Aletho News

12 Things Your Psychiatrist Was Trained Not to Tell You

An Essay on What the Fifteen-Minute Consultation Leaves Out

Lies are Unbekoming | September 10, 2026

What follows is twelve documented findings compressed into one sitting. It is written for the reader who has been prescribed one of these drugs, or is caring for someone who has, and who wants to know what the fifteen-minute consultation did not include. Every claim is drawn from the profession’s own literature, its own regulatory filings, its own package inserts, or the admissions of its own senior figures. Where an item is developed at greater length elsewhere in this series, that is noted. The purpose here is not depth on any single item. It is the cumulative weight of the twelve landing together.

Opening

Three percent of the 4,041 patients enrolled in the STAR*D trial remitted, stayed well, and remained in the study through the one-year follow-up.¹

The trial was announced with a cumulative remission figure of 67 percent.² When Ed Pigott and colleagues spent more than five years reanalyzing the data with fidelity to the original protocol, they found the 3 percent figure. When journalists put the 3 percent number to Maurizio Fava, one of the lead investigators, he acknowledged it was accurate. The investigators knew.³

The paper has not been retracted. It is still cited in psychiatric textbooks. The American Journal of Psychiatry ignored a petition signed by more than 1,800 people asking for retraction. The New York Times, repeatedly notified of the fraud, published the 70 percent figure again in a 2024 article praising the drugs.⁴

STAR*D was the largest depression trial ever conducted. It was funded by the National Institute of Mental Health. It was designed by the profession’s most senior researchers. What it proved, when honestly analyzed, was that the drugs did not work.

That fact has been available for over a decade. It has not reached the patients being handed the prescriptions.

The evidence throughout is drawn primarily from Peter Gøtzsche, Robert Whitaker, Peter Breggin, Gary Greenberg, David Healy, and Joanna Moncrieff. What the twelve items share is that none of them are contested at the level of documentation. They are contested only at the level of what the profession chooses to tell patients.

What They Told You Was True

The prescription is written on the basis of a mechanism, a diagnosis, and a trial. Each has failed on its own terms.

1. The chemical imbalance was never demonstrated

The theory that depression results from a deficiency of serotonin was never established in the scientific literature. Joanna Moncrieff and colleagues published a comprehensive umbrella review of the serotonin theory in 2022 and found no consistent evidence for its central claims.⁵ The theory was abandoned by serious researchers decades earlier. It continued to appear in direct-to-consumer advertising and patient education materials because it served a function. It explained why the pill was necessary and why the patient would need to keep taking it.

Steven Hyman, director of NIMH from 1996 to 2001, later observed that “the gold standard was the DSM criteria. It struck me as a fool’s errand to try to develop a biomarker for a fictive category.”⁶ The chemical imbalance was the mechanism proposed for a disease no one could measure, in a category no one could validate.

Chemical Imbalance: The Collapse of a Medical Myth

2. The DSM has no biological markers

After four decades and hundreds of millions of dollars in federal research, not one disorder in the Diagnostic and Statistical Manual of Mental Disorders has a confirmed biological test. Not depression. Not schizophrenia. Not bipolar disorder. Not ADHD. Not anxiety. Not any of the more than three hundred conditions the manual lists.

Robins and Guze proposed a five-step validation process in 1970: clinical description, laboratory studies, exclusion criteria, follow-up studies, family studies.⁷ The five steps were meant to establish, over time, which alleged disorders were real diseases and which were figments. Four decades later, Darrel Regier, who chaired the DSM-5 task force, told Psychiatric News that “validity tests have not lived up to the expectations of Robins and Guze.”⁸ Kenneth Kendler, the field’s leading nosologist, wrote that the diagnostic categories in use had been “heavily influenced by expert opinion” and were “fuzzy constructs that shift when viewed in different ways.”⁹

Thomas Insel, director of NIMH from 2002 to 2015, put it most directly in a 2005 address to the American Psychiatric Association: “The DSM-IV has 100 percent reliability and zero percent validity.”¹⁰ Reliability means clinicians using the same manual will arrive at the same diagnosis. Validity means the diagnosis corresponds to a real thing. Insel was telling the assembled profession that its manual sorted patients consistently into categories that did not exist.

