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Feeling Better, Getting Worse: How Psychiatric Drugs Create the Illusion They Cure

An Essay on Short-Term Improvement, Long-Term Dependence, and the Evidence Patients Never See

Lies are Unbekoming | April 9, 2026

Of 18,426 patients enrolled in 71 antidepressant trials — 67,319 pages of clinical data, a stack seven metres high, obtained from drug regulators and read for the first time by Peter Gøtzsche’s research group — 12 percent more dropped out while taking the drug than while taking placebo.¹

The psychiatrists’ position is that these drugs do more good than harm. The patients, through their behaviour, delivered the opposite verdict. They preferred the sugar pill.

Nobody who takes a psychiatric drug and reports feeling better is lying. The experience is real. But what produced it, what it is made of, and what it costs — none of this is what the patient was told. Six mechanisms account for almost everything people attribute to their medication. None of them require the drug to be treating a disease.

The Prescription

A person in distress sits across from a doctor. Fifteen minutes later they leave with a diagnosis and a prescription. They are told they have a chemical imbalance that the drug will correct. They may be told depression runs in families — that there is a genetic predisposition, a biological vulnerability they inherited. They are told to give it a few weeks.

The chemical imbalance theory has been abandoned by every serious researcher in the field.² No gene or set of genes for depression has ever been identified despite decades of searching and billions in funding. As Peter Breggin observed, there is no substantial scientific evidence that depression is genetic in origin — and telling patients otherwise leaves them convinced they are stuck with an innate defect, dependent on experts, and resigned to lifelong medication.⁴⁵ The drug was approved on the basis of trials lasting five to six weeks.³ Long-term effects have never been properly studied.⁴ And the condition being treated has a spontaneous remission rate so high that the head of the NIMH’s depression section once observed that most depressive episodes “will run their course and terminate with virtually complete recovery without specific intervention.”⁵

The patient knows none of this. They go home, swallow the pill, and wait.

The First Weeks: Time Heals What the Pill Takes Credit For

Depression, before pharmacology claimed it, was understood to be self-limiting. NIMH psychopharmacologist Jonathan Cole wrote in 1964: “Depression is, on the whole, one of the psychiatric conditions with the best prognosis for eventual recovery with or without treatment. Most depressions are self-limited.”⁶ His colleague Nathan Kline: “In the treatment of depression, one always has as an ally the fact that most depressions terminate in spontaneous remissions. This means that in many cases regardless of what one does the patient eventually will begin to get better.”⁷

Cole and Kline were not dissidents. They were among the most prominent figures in American psychopharmacology.

A study tracking eighty-four patients through untreated depressive episodes found that 23 percent recovered within one month, 67 percent within six months, and 85 percent within a year.⁸ Mark Posternak, the researcher, noted that his results confirmed Kraepelin’s century-old observation that untreated depression typically clears within six to eight months. Dean Schuyler, who headed the NIMH’s depression section, recognised the problem as early as 1974: spontaneous recovery rates were so high that it was difficult to “judge the efficacy of a drug, a treatment or psychotherapy in depressed patients.”⁹

Antidepressants take four to six weeks to produce their claimed effect. Spontaneous recovery begins immediately and continues at roughly 2 percent per week.¹⁰ A person who starts a drug during a depressive episode is beginning treatment at the moment when natural recovery is already underway. A month later, they feel better. The drug gets the credit. The calendar does not.

The Side Effects That Sell the Cure

In the NIMH’s review of all antidepressant studies, well-controlled trials showed 61 percent of drug-treated patients improved versus 46 percent on placebo — a net benefit of 15 percent.¹¹ Irving Kirsch, reviewing FDA data on Prozac, Effexor, Serzone, and Paxil, found the drug-placebo difference on the Hamilton Rating Scale was 1.8 points. The UK’s National Institute for Clinical Excellence had established 3 points as the minimum for clinical significance.¹² The best Danish meta-analysis found a difference of 2 points, and the smallest effect that can actually be perceived on this scale is 5 to 6 points.¹³

That is the margin on which billions of prescriptions rest.

