In the 1820s, when John Bostock first documented the condition in London, every case he could find was in the middle or upper classes. He inquired at the dispensaries and across the country and found, in his own words, no unequivocal case occurring among the poor.¹ Twenty years earlier, a new medical procedure had been introduced in England. The disease appeared in the class that received the procedure. Those who had not received it remained free of it. The procedure was Edward Jenner’s vaccination, the insertion of material from cowpox lesions into incisions in the human arm. The material’s origin was the cow.²
Hay fever did not exist in the medical literature before this. The first cases appeared in the population that had received the procedure. The mechanism by which injection of foreign protein produces sensitization to bystander substances was discovered before the end of the century, demonstrated in animal models repeatedly since, and conceded by establishment investigators in at least one specific case. The condition that tens of millions experience as a feature of biology is an artifact of the syringe.
The Disease That Did Not Exist
Bostock called it the Catarrhus Aestivus, summer catarrh.¹ He had experienced it himself since he was a young man. His symptoms began every June with heat and fullness in the eyes, irritation of the nose accompanied by sneezing, and tightness in the chest. The 1819 paper to the Medico-Chirurgical Society was an attempt to ask the other physicians of London whether they had seen anything similar. Nothing in the medical literature, ancient or modern, described the syndrome. None of the most eminent physicians of London, Liverpool, or Edinburgh had heard of anything like it.
By 1828 Bostock had assembled twenty-eight cases.¹ Every one of them was in the middle or upper classes. He initially attributed the trigger to the effluvium from new hay, and the name stuck. The condition was hay fever even after Charles Blackley demonstrated, in 1873, that the proximate trigger was pollen and not hay itself.³ Blackley, a Manchester physician who suffered from the condition, applied pollen to abraded patches of his own skin and observed the reaction. The proximate cause was identified. The originating cause was not asked.
What did become asked, in the half-century that followed Bostock’s first paper, was what kind of person developed hay fever. The answer was consistent. The condition was an affliction of the wealthy, of the urban, of the educated. The wheezing wealthy, in a pattern that became fashionable, would migrate every summer to the English coast, then to the Swiss Alps, and, by the late nineteenth century, to the White Mountains of New Hampshire, where the air was understood to be safe.³ Those who could not afford to leave continued, by every report, not to develop the condition. The nostrums prescribed when the patient could not travel included medicated cigarettes, powders, and salves.
The vocabulary used to describe what was happening did not yet exist. The word allergy was coined in 1906 by the Viennese pediatrician Clemens von Pirquet, in response to reactions doctors had observed in patients they had injected with horse serum. The word anaphylaxis had been introduced four years earlier by the French physiologist Charles Richet, describing a phenomenon he had produced by injecting sea anemone venom into dogs. The condition Bostock had documented in 1819 had been observed for eighty-five years without a category to file it under. It was, in the most literal sense, unprecedented in human medicine.
What had also happened in the decades preceding Bostock’s first paper was Edward Jenner’s introduction of the cowpox procedure.² Jenner published his findings in 1798. By 1801 James Smith had been appointed as the first United States Vaccine Agent. The first US Vaccine Act passed in 1813. Compulsory vaccination would spread across European jurisdictions through the rest of the century, with the United Kingdom’s Vaccination Act of 1853 making the procedure mandatory in England and Wales. Before any of those mandates were in place, the procedure had been adopted by those who could afford it and avoided by those who could not. The early vaccinations used arm-to-arm transmission from cowpox-affected milkmaids; by the mid-nineteenth century, industrial-scale production used calf-derived vaccine lymph directly. The constant across both methods was that material of animal origin was introduced past every layer of the body’s normal route of exposure.
Forrest Maready’s reconstruction of the historical record names what the documented sequence implies.² A disease that had no precedent in medicine appeared in London within a generation of the introduction of the cowpox procedure, in the class that received the procedure, in a city where the procedure had spread first. The mechanism by which such exposure produces sensitization to bystander substances had not yet been described. It would be, three quarters of a century later, by Charles Richet.
Richet, and Foreign Protein
In 1901 Charles Richet, working with Paul Portier aboard the yacht of the Prince of Monaco, was studying the toxicity of sea anemone venom. He injected small amounts into dogs to establish baseline responses. The first injections produced predictable effects. When he later attempted to inject the same dogs again, weeks after the first exposure, he found something he had not expected. The second injection, of a dose the dogs had previously tolerated, produced a violent and disproportionate reaction. The dogs collapsed. Some died within minutes.⁴
Richet named the phenomenon anaphylaxis, against protection, because the body’s response to the second exposure was the opposite of what immunization was meant to produce. Injection of foreign protein did not protect against subsequent exposure. It sensitized. The reaction was demonstrated across species and across protein sources, and the demonstration was reliable. The 1913 Nobel Prize in Physiology or Medicine was awarded to Richet for this work.⁴
The mechanism Richet described is the foundation of every allergic phenomenon documented since. Foreign protein introduced through injection, bypassing every layer of the body’s normal route of exposure, produces a sensitized state. On subsequent contact with the same material or with material closely resembling it, the body responds with escalating intensity. The mechanism does not require an inhaled antigen or a digestive failure. It requires only an injection and a second exposure. The clinical demonstration in human children had already been under way for more than a decade by the time Richet won his Nobel Prize.
The Diphtheria Antitoxin
The first mass clinical demonstration of Richet’s mechanism in human children did not wait for the Nobel committee. It had already been under way in routine pediatric practice for the better part of a generation.
In 1890 Emil von Behring and Shibasaburo Kitasato discovered that horses injected with diphtheria toxin produced a substance in their blood that neutralized the toxin. By collecting blood from the immunized horses, separating out the red cells, and filtering the remaining serum, a therapeutic preparation could be made. Children with diphtheria, injected with the horse serum, often recovered. Behring received the first Nobel Prize in Physiology or Medicine for this work, in 1901.⁵
The procedure became routine through the 1890s and the first years of the twentieth century. Children with diphtheria received it as treatment. Children in institutions, orphanages, and hospitals received it prophylactically when diphtheria appeared in the community. The serum being injected was horse serum: the antitoxin and every other protein the horse’s bloodstream had been carrying.
What the children began to show, with growing frequency, was a delayed systemic illness that did not fit any existing diagnostic category. Seven to twelve days after the injection, fever appeared, urticarial rashes spread across the body, joints swelled and ached, and the lymph nodes nearest the injection site enlarged. The illness lasted one to two weeks and resolved on its own. It bore no resemblance to diphtheria.
Clemens von Pirquet and Béla Schick, two pediatricians at the University Children’s Hospital in Vienna, began collecting the cases systematically. By 1905 they had analyzed over a hundred and published their findings as Die Serumkrankheit, Serum Sickness.⁵ The monograph documented what they observed. The illness was a response to the horse proteins in the serum. It was dose-related, with the worst reactions in the children who had received the most serum. Re-injection produced an accelerated response, sometimes within twenty-four hours of the second injection rather than the eight-to-twelve days of the first. In some cases the second injection produced sudden anaphylaxis and the child died within minutes.
The clinical phenomenon Richet had documented in dogs was being observed, in real time, in children injected with horse serum. In 1906 Pirquet coined the word allergy, from the Greek allos and ergon meaning altered reactivity, to describe what he and Schick had been observing. The word entered the medical vocabulary of the twentieth century. Within a generation it had been generalized far beyond the horse-serum context that produced it. It is the word used today, by the same medical tradition, to describe hay fever.
The diphtheria antitoxin episode established on the clinical record what Richet’s animal experiments had shown more cleanly. Foreign animal protein injected into children produced systemic reactions in a substantial fraction of recipients, intensifying with each successive exposure and sometimes killing the child outright on a second injection. This was not theoretical. It was the routine experience of pediatric practice for two decades, and it generated the vocabulary that the rest of the twentieth century would inherit.
The Adjuvant Mechanism
The next refinement was aluminum.
Vaccine science discovered in the 1920s that injecting a foreign protein alongside an aluminum compound produced a far more intense response than injection of the protein alone. The aluminum acted as what the field came to call an adjuvant, a helper. It provoked an inflammatory reaction at the injection site so intense that any other material present at that site was swept into the reaction. The body responded not just to the aluminum and not just to the protein, but to the combination.
The mechanism is the foundation of every laboratory model of allergic disease. The standard laboratory model of asthma is produced by injecting mice with ovalbumin alongside aluminum hydroxide. The same protocol, with different proteins, produces laboratory models of dust mite allergy, fish allergy, and other named allergic conditions. Allergy is not observed in nature and then replicated in the laboratory. Allergy is created in the laboratory by injection of foreign protein with adjuvant. The mechanism by which allergy is produced for study is the mechanism the syringe administers in clinical practice. The two procedures are the same procedure.
Aluminum exposure is also known to produce asthma in humans through other routes. The industrial-exposure literature has documented occupational asthma in aluminum smelters and aluminum welders for decades. The mechanism is not in dispute. What is in dispute is whether the same aluminum, injected into the bloodstream of children rather than inhaled by adults at work, has equivalent effects.
The Japanese DTaP case settled the question for one specific protein. Through the 1980s and into the 1990s, Japan revised the formulation of its diphtheria-tetanus-acellular-pertussis vaccine.³ The acellular version, the world’s first, contained gelatin as a stabilizer. Until 1993, Japanese children received a trivalent MMR vaccine before the DTaP series, and no anaphylactic reactions to the MMR were reported during that period. From 1994 the schedule was reversed, with DTaP given before the gelatin-containing MMR.
Japanese children began to react with anaphylaxis to the MMR. They began to react with anaphylaxis to gelatin-containing foods, to yogurt, to gummy sweets, to jelly desserts. Japanese investigators traced the chain. The DTaP, administered first, had sensitized the children to the gelatin present in the formulation. The MMR, given later, contained the same gelatin. The body had been primed by the first injection. The second exposure produced the reaction. Between 1997 and 2000, gelatin was removed from all the Japanese DTaP vaccines. The anaphylaxis to gelatin-containing MMR stopped.⁶
The conceded mechanism is exactly what Richet had described in 1901. Foreign protein, introduced at an injection site, produces sensitization to that protein. The body subsequently encounters the same protein through another route, including orally, and reacts. The Japanese investigators conceded the mechanism in the specific case of gelatin. They did not concede it for any other.
Hilleman, Adjuvant 65, and What Merck Knew
Maurice Hilleman, the chief vaccine developer at Merck through the second half of the twentieth century and the dominant figure in twentieth-century American vaccine production, understood the mechanism. In 1964 his team announced Adjuvant 65, an experimental influenza-vaccine adjuvant composed of eighty-six percent peanut oil emulsified with four percent aluminum monostearate.⁷ The formulation was developed because earlier oil-based adjuvants had produced persistent local reactions, tumors in animals, and what the literature of the period called autoimmune reactions. Hilleman’s group published the early clinical trials in the New England Journal of Medicine, the New York Times reported on the patent, and clinical testing proceeded through the late 1960s and into the 1970s.
Hilleman and his colleagues understood that the procedure they were testing would introduce intact peanut oil, alongside an aluminum compound, into the human arm. Allergic sensitization to the oil was acknowledged as a possibility. The reasoning at the time was that highly refined peanut oil would lack the proteins that drove an allergic response. The FDA disagreed: refined oils retained protein traces, and intramuscular injection rather than intravenous was the recommended route precisely because intravenous deposition risked greater absorption and a stronger reaction.
The 1973 WHO Scientific Group on Immunological Adjuvants, whose deliberations were published as Technical Report Series No. 595 in 1976, addressed the safety questions that adjuvants raised.⁸ The group examined what injection of adjuvants alongside antigens would produce, considered the route-of-administration variable, and reviewed contamination concerns. Adjuvant 65 itself was discontinued within a few years because of reactogenicity in human subjects.
The relevant point is not that Adjuvant 65 was licensed for general use. It was not. The relevant point is that the people building vaccine adjuvants understood, by the mid-1960s, that introducing food-derived oils into the human bloodstream alongside an aluminum compound carried a serious risk of allergic sensitization. They tested it anyway. They considered the risk acceptable. The schedule they helped design in the years that followed expanded steadily. Peanut allergy, a clinical rarity through the 1980s, became epidemic in the 1990s and 2000s.
The Pertussis Mouse
The animal-model literature on pertussis demonstrates the mechanism applied to airborne triggers.³ When researchers inject mice with pertussis, the mice subsequently react to airborne allergens they would not otherwise have reacted to. Pertussis toxin functions as an adjuvant in this experimental context, amplifying the body’s response to whatever proteins are present in the inhaled environment.
The animal-model and clinical-observation literatures converge on a single pattern. Inject foreign protein into a young animal, with or without a separate adjuvant, and the animal becomes sensitized to substances it would otherwise have tolerated. The procedure used to manufacture laboratory models of allergic disease is the procedure that produces clinical allergic disease in human beings.
Modern Schedule, Modern Numbers
The clinical evidence for the same mechanism in modern children is documented in the establishment’s own journals, though the literature is contested.
In 2005 the Journal of Allergy and Clinical Immunology, the flagship publication of American allergy medicine, published a study by Enriquez and colleagues based at Vanderbilt University.⁹ The cohort included 515 never-vaccinated children, 423 partially vaccinated children, and 239 fully vaccinated children in the United States. Among children with no family history of hay fever, parents of unvaccinated children were ten times less likely to report hay fever in their child. The probability that this finding occurred by chance was less than five in ten thousand. The lead author was based at Vanderbilt’s Division of Allergy, Pulmonary, and Critical Care Medicine. The paper was peer-reviewed in the allergy field’s central journal, and it remains in the literature.
The same year, the Archives of Disease in Childhood, the British pediatric journal of record, published a study by Bremner and colleagues using two large UK databases comprising more than 7,000 hay fever cases and matched controls.¹⁰ The investigators did not find that vaccinated children overall had higher hay fever risk than the unvaccinated. What they found was internal to the schedule. Children whose DTP series had been delayed beyond their first birthday had reduced odds of hay fever, and children whose first MMR had been delayed beyond age two had similarly reduced odds. The pattern was a dose-response on timing: the longer the schedule was deferred, the less hay fever appeared. The investigators acknowledged the finding and suggested it might reflect confounding by febrile illness during the delay. The pattern, however interpreted, is consistent with the Richet mechanism: timing of antigen exposure during early life shapes the subsequent allergic response.
Three years later, Pediatric Allergy and Immunology published the Bernsen finding.¹¹ Bernsen and colleagues compared pertussis exposure in vaccinated and unvaccinated children. The internal finding within the paper is the load-bearing one. In the unvaccinated group, there were no significant associations between pertussis exposure and the conditions labeled atopic. In the vaccinated group, the associations were positive across hay fever, asthma, and food allergies. The same bacterium, introduced through two different routes, produced two different outcomes. Encountered naturally, pertussis did not produce hay fever. Following pertussis vaccination, it did.
