In medicine, we love a good heroic story. A patient suffers a serious disease. A drug company produces a brilliant new drug which proves to be beneficial. Lives are saved. Everyone is happy. Another battle won in the war on disease. Science marches triumphantly forward.
But sometimes the real story is less heroic and far more awkward. And the major “advance” comes not from a new drug, but from the opposite: because patients stopped swallowing a drug that never should have been so widely used in the first place.
That is almost certainly the case of breast cancer in North America in the early 2000s.
The pivotal moment came in the summer of 2002 when a major randomized trial, called the Women’s Health Initiative (WHI) was published, aiming to answer a question which physicians had long pondered: was long-term use of hormone replacement therapy, typically prescribed for women going through menopause, good for the heart?
Up to that point, hormone therapy had been marketed as a kind of fountain-of-youth elixir for menopausal women. Promising to protect the heart, keep bones strong, preserve youthfulness, and generally smooth out biological inconveniences of aging, women were prescribed these drugs and stayed on them for years, sometimes for decades. At that time, there was considerable debate about long-term effects, with some experts claiming the heart protective-effects of hormones were so pronounced that even studying the issue was a waste of time.
Launched in 1997, the WHI enrolled more than 16,000 post-menopausal women to test the effects of combined estrogen-progestin. Another arm tested the effects of estrogen alone in 10,000 women who had undergone a hysterectomy. The larger trial was terminated three years earlier than originally planned, once the findings showed an increased risk of breast cancer, heart disease, stroke, and blood clots among participants. The smaller trial was also halted a year earlier than planned due to increased risk of stroke.
That was the day that the music died for hormone therapy.
Or at least we thought.
Within months women stopped taking and physicians stopped prescribing hormone therapy. The everyday use of this class of drugs fell dramatically, by roughly half within a year.
And then something remarkable happened.
Breast cancer incidence in the United States dropped. Some say that the rates had been in decline for several years, but the drop was significant, falling by roughly six to seven percent in 2003. It was one of the sharpest year-to-year declines ever observed. The drop was especially pronounced among women over 50 and in estrogen-receptor positive tumors, precisely the cancers most likely to be stimulated by hormones.
This wasn’t a subtle statistical wiggle. For epidemiologists, this was the sort of signal that almost never happens so cleanly in real life. Usually population health trends are messy, tangled up in dozens of possible explanations. There are long latency periods with cancer yet here a cause and effect appeared almost choreographed.
Drug exposure goes down. Disease incidence goes down, Just like that. Overnight, by stopping a drug we probably saw the most important advance in the fight against breast cancer in the last half century. But….
HRT Revisited
But today? Memories are short, and for many obstetricians, women’s health advocates, and even health reporters, it seems like the lessons from the WHI are being rewritten. The known and proven harmful effects of hormones on women’s health are undergoing a massive rewrite which is stimulating a resurgence in HRT.
This new Hormone Replacement Therapy conversation lately is captured in such articles as this piece from PBS; “How a Decades Old Study Gave Hormone Therapy a Bad Reputation,” which calls the WHI a “flawed” study. Other major media outlets like the New York Times, the Washington Post and TIME Magazine are eagerly celebrating the renewed interest in menopause, emphasizing that women’s health concerns are never adequately dealt with, and that HRT needs a second look.
The media attention was amped last year up when the FDA convened an Expert Panel on Menopause and Hormone Replacement Therapy for Women. That meeting led to the removal of the boxed warnings in November 2025 even though the labels still warn of the risk of uterine and endometrial cancer associated with estrogen-only HRT, which is typically prescribed to people who have had their uterus removed through a hysterectomy.
A lot of the hullabaloo over the removal of the FDA’s Black Box Warning on Hormone Therapy relied on a strange mix of both revisionism (the science has changed) and egalitarianism (women needed “more choice”). For the media, this was an easy sell.
The rationale used by the FDA committee and hormone aficionados everywhere was that the science has been fully reinterpreted, and “corrected.” Let’s be clear what has happened: there has been new “analyses” of the effects of hormones, but no new original research showing that the previous safety concerns are exaggerated.
Much of the renewed support for HRT uses the ‘window of opportunity’ argument that suggests that it is safe if a 50-year-old woman takes hormones, but in her 60’s it’s unsafe. Can we really accept that the effects of these drugs on women would be dramatically different at some sort of arbitrary age-related cutoff? That’s the line we are expected to believe.
But look at how that argument is easily confounded. If the drugs show a reduced harm in younger women that’s mostly because, for any disease, younger age usually means lower disease burden. The revisionists discredit the WHI even though there were thousands of women in their 50’s in that trial, and many of them were among those harmed.
A distinction needs to be made here, where one has to examine the exact reason why one is taking hormones. Is it to control menopausal symptoms (especially hot flashes, vaginal dryness) or to prevent diseases of aging (breast cancer, heart disease, dementia)?
The WHI study was aimed at determining the long-term, post-menopausal effects of the drug, and hence it was looking at the second question. As to the first question, hormones are undoubtedly effective for treating menopausal symptoms.
Symptomatic treatment is therefore behind the major push for the drugs these days. One doctor friend of mine told me that “every menopausal woman he knows is taking hormones,” implying that this was both right and natural. Another friend, who is turning 60 this year, just recently told me over coffee she’s been on the drugs for ten years and has no plans for stopping them, as she remembers how bad the sleeplessness and brain fog were when she was in menopause. This was a head-scratcher to me, left me wondering why her doctor isn’t concerned about the recent post-black box warning recommendations that if menopausal women are going to take hormones they should do so in the lowest dose possible, for the shortest period of time possible.
The message here: take these drugs, but not for long, and not in high doses. That’s the pharmaceutical equivalent of someone shouting “Danger!”
What pharmaceutical companies do best is not develop drugs, but develop drug markets and you see this on full display in the current menopausal makeover. With a highly malleable clientele, who have both money and motivation, the key obstacle is convincing prescribers that these women urgently need chemical assistance to get through this tough life transition, and that prescribing hormones is one way to fight back against the manosphere. Were it only so easy…
Revising the HRT market depends on the usual tactics: some high-octane marketing including funding pro-HRT “studies,” selectively publishing data that emphasize HRT’s benefits and downplay the harms, funding direct-to-consumer advertising campaigns wrapped in the justice angle, while sponsoring guideline panels and medical education for your and my doctors. By paying off key opinion leaders, and getting social media influencers slurping on the HRT taps the media serves up this revival as a “feel-good” story of female emancipation.
Let’s face it, menopause in 2026 is the sort of uplifting health story that the mainstream media has leaped on with uncommon gusto. In Canada, our public broadcaster, CBC, finds the subject so compelling it runs its own series (Small Achievable Goals) about menopause, organizes noontime Menopause Month call-in shows to dive into the many ‘equity’ issues related to menopause (like why are Canadian women paying out of pocket for menopause care from private practitioners?) and produces a litany of programs that are mostly repetitive recitations over the need to counter the “stigma” caused by menopause. We get it. Menopause is clearly not fun for many women and employers who don’t make concessions for suffering women need to be brought into the 21st century.
The punchline, however, always seems the same: Women are not being taken seriously when it comes to menopause and they’re mad as hell. And no one should stand in their way of getting full access to menopausal treatments, especially those prescribed medications produced by the biggest drug companies in the world. We have a term for this: Pinkwashing. In other words, taking corporate business objectives and painting them in a feminine way in order to show how much you care.
You don’t have to do a systematic review of the mainstream media’s menopause mongering, but even a quick global survey of the main English language outlets can identify some dominant themes. Even though millions of women stopped HRT in 2002, and breast-cancer incidence dropped significantly, not a single story in 2026, as far as I can tell, mentions this fact. It’s curious. Even though most epidemiologists who have examined these data say that all the evidence points towards HRT promoting breast-tumor growth.
The remake of HRT has certainly paid off. Overall HRT demand in North America has grown, driven by what the experts call “increased menopause awareness, guideline updates, and reduced stigma.” Data from insurance claims and health systems show hormone therapy use is steadily rising again after years of decline. Its use among women aged 45–65 increased about 20% between 2020 and 2023. This pink trend is occurring alongside a surge in menopause clinics, telehealth menopause services, and the growing pervasiveness of influencer physicians and social-media menopause advocates.
The HRT market in North America has grown steadily too, worth about $5 billion per year, dominated by drugs like Premarin (branded conjugated estrogens) made by Pfizer. Without any generic competition in the US until late 2025 Pfizer has been able to dominate the market, selling more than $100 million worth of Premarin in 2022 alone. Prempro (conjugated estrogens + medroxyprogesterone,) has been generically available since 2006 or so and has many other generic companies dominating the market due to much lower pricing.
Let’s recap.
Medicine has a long history of embracing interventions that appear beneficial at first glance, only to discover later that the harms outweigh the benefits. Hormone therapy for menopause became a textbook example. The dramatic changes in practice left us with one of the clearest natural experiments in modern epidemiology.
The Women’s Health Initiative revealed a risk.
Millions of women stopped taking the drug.
Breast cancer rates fell.
If you were designing a demonstration of how pharmaceutical exposure can shape population health, you could hardly script it better.
The lesson is not that all drugs are bad or that medical progress is an illusion. It’s that sometimes the most powerful intervention in medicine is restraint.
Before we celebrate the next pharmaceutical breakthrough it might be worth remembering that one of the biggest declines in a major, frequently fatal disease in modern history happened for a very simple reason: Millions of women stopped taking a pill.
Some clinicians and public-health researchers (myself among them) would argue that the media narrative minimizes known and proven downsides of these drugs, often trivializing or ignoring serious harms, including risks of stroke, blood clots, gallbladder disease, and increased breast cancer risk.
The swinging pendulum is now carving its frightful arc from fear and danger towards promotional enthusiasm, and women who are supposed to be beneficiaries of these changes will only suffer further.
Alan Cassels is a Brownstone Fellow and a drug policy researcher and author who has written extensively about disease mongering. He is the author of four books, including The ABCs of Disease Mongering: An Epidemic in 26 Letters.
In November 1992, the Journal of the American Medical Association published a paper titled “Evidence-Based Medicine: A New Approach to Teaching the Practice of Medicine.”¹ The authors, the Evidence-Based Medicine Working Group at McMaster University, led by Gordon Guyatt, announced a paradigm shift. The first paragraph named what was being replaced: “intuition, unsystematic clinical experience, and pathophysiologic rationale.”¹ The replacement was a hierarchy in which the randomised controlled trial sat at the top and clinical observation sat near the bottom.
The paper was not modest. It described its proposal in Kuhnian terms and predicted that the old approach — the physician’s accumulated judgement, the recognition of patterns across thousands of patients, the reasoning from mechanism and first principles — would be superseded.¹ Within a decade, the framework had been adopted across major medical journals, accreditation bodies, and clinical guideline organisations. In a 2007 BMJ poll of more than 11,000 readers asked to name the most important medical milestones since 1840, the sanitary revolution placed first, antibiotics second, anaesthesia third; evidence-based medicine appeared on the shortlist of fifteen.²
What was elevated to the top of the hierarchy was the one form of evidence pharmaceutical companies could afford to manufacture at scale. What was demoted to the bottom was everything they could not control. This was not the discovery of how medicine should be practised. It was the redefinition of what counted as knowing. The framework called itself evidence-based. What it actually was, was evidence-biased — a hierarchy in which what counted as evidence was determined, first, by who could afford to produce it.
The essay examines what that redefinition did, who it served, and the cost in lives.
Explain It to a Six-Year-Old
For a long time, children have learned about the world in many ways. Some things they see with their own eyes. Some things they hear from grandparents who have lived a long time. Some things they figure out by thinking carefully. Some things they know because they have tried them and watched what happened. All of these are ways of knowing.
One day, the school makes a new rule. From now on, the only things that count as knowing are things that have been seen in a special room, by a man with a clipboard, who writes down what he saw. Hearing from grandparents does not count anymore. Trying things and watching what happens does not count. Thinking carefully does not count. The teacher tells the children, “Those were just stories. Real knowing happens in the special room.”
The special room is very expensive. Only one company can afford to rent it. The company pays the man with the clipboard. The company decides what gets looked at in the room and what does not. Apples never go in the room. Sunlight never goes in the room. Grandmothers’ soup never goes in the room. So the school says, “We do not know if apples are good. We do not know if sunlight is good. We do not know if grandmothers’ soup is good. Nobody has seen them in the room.”
The company sells biscuits. The biscuits go in the room every day. The man with the clipboard writes down that the biscuits are good. The teacher tells the children, “We know the biscuits are good, because we saw them in the room.”
Some children eat the biscuits and get tummy aches. They tell the teacher. The teacher says, “Tummy aches have not been seen in the room. We do not know that the biscuits cause tummy aches.” When a doctor visits and says she has seen many children with tummy aches after eating biscuits, the teacher says the doctor is only telling stories. Stories do not count.
Years pass. The children eat more biscuits and fewer apples. Many of them are sick. The company is very rich. The teacher still says the only real knowing is the knowing that happens in the special room.
That is what happened to medicine in 1992.
What Sits at the Top of the Hierarchy
The EBM hierarchy of evidence places systematic reviews of randomised controlled trials at the apex. Beneath them sit individual RCTs, then cohort studies, then case-control studies, then case series, then expert opinion and clinical experience at the bottom.³
The framework is presented as neutral. It is not.
A randomised controlled trial of a pharmaceutical product costs between twenty and three hundred million dollars to conduct.⁴ The trial requires regulatory approval, site recruitment, statistical infrastructure, monitoring, data management, and publication support. The entities capable of funding such trials are, in practice, three: pharmaceutical companies, the National Institutes of Health, and a small number of large foundations whose priorities track institutional medicine. The pharmaceutical industry funds the majority of clinical research in the United States and a higher proportion of late-phase trials of new products.⁵
A trial of a whole food, a traditional practice, a non-patentable substance, a low-cost generic, or a non-pharmaceutical intervention almost never reaches the funding threshold the hierarchy requires. Substances and practices that produce no return on investment do not generate the evidence the framework recognises, and so they sit at the bottom of the hierarchy or fall off it entirely.
The hierarchy then performs a second move. When a question has not been studied at the top tier, the framework declares “insufficient evidence” or “no evidence of benefit.” Absence is treated as a finding. The reader is led to conclude that the unstudied intervention does not work, when what has actually been established is that no one has been willing to pay for the kind of study the framework demands.
The streetlight effect — searching for keys under the lamp because that is where the light is — is not a flaw of the framework. It describes how the framework operates by design. The hierarchy of evidence is a hierarchy of who can afford to generate evidence.
The Trials at the Top Are Built by the Sponsor
The architecture of the modern pharmaceutical trial is the second mechanism. The sponsor — the company that owns the product — controls the design.
The sponsor selects the primary endpoint. A trial of an antidepressant can be designed to measure a small change on a subjective rating scale at week six, rather than functional recovery at one year. A trial of a statin can be designed to measure relative risk reduction in cardiovascular events, rather than all-cause mortality. A trial of a cancer drug can be designed to measure progression-free survival — the time until the tumour grows on a scan — rather than overall survival.⁶ The endpoint determines what answer the trial is permitted to give.
The sponsor selects the comparator. A new drug compared against placebo where an effective comparator already exists tends to win. A new drug compared against an existing drug at the wrong dose, or in the wrong patient population, tends to win. The comparator becomes a design choice rather than a scientific reference.
The sponsor selects the population. Trials that approve drugs exclude the elderly, the polypharmacy patients, the pregnant, those with comorbid conditions, those with abnormal laboratory values, and those with histories of the very adverse events being assessed. The drug is then prescribed to the population that was excluded. The VIGOR trial of Vioxx excluded patients with significant cardiovascular risk; the drug was marketed and prescribed to a population dominated by such patients.⁷
The sponsor selects the duration. A trial of six weeks tells you nothing about a drug that will be taken for life. A trial of two years tells you nothing about lifetime cancer risk. Sponsors routinely halt trials early “for benefit” once a favourable interim result is reached, eliminating the longer follow-up that would have permitted assessment of late-emerging harms; the JUPITER statin trial discussed later was stopped at a median of 1.9 years rather than completing its planned four-year duration.⁸
The sponsor controls the data. Investigators at trial sites send data to the sponsor. The sponsor’s statisticians analyse it. The sponsor’s medical writers produce the manuscript. The 2017 Cochrane systematic review by Lundh and colleagues, examining 75 studies across multiple drug classes, found industry-sponsored research produces conclusions more favourable to the sponsor’s product than independently funded research of the same questions, with the effect persisting after adjustment for methodological quality.⁹ A 2003 BMJ analysis by Lexchin and colleagues found that industry-funded trials of new drugs produced results favourable to the sponsor’s product at roughly four times the rate of independently funded trials.¹⁰
The RCT does not measure efficacy. It measures what its sponsor designed it to measure.
What Happens to the Trials That Find Harm
The third mechanism concerns what happens to the data the sponsor would prefer not to publish.
In 2008, Erick Turner and colleagues at the Department of Veterans Affairs published an analysis in the New England Journal of Medicine of all FDA-registered trials of antidepressants conducted between 1987 and 2004 — 74 trials covering 12 drugs. The FDA records, obtained under freedom of information requests, showed 38 trials with positive results and 36 trials with negative or questionable results. Of the 38 positive trials, 37 were published. Of the 36 negative trials, 22 were not published at all, and 11 were published in a way that conveyed a positive outcome.¹¹ The published literature on antidepressants showed positive findings in 94% of trials. The actual data showed 51%.
This is publication bias as a system, not as accident. The same pattern has been documented for COX-2 inhibitors, antipsychotics, neuraminidase inhibitors, and statins.¹² Trials that find harm are buried. Trials that find benefit are amplified.
A second layer operates below publication. Ghostwriting — the practice of pharmaceutical companies producing manuscripts and recruiting academic authors to attach their names — has been documented across multiple drug classes. Internal Merck documents released in the Vioxx litigation showed company employees drafting clinical trial papers and review articles, then recruiting academic physicians to be listed as authors; in the litigation review by Ross and colleagues, the company author was frequently the first or last name on the draft before the academic name replaced it.¹³ Wyeth’s hormone replacement therapy promotion was supported by at least 26 ghostwritten papers published in the medical literature between 1998 and 2005, identified through documents released in litigation and analysed by Adriane Fugh-Berman.¹⁴
A third layer operates at the journals themselves. When a pharmaceutical company publishes a favourable trial in a major medical journal, it routinely purchases tens or hundreds of thousands of reprints of that article from the journal — reprints distributed to physicians by sales representatives as the academic credential for the product. Richard Smith, former editor of the BMJ, described medical journals in 2005 as “an extension of the marketing arm of pharmaceutical companies,” noting that reprint orders for industry-favourable studies can generate revenues sufficient to constitute a substantial share of a major journal’s income.¹⁵ The journals at the top of the EBM hierarchy depend financially on the companies whose products they evaluate.
The reader of the medical literature encounters what appears to be the considered opinion of an academic physician. The reader does not see the company writer who drafted the manuscript or the company statistician who selected the data presented.
“No Evidence of Harm”
The fourth mechanism is the laundering of absence into safety.
When a harm signal appears in post-marketing data, the framework processes it in stages. The harm is not yet established because no RCT has been designed to test for it. The harm cannot be established because the RCT that would test for it has not been conducted. The harm has not been confirmed because the studies that exist were not powered to detect it. The correlation between exposure and harm is not causation, because the gold-standard trial has not been performed. By the time the gold-standard trial is performed, if it ever is, the drug has been on the market for a decade and the harm is too widespread to deny.
Each stage uses the framework’s own standards to keep the product on the market. Each stage requires the evidence that the framework’s funding structure ensures will not be generated.
The phrase “no evidence of harm” does work the reader rarely notices. It does not mean studies were conducted and harm was not found. It usually means that studies sufficient to detect the harm were not conducted. The phrase converts absence into safety. The asymmetry is structural: “no evidence of benefit” is treated as a finding against an unfunded substance, while “no evidence of harm” is treated as a finding in favour of a marketed product.
The framework is unfalsifiable for the things it protects and fatal for the things it does not.
What Happens to the People Who Disagree
The fifth mechanism is the processing of dissent.
