The Top 10 Myths of Modern Psychiatry
An Essay
Over the past four decades, a particular story about mental illness has become cultural bedrock. Depression results from low serotonin. Schizophrenia is a genetic brain disease. Psychiatric medications correct underlying biological abnormalities, much like insulin for diabetes. Left untreated, mental disorders inevitably worsen. These claims appear in pharmaceutical advertisements, medical school curricula, and patient brochures distributed in psychiatrists’ waiting rooms.
The research literature tells a different story. What follows examines ten foundational claims of modern psychiatry against the evidence that has accumulated over fifty years of investigation. The findings do not come from fringe sources—they emerge from studies funded by the National Institute of Mental Health, the World Health Organization, and published in mainstream psychiatric journals.
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Myth 1: Mental Disorders Are Caused by Chemical Imbalances
According to the standard account, depression results from insufficient serotonin, schizophrenia from excess dopamine, and ADHD from inadequate dopamine. Psychiatric medications purportedly correct these imbalances the way thyroid medication corrects hypothyroidism.
Research has never demonstrated a chemical imbalance as the cause of any mental disorder. Joseph Schildkraut proposed the serotonin hypothesis of depression in 1965, but by the mid-1970s, researchers Joseph Mendels and Alan Frazer had concluded the theory arose from inadequate evaluation of contradictory findings. Kenneth Kendler, coeditor of Psychological Medicine, summarized the outcome of decades of research in 2005: “We have hunted for big simple neurochemical explanations for psychiatric disorders and have not found them.”
Several observations directly contradict the serotonin theory. Tianeptine, marketed as an antidepressant, actually lowers serotonin. Mirtazapine, another antidepressant, does not affect serotonin at all. Mice genetically depleted of brain serotonin behave normally. When antidepressants do raise serotonin levels, this change occurs within one to two days—yet the drugs take weeks to show any effect on depression scores, and that effect is barely distinguishable from placebo.
Despite the absence of supporting evidence, the chemical imbalance story has achieved remarkable penetration. Surveys show that 80 percent of patients taking antidepressants or mood stabilizers believe their medication corrects changes that occurred in their brain. Ninety-two percent of American university students report having heard that depression is caused by a chemical imbalance. A 2019 review of 39 popular health websites across ten countries found that 74 percent attributed depression to chemical imbalance or claimed that antidepressants could correct one.
Steven Hyman, former director of the National Institute of Mental Health, acknowledged in 1996 that patients do not start with chemical imbalances—the drugs create them. The brain compensates for the presence of a medication by altering its own chemistry. This compensatory response explains why withdrawal can be so difficult: the brain has adapted to the drug’s presence and requires time to readjust when the drug is removed.
Myth 2: Mental Disorders Are Primarily Genetic
Headlines regularly announce the discovery of genes for schizophrenia, depression, or bipolar disorder. The public has absorbed the message that mental illness runs in families because of hereditary factors.
The evidence does not support this conclusion. When one identical twin develops schizophrenia, the other twin—who shares 100 percent of their DNA—usually does not. If schizophrenia were primarily genetic, concordance rates in identical twins would approach 100 percent. Instead, they hover around 50 percent or lower, meaning that in most cases, having an identical twin with schizophrenia does not result in developing the condition yourself. As researchers R.C. Lewontin, Steven Rose, and Leon Kamin concluded in Not in Our Genes, twin data actually provide stronger evidence for environmental influences than genetic ones.
The most frequently cited genetic study of schizophrenia, the Danish-American adoption study led by Seymour Kety and colleagues at NIMH, contains a remarkable finding that rarely appears in summaries of the research. When the investigators examined rates of schizophrenia among biological relatives of adopted children who developed the condition, they found no increase among mothers, fathers, full brothers, or full sisters. The only elevated rate appeared among half-siblings on the father’s side—a finding so anomalous that it suggests either error or an environmental factor such as abuse within that family line.