A 2006 paper in the Journal of Allergy and Clinical Immunology by Flöistrup and colleagues examined 4,606 children in Steiner-school communities, largely unvaccinated, against 2,024 conventional controls across five European countries.¹² Children who had received MMR vaccination showed an increased risk of rhinoconjunctivitis, the clinical term for hay fever. Children who had experienced natural measles, by contrast, showed a reduced risk of IgE-mediated eczema. A 1999 Lancet paper by Alm and colleagues, comparing 295 anthroposophic children with 380 conventional controls, found that children who had never received MMR carried a reduced odds ratio for allergy in general.¹³
The literature is not univocal. Several mainstream reviews have found no association between vaccination and allergic disease, and a small number of studies have reported lower allergy rates in vaccinated children.¹⁴ The defenders of the schedule cite these findings as offsetting the positive studies. Several considerations weigh against treating the disagreement as a wash. The internal findings within the positive studies, the route-of-exposure contrast in Bernsen and the dose-response on timing in Bremner, are difficult to explain by confounding. The mechanism is established. The Japanese gelatin case is direct evidence of the mechanism operating in human children, with anaphylaxis appearing after the schedule change and disappearing after gelatin removal. The historical case from 1819 stands regardless of how the modern epidemiology shakes out: a disease that did not exist in the medical literature appeared, in a single generation, in the class that received the new procedure.
Broader catalogs of vaccinated-and-unvaccinated comparisons document the same pattern across multiple countries and investigators. Mawson’s 2017 cohort, the analyses compiled by Hooker and Miller in 2021, Lyons-Weiler and Thomas’s data from the Portland practice, Garner’s 2021 survey of more than a thousand unvaccinated American children, the Dutch NVKP 2006 data: each independent dataset converges on elevated allergic disease in the vaccinated.¹⁵ The aggregate weight of the evidence runs in one direction.
The convergence is acknowledged at the highest level of allergy organizations, though the implications are not. The World Allergy Organization reported in 2011 that the prevalence of allergic disease, with allergic rhinitis named explicitly among the conditions, was rising dramatically in both developed and developing countries.¹⁶ The increase was concentrated in children and in the previous two decades. The 2013 WAO White Book addressed the question of whether vaccination might be implicated. Its conclusion was that vaccination programs were essential and that the harms of denying them would exceed the costs of the allergy epidemic. The conclusion is the only statement in that section of the report that the authors do not reference.¹⁶ The WAO acknowledged the connection by raising it. They dismissed it without evidence.
Aluminum, Dose, and Asthma
The most recent of the establishment’s own findings on this terrain is the Daley study, published in Academic Pediatrics in 2022.¹⁷ The study was funded by the Centers for Disease Control and Prevention. Its authors included current and former CDC staff. Its data came from the Vaccine Safety Datalink, the CDC’s own pharmacovigilance system, covering seven large medical organizations.
The investigators followed 326,991 children born between 2008 and 2014. For each child, the cumulative aluminum exposure from vaccines received before age twenty-four months was calculated in milligrams. The outcome was persistent asthma diagnosed between ages two and five years, defined by the field’s tighter criteria: repeated clinical encounters plus at least two long-term controller medication dispenses.
The finding was a dose-response. For each one-milligram increase in vaccine-associated aluminum exposure before age two, the adjusted hazard ratio for persistent asthma was 1.26 in children with eczema and 1.19 in children without. Children who received three or more milligrams of vaccine-associated aluminum had a thirty-six percent higher risk of persistent asthma than children who received less than three milligrams.
The accompanying editorial, also in Academic Pediatrics, opened with the observation that “people only see what they are prepared to see.” The author called the findings “intriguing” while emphasizing that no determination of causation could be made from observational data. The CDC, in its public response, stated that it was “not changing the current routine childhood vaccination recommendations based on this single study.”
The Daley study did, as far as it could in an observational design, what the critics of all prior vaccine-and-allergy research had demanded. It used the CDC’s own data, the field’s tightest definition of asthma, a cohort of more than three hundred thousand children, and a continuous dose variable rather than a binary vaccinated-versus-unvaccinated comparison. The finding was a dose-response on aluminum, internal to the vaccinated population, by mainstream investigators publishing in a mainstream journal. The aluminum that Glenny had described in 1926 as boosting the body’s response to injected antigens is now documented, in a 2022 paper funded by the CDC, as boosting the body’s response to environmental antigens at a population scale. Hay fever and asthma belong to the same family of conditions; the aluminum that drives the asthma signal in the Daley cohort is the same aluminum that has been added to the schedule across the period in which hay fever has expanded.
What the Body Is Doing
The symptoms of hay fever are produced by the body, not by the pollen.
Daniel Roytas’s analysis of nasal secretions in respiratory illness documents what is actually found in the mucus.¹⁸ Histamine, bradykinin, prostaglandins, interleukins, cytokines, lysozymes, lactoferrin, hyaluronan, mucins, fibrinogen, immunoglobulins. These are the substances the mucous membrane releases when it encounters an irritant. Histamine produces nasal congestion, sneezing, and the throat irritation that pharmaceutical companies have spent a century selling drugs against. Bradykinin produces the same effects. Concentrations of bradykinin in nasal secretions during respiratory illness rise to thirty times normal levels.¹⁸
Both substances, when introduced into the airways of healthy volunteers, produce the symptoms of hay fever directly. No pollen is required. No allergen is required. The mucous membrane releases the inflammatory mediators when it is irritated, and the mediators produce the symptoms. The mediators are the body’s response. They are not the problem.
The body’s purpose in releasing them is documented. Histamine, bradykinin, and the other inflammatory chemicals in nasal mucus exist to expel material from the respiratory tract. The runny nose and the watering eyes that hay fever patients experience are the body’s mechanism for getting toxic material out. The symptom is the cleansing.
Roytas notes that medical papers have acknowledged the principle. Inhalation of non-infectious agents, irritants, allergens, chemicals, produces clinical illness indistinguishable from what the establishment calls infectious illness.¹⁸ The body responds to insult by mounting the same response, whatever the insult.
What hay fever sufferers are doing, when they take an antihistamine, is shutting down the mechanism by which the body expels the material it has reacted to. The chemical is retained. The membrane stays inflamed. The expulsion is suppressed. The reactive state is preserved.
What Medicine Says Is Happening
The official explanation for hay fever is that the body has made a mistake.
The mechanism, as the establishment presents it, runs as follows. A substance the body encounters, pollen or dust or dander or peanut protein, is identified by the body as harmful when it is in fact harmless. The body produces a specific protein, an immunoglobulin called IgE, in response to this misidentification. The IgE binds to receptors on cells called mast cells, located in connective tissue. When the body encounters the same substance again, the IgE on the mast cells signals them to release histamine and other inflammatory mediators. The mediators produce the symptoms.
Lester’s analysis identifies what is missing from this account.¹⁹ The roles of IgE and mast cells, as Lester documents, remain poorly understood by the establishment’s own admission. The protein medicine calls IgE has not been purified from human serum and characterized directly. It is inferred from laboratory tests that detect binding behavior, not from direct observation. What the antibody is, what it does, and whether the conventional account of its function corresponds to anything real in the body are questions the field treats as settled by convention rather than by evidence.
The deeper problem is the circular logic of the underlying framework. The American College of Allergy, Asthma, and Immunology acknowledges that hay fever symptoms can be triggered by common irritants such as cosmetics, laundry detergents, pool chlorine, perfumes, and hair sprays.¹⁹ The British National Health Service’s list of common allergens includes medications and household chemicals. The NHS then describes these allergens as substances “generally harmless to people who aren’t allergic to them.”¹⁹ The argument is that the substance is harmful only to the body that mistakenly identifies it as harmful. The framework defines its terms in a way that cannot be falsified. Whatever the body reacts to is, by definition, a thing it should not have reacted to, and the reaction is, by definition, a mistake.
The substances in question are not harmless. They are chemicals. Many of them are documented toxins. The body is not mistakenly identifying them as harmful. The body is responding to them as harmful because they are harmful. The framework that calls this response a malfunction has rotated the arrow of cause and effect. The body is doing what bodies do when they encounter material they cannot tolerate. The doing is then labeled the disease.
What is added to the picture by the vaccination history is the explanation of why some bodies cannot tolerate these substances while others can. The Richet mechanism, as demonstrated by Bostock’s cases, by the diphtheria antitoxin reactions, by the Japanese gelatin admission, by the converging modern epidemiology, is that the sensitized body responds to substances the unsensitized body does not. The sensitization comes from injection. The substance the sensitized body subsequently reacts to is whatever happens to be present in the air, in the cosmetics, in the food, in the environment. The proximate trigger is incidental. The originating cause is the syringe.
Why It Manifests
The terrain framework provides the missing layer of explanation. Sensitization is the precondition that explains why a body responds at all. Sensitization alone does not explain why a particular body responds today and not yesterday, in June and not December, after this exposure and not that one.
John Tilden, writing in the 1920s, documented the chain that connects systemic toxic load to mucous membrane response.²⁰ The body, as Tilden described it, vents accumulated toxins through whichever route remains available. The mucous membranes of the nose are one such route. What medicine calls a cold is the elimination of accumulated toxin through the nasal membrane. Repeated colds, when the underlying toxic load is not addressed, lead to thickening of the membrane, then to ulceration, then to bony spurs, then to what is named hay fever. In Tilden’s words: “The cause is the same from the first cold to hay fever.”²⁰
Henry Bieler, writing in the 1960s, named the same sequence from the local end. Hay fever, Bieler observed, develops after atrophy of the nasal and sinus mucous membranes.¹⁹ The membrane that has been repeatedly inflamed, scarred, and depleted no longer functions as a protective barrier. It reacts to substances it would once have tolerated. As Bieler put it: “When there is no catarrhal state, there is no hay fever.”¹⁹
Herbert Shelton’s account closed the loop on what produces and perpetuates the catarrhal state.¹⁹ Inhalation of toxic chemicals such as volatile organic compounds, fragrances, household products, and industrial pollutants induces nasal irritation and inflammation. When the exposure continues, and when the body’s response is suppressed pharmaceutically, the acute inflammation becomes chronic. The chronic catarrh becomes the conditions filed under allergic rhinitis, hay fever, and chronic sinusitis. Shelton named catarrhal inflammation a crisis of toxemia.¹⁹
The integrated picture: injection produces sensitization. The sensitized membrane is reactive. The reactivity is manifested when the body’s toxic load reaches a threshold, when the inhaled trigger meets a membrane already depleted, when the seasonal pollen meets a system already at its limits. The vaccinated person carries the originating cause. The dietary toxemia, the household chemicals, the industrial pollutants, the modern environmental burden carry the proximate triggers. The membrane atrophies through repeated exposure and repeated suppression. The June pollen, the September ragweed, the cat dander, the perfume, none of these is the disease. They are what the sensitized and depleted system can no longer tolerate.
The terrain framework explains the variability. Some vaccinated children develop hay fever. Some do not. Some develop it at five, some at fifteen, some lose it in middle age. The sensitization is the underlying precondition. The manifestation depends on the cumulative state of the terrain: the diet, the chemical exposures, the stress load, the cumulative toxic burden. A body that was sensitized but whose terrain remained strong may not manifest. A body whose terrain weakens through accumulated insult will.
What the Treatment Does
The treatment for hay fever is, in every modality the establishment offers, the suppression of the response the body is mounting to deal with the situation.
Antihistamines block the histamine that the membrane is releasing to flush the irritant out. The histamine is retained. The membrane stays inflamed. The expulsion is suppressed. Corticosteroids deliver synthetic versions of the body’s own anti-inflammatory hormone at concentrations that override the body’s regulation, shutting down inflammation by chemical force. Chronic use of nasal corticosteroids produces, in turn, mucosal atrophy, recurrent infections, and the slow erosion of the membrane’s structural integrity. The acute response is suppressed and the underlying terrain deteriorates.
Allergen immunotherapy, the procedure marketed as allergy shots, completes the circle. Patients sensitized through injection are treated by repeated injection of the substance they were sensitized to, in escalating doses, with the goal of reaching a tolerance state. The procedure is the same procedure that produced the disease, applied as the cure. The Richet mechanism is acknowledged in the design of the treatment. The clinical category, the mechanism, and the treatment all rest on the same observation: that injection produces sensitization, that the sensitized body reacts to subsequent exposure, and that further injection can modulate the response.
What the treatment does not do is identify and remove what made the membrane reactive in the first place. The household chemicals, the industrial fragrances, the dietary toxic load, the pharmaceutical burden, the original vaccination history, none of these enters the clinical encounter. The patient receives a prescription. The next prescription follows. The acute symptom becomes chronic. The detailed sequence by which acute conditions are driven into chronic states through pharmaceutical suppression is developed in the essay on inflammation, where Shelton’s catarrhal chain runs to its full progression.²¹
The Hygiene Hypothesis
The establishment’s competing explanation for the modern rise in allergic disease is the hygiene hypothesis. The argument, first articulated by David Strachan in 1989, was that hay fever and the wider atopic conditions had risen because modern children encountered fewer microbes in early life, and that the resulting underdevelopment of the body’s regulatory capacity left them prone to misdirected reactions.
The hypothesis was built specifically to explain hay fever.³ Strachan’s original findings concerned birth order, family size, and socioeconomic status as predictors of hay fever risk. The hypothesis has been adjusted and extended in the decades since. It cannot account for the 1819 first appearance, when the affluent classes who developed the condition had less rather than more hygiene than the rural poor who did not. It cannot account for the Bernsen finding that pertussis encountered naturally protects against atopy while pertussis injected produces it. The hygiene hypothesis is a theory in search of a mechanism. The mechanism that fits the data is the syringe.
What Hay Fever Is
The documented sequence is the one this essay has traced. A disease that had no precedent in the medical literature appeared in London within a generation of the introduction of a new injection procedure, in the class that received the procedure. The mechanism by which injection of foreign protein produces sensitization was demonstrated in children injected with horse serum, was awarded the Nobel Prize in 1913, and is now the standard laboratory protocol for manufacturing allergic disease for study. The Japanese investigators conceded the mechanism in the case of DTaP and gelatin: schedule change produced anaphylaxis, gelatin removal stopped it. The animal-model literature shows that injected microbial preparations function as adjuvants for airborne allergens the animal would otherwise have ignored.
Modern epidemiology documents the convergent pattern. Vaccinated children with no family history of hay fever are ten times more likely to develop it than children who were never vaccinated. The dose-response on timing is internal to the schedule. The same bacterium, when injected, produces atopy that normal exposure does not. The most recent and methodologically rigorous of these studies, funded by the CDC, found a dose-response on aluminum specifically: each milligram of vaccine-associated aluminum increased the persistent-asthma risk in young children.
