of the effects of antipsychotic drugs on brain volume” that states in its conclusion that: “Some evidence points towards the possibility that antipsychotic drugs reduce the volume of brain matter and increase ventricular or fluid volume. Antipsychotics may contribute to the genesis of some of the abnormalities usually attributed to schizophrenia.”

Then there’s the famous 2011 paper by Peter R. Breggin from the International Journal of Risk & Safety in Medicine 23 titled “Psychiatric drug-induced Chronic Brain Impairment (CBI): Implications for long-term treatment with psychiatric medication” that shows us that:

The clinical effect of chronic exposure to psychoactive substances, including psychiatric drugs, produces effects very similar to those of close-head injury due to traumatic brain injury (TBI) or the Postconcussive Syndrome. Generalized or global harm to the brain from any cause produces very similar mental effects. The brain and its associated mental processes respond in a very similar fashion to injuries from causes as diverse as electroshock treatment, closed head injury from repeated sports-induced concussions or TBI in wartime, chronic abuse of alcohol and street drugs, long-term exposure to psychiatric polydrug treatment, and long-term exposure to particular classes of psychiatric drugs including stimulants, benzodiazepines, lithium and antipsychotic drugs.

This research is backed up by numerous other papers, including that by Husa, A. P. and Moilanen, J. Published in 2017 in Psychiatry Research, 247, 130-138. Titled “Lifetime antipsychotic medication and cognitive performance in schizophrenia at age 43 years in a general population birth cohort” which suggests: “In this study higher lifetime cumulative dose-years of any antipsychotics were significantly associated with poorer global cognition at the age of 43 years in schizophrenia, when the most important confounding factors related to duration and severity of illness were controlled for. ... The cognitive effects of typical and atypical antipsychotics were similar.”

The long-term outcomes literature for drug treatment of schizophrenia is helpfully collected in the April 12th, 2015 section of the Mad in America website titled “Antipsychotics/Schizophrenia”, which states: “The long-term outcomes literature for antipsychotics, which has been compiled over a period of nearly 60 years, consistently tells of drugs that increase the likelihood that a person diagnosed with schizophrenia will become chronically ill. ... It seems paradoxical that drugs that ameliorate acute psychotic symptoms over the short term will increase the likelihood that a person so treated will fare poorly over the long term. But that disturbing fact showed up in the very first outcome studies, and has continued to show up ever since.”

This section highlights the original NIMH follow-up study of Nina R. Schooler and Solomon C. Goldberg published in the American Journal of Psychiatry 123 (1967): 986-995, titled “One Year After Discharge: Community Adjustment of Schizophrenic Patients”.  This NIMH study looked at one-year outcomes for 299 patients who had been treated either with neuroleptics or placebo upon their admission to a hospital. This was the first long-term study conducted by the NIMH, and the researchers found that patients who received placebo “were less likely to be rehospitalized than those who received any of the three active phenothiazines.”

In the late 1970s, two physicians at McGill University, Guy Chouinard and Barry Jones, released four papers identifying the biological changes induced in the brain by antipsychotics that led to the high relapse rates for drug-treated patients (“Dopaminergic Supersensitivity after Neuroleptics”, Muller, P. Psychopharmacology 60 (1978):1-11; “Neuroleptic-induced Supersensitivity Psychosis”,  Chouinard, G. American Journal of Psychiatry 135 (1978):1409-1410.; “Neuroleptic-induced Supersensitivity Psychosis”, Chouinard, G. American Journal of Psychiatry 137 (1980):16-20.; “Neuroleptic-induced Supersensitivity Psychosis, the “hump course” and tardive dyskinesia”, Chouinard, G. Journal of Clinical Psychopharmacology 2 (1982):143-4.).

Because the drugs dampen dopamine activity, the brain tries to compensate by becoming “supersensitive” to dopamine. In particular, the drugs trigger an increase in the density of dopamine receptors. This perturbation in dopamine function, over the long term, makes the patients more biologically prone to psychosis and to worse relapses upon drug withdrawal. Chouinard and Jones concluded: “Neuroleptics can produce a dopamine supersensitivity that leads to both dyskinetic and psychotic symptoms. An implication is that the tendency toward psychotic relapse in a patient who has developed such a supersensitivity is determined by more than just the normal course of the illness.”

However, since the early 1980s psychiatry has mostly ignored the problem of “neuroleptic-induced supersensitivity psychosis”. But since that time there have been a number of long-term outcome studies that have confirmed the fact that antipsychotics increase the likelihood a person will become chronically ill, including the paper by Anne-Noël Samaha and Philip Seeman in The Journal of Neuroscience, March 14, 2007 titled ““Breakthrough” Dopamine Supersensitivity during Ongoing Antipsychotic Treatment Leads to Treatment Failure over Time” which states in its results:

Our results suggest that an antipsychotic-induced increase in dopamine sensitivity might predispose certain individuals to psychotic relapse. ... Together, the present findings allow us to propose the following: (1) initially, antipsychotics block D₂ receptors, and increase dopamine and dopamine turnover in a system where levels of D₂ receptors and D₂^High receptors are normal. At this stage the balance of agonist (i.e., endogenous dopamine-related) drive and receptor blockade allows the antipsychotic to exert a net antidopaminergic effect. (2) With continued treatment, there is a decrease in turnover on the presynaptic side, D₂ blockade by antipsychotics is maintained, but both D₂ receptor numbers and D₂ High sites are elevated. At this later stage, endogenous dopamine drive is potentiated and can more readily oppose the antidopaminergic effects of the antipsychotic. This might explain why antipsychotics so often fail.

Indeed, during the 1990s, researchers using MRI technology discovered that antipsychotics shrink the frontal lobes and cause an enlargement of the basal ganglia. In the “Follow-up Magnetic Resonance Imaging” study of schizophrenia by Raquel E. Gur for Archives of General Psychiatry 55 (1998):145-152, researchers reported that the enlargement of the basal ganglia was associated with a worsening of both the positive and negative symptoms of schizophrenia. This was powerful evidence of how the drugs cause chronic illness over time. 

Finally (for the moment), from 2003 onwards, Nancy Andreasen, the former editor of the American Journal of Psychiatry, began reporting on her large MRI study of schizophrenia patients treated with antipsychotics, in the paper “Progressive Structural Brain Abnormalities and Their Relationship to Clinical Outcome” published in Arch Gen Psychiatry. 2003;60:585-594. She found that the patients progressively lost “frontal white matter volume,” and that this brain shrinkage was associated with a worsening of negative symptoms, increased functional impairment, and, after five years, cognitive decline. In a 2011 article titled “Long-term Antipsychotic Treatment and Brain Volumes” for Arch Gen Psychiatry. 2011;68(2):128-137, she reported that this shrinkage was drug-related. Use of the old neuroleptics, the atypical antipsychotics, and clozapine were all “associated with smaller brain tissue volumes,” with decreases in both white and grey matter. The severity of illness and substance abuse had “minimal or no effect” on brain volumes.