Gene-finding studies that make headlines are routinely contradicted by subsequent research. A 1988 Nature study claiming to locate a schizophrenia gene on chromosome 5 was refuted in the same journal issue by another research team that found no such linkage in a Swedish population. The original finding vanished, but the headlines proclaiming a genetic breakthrough had already reached the public.
A 2022 article by the Psychiatric Genomics Consortium claimed schizophrenia has 60-80 percent heritability. Yet analysis of the same group’s data suggests identified genes explain approximately 2 percent of the risk—meaning 98 percent of variance must be attributed to other factors. The strongest of those factors is trauma, which shows a clear dose-response relationship with psychosis: more severe trauma correlates with higher rates of psychotic experiences.
Telling patients their conditions are hereditary removes hope. Genes cannot be changed. Environments, relationships, and the effects of trauma can be addressed through intervention.
Myth 3: Psychiatric Diagnoses Are Valid Disease Categories
The Diagnostic and Statistical Manual of Mental Disorders (DSM) provides the diagnostic categories psychiatrists use to identify mental illness. Reliability—the extent to which different clinicians agree on a diagnosis—improved substantially with the DSM-III in 1980. Validity—whether these categories describe actual diseases with distinct causes and courses—is another matter.
The architects of the DSM-III understood this distinction. Robert Spitzer, who led the revision, hoped that reliable diagnostic categories would eventually be validated through laboratory findings, genetic markers, and biological tests. Nearly forty years later, Darrel Regier, vice-chair of the DSM-5 task force, acknowledged that validity tests “have not lived up to the expectations of Robins and Guze”—the researchers who proposed a path from reliability to validity in 1970.
Field trials for DSM-5 produced sobering results. Major Depressive Disorder achieved a kappa of 0.32, meaning clinicians agreed on this diagnosis at a level barely above chance. Generalized Anxiety Disorder scored 0.20. Schizophrenia, once considered reliably diagnosable, dropped from 0.81 in DSM-III trials to 0.46 in DSM-5 testing. The consistency psychiatrists could achieve in identifying depression and anxiety—two of the most common conditions they treat—proved strikingly poor.
The DSM’s own introduction contains a disclaimer: “There is no assumption that each category of mental disorder is a completely discrete entity with absolute boundaries dividing it from other mental disorders or from no mental disorder.” The manual’s architects knew they were creating conventions for communication, not carving nature at its joints. That caution has not prevented the categories from being treated as though they represent distinct biological conditions.
Paula Clayton, a Washington University psychiatrist and DSM-III Task Force member, discovered that recently bereaved people met all diagnostic criteria for Major Depressive Disorder. The symptoms of grief and the symptoms of clinical depression were indistinguishable by the DSM’s own standards. The committee responded by creating the “bereavement exclusion”—an acknowledgment that identical symptoms do not necessarily indicate disease. That exception has since been narrowed, and grief lasting more than two weeks can now qualify as a mental disorder.
Myth 4: Psychiatric Drugs Prevent Relapse
Relapse prevention studies appear to demonstrate that psychiatric medications keep patients well. The typical design: take patients who have stabilized on medication, randomly assign half to continue the drug and half to placebo, and observe who relapses first. Those withdrawn from medication relapse at higher rates, leading to conclusions that the drugs prevent recurrence of illness.
This methodology contains a fundamental flaw. Patients withdrawn from medication are not returned to their pre-drug state—they are experiencing drug withdrawal. The brain has adapted to the presence of the medication, and abrupt removal produces discontinuation effects that can mimic or trigger the very symptoms the drug was treating. Higher relapse rates in the placebo group may reflect withdrawal phenomena rather than return of underlying illness.
NIMH researchers discovered this pattern in the first follow-up studies of antipsychotics. Patients who had received placebo during initial treatment were less likely to be rehospitalized than those who had received active medication. Relapse rates rose in direct correlation with prior drug dosage: only 7 percent of those who had been on placebo relapsed, compared to 65 percent of those taking high doses before withdrawal.