A clinician who observes a pattern of harm in patients and reports it is reasoning from unsystematic clinical experience — the bottom of the hierarchy. The observation is dismissed as anecdotal. A researcher who publishes findings unfavourable to a major product class is subjected to coordinated response: methodological critique, accusations of conflict of interest, retraction campaigns, ridicule in the trade press, and loss of funding. A physician who treats outside guideline-driven protocols is referred to the medical board. A patient who reports the harm is told the condition is unrelated, idiopathic, or psychological.
Peter Gøtzsche, co-founder of the Cochrane Collaboration and author of multiple Cochrane reviews unfavourable to the pharmaceutical industry, was expelled from the Cochrane governing board in 2018 after publishing critical analyses of mammography screening, psychiatric drug regulation, and antidepressant suicidality.¹⁶ The expulsion processed dissent.
John Ioannidis, professor of medicine at Stanford and one of the most cited scientists in medical literature, published “Why Most Published Research Findings Are False” in PLoS Medicine in 2005, demonstrating from within the establishment that the statistical and structural assumptions of the published evidence base were unreliable.¹⁷ The paper was met with hostility from those it implicated and quietly absorbed by those it embarrassed. The framework continued unchanged.
David Healy, a psychiatrist and historian of antidepressants whose research had exposed the suicidality signal in SSRI trial data, was offered the chair of the Mood and Anxiety Disorders Programme at the University of Toronto’s Centre for Addiction and Mental Health in 2000. After a public lecture in which he discussed Prozac-induced suicidality, the appointment was withdrawn. The Centre received substantial funding from Eli Lilly, the manufacturer of Prozac.¹⁸ Nancy Olivieri, a haematologist at the University of Toronto, reported safety concerns about deferiprone, a thalassaemia drug manufactured by Apotex, after observing harm in her clinical trial. Apotex threatened legal action; the university, which was at the time negotiating a substantial donation from Apotex, did not defend her academic freedom.¹⁹ Both cases preceded the EBM apparatus’s deployment against later dissenters; both established the template.
The framework does not produce truth and then defend it against error. The framework produces orthodoxy and then defends it against observation.
Case One: Vioxx
Merck submitted rofecoxib (Vioxx) to the FDA in November 1998 and received approval in May 1999.²⁰ The drug was a COX-2 inhibitor — a new class of anti-inflammatory marketed as gentler on the stomach than older drugs. Before its withdrawal, more than 80 million people worldwide had been prescribed Vioxx.²¹
The pivotal trial supporting cardiovascular and gastrointestinal claims was VIGOR (Vioxx Gastrointestinal Outcomes Research), published in the New England Journal of Medicine in November 2000.²² The trial compared Vioxx against naproxen in 8,076 rheumatoid arthritis patients. The publication reported that Vioxx caused fewer serious gastrointestinal events than naproxen. The published paper also reported that patients on Vioxx had four times the rate of myocardial infarction; further analysis presented to the FDA Arthritis Advisory Committee in February 2001 determined the rate to be fivefold.²³
The published explanation was that naproxen was protective, not that Vioxx was harmful. The cardioprotective effect of naproxen had not been established at this magnitude before VIGOR and was not established afterwards.²⁴ The interpretation served the sponsor.
Internal Merck documents released in subsequent litigation showed company awareness of the cardiovascular signal predating VIGOR’s publication. Internal communications discussed how to manage the signal; the published trial reports did not communicate what the internal analyses had described.²⁵ Merck withdrew Vioxx in September 2004 after the APPROVe trial, designed to assess Vioxx’s effects on colorectal polyps, demonstrated a doubling of cardiovascular events.²⁶ FDA epidemiologist David Graham testified before the Senate Finance Committee that Vioxx had caused an estimated 88,000 to 139,000 excess heart attacks, of which 30 to 40 percent were fatal.²⁷ The lower bound was approximately 26,000 American deaths.
The trial that approved the drug satisfied every requirement of evidence-based medicine. It was randomised. It was controlled. It was published in the most prestigious medical journal in the world. It supported guideline recommendations and reimbursement decisions. The framework that produced it found nothing wrong with it.
The harm was visible in the data. The harm was known to the sponsor. The harm was published in a form that obscured its meaning. The framework continued to recommend the drug for almost five years. When the drug was withdrawn, the framework was not.
Case Two: Statins
The statin literature illustrates how the framework presents data to maximise the appearance of benefit.
Statins reduce LDL cholesterol. Whether they reduce all-cause mortality in primary prevention — in patients without established cardiovascular disease — has been contested in the literature for two decades.²⁸ The framework has resolved the contest in favour of mass prescription.
The presentational device is relative risk reduction. A statin trial reports that the drug reduces cardiovascular events by some percentage. The figure is technically accurate. What it conceals is the absolute risk reduction — the actual difference in event rates between the treated group and the untreated group.
In the JUPITER trial of rosuvastatin (2008), patients on the drug had a 1.6% rate of major cardiovascular events over 1.9 years. Patients on placebo had a 2.8% rate.²⁹ The relative risk reduction was 44%. The absolute risk reduction was 1.2%. The number needed to treat — the number of patients who must take the drug for one to avoid an event — was approximately 95 over two years. The other ninety-four took the drug and received no cardiovascular benefit from it.
The framework permits the relative figure to be reported in the headlines, the abstract, the press release, the guideline recommendation, and the prescribing conversation. The absolute figure appears, if at all, in the body of the paper. The patient is told the drug reduces heart attack risk by 44%. The patient is not told the drug reduces their personal two-year risk from 2.8% to 1.6%.
Adverse effects are processed through related machinery. Many statin trials use a run-in period — patients are given the drug before randomisation, and those who experience adverse effects are excluded before the trial begins.³⁰ Trials then report low rates of muscle pain, cognitive impairment, and new-onset diabetes. Surveys of statin users in real clinical practice — without the run-in selection — find muscle symptoms in 10 to 25 percent of patients, against trial-reported rates in the low single digits.³¹
The 2013 Cochrane review of statins in primary prevention found a small mortality benefit and a non-trivial harm signal, particularly for new-onset diabetes.³² The framework’s response was not to question primary prevention prescribing. It was to expand it. The 2013 ACC/AHA cholesterol guidelines lowered the threshold for statin prescription and added an estimated 13 million Americans to the eligible population.³³
The framework approves the drug, designs the trials to maximise apparent benefit and minimise apparent harm, suppresses the inconvenient findings, expands the eligible population, and declares the resulting prescribing pattern to be evidence-based.
Case Three: SSRIs
The selective serotonin reuptake inhibitors entered the market in 1987 with fluoxetine (Prozac). They were marketed on the basis of a “chemical imbalance” theory of depression — the claim that depressed patients had low serotonin and the drugs corrected the deficiency.³⁴ The theory was never demonstrated. A 2022 systematic umbrella review by Joanna Moncrieff and colleagues, published in Molecular Psychiatry, concluded that the evidence does not support the hypothesis that depression is caused by reduced serotonin activity or concentrations.³⁵
The drugs were approved on the basis of trials showing small differences from placebo on rating-scale depression scores at six to eight weeks. The Turner analysis cited earlier in this essay found that the published literature substantially overstated the actual trial outcomes; when unpublished trials were included, the apparent efficacy fell substantially, with roughly half the trials having failed to demonstrate benefit.¹¹ A 2008 meta-analysis by Irving Kirsch and colleagues using FDA data found that the difference between SSRIs and placebo on depression rating scales fell below the threshold for clinical significance for all but the most severely depressed patients.³⁶
The harms followed the framework’s standard sequence.
Sexual dysfunction was acknowledged in trial reports at rates of 2 to 16 percent, well below the 50 to 70 percent rates documented in subsequent clinical surveys.³⁷ Post-SSRI sexual dysfunction — persistent sexual dysfunction continuing after discontinuation — was denied for two decades. The European Medicines Agency added a warning label in 2019.³⁸ Patients reporting the syndrome had been told for two decades it was not a recognised condition.
Suicidality in children and adolescents was visible in the trial data from the early 1990s. The published literature did not communicate the signal. A 2004 FDA review of pediatric trials confirmed it, and the FDA added a black box warning in October 2004.³⁹ A 2016 BMJ analysis by Tarang Sharma, Peter Gøtzsche and colleagues, using clinical study reports rather than published papers, found the suicidality signal in adults as well — and found systematic misclassification of suicide attempts as “emotional lability” in the original trial reports.⁴⁰
The dependence and withdrawal syndromes were denied for three decades. SSRI manufacturers and prescribing guidelines characterised the discontinuation syndrome as a mild, transient phenomenon affecting a small minority of patients. A 2019 systematic review by James Davies and John Read found 56% of patients experience withdrawal effects when attempting to discontinue, with 46% of those affected describing the experience as severe.⁴¹ The UK Royal College of Psychiatrists revised its position later that year, acknowledging that withdrawal could be severe and prolonged.⁴² The acknowledgement came thirty-two years after the first SSRI was approved.
Around one in eight American adults now takes an antidepressant.⁴³ The framework that approved them functioned exactly as designed.
Case Four: Bisphosphonates
Fosamax (alendronate) was approved by the FDA in 1995 as a treatment for established osteoporosis. The market was small. In 1995, the number of American women with documented osteoporosis was a fraction of what the drug’s commercial prospects required.
The framework supplied the market. In 1994, a World Health Organization study group convened in Rome, financed by the pharmaceutical industry, produced arbitrary diagnostic cutoffs based on bone mineral density measured against the average of a healthy thirty-year-old white woman.⁴⁴ Bone density between one and 2.5 standard deviations below this reference was named “osteopenia.” Bone density more than 2.5 standard deviations below was named “osteoporosis.” The categories were statistical cutoffs imposed on a normally distributed biological variable; they were not derived from outcome data on who actually fractured. Anna Tosteson, a member of the original WHO group, later said the categories had been intended as population research tools, not individual diagnoses; the chair of the meeting, John Kanis, said the same.⁴⁵ A subsequent 1999 WHO panel on osteoporosis cost analysis included eleven members, eight of them employed by pharmaceutical manufacturers.⁴⁶
Merck did the rest. The company established the Bone Measurement Institute, a nonprofit that lobbied for insurance coverage of bone density testing and underwrote the placement of scanners in physician offices across the United States.⁴⁷ In 1997, the FDA cleared a lower 5 mg dose of Fosamax specifically for women with osteopenia. Approximately thirty percent of postmenopausal women now had a “disease” requiring early intervention.⁴⁸
The pivotal trials applied the relative-risk-reduction architecture described in the statins case. The Fracture Intervention Trial reported a 47% relative reduction in hip fracture and a 52% relative reduction in radiographic vertebral fracture in women with established osteoporosis.⁴⁹ The trial enrolled high-risk women in whom even modest relative reductions translated into modest absolute differences. It did not study the population in which the drug was subsequently prescribed in greatest numbers — women with osteopenia, who carried substantially lower baseline fracture risk. The framework approved the prescribing pattern anyway.
The drug’s mechanism of action determined what would follow. Bisphosphonates concentrate in bone and disable osteoclasts, the cells responsible for clearing old bone and allowing new bone to be laid down in response to mechanical load. Blocking the clearing side of the remodeling cycle while leaving the building side unopposed produces bones that are denser by measurement and more brittle by behaviour — old bone that should have been replaced accumulates as highly mineralised, structurally compromised material. The scan reads higher. The bone breaks more easily.
The harm signal emerged after the prescribing pattern was established. Reports of atypical femoral fractures — spontaneous breaks in the shaft of the thighbone, occurring with little or no trauma — appeared in the orthopaedic literature from 2007.⁵⁰ The drug marketed to prevent fractures was producing a different category of fracture in long-term users. The FDA issued a safety warning in October 2010 but did not retract the prescribing recommendation; osteonecrosis of the jaw was added as a separate documented harm.⁵¹ A 2011 JAMA study reported significantly elevated risk of subtrochanteric and femoral shaft fractures in long-term bisphosphonate users.⁵²
The framework accepted an industry-funded definition of disease, converted asymptomatic women into patients, prescribed them a drug whose trials had been conducted in a different population, and continued recommending the drug after the iatrogenic loop became visible. Nothing in this sequence required new science. It required only the framework’s willingness to treat industry-supplied definitions as medical knowledge, industry-funded trials of one population as evidence about another, and a metric the drug improved (density on the scan) as a proxy for the outcome the drug worsened (the strength of the bone under stress).
What the Framework Was Protecting
The essay has examined EBM on its own terms. By its own stated standards, the framework does not produce reliable knowledge, does not protect patients, does not exclude bias, and does not distinguish truth from manufactured evidence. Every claim it makes for itself can be inverted with examples from its own literature.
A deeper question remains.
EBM is the epistemological enforcement layer for a particular model of medicine. That model holds that the body is a malfunctioning machine, that illness is caused by external invaders or internal genetic defects, that the response to illness is the introduction of a patented chemical or biological product, that the practitioner’s task is to match product to diagnosis, and that the evidence required to justify the product is the kind of trial pharmaceutical companies are equipped to manufacture.
The framework’s structural bias against whole foods, traditional practices, low-cost interventions, and reasoning from mechanism is not incidental to this model. The pharmaceutical paradigm requires the bias to function. A framework that recognised the body’s intrinsic capacity for self-regulation and repair, that attended to the actual sources of damage — toxic exposure, nutritional depletion, electromagnetic burden, psychological strain — and that treated the practitioner’s task as the removal of obstacles rather than the introduction of products, would not need RCTs at the top of its hierarchy because it would not be generating products to be tested. It would be observing what the body does when the obstacles are removed.
EBM is not science being corrupted by industry. EBM is the epistemological form industry required. It was designed in the 1990s, codified in the 2000s, and operated at civilisational scale in the 2020s. The framework has done what its architecture predicted.
This is what political economist Toby Rogers, in testimony before the United States Senate in 2025, named epistemic capture — the colonisation of knowledge production itself rather than the regulation of its products.⁵³ When an industry captures regulation, it controls decisions. When an industry captures epistemology, it controls what is allowed to count as a fact. EBM is epistemic capture’s operating system in medicine. The same investment funds that hold major positions in the pharmaceutical companies whose products the framework evaluates also hold major positions in the publishers of the journals that perform the evaluation; the producer and the certifier of medical knowledge share their owners.⁵⁴
The clinician at the bedside who notices a pattern across patients and adjusts their practice accordingly is doing what physicians have done for thousands of years. The framework calls this anecdote and ranks it at the bottom of the hierarchy. The patient who recovers from a chronic condition through dietary change, sunlight, sleep, and the removal of pharmaceutical exposures is doing something the framework cannot measure, because the framework was not designed to measure it. The traditional practitioner whose people have used a plant for fifteen generations is reasoning from a form of evidence the framework excludes by definition.
What the framework calls evidence is what industry can pay for. What the framework calls anecdote is what the body actually does.
The 1992 paper announced a paradigm shift. The shift was real. The direction was not what the paper claimed. Medicine did not move from intuition to evidence. It moved from the physician’s accumulated judgement to the industry’s manufactured documentation. The hierarchy of evidence is the hierarchy of who paid for the study. Evidence-based medicine, examined as machinery, is evidence-biased medicine — biased structurally, by what gets funded; biased methodologically, by what gets measured; biased editorially, by what gets published; biased financially, by who owns the journals; biased institutionally, by what gets recommended after the harm has been documented. The bias is the framework.
The document is publicly available. The signatures are on it. The date is November 1992. Whatever the framework was sold as, the framework is what its architecture produced. What its architecture produced is in the medical journals, in the prescribing patterns, in the disability statistics, and in the cemeteries. It is also in the minds of two generations of doctors and patients who no longer believe their own observations count.
References
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Petersen M. “Hormones and Bones: How the Drug Companies Made Aging Into a Disease.” New York Times, November 16, 2003. See also Heaney RP et al. and consensus development conference: “Diagnosis, Prophylaxis, and Treatment of Osteoporosis.” American Journal of Medicine 94, no. 6 (June 1993): 646–650, and Kanis JA, WHO Study Group. “Assessment of Fracture Risk and Its Application to Screening for Postmenopausal Osteoporosis: Report of a WHO Study Group.” WHO Technical Report Series 843. Geneva: World Health Organization, 1994.
Spiegel A. “How a Bone Disease Grew to Fit the Prescription.” NPR Morning Edition, December 21, 2009.
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Moynihan R. “Osteoporosis and the Marketing of a Disease.” Therapeutics Initiative Workshop, University of British Columbia, October 2006. Fosamax sales figures: Merck Annual Reports, 1996–2005.
Black DM, Cummings SR, Karpf DB, et al. “Randomised Trial of Effect of Alendronate on Risk of Fracture in Women with Existing Vertebral Fractures.” The Lancet 348, no. 9041 (December 1996): 1535–1541. See also Black DM, Thompson DE, Bauer DC, et al. “Fracture Risk Reduction with Alendronate in Women with Osteoporosis: The Fracture Intervention Trial.” Journal of Clinical Endocrinology & Metabolism 85, no. 11 (November 2000): 4118–4124.
Neviaser AS, Lane JM, Lenart BA, Edobor-Osula F, Lorich DG. “Low-Energy Femoral Shaft Fractures Associated with Alendronate Use.” Journal of Orthopaedic Trauma 22, no. 5 (May 2008): 346–350. Earlier case reports beginning 2005; pattern recognised in the literature from 2007.
US Food and Drug Administration. “Safety Update for Osteoporosis Drugs, Bisphosphonates, and Atypical Fractures.” FDA Drug Safety Communication, October 13, 2010.
Park-Wyllie LY, Mamdani MM, Juurlink DN, et al. “Bisphosphonate Use and the Risk of Subtrochanteric or Femoral Shaft Fractures in Older Women.” JAMA 305, no. 8 (February 2011): 783–789. See also Dell RM, Adams AL, Greene DF, et al. “Incidence of Atypical Nontraumatic Diaphyseal Fractures of the Femur.” Journal of Bone and Mineral Research 27, no. 12 (December 2012): 2544–2550.
Rogers T. Testimony before the United States Senate Committee on Homeland Security and Governmental Affairs, September 10, 2025. See also Rogers T. “Big Pharma’s Epistemic Capture of Medical Research.” uTobian (Substack), September 2025.
Bazin X. Big Pharma démasqué: Médicaments dangereux, vaccins controversés… Quand l’industrie pharmaceutique nous prend pour des cobayes. Trédaniel, 2022. Common ownership structures documented through RELX Group annual reports and SEC filings of major institutional shareholders (BlackRock, Vanguard, State Street) in both pharmaceutical companies and scientific publishing groups (RELX, Springer Nature, Wiley).
Yesterday, almost 2,000 people, mostly young children, died of malaria because they could not access effective and relatively cheap treatment quickly enough. About 4,000 people died of tuberculosis (TB), including many young adults leaving orphans. This happens every day. Progress in reducing these numbers is stalling, as partly due to the continuing economic damage from the Covid-19 response.
In the past two weeks three tourists unfortunately died among about 150 passengers and crew on a cruise ship MV Hondius off the west coast of the African continent where most of those malaria and TB deaths occurred. The Hondius had a hantavirus outbreak, known to have infected less than 10 people but including at least two of those that died.
The World Health Organization (WHO) estimates that 10,000 to 100,000 hantavirus cases occur every year, spread across the Americas, Europe, Africa, and Asia. The current media coverage and WHO news conferences therefore concern about one-thousandth of the cases expected this year. The United States averages about 30 – they simply have not been newsworthy.
Hantavirus is transmitted from mice and rats through their feces, urine, saliva, or their bite. The Andean variety, which occurred on the cruise ship, can also sometimes transmit from a sick infected person. However, as the low number of cases on the ship demonstrates, the risk of human-human transmission is not great. It is, however, a nasty virus, with reported mortality around 15% of cases and sometimes significantly higher.
So, among the 170,000 average deaths in the world each day, and thousands from the WHO’s traditional focus diseases, why the excitement over Hantavirus? Why the pictures of hazmat-suited emergency response crews and desperate contact tracing, when we don’t usually notice? Why is the Director-General of the entire WHO spending so much time on this, when diseases of poverty are rising and basics such as nutrition funding are falling? A fascinating question.