Breggin identified why even this margin exists. He called it the “enhanced placebo effect.” A patient on a sugar pill senses, consciously or not, that nothing powerful has entered their system. An antidepressant produces noticeable physical effects — dry mouth, nausea, drowsiness, sexual dysfunction, weight change. The patient feels these and concludes, reasonably, that they are taking potent medicine. The side effects convince the patient the drug is real. This conviction amplifies the placebo response.¹⁴

Investigators tested this in at least seven studies comparing tricyclic antidepressants to “active” placebos — chemicals that produce unpleasant side effects like dry mouth but have no antidepressant properties. In six of the seven, there was no difference in outcomes.¹⁵ When both pills cause side effects, neither is superior. A Cochrane review confirmed the finding.¹⁶

The entire marginal advantage of antidepressants over placebo may be an artefact of broken blinding. Patients and clinicians can guess who is on the drug and who is on the sugar pill, because the drug has obvious physical effects. This knowledge contaminates every rating, every assessment, every reported outcome.

The NIH-funded St. John’s wort trial demonstrated this by accident. Because St. John’s wort causes side effects similar to an antidepressant, this trial was genuinely blinded — neither patients nor clinicians could tell who was taking what. Results: 24 percent of the herbal group had a full response, 25 percent of the Zoloft group, 32 percent of the placebo group. Zoloft did not outperform placebo. The investigators concluded that the herb was ineffective and neglected to mention that their own drug had failed the same test.¹⁷

The Flattening

Psychiatric drugs produce their effects the same way in patients, healthy volunteers, and laboratory animals. Gøtzsche, drawing on clinical trial data, lists what these effects actually are: numbing of feelings, emotional blunting, drowsiness, reduced concern about oneself and others, diminished capacity for sexual function and romantic attachment.¹⁸

These are not side effects. They are the effects. The drug does not selectively remove depression while leaving everything else intact. It reduces the brain’s capacity to generate emotional intensity across the board. A person who was in anguish may interpret this flattening as recovery. A clinician observing calmer behaviour will rate the patient as improved. Both are observing something real. Neither is observing the treatment of a disease.

Breggin made the point precisely: antidepressants reduce emotional responsiveness generally, which is why they are prescribed not only for depression but for anxiety, panic attacks, obsessive-compulsive behaviour, bulimia, chronic pain, and aggression. They are not treating different diseases through different mechanisms. They are producing the same blunting effect across all of them.¹⁹

The rating scales used to measure “improvement” cooperate with this illusion. The Hamilton Depression Rating Scale — the standard instrument — scores items like sleep quality, appetite, and psychomotor behaviour. A sedated patient who sleeps more and eats more registers as improved. Breggin observed that psychiatric improvement standards are often behavioural (”sleeps better,” “gaining weight”) rather than psychological (”feels better about life,” “actively building a better future”).²⁰ A tranquillised patient and a recovered patient score identically.

Patient self-ratings tell a different story. In Greenberg and Fisher’s meta-analysis of newer antidepressants, patient self-ratings showed virtually no benefit beyond placebo.²¹ The doctors see improvement. The patients, asked directly, do not.

In Denmark, researchers surveyed patients on antidepressants. Half agreed the drugs altered their personality and that they had less control over their thoughts and feelings. The psychiatrists who received these results refused to believe what their own patients told them, called the patients ignorant, and recommended “psychoeducation.”²² The patients’ relatives, independently surveyed, agreed with the patients.

Breggin described a further mechanism operating in some patients: mild organic brain syndrome. Antidepressants, through their general toxicity, can produce a delirium characterised by memory difficulties, confusion, impaired judgment, and mood instability. A patient in this state may experience artificial euphoria or generalised apathy and be evaluated as “improved” — because depression requires a relatively intact brain to sustain itself. Damage the brain sufficiently and the depression lifts, not because the distress has been addressed, but because the capacity to experience it has been impaired.²³ A Yale study found this drug-induced delirium appeared two to four weeks after starting treatment — the exact interval when “therapeutic response” is expected — in more than one-third of patients over age forty.²⁴

The Attempt to Stop

Months pass. Perhaps years. The patient decides to stop. They feel well. They are tired of the side effects. They may have read something that unsettled them.