Clearest of all, and most damning, in the 15-year outcomes study by Martin Harrow and Thomas H. Jobe for the Journal of Nervous and Mental Disease 195 (2007): 407-414., titled “Factors involved in outcome and recovery in schizophrenia patients not on antipsychotic medications: a 15-year multifollow-up study” we read that NIMH-funded researchers followed the long-term outcomes of schizophrenia patients diagnosed at two Chicago-area hospitals in the late 1980s, and found that at the end of 15 years, 40% of the schizophrenia patients who had stopped taking antipsychotics were recovered, versus 5% of those who had stayed on the drugs. Long-term outcomes for patients with “other psychotic disorders” were also much better for those off antipsychotics than for those who stayed on the medications.

As I wrote in one of the addendum sections of my other print book, the two-part childhood psychiatric autobiography, Consumption: Memories of my Childhood:

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 planning (Hagen et al., 2010; Keefe, Bollini, & Silva, 1999).

And:

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 life” (Breggin, 2008a.) … [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 antipsychotics (Hagen et al., 2010, p. 50.). These participants described the antipsychotics as resulting in “not feeling anything,” “feeling isolated,” “being completely numb,” and feeling like “a complete, drooling zombie”(Ibid.)

 And, disastrously:

...in Chapter 5, Williams highlights that “[Guy] Chouinard and his research team (Chouinard et al., 1978.) 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 today (Whitaker, 2010.) 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 ganglia (Chakos et al., 1994; Gur et al., 1998; Madsen, Keiding, Karle, Esbjerg, & Hemmingsen, 1998.) , changes which have been demonstrated to increase the severity of both positive and negative psychotic symptoms (Gur et al., 1998.) … 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.”

As further comment, one could consider Peter Kinderman’s introduction to the paradigm-shift necessary if psychological health treatment is to survive for the future (and firm critique of bio-reductionist psychiatry), A Prescription for Psychiatry, published by Palgrave Macmillan in 2014, where he writes, in Chapter 3:

...taken longer term, these drugs have serious, life-changing adverse effects. These negative effects, sometimes euphemistically called ‘side-effects’, can include a condition that resembles Parkinson’s disease – with shaking, muscular rigidity and problems with walking and movement – and even reduced brain size in people who have been taking ‘antipsychotic medication’ for a long time. Because they affect various physical systems, such as our heart, liver, and kidneys, as well as our brains, and because one of the common adverse effects is a significant gain in weight (itself physically dangerous [on account of diabetes]), these drugs can have a significant impact on our health. ... [T]hey don’t target biological abnormalities specific to psychosis, and don’t return people to ‘normal’. They just have the kinds of effects that psychoactive drugs are recognised to have. ...[They] can reduce emotional distress. ... but it is not quite the same thing as reducing psychosis. ...[Patients] will often find their fears much less preoccupying and distressing ... That sounds a lot like the effects of opioid street drugs like heroin.

He goes on to say on the following page:

...the emerging evidence, summarised in books by Richard Bentall, Robert Whitaker and Jo[anna] Moncrieff [See R. Bentall (2009) Doctoring the Mind: Why Psychiatric Treatments Fail; R. Whitaker (2010) Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs, and the Astonishing Rise of Mental Illness in America; and J. Moncrieff (2013) The Bitterest Pills: The Troubling Story of Antipsychotic Drugs] strongly suggests that for most people the long-term benefits of antipsychotic medication are significantly outweighed by their profound adverse effects. And it looks very much as if the levels of psychosis, and ‘relapse’ rates, are no higher in people who lead medication-free lives than in people who take antipsychotic medication on a long-term basis. In other words, these drugs don’t appear to prevent relapse. And because these drugs have very profound side-effects, those people who take the medication on a long-term basis often experience significant physical health problems, as well as emotional blunting, sedation and suppression of creativity and imagination.

Furthermore, regarding the newest range of atypical antipsychotics, often publicised by psychiatrists as ‘safe’ and ‘side-effects free’ (particularly with the increasingly prevalent use of aripiprazole – ‘Abilify’), in a paper titled “A systematic review of reported cases involving psychotic symptoms worsened by aripiprazole in schizophrenia or schizoaffective disorder” published by Hiroyoshi Takeuchi and Gary Remington on 5th July 2013 in Psychopharmacology  Volume 228, pages 175–185 we find, drawn from their methods, that:

A systematic literature search was conducted on August 18, 2012, using the PubMed and the EMBASE. Twenty-two cases met the following inclusion criteria: (1) diagnosis of schizophrenia or schizoaffective disorder, (2) worsening of psychotic symptoms associated with aripiprazole, and (3) aripiprazole dose ≤30 mg/day. Information about the causal relationship between aripiprazole and increased psychotic symptoms was extracted. The quality of the causal relationship was evaluated according to the modified guidelines for evaluation of drug-associated events and classified as “questionable,” “moderately suggestive,” or “highly suggestive.” 

In this case the results were as follows:

Patients were chronic in at least 15 cases, and prior antipsychotic dose exceeded recommended guidelines in 19 cases. Psychotic symptoms worsened after simply adding aripiprazole to the current regimen in eight cases. Besides psychotic symptoms, increasing agitation (nine cases), aggression (11 cases), and/or activation (seven cases) were reported. Clinical resolution occurred after aripiprazole discontinuation in eight cases. Regarding causal relationship, 11 cases were classified as “highly suggestive,” three as “moderately suggestive,” and eight as “questionable”

The experimenters’ conclusions were that:

Clinicians should be vigilant when adding aripiprazole to patients with chronic schizophrenia also receiving relatively high doses of other antipsychotics, and discontinuation of aripiprazole should be considered if psychotic symptoms and/or agitation/aggression/activation increase.

Damningly, we find in John Read’s international study for Schizophrenia Bulletin – the largest study of its kind to date, employing 650 people from 29 different countries – “Using open questions to understand 650 people’s experiences with antipsychotic drugs”, published on 12th February 2020, that more than half of antipsychotic users reported only negative experiences with the drugs. As Read himself commented bitterly:

I can’t believe I have patients walking around on 800mg of this stuff. There’s no way in good conscience I could dose this ... unless a patient consented to 20 hours of sleep a day. I’m sure there’s a niche market for this med though. There has to be a patient population that doesn’t want to feel emotions, work, have sex, take care of their homes, read, drive, go do things, and want to drop their IQ by 100 points.

However, it is unlikely day to day that clinicians will ever readily agree to reduce (or drop) use of an antipsychotic on their patients though, preferring instead to deny and double down even though the evidence of harm is mounting. As one participant in Read’s study confirmed: “I was not warned about the permanent/semi-permanent effects of antipsychotics which I got.” Another one noted: “Most doctors do not have a clue. They turn their backs on suffering patients, denying the existence of withdrawal damage.”

Of course, for these medications to have any real validity outside of the ‘drug-model’ I have explained above (as opposed to the ‘disease-model’), the biomedical hypothesis (swiftly raised to a theory, and then pursued mono-mindedly at the expense of any and all psychosocial interventions) would have to have some basis in reality. Increasingly though – and arguably rather obvious from the start of the damning migration away from psychological responses to mental illness in the early 1960s, themselves a brief window of air following the ‘electro-convulsive’ memory-obliterating tortures and grisly psychosurgeries of the first half of the 20th Century (much as ‘ECT’ has never been formally withdrawn from psychiatric treatments, conducted to this day in the United Kingdom, and psychosurgery – lobotomy – is still popular in some 21st Century Latin American countries) – evidence suggests that it doesn’t. One could at least begin dismantling psychiatry’s claims by reviewing Elliot Valenstein’s Blaming the Brain, where, as one example, he writes on pages 95-96:

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.