The WHO wants the United States and Argentina to rejoin, and WHO DG Tedros Ghebreyesus has raised this in his hantavirus briefings. Multilateral cooperation in global health has demonstrably helped in addressing malaria and TB in the past, but reliance on detached and homogenous WHO recommendations for Covid worked out really badly. The WHO is wisely claiming the MV Hondius is not heralding a pandemic, but nonetheless are making all the mileage they can from the fear created around this epidemiologically irrelevant event.
Just two weeks ago, African nations also rejected (again) a pathogen-sharing requirement for the WHO’s new Pandemic Agreement (treaty). This would require them to implement surveillance at their expense and provide data on pathogens to the WHO, which will then provide it to large Pharma companies to produce vaccines that the WHO will recommend and market.
Malaria and TB deaths should increase further through this process because the WHO wants over $10 billion from donor countries diverted to its pandemic agenda, and $20 billion spent by low- and middle-income countries to support it (the world spends about $3.5 billion on malaria each year). While malaria, TB, HIV, nutrition, and improving access to primary care clinics may be a greater priority for such countries, false charges of putting the world at risk by failing to sign the WHO’s Pandemic Agreement may eventually prove too much to withstand.
A further potential influence is conflict of interest, though its impact on the current situation is unclear. The WHO’s largest donor is now the Gates Foundation, a private operation directed by Bill Gates with a strong history of investment in the mRNA vaccine company Moderna. Moderna is working on a hantavirus mRNA vaccine, which is surprising from an investment perspective as the market seems small. How would a viable commercial market be ensured for a vaccine for such an obscure disease? This viable market requires large swathes of the population to be convinced that they are at far higher risk than they actually are, or coerced into taking it. In the United States the risk is about 1 case per 10 million people per year, with perhaps 1 per million to 1 per 100,000 globally.
A direct connection between Moderna’s market problem and the current hysteria does not need to be made. The point is that the WHO is now an organization in which its largest funder also has large, vested interests in the sales of specific health products. Through specified funding, the funder also determines which activities the WHO will undertake.
The WHO’s second largest funder over 2024-2025 was Gavi, a public private parentship for vaccines, again involving Gates and Pharma companies. Public-private partnerships, which the WHO has itself essentially become, are intrinsically designed around vested or conflicted interest – the justification for private companies expending resources is gain for their investors.
No sane approach would allow vested commercial private interests to determine global health policy. Pharma’s job is to maximize profit, while the WHO’s job is to maximize health and health equity. One of these must be failing.
A vast global health industry has been built in which private investors determine priorities, taxpayers foot most of the bill, and populations have become markets. As this plays out, public health messaging becomes increasingly incoherent and detached from reality until several cases of hantavirus among tourists on a cruise ship, out of up to 100,000 expected this year, appear as an international crisis.
The result is not just fear and confusion, but a massive institutional failure that allows huge numbers of children to die disregarded while public health workers don hazmat suits as media celebrities. We need to ask why. There is a path for an organization such as the WHO to act in an ethical, proportionate manner that serves humanity rather than parasitizing it. The hantavirus roadshow can be an impetus for change, but not to further enrich and empower those promoting it. We need to, as citizens and as a public health community, insist that institutions such as the WHO do better, or insist on replacing them with something better.
David Bell, Senior Scholar at Brownstone Institute, is a public health physician and biotech consultant in global health. David is a former medical officer and scientist at the World Health Organization (WHO), Programme Head for malaria and febrile diseases at the Foundation for Innovative New Diagnostics (FIND) in Geneva, Switzerland, and Director of Global Health Technologies at Intellectual Ventures Global Good Fund in Bellevue, WA, USA.
According to a recent report by the German online TKP, a movement is gaining momentum within the scientific community that threatens to dismantle the official IPCC narrative from the inside out. This rebellion is led by 46 scientists, many of whom have direct experience working with the Intergovernmental Panel on Climate Change, who are now publicly challenging the foundational claims that have dictated global policy for decades.
The heart of their argument lies in the fundamental failure of current climate models.
These prestigious researchers – among them Dr. Robert Balling, Dr. Lucka Bogataj, Dr. John Christy and Dr. Judith Curry – contend that the IPCC has relied on simulations that are heavily biased toward human-induced CO2 while systematically ignoring or downplaying natural variables. By prioritizing political consensus over raw data, these models have consistently overestimated global warming, creating a gap between alarmist predictions and the actual temperature trends observed over the last several years.
The scientists suggest that the “climate emergency” is less a scientific reality and more an ideological construct designed to drive the Net Zero agenda.
Power natural factors ignorerd by IPCC
Furthermore, this group highlights the critical role of natural drivers that are often missing from the mainstream conversation. They point to solar activity, atmospheric water vapor, and complex cloud cycles as the true drivers of Earth’s climate. By looking back at historical periods like the Medieval Warm Period, they argue that the planet’s current warming is well within the bounds of natural variability and is not the unprecedented catastrophe it is often portrayed to be.
Culture of scientific suppression
Perhaps most concerning is the article’s depiction of a scientific community under pressure. The rebelling scientists describe a culture of suppression where dissenting opinions are sidelined through the loss of funding, career gatekeeping, and media blackouts. This internal collapse suggests that the “science is settled” mantra is no longer sustainable.
Dogmna coming to an end
As these 46 voices come forward, they signal a shift toward a more skeptical, data-driven approach that prioritizes objective reality over the prevailing political narrative, suggesting that the era of unquestioned climate dogma may be coming to an end.
A reader wrote to me this week. Her question, in essence:
She knows someone trying to come off Seroquel safely. Does anyone know the deficiencies it might have caused? Are there books or functional doctors who work on that?
She is looking for a functional doctor. Someone to walk her person through the Seroquel taper the way a functional cardiologist walks a patient off statins, or a functional endocrinologist walks a patient off long-term steroids. She wants someone who understands what the drug has done to the body, can identify the depletions, can order the right tests, and can hold the patient’s hand through the worst of it.
That person does not exist. Not as a profession. Not as a network. Not in any country I have looked at.
The Assumption Hidden in the Question
Every other branch of medicine has a parallel network for patients who decide that what they have been prescribed is making them worse. Someone leaving conventional cardiology finds functional cardiologists, integrative GPs, nutritionists, lifestyle medicine doctors, chiropractors, osteopaths, and bodyworkers. The person leaving an oncologist finds clinics in Mexico and Germany, a literature on metabolic therapies, and dozens of practitioners whose practices are built around helping the patient leave the mainstream pathway.
These parallel networks are not perfect. They vary in quality. Some are captured by their own commercial pressures. But they exist. A patient can find them. A patient can book an appointment.
Now try the same exercise for someone on Seroquel. Or for someone six years into a benzodiazepine. Or two decades into an SSRI.
What they find is a peer forum, a free PDF from Denmark, and a book by a British psychiatrist whose own profession ignored the problem until he forced them to look at it. They find a small number of dissident practitioners, most of them retired or semi-retired, with waiting lists measured in months. They find a great many websites. They find almost no doctors.
My reader did not ask a strange question. She asked the normal question. The strangeness is that there is no normal answer.
What the Evidence Says About the Vacuum
The emptiness is documented in plain language by the clinicians who actually do this work.
Peter Breggin, who has been doing psychiatric drug withdrawal work for more than forty years, states it directly. It has become very easy for individuals to find clinicians who will prescribe psychiatric drugs, but it remains very difficult for patients to find help in reducing or withdrawing from them. He attributes this to a lack of peer support and training, which leaves most clinicians uncomfortable even responding to a patient’s request for reduction or withdrawal.¹
Peter Gøtzsche puts it more bluntly. Very few doctors know anything about withdrawal, and many make horrible mistakes. If they taper at all, they do it far too quickly, because the prevailing wisdom treats withdrawal as a problem only with benzodiazepines, and because the few guidelines that exist recommend tapering schedules that are dangerously fast.²
The largest survey of long-term users who tried to discontinue — Ostrow and colleagues, published in Psychiatric Services in 2017 — quantifies the vacuum. Of 250 adults with serious mental illness diagnoses who wanted to stop psychiatric drugs, 71% had been taking them for over nine years. Only 54% met their goal of completely discontinuing. Among those who attempted it, only 45% rated doctors as helpful during withdrawal. Sixteen percent began the process against their doctor’s advice. Twenty-seven percent did not tell their doctor, stopped seeing the doctor, or changed doctors. Self-education and contact with peers who had withdrawn were the most frequently cited sources of help.³
More than a quarter of the people who tried to come off went around their doctor or away from their doctor entirely. They were not helped by the profession that put them on the drug. In many cases they were actively avoided by it.
Gøtzsche documents something worse in Denmark. Researchers there tried to run a withdrawal trial involving patients on antipsychotics. The trial collapsed — not because the drugs failed to come off, but because patients were too frightened to participate. They had been told for so long that they would relapse without their medication that the prospect of stopping was, in itself, destabilising.² The profession had successfully convinced them that leaving was more dangerous than staying.
The Horowitz Exception
Mark Horowitz is a training psychiatrist at the NHS with a PhD in the pharmacology of antidepressants from King’s College London. He was prescribed an antidepressant in medical school. Fifteen years later, he tried to come off it following the standard guidelines his own profession had produced. He was blindsided by withdrawal symptoms so severe they forced him back onto the drug.⁴
Unable to find clinical support, he turned to an online peer community founded by Adele Framer — SurvivingAntidepressants.org — and discovered that the people there had worked out, through years of collective trial and error, what the psychiatric literature did not contain. The dose-response curve for these drugs is hyperbolic, not linear. Halving the dose at each taper step, as the official guidelines recommended, guaranteed a withdrawal crash at the bottom of the curve. The patients had figured it out. The profession had not.⁵
In 2019, Horowitz published this finding with David Taylor in The Lancet Psychiatry.⁵ In 2021, with Joanna Moncrieff, he set up England’s first psychiatric drug deprescribing clinic.⁴ In 2024, he and Taylor published The Maudsley Deprescribing Guidelines — the first clinical textbook on how to come off these drugs written within the British medical establishment.⁶
One clinician. One clinic. One book. For a problem that affects tens of millions of patients across every Western country.
Horowitz’s findings were accommodated only after the peer communities had been telling people the same thing for a decade, and after the evidence became too large to ignore. Joanna Moncrieff, Peter Gøtzsche, Peter Breggin, David Healy, and a small handful of others have done comparable work. They remain isolated. They have no referral network underneath them. They are not training a generation of younger clinicians to replace them.
The vacuum is not the temporary feature of a field that hasn’t yet matured. It is the product of active resistance from within the profession.
Why the Vacuum Is Structural
The parallel practitioner network that exists in cardiology, endocrinology, and oncology exists because those branches of medicine concede, even at their most conventional, that the body can heal. A functional cardiologist can hang a shingle because conventional cardiology admits that diet, exercise, stress, and sleep can reverse heart disease. The door is cracked open. The functional practitioner walks through.
Psychiatry does not open that door. Its official framework holds that the conditions it diagnoses are chronic, lifelong, and biologically driven. The Royal College of Psychiatrists, the American Psychiatric Association, and every major national equivalent tell patients that their “illness” requires long-term management, often lifelong, and that stopping medication invites relapse. The DSM categories are described as diseases. The drugs are described as treatments that correct an underlying dysfunction.
In this framework, no role exists for a practitioner who helps people leave. A practitioner who helps people leave is, by definition, someone who believes the drugs were not necessary in the first place, or are no longer necessary, or are causing more harm than the original distress. That practitioner is a heretic within the profession. Not a specialist filling a niche. A threat to the diagnostic framework itself.
The vacuum is not a gap in a functioning system. It is the absence that the system requires in order to continue functioning.
If the profession built a deprescribing subspecialty — trained practitioners, published guidelines, referral pathways, insurance codes — it would be admitting that a significant fraction of its patients never needed the drugs, were harmed by them, and can and should come off them. That admission would collapse the commercial and intellectual scaffolding of the field. The admission is not made. The subspecialty is not built. The patients are left to find their own way.
Gøtzsche puts it in one sentence. It seems, he writes, as if lifelong medication is tacitly assumed to be a good thing.² That is the explanation for the vacuum.
What the Reader Is Actually Asking For
When I translate my reader’s question into what it would take to answer it, the practitioner she is looking for would need to
understand what Seroquel has done to the body,
design a hyperbolic taper matched to this patient’s half-life and receptor profile,
order compounded doses or guide the making of them,
address the depletions that accumulate during years of antipsychotic exposure,
manage the return of sleep disruption, anxiety, and emotional intensity that follows removal of the drug,
and walk alongside for the twelve to thirty-six months this typically takes.
This is a real job. It is a needed job. It is nobody’s job.
No medical school trains for it. No residency offers it. No insurance code reimburses it. No malpractice carrier covers a psychiatrist who specialises in getting people off psychiatric drugs. No prescriber can build a practice around it without accepting the isolation and reduced income that come with practising outside the standard framework. No primary care doctor has the time, the knowledge, or the institutional cover to do it either.
The work exists. The workers do not.
The Reframe: This Was Never a Psychiatric Problem
The practitioner my reader is looking for does not exist because psychiatric drug recovery is not a psychiatric problem. The body’s task, once the drug is tapered off, is not a psychiatric task. It is a terrain task.
The drug was a toxic exposure — a sustained, daily, years-long exposure acting on a nervous system that was probably already carrying some combination of nutritional deficiency, accumulated toxic burden, disrupted sleep, chronic stress, and environmental insult before the prescription was ever written. Years of Seroquel add to that burden. They deplete the body in predictable ways: oxidative stress that consumes glutathione and antioxidant enzymes,⁷ mitochondrial damage, metabolic disruption producing weight gain, blood sugar dysregulation, and elevated lipids,⁸ and a cascade of effects on movement, cognition, and sleep architecture.
What the body needs, once the drug is being reduced, is not correction by a psychiatric specialist. It is removal of the toxic input and restoration of the conditions that allow repair — clean water, nutrient-dense food, mineral repletion, sunlight, sleep, movement, reduction of other ongoing toxic and stress inputs, and time.
The practitioners who support that work do exist. They are simply not labelled as psychiatric practitioners, because the work is not psychiatric. They are the terrain-oriented doctors, the New Biology practitioners, the functional medicine clinicians who understand mitochondrial recovery and mineral repletion, the nutritionists who work with detoxification, the bodyworkers who address the fascia and the lymph.
My reader asked whether there were functional doctors “on that topic.” The honest answer is that the topic, correctly named, is not psychiatric drug withdrawal. The topic is terrain restoration after a prolonged toxic exposure. That has practitioners. Those are the practitioners she needs.
The psychiatric part of the work — writing the taper prescription, adjusting compounded doses — is the smallest part, and it requires the least expertise. Any honest prescriber willing to listen to the patient and read the Horowitz guidelines can do it. The rest of the work, the terrain work, is what actually determines whether recovery happens.
A Practical Map
For my reader, and for anyone in her position, here is what the road actually looks like.
For the taper itself. Horowitz and Taylor’s Maudsley Deprescribing Guidelines is the single most important book.⁶ Breggin’s Psychiatric Drug Withdrawal covers the clinical management in detail, including a case involving Seroquel.¹ Gøtzsche’s Mental Health Survival Kit and Withdrawal from Psychiatric Drugs is plain-language and principles-based.² Sørensen, Rüdinger, Gøtzsche and Toft’s A Practical Guide to Slow Psychiatric Drug Withdrawal is free as a PDF from deadly-medicines.dk.⁹ These four texts contain most of what is known.
For the prescriber. You are probably looking for any doctor — primary care, psychiatrist, or integrative — willing to write the taper according to the schedule you bring them. You are not looking for the prescriber to design it. You are looking for them not to obstruct it. This is a much smaller ask, and much more achievable, than finding a specialist. Compounding pharmacies produce the small custom doses that manufactured pills cannot.
For the peer community. SurvivingAntidepressants.org is the largest and most rigorous. Benzo Buddies covers the benzodiazepine side. Mad in America (madinamerica.com) hosts an enormous archive of first-person accounts, research summaries, and practitioner interviews. The International Institute for Psychiatric Drug Withdrawal (iipdw.org) and the Inner Compass Initiative (theinnercompass.org) are both worth knowing. Ostrow’s survey found that peer contact and self-education were the two most frequently cited sources of help during withdrawal, rated more useful than doctors.³
For the terrain work. The New Biology Clinic (newbiologyclinic.com), built around the framework of Tom Cowan, Andy Kaufman, and colleagues, addresses the underlying causes that mainstream medicine will not examine. Kelly Brogan’s A Mind of Your Own is written by a psychiatrist who now works from a broadly terrain-compatible orientation and addresses coming off psychiatric drugs directly.¹⁰ Competent functional medicine practitioners who understand mitochondrial recovery, mineral repletion, and the role of ongoing toxic exposures can carry much of the load, though their familiarity with psychiatric drugs specifically will vary.
For the depletions. Long-term antipsychotic exposure is associated with oxidative stress consuming glutathione and related antioxidant systems.⁷ The commonly reported associated depletions, drawing from the broader clinical literature, include coenzyme Q10, magnesium, B vitamins (particularly B12 and folate), vitamin D, zinc, and omega-3 fatty acids. These are worth testing and repleting. They are not a substitute for the terrain work. They are part of it.
None of this replaces the specialist network that does not exist. It is what is actually available, and it is what actually works when people succeed — which many do.
For a Six-Year-Old
Your body knows how to get better. It has always known.
When something is hurting it, the body’s job is to repair. It does this on its own, every day, all the time. It does not need a special doctor to do it.
What it needs is good food, clean water, sleep, sunshine, and time. It needs whatever was hurting it to slowly, carefully, stop being there.
The slowly and carefully part matters. You cannot rip a plaster off a wound that has grown into the skin. You have to loosen it a little at a time, and let the skin heal as you go.
That is the whole of it.
Closing
My reader asked for leads to help someone detox from Seroquel safely, and for functional doctors who work on that topic. I have given her the leads I have. I have also told her that the functional doctors she is looking for, in the form she imagines them, do not exist — and will not exist, because the framework that would need to produce them has structural reasons not to.
The absence of a specialist network is not the absence of a path. The path exists. It is slower and harder than it should be. It requires self-education, peer support, a cooperative prescriber, a terrain-oriented practitioner, and time. Many people walk it. Many get to the other side. Ostrow’s survey of those who succeeded found that 82% were satisfied with their decision.³ Few psychiatric interventions can claim that.
What psychiatry will not provide, the body provides — once the exposure stops and the conditions for repair are restored. The doctor she is looking for does not exist. The recovery she is looking for does.
Nothing in this essay is medical advice. It is research and analysis. Anyone reducing or stopping a psychiatric drug should do so with qualified support and adequate time, informed by the texts and communities referenced above.
References
Breggin, Peter R. Psychiatric Drug Withdrawal: A Guide for Prescribers, Therapists, Patients and Their Families. New York: Springer, 2012.
Gøtzsche, Peter C. Mental Health Survival Kit and Withdrawal from Psychiatric Drugs. Ann Arbor: L H Press, 2022.
Ostrow, L., Jessell, L., Hurd, M., Darrow, S. M., & Cohen, D. “Discontinuing psychiatric medications: a survey of long-term users.” Psychiatric Services 68 (2017): 1232–8.
Horowitz, Mark A. Personal and professional biography. See markhorowitz.org and Simons, P., “Peer-support groups were right, guidelines were wrong: Dr. Mark Horowitz on tapering off antidepressants,” Mad in America, March 20, 2019.
Horowitz, Mark A., and David Taylor. “Tapering of SSRI treatment to mitigate withdrawal symptoms.” Lancet Psychiatry 6 (2019): 538–46.
Horowitz, Mark, and David M. Taylor. The Maudsley Deprescribing Guidelines: Antidepressants, Benzodiazepines, Gabapentinoids and Z-drugs. London: Wiley-Blackwell, 2024.
Salim, Samina. “Oxidative Stress and Psychological Disorders.” Current Neuropharmacology 12, no. 2 (2014): 140–147.
Lieberman, J. A., et al. “Effectiveness of antipsychotic drugs in patients with chronic schizophrenia” (CATIE study). New England Journal of Medicine 353 (2005): 1209–1223.
Sørensen, A., Rüdinger, B., Gøtzsche, P. C., and Toft, B. S. A Practical Guide to Slow Psychiatric Drug Withdrawal. Copenhagen, 2020. Available at deadly-medicines.dk.