This finding has been replicated with antidepressants. When patients discontinue antidepressant medication, they face elevated relapse rates. But the relapse occurs in the context of neurological changes the drug itself has produced. Giovanni Fava, editor of Psychotherapy and Psychosomatics, has argued that antidepressants may sensitize the brain to depression, making future episodes more likely. Ross Baldessarini at Harvard reached similar conclusions: interrupting drug treatment produces complications that would not occur if the drug had never been started.
Research comparing patients who were never medicated to those who took and then discontinued medication would clarify this question. Such studies remain rare.
Myth 5: Long-Term Treatment Improves Outcomes
The assumption that continuous medication produces better long-term outcomes underlies treatment guidelines recommending maintenance therapy for years or indefinitely. The evidence points in a different direction.
Martin Harrow, a psychologist at the University of Illinois, followed 64 schizophrenia patients for fifteen years in an NIMH-funded study. At the fifteen-year mark, 40 percent of those who had stopped taking antipsychotics were in recovery, compared to 5 percent of those who remained on medication. The medicated group also showed a threefold higher rate of uniformly poor outcomes. Those who discontinued medication and recovered often left the mental health system entirely—finding employment, some in professional careers, and no longer identifying as mentally ill. Long-term antipsychotic use also carries the risk of tardive dyskinesia—a largely irreversible neurological disorder causing involuntary movements—which affects 40 to 60 percent of chronically treated patients according to the American Psychiatric Association’s own task force.
The World Health Organization conducted two major studies comparing schizophrenia outcomes across countries. Patients in India, Nigeria, and Colombia showed dramatically better outcomes than those in the United States and Europe. The difference in medication use was striking: only 16 percent of patients in developing countries were regularly maintained on antipsychotics, compared to the near-universal medication rates in wealthy nations.
Depression shows a similar pattern. Prior to the introduction of antidepressants, depression was characterized as an episodic disorder. Studies of hospitalized patients showed that approximately half who experienced a first episode would never be rehospitalized. Contemporary studies of medicated depression show far higher rates of recurrence and chronicity.
The evidence on ADHD and stimulant medications tells the same story. Before the NIMH launched its major study of ADHD treatment in the 1990s, the investigators acknowledged in their planning documents that “the long-term efficacy of stimulant medication has not been demonstrated for any domain of child functioning.” The 1994 APA Textbook of Psychiatry stated plainly: “Stimulants do not produce lasting improvements in aggressivity, conduct disorder, criminality, education achievement, job functioning, marital relationships, or long-term adjustment.”
The NIMH’s Multimodal Treatment Study of ADHD (MTA) followed 579 children comparing medication, behavioral therapy, combined treatment, and routine community care. At fourteen months, the investigators declared victory for stimulants based on reduced hyperactivity scores. The study was then converted to naturalistic follow-up, tracking children regardless of whether they continued medication.
At three years, the results reversed. Medication use had become “a significant marker not of beneficial outcome, but of deterioration.” Children who remained on stimulants showed worse hyperactivity and impulsivity than those who had stopped. They had higher delinquency scores, meaning more trouble at school and with police. They were shorter and weighed less than their unmedicated peers. At six and eight years, there were no differences between groups in school grades, arrests, or psychiatric hospitalizations.
William Pelham, one of the principal investigators, summarized the findings: “We had thought that children medicated longer would have better outcomes. That didn’t happen to be the case. There were no beneficial effects, none. In the short term, [medication] will help the child behave better, in the long run it won’t. And that information should be made very clear to parents.”
The children themselves consistently report disliking the medications. Researchers found “a pervasive dislike among hyperactive children for taking stimulants.” Children on Ritalin rated themselves as less happy and more dysphoric. Observers noted they became “passive, submissive,” “socially withdrawn,” and sometimes “zombie-like.” One researcher noted the drugs reduced “curiosity about the environment.” Another observed that medicated children “lose their sparkle.” The drugs work for teachers seeking classroom compliance; whether they benefit the child is another question.
An NIMH study of naturalistic outcomes compared depressed patients who received treatment to those who did not. At six years, treated patients were three times more likely to have ceased functioning in their principal social role and nearly seven times more likely to become incapacitated. The untreated group showed no significant decline in socioeconomic status; 59 percent saw their incomes rise.