Valenstein goes on to explain, on page 96, referencing a parallel to  the ‘hard problem’ of consciousness (famously put forward by the Australian philosopher of mind, David Chalmers):

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.

The crux of his powerful argument is displayed – again to only provide a single example from an extensive piece of empirical reasoning – by the following research from page 113 (which has been available a while, suggesting that the monolithic psychiatry industry is ignoring it rather than accepting that there is a serious problem):

…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 (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.)

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 (A. Carlsson, Early psychopharmacology and the rise of modern brain research. Journal of Psychopharmacology, 1990, 4, 120-26 ... 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.)

Other (PET) studies fail to find high numbers of any dopamine receptors in schizophrenics (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).

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 clear 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.”

Peter Breggin’s Toxic Psychiatry, and the many book presentations of Joanna Moncrieff, such as her two-part work with Jacqui Dillon, Ewen Speed, and Mark Rapley, De-medicalizing Misery, are also worth evaluating, and especially Jay Joseph’s twin-studies exposures in The Gene Illusion and The Trouble with Twin Studies, where the ‘Equal Environment Assumption’, where reared together MZ pairs (monozygotic  - identical - twins) are compared with reared together same-sex DZ pairs (dizygotic – fraternal – twins), works on the assumption that they grow up experiencing roughly equal shared home environments. Twin researchers believe that MZTs share 100 percent of their segregating genes. In contrast, DZTs share only 50 percent on average,  so their conclusion is that the more remarkable resemblance of MZTs versus DZTs indicates that the behaviour has a significant genetic component. Thus, given that their environment is considered equal, the more remarkable behavioural resemblance of MZT versus DZT pairs can only be caused by genetic factors.

However, as Joseph rightly expands upon, “by the mid-1960s, it was clear to most critics that the twin method was based on the “fallacy” that MZT and DZT environments were equal (Bleuler 1978, Penrose 1973, Stocks, 1993)”.

Joseph quotes the Finnish schizophrenia twin researcher Pekka Tienari in saying:

It is doubtful … whether the difference in concordance rate between identical and fraternal groups of twins can, as such, be ascribed to hereditary factors. In all likelihood,  the environment, too, is more similar in the case of identical than in the case of fraternal twins … Furthermore, it is obvious that the intensity of the mutual relationship of identical twins in considerably greater than that of siblings in general and, also, of fraternal twins … It is apparent that the differences in  concordance rates between groups of identical and fraternal twins, as well as between female and male twin pairs, are partly attributable to environmental (psychological) factors. (Tienari, 1963, pp. 119-121)

Joseph explains, however, that despite this acknowledgment by critics, “twin researchers were successful in preserving the twin method mainly on the basis of: (a) using circular arguments and committing other logical fallacies; (b) changing the definition of the EEA; or (c) denying, ignoring, or downplaying the evidence that MZT and DZT environments are different (Joseph 2004, 2010a, 2012; Lewontin, Rose, & Kamin, 1984; Pan Kemker, Ross, & Golden, 1996)”.

He ends by suggesting that “we can conclude that previously reported twin method MZT-DZT comparisons in the social and behavioural science have recorded nothing more than the role of non-genetic influences on human behavioural characteristics. Critics have argued for decades that the twin method is unable to disentangle the potential roles of genetic and environmental influences … [This] does not mean that twin studies “overestimate heritability” or that researchers should assess the EEA on a study-by-study basis, but instead indicates that the twin method is no more able than a family study to disentangle the potential influences of genes and environment. … This leads to the conclusion that genetic interpretations of all past, present, and future MZT-DZT twin method comparisons in the social and behavioural sciences must be rejected outright.”

As Jay Joseph informs us in the conclusions of his follow-up research account, The Missing Gene, having just explained why there is little evidence in support of psychiatry’s genetic claims being more than pseudoscience, in thorough detail and with much rigorous evaluation of multiple examples, “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.”

There is much now available in the research papers world expressing why the claim that there is a gene for schizophrenia and other mental disorders (or the phenomenon of multiple gene action) is fallacious. Again, just as a start, one could consider the scientific article in the American Journal of Psychiatry (Am J Psychiatry 2008; 165:497–506, available from ajp.psychiatryonline.org) titled “No Significant Association of 14 Candidate Genes With Schizophrenia in a Large European Ancestry Sample: Implications for Psychiatric Genetics”, by Alan R. Sanders, et al., which states in its results:

Neither experiment-wide nor gene-wide statistical significance was observed in the primary single-SNP analyses or in secondary analyses of haplotypes or of imputed genotypes for additional common HapMap SNPs. Results in SNPs previously reported as associated with schizophrenia were consistent with chance expectation, and four functional polymorphisms in COMT, DRD2, and HTR2A did not produce nominally significant evidence to support previous evidence for association. 

In its conclusion, the article still adopts the weary psychiatric researcher trope of over-optimistically clutching at straws for the future, in case things may somehow get better then on account of genome-wide association methods (themselves comprehensively debunked by Jay Joseph in Schizophrenia and Genetics: The End of An Illusion, 2023), but it is clear for the moment that they have been forced reluctantly to concede defeat:

Our results suggest that, taken together, common DNA variants in these 14 genes are unlikely to explain a large proportion of the genetic risk for schizophrenia in populations of European ancestry. More robust findings are likely to be discovered using genome-wide association methods and, as our knowledge of the biology of mental illness continues to improve, focused studies of genes based on more precise mechanistic hypotheses. Nevertheless, although larger samples could possibly detect small genetic effects that were missed in this experiment, our findings suggest it is unlikely that true associations exist at the population level for the alleles that have formed the basis for the large candidate gene literature for these 14 postulated schizophrenia candidate genes.

Briefly, one could further consider the paper by Barondes, S. et al. (1999) titled An Agenda for Psychiatric Genetics. From Arch. Gen. Psych. 56: 549-552. (“genetically influenced psychiatric disorders have so far been resistant to analysis”), or the January 20th, 2024 article by Peter Simmons for the Mad in America website, titled “Searching for the “Psychiatric Yeti”: Schizophrenia Is Not Genetic”, reviewing the work of schizophrenia researcher E. Fuller Torrey.

Torrey further quotes from researchers Rudolf Uher and Michael Rutter, writing in 2012 in Vol. 24, Issue 6 of the International Review of Psychiatry (“Basing psychiatric classification on scientific foundation: Problems and prospects”), as they admit:

It can be summarized that molecular genetic studies of psychiatric disorders have done a lot to find very little. In fact, in the era of genome-wide association studies, psychiatric disorders have distinguished themselves from most types of physical illness by the absence of strong genetic associations.

 As is clear, there is quite a lot available to explore on this topic, if only more of the general public would. I could easily go on, for many pages, but enough has been introduced for now to provide something to work with. 