The APA response was to convene committees to plan the DSM-5. The committees did not find biological markers. They could not have. The categories were not built to have biological markers. They were built from clinical description alone. The manual reifies its own criteria.

The consequence for the patient is direct. When the doctor says “you have major depressive disorder,” the patient hears a diagnosis in the sense that a diabetes diagnosis is a diagnosis: a measurable biological state with a known mechanism. What the patient has actually received is a checklist tally. Five of nine symptoms present for two weeks. That is the whole test. There is no blood work, no scan, no biomarker. The diagnostic bible of American psychiatry sits on the shelf as an artifact of expert agreement, not a description of nature.

Manufacturing Madness: The DSM as Instrument of Social Control

3. STAR*D was manipulated

The opening figures bear structural repetition: 3 percent versus 67 percent, admitted by the lead investigator, still not retracted, still cited. Ed Pigott’s reanalysis was published in BMJ Open in 2023.¹¹ The investigators, when confronted, doubled down on the fraud in the American Journal of Psychiatry rather than correct it.¹² The owner of the journal, the American Psychiatric Association, did nothing.

Peter Gøtzsche has documented the specific manipulations. The “remission” threshold was set so low that a patient scoring 7 on the Hamilton depression scale, including endorsement of “feels like life is not worth living,” was counted as symptom-free.¹³ Patients who exited the study were assumed to have remitted at the same rate as those who stayed, a statistical fiction that inflated the numbers by an order of magnitude. Eleven prespecified outcomes were never reported. Suicidal ideation was reported at 0.7 percent in one paper and ten times that in others by the same authors.

The trial that was supposed to establish the effectiveness of antidepressants in real-world practice established the opposite. The profession’s response was to continue citing the announced figure.

Is Psychiatry a Crime Against Humanity? (2024)

What Happens on the Drug

The prescription arrives with the phrase “you may notice some side effects.” The phrase does the work of concealment. Three effects, in particular, are not warned about with the seriousness they warrant.

4. Akathisia carries documented suicide risk

Akathisia is a state of extreme inner restlessness produced by antidepressants, antipsychotics, and antiemetics. The Greek term means inability to sit still. The patient may pace, fidget, wring hands, or endlessly walk. The condition may also present without visible motor symptoms, as unbearable internal agitation the observer cannot see.¹⁴

In 1990, Martin Teicher and colleagues at Harvard published five cases of patients who developed intense suicidal preoccupations on fluoxetine, all associated with akathisia, all resolving when the drug was stopped and returning when it was restarted.¹⁵ Rothschild and Locke published the rechallenge study in 1991: three patients who had made serious suicide attempts on fluoxetine, all rechallenged under controlled conditions, all developing akathisia and becoming suicidal again. One patient said in retrospect: “I tried to kill myself because of these anxiety symptoms. It was not so much the depression.”¹⁶

A study of psychiatric inpatients found that 79 percent of those who had attempted suicide were experiencing akathisia at the time.¹⁷ Another found that half of all fights on a psychiatric ward were akathisia-related. Haloperidol at moderate to high doses made half the patients markedly more aggressive, sometimes to the point of wanting to kill their psychiatrists.

The FDA’s 2004 black-box warning on antidepressants describes what Breggin has called the stimulant syndrome: anxiety, agitation, panic attacks, insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia, hypomania, mania.¹⁸ The label warns that these can occur in nonpsychiatric patients, meaning the drug produces the syndrome by itself, not by unmasking a preexisting condition.

Gøtzsche’s team examined manufacturer trial data and found akathisia miscoded as “hyperkinesia” in Zoloft trials. In paroxetine trials they found not a single case of akathisia recorded, which is statistically impossible given the drug class.¹⁹ The miscoding was systematic.