Whatever word a reader chooses for the documented sequence, coincidence, correlation, contributing factor, primary cause, the documentation exists. The records exist. The studies exist in the establishment’s own journals, by the establishment’s own investigators. The body is not malfunctioning. The body is responding to having had foreign protein inserted past every layer of its protective architecture by a procedure that promised protection and delivered sensitization. Hay fever is the response. The syringe is the cause.
Author’s Note
Hay fever is not treated here as an exception within the framework of allergic disease but as the originating case. The condition the establishment files under allergic rhinitis was the first disease for which the words allergy and anaphylaxis had to be coined. The vocabulary of modern allergy medicine was created in direct response to the reactions doctors observed in patients they had injected.
Where this essay cites establishment research, it uses the establishment’s terminology. IgE, mast cell, allergen, immune response. These terms appear in attributed register, as the constructs by which mainstream medicine accounts for what it observes. In the terrain framework that grounds the analysis, those constructs do not name confirmed biological entities. They name conventions of interpretation. The body does not attack itself. The body does not make a mistake. The body responds to having been sensitized and to having been continuously exposed to substances it cannot tolerate. The conventional account inverts cause and effect.
The remedy does not exist in the pharmacy. A body sensitized through injection, depleted through dietary toxic load, irritated through environmental chemical exposure, and suppressed through pharmaceutical intervention cannot be restored through additional intervention. The remedy is to stop the procedure that produced the condition and to begin the long process of detoxifying and rebuilding what has been damaged. Nothing here is medical advice. The intent is to provide the documented historical and clinical record that the conventional account of hay fever omits.
Explain It To A Six-Year-Old
A long time ago, before doctors started doing it, almost nobody got hay fever. Then doctors started giving people a shot in the arm. They thought the shot would keep people from getting sick. The shot put stuff into the body that the body had never seen before, and the body got confused.
When the body is healthy, it knows what belongs and what does not. It breathes in flowers and dust and grass and air, and it sorts them out fine. When the doctors put stuff straight into the arm with a needle, the body had to figure out what was happening without being able to use its usual ways of checking. So it started to react.
After the shot, some bodies started to get itchy and sneezy when they breathed in things that used to be fine. Pollen from grass, dust, pet fur. The body would say, wait, that looks like something I had to deal with before, when the doctor stuck the needle in. And it would start sneezing and the eyes would itch and the nose would run.
Hay fever is the body doing its job. It is trying to wash away things it thinks are dangerous. The runny nose washes things out, and so do the watering eyes, and the sneezing pushes things away.
Medicine usually gives people pills to stop the runny nose and the sneezing. The pills do not fix the problem. They just hide what the body is trying to do. The real problem is that the body was confused in the first place by the shot.
If you have hay fever, your body is not broken. Your body is working. It is reacting to something that scared it a long time ago.
References
¹ Bostock, J. (1819). Case of a Periodical Affection of the Eyes and Chest. Medico-Chirurgical Transactions, 10, 161–165; and Bostock, J. (1828). Of the Catarrhus Aestivus, or Summer Catarrh. Medico-Chirurgical Transactions, 14, 437–446.
² Maready, F. Crooked: Man-Made Disease Explained. Feels Like Fire, 2018.
³ Fraser, H. The Peanut Allergy Epidemic: What’s Causing It and How to Stop It. Skyhorse Publishing, third edition, 2017.
⁴ Richet, C. Nobel Lecture: Anaphylaxis, delivered 11 December 1913. Nobel Prize in Physiology or Medicine awarded for work on anaphylaxis.
⁵ Behring, E. von, and Kitasato, S. (1890). Ueber das Zustandekommen der Diphtherie-Immunität und der Tetanus-Immunität bei Thieren. Deutsche medizinische Wochenschrift, 16, 1113–1114; and von Pirquet, C., Schick, B. (1905). Die Serumkrankheit. Vienna: Franz Deuticke. Translated by Schick as Serum Sickness, Baltimore: Williams & Wilkins, 1951.
⁶ Nakayama, T., Aizawa, C., Kuno-Sakai, H. (1999). A clinical analysis of gelatin allergy and determination of its causal relationship to the previous administration of gelatin-containing acellular pertussis combined with diphtheria and tetanus toxoids. Journal of Allergy and Clinical Immunology, 103, 321–325; Kuno-Sakai, H., Kimura, M. (2003). Removal of gelatin from live vaccines and DTaP — an ultimate solution for vaccine-related gelatin allergy. Biologicals, 31(4), 245–249.
⁷ Weibel, R.E., Woodhour, A.F., Stokes, J., Metzgar, D.P., Hilleman, M.R. (1967). New Metabolizable Immunologic Adjuvant for Human Use: Evaluation of Highly Purified Influenza-Virus Vaccine in Adjuvant 65. New England Journal of Medicine, 276, 78–84; Hilleman, M.R. (1966). Critical appraisal of emulsified oil adjuvants applied to viral vaccines. Progress in Medical Virology, 8, 131–182.
⁸ World Health Organization Scientific Group on Immunological Adjuvants. Immunological Adjuvants: Report of a WHO Scientific Group. WHO Technical Report Series No. 595, Geneva, 1976.
⁹ Enriquez, R., Addington, W., Davis, F., Freels, S., Park, C.L., Hershow, R.C., Persky, V. (2005). The relationship between vaccine refusal and self-report of atopic disease in children. Journal of Allergy and Clinical Immunology, 115(4), 737–744.
¹⁰ Bremner, S.A., Carey, I.M., DeWilde, S., Richards, N., Maier, W.C., Hilton, S.R., Strachan, D.P., Cook, D.G. (2005). Timing of routine immunisations and subsequent hay fever risk. Archives of Disease in Childhood, 90, 567–573.
¹¹ Bernsen, R.M.D., Nagelkerke, N.J.D., Thijs, C., van der Wouden, J.C. (2008). Reported pertussis infection and risk of atopy in 8- to 12-yr-old vaccinated and non-vaccinated children. Pediatric Allergy and Immunology, 19(1), 46–52.
¹² Flöistrup, H., Swartz, J., Bergström, A., Alm, J.S., Scheynius, A., et al. (2006). Allergic disease and sensitization in Steiner school children. Journal of Allergy and Clinical Immunology, 117(1), 59–66.
¹³ Alm, J.S., Swartz, J., Lilja, G., Scheynius, A., Pershagen, G. (1999). Atopy in children of families with an anthroposophic lifestyle. Lancet, 353(9163), 1485–1488.
¹⁴ For mainstream reviews finding no association or protective effects, see Grüber, C., Lau, S., Sommerfeld, C., Wahn, U. (2002), and Nilsson, L., Kjellman, N.I., Björkstén, B. (2003). The aggregate analysis sits within ongoing methodological dispute over case ascertainment and confounding by socioeconomic and care-seeking variables.
¹⁵ Kennedy, R.F., Jr., and Hooker, B.S. Vax-Unvax: Let the Science Speak. Skyhorse Publishing, 2023. The original studies catalogued therein include Mawson et al. (2017), Hooker and Miller (2021), Lyons-Weiler and Thomas (2020), Garner (2021), and the Dutch NVKP 2006 dataset.
¹⁶ Bailey, M. The Final Pandemic: An Antidote to Germ Theory. Independently published, 2023. Citing World Allergy Organization, White Book on Allergy: Update 2013; and Pawankar, R., Canonica, G.W., Holgate, S.T., Lockey, R.F., editors, WAO White Book on Allergy, World Allergy Organization, 2011.
¹⁷ Daley, M.F., Reifler, L.M., Glanz, J.M., Hambidge, S.J., Getahun, D., Irving, S.A., Nordin, J.D., McClure, D.L., Klein, N.P., Jackson, M.L., Kamidani, S., Duffy, J., DeStefano, F. (2023). Association Between Aluminum Exposure From Vaccines Before Age 24 Months and Persistent Asthma at Age 24 to 59 Months. Academic Pediatrics, 23(1), 37–46.
¹⁸ Roytas, D. Can You Catch a Cold? Untold History and Human Experiments That Challenge the Theory of Viral Contagion. Humanley, 2024.
¹⁹ Lester, D., and Parker, D. What Really Makes You Ill? Why Everything You Thought You Knew About Disease Is Wrong. Independently published, 2019. Citing Bieler, H. Food Is Your Best Medicine; and Shelton, H. Natural Hygiene: Man’s Pristine Way of Life.
²⁰ Tilden, J.H. Toxemia Explained: The True Interpretation of the Cause of Disease. Originally published 1926; reprinted FQ Classics, 2007.
²¹ Unbekoming. What Is Inflammation? Substack essay.
Additional Sources
What Is Inflammation? The acute-to-chronic suppression chain described in this essay, the trajectory from catarrhal response through pharmaceutical suppression to chronic disease, is developed in full in the inflammation essay.
What Is Asthma? The atopic disease that sits beside hay fever in the modern epidemiology, with the strongest vaccinated-and-unvaccinated signal in the literature.
What Is Eczema? The third member of what the establishment calls the atopic triad, with the same originating mechanism and the same modern epidemiology.
Maready, F. Crooked: Man-Made Disease Explained. The book-length treatment of the historical case for vaccination as the originating cause of allergic disease, including the Bostock chronology and the diphtheria antitoxin documentation.
Fraser, H. The Peanut Allergy Epidemic. The book-length treatment of the modern allergic disease epidemic, including the Richet mechanism and the Japanese gelatin admission.
Kennedy, R.F., Jr., and Hooker, B.S. Vax-Unvax: Let the Science Speak. The compilation of vaccinated-and-unvaccinated comparison studies cited in Movement 3.
Miller, N.Z. Critical Vaccine Studies: 400 Important Scientific Papers Summarized for Parents and Researchers. The compilation that catalogs the Enriquez, Bremner, Bernsen, Flöistrup, and Alm papers among many others.
Bailey, M. The Final Pandemic: An Antidote to Germ Theory. The terrain-framework treatment that documents the WAO admissions and the broader vaccine-allergy literature.
The Vaccines and Related Biological Products Advisory Committee (VRBPAC), which reviews scientific data on the safety and effectiveness of vaccines and other therapeutics on behalf of the U.S. Food and Drug Administration (FDA), voted 9-0 in dual votes to recommend approval of the vaccine for the 50-64 and 65-plus age groups.
Today’s votes took place after several hours of presentations based on the findings of Moderna’s Phase 4 clinical trial data for its mRNA-1010 vaccine. The trial compared the efficacy of mRNA-1010 to that of a conventional, non-mRNA flu vaccine.
Daniel O’Connor, founder and CEO of TrialSite News, told The Defender today’s favorable votes “may reflect the committee’s view that the benefit-risk profile is acceptable.” However, the vote “does not erase the fundamental concerns surrounding this application.”
“Significant questions remain about comparator selection, study design and whether the reported efficacy advantage represents a clinically meaningful improvement for patients or simply a statistical advantage within the framework of the trial,” O’Connor said.
According to an FDA briefing document prepared in advance of today’s meeting, “no major deficiencies were identified” with the vaccine for adults 50 and over. Citing the clinical trial data, the document states that the mRNA-1010 vaccine had a 26.6% relative efficacy rate in adults 50 and over, with similar rates for adults 65 and up.
The mRNA-1010 vaccine also showed a higher immune response than Sanofi’s Fluzone vaccine, the document noted. According to Fierce Biotech, these results met all of the FDA’s “pre-specified criteria for success” and bolstered Moderna’s application for approval.
Karl Jablonowski, Ph.D., senior research scientist for Children’s Health Defense, said today’s vote shifts mRNA-1010 safety monitoring to after licensure.
“VRBPAC meetings proceed to the beat of the rubber stamp. The unanimous vote guarantees a lot of really good questions of harm will have to be answered in the post-marketing period, when that harm manifests in the population,” Jablonowski said.
Moderna seeks traditional approval for the mRNA-1010 vaccine for the 50-64 age group and accelerated approval for the 65-plus age group.
Fierce Biotech reported that the FDA uses VRBPAC meetings to “seek outside counsel on tough or high-profile regulatory decisions.”
The FDA will make an approval decision on mRNA-1010 by Aug. 5 — and while the agency is not bound to VRBPAC’s votes, it “often follows the opinions” of its advisory committees.
Moderna’s stock was up over 4% in trading immediately after the vote, and up 3.50% at the close of market.
mRNA vaccine had higher rate of adverse events than conventional flu shot
According to MedPage Today, all current flu vaccines are “manufactured using egg-based, cell-culture based, or recombinant production technologies” — a production process that could result in “egg-adaptive mutations” and which makes it slow to reformulate vaccines when they don’t match currently circulating flu strains.
In their briefing document, FDA scientists suggested that “high-volume manufacturing” of a flu vaccine “capable of rapid strain reformulation is … needed.”
However, the briefing document did identify some concerns with mRNA-1010. FDA scientists noted the higher rate of solicited adverse events among clinical trial participants who received mRNA-1010 — and the higher number of unspecified deaths and serious adverse events related to anemia or urinary tract infections.
The document also noted that “efficacy in immunocompromised individuals and very frail older adults has not been established” — which is “significant because these populations face the highest absolute risk of severe influenza-related complications and may respond differently to mRNA-based vaccine platforms.”
Several experts told The Defender that Moderna’s mRNA-1010 vaccine poses risks. “Throughout the study, solicited adverse events are almost, and in some cases more than, double that of the comparator,” Jablonowski said.
The briefing document acknowledged a higher rate of solicited adverse reactions for mRNA-1010 vaccine recipients than among the conventional flu vaccine recipients. According to the Association of Health Care Journalists, solicited adverse events are “those that the trial investigators specifically ask participants about because they are either expected or likely based on known reactions to other vaccines.”
Unsolicited (unexpected) adverse events, serious adverse events, adverse events of special interest and deaths “were balanced between treatment groups,” and “no cases of myocarditis or pericarditis were identified within 42 days postvaccination,” the document states.
Immunologist and biochemist Jessica Rose, Ph.D., said this period is too small to detect long-term risks. “There is no way to know what the long-term adverse events will encompass,” she said.
Dr. Angus Dalgleish, professor emeritus of oncology at City St. George’s, University of London, said, “There is no need for any specific flu vaccine.” He cited the high number of serious adverse events related to the mRNA COVID-19 vaccines.
“The case for mRNA gene therapies for any infectious disease can never be approved with current technology, given the totally unacceptable serious side effect risks,” Dalgleish said.