Brogan, Kelly. A Mind of Your Own: The Truth About Depression and How Women Can Heal Their Bodies to Reclaim Their Lives. New York: HarperCollins, 2016.
Gøtzsche, Peter C. Is Psychiatry a Crime Against Humanity? Copenhagen: Institute for Scientific Freedom, 2024.
Whitaker, Robert. Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs, and the Astonishing Rise of Mental Illness in America, 2nd ed. New York: Broadway Paperbacks, 2015.
Davies, J., and J. Read. “A systematic review into the incidence, severity and duration of antidepressant withdrawal effects: Are guidelines evidence-based?” Addictive Behaviors 97 (2019): 111–121.
Editor’s note: I have long resisted the climate manipulatioin idea but this seems convincing.
Below is an automated translation of an article from the French weekly RIVAROL, one of the last far-right publications in France, which is beset by lawsuits and has lost its press accreditation (and the tax advantages that came with it). It is a paper publication, but it can no longer appear on newsstands, so Rivarol has opted for the PDF format.
The article deals with a subject that we don’t see surfacing much in the American far-right press: drought and climate control as an already existing weapon, discreetly – but intensively – used by the Americans against Iran.
RIVAROL is not a scientific journal, but that being said, the facts are troubling and we must force our opponents to respond:
Why is it that the end of the Iranian drought coincides with the destruction of the ring of American radar installations in the Arabian Peninsula? Doesn’t this confirm what President Mahmoud Ahmadinejad had already said long ago about manipulating climate to pursue political interests?
While Iran rains missiles down on its enemies, the rain returns to Iran. Coincidence?
§§§§§
Iran’s first victory against the climate conspiracy
AN ABNORMAL DROUGHT THAT DRAGGED ON
About fifteen years ago, the then-President of Iran, Mahmoud Ahmadinejad, repeatedly claimed that Western powers (under American influence) were “stealing” rain from Persia and much of the Middle East (including Iraq). Naturally, at that time, almost everyone in the West considered the strongman of Tehran a crackpot, a conspiracy theorist who, moreover, had the misfortune, it was assumed, of being a notorious historical revisionist.
Westerners continue to silence or deny what Mahmoud had calmly stated. In 2018, Iran officially accused the United Arab Emirates and Israel of stealing its rains, when the senior official of the Islamic Revolutionary Guard Corps, Brigadier General Gholam Reza Jalali, declared: “Israel and another country are working together to prevent Iranian clouds from raining.”
The New York Times reported that the country Jalali did not name was the United Arab Emirates, which has launched a cloud seeding program by injecting chemicals into clouds in an attempt to induce rain in its favor, but also to prevent rainfall in Iran.
Today, however, many Middle Eastern elites are talking about the extreme drought and equally abnormal heat that have plagued the region for ages. We also recall that before the war against Iran, the country had suffered for years from a dramatic water shortage that directly endangered the people, especially the nation’s capital, whose inhabitants (and first and foremost the government) were ready to flee rather than become parched or dry out like old stones.
THE RETURN OF THE RAIN
And then, suddenly, a miracle amidst the misfortunes! In Iran, the clouds finally wept, abundantly and regularly, and temperatures returned to normal (dropping by an average of five degrees Celsius). A few days after the first Iranian strikes against American bases located in the United Arab Emirates and elsewhere on the Arabian Peninsula, the regional climate changed completely.
Initially stunned, the population could observe over the following weeks the gradual filling of natural and reservoir lakes, the return of life to rivers, streams, and springs, the greening and re-greening of meadows, and the return of flora and fauna familiar from the past. In five or six weeks, enormous water reservoirs were filled, and large hydroelectric facilities had to release water to prevent overflows.
The authorities finally called on all Iranian farmers to sow as much wheat as possible and to plant without worry, since water would certainly not be lacking during the summer season. The return of a “normal” spring was not an accident, and this understanding is now shared by everyone in Tehran, Baghdad, and Afghanistan.
According to Iranian officials, including ambassadors (stationed in the greater region), this new rain that has nourished the land is not providential but the result of Iran’s bombings of the gigantic American radars which were simultaneously being used as HAARP systems, tools quite capable of locally modifying the climate.
The Iranian embassy in Kabul posted this unambiguous tweet: “Iran, after destroying a secret cloud seeding and climate manipulation center in the United Arab Emirates, saw everything change overnight. Once this secret center was destroyed, the region’s weather map completely reversed, and now it rains every week in Turkey, Iran, and Iraq, with temperatures dropping by 5 degrees. I don’t know if what they’re saying is true, but there’s a change that everyone is noticing, and temperatures in Iraq haven’t been like this for decades.”
Before the war, and Tehran’s audacious response, two major American activities were likely to alter the climate of the Middle East, not inadvertently but intentionally.
CHEMTRAILS AND WAVES
Until the outbreak of the conflict, military aircraft of the United States and their allies released daily, or several times a week (there are many testimonies on this point), trails which are aptly called chemtrails which covered the sky in a few hours with a milky coating generating a scientifically proven greenhouse effect.
Those with a bit of curiosity observe this same phenomenon in Europe and recall that the contrails left behind by all the planes in the last century lasted no more than a few dozen seconds. Never before had these contrails remained in our atmosphere for more than a minute; never had the sky turned whitish after a flurry of flights. Never.
This has been the case regularly since the 2000s, particularly since the deadly heatwave of 2003. Summers have been hotter, all seasons have suddenly been hotter, sometimes extraordinarily dry, to the point of a telluric change in some regions which has caused the fracturing of tens of thousands of houses built on clay soil.
Most of the hundreds of thousands of daily flights around the world do not produce chemtrails. Just a few hundred aircraft (not commercial airliners, of course) are enough to locally alter the climate, here or there, and cause temperatures to skyrocket. Keen observers will have noticed that these trails crisscross the sky in very calm weather, when their sponsors are certain they won’t be too widely dispersed and therefore ineffective.
As unpleasant as they may be, heat waves, droughts, and mild winters are messages meant for the brainwashed Westerners. They must admit that everything is out of whack because of their own activities, that the Earth is dying because of the carbon dioxide they emit with their diesel cars, their gas boilers, their incessant flatulence, and their horrendous meat-based diet.
The message is crystal clear: you small-time European consumers, you see the damage you’re causing, you careless fools! There are no seasons anymore, you bunch of idiots! The carp have no oxygen in the ponds, the trout have no current in the rivers, the grass is yellow in June, Grandma is suffocating in July, we’re dying of heat in Nantes, everything’s gone to hell. Scrap your gas-powered car, scrap your gas appliances, buy an electric car or a heat pump as soon as you can, install solar panels, demand the energy transition for everyone!
THE IRANIAN TARGET
In the Middle East, there was no message. No one was urging its inhabitants to abandon oil and internal combustion engines. Iran and its surrounding regions were simply a target. A target to be weakened, starved, and destabilized. So that only discontent could flourish, so that hatred against the regime could explode. In addition to the countless economic sanctions imposed upon it, Iran had thus been the target of climate attacks for many years.
For decades, military scientists have known how to dry out and heat entire regions by dusting their airspace with tiny metallic particles (aluminum and others) and water vapor. These particles are agitated by radar waves (which travel at the speed of light) and thus heat up. This temperature increase at the core of the clouds prevents the suspended water from freezing, thus preventing precipitation.
By preventing the movement of crop-dusting aircraft and by neutralizing giant radars (by destroying them), Iran has freed itself (momentarily?) from this “climate” trap.
BETWEEN CONSPIRACY AND CONSPIRACY THEORIES, A TRAP AGAINST IRAN
Tehran, long convinced of the existence of this plot orchestrated by the American-Zionist axis, could not, however, intervene sooner. It would have had to attack both the Americans and the United Arab Emirates first. And no one, apart from the Iranian elite and those in the know, would have believed the motive for its attack: a return to normalcy.
In its self-defense, the Persian regime was able to destroy the massive radar systems in a seemingly, ostensibly, rational move. It was the radars themselves that were eliminated, not radars also used as instruments projecting microwaves to deplete Iran’s resources. The damning accusation of conspiracy could not be leveled against it.
By holding out for so long, by resisting for so long the sanctions and social unrest orchestrated by the enemy, by enduring for so long this extraordinary drought, Iran has won the battle against “conspiracy theories” by avoiding appearing as one of its most obsessive proponents.
We know that Iran quite legitimately believed in this conspiracy, but a war waged to officially combat it would not have been accepted by everyone in a world saturated in the media (even outside the West) and the demonization of “conspiracy theories.” Climate warfare could have brought Iran to its knees, but it was its enemy, who needed this war (which it tried by all means to provoke), who struck first. This is Iran’s greatest success to date.
Nevertheless, it is difficult to believe that the American-Zionist axis has surrendered in this war. Is it trying, or will it try, to rebuild radars designed to manipulate the climate in the same way, or will it use other radars located on other continents? Will it use drones to spray its chemical potion? In short, is the climate war truly over?
If it is not already doing so, Iran now has every interest in communicating on this issue so that it is taken seriously by people around the world. A difficult but vital task.
TheNew York Times(NYT) reports in “A New Idea to Save the Climate? Dam the Bering Strait.” that scientists have proposed building a 50-mile-long dam between Alaska and Russia to stabilize the Atlantic Meridional Overturning Circulation (AMOC) in order to prevent climate catastrophe. This is a seriously risky idea. The proposal is not an engineering plan grounded in observational need, but rather is computer-model thought experiment based on speculative tipping-point scenarios not justified by data concerning the AMOC or an understanding of what the possible future consequences might be for humans, the oceans, and sea life.
The author describes an article published in Science Advances where the idea of a cross continental dam across the Bering Strait is proposed as a “proof of concept,” noting that the dam could, under certain modeled conditions, prevent an AMOC collapse. It further explains that the findings come from a computer model of Earth’s climate, not from direct evidence that the AMOC is about to fail. That distinction is critical.
As Climate Realism has reported in dozens of articles, the AMOC has been the subject of repeated alarmist headlines over the past decade. Some studies have projected weakening. Others have suggested relative stability. Still others have found mechanisms, such as Southern Ocean wind-driven upwelling, which may be strengthening the AMOC. The scientific literature has moved in three directions: collapse, steady-state persistence, and even partial strengthening depending on assumptions.
What has not emerged is observational evidence of imminent shutdown.
The NYT acknowledges that “the uncertainty is very, very large,” quoting a climate scientist who says researchers do not know how close the AMOC is to collapse.
The proposed intervention outlined in the study would block the Bering Strait to alter freshwater flows between the Pacific, Arctic, and Atlantic Oceans. The model simulations suggest that if the AMOC is still strong, closing the strait might help maintain salinity and stabilize circulation. But if the AMOC is already weak, the same intervention could accelerate collapse.
In other words, the intervention could help, harm, or do nothing depending on timing and initial conditions.
That is not a control mechanism; it is a Las Vegas style gamble on a global scale.
The proposal relies on climate model outputs run under specific forcing assumptions. Models are useful tools, but they are not reality. Ocean circulation at the scale of the AMOC involves complex thermohaline processes, wind forcing, stratification, and deep-water formation, most of which aren’t well understood and, at best if accounted for at all in climate models, are only imperfectly represented even in state-of-the-art systems.
Moreover, the underlying modeling framework uses coarse resolution that does not fully resolve the Bering Strait’s dynamics, instead parameterizing throughflow behavior. From that abstraction comes a proposal to physically block a major ocean gateway. The AMOC is critical to coastal communities and the health and lifecycles of sea life. There is no evidence the models accounted for ancillary impacts on these communities or species – the only focus was keeping the AMOC from collapsing, though, it turns out, the proposed cure may, in fact, cause the collapse.
The scale of the proposal itself should give pause. An 80-kilometer barrier in Arctic conditions across an international boundary is not comparable to ordinary coastal infrastructure. The NYT notes that once built, such a structure “couldn’t easily be taken down.” Geoengineering does not come with an undo button.
The Bering Strait is also a biological choke point linking Pacific and Arctic ecosystems. Blocking it would alter nutrient transport, salinity gradients, and marine migration pathways. The ecological consequences are acknowledged only briefly in the NYT coverage, yet they could be profound.
There is also a glaring contradiction embedded in this narrative. For years, readers have been told that the AMOC is fragile, sensitive to freshwater perturbations, and prone to tipping points. If that is true, why would deliberately shutting off a major ocean exchange be considered a sane idea? If the system is robust enough to tolerate such intervention, then perhaps the entire AMOC collapse narrative deserves reconsideration.
The Intergovernmental Panel on Climate Change (IPCC) Sixth Assessment Report (AR6) states that while AMOC weakening is likely under high-emissions scenarios – scenarios which are not just improbable but likely impossible, there is low confidence in a collapse before 2100. That is a far cry from imminent shutdown requiring Arctic mega-dams. The NYT article concedes that scientists do not know how close the AMOC is to collapse.
What we are seeing is a pattern. As climate modeling grows more dramatic, proposed interventions grow more extreme: carbon capture and permanent storage; solar radiation blocking; and now ocean dams. Each rest on the assumption that models reliably predict nonlinear system behavior decades in advance.
Before entertaining planetary-scale geoengineering, a simpler question should be asked: where is the observational evidence of near-term failure? The RAPID array has been monitoring the AMOC since 2004 and shows variability but not collapse. Paleo records indicate multidecadal fluctuations long before industrial emissions.
Ocean circulation is complex. Uncertainty is high. Models disagree. And now, on that uncertain foundation, we are asked to consider blocking an ocean strait. This is mad scientists from the movies type stuff. The NYT shouldn’t have even given this proposal an audience.
This is not sober climate reporting by TheNew York Times. It amplifies a speculative modeling exercise as if it were visionary thinking. When the cure involves restructuring planetary oceanic circulation based on uncertain and likely flawed simulations, skepticism is not denial, it is prudence in the face of a crazy idea with unknown consequences. The evidence that humans actually control the climate is exceedingly weak, but this proposal, if enacted, would certainly cause unforetold and unpredictable climate disruptions that we haven’t even begun to consider.
Crazy plans don’t become reasonable just because some group of scientists propose them. And crazy plans, just because they are floated, don’t necessarily merit the attention of a major media outlet, promoting it as a reasonable idea.
Federal health officials under the Biden administration failed abysmally to look for COVID-19 vaccine safety signals, according to congressional testimony delivered today by Children’s Health Defense (CHD) Senior Research Scientist Karl Jablonowski.
The government’s vaccine safety monitoring “over the past several years has been insulting, and many people are injured,” Jablonowski wrote in his written testimony.
History repeats itself if we don’t learn our lessons, Jablonowski warned.
Jablonowski, who holds a doctorate in biomedical and health informatics from the University of Washington’s School of Medicine, spoke as a witness at the U.S. Senate Permanent Subcommittee on Investigations hearing, “Unmasked: How Biden Health Officials Purposely Turned a Blind Eye Toward COVID-19 Vaccine Safety Signals.”
Hours before the hearing, Sen. Ron Johnson (R-Wis.), subcommittee chair, released a report detailing how Biden-era federal health officials refused to use a state-of-the-art statistical tool for detecting COVID-19 vaccination signals in VAERS — even though they knew the tool they were using was too broken to pick up on safety signals, including sudden cardiac death.
Johnson’s report, which cited roughly 600 pages of emails, revealed that in 2021, officials with the U.S. Food and Drug Administration (FDA) told an FDA researcher to “cease and desist” using the state-of-the-art tool to analyze COVID-19 vaccine injury reports in the Vaccine Adverse Event Reporting System (VAERS).
FDA was ‘blind’ to COVID vaccine injury reports in VAERS
In his testimony, Jablonowski detailed how each of the federal government’s three vaccine safety monitoring systems — VAERS, V-safe and Vaccine Safety Datalink (VSD) — had “pitfalls” and “failed” to adequately assess safety issues with the COVID-19 vaccine and other vaccines.
The failures of vaccine safety monitoring “can be, and were, catastrophic,” he said.
For instance, the FDA insisted on monitoring COVID-19 vaccine reports using a method that it knew didn’t work. The FDA knew the method was likely to give inaccurate results if similar vaccines — such as the Pfizer and Moderna COVID-19 vaccines — were included in the dataset. This is called masking.
“The FDA was completely blind to COVID-19 vaccine adverse events,” Jablonowski wrote. He said the FDA could have used an improved statistical method accounting for masking.
A 2022 peer-reviewed paper in Drug Safety showed that the improved method detected roughly 25 statistically significant COVID-19 vaccine safety signals — including sudden cardiac death, Bell’s palsy and pulmonary infarction — that the FDA’s older method missed.
In an earlier interview with The Defender, Jablonowski explained why it was so harmful for the FDA to continue using the older method:
“Imagine a night watchman has to find something on the ground. But instead of holding a flashlight, he is wearing sunglasses. In the morning, he says he didn’t find anything. That’s true, but it’s because he was using a tool that impeded his ability to see.”
As of March 27, 1,675,590 adverse events were reported to VAERS following COVID-19 vaccination, according to OpenVAERS. That number includes over 39,077 reports of death, 29,200 reports of myocarditis or pericarditis, and 18,009 reports of Bell’s palsy.
A national survey conducted in November 2025 found that roughly 1 in 10 U.S. adults who received the COVID-19 vaccine experienced “major” side effects.
V-safe was designed to collect ‘inconsequential’ data
Jablonowski told lawmakers that the Centers for Disease Control and Prevention’s (CDC) COVID-19 vaccine safety monitoring tool, V-safe, was designed to collect only “inconsequential” information that no one really cares about.
The V-safe app invited COVID-19 vaccine recipients to check off boxes to indicate what, if any, side effects they experienced after getting the shot.
However, the box options were for common short-term vaccine side effects that most people would consider “inconsequential,” such as chills, headache, joint pain, muscle or body aches, fatigue or tiredness, nausea, vomiting, diarrhea, abdominal pain or rash.
If a person experienced a more serious problem, they had to manually type it into the “other” text field, Jablonowski noted. He said:
“It is with horror that we find 366 individuals typed ‘myocarditis’ in the ‘other’ free-text field, a condition requiring a medical diagnosis. The horror is amplified by the nearly 50,000 registrants who typed ‘chest pain’ into the ‘other’ free-text field.”
Vaccine Safety Datalink is off-limits to independent researchers
Jablonowski also detailed how VSD, a collaborative database of patient information from 13 integrated healthcare organizations covering over 15.5 million people, also fails the public.
VSD data can ostensibly be used to detect vaccine safety issues in near-real time, Jablonowski said.
The problem is that only a small handful of scientists are ever allowed to look at the data. Jablonowski said:
“This many million-dollar taxpayer funded resource is not available to any scientist outside of the 13 Managed Care Organizations (MCO) or the federal government without independent IRB [independent review board] applications approved by all 13 MCOs, an estimated $250,000 per project.”
In other words, independent researchers are realistically barred from analyzing the data. “Transparency is simply unattainable,” Jablonowski said.
The World Health Organization’s current asthma fact sheet states that “many factors have been linked to an increased risk of developing asthma, although it is often difficult to find a single, direct cause.”¹ The United States National Heart, Lung, and Blood Institute puts it more plainly: “The exact causes for developing asthma are unknown and may be different from person to person… Because the exact cause is unknown, you may not be able to prevent asthma in yourself or your children.”² The United Kingdom’s National Health Service agrees: “The exact cause of asthma is unknown.”³ The Mayo Clinic concurs for childhood asthma specifically: “causes aren’t fully understood.”⁴ The Cleveland Clinic is briefer: “Experts aren’t sure what causes asthma.”⁵
In 2018, a twenty-three-author Commission published in The Lancet proposed something more radical. After reviewing the state of the field, the authors concluded that the word “asthma” should be retired. It was, they argued, “a label for a heterogeneous mix of pathologically distinct processes poorly represented by our current physiological and symptom-based classification system.” They noted that progress in reducing asthma admissions and mortality had stalled in the prior decade.⁶ The Commission’s lead author, Ian Pavord, is among the most cited respiratory physicians in the world. His position, after a career studying the condition, was that the condition does not exist as a coherent diagnostic entity.
The Global Asthma Report places worldwide prevalence at approximately 262 million people.⁷ Every one of them has been given a diagnosis whose name the field’s senior authorities propose to abandon, for a condition whose cause the field’s public-facing institutions declare beyond their capacity to identify.