The FDA-approved label for Zyprexa describes akathisia as “extreme inner anxiety and restlessness.” At least one psychiatric textbook labeled it “agitated depression,” folding the drug’s most dangerous effect back into the diagnosis it was prescribed to treat. The patient who reports the akathisia is told the underlying illness has worsened. The dose is increased.

Mental Health Survival Kit and Withdrawal from Psychiatric Drugs (2022)

5. Benzodiazepine dependence begins at prescribed doses

The FDA-approved label for Xanax states that withdrawal symptoms, including seizures, have been reported after only brief therapy at doses within the recommended range for treating anxiety.²⁰ In the eight-week trials used for FDA approval, patients were worse off at eight weeks than before starting the drug. Between 7 and 29 percent of patients could not withdraw after only six to eight weeks of exposure.²¹

If you are currently taking a benzodiazepine, do not stop it abruptly. Abrupt cessation can produce seizures. Item 12 addresses what safe withdrawal actually requires.

Heather Ashton, the British psychiatrist who ran a benzodiazepine withdrawal clinic at the University of Newcastle for decades, documented that long-term users often required a year or more to taper.²² Some experience withdrawal symptoms lasting years after cessation. Cognitive impairment, depression, and anxiety worse than the original condition are common outcomes of long-term use.²³ Gøtzsche, who has decades of clinical pharmacology experience, has noted that patients report benzodiazepine withdrawal as often worse than heroin. Heroin abstinence symptoms resolve within days. Benzo withdrawal can persist for years.

Anxiety Uncovered: The Truth About Benzodiazepines and Real Solutions

6. ADHD stimulants produce the symptoms they treat on withdrawal

The DSM has a category for stimulant withdrawal, which lists depression, anxiety, irritability, sleep problems, fatigue, and agitation as the withdrawal syndrome after “several days or longer” of use. Rebound hyperactivity, talkativeness, and inattention are documented after a single dose in a placebo-controlled NIMH study of normal children ages 6 to 12.²⁴ Ten of fourteen children in that study showed marked behavioral rebound; three developed euphoria.

If a child is currently taking a stimulant, do not stop it abruptly. Rebound and withdrawal effects are commonly mistaken for a worsening of the original condition. Item 12 addresses safe withdrawal.

The teacher observes the child on Monday morning after a weekend off the drug, notices the child is more scattered and irritable than usual, and concludes the child needs the medication. The child is in withdrawal. The dose is increased. Peter Breggin’s observation from the early 1990s stands unchanged three decades later: if the child continues on Ritalin because they continue to have problems focusing, the disorder may be the drug’s effect.²⁵ Drug-induced inattention becomes the reason to continue and increase the drug.

The Multimodal Treatment Study of ADHD, the largest NIMH-funded stimulant trial, tracked children through eight years of follow-up. By three years, the medicated children showed no advantage over the non-medicated on any measure. They were, however, 2 cm shorter and 2.7 kg lighter than their unmedicated peers, a growth suppression the FDA eventually required on the label.²⁶

The Arithmetic Pill: ADHD, ADD, and the Evidence

What Happens to Your Brain

The drugs act on the brain and the brain responds. What the brain does under sustained chemical assault is documented in the profession’s own imaging studies.

7. Antipsychotics shrink brain tissue on MRI

Nancy Andreasen, editor-in-chief of the American Journal of Psychiatry from 1993 to 2005, began a longitudinal MRI study of over 500 first-episode schizophrenia patients in 1989. In 2003, she reported that frontal lobe white matter volume decreased progressively over the years of treatment.²⁷ In 2011, her team published in Archives of General Psychiatry the finding that antipsychotic exposure was directly associated with volume loss.²⁸ In a 2008 interview with the New York Times, Andreasen stated it plainly: “The more drugs you’ve been given, the more brain tissue you lose.”²⁹

Fusar-Poli and colleagues confirmed the pattern in a 2013 meta-analysis of longitudinal MRI studies.³⁰ The 2009 Navari and Dazzan review reported that both older and newer antipsychotics produce gross changes in brain volume in selected regions.³¹ In monkey studies, haloperidol and olanzapine produced substantial reductions in both grey and white matter, and reduced glial cell numbers.³²

Andreasen’s original interpretation was that the shrinkage reflected the disease. The follow-up data forced her to concede the drug was the cause.

Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs, and the Astonishing Rise of Mental Illness in America (2010)

8. Tardive dyskinesia is permanent

Tardive dyskinesia is a drug-induced movement disorder produced by antipsychotics. It can affect any voluntary muscle: face, tongue, neck, torso, extremities, diaphragm, vocal cords. The condition presents as involuntary jerky movements, slower writhing movements, painful spasms, or restlessness the patient cannot control. The mechanism is understood. Antipsychotics block dopamine receptors in a brain region called the basal ganglia. Over time the brain compensates by growing more of those receptors. When the drug dose is reduced, or when the extra receptors eventually outnumber the block, the excess drives the involuntary movements.

The prevalence is not marginal. DSM-IV-TR sets the annual incidence at 3 to 5 percent per year in young adults and 25 to 30 percent per year in older patients.³³ These are cumulative rates. A young adult after three years of exposure has a 9 to 15 percent risk. An older patient after three years has a 75 to 90 percent risk. Prevalence in outpatient clinics runs above 40 percent. In long-term facilities, above 50 percent.³⁴ There is no established treatment. Most cases are permanent.

The condition often extends beyond motor symptoms. Gualtieri and Barnhill observed that “in virtually every clinical survey that has addressed the question, it is found that TD patients, compared to non-TD patients, have more in the way of dementia.”³⁵ Breggin has called this tardive dementia. Tardive akathisia and tardive psychosis have also been documented, representing further permanent damage to the higher brain function of patients whose brains were supposed to be helped.

The condition is frequently masked by the drug that caused it. Increasing the dose suppresses the visible movements while the underlying damage progresses. Reducing the dose brings the movements out, which the prescriber may interpret as evidence that the patient still needs the medication. The patient’s brain, already damaged, is offered more of what damaged it.

The neurological literature has documented tardive dyskinesia for over five decades. It is required disclosure on antipsychotic labels. It is not routinely disclosed at the point of prescription.

Toxic Psychiatry

9. ECT causes documented brain damage

Electroconvulsive therapy applies electrical current to the head sufficient to produce a grand mal seizure. In modern practice, the patient is anesthetized and given a muscle relaxant to prevent the visible convulsion. The electrical dose is often increased to compensate for the seizure threshold raised by the anesthesia. Multiple treatments are given, typically 8 to 16 per course, sometimes more.

Autopsy studies dating to the 1940s documented brain necrosis in patients who died following ECT.³⁶ Animal studies documented brain damage. The brain’s response to ECT is an acute organic brain syndrome, medically indistinguishable from severe head injury. In neurological terms, multiple continuous seizures without full recovery of consciousness constitute status epilepticus, a medical emergency defined by its risk of permanent brain damage.

The memory loss is documented in every serious study that has looked for it. Larry Squire and Pamela Slater reported an average of 27 months of retrograde amnesia surrounding treatment.³⁷ Freeman and Kendell, using face-to-face interviews conducted by the treating doctors themselves (a design that biased strongly against reporting), found that 74 percent of patients reported memory impairment and 30 percent said their memory function was permanently affected.³⁸ Squire and Slater’s own longer follow-up found that 55 percent of patients felt they had not regained normal memory function over the years.

Gøtzsche summarizes the current literature: with strict definitions of memory loss, 29 to 55 percent of patients are affected. With looser criteria, 51 to 79 percent.³⁹ Death rates from ECT, according to a systematic review by John Read and colleagues, run at approximately 1 per 1,000 treatment courses, ten times higher than the American Psychiatric Association’s stated figure.⁴⁰

The efficacy evidence is thinner than the harms evidence. The 1985 NIMH Consensus Conference on ECT accepted the finding that no controlled study showed benefit beyond four weeks. The four-week window corresponds to the acute organic brain syndrome, during which severe brain dysfunction produces the euphoria or apathy interpreted as improvement.⁴¹ Once the brain begins to recover, the depression returns. If the patient is given more ECT, the brain damage accumulates. If the patient is not given more ECT, the profession points to the returning depression as evidence the disease was chronic.