Rose agreed. She said that since mRNA-1010 is based on the same “flawed” platform as the COVID-19 shots, she anticipates “exactly the same problems as for the COVID shots, as per the millions of reported adverse events to pharmacovigilance databases.”
FDA glosses over safety concerns
These concerns are similar to those expressed when Moderna first filed its application for licensure in December 2025 and which contributed to the FDA declining to review the company’s application in February.
In a “refusal-to-file” letter signed by Dr. Vinay Prasad, then-director of the FDA’s Center for Biologics Evaluation and Research, which oversees vaccines, the agency cited Moderna’s failure to perform an “adequate and well-controlled” clinical trial and its failure to use the “best-available standard of care” during the trial process.
In February, STAT reported that Prasad overruled senior FDA vaccine reviewers, who were ready to review Moderna’s application. However, Andrew Nixon, a spokesperson for the U.S. Department of Health and Human Services, told STAT at the time that the claim was “categorically false.”
In response to Moderna’s claim that mRNA-1010 had a 26.6% higher relative efficacy rate than the existing Fluzone vaccine, former pharmaceutical research and development executive Sasha Latypova wrote on Substack that this is significantly lower than the 95% relative efficacy claimed for the mRNA COVID-19 vaccines during Phase 3 clinical trials.
Jablonowski told The Defender in February that the mRNA-1010 clinical trial data show that mRNA recipients had a 329% higher chance of sustaining a serious adverse event and a 278% higher chance of experiencing an unsolicited adverse event — referring to a condition that was not expected or previously known.
However, the FDA’s briefing document found that mRNA-1010’s safety profile was “acceptable for the intended population” and that there was no causal relationship between the vaccine and the unspecified deaths and cases of anemia and urinary tract infections identified during the clinical trial.
The document said these adverse events are “unlikely to represent a vaccine safety signal” and that the risk of rare adverse events should be tracked through post-licensure monitoring.
But according to Jablonowski, conventional flu vaccines have shown they have negative efficacy — placing the vaccinated at higher risk of flu than the unvaccinated. He said this makes any comparison between the candidate mRNA vaccine and existing vaccines invalid.
“If the current flu vaccines have negative efficacy, a placebo would be more efficacious. … In the 2024-2025 season, the Cleveland Clinic found a negative 27% efficacy,” Jablonowski said.
‘They’re promoting the platform’
The FDA’s decision to decline review of Moderna’s application led to an uproar within the pharmaceutical and public health spheres. Within two weeks, the FDA accepted the company’s application for licensure of mRNA-1010. Leadership shake-ups at the FDA soon followed.
Some experts suggested that political pressure — and corporate lobbying — contributed to the FDA’s about-face.
Blackstone, a New York-based investment firm, is the world’s largest alternative assets manager, with a portfolio exceeding $1 trillion. In 2024, the company launched an ongoing, $750 million investment in Moderna, explicitly to support the development of its mRNA flu shot.
Aside from its financial might, Blackstone is also closely connected to the Republican Party and the Trump administration, through significant donations from its executives and employees and through its ties with prominent lobbying firms linked to Republicans — and Big Pharma.
In turn, Blackstone’s CEO and co-founder, Stephen A. Schwarzman, has close ties to President Donald Trump and his administration, while members of Blackstone’s Life Sciences division have ties with several vaccine makers, including Pfizer.
In a post on X, Max Bayer, a science reporter with Endpoints News, noted that today’s meeting included the participation of a non-voting pharmaceutical industry representative and that “no waivers were issued for conflicts of interest.”
Rose suggested that these moves signal a desire on the part of the FDA to continue promoting mRNA vaccine technology.
“They’re promoting the platform,” Rose said. “People who acknowledge risk who oppose using an unsafe and ineffective platform are a problem for the industry players aligned with pushing this technology forward.”
A journalist from The Guardian recently contacted me for a comment on vaccine-related studies I have previously cited in my work. The publishers of these studies have decided—years after publication—that these studies were so flawed and “dangerous to public health” that they needed to be retracted or investigated. The journalist wanted to know if I would amend my book and my recent ACIP presentation now that these studies were under attack.
My response:
“I welcome the media noting the targeted assassination of articles that do not fit the religious belief of vaccine proponents; this is also exemplified by the media’s lack of interest in the hundreds of other articles, reviews, and trial documents from my book and ACIP presentation which make plain that the claim vaccines are ‘safe and effective’ is not supported by the available evidence.”
So which studies are under fire? You won’t be surprised that they are on some of the biggest hot-button topics when it comes to vaccine injury:
2. RETRACTED: Hepatitis B Vaccination of Male Neonates and Autism Diagnosis, NHIS 1997–2002 (Carolyn Gallagher & Melody Goodman, 2010). This paper was published sixteen years ago. Sixteen years. And only now was it retracted after the publisher claimed that “due to fundamental methodological flaws the study’s conclusions are unsound.” The authors stand behind the study and noted “many of the recent criticisms of the paper are consistent with what we recognized and noted at the time.”
Behind each of these attacks is a plain desire to wipe from the record any evidence of vaccine harm and to chill the publication of any future studies that report vaccine harm.
Every scientist who values scientific integrity should publicly denounce these tactics. Anything less is not science. It is ideology.
Controversy over a BMJ paper examining excess mortality trends during the COVID-19 pandemic remains unresolved more than two years after publication, Steve Kirsch reported on Substack.
Dutch researcher Saskia Mostert, M.D., Ph.D., led the study, which was published in BMJ Public Healthin May 2024.
Mostert’s team analyzed excess mortality data from 47 Western countries and reported that elevated death rates persisted through 2022 and 2023 despite the end of pandemic restrictions and the widespread availability of COVID-19vaccines.
The authors argued that the findings warranted further investigation into potential contributing factors, including pandemic-era policies, healthcare disruptions and mass vaccination programs.
The paper was attacked on PubPeer and Retraction Watch, two platforms that have become the driving force behind many recent retractions of peer-reviewed scientific papers whose findings challenge the mainstream narrative on vaccines, COVID-19 treatments and aluminum, among others.
Critics did not dispute the paper’s core findings that excess mortality was high and remained elevated in many Western countries during the study period. Instead, they criticized the paper’s discussion of the COVID-19 vaccines, saying it implied there was a causal link between the shots and excess death and encouraged readers to infer causation.
Several critics called for the paper to be retracted.
In response to these and other mainstream criticism of the paper, BMJ Public Health issued a statement saying that media reports had misrepresented the findings. However, in mid-June 2024, the journal stamped the article with an “expression of concern.”
The journal said its “integrity team and editors” were investigating issues “regarding the quality and messaging of this work.” It also said the Princess Máxima Center, where three of the four study authors were based, was investigating the study.
BMJ Public Health added that the study does not support the claim that vaccines are a major contributor to excess deaths.
The BMJ typically waits for the home institution’s findings before taking action, according to Kirsch. He said the Princess Máxima Center hasn’t yet sufficiently explained what was wrong with the study.
BMJ updated the expression of concern in January 2025, stating that it was awaiting the findings and that the institution had no update regarding when the information would be sent. The Princess Máxima’s website says the investigation is “complete but not yet finalized.”
“After more than two years, the ‘issues’ with the paper have not been revealed,” Kirsch wrote. He said that the center’s investigation revealed that the data and methodology are real and the authors committed no fraud.
“The institution just didn’t like the political implications of being associated with a paper that called the safety of the COVID vaccine into question.”
Princess Maxima Center did not respond to The Defender’s request for comment.
Study used proper methods, reported valid findings
All-cause mortality expert Denis Rancourt, Ph.D., told The Defender that the authors conducted their analysis, “using a correct method and without error.”
“Those results are robust and are corroborated and expanded upon by others,” Rancourt said. All-cause mortality is an important metric that is valid regardless of different opinions about what drives that mortality, he added.
Rancourt said the researchers discussed their results in relation to a broad range of published studies.
The push for retraction was based on how the media and social media commenters interpreted the discussion — not based on what the authors actually did in the paper.
“This is a regressive reason to start unpublishing papers,” he said, adding:
“The large industry of unpublishing shows that our society has moved away from independent thought (intellectual literacy) and towards excessive reliance on the pronouncements from high-status sources. I include scientists themselves in the said society.”
All-cause mortality identified in the paper ‘unprecedented and raises serious concerns’
The original paper showed that excess mortality in 2020 was documented in 41 of the 47 countries the authors analyzed. Over the next two years, that number increased to 42 and 43 countries in 2021 and 2022, respectively.
Overall, there were 3,098,456 excess deaths from Jan. 1, 2020, to Dec. 31, 2022, with just over 1 million of those occurring in 2020.
“This is unprecedented and raises serious concerns,” said researchers, who analyzed all-cause mortality reported in the Our World in Data database.
“In 2021,” they wrote, “the year in which both containment [i.e., lockdown] measures and COVID-19 vaccines were used to address virus spread and infection, the highest number of excess deaths was reported: 1,256,942 excess deaths.”
They reported that in 2022 — “the year in which most containment measures were lifted and COVID-19 vaccines were continued” — there were 808,392 excess deaths.
The authors pointed out that during the pandemic, politicians and the media emphasized: “on a daily basis that every COVID-19 death mattered and every life deserved protection through containment measures and COVID-19 vaccines.”
“In the aftermath of the pandemic, the same moral should apply,” the authors said. “Every death needs to be acknowledged and accounted for, irrespective of its origin.”
The authors called for government transparency in cause-of-death data so researchers can do “direct and robust analyses to determine the underlying contributors.”
This also means that autopsies need to be done to determine the exact reason for death, they added.
The authors noted that the data they analyzed may not have recorded all actual deaths because “countries may lack the infrastructure and capacity to document and account for all deaths.”
Record-keeping mishaps or delays may also cause deaths to go unrecorded.
The Centers for Disease Control and Prevention’s (CDC) recent decision to award Pfizer $1.24 billion for COVID-19 vaccines has renewed debate over the government’s continued investment in mRNA technology.
The contracts, awarded on June 1, include about $735.7 million for pediatric COVID-19 vaccines and nearly $505.3 million for adult doses for fiscal year 2026-2027.
Critics say the funding reflects a continued commitment to vaccines associated with high rates of serious injuries and deaths, and a lack of adequate safety testing and monitoring.
Public health experts argue the investment is necessary to protect vulnerable populations and prepare for future outbreaks.
The latest contracts come as mRNA technology expands beyond COVID-19.
A recent review in Human Vaccines & Immunotherapeutics found that mRNA-based therapeutics were identified in more than 550 registered clinical trials. The authors reported that more than 90% of the projects involved mRNA vaccines and that most products remain in early-stage testing before broader adoption.
‘Unnecessary and often harmful injections’
The procurement of monetary resources signals that federal officials intend to continue investing heavily in mRNA technology despite declining public demand and ongoing controversy over vaccine safety monitoring, critics say.
Jeffrey Tucker, president and founder of the Brownstone Institute, told The Defender there was “no scientific justification” or “market demand” for the latest mRNA vaccine funding.
“This raises a serious question concerning how these captured agencies really work,” Tucker said. “We are talking about vast amounts of tax dollars flowing to support unnecessary and often harmful injections.”
“This is $1.24 billion for what is essentially a cold in minor children,” said Children’s Health Defense Chief Scientific Officer Brian Hooker.
Daniel O’Connor, publisher of TrialSite News, which covers global biomedical and clinical research, told The Defender Americans “better start asking the hard questions.”
“If demand is falling, safety questions remain contested and many reporting vaccine injuries say they’ve been left behind, why is Washington committing another $1.24 billion to vaccine procurement instead of first providing a transparent accounting of need, benefit, risk, and responsibility?”
‘COVID-19 has not disappeared’
Public health experts disagreed, saying their support of vaccinations is supporting the prevention of future pandemics.
Dr. Krutika Kuppalli, an associate professor in the Department of Internal Medicine at University of Texas Southwestern Medical Center, in Dallas, told The Defender that the monetary installments will help stave off another public health crisis because “COVID-19 has not disappeared.”
“While the emergency phase of the pandemic is over, the virus continues to cause significant illness, hospitalizations and deaths each year,” she said. “This investment reflects the reality that vaccines remain one of our most effective tools for preventing severe disease, particularly among those at highest risk. Maintaining access to updated vaccines is an important part of ensuring the country remains prepared for future COVID-19 surges.”
Dr. William Schaffner, an infectious disease specialist and professor at Vanderbilt University Medical Center in Nashville, Tennessee, said the contracts will ensure “continuing availability of safe and effective COVID vaccines through the next two years.”
“COVID vaccines have repeatedly been demonstrated to provide protection against the most severe manifestations of COVID infection: hospitalization, intensive care unit admission and death,” Schaffner said. “This is particularly applicable to those persons at increased risk of becoming seriously ill: persons age 65 and older, anyone with a chronic medical condition, persons who are immunocompromised and persons who are pregnant.”
However, some studies suggest claims that the COVID-19 vaccines saved millions of lives are based on flawed models and incorrect calculations.
Legality of funding in question
The contracts also raise questions about federal vaccine spending.
Under the CDC’s Vaccines for Children (VFC) Program, the federal government agrees to buy and provide free vaccines through negotiated contracts for eligible children.
Current CDC price schedules list Pfizer COVID-19 vaccines at roughly $69 to $91 per dose, depending on the formula, while Moderna doses range from about $78 to $83.
Dr. Robert Malone, a pioneer and expert in mRNA vaccines, however, questioned the legal authority to use federal funding for the Pfizer contracts because the purchase wasn’t approved by the CDC’s Advisory Committee on Immunization Practices (ACIP).
“Use of VFC funds requires ACIP authorization,” he said. “But there is no ACIP.”
The injunction stemmed from a lawsuit filed by the American Academy of Pediatrics (AAP) against Kennedy and the U.S, Department of Health and Human Services (HHS). The AAP accused Kennedy of violating procedures when he fired previous ACIP members and replaced them.
The ruling effectively paralysed ACIP and cast doubt on the legitimacy of its membership structure.
Requests for comment from ACIP went unanswered.
‘We are a long way from reckoning’
The CDC has maintained that authorized COVID-19 vaccines underwent extensive safety review and that the benefits outweigh known risks.
However, during a Capitol Hill meeting this week, Sen. Ron Johnson (R-Wis.) referred to reported COVID-19 vaccine injuries as the “biggest government scandal in my lifetime.”
“What about all the injection-injured?” he said. “Until this government and this administration acknowledge those injuries, acknowledge the harm caused by these injections, and I would say federal health agencies also acknowledge the harm done by childhood vaccines, we are a long way from reckoning.”
In April, Johnson released a report revealing that Biden-era health officials rejected a state-of-the-art statistical tool for detecting COVID-19 vaccine safety signals — and instead deliberately continued using a broken method because they didn’t want to “feed in to [sic] anti-vaccination rhetoric.”