Within days: headaches, dizziness, nausea, insomnia, agitation, anxiety, confusion, fatigue, flu-like symptoms, electric shock sensations. As many as 50 percent of patients who stop antidepressants experience these withdrawal effects.²⁵

The symptoms vanish when the drug is restarted. The trap closes.

Patient and doctor both conclude that the return of distress proves the drug was treating a real condition. The depression has “come back.” The drug is “needed.” But the symptoms are not relapse. They are withdrawal. The brain, having adapted to the presence of a chemical that altered its neurotransmitter activity, protests the chemical’s removal.

Gøtzsche coined a term for this: “abstinence depression.” A depression that occurs in a patient who is not currently depressed but whose drug is stopped too quickly. Its hallmark: symptoms appear rapidly after discontinuation and disappear within hours when the full dose is resumed. A real depressive episode does not respond to a pill within hours. The speed of response is the diagnostic marker that separates withdrawal from genuine relapse.²⁶

He demonstrated this with a cold turkey trial. Stable, well patients were secretly switched to placebo for 5 to 8 days. Twenty-five of 122 patients on sertraline or paroxetine met criteria for depression during that window. Gøtzsche calculated the expected number of genuine relapses in such a short period, based on known relapse rates from an adolescent depression study: 0.03. Effectively zero. Every one of the twenty-five “relapses” was a withdrawal reaction.²⁷

The profession does not call these symptoms “withdrawal.” It calls them “discontinuation syndrome.” Gary Greenberg described this renaming for what it is: in any other context, a malaise that appears when you stop a drug and disappears when you restart it is called dependence with withdrawal. Calling it “discontinuation syndrome” keeps antidepressants at a comfortable distance from alcohol, benzodiazepines, and opioids.²⁸

The clinical consequences are specific. Breggin described the vicious circle: a patient attempts to stop the drug and experiences withdrawal. The treating professionals mistake withdrawal for relapse. The drug is reinstated. The patient — who might have recovered fully without the medication — is now physiologically dependent on a chemical they were told was safe to stop at any time.²⁹ A study of twenty-two children withdrawn from the tricyclic Tofranil documented this pattern: staff attributed the children’s withdrawal symptoms to “mental illness,” to stress, to allergies, even to viral illness. Antidepressants were restarted in children who were “mistakenly diagnosed as relapsing during the withdrawal period.”³⁰

Gøtzsche reviewed the five most-used psychiatry textbooks in Denmark and found that their withdrawal guidance is wrong and frequently dangerous. Doctors taper too quickly and in linear fashion rather than the exponential taper the drugs’ pharmacology demands. None of the textbooks acknowledged that withdrawal symptoms and disease symptoms are often identical.³¹

The Long Decline

European psychiatrists began noticing the pattern in the 1960s. German physician H. P. Hoheisel reported in 1966 that antidepressant exposure appeared to be “shortening the intervals” between depressive episodes. A Yugoslavian doctor observed the drugs were causing “chronification” of the disease. Bulgarian psychiatrist Nikola Schipkowensky agreed: the tricyclics were inducing “a change to a more chronic course.”³²

Dutch physician J. D. Van Scheyen examined ninety-four depressed patients over five years. Long-term antidepressant medication, he found, “exerts a paradoxical effect on the recurrent nature of the vital depression” — the drugs increased the rate of recurrence and shortened the time between episodes.³³

In 1994, Italian psychiatrist Giovanni Fava forced the question into the open. The drugs, he argued, perturb neurotransmitter systems in ways that produce compensatory brain changes. When the drug is stopped, these changes operate unopposed, producing withdrawal and increasing vulnerability to relapse. The longer someone takes the drug, the worse this becomes. Antidepressants, Fava concluded, “may propel the illness to a more malignant and treatment unresponsive course.” He raised the possibility that the drugs cause “irreversible receptor modifications” that “sensitize” the brain to depression.³⁴

Ross Baldessarini of Harvard confirmed it: half of all patients withdrawn from antidepressants relapsed within fourteen months, and the longer a person had been on the drug, the higher the relapse rate upon withdrawal.³⁵