The Comparison
The comparison that would answer the question has been done. It was not done by the WHO, the NIH, the CDC, or any major academic medical center. It was done by an independent researcher named Joy Garner, who spent several years assembling the Control Group Survey — a nationwide study of entirely unvaccinated Americans across forty-eight states, conducted in 2019 and 2020, with a 0.178% random sample of the unvaccinated population in all age groups, published in 2022.⁸
Among adults with zero exposure to any vaccines, no Vitamin K injection at birth, and no maternal vaccination during pregnancy, the rate of any chronic condition was 2.64%. Among the general adult population — 99.74% of whom have some vaccine exposure — the rate is 60%. The survey calculated the statistical odds that vaccines are not the cause of over 90% of the disabling chronic conditions suffered by Americans over eighteen at 1 in 245,083,100,778,672,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000. The p-value for that calculation is less than 4.08×10⁻⁶³.⁸ In particle physics, the threshold for declaring a theoretical particle discovered is 1 in 3,500,000. The Control Group result exceeds that threshold by fifty-seven orders of magnitude.
Asthma was among the specific conditions showing the differential. So were eczema, allergies, developmental disabilities, autism, ADHD, epilepsy, and cancers. The 99% confidence interval spanned less than 0.04% from the sample means.⁸
The establishment’s response has been silence. The Control Group Survey is not cited in any WHO fact sheet, any NIH publication, any GINA guideline, or any CDC document. It is not taught in any medical school. The data collection methodology — handwritten surveys, postmarked envelopes, in-person interviews — was designed to meet the federal rules of evidence for admissibility in product safety actions, not to be published in The New England Journal of Medicine. Garner built the survey to survive legal scrutiny rather than journal peer review, because she understood what the survey would encounter.
The published twelve-study convergence tells the same story. Kemp and Pearce in New Zealand in 1997: 23% of DPT/polio vaccinated children had asthma; zero unvaccinated.⁹ Odent in JAMA in 1994: pertussis-vaccinated children had asthma at 10.7% versus 2.0% in the unvaccinated.¹⁰ McKeever in 29,238 British children in 2004: hazard ratio of 14 for DPPT and 3.5 for MMR.¹¹ Enriquez at Vanderbilt in 2005: relative risk of 11.4 for asthma in vaccinated children.¹² Mawson in 2017 in American homeschooled children aged 6–12: allergic rhinitis rate of 10.4% versus 0.4%, a 26-fold difference.¹³ Lyons-Weiler and Thomas in 2020, working from Dr. Paul Thomas’s own pediatric practice records of 3,324 children over ten years: office-visit relative risks of 16.0 for asthma, 20.6 for allergic rhinitis, 11.3 for sinusitis, and 6.5 for breathing issues.¹⁴
The response to Thomas’s publication is diagnostic. The Oregon Medical Board suspended his license in December 2020, emergently and without filing charges, citing his vaccination practices. He lost his license, his hospital privileges, his board certifications, his health plan contracts, and his ability to practice medicine. His January 2022 trial before the Board was estimated to cost him over $250,000 in legal fees.¹⁴
The cause is not unknown. The comparison has been done. The comparison shows that the unvaccinated do not develop asthma at anything approaching the rate of the vaccinated. When a physician publishes the comparative data from his own practice, the institutional response is professional destruction, not investigation. The “unknown cause” formulation is not an admission of ignorance. It is a refusal to fund, publish, or practice the comparison that has already answered the question.
The Method
The establishment’s position is that the mechanism by which injection could produce asthma is speculative. The position is untenable because the establishment itself uses injection to produce asthma in laboratory animals — and has for decades.
The standard protocol for inducing allergic airway disease in a mouse is to sensitize the animal by intraperitoneal injection of ovalbumin (a protein antigen from chicken egg) adsorbed to aluminum hydroxide, followed by airway challenge with the same antigen. The mouse develops airway eosinophilia, elevated IgE, mucus hyperproduction, and airway hyperresponsiveness to methacholine. This is the stock method of every laboratory studying allergic asthma. Wilson and colleagues demonstrated in 2009, in the American Journal of Respiratory and Critical Care Medicine, that the same aluminum-adjuvanted route produces Th17-dependent neutrophilic airway hyperresponsiveness.¹⁵ Mishra and colleagues in 2015, in Nature Communications, demonstrated the same mechanism for house dust mite sensitization.¹⁶
Aluminum hydroxide is the most common vaccine adjuvant in the pediatric schedule. It is the same substance that, when injected into mice with a protein antigen, produces the murine model of the human condition. The formula is not contested. It is described in published protocols, used in thousands of studies, and produces the condition reliably.
The occupational confirmation is in the human literature. In 1994, Desjardins and colleagues at the University of Montreal published a study in the American Journal of Respiratory and Critical Care Medicine titled “Aluminium potroom asthma confirmed by monitoring of forced expiratory volume in one second.” Workers in aluminum smelters developed asthma from inhalation exposure to aluminum fluoride fumes. The condition has its own name in occupational medicine: potroom asthma.¹⁷ Kongerud’s 1994 Norwegian cohort study documented the same relationship: a close correlation between fluoride exposure levels and work-related asthmatic symptoms, confirmed by serial peak flow monitoring.¹⁸
In 2023, Matthew Daley and colleagues at Kaiser Permanente Colorado published in Academic Pediatrics the largest study yet conducted on cumulative vaccine aluminum exposure and asthma. The cohort was 326,991 children drawn from the CDC’s own Vaccine Safety Datalink. The exposure was total aluminum from vaccines administered before 24 months. The outcome was persistent asthma diagnosis at 24–59 months. Children exposed to more than 3 mg of vaccine aluminum were 36% more likely to develop persistent asthma (95% CI 1.21–1.53). Among children with eczema — the group Lester and Parker identify as having the compromised skin elimination pathway that forces toxic burden toward the lungs — those exposed to more than 3 mg of aluminum were 61% more likely to develop persistent asthma (95% CI 1.04–2.48).¹⁹
The CDC’s own database. Kaiser Permanente’s own lead author. An establishment journal. The signal survived the filtering. Aluminum causes asthma in adult workers through inhalation. Aluminum causes asthma in mice through injection with a protein. Aluminum causes asthma in children through injection with proteins, at a dose-response curve documented inside the establishment’s own dataset.
Charles Richet demonstrated in 1901 that injection of foreign proteins creates sensitization — a heightened response on subsequent exposure. The experiments were reproducible across species. The mechanism was universal. Richet won the 1913 Nobel Prize in Physiology or Medicine for this work.²⁰ Vaccines are injections of foreign proteins with adjuvants whose explicit function is to provoke an inflammatory response that would not otherwise occur. The consequence of injecting foreign proteins with aluminum — allergy, asthma, airway hyperresponsiveness — was predictable from the Nobel-winning research of 1901. The American schedule is now over seventy doses before adulthood.
The Drugs That Suppress
Having produced the condition, medicine treats it. The first-line controller is an inhaled corticosteroid. The first-line rescue for a century was a β-agonist bronchodilator. Both categories are associated with documented, regulator-acknowledged harm at scale.
Todd and colleagues in 2002 surveyed UK consultant pediatricians. They documented 33 biochemically confirmed adrenal crises among patients on inhaled corticosteroids — 28 children (mean age 6.4 years; one death) and 5 adults. Thirty of the 33 patients were on fluticasone at routinely prescribed pediatric doses.²¹ Kelly and colleagues, reporting for the Childhood Asthma Management Program Research Group in The New England Journal of Medicine in 2012, demonstrated that budesonide 400 μg/day for four to six years in prepubertal children produced a permanent 1.2 cm reduction in adult height.²² Israel and colleagues in 2001 showed dose-dependent hip bone mineral density loss in premenopausal women on inhaled corticosteroids, independent of oral steroid use.²³ Garbe and colleagues in JAMA in 1998 showed that more than three years of inhaled corticosteroid use tripled the risk of cataract extraction in the elderly.²⁴ Qian, Suissa, and Ernst in 2017 showed a relative risk of 1.83 for pneumonia in asthma patients on current inhaled corticosteroids.²⁵
In 2022, Kachroo and colleagues published in Nature Medicine a multi-cohort metabolomic study of more than 14,000 people. They demonstrated dose-dependent adrenal suppression in users of inhaled corticosteroids. The finding was not confined to high-dose users.²⁶
The FDA label on every inhaled corticosteroid names these harms. Flovent HFA: “It is possible that systemic corticosteroid effects such as hypercorticism and adrenal suppression (including adrenal crisis) may appear in a small number of patients.” Arnuity Ellipta: “Deaths due to adrenal insufficiency have occurred during and after transfer from systemic corticosteroids.”²⁷ The Mayo Clinic’s public information page on Cushing’s syndrome states: “Cushing syndrome can happen from taking glucocorticoid medicines. These are often used to treat inflammatory diseases such as rheumatoid arthritis, lupus and asthma… Any form of glucocorticoid, if taken in large amounts for a long time, can cause Cushing syndrome.”²⁸ The NIH MedlinePlus page on exogenous Cushing’s syndrome names inhalers explicitly among the causes.²⁹
A syndrome caused by a class of drug is listed on the drug’s own label as a side effect. The drug remains first-line therapy. The condition it is prescribed to treat is declared of unknown cause.
Between 1961 and 1967, asthma deaths rose sharply across six countries — England, Wales, Ireland, Australia, New Zealand, Norway, Scotland. The rise was concentrated in 5- to 34-year-olds. The British mortality toll alone was approximately 3,500 excess asthma deaths during that period. In children aged 10 to 14 during the epidemic years, asthma became the fourth leading cause of death. In 1972, Paul Stolley of Johns Hopkins identified the cause: a reformulated isoprenaline inhaler sold in the Commonwealth countries at five times the concentration of the North American version. Stolley’s verdict: “the worst therapeutic drug disaster on record. There’s nothing else — not even thalidomide — that ranks with it.”³⁰
The industry and regulatory response was denial, delay, and quiet reformulation. No manufacturer was held criminally liable. No executive faced professional consequences. The episode is not taught in medical schools as the defining case of regulatory capture it represents.
From 1976, New Zealand held the world’s highest asthma death rate. Crane, Pearce, and colleagues demonstrated in The Lancet in 1989 that prescribed fenoterol was the cause; in the most severe asthmatics, the relative risk of death from fenoterol was 13.3.³¹ Pearce and colleagues reported in 1995 that the New Zealand asthma death rate fell by approximately 50% within a year of fenoterol’s restriction.³² The 2006 Salmeterol Multicenter Asthma Research Trial (SMART), published in Chest, documented 13 asthma-related deaths in the salmeterol arm versus 3 in the placebo arm — a relative risk of 4.37 (95% CI 1.25–15.34). The African-American subgroup relative risk was 4.10.³³
In February 2010, the FDA issued a Drug Safety Communication requiring boxed warnings on all long-acting β-agonist products and stating that “LABAs should not be used as first-line therapy for asthma.”³⁴ In April 2019, the Global Initiative for Asthma reversed half a century of first-line prescribing practice. In the words of the guideline body’s own authors, writing in the European Respiratory Journal: “In April 2019, GINA published new recommendations that might be considered the most fundamental change in asthma management in 30 years… For safety, GINA no longer recommends treatment of asthma in adolescents and adults with SABA alone.”³⁵
Three mortality epidemics across fifty years. A more potent bronchodilator is introduced commercially, deaths rise, researchers in the affected country identify the drug as the cause, the industry denies, regulators delay, the drug is eventually restricted or relabelled. GINA’s 2019 reversal is the formal admission that short-acting β-agonist monotherapy — the treatment standard for most asthmatics for most of the twentieth century — had been killing asthmatics. The admission carries no acknowledgement of the cumulative death toll. The admission carries no acknowledgement that the condition being treated may itself be the consequence of other pharmaceutical and industrial exposures.
The Physician They Refused to Read
Dr. Henry Bieler was an American physician who practiced in Pasadena, California, from the 1920s until his death in 1975. His 1965 book Food Is Your Best Medicine remains in print. His patients included Gloria Swanson and Greta Garbo. He did not practice within the pharmaceutical paradigm. He was dismissed by organized medicine as a nutritionist and quack.
Bieler’s clinical framework was the terrain position articulated in specific biochemical terms. Disease arose, he wrote, from toxemia — the accumulation of metabolic waste beyond the body’s capacity to eliminate it. The liver was the master chemist. When the liver was overwhelmed, the endocrine glands were forced into “vicarious elimination,” pushing acid waste through secondary organs. The skin eliminated through eczema and rashes. The mucous membranes eliminated through catarrh and sinusitis. The lungs eliminated through what medicine named bronchitis, pneumonia, and asthma.³⁶
On asthma specifically, Bieler was clinical and direct. The asthmatic was a person whose liver had failed to keep pace with the toxic burden, whose adrenal glands were being driven to exhaustion compensating, and whose bronchial mucosa had become the path of elimination. He observed that “the adrenal activity in asthma patients is much below normal.” He wrote: “I have found that a rational and often successful treatment depends first upon detoxicating the patient.”³⁶ His protocols involved fasting, alkalizing vegetable broths (the Bieler broth — zucchini, green beans, celery, parsley — restored sodium-potassium balance for stressed adrenal glands), and strict avoidance of drugs, particularly cortisone and its analogues. He named cortisone, adrenaline, antibiotics, and caffeine together as “whips to an already-exhausted adrenal cortex” — producing temporary symptom suppression at the cost of deeper glandular collapse.³⁶
His patients recovered.
Bieler was writing in 1965. Inhaled corticosteroids were introduced commercially in 1972 (beclomethasone dipropionate), positioned as first-line asthma therapy, and have remained the cornerstone of the GINA treatment schedule ever since. Bieler’s specific clinical observation — that corticosteroids whip an already-exhausted adrenal cortex toward deeper failure — was untested in the mainstream literature until 2022, when Priyadarshini Kachroo and colleagues published their Nature Medicine metabolomic study of more than 14,000 ICS users and documented exactly what Bieler had described: extensive, dose-dependent adrenal suppression from inhaled corticosteroid therapy in asthma.²⁶
Fifty-seven years separate Bieler’s observation from its confirmation. No practice has changed. No asthma guideline references Bieler. No medical school teaches his framework. The confirmation was published; the implication was ignored. The physician who named the mechanism in 1965 is still dismissed as a quack. The Nature Medicine paper that confirmed his finding in 2022 did not prompt any reconsideration of the drug category whose harm it documented. The iatrogenic cascade continues. Asthma is treated with inhaled corticosteroids. The corticosteroids suppress the adrenals. Adrenal insufficiency is documented. The adrenal insufficiency is managed with additional steroids. The asthmatic accumulates prescriptions, diagnoses, and deficiencies across a lifetime.
Bieler did what the establishment refused to do. He investigated the cause. He named it. He published the findings. He treated patients within the framework. He was vindicated in 2022 by the establishment’s highest-impact biomedical journal. The practice has not moved.
The Full Terrain
Bieler’s framework — shared with Tilden, Shelton, Williams, and the broader Natural Hygiene lineage — identifies four categories of insult: toxic exposure, nutritional deficiency, electromagnetic exposure, and psychological strain. The material this essay has documented so far — the vaccine-aluminum mechanism, the corticosteroid cascade, the β-agonist epidemics — sits inside the first category, and more specifically in the iatrogenic subset of the first category. Asthma is not caused solely by pharmaceutical intervention. Asthma is the expression of accumulated toxic burden through the respiratory system, and pharmaceutical intervention is one source of that burden among several.
Paracetamol
Richard Beasley and the International Study of Asthma and Allergies in Childhood (ISAAC) Phase Three cohort published in The Lancet in 2008 the largest study ever conducted on paracetamol (acetaminophen) and childhood asthma. The cohort was 205,487 children from thirty-one countries. Paracetamol given for fever in the first year of life was associated with an odds ratio of 1.46 (95% CI 1.36–1.56) for asthma at six to seven years of age. High current use was associated with an odds ratio of 3.23 (2.91–3.60). The population-attributable risk for severe asthma symptoms was 22–38%.³⁷ Beasley’s 2011 ISAAC follow-up in adolescents, published in the American Journal of Respiratory and Critical Care Medicine, found a high-current-use odds ratio of 2.51 and a population-attributable risk for severe asthma of 38–43%.³⁸ Shaheen’s 2000 Thorax study showed dose-response in adults: weekly paracetamol use produced an odds ratio of 1.79; daily use, 2.38.³⁹ Shaheen’s 2002 Thorax study showed that frequent late-pregnancy paracetamol use was associated with a doubling of childhood wheeze risk (OR 2.10, 95% CI 1.30–3.41).⁴⁰ The proposed mechanism is glutathione depletion — paracetamol’s metabolite NAPQI consumes the master antioxidant, leaving the airway epithelium oxidatively vulnerable.⁴¹
Pediatric aspirin use in the United States collapsed between 1980 and 1986 following the Reye’s syndrome warnings. Paracetamol filled the void. Varner and colleagues observed in 1998 that the collapse of pediatric aspirin use was paralleled by a documented acceleration in childhood asthma prevalence.⁴² The correlation does not establish causation on its own; Beasley 2008 and the subsequent ISAAC data provide the mechanistic and epidemiologic anchor. The 2016 AVICA trial, published in The New England Journal of Medicine, tested paracetamol versus ibuprofen in already-asthmatic children and found no difference in exacerbations.⁴³ The trial did not address the question that matters: whether paracetamol causes incident asthma. Beasley’s 2008 Lancet finding, covering over 205,000 children across more than thirty countries, remains the definitive population study, and it identifies paracetamol as a risk factor for 22–38% of severe childhood asthma.
The WHO’s 2008 guidance cited in Beasley states that paracetamol “should not be used routinely, but should be reserved for children with a high fever (38.5°C or above).” This guidance is not implemented in most pediatric practice. The GINA strategy report advises: “where possible, avoid the use of acetaminophen and broad-spectrum antibiotics during the first year of life.” The FDA has issued no asthma-specific warning.
Chemical Inhalation
Occupational asthma is the most common occupational lung disease in industrialized countries. The American Thoracic Society and European Respiratory Society published a joint consensus statement in 2019 concluding that approximately 16% of adult-onset asthma is caused by workplace exposures.⁴⁴ Torén and Blanc’s earlier 2009 systematic review identified a median population-attributable risk of 17.6%.⁴⁵ More than three hundred chemical agents have been implicated. Isocyanate asthma in industrial workers. Baker’s asthma from flour dust. Persulfate asthma in hairdressers. Potroom asthma in aluminum smelters. Cleaning product asthma in healthcare workers.
Zock and colleagues in 2007, in the American Journal of Respiratory and Critical Care Medicine, published an international longitudinal cohort study of adult-onset asthma and home use of cleaning sprays. Weekly use of cleaning sprays was associated with a doubling of physician-diagnosed asthma incidence (RR 2.11, 95% CI 1.15–3.89). The study estimated that the use of cleaning sprays at least four days a week could account for up to 15% of adult asthma cases.⁴⁶
The chemicals recognized as causing occupational asthma are present in homes. Bleach and quaternary ammonium compounds in cleaning products. Isocyanates in spray-foam insulation and home-applied paints. Formaldehyde and volatile organic compounds from particleboard, new carpet, and some candles. Scented air fresheners — the highest-risk product category in Zock’s 2007 cohort, with a relative risk of 1.71 — react with indoor ozone to form formaldehyde and secondary organic ultrafine particles. Persulfates in home hair-bleaching kits. If the 15% home-cleaning-spray and 16% occupational attributable fractions are additive rather than overlapping, the total chemical-exposure-attributable asthma approaches 30% of adult-onset cases — before anyone counts fragrance chemicals, scented candles, off-gassing furniture, or particleboard construction materials.
The establishment literature attributes this cluster of cases to “environmental triggers” and refers patients for avoidance counselling. The broader implication — that asthma is the respiratory expression of industrial chemical inhalation, and that the industrial chemicals in question remain commercially available, unregulated in most domestic applications, and heavily marketed to the same demographics that show the highest asthma rates — does not appear in clinical guidelines.