The APA’s 1990 task force report on ECT omitted essentially the entire literature documenting memory loss and brain damage.⁴² The literature it omitted included the work of Squire, Slater, Janis, Friedberg, Breggin, and even the APA’s own previous 1978 report, which contained more information on memory loss than the 1990 update. In psychiatry, science sometimes runs backward.

What Happens When You Try to Leave

At some point the patient decides they no longer want to be on the drug. The system was not built to help them leave.

10. SSRI discontinuation can last years

The FDA-approved labels describe “discontinuation syndrome.” Patients and doctors alike were told the symptoms would last a few weeks and resolve. The systematic review by Davies and Read, published in 2019, established that this was false. Withdrawal symptoms are more common than reported, more severe than reported, and last far longer than reported. In one survey of 580 patients, 16 percent reported withdrawal symptoms lasting over three years.⁴³

If you are currently taking an SSRI or SNRI, do not stop it abruptly. Withdrawal reactions can include severe agitation, akathisia, suicidal ideation, and violence. Item 12 addresses the resources for safe tapering.

The Dutch tapering-strip program run by Peter Groot and Jim van Os has documented the shape of the problem. Of 895 patients on antidepressants, 62 percent had previously tried to withdraw without success. Using hyperbolic dose-reduction strips, 71 percent were able to withdraw within a median of 56 days.⁴⁴ Venlafaxine required 90 percent of patients to start at the lowest available dose and taper over three months. Some patients required more than six months. Dutch insurers refused to reimburse extended tapering because “there is no evidence in the literature” for its necessity, a circular defense against the very treatment the literature was documenting.

The withdrawal is routinely misinterpreted as return of the underlying illness. The patient is told they were unwise to stop and needs to remain on the drug indefinitely. Breggin’s term for this pattern is medication spellbinding. The drug produces effects the patient attributes to the disease.

11. Long-term outcomes are worse with the drugs than without them

The 1997 British study of a large inner-city primary care facility followed 95 never-medicated depressed patients and 53 drug-treated ones. Symptom reduction at six months: 62 percent for the never-medicated, 33 percent for the drug-treated.⁴⁵ A World Health Organization study of 640 depressed patients found that medicated patients had worse general health and were more likely to still be mentally ill at one year.⁴⁶ A Canadian five-year study of 9,508 depressed patients: 19 weeks of depression per year for the medicated, 11 for the unmedicated.⁴⁷ An NIMH study of 547 patients: medicated patients were three times more likely to lose their principal social role and nearly seven times more likely to become incapacitated at six years.⁴⁸

Rif El-Mallakh reported that 40 percent of patients on antidepressants end up in a chronically depressed “treatment resistant” state.⁴⁹ Giovanni Fava documented that drug changes induced by antidepressants “may propel the illness to a more malignant and treatment unresponsive course.”⁵⁰

The pattern extends to antipsychotics. Martin Harrow’s 15-year follow-up of first-episode psychosis patients found that those not on antipsychotics had significantly better outcomes and were far more likely to be in recovery.⁵¹ Lex Wunderink’s 7-year Dutch trial randomized first-episode psychosis patients to maintenance antipsychotics or dose reduction and discontinuation. The reduction group had double the recovery rate.⁵² Bockoven had documented in 1975 that rehospitalization rates rose after the introduction of antipsychotics and that medicated patients were more socially dependent than those treated in the pre-drug era.⁵³

The pattern is consistent across drug classes and across decades. Longer exposure produces worse outcomes. The drugs sensitize the brain and convert episodic distress into chronic dysfunction. The profession’s response has been to rewrite the natural history of the conditions to match the drug-damaged outcomes. The 1999 American Psychiatric Publishing Textbook of Psychiatry declared that older studies showing depression was self-limiting had been “disproved.” Depression became “a highly recurrent and pernicious disorder.”⁵⁴ The drugs had made it so.