When Brown University psychiatrist Michael Posternak tracked untreated depression in 84 patients who relapsed but did not resume medication, 23 percent recovered within one month, 67 percent within six months, and 85 percent within a year. This confirmed what Emil Kraepelin had observed a century earlier about the natural course of depression. As Posternak noted, if 85 percent of untreated patients recover within a year, “it would be extremely difficult for any intervention to demonstrate a superior result.”
Myth 6: Antidepressants Prevent Suicide
The belief that antidepressants reduce suicide risk provides a primary justification for their widespread use. Clinical trial data indicate the opposite.
In 2004, the FDA conducted a meta-analysis of 24 pediatric antidepressant trials involving 4,582 patients. Children and adolescents taking antidepressants showed twice the rate of suicidal thinking and behavior compared to those on placebo. The probability of this result occurring by chance was 1 in 20,000. The finding was so robust that it emerged despite the fact that the trials were designed and conducted by drug companies with no interest in detecting this effect.
Thomas Newman, an epidemiologist on the FDA advisory committee, calculated the statistical significance himself because the FDA had not provided it. He noted that such a dramatic result emerged “for an outcome that the sponsors of the trials were not looking for, and presumably did not wish to find.”
FDA analysis of adult trials showed similar patterns. Paxil produced a statistically significant increase in suicidality across all ages and diagnostic categories. Depressed patients taking Paxil were 6.4 times more likely to develop suicidal thoughts or behavior than those taking placebo. If depression itself caused this suicidality, the placebo group—lacking the supposed benefit of medication—should have fared worse. They fared better.
No completed suicides occurred in either the drug or placebo groups in the pediatric trials. This absence does not indicate safety—actively suicidal patients were excluded from enrollment, participants received close monitoring, and trial duration was brief. What it does demonstrate: leaving depressed children unmedicated for the short duration of a clinical trial did not produce suicides.
The black-box warnings now required on antidepressant labels reflect regulatory acknowledgment that these drugs increase suicidality in children, adolescents, and young adults. The Canadian regulatory agency went further, warning that patients of “all ages” taking these drugs “may experience behavioural and/or emotional changes that may put them at increased risk of self-harm or harm to others.”
The risk extends beyond suicide to violence against others. Reports of SSRI-induced violence appeared soon after Prozac reached the market in 1988. Teicher and colleagues published a landmark 1990 paper describing patients who developed akathisia—a severe inner restlessness—on Prozac, became obsessively suicidal, experienced relief when the drug was stopped, and relapsed when it was resumed. One patient reported: “I tried to kill myself because of these anxiety symptoms. It was not so much the depression.”
Akathisia can drive people to actions destructive to themselves or others. The mechanism parallels amphetamine-induced violence, which permeates the research literature on stimulant drugs. During Japan’s 1954-56 amphetamine epidemic, more than 50 percent of murders in a two-month period were connected to amphetamine use.
In 2001, a Texas jury awarded $6.4 million in a case where Donald Schell, age 60, took two doses of Paxil before shooting his wife, daughter, and granddaughter to death. The Prozac Survivors Support Group documented 133 cases of crime and violence during 1991-92, including 14 murders. Studies of children found that 22 percent of SSRI-treated patients experienced adverse psychiatric events, with 10 percent becoming psychotic and 6 percent manic. Eight percent of children on antidepressants developed mania or hypomania compared to 0.2 percent on placebo.
The FDA’s current antidepressant labels warn of “irritability, hostility, aggressiveness, impulsivity, akathisia (psychomotor restlessness), hypomania, and mania”—symptoms that constitute, as one researcher noted, a virtual prescription for violence. Health Canada’s warning explicitly states that patients may experience changes “that may put them at increased risk of self-harm or harm to others.”
Evidence suggests psychotherapy halves suicide risk. This finding receives little attention compared to the promotion of pharmaceutical interventions.