The profession’s response was not investigation. Donald Klein of Columbia University told Psychiatric News: “The industry is not interested, the NIMH is not interested, and the FDA is not interested. Nobody is interested.”³⁶

Instead, the history was rewritten. The pre-drug studies showing that depression was episodic and self-limiting were declared “flawed.” The 1999 APA Textbook of Psychiatry stated that it was previously believed “most patients would eventually recover from a major depressive episode. However, more extensive studies have disproved this assumption.” Depression was now “a highly recurrent and pernicious disorder.”³⁷

The drugs worsen the long-term course of the illness. Rather than withdraw the drugs, the profession rewrote the natural history of the illness to match the drug-damaged outcomes.

The long-term studies are unambiguous. British researchers found that never-medicated depressed patients experienced a 62 percent symptom reduction in six months; drug-treated patients, 33 percent.³⁸ A WHO study found that patients diagnosed and treated with psychiatric drugs fared worse — in both depressive symptoms and general health — over one year than those not exposed to the drugs.³⁹ In a five-year study of 9,508 depressed patients, those on antidepressants were symptomatic nineteen weeks per year, versus eleven weeks for those on no medication.⁴⁰ An NIMH study found the eighteen-month stay-well rate was highest for cognitive therapy (30 percent) and lowest for antidepressants (19 percent).⁴¹

The STAR*D trial — $35 million of NIMH money, over four thousand “real-world” patients — was announced with the claim that about 70 percent of those who stayed in the study “became symptom-free.” Ed Pigott and colleagues spent more than five years analysing the actual data. The real figure: 3 percent of patients who entered the trial remitted, stayed well, and remained in the study during the one-year follow-up. Confronted with the 3 percent number, investigator Maurizio Fava acknowledged it was accurate. The investigators had known all along.⁴²

The Patients Vote

Those 18,426 patients across Gøtzsche’s 71 trials voted with their feet. Twelve percent more chose to stop taking the drug than chose to stop taking placebo.¹ The finding is worse than it appears, because some of the patients randomised to placebo were suffering cold turkey withdrawal from drugs they had been taking before the trial. Even with this handicap, the placebo group was more willing to continue.

Gøtzsche’s team attempted to assess quality of life — the outcome that matters most to patients. The data was virtually non-existent. Out of 131 studies, three had published quality-of-life results. The data was not missing because it was not collected. It was missing because the results were unfavourable.⁴³

A Danish parliamentarian asked the Minister of Health whether it was reliable to conclude that antidepressants improved quality of life when only three of 131 studies had published data on the question. The minister referred the question to the drug agency, which replied that an effect on quality of life had been found in the studies where it was measured. Quality of life was measured in far more studies than those that published their findings.⁴⁴

What Was Not Disclosed

The feeling was real. It was produced by the natural passage of time and the body’s tendency toward spontaneous recovery. By the placebo effect of receiving treatment from an authority figure. By the enhanced placebo effect of a pill that produces noticeable physical sensations. By emotional blunting that reduced the capacity to feel distress along with the capacity to feel everything else. And in some patients, by a mild organic brain dysfunction that made the sustained experience of depression temporarily impossible.

When it came time to stop, the drug produced withdrawal symptoms indistinguishable from the original condition. Patient and doctor both interpreted this as proof that the disease had returned and the medication was needed for life. The dependence was renamed “discontinuation syndrome.”

For those who stayed on, the drug altered brain chemistry in ways that increased vulnerability to future episodes, shortened the intervals between them, and converted an episodic, self-limiting condition into a chronic one. This conversion was attributed not to the treatment but to a revised understanding of the disease. The textbooks were rewritten to match the drug-damaged outcomes.

At no point was the patient given accurate information. Not about the spontaneous remission rate. Not about the drug’s negligible advantage over placebo. Not about the blunting. Not about the withdrawal. Not about the long-term prognosis.

Three percent of STAR*D patients recovered and stayed well. The investigators announced 70 percent. Sixty-seven thousand pages of clinical trial data sat unread until one research group opened them and discovered that patients preferred placebo. Quality of life data was collected and buried. The profession was told the drugs were sensitising the brain to depression and responded that nobody was interested in investigating.