During an April 29 hearing, Johnson revealed that a longtime U.S. Food and Drug Administration (FDA) medical officer, Ana Szarfman, M.D., Ph.D., repeatedly warned colleagues that the agency’s approach to safety monitoring could miss serious safety signals due to a problem known as “masking.” Masking occurs when other vaccines obscure risks tied to a specific product.
Johnson said FDA officials brushed aside Szarfman’s warnings.
The CDC, HHS and Pfizer did not immediately respond to requests for comment regarding the contracts.
In 2022, the New England Journal of Medicine published the results of the NordICC trial — the first randomised controlled study of colonoscopy screening ever conducted. Over 84,000 people were followed for ten years. The trial found an 18% reduction in cancer incidence and no significant reduction in cancer deaths. To prevent a single case of colorectal cancer, 455 people had to be invited for screening. To prevent a single death, the numbers were statistically indistinguishable from zero.¹
This is the pattern.
Across the major screening programmes — mammography, PSA, Pap, colonoscopy, lung CT — when the question is whether the screened population actually outlives the unscreened population, the benefit largely disappears.² The statistic the programmes advertise is disease-specific mortality: deaths from the disease the test is looking for. The statistic they bury is all-cause mortality: whether the screened group, taken as a whole, lives longer. The two numbers are not the same. You can reduce deaths from one disease while total deaths remain flat — because treatment has killed as many people as the disease prevented, or because the disease you found was never going to kill anyone.²
The screened do not live longer than the unscreened. They are more likely to spend their remaining years monitored, biopsied, cut, and medicated for conditions that would not have harmed them. This essay catalogues twelve tests that produce that conversion, organised by the four mechanisms through which it is achieved.
The Frame
Five concepts make the rest of this essay readable.
Disease-specific versus all-cause mortality. A screening programme can reduce deaths from breast cancer while total deaths remain unchanged. This happens when treatment kills as many people as the disease — through surgical complications, radiation-induced secondary cancers, cardiovascular effects of chemotherapy, or the cascade of follow-up procedures that screening triggers. Only all-cause mortality reveals whether the programme, taken as a whole, extended life.² Trials that report disease-specific reductions without corresponding all-cause reductions are reporting a redistribution of deaths.
Lead-time bias. A cancer destined to kill at age 70 appears as a three-year survival if found at age 67 through symptoms, and a seven-year survival if found at age 63 through screening. The patient dies at the same age in both cases — the clock simply started earlier. Five-year survival statistics, the most commonly cited evidence for screening success, are inevitably improved by earlier detection, even when no life is extended by a single day.² Kidney cancer five-year survival improved from 50% to 60% as imaging found more small tumours; the death rate from kidney cancer remained unchanged.²
Length bias. Aggressive cancers grow fast, become symptomatic between screening intervals, and reach the patient through the clinic rather than the screening room. Indolent cancers linger for years in the detectable phase, making them easy targets. The cancers screening preferentially catches are the ones least likely to kill. The ones most likely to kill evade it.²
Overdiagnosis, and the autopsy reservoir behind it. Approximately 40–70% of older men have prostate cancer at autopsy, while only about 3% die from it.² Up to 39% of middle-aged women show evidence of breast cancer at autopsy; lifetime risk of dying from it is under 4%.² Thyroid cancer appears in 36–100% of carefully examined autopsies, depending on how many microscope slides the pathologist prepares.² Polyps are found in 32–50% of older adults; only 5% develop colorectal cancer.³ The reservoir of detectable-but-harmless abnormality is vast. Every screening test dips into it. Every person pulled from it becomes a cancer patient who can only be harmed by treatment, because they were never at risk.
The threshold. The cutoff that separates well from sick is set by a committee, not by biology. In every screening category, the threshold has been lowered — by panels whose members hold financial relationships with the manufacturers of the drugs and devices used to treat the redefined condition.⁴ The 1988 cholesterol panel. The 1994 WHO bone density panel.⁵ The 2003 American Diabetes Association threshold for impaired fasting glucose.⁶ The 2017 American College of Cardiology hypertension revision.⁷ The lowered PSA cutoff. Each revision converts millions of well people into patients overnight. No one inside their body changed.
The early-detection objection — that finding disease earlier must, by intuition, help — fails on this evidence. It assumes that everything labelled cancer or pre-cancer will progress; the autopsy data say otherwise. It assumes that finding more is finding harm prevented; the mortality data say otherwise. It assumes that the people setting the thresholds are disinterested; the disclosures say otherwise.
Group A — Threshold Manipulation
The number creates the disease.
The first three screenings illustrate the cleanest mechanism in the catalogue. The cutoff changes while the body does not, and the well become the sick by committee vote. The drug to treat the redefined condition is manufactured by the company whose representative sat on the panel that lowered it.
1. Bone Density (DEXA) and the Manufactured Pre-Disease
In 1994, a World Health Organization panel redefined osteoporosis based on bone mineral density measured by DEXA scan.⁵ The reference standard was the bone density of a healthy 35-year-old woman. By this definition, any woman whose bones had decreased from their youthful peak — which describes virtually every woman over 50 — could be diagnosed with osteopenia or osteoporosis. The condition “osteopenia” did not exist as a clinical category before this redefinition.⁸ Internal Merck memos described the company’s excitement about the new diagnostic category and the market it would create for Fosamax.⁸
The DEXA scan measures bone mineral density. That is all it measures. It cannot assess the collagen matrix — the protein scaffolding on which the minerals deposit. A baby has very low bone mineral density and rarely fractures. An elderly woman with osteoporosis may have adequate minerals deposited in the wrong locations, including her arteries. Bone strength is a property of the matrix as much as of the minerals; the DEXA captures only one of the two and is treated as if it captured both.³
Bisphosphonate drugs raise the number the DEXA measures. They do not so much prevent fractures as change the kind of fracture. Documented harms include osteonecrosis of the jaw — the jawbone literally dying — and atypical femur fractures, where the thigh bone snaps under minimal stress in patients taking drugs prescribed to prevent fractures.⁹,¹⁰ The absolute fracture reduction in randomised trials is 1–2%. Fifty to a hundred women must be treated for years to prevent a single hip fracture, while every one of them carries the risks above.⁸
What to Ask Before Your Next Bone Density Scan – Unbekoming
2. Cholesterol
The cholesterol threshold for statin prescription has been lowered repeatedly since 1988, by panels whose members held financial relationships with the manufacturers of the drugs being recommended.⁴ The 2004 National Cholesterol Education Program guidelines tripled the number of Americans classified as needing treatment. The Washington Post reported the panel’s undisclosed conflicts. The guidelines remained unchanged.⁴
The cholesterol hypothesis has the unusual property of being unfalsifiable. The MRFIT trial followed 361,662 men and found that those with cholesterol below 170 had double the death rate from cerebral haemorrhage of those with higher levels; below 160 the death rate quadrupled.¹¹ The Sydney Diet Heart Study, recovered and reanalysed by Christopher Ramsden, found that men who replaced saturated fats with vegetable oils had a 62% higher death rate.¹² The Minnesota Coronary Survey, hidden for decades, showed that for every 30 points cholesterol decreased, mortality increased by 22%.¹¹ None of this has altered the trajectory of the threshold or the prescription.
The statin absolute risk reduction in primary prevention — people without existing heart disease — is approximately 1–2% over five years.¹³ Advocates present this as a 30–40% reduction by using relative risk. The numbers describe the same trial result. The first is what the patient experiences; the second is what the press release says. Patients are not shown the first.
Statins raise blood glucose. The Crestor label states that statin-induced glucose elevations “may exceed the threshold for the diagnosis of diabetes mellitus.” The warning was added decades after approval, after the diabetes signal had become too large to ignore.¹¹ The statin prescribed for the lowered cholesterol threshold thus produces the prediabetes captured by the next lowered threshold.
In 2003, the American Diabetes Association lowered the threshold for impaired fasting glucose from 110 mg/dL to 100 mg/dL.⁶ The category “prediabetes,” as it functions clinically today, did not exist before this revision. Millions of additional Americans were added to the surveillance rolls. None of their blood sugar changed. A committee’s definition of normal changed.
Prediabetes is not diabetes. Many people classified as prediabetic will never develop diabetes. The label nevertheless creates patients — patients who are monitored, tested, counselled, and increasingly prescribed metformin for a number on a lab report. Metformin causes gastrointestinal distress in up to 25% of patients.¹⁴ These symptoms are typically addressed with additional medication, or attributed to irritable bowel syndrome, which becomes its own diagnostic pathway.
The label persists across the life cycle. A woman diagnosed with gestational diabetes during pregnancy — using the same threshold-lowering mechanism, which catches around 18% of pregnant women on current criteria — returns six weeks postpartum for a repeat glucose tolerance test.¹⁵ The test is unchanged. Her physiology is largely unchanged. She is re-labelled “glucose intolerant” or “prediabetic” and enters lifelong annual surveillance. The temporary pregnancy label becomes a permanent metabolic identity.¹⁵
The fasting insulin test, which would actually reveal metabolic dysfunction, is rarely ordered.¹¹ The fasting glucose, which lags behind insulin dysregulation by years, is the screening test of record. The earlier marker is upstream and dietary; the later marker is downstream and pharmaceutical. The system selects for the marker that supports its intervention.
The Mother Who Remains: How Medicine Captures Women After Birth (Part 8) – Unbekoming
Group B — Overdiagnosis
Finding what would never have harmed you.
The next three screenings do not invent the condition by adjusting a threshold. They find conditions that exist by the pathology textbook’s definition but would never have caused symptoms or death. Overdiagnosis is the bulk of what these programmes produce, not a marginal side-effect of them.
4. Mammography
The 25-year Canadian National Breast Screening Study, published in the BMJ in 2014, followed nearly 90,000 women. It found no significant reduction in breast cancer mortality from mammographic screening.¹⁶ The 2013 Cochrane Review of randomised trials reached the same conclusion.¹⁷ The relative risk for all-cause mortality in well-conducted trials is 1.01 (95% CI 0.99 to 1.04) — no significant difference between the screened and the unscreened.¹⁷
What screening does find, reliably, is ductal carcinoma in situ. DCIS was a rare diagnosis before the 1980s. It now accounts for a significant proportion of all screen-detected breast cancers. Studies following women whose DCIS was missed at biopsy show that 75–90% never develop invasive cancer over 10–20 years.¹⁸ The condition is treated nonetheless — with surgery, radiation, and in some cases chemotherapy. Nearly half a million women have been diagnosed and treated for DCIS since widespread mammography began.¹⁸ The cancers they were treated for would, in the great majority of cases, never have harmed them.
Up to 60% of women who undergo annual mammograms for a decade experience at least one false positive.¹⁸ Each false positive triggers additional imaging, biopsy, and the psychological burden of waiting. A single mammogram delivers radiation equivalent to approximately 100 chest X-rays, concentrated on compressed breast tissue.¹⁸ Over a decade of annual screening that is 1,000 chest X-rays’ worth of ionising radiation aimed at the tissue the screening is supposedly protecting. A 2012 BMJ study found that women with BRCA variants who underwent mammograms before age 30 had an increased risk of developing breast cancer compared to those who did not.¹⁹
What to Ask Before Your Next Mammogram – Unbekoming
5. Colonoscopy
The NordICC trial, with which this essay opened, was published in the New England Journal of Medicine in 2022. It followed over 84,000 people for ten years and found an 18% reduction in cancer incidence and no significant reduction in cancer deaths.¹ Until 2022, gastroenterology had no randomised trial supporting the procedure it had been recommending for decades.
The paradox is structural. Polyps are found in 32–50% of older adults. About 5% of people develop colorectal cancer.³ The vast majority of polyps removed during colonoscopy were never destined to cause harm. The procedure removes them anyway, and each removal leaves a wound in the protective mucosal layer. A 2019 study in Gastroenterology proposed an additional mechanism — iatrogenic tumour seeding via the scope itself, where cancerous cells stick to the biopsy forceps or are aspirated into the scope’s channel and redeposited elsewhere in the colon as the scope is withdrawn.³
The bowel preparation devastates the microbial ecology of the colon. Polyethylene glycol prep causes an “instant and substantial change” in gut microbial balance.³ Beneficial populations decrease significantly. The microbiome rebounds over weeks or months but may never return precisely to its original composition. Repeated colonoscopies across decades may leave the colon both microbiologically disturbed and physically scarred — creating, plausibly, the conditions in which polyps continue to form.
Complication rates from a Canadian population study of 97,204 outpatient colonoscopies: significant bleeding in 1 in 600; perforation in 1 in 1,200; death from the procedure in 1 in 14,000.³ These are surgical-intervention rates, not the rates of a benign screening test. The procedure generates approximately $4 billion annually in the United States.³
The Colonoscopy Cartel: How Routine Screening Became a Business Model – Unbekoming
6. CT Scan — The Screening Test That Causes the Disease It Looks For
A 2025 study in JAMA Internal Medicine projected that the 93 million CT scans performed in the United States in 2023 will ultimately cause approximately 103,000 future cancers — roughly 5% of all new cancer diagnoses each year.²⁰ CT usage has grown from 3 million scans in 1980 to over 90 million today, a thirty-fold increase. Medical imaging is now the primary source of radiation exposure for most Americans beyond natural background.
The radiation epidemiology is no longer in dispute. The Taiwanese registry study found that CT exposure was associated with a 2.55-fold increase in thyroid cancer risk and a 1.55-fold increase in leukaemia risk, with clear dose-response relationships.²¹ The British NHS registry study of 178,604 children found that those exposed to cumulative doses of 30 mGy demonstrated a threefold increased risk of leukaemia; exposure to 50 mGy showed similarly elevated brain tumour risk.²² Five to ten head CT scans in children under fifteen can accumulate sufficient radiation to significantly increase lifetime cancer risk.²²
Approximately 25% of CT scans reveal incidental findings — unexpected abnormalities unrelated to the original reason for imaging.²¹ The Emory University radiologist who underwent virtual colonoscopy after a routine annual physical illustrates the cascade in its full form. The scan found no colon problem but identified a kidney mass, a 2-cm liver mass, and multiple lung nodules. Further scans showed the kidney mass was a cyst. High-resolution lung scans revealed seven to eight nodules. CT-guided liver biopsy was inconclusive. PET scan was negative. Surgeons performed video-aided thoracoscopy, collapsing part of his lung to remove three small lung sections. He awoke after five hours of surgery with a chest tube, bladder catheter, central venous line, arterial catheter, spinal catheter, oxygen, heparin, prophylactic antibiotics, and patient-controlled narcotics. Five weeks before he returned to near-normal function, except for permanent rib pain from surgically interrupted nerves. The diagnosis: histoplasmosis — a common, usually asymptomatic fungal exposure.²,²³
38% of CT scans in some clinical settings are ordered for legal protection rather than clinical necessity. Only 2.2% of defensively ordered scans change patient management. Physicians who own imaging facilities order twice as many CT scans as those without financial stakes.²¹
The positive result that escalates into iatrogenic harm.