Myth 7: ECT Is Safe and Effective
Electroconvulsive therapy induces grand mal seizures by passing electricity through the brain. Proponents describe it as a safe and effective treatment for severe depression. Research on efficacy and safety tells a more complicated story.
Controlled studies comparing ECT to simulated ECT—in which patients undergo the same procedure without receiving electrical current—show benefits lasting no more than four weeks. At the 1985 NIH Consensus Conference on ECT, psychologist Edward Opton presented a review of controlled trials demonstrating this limitation. When no assembled shock doctors could produce contradicting evidence, the consensus panel accepted his conclusion.
Four weeks corresponds to the period of maximum brain dysfunction following ECT. Patients emerge from treatment with an acute organic brain syndrome—the brain’s typical response to severe trauma. Symptoms include disturbed memory, impaired comprehension, confusion, and motor disturbances. ECT advocate Richard Abrams acknowledged in his 1988 textbook that patients recovering from ECT “understandably exhibit multiform abnormalities of all aspects of thinking, feeling, and behaving.”
Memory loss is not a rare side effect but a common outcome. In one survey, 74 percent of patients reported memory impairment following ECT, and 30 percent described their memory as permanently affected. Larry Squire and Pamela Slater found that patients questioned seven months after treatment reported memory loss spanning an average of 27 months surrounding the treatment period.
The comparison to head injury is instructive. Neurology recognizes that even mild head trauma frequently produces lasting problems with memory, concentration, and problem-solving. Many patients describe feeling fundamentally changed. ECT delivers a more severe insult than most closed-head injuries, yet its proponents maintain that the resulting symptoms represent therapeutic response rather than damage.
Animal studies consistently demonstrate that electrically induced seizures produce brain cell death and structural changes. The American Psychiatric Association’s 1990 task force report on ECT did not mention the most relevant animal research or the landmark human studies on memory dysfunction. This selective presentation of evidence serves professional interests more than patient welfare.
Myth 8: Withdrawal from Psychiatric Drugs Is Easy
Patients are often told they can stop psychiatric medication whenever they choose, with minimal difficulty. Clinical experience and research demonstrate otherwise.
Estimates suggest that 50 percent or more of patients stopping antidepressants experience withdrawal symptoms. These include headaches, dizziness, fatigue, nausea, tremors, anxiety, agitation, and disturbing dreams. The symptoms resolve when the drug is resumed, leading many patients to conclude their depression has returned and that they require medication indefinitely.
Drug companies and many psychiatrists call these effects “discontinuation syndrome” rather than withdrawal—a terminological choice that obscures the parallel with other drugs of dependence. When a drug produces symptoms upon cessation that resolve upon resumption, standard pharmacology recognizes this as withdrawal. The semantic distinction between “discontinuation syndrome” and “withdrawal” serves marketing purposes.
A systematic review found that withdrawal symptoms were reported by a much higher percentage of patients than guidelines acknowledged, were often severe, and could last months or years. Standard medical advice to taper over two to four weeks proves inadequate for many patients. Research by Mark Horowitz and David Taylor, published in Lancet Psychiatry, demonstrated that the relationship between dose reduction and receptor occupancy is hyperbolic, not linear. Reducing from 20mg to 10mg of an SSRI does not halve receptor occupancy—it reduces it only marginally. Effective tapering requires progressively smaller reductions over extended periods, sometimes years.
Children are not spared. A review of 22 children withdrawn from tricyclic antidepressants found that each experienced multiple withdrawal symptoms including gastrointestinal complaints, drowsiness, decreased appetite, tearfulness, and agitation. Mental health professionals frequently attributed these symptoms to mental illness, stress, or viral infection rather than drug withdrawal, leading to reinstatement of medication.
The Royal College of Psychiatrists and other professional bodies have begun acknowledging that withdrawal can be prolonged and severe. This represents a reversal from decades of minimization. Patients and peer support groups recognized the problem long before professional organizations did.
Myth 9: Untreated Mental Illness Inevitably Worsens
The claim that untreated mental illness follows a deteriorating course provides justification for early and aggressive intervention. Historical and contemporary evidence contradicts this assumption.