It would indeed be a bonus to the serious ongoing societal problem of mental health stigma among the public (and professionals) if it can be put to psychiatrists that their nefarious theory is incorrect, as, as has been researched by Nicholas Rüsch, et al., in his National Institute of Health public access paper for  Psychiatry Res. 2010 October 30; 179(3): 328–332. (doi:10.1016/j.psychres.2009.09.010), titled “Biogenetic models of psychopathology, implicit guilt, and mental illness stigma”:

[some] research has cautioned that emphasizing biogenetic aspects of mental illness could produce the impression that mental illness is a stable, intrinsic aspect of a person (“genetic essentialism”), increasing the desire for social distance. ... Considering these mixed consequences of genetic models, the desire for social distance is a closer proxy of discriminating behavior than perceived responsibility; furthermore, behavioral consequences are likely to be more harmful for stigmatized individuals than personally held views about responsibility. Therefore, the current findings suggest that among members of the general public the negative effects of endorsing genetic models seem to outweigh the positive.

For the diagnosed individuals themselves:

First, unlike the general public, there was no evidence that endorsement of genetic causation was associated with lower explicit feelings of responsibility or weaker automatic associations between mental illness and guilt. Instead, the negative implications of a genetic essentialist view seemed to be evident, in that both greater explicit fear toward persons with mental illness and stronger automatic me-guilty associations were found among diagnosed participants who endorsed the genetic model. Perhaps because genetic qualities can be seen as deeply defining (indeed, constituting a person's essence; Keller, 2005), individuals who view their psychiatric disorder as genetic in origin may develop an irrational sense of implicit guilt because the disorder comes to be seen as a fundamental, and perhaps immutable, identity-defining trait. For stigmatized individuals, a dominant genetic view of their illness may make it difficult to develop their own narrative taking into account non-genetic factors in a more balanced fashion (Lysaker et al., 2007).

Unfortunately, these findings confirm a pessimistic prediction of the genetic essentialism perspective, in that endorsement of the genetic model was associated with increased desire to avoid persons with mental illness among the general public, and with greater explicit fear and implicit guilt among the diagnosed sample.

They conclude:

With respect to self-stigma in people with mental illness, biogenetic illness models could also lead diagnosed individuals to implicitly feel fundamentally flawed and guilty for their condition. This is consistent with previous findings that persons with schizophrenia prefer psychosocial over biogenetic explanations for their condition (Holzinger et al., 2001, 2003). People with mental illness possibly prefer psychosocial models because, among other reasons [emphasis mine: those reasons being a matter of the truth!], these models are less associated with implicit guilt or fear of their in-group members. Biogenetic models of mental illness have further been criticized by proponents of a recovery-oriented approach because they do not reflect subjective experience or meaning, central features of living with a mental illness, and are often deficit-oriented, thereby facilitating stigma (Slade, 2009). Consumers, relatives, and mental health professionals alike should therefore be cautious in promoting explanations that exclusively focus on biogenetic factors when trying to help consumers to cope better with their mental illness.

Jay Joseph goes on, in The Missing Gene, to catalogue psychiatry’s glaring research errors (his final sentiment echoed by Jonathan Latham in his 2011 article for The Guardian, titled “The failure of the genome”):

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 researchers’ beliefs than from the data itself; the interpretation of family data as evidence in support of genetics; textbooks’ creation of myths about “landmark” psychiatric genetic studies and the “overwhelming” 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 major mental disorders are unlikely to exist.

I asked my latest psychiatrist, in not quite so many words, if she thought my father's utter dismissal with scoffing contempt of my every opinion from year dot could be responsible for a great deal of my mental collapse worries, even from before Abby's feckless aura of intense, non-stop petulant argumentative chaos and the Terrorist/Reckless Terrorist-enabler accusation stress. The latter conclusion is the reason for the official charges, for the ownership and transmission of that contraband defence literature by the likes of Ragnar Benson and Kurt Saxon – notorious names in the American survivalist community – but in practice the former erroneous slur takes complete precedence in how I was (and still am) judged by those aware of the arrest, friends, family, and especially local State service acquaintances. My father himself said to me at the time “you know, perhaps it’s for the best that you go to jail, given all you’ve done...”, words which totally destroyed me

Did my father’s all-out ridicule of my intelligence, and critical cold shoulder towards my creative works, and bouts of physical violence and sadistic bullying, when I was 18 and 5 respectively, and inability to ever say ‘I love you’ to me, and his snide, insulting, belittling – humiliating – remarks if I disagreed with him, especially in public (although familiar over the phone these days), and all this for the first 29 years of my life (though ongoing up until he got too old and sick to continue effectively), have anything to do with my problems did she think?

Did his total gaslighting denial and consistent downplaying of my history of sexual abuse at the hands of a couple of other abusive humans have any part to play? I was abused in harrowing fashion once – so much so that to this day I have total amnesia over the events past a certain point, other than to experience the ramifications of prolonged rectal bleeding later – when I was very small, by a gang of untraceable paedophilic foreigners (I was too young to identify them accurately, beyond their races, and the attack happened in near-darkness, under cover of trees), then again three main times by a savage Pakistani moron less than a year older than my age, in a posh country house bedroom from 11 to 13 (and indeed at my own parents’ house!), where, on one occasion, I learned, unfortunately, what excrement tastes like, having had it forced in my mouth scant weeks before being anally (re-)raped whilst asleep, not that that teenage abuser didn’t just mock me regularly when in company and batter the hell out of me on the sly, the mockery lingering for years afterward.

I remember the further horror and shame of not only being groped across my genitals and the frottage of his sweating, stinking body on my upper thigh but the force directed at me to touch his genitals also, on fear of violence. Smearing me in bloody pus and excrement from the dead chicks in his mother’s outhouse incubator was another particularly unpleasant moment. There was the time he insisted on playing a game, accompanied by his Gypsy neighbour, in which they tied me to his bedpost and whipped me painfully with a skipping rope.

He turned out to be an exceedingly sick individual behind closed doors, not that it ever came out in the company of his laddish European peers, a very popular and well-respected student among the cool set. My mother informed me once that she was cooking in our kitchen during a visit by him and had felt him deliberately rub up against her from behind also. I remember at 14, when his mother, a Western woman married to his Pakistani father, would accompany her son into their downstairs toilet and wipe his arse for him on command. She’d been at this for years. I hung around with him for too long, still. Generally, day-to-day, it would just be mockery, put-downs, and jokes in company at my expense.

Public school was a nightmare for me, my first steady experience of terrible loneliness and a source of daily fear and sadness; bullied relentlessly for almost ten years, day in and day out, never accepted by the other pupils, and always an ostracised outsider, quiet, timid, and increasingly morose. I spent my time reading in the school library, or taking long walks or runs out into the surrounding countryside, sitting down in the long grass by the river and writing little nature sonnets in Romantic poetry in my notepad based on what I observed, or drawing and sketching for hours, fantasy art and illustration based on British artists such as Rodney Matthews and Ian Miller, and inspired by the classical Flemish resonances of Jacek Yerka’s intricate, brooding surrealist paintings.