The next three screenings illustrate what happens after a positive result. Each programme has its own version of the cascade, but the structure is consistent: the abnormal finding triggers a sequence of procedures whose cumulative harm to the well far exceeds any benefit to the few who genuinely had the disease being screened for.
7. PSA Testing
Richard Ablin, who first identified a prostate-specific antigen in 1970, called the use of PSA for population screening a “profit-driven public health disaster” in a New York Times op-ed in 2010.²⁴ He wrote against the screening test most associated with his name for the rest of his career. The screening continued.
PSA is prostate-specific, not cancer-specific. The protein is produced by all prostate tissue — cancerous, enlarged, inflamed, and normal. An elevated PSA can mean prostate cancer. It can also mean benign prostatic hyperplasia, prostatitis, recent ejaculation, a urinary tract infection, or simply a larger prostate. No PSA threshold reliably separates cancer from non-cancer, and no threshold separates cancers that will kill from cancers that will not.²⁵
The threshold of 4.0 ng/mL was, by the account of New York Times reporting, chosen “just sort of arbitrarily.” William Catalona’s 1991 New England Journal of Medicine paper established it without reporting false positive rates — a basic requirement for any screening test.²⁵,²⁶ The world adopted the number.
75% of men with elevated PSA do not have cancer. Between 30 and 100 men are overdiagnosed and overtreated for every life saved.²⁵ The 2012 Prostate Cancer Intervention Versus Observation Trial (PIVOT) and the Scandinavian Prostate Cancer Group Study found no significant survival benefit from radical prostatectomy compared to watchful waiting.²⁵ The surgery causes permanent urinary incontinence in 20–30% of men and erectile dysfunction in 60–80%.²⁵ Active surveillance is appropriate for roughly 99% of low-risk cases.²⁵
30 million American men are screened each year. The screening triggers approximately one million biopsies. At least 750,000 of those biopsies find no cancer. The programme generates $3 billion annually.²⁵ When the US Preventive Services Task Force recommended against routine screening in 2012, urology associations mobilised lobbying efforts to preserve the status quo.
The PSA cascade leads to the biopsy. Standard transrectal biopsy routes 10–18 needles through the rectal wall into a sterile organ. The needle carries with it the bacteria living in the rectum. Published infection rates after transrectal biopsy reach 5.4%. Sepsis rates range from 0.2% to 9.4% depending on the setting. Between 50,000 and 150,000 men are hospitalised worldwide each year for post-biopsy infection.²⁷
The standard antibiotic prophylaxis is a fluoroquinolone. Approximately 22% of men undergoing this biopsy carry fluoroquinolone-resistant E. coli in their gut flora; the prophylactic antibiotic does not work for one in five men.²⁸ The 2022 GRAM Report in the Lancet estimated that nearly 5 million deaths worldwide in 2019 were closely associated with antimicrobial resistance, with E. coli identified as the most significant contributing organism.²⁹ Transrectal prostate biopsies continue to be performed in this resistance landscape.
A different route exists. Transperineal biopsy enters the prostate through the perineal skin, bypassing the rectum entirely. The 2024 meta-analysis published in Prostate Cancer and Prostatic Diseases found that the transperineal approach reduces infectious complications by 77%.³⁰ The transperineal route has been available for decades. The transrectal route, with its known infection profile, remains the default in most clinics.
The broader complication profile is less dramatic but affects more men. Hematuria. Hematospermia. Rectal bleeding, with severe haemorrhage in up to 1% of cases. Lower urinary tract symptoms in up to 25% post-procedure.²⁷ Tuncel and colleagues found that 41% of men reported erectile dysfunction one month after biopsy, with 15% still affected at six months.³¹ A prostate cancer diagnosis itself, even when made for an indolent cancer that would never have caused symptoms, increases cardiovascular events (relative risk 1.3) and suicide risk (relative risk 2.6) within the first year of diagnosis.³² These outcomes do not appear on the consent form. A 1999 study in Effective Clinical Practice found that 31% of men who received a PSA test were unaware their physician had ordered it; of those who were aware, only 47% recalled any discussion of risks and benefits.³³
Through the Wall: The Prostate Biopsy and What No One Mentions – Unbekoming
9. Pap Smear and HPV Testing
Angela Raffle’s 2003 study in the British Medical Journal calculated the arithmetic of cervical screening. One thousand women must be screened for 35 years to prevent one death from cervical cancer. Of those 1,000 women, 150 will receive a stress-causing test result during those 35 years. About 50 will undergo cancer treatment they did not need. Fifty women treated unnecessarily for every death prevented.³⁴
The cascade from abnormal Pap to LEEP runs like this. A woman with no symptoms is screened. The cytology shows abnormal cells. She receives a letter or a call. The words used vary; the message is consistent: something is wrong, further investigation is needed. The waiting period is filled with anxiety, internet searches, and the imagining of worst cases. She undergoes colposcopy. Tissue is removed for biopsy. The cervix has nerve endings; the biopsy is painful, with bleeding and cramping. If the pathology shows precancerous changes, treatment is recommended — typically LEEP (loop electrosurgical excision procedure) or cone biopsy. A portion of the cervix is cut away.²
The harm extends to future pregnancies. LEEP and cone biopsy shorten and weaken the cervix. The woman who underwent the procedure is at increased risk of preterm birth in subsequent pregnancies. Her premature infant may require neonatal intensive care, which initiates its own cascade. A screening test administered to an asymptomatic woman has produced not only her own anxiety, procedures, and tissue loss, but increased risk to a future child.²
The new HPV DNA testing — adopted as first-line screening in Australia in 2017 and increasingly in the United States — finds the marker that most sexually active women carry. The Pap looked for abnormal cells. The HPV DNA test looks for sequences attributed to HPV. The yield of positives expands accordingly. Over 99% of those who test positive for HPV markers never develop cervical cancer.² Switching from cytology to PCR-based HPV testing broadens the pool of positives feeding the treatment cascade rather than improving the discrimination of the test.
The HPV Lie: Pap Smears, Gardasil, and a Cancer Caused by Something Else – Unbekoming
Beyond the Threshold: When the Marker Is the Construct
The first nine entries indict screening on the establishment’s own data — the studies, the trials, the autopsy reservoirs, the conflicts of interest disclosed in the papers themselves. The next three entries ask something deeper: whether the marker the test detects has any necessary connection to the disease the test claims to predict, or whether the marker itself is an artefact of a methodology that produces what it looks for.
Group D — Tests That Measure Nothing Real
The marker is a construct.
10. PCR
Kary Mullis won the 1993 Nobel Prize in Chemistry for inventing the polymerase chain reaction. He spent much of the remainder of his career warning that PCR should not be used for diagnostic purposes. “PCR is just a process that allows you to make a whole lot of something out of something,” Mullis said in 1997. “It doesn’t tell you that you are sick, or that the thing that you ended up with was going to hurt you or anything like that.” In another formulation: “With PCR, if you do it well, you can find almost anything in anybody.”³⁵
PCR doubles the targeted nucleotide sequence with each cycle. After 20 cycles, a millionfold amplification. After 30 cycles, a billionfold. At 40 cycles, a trillionfold.³⁵ The MIQE guidelines — the internationally recognised standard for PCR methodology — state that “Cq values higher than 40 are suspect because of the implied low efficiency and generally should not be reported.”³⁶ Harvard epidemiologist Michael Mina, quoted in the New York Times in August 2020, said he would set the threshold at 30 or even less.³⁷ The Corman-Drosten protocol, which became the basis for COVID-19 PCR testing worldwide, used 45.³⁸
The 2006 Dartmouth-Hitchcock incident demonstrated the mechanism in miniature. Hospital staff developed a persistent cough. A rapid molecular test was deployed. 142 staff tested positive for pertussis. Nearly 1,000 were taken off work. Thousands received antibiotics. 3,599 doses of pertussis vaccine were administered. By year’s end, the established gold-standard culture results returned. Not a single case of pertussis was confirmed. The outbreak had been manufactured by the test.³⁵
In May 2020, Tanzania’s President John Magufuli submitted samples from a papaya, a quail, and a goat to the national laboratory under false names. The papaya and the goat tested positive for COVID-19.³⁵ The 27 different PCR test manufacturers examined in Dutch court proceedings all carried the same product disclaimer: “Research Use Only (RUO), not for diagnostic purposes.”³⁵
The WHO’s August 2020 case definition completed the circle: “a person with laboratory confirmation of COVID-19 infection, irrespective of clinical signs and symptoms.”³⁵ A person with no symptoms was a confirmed case of disease on the basis of a biochemical reaction in a laboratory.
The antibody test inverts traditional immunology. The presence of antibodies was historically interpreted as evidence of recovery and protection: the body had encountered something, responded to it, and was now resistant. HIV testing reinterpreted a positive antibody result — for the first time in the history of immunology — as evidence of an active, ongoing, deadly infection rather than a successful response.³⁵
The reliability of the reinterpretation depends on whether the test detects antibodies specific to the claimed agent. The HIV antibody test manufacturer’s insert states: “There is no recognized standard for establishing the presence or absence of antibodies to HIV-1 and HIV-2 in human blood.”³⁵ The German weekly Die Woche ran a headline calling this “The AIDS Test Lottery,” reporting that “the antibody tests do not measure what they should: HIV infection. They also react to people who have overcome a tuberculosis infection.”³⁵
Nancy Banks compiled a list of more than sixty conditions known to cause false-positive HIV antibody results — kidney failure, tuberculosis, flu, flu vaccination, tetanus vaccination, malaria, haemophilia, leprosy, and pregnancy in women who have given birth multiple times.³⁹ The proteins in the test, Banks writes, “are cellular in origin and are not specific to HIV.” The calibration was circular: proteins that caused the strongest reaction in seriously ill AIDS patients were selected to define the test. That those proteins had any connection to a retrovirus of any type was never independently established.³⁵
The monoclonal antibodies that became the diagnostic industry’s stock in trade were developed in 1975 through hybridoma technology — fusion of cancerous myeloma cells with mouse spleen cells. These are laboratory-manufactured chimeras that exist nowhere in nature. Harvard’s Clifford Saper has confirmed that they bind indiscriminately to similar protein sequences rather than to a single specific target.⁴⁰ Children born with agammaglobulinaemia, who produce none of what immunology calls antibodies, recover from illness normally.⁴⁰ The British Medical Research Council’s 1950 Report #272 found no correlation between antibody count and susceptibility to diphtheria.⁴⁰
The antibody test is the mechanism by which a healthy person becomes a sick one on paper. It measures cross-reactive binding to uncharacterised proteins and reports the binding as specific recognition of a pathogen.
The Antibody Deception: Invisible Enemies, Visible Lies – Unbekoming
12. BRCA Testing and Prophylactic Mastectomy
In 1994, Yoshio Miki and colleagues published in Science the identification of a gene they named BRCA1, associated with breast cancer in selected families.⁴¹ The 80–87% lifetime risk figure that drives prophylactic mastectomy decisions today derives from families chosen for inclusion because they had extreme cancer clustering — six, eight, ten cases across generations. This is ascertainment bias. A 2007 simulation analysis in the Journal of Medical Genetics quantified its magnitude: risk estimates from clinically ascertained families are inflated by a factor of two to three.⁴² A 2019 study in the European Journal of Human Genetics found the bias to be pervasive and unacknowledged.⁴³ The corrected estimates were rarely communicated to women making surgical decisions.
35–55% of BRCA variant carriers never develop breast cancer. The papers themselves document women carrying clearly “deleterious” mutations who lived to age 80 without malignancy.⁴¹ Compare this with Huntington’s disease, the case mainstream genetics treats as definitive — penetrance reportedly approaching 100% in carriers of the expanded repeat. A sequence variant that fails to produce the disease in half its carriers cannot be the cause of the disease; at most, it is a correlate in pre-selected families.
The 2002 BMJ study by Metcalfe and colleagues examined women who had already undergone prophylactic bilateral mastectomy after BRCA testing. Most overestimated their cancer risk by more than 90% compared with computer-generated estimates.⁴⁴ Twenty-two of seventy-five women believed their risk was 100%. The eighteen women with the lowest computed risk — those with limited family history — believed their risk was highest, averaging 80% when the models gave 12%. Their belief was wrong by a factor of seven. The machinery that produced the belief — the testing, the counselling, the risk communication — failed them. They removed healthy breasts.
The original BRCA papers carry conflict-of-interest disclosures. The race to identify the genes was explicitly a race to patent them. Myriad Genetics won and held a monopoly on the test until the 2013 Supreme Court ruling in Association for Molecular Pathology v. Myriad Genetics.⁴⁵ At peak, BRCA testing alone generated over $500 million annually. Preventive surgeries, surveillance, and PARP inhibitors added billions.
Healthy women with no symptoms are routed toward mastectomy and oophorectomy on the basis of a probability inflated by ascertainment bias, applied to laboratory markers whose causal connection to the cancer has never been established outside the families originally selected for clustering. They are not given the corrected numbers. They are not told that 35–55% of carriers never develop the disease. They are told they have a gene that causes cancer, and they are routed to the operating theatre.
The BRCA Gene and the Women Who Lost Their Breasts to a Hypothesis – Unbekoming
What the Twelve Have in Common
Twelve tests. Four mechanisms. One output: more patients.
The threshold-manipulation group converts the well into the sick by lowering the cutoff. The drug to treat the new diagnosis is manufactured by the company whose representative sat on the panel that lowered the cutoff. The body is unchanged.
The overdiagnosis group finds conditions that exist by the textbook definition but would never have caused symptoms or death. The mammogram finds DCIS that would have resolved or remained dormant. The colonoscopy finds polyps that were never destined to become cancer. The CT scan finds incidentalomas that lead to thoracic surgery for histoplasmosis.
The cascade group illustrates what a positive result produces. The PSA leads to the biopsy that leads to the sepsis that leads to the radical prostatectomy that leads to the incontinence and impotence — for cancers that, in autopsy series, are present in 70% of men over 80 and kill 3%. The Pap smear leads to the colposcopy that leads to the LEEP that leads to the preterm birth in a future pregnancy. The biopsy needle is the test as injury.
The marker-as-construct group asks the deeper question of whether the test detects what it claims to detect. PCR amplifies fragments and is read as detection of a whole organism it never isolates. The antibody test picks up cross-reactive binding and reports it as specific recognition. The BRCA test identifies a correlate in pre-selected families and frames it as a deterministic cause.