Damp Buildings and Mould
The World Health Organization’s 2009 Guidelines for Indoor Air Quality: Dampness and Mould concluded that microbial pollution in damp buildings causes “increased prevalences of respiratory symptoms, allergies and asthma as well as perturbation of the immunological system.”⁴⁷ The 2004 Institute of Medicine report Damp Indoor Spaces and Health found sufficient evidence of association between damp indoor environments and upper respiratory tract symptoms, cough, wheeze, and asthma symptoms in sensitized asthmatics.⁴⁸ Mendell and colleagues’ 2011 review in Environmental Health Perspectives went further: the epidemiologic evidence “strongly suggested causation” of asthma exacerbation in children by indoor dampness and mould.⁴⁹ Pekkanen’s 2007 Finnish cohort study documented a dose-response relationship: civil-engineer-verified moisture damage produced an asthma odds ratio of 4.0 in the highest-exposure group.⁵⁰ Kercsmar’s 2006 randomized remediation trial, published in the same journal, showed approximately 90% reduction in asthma acute-care visits among children whose homes underwent moisture remediation.⁵¹
The tight building envelopes that followed the 1973 oil crisis — designed to reduce energy losses — reduced indoor air exchange. Moisture accumulated. Mould colonized. The timing matches a component of the 1980s asthma prevalence inflection. The WHO and the IOM have been clear about the causation. No national public health campaign in any country has matched the scale of the exposure.
Nutritional Depletion
The one asthma intervention with Cochrane-grade evidence and formal endorsement by every major guideline body is not a drug. It is a nutrient. Intravenous magnesium sulfate, administered in the emergency department to asthmatics who have failed to respond to oxygen, nebulized β-agonists, and IV corticosteroids, reduces hospital admissions. The 2014 Cochrane review covering fourteen trials and 2,313 adults produced an admission odds ratio of 0.75 (95% CI 0.60–0.92), high-quality evidence.⁵² The 2016 pediatric Cochrane review showed an admission odds ratio of 0.32 (0.14–0.74).⁵³ The British Thoracic Society, NICE, GINA, and the NHLBI all endorse IV magnesium sulfate as adjunct therapy in severe acute asthma. The recommended dose is 1.2 to 2 grams infused over twenty minutes.
A nutrient rescues asthmatics from their drugs’ failures. The clinical implication — that chronic magnesium depletion contributes to bronchial hyperreactivity, and that supplementing magnesium might prevent attacks rather than merely rescue from them — is not taught. The commercial asthma market is sized around pharmaceutical therapy; nutrient therapy is not patentable.
Litonjua’s 2016 VDAART randomized trial in JAMA showed a 6.1% absolute reduction in asthma/recurrent wheeze at age three in children whose mothers had received 4,400 IU daily vitamin D during pregnancy compared to 400 IU.⁵⁴ Hodge’s 1996 Sydney cohort showed a fivefold reduction in current childhood asthma with regular oily fish consumption (OR 0.26, 95% CI 0.09–0.72).⁵⁵ Loss’s 2011 GABRIELA study showed that raw farm milk consumption reduced asthma by approximately 40% (adjusted OR 0.59); boiled farm milk showed no protective effect.⁵⁶ Hemilä’s 2013 meta-analysis in BMJ Open showed vitamin C produced a 48% reduction in exercise-induced bronchoconstriction.⁵⁷
Asthmatic airways are systems under metabolic strain. The strain responds to specific nutritional support. None of these interventions are pharmaceutical. None generate substantial revenue. None are prioritized in guideline algorithms.
Electromagnetic Exposure
The terrain framework identifies four categories of insult. Three have been documented thoroughly in this essay: toxic exposure (iatrogenic and environmental), nutritional deficiency, and — through the nineteenth-century nervous-disease literature discussed below — psychological strain. The fourth is electromagnetic exposure. The respiratory-specific peer-reviewed evidence for RF-EMF as a direct asthma cause is currently weak. No controlled human provocation trial has been published. No WHO, CDC, NIH, ATS, or GINA document identifies RF-EMF as an asthma risk factor. This is a genuine evidentiary gap.
What exists is a plausible mechanism — Pall’s 2013 Journal of Cellular and Molecular Medicine review documents voltage-gated calcium channel activation by non-thermal EMF exposure, producing NO/peroxynitrite pathway signalling, oxidative stress, and mast-cell and inflammatory activation.⁵⁸ The ecological correlation between the rollout of successive wireless infrastructure generations (2G, 3G, 4G, 5G) and the acceleration in asthma prevalence exists in descriptive data but has not been subjected to rigorous time-series analysis. The terrain framework’s position is that EMF belongs on the investigation list. The establishment’s position is that the question is not worth asking — the same agnotological posture documented throughout this essay.
The hypothesis advanced by Arthur Firstenberg in The Invisible Rainbow — that the 1918 respiratory mortality event coincided with the global rollout of high-power radio — is contested on dosimetry grounds and remains outside established evidence.⁵⁹ It is named here for the reader’s awareness, not endorsed. The terrain framework’s inclusion of EMF as an insult category rests on mechanistic plausibility and ecological pattern, not on direct respiratory provocation data.
The Nineteenth-Century Baseline
Asthma is not a timeless condition. The Victorian medical literature describes asthma as rare enough to warrant case-by-case chapter-length treatment. Henry Hyde Salter’s 1860 monograph On Asthma: Its Pathology and Treatment is the foundational nineteenth-century text; Salter’s position was that asthma is “essentially, and, with perhaps the exception of a single class of cases, exclusively a nervous disease.”⁶⁰ George Miller Beard’s 1881 American Nervousness, Its Causes and Consequences folded asthma into neurasthenia, the syndrome Beard argued was produced by the pressures of “modern civilization” — which he enumerated as steam-power, the periodical press, the telegraph, the sciences, and the entry of women into public life.⁶¹ Sir William Osler’s 1892 Principles and Practice of Medicine treated asthma in a five-page chapter, noting that “all authors agree that there is, in a majority of cases of bronchial asthma, a strong neurotic element.”⁶²
The prevalence implied by this literature is small. Salter, Beard, and Osler wrote as if asthma were a condition most physicians would encounter only occasionally. Nothing in their texts suggests the 1-in-13 prevalence of the current American population. The inflammatory-disease paradigm that now defines asthma is forty years old — Laitinen’s 1985 bronchial biopsy study, followed by Djukanović’s 1990 consolidation, together shifted the definition from nervous disorder to chronic airway inflammation.⁶³ ⁶⁴ The Lancet Commission’s 2018 proposal to retire the word “asthma” is the implicit admission that the inflammatory paradigm has also failed to explain the condition or reduce its burden.
Victorian medicine associated asthma with affluence and urban living. Heavy textiles, carpets, upholstery. Coal-smoke interiors. Indoor pollution from lamp oil, dust mites in horsehair mattresses, chimney soot. The nervous-disease framing was not simply prescientific — it named something the modern inflammatory paradigm has obscured. Asthma rose in the populations exposed to industrial indoor environments. The rise accelerated across the twentieth century as industrial chemistry extended its reach into every domestic product. The twenty-first century’s further acceleration — from approximately 3% of American children in 1980 to 8–10% of the American population today — tracks the expansion of the pharmaceutical schedule, the pediatric paracetamol shift, the ultraprocessed food transition, the wireless rollout, and the tight-envelope mould-friendly housing stock that followed 1973. The nineteenth-century baseline is what asthma looks like before these exposures. The Control Group Survey’s 2.64% figure is what it looks like when those exposures are refused.
The Next Move
The word “asthma” may not survive this decade. The 2018 Lancet Commission has already proposed retiring it. A new label is being prepared: autoimmune airway disease. Paul Thomas, in Vax Facts, observes: “In recent years, research has indicated that, contrary to long-standing belief, asthma may be an autoimmune condition. There are now over 100 conditions that are considered autoimmune. Vaccines may well be the single most important cause of autoimmune conditions.”⁶⁵
When evidence accumulates that cannot be explained within the existing framework — and the evidence that injection produces airway hyperresponsiveness is accumulating — the solution is not to follow the evidence to the cause. The solution is to rename the condition in a way that removes the cause from the frame.
Autoimmunity — the body attacking itself — achieves this precisely. The injection disappears. The chemical exposures disappear. The paracetamol, the corticosteroids, the β-agonists disappear. What remains is the body, malfunctioning, requiring lifelong immunosuppression. The patient who asked “what am I being exposed to?” is offered instead the question “what is wrong with me?” The framing erases causation. The body is responding, correctly, to injuries it is being asked to absorb.
When the next headline announces that asthma has been reclassified as autoimmune, the reader will know what is being said. The injection that caused the sensitization Richet described in 1901 is being renamed. The chemical that the establishment’s own laboratories use to manufacture the condition in mice is being exonerated. The physician who treated asthma through detoxification sixty years ago, and whose specific clinical observation was confirmed by Nature Medicine in 2022, is still a quack. The mechanism is known. The mechanism has been known. What is being renamed is not the disease. What is being renamed is the body’s entirely appropriate response to a century of injuries.
Explain It To A 6 Year Old
Two children are born on the same day in the same city. Their mothers meet in the hospital. They live in neighbouring houses. They breathe the same air and drink the same water. They go to the same school.
One of them gets the vitamin K shot at birth. He gets all the injections the doctors offer — dozens of shots before he starts school. When he has a fever, he gets paracetamol. When he has an ear infection, he gets antibiotics. When he is nine, he is diagnosed with asthma. He gets a blue inhaler and a brown inhaler. He gets steroid tablets when the asthma is bad. By the time he is twenty, he has asthma, eczema, allergies, and digestive problems. His grandmother worries about him.
The other child gets none of these things. Her parents looked at the schedule and said no. She has fevers; they do not give her paracetamol. She gets ear infections; she gets better. She does not develop asthma. She does not develop eczema. She does not develop allergies. When she is twenty, she is well. Her grandmother does not worry.
The grown-ups in the city — the doctors, the journalists, the health authorities — say they do not know why one child has asthma and the other does not. They say it might be genetic. They say it might be bad luck. They say the cause of asthma is mysterious. They do not do the comparison. When a researcher does the comparison anyway, her study is not cited in any fact sheet. When a doctor in Oregon does the comparison from his own practice and publishes the results, his licence is taken away.
The cause is not mysterious. The grown-ups know. They have always known. They have written it in their own laboratory papers. They mix aluminum with a protein and inject it into a mouse, and the mouse becomes asthmatic. They put aluminum dust in the air of a factory, and the workers become asthmatic. They inject aluminum into children, and the children become asthmatic, at a rate that goes up with the dose, in a study run by Kaiser Permanente and published in their own journal.
The difference between the two children is not genetic. It is not bad luck. It is not a mystery. It is a decision. One set of parents said yes to everything the grown-ups offered them, and their child is sick. The other set of parents said no, and their child is well. The decision is available to every parent in the city. It has always been available. It has never been advertised.
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Todd GRG, Acerini CL, Ross-Russell R, Zahra S, Warner JT, McCance D. “Survey of adrenal crisis associated with inhaled corticosteroids in the United Kingdom.” Archives of Disease in Childhood 2002;87(6):457–61.
Kelly HW, Sternberg AL, Lescher R, et al.; CAMP Research Group. “Effect of inhaled glucocorticoids in childhood on adult height.” New England Journal of Medicine 2012;367(10):904–12.
Israel E, Banerjee TR, Fitzmaurice GM, Kotlov TV, LaHive K, LeBoff MS. “Effects of inhaled glucocorticoids on bone density in premenopausal women.” New England Journal of Medicine 2001;345(13):941–47.
Garbe E, Suissa S, LeLorier J. “Association of inhaled corticosteroid use with cataract extraction in elderly patients.” JAMA 1998;280(6):539–43.
Qian CJ, Coulombe J, Suissa S, Ernst P. “Pneumonia risk in asthma patients using inhaled corticosteroids: a quasi-cohort study.” British Journal of Clinical Pharmacology 2017;83(9):2077–86.
Kachroo P, Stewart ID, Kelly RS, et al. “Metabolomic profiling reveals extensive adrenal suppression due to inhaled corticosteroid therapy in asthma.” Nature Medicine 2022;28(4):814–22.
FDA label information for Flovent HFA (fluticasone propionate) and Arnuity Ellipta (fluticasone furoate), accessed via accessdata.fda.gov.
Mayo Clinic. Cushing syndrome. mayoclinic.org/diseases-conditions/cushing-syndrome.
National Library of Medicine. Exogenous Cushing syndrome. MedlinePlus, medlineplus.gov/ency/article/000410.htm.
Stolley PD, Schinnar R. “Association between asthma mortality and isoproterenol aerosols: a review.” Preventive Medicine 1978;7(4):519–38. Also Speizer FE, Doll R, Heaf P, Strang LB. “Investigation into use of drugs preceding death from asthma.” BMJ 1968;1(5588):339–43; Inman WH, Adelstein AM. “Rise and fall of asthma mortality in England and Wales in relation to use of pressurised aerosols.” Lancet 1969;2(7615):279–85.
Crane J, Pearce N, Flatt A, et al. “Prescribed fenoterol and death from asthma in New Zealand, 1981–83: case-control study.” Lancet 1989;1(8644):917–22.
Pearce N, Beasley R, Crane J, Burgess C, Jackson R. “End of the New Zealand asthma mortality epidemic.” Lancet 1995;345(8941):41–44.
Nelson HS, Weiss ST, Bleecker ER, Yancey SW, Dorinsky PM; SMART Study Group. “The Salmeterol Multicenter Asthma Research Trial: a comparison of usual pharmacotherapy for asthma or usual pharmacotherapy plus salmeterol.” Chest 2006;129(1):15–26.
US Food and Drug Administration. Drug Safety Communication: New safety requirements for long-acting inhaled medications called long-acting beta-agonists (LABAs). 18 February 2010.
Reddel HK, FitzGerald JM, Bateman ED, et al. “GINA 2019: a fundamental change in asthma management.” European Respiratory Journal 2019;53(6):1901046.
Bieler HG. Food Is Your Best Medicine. New York: Random House, 1965. See also Bieler HG. Dr. Bieler’s Natural Way to Sexual Health. Los Angeles: Charles Publishing, 1972. The broader philosophical predecessors are Tilden JH, Toxemia Explained (Denver, 1926), and Shelton HM, Fasting Can Save Your Life (Natural Hygiene Press, 1964).
Beasley R, Clayton T, Crane J, et al. “Association between paracetamol use in infancy and childhood, and risk of asthma, rhinoconjunctivitis, and eczema in children aged 6–7 years: analysis from Phase Three of the ISAAC programme.” Lancet 2008;372(9643):1039–48.
Beasley RW, Clayton TO, Crane J, et al. “Acetaminophen use and risk of asthma, rhinoconjunctivitis, and eczema in adolescents: International Study of Asthma and Allergies in Childhood Phase Three.” American Journal of Respiratory and Critical Care Medicine 2011;183(2):171–78.
Shaheen SO, Sterne JA, Songhurst CE, Burney PG. “Frequent paracetamol use and asthma in adults.” Thorax 2000;55(4):266–70.
Shaheen SO, Newson RB, Sherriff A, et al. “Paracetamol use in pregnancy and wheezing in early childhood.” Thorax 2002;57(11):958–63.
Nuttall SL, Williams J, Kendall MJ. “Does paracetamol cause asthma?” Journal of Clinical Pharmacy and Therapeutics 2003;28(4):251–57.
Varner AE, Busse WW, Lemanske RF Jr. “Hypothesis: decreased use of pediatric aspirin has contributed to the increasing prevalence of childhood asthma.” Annals of Allergy, Asthma & Immunology 1998;81(4):347–51.
Sheehan WJ, Mauger DT, Paul IM, et al. “Acetaminophen versus ibuprofen in young children with mild persistent asthma.” New England Journal of Medicine 2016;375(7):619–30.
Blanc PD, Annesi-Maesano I, Balmes JR, et al. “The occupational burden of nonmalignant respiratory diseases. An Official American Thoracic Society and European Respiratory Society Statement.” American Journal of Respiratory and Critical Care Medicine 2019;199(11):1312–34.
Torén K, Blanc PD. “Asthma caused by occupational exposures is common: a systematic analysis of estimates of the population-attributable fraction.” BMC Pulmonary Medicine 2009;9:7.
Zock JP, Plana E, Jarvis D, et al. “The use of household cleaning sprays and adult asthma: an international longitudinal study.” American Journal of Respiratory and Critical Care Medicine 2007;176(8):735–41.
World Health Organization Regional Office for Europe. WHO Guidelines for Indoor Air Quality: Dampness and Mould. Copenhagen: WHO, 2009.
Institute of Medicine. Damp Indoor Spaces and Health. Washington, DC: National Academies Press, 2004.
Mendell MJ, Mirer AG, Cheung K, Tong M, Douwes J. “Respiratory and allergic health effects of dampness, mold, and dampness-related agents: a review of the epidemiologic evidence.” Environmental Health Perspectives 2011;119(6):748–56.
Pekkanen J, Hyvärinen A, Haverinen-Shaughnessy U, Korppi M, Putus T, Nevalainen A. “Moisture damage and childhood asthma: a population-based incident case-control study.” European Respiratory Journal 2007;29(3):509–15.
Kercsmar CM, Dearborn DG, Schluchter M, et al. “Reduction in asthma morbidity in children as a result of home remediation aimed at moisture sources.” Environmental Health Perspectives 2006;114(10):1574–80.
Kew KM, Kirtchuk L, Chang CC. “Intravenous magnesium sulfate for treating adults with acute asthma in the emergency department.” Cochrane Database of Systematic Reviews 2014;5:CD010909.
Griffiths B, Kew KM. “Intravenous magnesium sulfate for treating children with acute asthma in the emergency department.” Cochrane Database of Systematic Reviews 2016;4:CD011050.
Litonjua AA, Carey VJ, Laranjo N, et al. “Effect of prenatal supplementation with vitamin D on asthma or recurrent wheezing in offspring by age 3 years: the VDAART randomized clinical trial.” JAMA 2016;315(4):362–70.
Hodge L, Salome CM, Peat JK, Haby MM, Xuan W, Woolcock AJ. “Consumption of oily fish and childhood asthma risk.” Medical Journal of Australia 1996;164(3):137–40.
Loss G, Apprich S, Waser M, et al. “The protective effect of farm milk consumption on childhood asthma and atopy: the GABRIELA study.” Journal of Allergy and Clinical Immunology 2011;128(4):766–73.e4.
Hemilä H. “Vitamin C may alleviate exercise-induced bronchoconstriction: a meta-analysis.” BMJ Open 2013;3(6):e002416.
Pall ML. “Electromagnetic fields act via activation of voltage-gated calcium channels to produce beneficial or adverse effects.” Journal of Cellular and Molecular Medicine 2013;17(8):958–65.
Firstenberg A. The Invisible Rainbow: A History of Electricity and Life. AGB Press, 2017; reissued Chelsea Green, 2020.
Salter HH. On Asthma: Its Pathology and Treatment. London: John Churchill, 1860; 2nd edition London 1868; 1st US edition Philadelphia: Blanchard & Lea, 1864.
Beard GM. American Nervousness, Its Causes and Consequences. New York: G.P. Putnam’s Sons, 1881.
Osler W. The Principles and Practice of Medicine. 1st edition. New York: D. Appleton & Co., 1892. Asthma: pp. 497–501.
Laitinen LA, Heino M, Laitinen A, Kava T, Haahtela T. “Damage of the airway epithelium and bronchial reactivity in patients with asthma.” American Review of Respiratory Disease 1985;131(4):599–606.
Djukanović R, Roche WR, Wilson JW, et al. “Mucosal inflammation in asthma.” American Review of Respiratory Disease 1990;142(2):434–57.
Thomas P. Vax Facts. Paul Thomas MD. See drpaulsfight.com for Thomas’s case history. The autoimmune reframing is also discussed in Jackson M, Asthma: The Biography (Oxford University Press, 2009).