As a child, I took violin and viola lessons and participated in a children’s orchestra and a string quartet; my favourite string recital was a performance of Fratres by Arvo Pärt. Additionally, at 13, I learnt to play the bagpipes from a friend of the family, composing my melodies with a biro on the staves at the rear of my piping tutor books, based on the marches, retreats, and strathspeys I already enjoyed playing, such as The Earl of Mansfield, The Green Hills of Tyrol, or Dorrator Bridge. I regularly participated in local country dances and piped at a Burns Night supper as a 16-year-old with my now-trained lung capacity.

At home, I continued to read, draw, and explore nature, looking forward to weekend walks with my parents through Danbury Woods and the lakes at Twitty Fee or cycling down the country lanes outside my village, watching the fish in the pond at the top of my street, or feeding the ducks at the waters of the village green, walking across the fields and meadows of cows, sheep, and horses close beside me, or flying kites on the hills of Hylands Park, exploring the ageing stones and statues by the stately home gardens. 

The school was always abysmal for me, though, and a prolonged, painful experience. I got on with all but one of the teachers and focused on my academic work, having no real choice otherwise, given the hell of everything else, but I still found the work quite enjoyable. It was never enough to make up for my horror around the other pupils. I sometimes wonder if my grades could have been higher were I not always so set-upon, scared, low, distracted, hurt, and worried.

I was pleased when I won an academic scholarship that cut my school fees significantly and then admission to the highest sets, with steady good marks and class prizes. Still, my GCSE results disappointed me, as did my A levels, and I felt I could have done much better and had no confidence in my academic abilities. I still don’t really. A 2:1 bachelor’s degree at university made me particularly displeased with myself. Having to postpone my master’s degree in Formal Linguistics in the second year on account of a returning heavy depression upset me greatly as someone who has never had much faith in myself.

Though my parents sometimes complimented my grades, and teachers seemed pleased enough, I’m not used to receiving praise or compliments. For most of my adult life, it’s been quite the opposite. I can’t remember any adult friends ever having a particularly kind word for me, much as a few enjoyed my company. As far as I remember, I’ve never received a compliment from Abby, neither physically nor over my mental qualities, and she doesn’t take any interest in my thoughts, interests, creative works, or constructions. I’m used to being chided, joked over, or ridiculed. I think I have some reputation with others for being bumbling or slow-witted, somehow a bit of a moron, almost like a special needs case. I notice this in their general interactions, at least.

 I’m used to new friends trying to push their luck or testing limits and bossing me about. I can’t comment too much on this as I don’t know many people in close contact. I could count genuine friendships I’ve made over 20 years since school on the fingers of one hand (and some of those people are dead), much as I’ve interacted with quite a few acquaintances. I don’t know anyone anymore who I would consider close to me (bar one very obliging ‘penpal’ friend and fellow independent researcher, over 8000 miles away from me across the Atlantic). Now and again, I see one person face to face, but it’s incredibly one-sided, and I seldom get to express much from my perspective.

I am not used to meeting people who can understand that human day-to-day discussion does not rely on full lockstep pre-agreement or even an immediate drive for instantaneous agreement at all and that it is indeed - or was once - perfectly possible to converse with someone who disagrees with you on your perspectives, either in their general awareness of your ideas, or in the shared conversation itself, without the need for temper tantrums, hysterical meltdowns, an old lady’s scolding, and chiding, demands that you stop talking altogether, massively disproportionate defensiveness and high emotional zealotry or entitled presumption, and anxiety over being exposed to thought itself, and this latter-day low trust society’s paranoiac obsession over punitively micromanaging others’ suspected offence-causing that, presenting these factors in totality, renders genuine sensible communication a thing of the past, much as people still like to fill the air with themselves in company.

I no longer have a shared frame of reference, knowing from experience that they have no background knowledge of anything I want to say and no curiosity or inclination to inform themselves about it. It’s not just that I must listen to their ignorance and childishness; it’s that I’m ‘not allowed’ by them to talk on anything substantial, anything “deep and heavy,” as I’ve heard them say – and this is an observation I’ve been making from a long time before they ever started to erroneously associate me and my contemporary self-study perspectives with ‘the Far Right,’ having noticed it even before reaching adulthood whenever I mentioned interests in science, reading, philosophy, the natural world, art, and especially poetry.

I barely speak these days, frustrated and sad that my thoughts and interests always remain inside, unshared; any confidence I had clawed back by early adulthood is now at rock bottom again. Almost all the time, I’m just listening as others rattle on and on, hardly noticing that all I’m doing is humouring them. Weary monosyllabic responses, mute, gloomy, unsmiling, having not laughed in many years, forcing myself to answer politely, to feign some interest, bored to death by their monotony and overwhelmed by the disappointing crassness, the abundant cliché statements of the eternal ignorance which they always think are so novel or even the legitimate inventions of a discrete individual ‘my opinion’ that somehow can’t be perceived by them as one already shared by 50 million other identical people, preparing my familiar “oh, I’m OK” response for the opening seconds of each meeting, delivered softly, barely audible, a formal concession to pacify them, knowing from experience that they’re not looking for me to say otherwise.

 It's impossible to gain confidence knowing others are not interested in anything you have to offer and are unwilling to tolerate you expressing what you like, think, or feel. They genuinely don't care. As we may recall, the experience of lifelong lonely ostracism didn't do the philosopher Friedrich Nietzsche any good psychologically. Stephan Zweig's writings, in his condensed book of the same title, go into far more detail on the scope of Nietzsche's loneliness. In one particularly stirring poetic passage, Zweig encapsulates the full horror of the genius philosopher's inevitable, long-fermented 1889 breakdown:

And this fever swells, seething under the surface before suddenly erupting. Observing the writings and letters of Nietzsche’s last years, one notes the pulsation of blood as if at a higher altitude: the hearts of Alpine climbers and aviators which are under duress have felt these sharp hammer blows; the last letters of Kleist betray this frenzied hammering, this fraught tone, the ominous roaring and friction noise of a machine about to malfunction … He cannot wait any longer for his proposed The Will to Power to come together as he envisaged it, so he tears it into fragments and hurls them like so many flaming torches into the darkness of his epoch … darkness is raised over him and it is like that mighty rumble which announces the oncoming storm; then laughter flickers up, a glaring, evil, raving laughter … but the song becomes more volatile, the laughter ever more piercing in the glacial silence and lost in his own entrancement he lifts his hands, dithyrambic his foot twitches; and suddenly the dance begins, the dance around the abyss, the abyss of his own downfall.

In the easy words of my Dad, spoken around 2016, "Everyone has problems in their life. I don't know what you've got to complain about, Benjamin; you've never suffered." This glib, matter-of-fact, thoroughly dishonest statement enraged me. Yes, I knew many have indeed had serious problems and continue to have them. I didn't think it necessary to add, though, as it was apparent. I was taken aback that he couldn't see a scale to that acknowledgment, though, as opposed to a blanket egalitarianism, some way to accept that some problems are worse than others, and, besides, that suggests that we should acknowledge discrete sets of issues to be solved in the case of any individual within that "everyone," and with some hierarchical assessment, some empirical triage, not a vague arbitrary act of mass passing the buck. I found his lack of empathy disconcerting, and I failed to see how accepting that others suffer too barred him from considering my discrete problems. Whose father is he?