12. Tapering protocols do not exist in most medical schools

The prescriber who put the patient on the drug is typically not trained in how to help them come off it. Withdrawal is not covered in the standard psychiatric curriculum. The tapering approach with the strongest evidence base is hyperbolic dose reduction, developed by Mark Horowitz and Joanna Moncrieff and published in Lancet Psychiatry in 2019.⁵⁵ The approach requires micro-dose reductions of a few percent at a time, made possible by liquid formulations or compounded tapering strips. Standard tablets do not come in the small doses required.

Peter Gøtzsche’s team spent two years trying to publish a Cochrane review protocol on antidepressant withdrawal support. The Cochrane depression group, chaired by Rachel Churchill, raised objections through 12,044 words of feedback across 86 numbered points, then rejected the protocol.⁵⁶ Cochrane refused to publish a review on how to help patients safely withdraw from a class of drugs prescribed to hundreds of millions of people worldwide. Gøtzsche’s PhD student Anders Sørensen mentored 30 consecutive patients through withdrawal in his unpaid spare time and documented the results, because it was the only way to do the work.

The insurance system compounds the problem. Dutch national health insurance refuses to reimburse extended tapering on the grounds of insufficient evidence, though the evidence exists and the insurers know it does. American insurers do not cover compounded formulations. The tapering strips developed at the Amsterdam pharmacy (taperingstrip.org) are available to prescribers in any country, but the patient must find a prescriber willing to order them, which many will not.

The knowledge exists. The Ashton Manual for benzodiazepine withdrawal has been public since 2002.⁵⁷ The Horowitz-Moncrieff hyperbolic tapering literature is in peer-reviewed journals. Mad in America hosts a withdrawal community with thousands of patients’ documented experiences. Breggin’s Psychiatric Drug Withdrawal was published in 2013.

None of it is on the psychiatric residency reading list. The doctor who wrote the prescription is, in most cases, not the doctor who can help the patient stop taking it. The patient is on their own.

What This Does Not Mean

The most common defense of the current prescribing paradigm is that the drugs help some patients, and that essays like this one endanger those patients by encouraging them to stop.

Some patients do report subjective benefit on these drugs. That is not disputed. What is not established is that this benefit exceeds placebo by a clinically meaningful margin, or that it survives the long-term outcomes documented in Item 11.

The safety caveats throughout this essay, and the resources listed below, exist precisely because abrupt cessation is dangerous. Nothing here recommends abrupt cessation. What is recommended is informed choice, which requires the twelve findings to be visible before the prescription is written or renewed. A patient who wishes to continue after seeing the twelve findings has made a different decision from a patient who was never shown them.

Resources

For patients currently on psychiatric drugs who wish to withdraw, resources exist outside the mainstream medical system. The Ashton Manual (benzo.org.uk/manual/) remains the standard reference for benzodiazepine tapering. The Horowitz-Moncrieff papers on hyperbolic tapering in Lancet Psychiatry (2019) provide the scientific basis for SSRI withdrawal. Mad in America (madinamerica.com) hosts an active community of patients who have withdrawn or are withdrawing. The Amsterdam tapering strip program (taperingstrip.org) makes hyperbolic dose reduction physically possible for antidepressants that do not come in the required small doses. Breggin’s Psychiatric Drug Withdrawal (2013) provides detailed clinical protocols. None of the above require permission from the prescribing physician. All require time and typically a support person. None should be attempted abruptly.

Closing

The twelve findings above are documented. They are not concealed by conspiracy. They sit in FDA labels, peer-reviewed journals, systematic reviews, and the admissions of senior figures within the profession. What conceals them is training.