Background and framework sources
Cowan TS, The Contagion Myth (Skyhorse, 2020); Bailey M, The Final Pandemic: An Antidote (2022); Lester D, Parker D, What Really Makes You Ill? Why Everything You Thought You Knew About Disease Is Wrong (Independently Published, 2019); Trebing WP, Good-Bye Germ Theory (Xlibris, 2006); Engelbrecht T, Köhnlein C, Bailey S, Virus Mania, 3rd edition (Books on Demand, 2021); Roytas D, Can You Catch a Cold? (2024); Williams U, Terrain Therapy (2022); Maready F, Crooked (Feels Like Ghosts, 2018); Fraser H, The Peanut Allergy Epidemic, 3rd edition (Skyhorse, 2017); Kennedy RF Jr., Vax-Unvax (Skyhorse, 2023); Miller NZ, Miller’s Review of Critical Vaccine Studies (New Atlantean Press, 2016); Humphries S, Bystrianyk R, Dissolving Illusions: Disease, Vaccines, and the Forgotten History (2013); Bystrianyk R, Humphries S, Turtles All the Way Down: Vaccine Science and Myth (2019); Handley JB, How to End the Autism Epidemic (Chelsea Green, 2018).
A woman films herself from a hospital bed. Her left side will not move. Her speech is slurred. She took the COVID vaccine three weeks earlier and had a stroke within days. The camera shakes because she is holding it with the hand that still works. And she says, into the lens, that she is glad she took it. Because it could have been worse.
By every ordinary standard of how people respond to injury, the woman in the bed should be angry. She should want to know what happened to her body, who gave her the injection, what was in it, why she was not warned. Instead she is defending the thing that harmed her, and she is doing it sincerely, from a bed she may never leave.
The pattern repeated at scale throughout 2021 and 2022. Myocarditis in young men, received with gratitude. Sudden hearing loss, received with gratitude. Menstrual disruption, miscarriage, Bell’s palsy, shingles, tinnitus, cognitive fog — received with gratitude. The injured gave television interviews thanking the health authorities. They wrote newspaper columns urging others to take the product that had injured them. They volunteered at vaccination centres. The more severe the injury, the more fervent the testimony.
The COVID case is the clearest and most recent instance of something older. Chemotherapy patients credit the treatment with saving them while enduring a devastation that is the treatment.¹ Flu shot recipients who get the flu report that the shot made it milder — a claim no one can check. Statin patients who develop muscle weakness, diabetes and cognitive decline continue taking the drug in gratitude for a heart attack that may never have been coming.² SSRI patients who cannot feel, cannot sleep without the pill, cannot leave the house without the prescription, describe the drug as having saved their lives.³ Parents whose children regress after vaccination defend the schedule that preceded the regression.
The gratitude is real. That is what makes it devastating. These patients are not lying or performing. They feel what they say they feel. They are captured, and the gratitude is what their captivity looks like when it speaks.
What follows rests on one claim. The phenomenon is an engineered room, not a cognitive error or a cultural drift. Four walls stand around the captured person, each sealing a different exit, built by identifiable actors serving documented interests. The same four walls stand around every major medical intervention of our time.
The essay names the walls, shows them at work across several medical domains, names their architects, and ends where it must — with the one act that brings them down.
2. The Sealed Room
Four walls hold the captured person in place. Each seals a different kind of escape. Together they form a room from which the individual patient, acting alone, cannot exit. The walls fail only at population scale, and only when enough of the captured begin to speak at once — a condition the later sections will examine.
Wall One — The Counterfactual Shield. The intervention is defended by an imagined alternative that never happened. It would have been so much worse without it. The worse outcome is unfalsifiable. It did not occur and cannot be examined. It exists only as a claim, and a claim that cannot lose.
Wall Two — Injury as Vindication. Actual harm from the intervention is converted, at the moment of appearance, into evidence the intervention was necessary. Side effects become signs the drug is working. Adverse events become imagine how bad it would have been otherwise. The harm is recruited to defend the thing that caused it.
Wall Three — The Sunk Cost Bind. The patient has submitted their body to risk, cost, violation. The psychological price of admitting the submission was unnecessary — or worse, actively harmful — is unbearable. Every subsequent piece of evidence gets reorganised to vindicate the original decision, and the reorganisation strengthens with time.
Wall Four — The Tribal Seal. The intervention is tribal. Taking it is membership. Refusing it is defection. Honest testimony about injury breaks ranks with the tribe that formed around the intervention. The social cost of speaking is exile, so the injured stay silent, or perform gratitude to remain inside.
The walls appear here in the order the captured person meets them psychologically. Wall One is intellectual — it is installed before anything happens, as the framing of the intervention. Wall Two is empirical — it activates when harm arrives, renaming it before the patient can. Wall Three is interior — it operates in the self, on the self. Wall Four is social, and it closes the last door, the one that opens onto another person.
The sections that follow examine the walls one by one, and then name the people who built them.
3. Wall One: The Counterfactual Shield
A man takes the COVID vaccine in March 2021 and does not get COVID for the next year. He reports that the vaccine worked.
A woman takes the same vaccine and gets COVID in September. She reports that the vaccine worked, because it would have been worse without it.
A second woman ends up in hospital with COVID in October. She reports that the vaccine worked, because without it she would have died.
A third ends up on a ventilator, survives, and reports that the vaccine saved her life.
Every possible outcome confirmed the intervention. The counterfactual shield is the mechanism that made this possible. For each real outcome, an imagined worse outcome was available for comparison, supplied by the same system that administered the injection. The patient did not compare their actual experience to another actual experience. They compared it to a hypothetical that could never be tested.
This is the structure of every statin prescription. The patient cannot feel cholesterol. They cannot feel the heart attack that did not occur. What they can feel is the muscle pain, the fatigue, the cognitive changes, the new diabetes — and they are told this is the acceptable cost of preventing something invisible. Prevention is the absence of an event, which means the benefit can never be observed, only claimed. Every year without a heart attack is credited to the drug. When a heart attack arrives anyway, the cardiologist explains how much worse it would have been.
The shield needs a particular statistical apparatus to stand. The patient does not invent the imagined alternative from nothing; it is delivered to them, precisely calibrated, by the medical literature. Relative risk reduction is the instrument. A drug that cuts heart attacks from two per hundred to one per hundred is described as producing a fifty percent reduction. The absolute change — one person in a hundred — is rarely spoken. The patient hears fifty percent and pictures a world in which they were twice as likely to die. The shield, built from numbers the patient cannot audit, is in place before the first dose.
Notice what the wall does with time. It is installed before the intervention. The patient arrives already committed to the counterfactual, and every subsequent event gets filtered through it. The shield is not a defence the patient raises under challenge. It is the prior condition of the encounter.
COVID delivered this with unprecedented coordination. The vaccine reduced severe illness by ninety-five percent.⁴ The number appeared in advertising, press conferences, pharmacy windows, social media posts. It was a relative risk reduction calculated from a trial of approximately forty thousand people in which one hundred and seventy total COVID cases occurred.⁴ The absolute reduction was roughly zero point eight percent. The ninety-five percent was mathematically real and useless to any individual patient, but it did the only thing it needed to do — it installed the counterfactual. By the time a person rolled up their sleeve, the severe illness they had been rescued from was already in their head. Every later event could only confirm it.
A patient who wants to question the shield has no tools. They cannot run the experiment on themselves. They have no access to an un-treated version of their own body. They can only trust the number, and the number was given to them by the people who sold the intervention.
4. Wall Two: Injury as Vindication
The second wall turns on when the intervention produces harm. It renames the harm, before the patient can examine it, as evidence the intervention was needed.
Chemotherapy is where this wall stands most nakedly. The treatment produces hair loss, nausea, vomiting, bone marrow suppression, secondary cancers, organ damage, cognitive decline, and in a significant fraction of patients death directly attributable to the treatment itself rather than the disease.¹ Every one of these effects is explained to the patient in advance as a sign the treatment is working. Worse side effects mean the cancer is being fought harder. The patient who is destroyed by the treatment is told, and comes to believe, that the destruction is evidence of the drug doing its job.
In any other domain, a substance that caused hair loss, marrow suppression, neuropathy and death would be called poison. In oncology, it is called treatment, and the symptoms of poisoning are called response. A patient loses her hair and is congratulated. A patient vomits for six hours and the oncologist nods with satisfaction. A patient’s white cell count collapses and the number is entered into a chart labelled progress.
The vindication continues after the treatment ends. Survivors describe the treatment as having saved them, even though the untreated survival rate for many cancers — particularly low-grade and early-stage — is substantial and, in some studies, superior.¹ Patients who do not survive are said to have succumbed to the disease. The treatment itself, in the grammar of the explanation, cannot lose. Recovery means the treatment worked. Decline means the cancer was too aggressive. Death from treatment-induced organ failure becomes death from cancer. The death certificate rarely names the chemotherapy.
The same inversion ran through the COVID rollout with identical logic. Myocarditis in a young man after the second dose was classified as mild and self-limiting, and official guidance explicitly declined to treat it as a reason to halt the programme.⁵ The injury was converted, in real time, from a reason to stop into what officials called a sign the body was responding as intended. A teenage boy who developed pericarditis was described as fortunate to have been vaccinated, because imagine how bad it would have been otherwise. The inversion operated not only in the patient but in the cardiologist giving the diagnosis, in the journalist writing the story, in the regulator reviewing the report. The injury was never an injury. It was always a sign.
Pfizer’s own documents, obtained by court order after the FDA requested seventy-five years to release them, list over one thousand two hundred distinct adverse events in the first twelve weeks of the rollout.⁶ The company had to hire more than two thousand additional staff to manage the caseload. Of two hundred and seventy pregnant women who reported injury, only thirty-two were followed up, and twenty-eight of their babies died — an eighty-seven point five percent fetal death rate in the followed cohort.⁶ These numbers were not volunteered by Pfizer. They were extracted through litigation. In the public conversation of 2021 and 2022, the events they describe were either denied or converted into evidence the programme was working.
The wall holds because the patient has no independent framework from which to resist it. When the oncologist says hair loss is good, the patient has no counter-language. When the cardiologist says myocarditis is mild, the young man has no access to population data. When the physician calls the side effects signs of the body responding properly, the patient accepts it because no other account is available in the room. The injury is named by the apparatus that produced it, and the name replaces the thing.
By the time the patient might think to examine the injury on their own terms, the third wall has already closed behind them.
5. Wall Three: The Sunk Cost Bind
The third wall stands inside the patient rather than outside, which is why it is the hardest to see. From inside, it feels like the patient’s own mind.
Consider a woman who has taken a selective serotonin reuptake inhibitor for fifteen years. She began after a divorce. The initial diagnosis was depression. She was told her brain had a chemical imbalance that the medication would correct.³ Within weeks she felt a kind of emotional flattening that her doctor called the medication working. She stayed on it. Over years she noticed she could not cry at funerals, could not feel desire, could not grieve her mother’s death when it arrived. She tried twice to come off the drug. Both times the withdrawal was catastrophic — electric shocks in her head, intrusions of suicidal thought, panic that kept her awake for days — and both times she went back on, convinced by the severity of the symptoms that she needed it.
Ask this woman whether the medication saved her and she will say yes. She will say it without hesitation and without calculation. She will also say she does not know who she was before it, because the person who took the first pill is no longer available for comparison. Fifteen years of her life have been built around the diagnosis and the drug. Her identity contains the diagnosis. Her marriage, her friendships, her children’s memories of their mother all include the medication as a feature of her personality.
To admit the medication was not needed — that her grief had been grief, that the withdrawal was the drug rather than the return of her underlying condition, that the emotional flattening was damage rather than improvement — would require her to accept that fifteen years of her life were spent inside a false frame. She would have to grieve what the medication took from her. She would have to face her absence from her children, her distance in her marriage, her unfelt goodbye to her mother. The cost of that reckoning is more than most people can pay. So she stays on the drug and says it saved her life. The gratitude is real because the cost of it being otherwise is unbearable.
Wall Three most resembles ordinary human psychology, which is why it reads as personal rather than architectural. Everyone has known some version of it — the defence of a choice after it has gone wrong, memory quietly rewriting itself to fit where money and years have already been spent. What makes the medical version structural is the scale of what has been paid in and the absence of any exit that does not require grieving it.
A man who has taken statins for twenty years, and who has watched his strength fade, his memory slip and his diabetes arrive — the exact trio the drug is known to cause² — is asked whether the statins helped. He says yes. He has to say yes. Saying no would mean accepting that two decades of growing weakness were caused by the drug he took to protect himself. It would mean admitting the heart attack he was preventing may never have been coming, that the cholesterol number he was taught to fear was a fabricated risk marker, that the man he became — slower, forgetful, diabetic — is a product of a prescription rather than of ageing. The alternative is gratitude, and he is grateful.
A mother whose child regressed after the MMR vaccination is asked whether she regrets it. Most of the time she says no. She says the vaccine was necessary. She says the autism was coming anyway. Admitting otherwise would mean accepting that she brought her child to be injured, held him down while the injection was delivered, paid for it and thanked the paediatrician afterwards. The grief on the other side of that admission is more than most parents can carry, and the wall is shaped precisely so she does not have to carry it. She can stay grateful. Her paediatrician will reinforce the gratitude. Her friends will reinforce it. The media will reinforce it. Wall Four will hold her there.
Wall Three has a property worth naming directly. It thickens with time. The longer the patient has been inside the frame, the higher the cost of leaving it becomes, and so the more fervent the defence. This is why the elderly chemotherapy survivor speaks with more heat about the drug that saved her than the recent survivor does. This is why the twenty-year statin patient is more certain of the drug’s necessity than the one-year patient. The wall grows. At some point it becomes unbreachable by any means available to the patient alone.
What completes the bind is that the captured person becomes a recruiter. The grateful SSRI patient urges her grieving friend to see a psychiatrist. The grateful chemotherapy survivor tells the newly diagnosed to accept the protocol. The grateful vaccinated parent shames the unvaccinated one at the school gate. Each captured person, defending their own wall, helps build walls around others — because their own wall depends on the walls around others holding. If the friend refuses medication and flourishes, fifteen years come into question. So the friend must be pressured, shamed, or cut off. The sunk cost in one person becomes the tribal pressure on the next, which brings the architecture to its final closure.
6. Wall Four: The Tribal Seal
The fourth wall operates outside the patient, in the community. It is the social enforcement of the narrative the patient has begun to perform, and it closes the last available exit.
Throughout 2021 this wall stood in open view. Taking the COVID vaccine was an act of public membership — selfies from vaccination centres, profile frame overlays, stickers worn on lapels, doses announced on social media. Refusing was public defection. The refusers lost jobs. They were barred from restaurants, gyms, concert venues, churches, universities, sometimes from hospitals even as visitors. They were removed from family gatherings. They were called murderers on national television by the president of France, by the prime minister of Canada, by physicians on major networks. Official communications described them as a selfish minority whose refusal was costing the compliant their freedom.
Inside that environment, an injured person who testified honestly about their injury was not merely raising a medical concern. They were defecting. Their testimony confirmed what the refusers had been saying. Their testimony was a gift to the outgroup. The tribe could not absorb it, because tribal cohesion depended on the intervention being unquestionable. So the injured were managed. Sometimes through silence — their accounts went unpublished, their videos removed, their doctors declining to code the injury as vaccine-related. Sometimes through reframing — the injury classified as COVID, as long COVID, as coincidence, as pre-existing. Sometimes through direct punishment — the injured person who insisted on naming the cause was accused of spreading misinformation, of harming public health, of serving the outgroup.
Every injured person watched this happen to others before it happened to them, and the lesson was not subtle. Most adjusted. They stopped describing their injury as an injury. They began describing it as unfortunate but acceptable. They began saying the words that returned their membership: I’m glad I took it. It could have been worse. The gratitude was not only psychologically needed. It was socially required.
Wall Four is not specific to COVID. It has stood around childhood vaccination for decades.⁷ A parent who questions the schedule loses access to paediatric practices that refuse unvaccinated patients. She is asked to leave mothers’ groups. Family members cut her off on the grounds that her choice endangers their vaccinated grandchildren. Her children are barred from schools. Any paediatrician willing to accommodate her operates under constant professional threat. Entire parenting communities organise around the vaccination question, and the penalty for dissent is exile. Parents whose children regress after vaccination, and who begin to suspect a causal link, face a choice between silence and exile. Most choose silence. Many perform gratitude instead, because gratitude reopens the community. The mother who says I’m so glad we vaccinated; his regression was just coincidence keeps her paediatrician, her friends, her family. The mother who says I believe the vaccine injured my child loses all of them.
The same seal stands around psychiatric medication, around cancer treatment, around mainstream obstetric care. In each, the patient who voices doubt is pressured first by the clinician, then by the family, then by the wider community that has already accepted the intervention as standard. Doubt is not only intellectually costly. It is socially costly, and the social cost arrives first. By the time the patient has finished working through their own doubts, the tribal apparatus is already at work on them, and the route back into membership requires the precise language of the first two walls. I’m so glad I took it.
What makes Wall Four the final seal is that it closes the one exit the other walls do not reach — the exit through honest testimony to another person. An intellectually awakened patient, who has seen through the counterfactual shield, recognised the injury as injury and refused to let sunk cost rewrite their history, still cannot speak, because speaking costs their community. The wall holds them silent. And in silence, the other three walls rebuild. The shield recloses. The injury reverts to vindication. The sunk cost reasserts its grip. The captive, left alone with the structure, returns to gratitude — because gratitude is the one posture that lets them remain intact on every side at once.
7. The Architects
The walls do not grow. They are built, funded, and maintained by identifiable actors working in documented financial arrangements. Nothing here is hidden. Everything is filed, recorded, disclosed in annual reports, visible in congressional testimony, available by Freedom of Information request. The architects have names and budgets.
Wall One — Who Builds the Counterfactual Shield
The shield is built from clinical trials and the statistical practices that translate trial results into claims patients can repeat to themselves. Most clinical trials are now run by for-profit Contract Research Organisations in jurisdictions with minimal oversight.⁸ Forty percent of medical journal articles are ghostwritten by the pharmaceutical industry.⁸ Authors with industry conflicts of interest are twenty times less likely to publish negative findings.⁸ Richard Horton, editor of The Lancet, has written that perhaps half the scientific literature is simply untrue.⁸ Marcia Angell, former editor of the New England Journal of Medicine, has written that the profession has been bought.⁸
The statistical habit that builds the counterfactual — relative risk reduction as the default metric — is a choice, not a necessity. Absolute risk reduction tells the patient what actually changes for them. Relative risk reduction amplifies the apparent effect. Every major drug marketing campaign of the last forty years has preferred the relative figure. The FDA permits it. Journals publish it. Physicians pass it along to patients who cannot tell the two apart.
For COVID, the ninety-five percent figure came from a trial of roughly forty thousand participants that recorded a total of one hundred and seventy COVID cases — one hundred and sixty-two in the placebo arm, eight in the vaccinated arm.⁴ The trial was not designed to measure transmission, hospitalisation, or death.⁴ Pfizer’s own documents show the company knew the lipid nanoparticles crossed the blood-brain and blood-testicular barriers, accumulated in ovaries and testes, and had caused reproductive harm in earlier nanoparticle studies — and proceeded without reproductive toxicity studies, citing urgency.⁶ The shield that reached hundreds of millions of minds was built from this data, presented in relative terms, and installed before the first injection.
Wall Two — Who Converts Injury Into Vindication
The apparatus that turns harm into proof operates across three layers: pharmacovigilance, physician training, and media framing.
Pharmacovigilance is structurally designed to undercount. The U.S. Vaccine Adverse Event Reporting System is passive; physicians are not required to file, and most do not. A Harvard Pilgrim Health Care study, funded by the federal government, concluded that fewer than one percent of vaccine adverse events are reported.⁹ If that figure is correct, official vaccine injury numbers understate real injury by a factor of one hundred. The study was delivered to the CDC, which declined to act on it and declined to implement active surveillance. The undercount is the default.
Physician training teaches doctors to name injuries in ways that protect the intervention. Hair loss is treatment response. Myocarditis is mild and self-limiting. Autism is coincidental regression that would have happened anyway. Death during treatment is disease progression. Medical school curricula are funded, in part, by the pharmaceutical industry.¹⁰ Two-thirds of medical school department chairs have financial ties to pharmaceutical companies.⁸ Continuing medical education — the system through which practising doctors update their knowledge — is dominated by industry-funded programmes. The doctors performing the reframing are not reading from a cynical script. They have been trained to see what they say they see.
Media framing completes the conversion. Pharmaceutical companies are the largest advertiser on American evening news.¹⁰ Twenty-seven billion dollars flows annually into pharmaceutical marketing — more than the entire NIH budget.⁸ The major news divisions are owned by investment firms — BlackRock, Vanguard — that also hold substantial stakes in pharmaceutical companies. When a young man develops myocarditis after a COVID shot and his story reaches the local news, the frame — rare, mild, unrelated to vaccination, which remains safe and effective — is not written in the newsroom. It arrives through press releases, expert contacts, and editorial relationships supplied by the same apparatus that sold the intervention.