 I don't know if my life experiences are uncommon, but I've never met anyone with my history (which includes severe autophagia – i.e. not fingertip nibbling territory: you will not find an example online in Wikipedia’s article on the subject that manages to encapsulate just what I could be known to do – and some truly barbaric episodes of grotesque self-harm). I wasn't sure if he tacitly meant 'and their problems aren't worth me worrying about either,' simply washing his hands of the world altogether. I've often wondered what marks me out as his son at all. There's no express loyalty. I'm another face in the crowd, and I don't fit the popular critical intersectionality of his newspaper-derived opinions, not a member of any of the prosperous victim groups his columnists encourage him to fret over.

In perhaps the most soul-destroying betrayal of all, I remember the derogatory joke about me that my father shared to that Pakistani abuser, standing on the summer beach together, a joke well received, as both began to laugh at me in my face, and yet, from the very onset of an official NHS acknowledgement of my severe mid-adolescent suicidal depression, when it had become so awful that I could no longer hide it, up to the periodic psychoses of the present day, his first port of call always being that love of telling me to take medication, to the near-point of forcing it down my throat by threatening to break contact if I refuse, unable somehow to see what has caused the harm, in the outside pain of school trauma and of sexual abuse, but much more so in an unsupportive and oppressive family that ignored any pain from outside and yet bullied me privately just as much, causing even deeper emotional scarring, driving me to grim self-loathing and humiliation, the death of ego and all self-esteem and pride, my lifetime experiencing this in their company, and what could be done personally by him to address the damage inflicted by him, not merely some mysterious reliance on the dispassionate abstractions of genetics, neurology, and cognitive science as he continues to put me in the ground, standing by distant and unconcerned as others, with his obliging consent and approval, increasingly take the reins also. 

As my mother often told me, if I became shocked at his feminist pandering and the tolerant leeway he granted to abusive girlfriends, “Dad prefers girls to boys.” Level-toned and matter-of-fact, as if what she was saying was a perfectly reasonable justification, I wasn’t sure if her regular reply ‘explanation’ was a subtle jab at me also.

Officially, having swiftly abandoned Major Depressive Disorder for something even more derogatory, they referred to what should have been evident to them merely as a very bad depression as Borderline Personality Disorder/Emotionally Unstable Personality Disorder for the first few years, with brief interludes two years in with a short-term private therapist/hypnotherapist (brief though very kind; the nicest professional I’ve ever been under – I liked Maggie Chapman: until I benightedly tried to get back in contact many years later, and royally put my foot in it in a psychotic fluster, that is), who considered Dissociative Identity Disorder, especially when I mentioned a tentative need to discuss some particularly unpleasant preadolescent sexual abuse, and something else even earlier that I wasn’t ever sure how to describe, and with some very abstract comments, vague as could be, hoping the other person would ‘get the hint’, not that the NHS thought much of this private diagnosis potential, having not asked me a single question on my early life, not once, continuing instead with Bipolar Disorder before changing their minds, and leaving my diagnosis undefined from there on in, speculating over Schizoaffective Disorder also in recent years, and seeming to home in on that potential, much as there were three or four months when PTSD was on the cards until they decided that couldn’t be right as I hadn’t fought in a war. 

It seems that all their behaviourist methodology could do was spot my latter-day episodes of full-blown psychosis (present from my middle to late 20s; before then my symptoms were simply neurotic/depressive, if extreme). The easy – perhaps convenient – arrival of this set of symptom observations blotted out any further hope that they could review my life in more detail, evidently content that they could now slot me neatly into a box, impatient as always to proceed with ‘business as usual’, and thus get on with the sole anticipated exercise of pouring toxic medications down my throat, ad infinitum. To paraphrase a famous quotation reflecting on cognitive biases by 1960s philosopher Abraham Kaplan (though popularised by psychologist Abraham Maslow in 1966), if one makes themselves into a hammer, everything else soon comes to resemble a nail. The archaic English expression “a Birmingham screwdriver” (meaning a metaphorical hammer also – one tool for all purposes) springs to mind.

The wretched diagnostic system annoys me and doesn’t say much about their competence in evaluating people if they have to change their minds that much (they were right in the damn first place – I was severely unhappy). They might as well throw the entire DSM out the window anyway as a stupid, rigged example of politicised democratic theorising behind the closed doors of their tripartite mono-discipline (psychiatry, clinical psychology, psychoanalysis), and, explicitly, in the upstairs offices of the American Psychiatric Association, a mere popularity contest vote for whatever new fad they fix on. As Eliot Valenstein reflects on, on pages 159-160 of Blaming the Brain:

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.)

He goes on to add, on pages 160-161:

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))

There is much to be said for sociobiology, Mendelian genetics, and Darwinian evolution. Still, evolutionary psychology, too, has dropped the ball in its accelerated 21st Century research tangent on account of a pandering to pharmacological psychiatric orthodoxy, the latter facilitated by a mere abstract literary idealism after all, and one that its practitioners arbitrarily impose on their victims, utilising no genuine power of observation otherwise, and ignoring all personal testaments and empirical rebuttals contradictory to this purely literary theorising, un-empirical from the outset beyond a stubbornly maintained and dogmatic corporate research confirmation bias that strips its mercantile, heavily marketed progress of all scientific rigour. This inadequate theory, fundamentally unfalsifiable by the conditions of the standard academic principle invented by Karl Popper, is thus a pseudoscience, as explained by the article Unfalsifiability in Psychiatry, taken from the anthology Day of Wrath published by César Tort, also available in the 2026 English Edition of book II of Tort’s magnum opus 12-book autobiography Whispering Leaves, titled How to Murder Your Child’s Soul, as the addendum chapter ‘Why Psychiatry is a Pseudo-science’, on page 155.

Tort writes, on page 157-158:

In The Logic of Scientific Discovery philosopher of science Karl Popper tells us that the difference between science and pseudoscience lies in the power of refutability of a hypothesis.

Despite its academic, governmental, and impressive financial backing in the private sector, psychiatry does not rest on a body of discoveries experimentally falsifiable or refutable. In fact, the central hypothesis in psychiatry, a biomedical entity called mental illness – say ‘schizophrenia’ – cannot be put forward as a falsifiable or refutable hypothesis.

Let us consider the claim that psychiatrists use drugs called neuroleptics to restore the brain chemical imbalance of a schizophrenic. A Popperian would immediately ask the questions: (1) What exactly is a brain chemical imbalance? (2) How is this neurological condition recognised among those who you call schizophrenics and which lab tests are used to diagnose it? (3) What evidence can you present to explain that the chemical imbalance of the so-called schizophrenic has been balanced as a result of taking the neuroleptic?

In other words, if they believed that genetically unstable brain chemistry abnormalities from birth were a valid hypothesis justifying their treatment model, they would develop a neurological test to apply to their patients before pushing these arrays of corporate drugs on them to establish a baseline, let alone if there is any change to be observed at all compared with what they decide are healthy brains, a matter of clinical safety as much as a tailored intervention for the neurological and hormonal specifics of any patient in question.