Before the introduction of psychiatric medications, depression was understood as a self-limiting condition. NIMH officials in the 1960s and 1970s described it as “one of the psychiatric conditions with the best prognosis for eventual recovery with or without treatment.” Jonathan Cole wrote in 1964 that most depressions are “self-limited.” Nathan Kline observed that “most depressions terminate in spontaneous remissions,” making it difficult to evaluate any treatment.
Studies from the pre-drug era support this view. Kraepelin found that 60 percent of depressed patients experienced only a single episode. A study of 2,700 patients hospitalized between 1909 and 1920 found that more than half admitted for first episodes never experienced another. Swedish physician Gunnar Lundquist followed 216 patients for 18 years and found that 76 percent became “socially healthy” and resumed their usual work.
Schizophrenia, considered the most severe psychiatric condition, also shows evidence of recovery without continuous medication. The World Health Organization’s international studies found recovery rates in developing countries—where most patients received little or no medication—that far exceeded outcomes in medicated Western populations.
The claim that psychosis causes progressive brain damage requiring immediate pharmaceutical intervention lacks support. Nancy Andreasen’s MRI research found that brain volume reductions in schizophrenia patients correlated with antipsychotic medication exposure, not with duration of untreated psychosis. The drugs, not the condition, appeared responsible for the observed changes.
Contemporary outcomes may be worse than historical ones precisely because of treatment. The transformation of depression from an episodic to a chronic condition coincides with the widespread adoption of antidepressant medication. Whether the drugs cause chronicity or simply correlate with it remains debated, but the pattern contradicts claims that treatment prevents deterioration.
Myth 10: The Problem Is Undertreatment
Psychiatric organizations consistently argue that too few people receive treatment and that expanding access would reduce the burden of mental illness. Disability statistics tell a different story.
In 1955, approximately 355,000 Americans were hospitalized with psychiatric disorders—roughly 1 in 468 of the population. By 2007, nearly 4 million Americans were receiving federal disability payments due to mental illness—approximately 1 in 76. This represents a sixfold increase in disability rates during an era of massive expansion in psychiatric treatment.
The pattern holds across diagnoses and countries. In Britain, days of incapacity due to depression tripled between 1984 and 1999, from 38 million to 117 million. Iceland reported that disability due to depression nearly doubled between 1976 and 2000, despite increased antidepressant use. If medications were effective at the population level, the investigators reasoned, “disability, morbidity, and mortality due to depressive disorders” should have decreased.
Studies examining the relationship between treatment and disability find troubling associations. Canadian workers who went on short-term disability for depression and took antidepressants were twice as likely to progress to long-term disability compared to those who did not take medication. The STAR*D trial—the largest study of antidepressant effectiveness ever conducted—found that only 3 percent of patients who entered treatment remained well at the one-year follow-up.
The increase in childhood mental illness is particularly striking. Between 1987 and 2007, the number of children receiving Supplemental Security Income for mental illness rose from 16,200 to 561,569—a 35-fold increase. Bipolar disorder in children, virtually unheard of before the 1990s, increased 40-fold between 1994 and 2003. ADHD diagnoses expanded from roughly 1 percent of children to 10 percent or more.
These figures are not consistent with undertreatment. They suggest that the expansion of psychiatric diagnosis and medication has not reduced disability—and may have contributed to it.
What the Evidence Suggests
The research reviewed here does not support the conclusion that psychiatric treatment should be abandoned. It does suggest that the dominant paradigm—early diagnosis, long-term medication, biological explanations—may produce outcomes worse than alternatives.
Studies consistently show better results for patients who use psychiatric medications selectively or briefly rather than continuously. The WHO schizophrenia studies, Harrow’s fifteen-year follow-up, and naturalistic depression research all point in this direction. Psychotherapy for depression produces outcomes comparable to medication in the short term and superior outcomes in the long term, without the risks of withdrawal or chronicity.