Psychiatric residency does not require reading Whitaker or Breggin or Gøtzsche. It does not require examining the primary trial data on the drugs the resident will spend a career prescribing. It requires reading the textbooks the profession publishes about itself, the same textbooks that praised electroconvulsive therapy while omitting the memory-loss literature and that continue to cite the STAR*D 67 percent figure. The continuing medical education the practicing psychiatrist attends is funded largely by the pharmaceutical industry, whose interest in the twelve findings is that they should not surface. The drug representatives who visit the office once a month are the primary source of pharmacological information for many prescribers.

The doctor across from the patient in the fifteen-minute consultation is often not withholding information out of malice. The doctor does not have it. What was left out of the training reproduces itself in every consultation the doctor conducts for the rest of the career.

The training explains the local silence. It does not explain how the whole enterprise reached the point where twelve findings of this severity could accumulate without institutional response. That answer comes from someone who ran the enterprise.

Thomas Insel directed the National Institute of Mental Health from 2002 to 2015. He controlled the American federal research budget for psychiatry for thirteen years. He was, in that period, the single most powerful figure in American psychiatric science.

Reflecting on his tenure after leaving the position, he made the following observation, widely reported and repeated in the years since:

I spent 13 years at NIMH really pushing on the neuroscience and genetics of mental disorders. And when I look back on that I realize that while I think I succeeded at getting lots of really cool papers published by cool scientists at fairly large costs, I think $20 billion, I don’t think we moved the needle in reducing suicide, reducing hospitalizations, improving recovery for the tens of millions of people who have mental illness.⁵⁸

Twenty billion dollars over thirteen years, and the head of the enterprise said it moved nothing on suicide, hospitalization, or recovery.

That is not the assessment of a critic. That is the man who ran the enterprise, describing the enterprise, from inside it. Insel went on to write a book defending psychiatric drugs, so the admission cannot be attributed to conversion or apostasy. He continues to believe in the paradigm. He just concedes it produced nothing.

The twelve items above sit inside that enterprise. What the psychiatrist was trained not to tell the patient is what the man who ran it for thirteen years, on his own accounting, could not deny.

How to Explain It to a Six-Year-Old

Imagine a garage that has been fixing cars for many years. Every car that leaves the garage has a bumper sticker that says FIXED.

One day someone counts. Out of every hundred cars leaving the garage, only three actually work. Ninety-seven do not.

The garage keeps operating. The mechanics keep putting on the FIXED stickers. The owner keeps telling everyone the garage fixes seven cars out of every ten.

When someone points out that the real number is three out of a hundred, the owner says yes, he knows the real number is three. He does not correct the seven-out-of-ten claim. He does not put up a new sign. He keeps the stickers.

The people bringing in their cars do not know about the three. They see the FIXED sticker and they drive off. Some of the cars catch fire on the highway. Some of the brakes fail. Some of the cars will not start again once they are turned off.

When people bring the broken cars back, the garage says the problem is not with the fix. The problem is with the car.

That is the garage. The cars are patients. The stickers are prescriptions. The garage is a whole profession.

References

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36. Summarized in Gøtzsche PC. Is Psychiatry a Crime Against Humanity? Institute for Scientific Freedom; 2024. Historical citations include Alpers BJ (1946) and subsequent European autopsy series.
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56. Gøtzsche PC. Is Psychiatry a Crime Against Humanity? Institute for Scientific Freedom; 2024, chapter on Cochrane.
57. Ashton H. Benzodiazepines: How They Work and How to Withdraw. Newcastle upon Tyne: University of Newcastle; 2002.
58. Insel T, quoted in Rogers A. Star neuroscientist Tom Insel leaves the Google-spawned Verily for … a startup? Wired 2017; May 11. See also Whitaker R’s coverage in Mad in America, and Levine B. How to explain top psychiatrists’ “Dr. Strangelove exuberance” unchecked by reality. Mad in America 2025; June 6.

September 27, 2026 Posted by aletho | Deception, Science and Pseudo-Science, Timeless or most popular | Haloperidol, SSRIs, Xanax, Zoloft, Zyprexa | Comments Off on 12 Things Your Psychiatrist Was Trained Not to Tell You