We administer standard scans, physical examinations, blood tests, and the like, after all, prior to placing conventionally unwell general hospital patients on their specific healing medications. We continue to monitor progress with regular tests after that, and we withdraw their treatments in the cases of a developing danger, co-morbidity complications, or for reasons of simple inefficacy.

Where does one begin with practically measuring this imbalance hypothesis? Which generation do we root it in? How far back in one’s family? Where does the buck stop? It’s all a moot point, as mental illness is not a biological disease and is not hereditary. Any continued intergenerational trauma can be put down to the experiences of offspring in the homes of poorly-treated traumatised adults: if one does not process their trauma in time within their lifetime, by getting to the root of the problem – identifying the perpetrators – they are liable to misdirect their  anger onto the wrong targets, often their child, co-worker, or spouse. A good example of this, taken to extremes, is the tragic case of the serial-killer Jeffrey Dahmer, ferociously abused by his father in childhood, but who thoroughly repressed that knowledge in later life, continuing to praise and defend his guilty parent, only to commit atrocious crimes against unconnected lovers. 

My hypothetical brain chemicals imbalance test has never been written into any formal psychiatric treatment methodology. All the psychiatric doctors ever had was the office-based group literary theorising describing the behaviours of their patients. Their lucrative drug industry partners are monitoring the results of their labours to 'fix' what they have never been able to prove objectively is even there, much as the distress responses are real enough.

The soundness of your theoretical model and the metrics you assign to your methodology will define your results, as will your rigid adherence to that theoretical model. In this example, terrible real-world consequences have been caused by this arrogance, a continuing problem. More than reforming or revolutionising this discipline, I believe an entirely new means of thinking should be adopted, and a complete paradigm shift should be implemented.

The previous acknowledgement taken into account, it is obvious to note that the external chemicals imparted by a regular daily application of these pharmaceuticals are the only effective method – albeit inadvertent to some degree (it can still be argued that they are consciously – cynically – drugging to sedate ‘rebellious’ teenagers, in order to preserve society’s status quo), an unplanned consequence of their dogged decision-making – by which one could substantially alter a person's physical brain chemistry in the long-term (as with food and drink consumables, oral stimulants, and illegal narcotics), given that at the historical instance of the psychological model's flip into bio-reductionist pharmacological psychiatry in the years of the mid-to-late 20th Century there is not one recorded historical example of an empirical baseline test conducted officially by psychiatry to objectively establish what, in human biology,  a standard 'chemical balance' is either.

That it is the long-term usage of these very drugs themselves contributing to brain shrinkage and brain damage, and the cognitive symptoms of early onset dementia, as much as an array of physically incapacitating neurological traumas shouldn't just be a terrible irony for highlighting the ridiculous, given that the main body overseeing their forceful administration is guilty long-term of conducting modern systemic torture in practice, a State organ of punitive medicine for the maintenance of citizen ideological conformism.

It's not that they couldn't have noticed this glaring error in their ostensible medical science's rigour, as much as that they don't care. They are too powerful as an institution, and it is doubtful that they can ever be reasoned with from outside their discipline, especially by their patients, held legally to Hippocratic account, or indeed brought to justice at the level of their entire profession's continued existence.

No matter how much one skews the almost comprehensively internalised peer-reviewed research, or how much big-budgeted high energy and copious time one's multinational bio-pharma cartel invests in psychologically and financially manipulating the researchers and evaluators they can employ, dazzle, bribe, blackmail, or otherwise sweet-talk, flatter, and pal up to (to create 'true believers'- a good pool to have access to when marketing a product) the approved drugs themselves still do not provide positive therapeutic results significantly better than those results provided by placebos.

See the August 2nd, 2022 study in the British Medical Journal by Marc B. Stone, et al., titled “Response to acute monotherapy for major depressive disorder in randomized, placebo controlled trials submitted to the US Food and Drug Administration: individual participant data analysis”, showing in its conclusion that only “about 15% of participants have a substantial antidepressant effect beyond a placebo effect in clinical trials”.

Similar evidence dealing instead with antipsychotics, can be found in the May 7th review paper on JAMA Psychiatry by Lasse Brandt, et al., titled “Antipsychotic Acute-Phase Treatment in Individuals With and Without Recent Treatment: An Individual Participant Data Meta-Analysis” and the extensive meta-analysis in the American Journal of Psychiatry, 2017, Oct 1;174(10):927-942, by Stefan Leucht, et al., available on the National Library of Medicine website, titled “Sixty Years of Placebo-Controlled Antipsychotic Drug Trials in Acute Schizophrenia: Systematic Review, Bayesian Meta-Analysis, and Meta-Regression of Efficacy Predictors.”

As Robert Whitaker notes in his related  Mad in America website article of June 1st, 2025:

The authors of the JAMA Psychiatry article conclude that their findings show that antipsychotics are effective over the short-term, which is the same conclusion made by the authors of the 2017 meta-analysis. They do so because both analyses tell of a “statistically significant” drug-placebo difference in the reduction of symptoms on the Positive and Negative Syndrome Scale (PANSS.) What the investigators in each study fail to note is that the drug-placebo difference is quite small (less than 10 points on a 210-point scale), and doesn’t rise to the level of a “minimum clinically important difference.” Indeed, a 9-point drug-placebo difference on the PANSS scale is so small that it most likely wouldn’t be clinically noticeable by either the patient or provider.

Anyone in the non-academic community (and some within it) who says they have personal evidence or experience that these wretched medications work effectively is guilty of merely seeing what they want to see and not what is occurring.

 Usually, this unshakeable loyalty to their medications' success rate and 'breakthrough' clinical excellence is observed in routine care workers and nursing staff, all those who, when you call them out over another useless product, say, "It's okay, that was that one, but… this new one is the latest thing, it's just on the market, in my personal experience it's really, really good..."

The types whom one finds they just cannot reason with, although sadly even patients can be conditioned to toe the line on this over-optimistic wishful-thinking at a conviction level closest to a fundamentalist's religious belief, these already-vulnerable people manipulated psychologically to think that they are getting better for this reason, or even this reason alone, and thus deceiving themselves to the reality that, if improving at all – a rare occurrence in the mental health world – they are most likely improving regardless of – and despite – bio-psychiatric psychopharmacological intervention.

Later on page 158 of How to Murder Your Child’s Soul, César Tort encapsulates the arrogance – the best long-term expression I have to describe these professionals – of academic psychiatry (as I was soon to discover again for myself in the meeting), and the sheer quasi-religious devotion of its adherents to a model that is – and always has been – irrevocably flawed:

[Nancy] Andreasen [editor of the American Journal of Psychiatry] is recognising that that her profession is incapable of responding to the second and third questions above.. How, then, have she and her colleagues convinced themselves restore to balance the ‘chemically unbalanced’ brains of schizophrenics? Furthermore, why does Andreasen state so confidently at the beginning of the section in Brave New Brain that addresses the question of what causes schizophrenia that the disorder ‘is not a disease that parents cause’?