The patient was told they had a chemical imbalance. They were told the drug would correct it. They were told depression ran in their family and that they were genetically predisposed. They were told to give it a few weeks. Every element of that narrative has been contradicted by the profession’s own research.

The feeling was real. What produced it was not what they said.

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References

1. Sharma, T., et al. “Drop-out rates in placebo-controlled trials of antidepressant drugs.” Int J Risk Saf Med 30 (2019): 217–232. Discussed in Gøtzsche, P.C. “Is psychiatry a crime?” (2024), p. 21.
2. Moncrieff, J., et al. “The serotonin theory of depression: a systematic umbrella review of the evidence.” Molecular Psychiatry (2022). See also Lacasse, J.R., Leo, J. “Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature.” PLoS Med (2005).
3. Breggin, P.R. Toxic Psychiatry. New York: St. Martin’s Press, 1991, pp. 160–163.
4. Deshauer, D., et al. “Selective serotonin reuptake inhibitors for unipolar depression.” Canadian Medical Association Journal 178 (2008): 1293–1301.
5. Schuyler, D. The Depressive Spectrum. New York: Jason Aronson, 1974. Cited in Whitaker, R. Anatomy of an Epidemic. New York: Broadway Paperbacks, 2010, p. 150.
6. Cole, J. Cited in Whitaker, Anatomy of an Epidemic, p. 150.
7. Kline, N. Cited in Whitaker, Anatomy of an Epidemic, p. 150.
8. Posternak, M.A., et al. “The naturalistic course of unipolar major depression in the absence of somatic therapy.” J Nerv Ment Dis 194 (2006): 324–329. Cited in Whitaker, Anatomy of an Epidemic, pp. 163–164.
9. Schuyler, D. Cited in Whitaker, Anatomy of an Epidemic, p. 150.
10. Posternak, J Nerv Ment Dis (2006).
11. NIMH review of antidepressant studies. Cited in Whitaker, Anatomy of an Epidemic, p. 151.
12. Kirsch, I., et al. “Initial severity and antidepressant benefits.” PLoS Medicine 5 (2008): e45. Cited in Whitaker, Anatomy of an Epidemic, pp. 152–153.
13. Jakobsen, J.C., et al. “Selective serotonin reuptake inhibitors versus placebo.” BMC Psychiatry 17 (2017): 58. Leucht, S., et al. “What does the HAMD mean?” J Affect Disord 148 (2013): 243–248. Cited in Gøtzsche, “Is psychiatry a crime?” p. 19.
14. Breggin, P.R. Toxic Psychiatry, pp. 159–160.
15. Whitaker, Anatomy of an Epidemic, p. 151.
16. Moncrieff, J., Wessely, S., Hardy, R. “Active placebos versus antidepressants for depression.” Cochrane Database Syst Rev (2004): CD003012.
17. Hypericum Depression Trial Study Group. “Effect of Hypericum perforatum in major depressive disorder.” JAMA 287 (2002): 1807–1814. Cited in Whitaker, Anatomy of an Epidemic, p. 153.
18. Gøtzsche, P.C. “Is psychiatry a crime?” (2024), p. 9.
19. Breggin, P.R. Toxic Psychiatry, pp. 163–164.
20. Ibid., pp. 160–161. Fisher, S. and Greenberg, R. The Limits of Biological Treatments for Psychological Distress. Hillsdale, NJ: Erlbaum, 1989.
21. Greenberg, R., et al. Meta-analysis of newer antidepressant drugs. Cited in Breggin, P.R. Talking Back to Prozac. New York: St. Martin’s Press, 1994, pp. 89–92.
22. Kessing, L., et al. “Depressive and bipolar disorders: patients’ attitudes and beliefs towards depression and antidepressants.” Psychological Medicine 35 (2005): 1205–1213. Cited in Gøtzsche, “Is psychiatry a crime?” p. 21.
23. Breggin, Toxic Psychiatry, pp. 164–166.