Wall Three — Who Reinforces the Sunk Cost
The sunk cost bind is thickened by patient advocacy groups and chronic disease management organisations, most of which are funded, directly or indirectly, by the pharmaceutical industry. Depression advocacy organisations receive substantial funding from SSRI manufacturers. Cancer advocacy organisations receive funding from chemotherapy manufacturers. The official vaccine safety organisations — not the dissident ones — receive funding from vaccine manufacturers, or from the CDC, which is itself funded in part by industry through its foundation.⁸
These organisations produce the narratives that keep the bind in place. The chemotherapy survivor community is built around the claim that the treatment saved them; dissenting voices are marginalised. The depression survivor community is built around the claim that medication saved them; those who question the diagnosis or the drug are accused of encouraging suicide. The vaccinated parent community is built around the claim that vaccines are necessary; parents who describe injury are labelled anti-vaccine and removed. In each case, the community functions as a structure that reinforces the patient’s need to stay grateful.
Chronic disease management delivers the reinforcement annually. The decade-long statin patient is told, at every physical, that her cholesterol is still elevated and she should continue the drug. The SSRI patient who describes emotional flatness is told the dose may need adjusting. A patient reporting withdrawal symptoms is told she is experiencing the return of her underlying condition. The clinical encounter reinforces the sunk cost every time she walks in. Her doubts, if she has any, are resolved by the clinician in favour of continued treatment.
Wall Four — Who Builds the Tribal Seal
The seal is built through public health communication, employer mandates, regulatory policy, media coordination, and the enforcement infrastructure of digital platforms.
COVID-era public health communication was produced and coordinated across federal agencies, corporate media, social media companies, and advertising campaigns. The specific framing — that the unvaccinated endangered the vaccinated, that refusal was antisocial, that vaccination was a civic duty — was not organic. It was produced. The Biden administration funded a multi-hundred-million-dollar campaign to promote vaccination.¹¹ Equivalent campaigns ran in every Western country. The narrative was coordinated enough that the same talking points surfaced nearly simultaneously across English-language media in multiple nations.
Employer mandates provided the enforcement. Workers were required to accept the injection as a condition of employment. Refusers were dismissed, often for cause, stripped of unemployment benefits and professional licences. Healthcare workers, teachers, service members, and federal contractors faced mandates that ended careers built over decades. The mandates did not issue from a vacuum. They were produced by regulatory decisions, legal memoranda, and executive orders that made refusal economically catastrophic.
Platform moderation finished the seal. Social media companies, under pressure from federal officials, removed accounts, posts and videos describing vaccine injury.¹¹ The label misinformation was applied to accurate first-person accounts. Fact-checking systems, funded in part by industry-adjacent foundations, rated injury reports false. The injured could not speak publicly about their own injury without suppression. In the digital age, the fourth wall was algorithmic.
Opioids: The Paradigm Run to Completion
The four walls can be seen at their fullest — and their eventual failure — in the OxyContin case, because that one ran all the way to the end.
Purdue Pharma received FDA approval for OxyContin in 1995. The approval process included language, permitted by the FDA, describing the drug as less addictive than other opioids because of its delayed-release formulation. The language was not supported by evidence. It was promotional text permitted into the regulatory record.¹² The company built a sales force that trained physicians to prescribe OxyContin for chronic pain, funded pseudo-science suggesting that patients seeking more of the drug were suffering from pseudo-addiction to be treated with higher doses, and paid consultants and patient advocacy groups to reinforce the claim that OxyContin was safe.¹²
The counterfactual shield was installed: patients were taught that without adequate pain management they would suffer unnecessarily. Wall Two took over when harm arrived: patients who developed tolerance and needed higher doses were told they had pseudo-addiction and required more of the drug, not less. Wall Three tightened as the months passed: patients who had been on OxyContin for years had organised their lives around it and could not stop without devastating withdrawal, and the withdrawal was interpreted as proof they had needed the drug all along. Wall Four held: patients who became dependent were categorised as addicts — a moral failing, a personal weakness — a category that separated them from each other and from the community that might otherwise have listened to them.
Patients thanked the physicians who prescribed it. They gave interviews thanking Purdue. Many became dependent and many of them died, and among those who died some were still grateful at the end. Then the bodies became too many to hide. Hundreds of thousands of deaths, families documenting the progression from legitimate prescription to heroin to fentanyl, internal Purdue documents forced into the open through litigation, Sackler family settlements, DEA investigations and congressional hearings. The walls came down twenty years late, with bodies stacked against them.
The lesson of OxyContin is not that the system corrects itself. The system corrects only when the damage becomes too visible to contain, and by then most of the damage is already done. Everything known at the end was knowable at the beginning. The FDA had the data. Purdue had its internal memoranda. The paid consultants had the complaints. The patients did not know, because the four walls stood around them, and most of them died grateful.
8. What the Captured Person Is Owed
If the architecture is engineered, the captured person is not a fool. They were not gullible or poorly educated. They were inside a structure built by specific actors for specific reasons, and its purpose was to produce exactly the response they gave — gratitude from the injured, defence from the captured, compliance from the well.
This is the first thing they are owed: the return of their dignity. The woman in the hospital bed who thanked the vaccine that stroked her is not a fool. She is inside the room, and her gratitude is the designed output of a designed apparatus. The same goes for the chemotherapy survivor who credits the poisoning, the parent who defends the schedule, the grandfather on his twentieth year of statins, the widow who still has OxyContin in the cupboard. None of them failed. A structure was built around them. The structure is what failed, because it was never designed to succeed at healing. It was designed to succeed at extraction, and at that it succeeded brilliantly.
The second thing they are owed is clarity about what their gratitude costs. When the injured cannot testify honestly about their injury, the injury does not appear in the record. It never becomes a safety signal, never gets studied, never reaches the next person considering the same intervention. The apparatus that produced the injury continues to produce it. The signals that might have shut down OxyContin in 1997 rather than 2017 were there in 1997, in the voices of the first dependent patients. Those voices were absorbed into the gratitude of the captured and converted into testimonials. The delay cost hundreds of thousands of lives.
The captured person’s dissenting voice is the most valuable instrument in medicine. Grateful testimony has been manufactured at scale for a century — that is what the previous sections have shown. What cannot be manufactured is the captured person turning, after years of defending the injury, and naming it. Once one captured person speaks that way, others recognise themselves in the testimony, and the walls begin to fail at the only point where they can fail — in the social layer, from inside the community. The injured testifying to the injured breaks the tribal seal. The tribal seal failing exposes the sunk cost. The sunk cost examined reveals the injury as injury rather than as vindication. The injury named dissolves the shield. The walls depend on each other, and the one that gives first is the fourth, because the fourth is the only one where another person’s voice can reach.
This is why the essay closes here, and not with a call to action. There is nothing general to be done. There is only the specific, costly, socially expensive act of breaking the silence — by the captured person who survives long enough to recant their gratitude, or, where the captured cannot speak, by those close enough to them to testify on their behalf. That single act, repeated, is the entire dismantling. It is what the apparatus was never designed to process, and it is the only thing that has ever worked against it. The OxyContin walls came down because the families of the dead spoke for those who could no longer speak. The Vioxx walls came down because injured patients outlived the cover-up long enough to name it. The DES walls came down because the daughters, injured in utero by what their mothers had been given, lived to testify to the inheritance. The machine ran, in each case, until the testimony arrived from someone it could not silence. Then it stopped.
The captured person speaking honestly is not an act of politics or rebellion. It is accurate description. What was done to the body was real, the captivity that followed was real, and the people who built it can be named. Under the gratitude is a person who has the right to say, at last, what actually happened.
That voice is what the room was built to prevent. It is also the only thing that has ever brought a room like this down.
References
Thomas Cowan, discussed in When Your Body Whispers, Listen: The Intelligence of Symptoms. New England Journal of Medicine finding on breast cancer overdiagnosis: approximately 1.3 million American women overdiagnosed over thirty years. On lead-time bias and survival statistic manipulation in early-stage cancer screening, see H. Gilbert Welch and colleagues’ work on overdiagnosis.
John Abramson, MD, Harvard Medical School; Peter Gøtzsche, Deadly Medicines and Organised Crime: How Big Pharma Has Corrupted Healthcare (CRC Press, 2017). On the chronic disease cascade around statins — muscle pain, memory effects, diabetes — see Extraction: The Middle Class as Colony.
Andrew Kaufman, MD, on SSRI mortality and pediatric prescribing pressures; Peter Breggin’s work on the suicide signal eventually acknowledged in black box warnings. On identity capture around psychiatric diagnosis, see Four Causes, Seventy Thousand Diseases.
Pfizer BNT162b2 Phase 3 trial data as summarised in the Pfizer Document Analysis Report (War Room/DailyClout, December 2022). The 95% relative risk reduction figure was calculated from 170 total COVID cases in a trial of approximately 40,000 participants.
CDC and FDA advisory communications on post-vaccination myocarditis, 2021–2022, including the June 2021 ACIP meeting that concluded benefits outweighed risks for adolescents and young adults. Critical account: Peter McCullough, MD, and Nicolas Hulscher’s published work on vaccine-associated myocarditis.
Pfizer Document Analysis Report, War Room/DailyClout (December 2022), summarising the FDA-released Pfizer clinical trial documents obtained through court order after the FDA requested 75 years to release them.
Turtles All the Way Down: Vaccine Science and Myth (2019). The 2013 Institute of Medicine report acknowledged that the childhood vaccination schedule as a whole has not been properly studied for safety.
Peter Gøtzsche, Deadly Medicines and Organised Crime (2017); Marcia Angell, The Truth About the Drug Companies; Richard Horton, The Lancet, 2015. Aggregated in Extraction: The Middle Class as Colony.
Lazarus R et al., “Electronic Support for Public Health–Vaccines Adverse Event Reporting System (ESP:VAERS),” Harvard Pilgrim Health Care, funded by AHRQ, 2010. Finding: fewer than 1% of vaccine adverse events are reported.
Abramson J and Starfield B on the purpose of commercially funded clinical research. FDA revolving door: nine of the last ten FDA commissioners as of 2019 joined pharmaceutical companies after leaving the agency. Congressional capture: more than two-thirds of Congress took money from the pharmaceutical industry in 2020.
Missouri v. Biden (2023) and related federal court findings on federal coordination with social media platforms to suppress COVID-related speech, including first-person vaccine injury accounts. Twitter Files disclosures, December 2022 – March 2023.
Patrick Radden Keefe, Empire of Pain: The Secret History of the Sackler Dynasty (2021); Barry Meier, Pain Killer: An Empire of Deceit and the Origin of America’s Opioid Epidemic (updated edition, 2018); internal Purdue Pharma documents released through multi-state litigation and the 2020 Department of Justice settlement.
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.
References
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.
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).
Breggin, P.R. Toxic Psychiatry. New York: St. Martin’s Press, 1991, pp. 160–163.
Deshauer, D., et al. “Selective serotonin reuptake inhibitors for unipolar depression.” Canadian Medical Association Journal 178 (2008): 1293–1301.
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.
Cole, J. Cited in Whitaker, Anatomy of an Epidemic, p. 150.
Kline, N. Cited in Whitaker, Anatomy of an Epidemic, p. 150.
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.
Schuyler, D. Cited in Whitaker, Anatomy of an Epidemic, p. 150.
Posternak, J Nerv Ment Dis (2006).
NIMH review of antidepressant studies. Cited in Whitaker, Anatomy of an Epidemic, p. 151.
Kirsch, I., et al. “Initial severity and antidepressant benefits.” PLoS Medicine 5 (2008): e45. Cited in Whitaker, Anatomy of an Epidemic, pp. 152–153.
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.
Breggin, P.R. Toxic Psychiatry, pp. 159–160.
Whitaker, Anatomy of an Epidemic, p. 151.
Moncrieff, J., Wessely, S., Hardy, R. “Active placebos versus antidepressants for depression.” Cochrane Database Syst Rev (2004): CD003012.
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.
Gøtzsche, P.C. “Is psychiatry a crime?” (2024), p. 9.
Breggin, P.R. Toxic Psychiatry, pp. 163–164.
Ibid., pp. 160–161. Fisher, S. and Greenberg, R. The Limits of Biological Treatments for Psychological Distress. Hillsdale, NJ: Erlbaum, 1989.
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.
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.
Breggin, Toxic Psychiatry, pp. 164–166.
Davies, R., et al. “Confusional Episodes and Antidepressant Medication.” American Journal of Psychiatry (July 1971). Cited in Breggin, Toxic Psychiatry, pp. 165–166.
Greenberg, G. Manufacturing Depression. New York: Simon & Schuster, 2010, pp. 281–282.
Gøtzsche, “Is psychiatry a crime?” pp. 104–105.
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.
Greenberg, Manufacturing Depression, pp. 281–282.
Breggin, P.R. Toxic Psychiatry, pp. 169–171.
Law, W., III, et al. American Journal of Psychiatry (May 1981). Cited in Breggin, Toxic Psychiatry, pp. 169–170.
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.
Hoheisel, Schipkowensky, and others cited in Whitaker, Anatomy of an Epidemic, pp. 155–156.
Van Scheyen, J.D. Cited in Whitaker, Anatomy of an Epidemic, p. 156.
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.
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.
“Editorial sparks debate on effects of psychoactive drugs.” Psychiatric News, May 20, 1994. Cited in Whitaker, Anatomy of an Epidemic, p. 159.
Hales, R., ed. Textbook of Psychiatry. Washington, DC: American Psychiatric Press, 1999, p. 525. Cited in Whitaker, Anatomy of an Epidemic, pp. 159–160.
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.
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.
Whitaker, Anatomy of an Epidemic, pp. 168–169.
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.
Pigott, H.E., et al. “Efficacy and effectiveness of antidepressants.” Psychother Psychosom 79 (2010): 267–279. Gøtzsche, “Is psychiatry a crime?” pp. 27–28.
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.
Gøtzsche, “Is psychiatry a crime?” p. 22.
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).
The mental health system is failing children by treating everyday struggles as “chronic illness requiring lifelong pharmaceutical treatment,” former psychiatric patient Laura Delano told lawmakers this week.
Delano said many challenges people face are “rooted in nutrition, sleep, stress, trauma, substance use, relationships, vocation, environment, economics, meaning, faith and purpose.” Yet the system often reduces those issues to medical diagnoses, she said.
Drawing on her own 14 years in the mental health system, Delano told lawmakers her experience reflects a broader trend.
Now the founder of Inner Compass Initiative and author of “Unshrunk: A Story of Psychiatric Treatment Resistance,” Delano said more Americans are seeking mental healthcare than ever, but outcomes — including suicide rates among young people — continue to worsen.
‘Two meds became three, four, five. My life unraveled’
Delano said she began treatment at 13. She was diagnosed with bipolar disorder and told she would need medication for life.
“You’re told this is an incurable illness. You’ll have this for the rest of your life. It’s manageable with medications, but you will never not have it,” she said. “And that’s the story that many, many people are being told about these conditions, which is simply not true.”
Over time, her diagnoses expanded and her prescriptions multiplied.
“Two meds became three, four, five,” she said. “My life unraveled.”
She said she gained weight, developed chronic health issues and became “increasingly anxious and suicidal.”
“Eventually, I couldn’t work or take care of myself,” she said.
“Nobody told me” that many psychiatric drugs were approved based on trials lasting “on average 6 to 12 weeks,” or that the long-term effects of taking multiple drugs together have “never been properly established.”
She said she wasn’t warned that medications could cause “serious physical health problems,” impair sexual function or, in some cases, increase suicidal thoughts.
When she tried to stop taking the drugs, she said she experienced withdrawal symptoms, but was told it was a relapse.
“Nobody told me that what I experienced … was withdrawal,” she said. “Instead, I was told that my worsening state meant my illness was so severe that it was now resistant to any treatment.”
At 25, Delano said she believed there was no hope. She attempted suicide.
‘This is the next opiate crisis, and I think it’s bigger’
Delano’s testimony comes as mental health outcomes worsen, even as diagnoses and prescriptions keep rising.
From 2007 to 2021, the suicide rate among people ages 10-24 increased by 62%. In 2023, over 49,000 Americans died by suicide — the highest number on record, and about 20,000 more than in 2000.
Among adolescents in 2024, 2.6 million reported serious suicidal thoughts, 1.2 million made a plan, and 700,000 attempted suicide.
At the same time, diagnoses have surged. Today, about 23.4% of U.S. adults — roughly 61.5 million people — experienced mental illness. This includes more than 36% of young adults.
Medication use has climbed alongside those numbers.
Since 2006, the use of SSRIs in children has more than doubled. A December 2025 report found that 6.1 million U.S. children ages 17 and under are taking at least one psychiatric drug.
“This is the next opiate crisis, and I think it’s bigger,” Delano said.
Doctors are increasingly medicalizing ‘normal human unhappiness’
Other experts at the roundtable raised similar concerns about diagnosis and treatment.
Dr. Sally Satel, a psychiatrist and senior fellow at the American Enterprise Institute, said clinicians often blur the line between clinical depression and life challenges.
“I can’t tell you how many people … once got a diagnosis [of depression], but their diagnosis is really demoralization,” she said.
“Do we need medications for that?” Satel asked. In some cases, what patients need to hear is, “Your life is difficult. You’re actually having a rational response to a difficult life,” she said.
Satel also said psychiatrists do not prescribe most psychiatric medications.
Primary care providers and midlevel practitioners write many of the prescriptions, she said. “That’s definitely … a problem.”
“We are overdiagnosing,” she added. “We’re turning … normal human unhappiness into … diagnoses that we then prescribe medications for that probably won’t work.”
‘Doubling down on what we’re doing … is not going to get us anywhere’
Dr. David Hyman, a physician and legal scholar, drew a similar distinction.
“Sadness and depression are two different things,” he said. Treatment — and not necessarily with medication — should focus on the latter, he added.
He also warned against a system that increasingly defaults to prescribing. “Doubling down on what we’re doing, which isn’t working, is not going to get us anywhere better than where we are,” he said.
While medications must show safety and efficacy to gain approval, he said, there is no consistent system to study the long-term effects or what happens when patients stop taking them.
“There’s not a mechanism or systematic reevaluation of things after they’ve been approved,” he said.
Tapering can take ‘not just months, but years’
Delano said that gap is especially clear when patients try to taper off medications.
Asked how often patients receive full information about their diagnosis and medications, she said: “From what I’ve seen, never.”
“It took 13 years to realize I needed to get out,” Delano said. But getting off the drugs is “incredibly difficult.”
“We have a system set up that makes it incredibly easy to start these drugs that were really only ever studied for … short-term use,” she said. “Yet, most people stay on them long term for years and have zero safe off-ramps.”
Without clear guidance, people often stop too quickly, feel worse and assume they need the drugs indefinitely, she said.
Delano called for updated drug labels, public education and clinical guidelines for gradual tapering.
She stressed that these medications can create physical dependence. “Not addiction, it’s different than addiction,” she said. It’s a biological effect that can make stopping difficult.
“It sounds so unfathomable that a capsule … might require chipping away … over not just months, but years,” she said. Yet for some patients, that level of gradual tapering is necessary, she added.
Now 16 years off psychiatric medications, Delano said her experience drives her work.
“It’s urgent that we better understand what is happening in people’s brains and bodies from using these medications long term and from trying to get off them,” she said.
Watch an excerpt from the subcommittee hearing here:
Eli Clifton and Ian Lustick Reveal How The Israel Lobby Paved The Way For A U.S. War On Iran
By Justin K.P. | The Dissident | August 11, 2026
Investigative journalist Eli Clifton and political scientist Ian Lustick have released a detailed history of the Israel lobby’s influence on U.S. foreign policy titled “Israel’s Lobby: America in the Grip of a Foreign Power”.
The book contains a detailed history of the Israel lobby’s influence over various U.S. administrations going back to its creation.
Among the book’s most interesting revelations is how the Israel Lobby pushed anti-Iran propaganda in the United States in order to destroy U.S. diplomacy with Iran. … continue
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