Speaking in Popperian terms, the answer is: by contriving a non-falsifiable or irrefutable hypothesis. In contrast to neurologists, who can demonstrate the physiopathology, histopathology or the presence of pathogen microorganisms, Andreasen and other psychiatrists recognise that they cannot demonstrate these biological markers – faulty genes or chemical imbalances – that they postulate in the major disorders classified in the current edition of the Diagnostic and Statistical Manual of Mental Disorders. If they could do it, psychiatry as a speciality would have disappeared and its body of knowledge merged into neurological science. What psychiatrists do is state that after almost a century of research in, for instance, schizophrenia, the medical aetiology of the ‘disease’ is still ‘unknown’ and they make the same claim about the most well-known behaviours in the DSM.

The psychiatrist barely paused before replying to me. She assured me, without evidence, that my own personal life history reasons (which, admittedly, I did not get the chance to express to anywhere near the same level of detail as above) and the theory-critical research – I’ve been known to print off these papers and bring them to clinic meetings with me, only for them to be totally ignored – I put as questions to her as to why I am often unwell were impossible. She was very emphatic about that. She didn't tell me the constant restlessness of akathisia, the painful, clammy fingertip rubbing and jerky, neurological damage, facial twitches of tardive dyskinesia, the excessive weight gain, the muted, alien emotional numbness, and the months of rage-inducing erectile failure commencing when I did take them were a lingering side-effect either – I'm near-fully impotent these days, and cannot climax. She didn't deny some of this when confronted, but she didn't give any indication that it bothered her and breezed on to recommend treatment as usual.

More than once, I've been cheerfully informed in response, "Oh, that's OK!" as if somehow one could consider themselves personally in the wrong or worry that they could be putting out their mental health workers by passively experiencing terrible side effects. Is that OK? It does suggest they don't give a damn about you.

I was left wondering if they were even familiar with the official terminology that I had employed to describe the ‘pyramidal’ – to employ their industry euphemism – effects (them being the only tangible effects I experienced from them from the fourteen or so on-off years in total when I was willingly subjected to their range of SSRIs, mood stabilisers, and second and third generation ‘anti-psychosis’ neuroleptic drugs daily after all, as opposed to, say, preventing psychosis from occurring, much as it's worth noting that I was first presented with a great many of them an entire decade before it ever did).

In the unhelpfully titled Madness and Genetic Determinism: Is Mental Illness in Our Genes? Patrick D. Hahn reinforces Jay Joseph’s research (from The Trouble with Twins Studies: A Reassessment of Twin Research in the Social and Behavioural Sciences, 2015) in proving that twin studies research is fundamentally flawed and that the evidence in favour of genetic influences is much weaker than mainstream sources report, the actual primary cause of mental problems (‘illness’ is not the correct concept) also explained in 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, and his colleagues, 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 institutionalisation, 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 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, by 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 unleashed on the child at any moment. Delusions are a cognitive attempt to make sense out of the paranoid emotional state.

Indeed, an Irish study published in July 2013 in the American Journal of Psychiatry 170, no. 7,  by Ian Kelleher, et al., titled “Childhood Trauma and Psychosis in a Prospect Cohort Study: Evidence, Challenges, Implications”:

Not only found a dose-response between bullying and physical abuse and psychotic symptoms, but also found that when the abuse stopped, the occurrence of psychotic symptoms dropped sharply.

And as Peter Bebbinton wrote in the conclusion of his  editorial for Epidemiologia e Psichiatria Sociale, 18, 4, 2009, published online by Cambridge University Press, titled “Childhood sexual abuse and psychosis: aetiology and mechanism”:

There is now considerable evidence of an association between child sexual abuse and psychosis. This relationship is at least as strong as, and may be stronger than, that with other mental disorders. There may be a specific relationship with hallucinations. A history of severe trauma is common in people who develop psychosis, but the link between child sexual abuse and psychosis may be particularly strong, because of the age of the victim and the especially intrusive nature of the abuse. The mechanism of effect may overlap considerably with the triggering action of life events occurring in close proximity to the onset of psychosis. However, we also need an account of the maintenance of effect of child sexual abuse that can explain the establishment of a vulnerability that persists, sometimes for many years, before the actual onset of disorder. This may result from the impact of a series of intervening events and circumstances, and may be facilitated by processes like impaired coping responses, impaired access to appropriate social support, and revictimisation.

Hahn himself 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.

There is also further evidence in this chapter of Hahn’s book discussing schizophrenogenic maternal relationships, where we are reminded that “the mother-child relationship is the most important human relationship there is.” Hahn asks us, “Is it really such a stretch to suggest that bad consequences may follow when this relationship goes awry?”

Much as this accurate taboo explanation for ‘mental illness’ has fallen out of favour in general, I wonder tentatively why more has not been written in the latter-day academic research on a paternal equivalent. 

Despite much press, this paradigm of parental abuse has never officially been debunked in a scientific manner: I am not counting the many angry unsubstantiated assertions made by threatened biomedical psychiatrists and the incessant copy-cat  repetitions of these assertions down they years by those laymen and medical professionals engaged in assumptive damage control and groupthink, those with an axe to grind and with nothing to back them up but their self-righteousness and blunt, knee-jerk incredulity, nor am I counting the firm, denialist lies and self-deceptions of guilty narcissistic parents put on the spot, or the deluded claims of repressed victims duped by psychiatric propaganda, those who do not even realise that they are victims of parental child abuse, despite all psychological analysis of context suggesting that they are – trauma-model psychiatrist Colin Ross’ writings in The Trauma Model: A Solution to the Problem of Comorbidity in Psychiatry, published in 2007, on an ‘attachment to the perpetrator’ cover the reasons for this final tragic and frustrating scenario well (the very unhelpfully named The Genetics of Schizophrenia, published by Ross in 2020 is also a useful little book for dispelling psychiatric genetics research, at fundamental theory level, if also flawed in places, with some very left-field speculations over electric-fields, again somewhat guilty of the ‘just in case’ clutching at straws mentality common to researchers who do not want to admit that mental problems are psychological in nature) .

I conclude that modern researchers are just too cowardly – too afraid of the reception (and the subsequent loss of funding?) – to go the final mile into historical territory already well-mapped by the psychological theorists and renegade psychiatrists Alice Miller, Silvano Arieti, R. D. Laing, Harry Stack Sullivan, and Theodore Lidz, and by the painful autobiographical truths of long term psychosis sufferer John Modrow, exposed in his How to Become a Schizophrenic, or perhaps to review Morton Schatzman’s notable case history analysis, Soul Murder, on the tragic life of the late-Victorian schizophrenia patient Daniel Paul Schreber, and his early experiences at the hands of his brutal authoritarian father, as further documented – if one has the analytic patience and basic compassion to read between the lines – in his florid autobiographical diary, Memoirs of My Nervous Illness.

For more detailed information on my own life history, and for a bibliography of classic academics who did have the integrity to admit that this child abuse is predominantly parental abuse, see my other book, Consumption: Memories of my Childhood, available on the Lulu Publishing website. Alternatively, a definitive argument for parental responsibility for the abuse of children is found in How to Murder Your Child’s Soul, by César Tort, also available from Lulu.