24. Davies, R., et al. “Confusional Episodes and Antidepressant Medication.” American Journal of Psychiatry (July 1971). Cited in Breggin, Toxic Psychiatry, pp. 165–166.
25. Greenberg, G. Manufacturing Depression. New York: Simon & Schuster, 2010, pp. 281–282.
26. Gøtzsche, “Is psychiatry a crime?” pp. 104–105.
27. Rosenbaum, J.F., et al. “Selective serotonin reuptake inhibitor discontinuation syndrome.” Biol Psychiatry 44 (1998): 77–87. Analysis in Gøtzsche, “Is psychiatry a crime?” pp. 104–105. Expected relapse rate calculated from Lewinsohn, P.M., et al. J Am Acad Child Adolesc Psychiatr 33 (1994): 809–818.
28. Greenberg, Manufacturing Depression, pp. 281–282.
29. Breggin, P.R. Toxic Psychiatry, pp. 169–171.
30. Law, W., III, et al. American Journal of Psychiatry (May 1981). Cited in Breggin, Toxic Psychiatry, pp. 169–170.
31. Gøtzsche, “Is psychiatry a crime?” pp. 104–105. See also Gøtzsche, P.C. Mental Health Survival Kit and Withdrawal from Psychiatric Drugs. Ann Arbor: L H Press, 2022.
32. Hoheisel, Schipkowensky, and others cited in Whitaker, Anatomy of an Epidemic, pp. 155–156.
33. Van Scheyen, J.D. Cited in Whitaker, Anatomy of an Epidemic, p. 156.
34. Fava, G. “Do antidepressant and antianxiety drugs increase chronicity in affective disorders?” Psychotherapy and Psychosomatics 61 (1994): 125–131. Fava, G. “Holding on: depression, sensitization by antidepressant drugs, and the prodigal experts.” Psychotherapy and Psychosomatics 64 (1995): 57–61. Cited in Whitaker, Anatomy of an Epidemic, pp. 157–159.
35. Viguera, A. “Discontinuing antidepressant treatment in major depression.” Harvard Review of Psychiatry 5 (1998): 293–305. Cited in Whitaker, Anatomy of an Epidemic, p. 156.
36. “Editorial sparks debate on effects of psychoactive drugs.” Psychiatric News, May 20, 1994. Cited in Whitaker, Anatomy of an Epidemic, p. 159.
37. Hales, R., ed. Textbook of Psychiatry. Washington, DC: American Psychiatric Press, 1999, p. 525. Cited in Whitaker, Anatomy of an Epidemic, pp. 159–160.
38. Ronalds, C., et al. “Outcome of anxiety and depressive disorders in primary care.” British Journal of Psychiatry 171 (1997): 427–433. Cited in Whitaker, Anatomy of an Epidemic, p. 162.
39. Goldberg, D., et al. “The effect of detection and treatment on the outcome of major depression in primary care.” British Journal of General Practice 48 (1998): 1840–1844. Cited in Whitaker, Anatomy of an Epidemic, p. 168.
40. Whitaker, Anatomy of an Epidemic, pp. 168–169.
41. Shea, M.T., et al. “Course of depressive symptoms over follow-up.” Archives of General Psychiatry 49 (1992): 782–787. Cited in Whitaker, Anatomy of an Epidemic, p. 156.
42. Pigott, H.E., et al. “Efficacy and effectiveness of antidepressants.” Psychother Psychosom 79 (2010): 267–279. Gøtzsche, “Is psychiatry a crime?” pp. 27–28.
43. Paludan-Müller, A.S., et al. “Extensive selective reporting of quality of life in clinical study reports and publications of placebo-controlled trials of antidepressants.” Int J Risk Saf Med 32 (2021): 87–99. Discussed in Gøtzsche, “Is psychiatry a crime?” pp. 21–22.
44. Gøtzsche, “Is psychiatry a crime?” p. 22.
45. Breggin, P.R. Talking Back to Prozac. New York: St. Martin’s Press, 1994, pp. 73–74. See also Breggin, Toxic Psychiatry, pp. 109–141 (chapter on genetics of psychiatric disorders).

April 11, 2026 - Posted by aletho | Deception, Science and Pseudo-Science, Timeless or most popular | SSRIs