For those already taking psychiatric medication, the research suggests that careful, gradual withdrawal—extending over months or years rather than weeks—allows many patients to discontinue successfully. Peer support and informed clinical guidance improve outcomes. The assumption that medication must continue indefinitely deserves questioning.
The evidence indicates that mental distress is not primarily biological in origin. Trauma, adversity, and social conditions show stronger associations with psychiatric diagnoses than genetics or brain chemistry. Interventions addressing these factors may prove more effective than those targeting hypothetical biological abnormalities.
What emerges from the research is not a case against psychiatry but a case against certainty. The confident claims that have shaped public understanding and clinical practice rest on evidence far weaker than typically acknowledged. Patients deserve access to this information when making decisions about their care.
The sources for this essay include peer-reviewed research published in mainstream psychiatric journals, NIMH-funded studies, World Health Organization investigations, and FDA analyses.
References
Books
Breggin, P.R. (1991). Toxic Psychiatry. New York: St. Martin’s Press.
Breggin, P.R. (2001). Talking Back to Ritalin. Cambridge, MA: Perseus Publishing.
Breggin, P.R. & Breggin, G.R. (1994/2014). Talking Back to Prozac. New York: Open Road Media.
Gøtzsche, P.C. (2015). Deadly Psychiatry and Organised Denial. Copenhagen: People’s Press.
Greenberg, G. (2010). Manufacturing Depression. New York: Simon & Schuster.
Greenberg, G. (2013). The Book of Woe. New York: Plume.
Szasz, T. (1961/2010). The Myth of Mental Illness. New York: Harper Perennial.
Valenstein, E.S. (1998). Blaming the Brain. New York: Free Press.
Whitaker, R. (2010). Anatomy of an Epidemic. New York: Broadway Books.
Key Studies
Harrow, M. & Jobe, T.H. (2007). “Factors involved in outcome and recovery in schizophrenia patients not on antipsychotic medications.” Journal of Nervous and Mental Disease, 195, 406-414.
Horowitz, M.A. & Taylor, D. (2019). “Tapering of SSRI treatment to mitigate withdrawal symptoms.” Lancet Psychiatry, 6, 538-546.
Jablensky, A. et al. (1992). “Schizophrenia: manifestations, incidence and course in different cultures.” WHO ten-country study. Psychological Medicine, Monograph Supplement 20.
Moncrieff, J. et al. (2022). “The serotonin theory of depression: a systematic umbrella review of the evidence.” Molecular Psychiatry, 27, 3243-3256.
MTA Cooperative Group (1999). “A 14-month randomized clinical trial of treatment strategies for ADHD.” Archives of General Psychiatry, 56, 1073-1086. See also Jensen et al. (2007) for 3-year follow-up and Molina et al. (2009) for 8-year follow-up.
Posternak, M.A. et al. (2006). “The naturalistic course of unipolar major depression in the absence of somatic therapy.” Journal of Nervous and Mental Disease, 194, 324-329.
Teicher, M.H. et al. (1990). “Emergence of intense suicidal preoccupation during fluoxetine treatment.” American Journal of Psychiatry, 147, 207-210.
Regulatory Sources
FDA (2004). Meta-analysis of pediatric antidepressant trials leading to black-box warning on suicidality.
GlaxoSmithKline (2006). “Dear Healthcare Provider” letter on Paxil and adult suicidality.
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The biggest error in psychiatry is that it takes a spiritual nature, looks to make it physical and chemical and unleashes more harm than good.
I argue our mind is this etheric vehicle we interact with, providing us with a plethora of info all at once. Unless we know for to decipher these thoughts, feelings, etc, we can be overwhelmed and some cases, snap.
This is a spiritual nature we live in and when we can see nature in everything, including the mind, everything becomes unlocked.
Here’s some older archived pieces I’ve written specifically on the mind:
https://unorthodoxy.substack.com/p/how-to-train-your-mind-part-one
https://unorthodoxy.substack.com/p/how-to-train-the-mind-part-2
Thanks for this piece. Love this work!
Very nice and insightful overview!