Each of these tests was developed for a specific clinical purpose: PSA to monitor men already diagnosed with prostate cancer, mammography to investigate palpable breast lumps, colonoscopy to assess symptomatic patients. They worked reasonably well within that scope. Repurposed to screen the asymptomatic, on the intuition that earlier detection must help, they fail because most of what they find is pseudodisease and the cascades they trigger produce harm exceeding any benefit to the few with genuine disease.²
The reservoir is vast. Seventy percent of men in their seventies harbour prostate cancer at autopsy. Up to 39% of middle-aged women show evidence of breast cancer at autopsy. Polyps are present in half of older colons. Thyroid cancer appears in nearly every carefully examined thyroid.² Every screening test dips into this reservoir. Every person pulled from it becomes a patient who cannot benefit from treatment, because they were never at risk.
The financial architecture is consistent across the catalogue. Colonoscopy generates $4 billion annually in the United States.³ PSA produces $3 billion.²⁵ CT scanning is a multi-billion-dollar industry.²¹ The DCIS treatment cascade — surgery, radiation, follow-up — runs to tens of thousands of dollars per case across hundreds of thousands of cases.¹⁸ BRCA testing exceeded $500 million annually at peak; the downstream surgeries and PARP inhibitors add billions. Each abnormal result triggers a sequence of follow-up procedures that generates more revenue. No conspiracy is required — only that every participant follow their own incentives.
The system is sustained, in large part, by the people it overdiagnosed. Every person overtreated for pseudodisease becomes, in their own telling, a survivor. They believe the screening saved their life, and they say so — to their families, to their neighbours, at fundraisers, and before parliaments. The screening programmes’ most effective advocates are the women whose healthy breasts were removed for a non-progressing DCIS, the men whose prostates were taken out for indolent cancers that would never have killed them, the people who were treated for a disease they never had and now organise their identity around the rescue. They are not lying. The framework that taught them to be grateful cannot acknowledge their mistake without dismantling itself.
How to Explain This to a Six-Year-Old
Some grown-ups have machines that look inside your body to find things that might be dangerous. They say finding things early is good, and going to the doctor sounds safe.
Here is what they don’t tell you. The machines find lots of small things that were never going to hurt you. Sometimes they find nothing at all and say they found something. Sometimes they find a piece of something and pretend it is the whole bad thing.
Once the machine says it found something, the grown-ups cut it out, or give you medicine to fight it, or make you come back every year to check. The cutting and the medicine often hurt you more than the thing would have.
The grown-ups also have a rule about what counts as sick. They get to change the rule. Every few years they change it so that more people are called sick. The people who change the rule are often paid by the companies that sell the medicine for being sick.
You can feel fine on Monday and be called sick on Tuesday, and nothing inside you changed. Only the rule changed.
Closing
The body that was well on Monday is a patient on Tuesday. Nothing inside it changed. The number on the chart changed.
A committee lowered a cutoff. A scan found a shadow. A biopsy went through the wall and brought back what it always brings back. A PCR amplified a fragment 35 trillion times and the result was labelled detection of a virus. A sequence variant labelled BRCA1, present in hundreds of thousands of women, was assigned a probability inflated by ascertainment bias and then offered as the basis for removing healthy breasts.
The twelve tests are not twelve separate stories. They are one story in twelve forms — the conversion of the well into the patient. The conversion is achieved through thresholds set by people who profit when the threshold moves; through overdiagnosis of conditions that would never have mattered; through cascades that begin with a positive result and end in the operating theatre or the morgue; and through markers whose existence, as the test claims them, is itself unverified.
The screened do not live longer than the unscreened. The trials are explicit on this point. The benefit the programmes advertise is disease-specific mortality; the number they bury is all-cause mortality. Moving the first without moving the second relocates death rather than preventing it.
The information needed to see this is not behind a paywall. It sits in the journals the physicians ordering these procedures subscribe to and cite — the NEJM, the BMJ, JAMA, the Cochrane reviews. It appears in the disclosures attached to the original papers, the financial filings of the companies that hold the patents, the consent forms no one reads aloud, the package inserts no one is handed, and the policy documents no one quotes back at the practice.
The document exists. The data exists. Most patients who go through these procedures never see them.
References
Bretthauer M, Løberg M, Wieszczy P, et al. Effect of colonoscopy screening on risks of colorectal cancer and related death. New England Journal of Medicine. 2022;387(17):1547–1556.
Welch HG. Should I Be Tested for Cancer? Maybe Not and Here’s Why. University of California Press, 2004. Welch HG, Schwartz L, Woloshin S. Overdiagnosed: Making People Sick in the Pursuit of Health. Beacon Press, 2011.
Source materials on colonoscopy screening, including: Bretthauer et al. (2022), as in reference 1; Gastroenterology (2019) on iatrogenic tumour seeding via colonoscope; Canadian population study of 97,204 outpatient colonoscopies on complication rates; Yoho R. Butchered by Healthcare, on procedure economics.
Lenzer J. Majority of panelists on cholesterol guidelines have current or recent ties to drug industry. BMJ. 2004;328(7452):8. See also Abramson J, Wright JM. Are lipid-lowering guidelines evidence-based? The Lancet. 2007;369(9557):168–169.
Kanis JA, Melton LJ III, Christiansen C, Johnston CC, Khaltaev N. The diagnosis of osteoporosis. Journal of Bone and Mineral Research. 1994;9(8):1137–1141. WHO Study Group on Assessment of Fracture Risk. Assessment of fracture risk and its application to screening for postmenopausal osteoporosis. WHO Technical Report Series 843, 1994.
Genuth S, Alberti KG, Bennett P, et al. Follow-up Report on the Diagnosis of Diabetes Mellitus. Diabetes Care. 2003;26(11):3160–3167.
Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults. Journal of the American College of Cardiology. 2018;71(19):e127–e248.
Source materials on bisphosphonates and bone density, drawing on Cowan T, clinical writing and webinars; Dean C. Death by Modern Medicine; and internal Merck communications regarding Fosamax marketing as discussed in The Architecture of Deception.
Shane E, Burr D, Abrahamsen B, et al. Atypical subtrochanteric and diaphyseal femoral fractures: Second report of a task force of the American Society for Bone and Mineral Research. Journal of Bone and Mineral Research. 2014;29(1):1–23.
Khan AA, Morrison A, Hanley DA, et al. Diagnosis and management of osteonecrosis of the jaw: a systematic review and international consensus. Journal of Bone and Mineral Research. 2015;30(1):3–23.
Kendrick M. The Great Cholesterol Con: The Truth About What Really Causes Heart Disease. John Blake Publishing, 2008. Kendrick M. The Clot Thickens: The Enduring Mystery of Heart Disease. Columbus Publishing, 2021. Ravnskov U. The Cholesterol Myths. NewTrends Publishing, 2000. MRFIT data and Crestor labelling as discussed in these works.
Ramsden CE, Zamora D, Majchrzak-Hong S, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968–73). BMJ. 2016;353:i1246. Ramsden CE, Zamora D, Leelarthaepin B, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ. 2013;346:e8707.
Abramson JD, Rosenberg HG, Jewell N, Wright JM. Should people at low risk of cardiovascular disease take a statin? BMJ. 2013;347:f6123.
McCreight LJ, Bailey CJ, Pearson ER. Metformin and the gastrointestinal tract. Diabetologia. 2016;59(3):426–435.
Source materials on gestational diabetes thresholds and postpartum glucose surveillance from Medicalized Motherhood, including current ACOG and ADA screening protocols.
Miller AB, Wall C, Baines CJ, Sun P, To T, Narod SA. Twenty-five year follow-up for breast cancer incidence and mortality of the Canadian National Breast Screening Study: randomised screening trial. BMJ. 2014;348:g366.
Gøtzsche PC, Jørgensen KJ. Screening for breast cancer with mammography. Cochrane Database of Systematic Reviews. 2013;6:CD001877.
Source materials from Breast Cancer: What They Didn’t Tell You and The Screening Trap, drawing on Welch HG and colleagues on DCIS overdiagnosis; BMJ 25-year follow-up (Miller et al. 2014); and false-positive rate analyses from US and UK screening programs.
Berrington de González A, Reeves G. Mammographic screening before age 50 years in the UK: comparison of the radiation risks with the mortality benefits. British Journal of Cancer. 2005;93(5):590–596. See also: Pijpe A, Andrieu N, Easton DF, et al. Exposure to diagnostic radiation and risk of breast cancer among carriers of BRCA1/2 mutations: retrospective cohort study (GENE-RAD-RISK). BMJ. 2012;345:e5660.
Smith-Bindman R, Chu PW, Azman Firdaus H, et al. Projected lifetime cancer risks from current computed tomography imaging. JAMA Internal Medicine. 2025.
Source materials from The Screening Trap, including Taiwanese registry analyses of CT-associated cancer risk; defensive medicine ordering rates; self-referral ordering studies; and Cedars-Sinai radiation overexposure incident (2008–2009).
Pearce MS, Salotti JA, Little MP, et al. Radiation exposure from CT scans in childhood and subsequent risk of leukaemia and brain tumours: a retrospective cohort study. The Lancet. 2012;380(9840):499–505.
Welch HG. Should I Be Tested for Cancer? Maybe Not and Here’s Why, on the Emory University radiologist case of incidentaloma cascade following virtual colonoscopy.
Ablin RJ. The Great Prostate Mistake. The New York Times. March 9, 2010.
Source materials from The PSA Trap and The Screening Trap, drawing on Catalona WJ et al. (1991), New England Journal of Medicine, original PSA threshold paper; Wilt TJ et al. PIVOT trial, NEJM 2012; Bill-Axelson A et al. Scandinavian Prostate Cancer Group Study; and US Preventive Services Task Force recommendation statements.
Catalona WJ, Smith DS, Ratliff TL, et al. Measurement of prostate-specific antigen in serum as a screening test for prostate cancer. New England Journal of Medicine. 1991;324(17):1156–1161.
Loeb S, Vellekoop A, Ahmed HU, et al. Systematic review of complications of prostate biopsy. European Urology. 2013;64(6):876–892.
Taylor AK, Zembower TR, Nadler RB, et al. Targeted antimicrobial prophylaxis using rectal swab cultures in men undergoing transrectal ultrasound guided prostate biopsy is associated with reduced incidence of postoperative infectious complications and cost of care. Journal of Urology. 2012;187(4):1275–1279. See also: Taylor S, Margolick J, Abughosh Z, et al. Ciprofloxacin resistance in the faecal carriage of patients undergoing transrectal ultrasound guided prostate biopsy. Journal of Urology. 2011 (PMID:21958149) — the source for the ~22% fluoroquinolone-resistance prevalence in gut flora prior to transrectal biopsy.
Antimicrobial Resistance Collaborators. Global burden of bacterial antimicrobial resistance in 2019: a systematic analysis. The Lancet. 2022;399(10325):629–655.
Wolff EM, Tafuri A, Mazzone E, et al. Infectious complications following transperineal prostate biopsy with or without periprocedural antibiotic prophylaxis — a systematic review including meta-analysis. Prostate Cancer and Prostatic Diseases. 2024. See also: Hu JC, Tosoian JJ, Qi J, et al. Transperineal vs transrectal prostate biopsy — the PREVENT randomized clinical trial. JAMA Oncology. 2024;10(10):1590–1593.
Tuncel A, Toprak U, Balci M, et al. Impact of transrectal ultrasound-guided prostate biopsy on erectile function in patients with lower urinary tract symptoms. Journal of Andrology. 2008;29(3):344–348.
Fang F, Keating NL, Mucci LA, et al. Immediate risk of suicide and cardiovascular death after a prostate cancer diagnosis: cohort study in the United States. Journal of the National Cancer Institute. 2010;102(5):307–314.
Federman DG, Goyal S, Kamina A, Peduzzi PN, Concato J. Informed consent for PSA screening: does it happen? Effective Clinical Practice. 1999;2(4):152–157.
Raffle AE, Alden B, Quinn M, Babb PJ, Brett MT. Outcomes of screening to prevent cancer: analysis of cumulative incidence of cervical abnormality and modelling of cases and deaths prevented. BMJ. 2003;326(7395):901.
Bailey M, Bailey S. The Final Pandemic: An Antidote to Medical Tyranny. 2022. Engelbrecht T, Köhnlein C, Bailey S, Bailey M, Scoglio S. Virus Mania. 3rd English Edition, 2021. Mullis K. “Corporate Greed & AIDS” talk, Santa Monica, California, 1997. Multiple Mullis quotations on PCR limitations as documented in these sources.
Bustin SA, Benes V, Garson JA, et al. The MIQE guidelines: minimum information for publication of quantitative real-time PCR experiments. Clinical Chemistry. 2009;55(4):611–622.
Mandavilli A. Your coronavirus test is positive. Maybe it shouldn’t be. The New York Times. August 29, 2020. Quoting Michael Mina, Harvard T.H. Chan School of Public Health.
Corman VM, Landt O, Kaiser M, et al. Detection of 2019 novel coronavirus (2019-nCoV) by real-time RT-PCR. Eurosurveillance. 2020;25(3):2000045.
Banks NT. AIDS, Opium, Diamonds, and Empire: The Deadly Virus of International Greed. iUniverse, 2010.
Stone M. The Antibody Deception: Invisible Y’s That Don’t Exist. Source for the Saper observation on monoclonal antibody binding; on agammaglobulinaemia recovery; and on British Medical Research Council Report #272 (1950).
Miki Y, Swensen J, Shattuck-Eidens D, et al. A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1. Science. 1994;266(5182):66–71.
Goldgar D, Venne V, Conner T, Buys S. BRCA phenocopies or ascertainment bias? Journal of Medical Genetics. 2007;44(8):e86.
Ranola JMO, Tsai GJ, Shirts BH. Exploring the effect of ascertainment bias on genetic studies that use clinical pedigrees. European Journal of Human Genetics. 2019;27(12):1800–1807.
Metcalfe KA, Liede A, Hoodfar E, Scott A, Foulkes WD, Narod SA. An evaluation of needs of female BRCA1 and BRCA2 carriers undergoing genetic counselling. Journal of Medical Genetics. 2000;37(11):866–874. Metcalfe K, Narod SA, et al. Women who undergo prophylactic bilateral mastectomy overstate risk of cancer. BMJ. 2002;325(7369):921.
Association for Molecular Pathology v. Myriad Genetics, Inc., 569 U.S. 576 (2013).
Sudden Infant Death Syndrome is officially defined as “the sudden death of an infant under one year of age, which remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of the clinical history.”¹
By its own definition, it is a non-explanation. A baby cannot be diagnosed with SIDS while alive. SIDS cannot kill a baby. The category exists to receive deaths whose cause cannot be officially acknowledged.
Before 1969, this category did not exist. Before organized vaccination programs expanded in the 1960s, what was then called crib death was so rare that it was not mentioned in infant mortality statistics.² The term Sudden Infant Death Syndrome was created in 1969 in response to a rise in unexplained infant deaths that coincided with expanded vaccination campaigns. By 1972, SIDS had become the leading cause of post-neonatal mortality in the United States, the leading cause of death between 28 days and one year of age.³ A category that had not existed three years earlier had become the dominant verdict on dead infants.
There are 130 official ways for an infant to die, as categorized in the International Classification of Diseases. There is no official way to die from a vaccine. That classification was removed in 1979.⁴ Medical examiners working since then have been given a manual that contains every imaginable cause of infant death except the one that the public record, the manufacturer’s own clinical trial data, and a half-century of clustering evidence all point to.
Before SIDS Existed
The 1967 Pediatrics review by Maria Valdes-Dapena examined the world literature on sudden unexpected infant deaths from 1954 to 1966. The review documented a rising phenomenon in industrialized nations, with the author professing herself “woefully ignorant” of the cause.⁵ The deaths were already occurring. They had not yet been categorized.
A causal connection to vaccination was made early. Within fifteen years of the Valdes-Dapena review, William Torch presented findings at the 1982 American Academy of Neurology Conference identifying DPT vaccination as a potential cause of the deaths the new category had been created to receive.⁶ The category was new. The deaths were not. What was new was the schedule that produced them and the institutional naming that made them legible only as a syndrome of unknown origin.
In 1969, when the term Sudden Infant Death Syndrome was created, the United States was four years past the introduction of the measles vaccine and five years past the licensing of the oral polio vaccine. DPT was being administered at expanded coverage. Mumps and rubella vaccines had been licensed. The childhood schedule was growing rapidly. Pre-1969, organized vaccination of infants was limited; crib death was rare and unstratified.² The temporal alignment between the expansion of the schedule and the creation of the category to absorb the resulting deaths went unnoticed because nobody was looking. There was no institutional reason to look.
In 1973, the National Center for Health Statistics, operated by the CDC, created a new cause-of-death category specifically for SIDS.² Certifiers were required to use it. By the late 1970s, the institutional infrastructure was nearly complete. What remained was the elimination of the alternative.
The 1979 revision of the International Classification of Diseases eliminated all cause-of-death classifications associated with vaccination.⁴ Previous versions of the ICD had listed “prophylactic inoculation and vaccination” as a separate cause-of-death category, with subcategories for deaths caused by specific vaccines. The 1979 revision and every subsequent update removed these. Since 1979, medical certifiers have had no code to assign vaccine-related deaths to. They are required, by the structure of the manual they use, to assign the death to a different category.
The asymmetry this produces is striking. The same federal government that maintains the ICD code structure also operates the National Vaccine Injury Compensation Program, established by the National Childhood Vaccine Injury Act of 1986. As of May 2021, the Vaccine Injury Compensation Program had awarded more than $4.5 billion in compensation for vaccine injuries and deaths.⁷ The federal government, in one capacity, compensates families for deaths caused by vaccines. The same federal government, in another capacity, removes the cause-of-death code that would allow those deaths to be officially documented in mortality statistics. The compensation requires the cause; the mortality statistics deny it. Both are operated by the same institution.
This structure has been in place for forty-six years. Every infant death that has occurred in temporal proximity to vaccination since 1979 has been recorded under a different code than the one that would name what happened. SIDS, “accidental suffocation,” “unknown cause,” “unspecified viral disease,” “diseases of the blood,” “cardiac arrest,” and “shaken baby syndrome” are among the 130 categories that have absorbed these deaths.² The codes operate as containers. The volume of what they contain has grown as the schedule has grown.
The Pattern That Should Not Exist
The strongest single piece of evidence for what SIDS contains is the temporal distribution of infant deaths relative to vaccination. Neil Miller’s 2021 analysis of the Vaccine Adverse Event Reporting System database, published in Toxicology Reports, examined 2,605 infant deaths reported between 1990 and 2019.⁸ The findings were specific and statistically definitive.
Of all reported infant deaths, 58% occurred within three days of vaccination, and 78.3% occurred within seven days. For the subset of deaths labeled SIDS specifically, 51% occurred within three days and 75.5% within seven days. The highest single-day count was day two after vaccination, with 760 reported infant deaths. The expected count for any single day if the deaths were randomly distributed across the sixty-day post-vaccination window analyzed would be approximately 43. Day two showed a 69-fold elevation over chance.⁸
The statistical significance was p < 0.00001. The probability that the observed clustering occurred by chance is less than one in 100,000.
In concrete terms: each day represents 0.27% of the year, and a seven-day window represents 1.9% of the year. If infant deaths bore no temporal relationship to vaccination, the proportion of deaths falling within seven days of a vaccination event would approximate the proportion of days the window represents. The observed figure is 78.3%. That is forty-one times the baseline expectation. The biological mechanism describes how the deaths occur. The temporal density demonstrates that they occur because of the intervention they cluster around.
The pattern was identified before Miller’s analysis. In 1982, William Torch presented data on seventy SIDS cases reported in Nevada. 6.5% of infants died within twelve hours of DPT vaccination, 13% within twenty-four hours, 26% within three days, and 37%, 61%, and 70% within one, two, and three weeks respectively.⁶ The clustering was visible in 1982. It has been visible for forty-three years.
In 1987, Alexander Walker of the Boston University Medical Center and the Harvard School of Public Health published findings in the American Journal of Public Health on US children born between 1972 and 1983 who received the diphtheria-tetanus-whole cell pertussis vaccine. Infants weighing more than 2,500 grams at birth experienced 7.3 times more SIDS within three days of DTP vaccination than during a period starting thirty days after vaccination. The 95% confidence interval ranged from 1.7 to 31.⁹ The lead author was affiliated with Harvard and the finding was published in a major public health journal. The institutional reaction was silence.
The manufacturer’s own data confirms what the epidemiological data shows. A confidential GlaxoSmithKline clinical study report on the hexavalent vaccine, made publicly available by an Italian court, documented that 65 of 67 sudden infant deaths occurring during the trial (97%) occurred within the first ten days after vaccination. Just two deaths occurred in the next ten days.¹⁰ Across the manufacturer’s own data, 62.7% of sudden infant deaths occurred within three days of vaccination and 89.6% within seven days. Six of the eight sudden deaths in children during their second year of life occurred within three days of vaccination.¹⁰ The manufacturer concluded that the vaccine did not increase the risk of sudden death. European regulators accepted the conclusion.
Independent autopsy findings confirm the relationship at the level of individual cases. Zinka and colleagues, publishing in Vaccine in 2006, documented six cases of sudden infant death occurring within forty-eight hours of hexavalent vaccination. Autopsies showed unusual neuropathology in the brains of these infants. The authors calculated a 13-fold increase in the risk of sudden death after hexavalent vaccination compared with an earlier period before the multi-dose vaccine was available.¹¹ D’Errico and colleagues, in 2008, examined a three-month-old infant who died within twenty-four hours of hexavalent vaccination. They concluded that acute respiratory failure due to post-vaccination shock was the cause of death.¹² Ottaviani and colleagues, in Virchows Archiv in 2006, documented a separate case of sudden infant death shortly after hexavalent vaccination, identifying the vaccine as the likely trigger of the lethal outcome.¹³
In 1978 and 1979, eleven infants in Tennessee died within eight days of DPT vaccination. Five died within twenty-four hours. Nine of the eleven had received their vaccine from the same lot, Wyeth Lot #64201.² A subsequent investigation confirmed a greater-than-expected relationship between the lot and the deaths. The FDA initially stated that a causal relationship could not be totally excluded. Later statements walked this back to “experts did not find evidence of a cause-effect relationship.” The CDC ultimately classified the deaths as coincidence.² Internal memos from the manufacturer, surfaced afterward, revealed a new shipping policy: no geographical location would receive all of its DPT vaccine from a single lot, ensuring that any future clustering would be statistically diluted across regions. The structural ability to detect hot lots was deliberately broken.
In a 2017 case before the National Vaccine Injury Compensation Program, the Special Master awarded compensation to the parents of a four-month-old infant who died the day after receiving seven vaccines. The ruling concluded that vaccines “likely did play a critical role in this child’s death” by stimulating inflammatory cytokines that suppressed the respiratory system and prevented normal response to carbon dioxide accumulation.¹⁴ The vaccine court awarded the compensation. The death certificate listed something else.
The Brainstem and the Empty Autopsy
The clustering data demonstrates that the deaths occur. The mechanism explains how, and the convergence of two independent mechanistic accounts on the same anatomical target, the brainstem respiratory control region, also explains why the autopsy finds nothing.
The first account begins with what aluminum does in tissue. Aluminum adjuvants are present in multiple vaccines administered during the first eighteen months of life, including hepatitis B, DTaP, Hib (some formulations), pneumococcal conjugate, and hepatitis A.¹⁵ The total dose of injected aluminum received by a fully vaccinated child has approximately quadrupled since the 1980s, from around 1,000 micrograms by age eighteen months under the schedule in place before the 1986 NCVIA to over 4,000 micrograms today.¹⁵ Aluminum is biopersistent. Gherardi and colleagues, publishing in Frontiers in Neurology in 2015, documented that aluminum hydroxide particles persist at injection sites and undergo slow CCL2-dependent translocation from muscle to brain via macrophage transport.¹⁶ Christopher Exley’s work in 2018 documented elevated aluminum levels in the brain tissue of individuals diagnosed with autism, demonstrating that injected aluminum reaches and persists in the brain.¹⁷ Khan and colleagues in 2013 documented the mechanical pathway of this translocation: biopersistent particles taken up by phagocytes, transported through lymphatic and circulatory routes, deposited in distant tissues including the central nervous system.¹⁸ Yao and colleagues, in 2015, showed that hepatitis B vaccination of postnatal rats modulates hippocampal synaptic plasticity and produces a four-fold elevation in the inflammatory cytokine IL-6, demonstrating that the vaccines themselves, not just isolated aluminum, produce these effects in the developing brain.¹⁹
When an infant receives multiple aluminum-containing vaccines simultaneously, the inflammatory cascade is rapid and substantial. Microglia in the brainstem become activated. Activated microglia release glutamate and other excitotoxic compounds, along with pro-inflammatory cytokines, into the surrounding tissue.²⁰ The brainstem contains the respiratory control center. When microglial activation in this region releases excitotoxins, the infant’s breathing is suppressed. If the suppression is severe enough and sustained enough, the infant stops breathing. The neuropathologist Dr. Douglas Miller, in expert testimony cited in the Vaccine Injury Compensation Program ruling and Neil Miller’s 2021 analysis, described how vaccine-induced inflammatory cytokines act as neuromodulators in the infant medulla, producing an abnormal response to accumulating carbon dioxide and disorganizing respiratory control.⁸
This explains the first part of the autopsy’s silence. The pathologist who examines a baby that has died of inflammatory respiratory failure is looking for visible tissue damage: discrete lesions, hemorrhage, structural anomaly. The mechanism described does not produce visible damage in the timeframe required for death. Microglial activation triggers the excitotoxin release, the respiratory center fails, and the infant dies before any histological signature of the cytokine surge would form.²⁰ The pathologist sees a baby that has stopped breathing for no apparent reason. The cause is dispersed at a biochemical timescale the autopsy cannot resolve.
The second account begins from a different starting point and arrives at the same anatomical region. Andrew Moulden, a Canadian neurologist with PhD-level training in clinical-experimental neuropsychology, developed what he called the Moulden Anoxia Spectrum Syndromes framework.²¹ Moulden’s central observation was that injected substances disrupt the electrostatic stability of blood flow. Aluminum, which carries a positive trivalent charge, has approximately eighty-four times the agglomeration-inducing capacity of sodium. It is, in industrial terms, a flocculant, the same agent used in water treatment plants to cause suspended particles to clump and settle. Injected into human tissue and bloodstream, aluminum produces the same effect: red blood cells, white blood cells, and other formed elements clump together. The blood sludges.
The microcirculation in the brainstem (the network of capillaries supplying the respiratory control region) operates at a scale where red blood cells must pass through capillaries in single file. When the blood sludges, this single-file passage is obstructed. The result is microscopic ischemia: regions of tissue receiving insufficient oxygen because the blood cannot flow through the capillaries that supply them.²¹
The human body has blood pressure receptors. It does not have blood flow receptors.²¹ This anatomical fact is critical. When microcirculation fails at the capillary level but the larger arteries continue to maintain pressure, no warning signal is generated. The brainstem can be suffering ischemic damage in its watershed end-vascular territories (the most poorly supplied regions, including those controlling automatic respiration) while the body’s monitoring systems detect no problem. The damage is, in Moulden’s analysis, sub-clinical to the body itself.
This explains the second part of the autopsy’s silence. The damage Moulden described occurs at the level of the microcirculation, well below the resolution of conventional neuroimaging. There is no infarct visible on MRI. There is no hemorrhage to find. And in death, the body has no blood flow at all. The difference between sludged microcirculation in life and the post-mortem absence of circulation is not detectable by examination of the dead tissue. The lesion is invisible by structural design.
The two accounts converge on a single anatomical target, the brainstem respiratory control region, by different routes. The inflammatory pathway explains why activated microglia in this region kill the infant. The microcirculation pathway explains why ischemia in this region kills the infant. Both are caused by injected aluminum, both produce respiratory arrest, and neither leaves damage detectable at the resolution the autopsy uses to look.
When the official definition of SIDS requires that death “remain unexplained after a thorough case investigation, including performance of a complete autopsy,” the definition is describing a death that occurred via mechanisms structurally invisible to the investigation it requires. The autopsy comes up empty because the investigation tools cannot see what killed the baby. The verdict of “unexplained” is the predictable output of looking for the wrong kind of damage at a scale the instruments were never designed to resolve.
What Happens When You Remove the Cause
The convergent mechanism predicts a specific real-world outcome: if vaccinations are reduced, delayed, or interrupted, the deaths the SIDS category absorbs should decline. The historical and contemporary record contains multiple natural experiments testing this prediction. Each confirms it.
Japan, 1975. Between 1970 and 1974, Japanese authorities documented thirty-seven sudden infant deaths following pertussis vaccinations. In response, the Japanese government raised the age of DPT vaccination from three months to two years.²² The result, documented across the following decade, was dramatic.
Sudden vaccine-related deaths dropped from 1.47 per million doses to 0.15 per million doses, a 90% decline.²² The category of “sudden death” following vaccination, in the analysis of Cherry and colleagues published in Pediatrics, “disappeared following both whole-cell and acellular vaccines when immunization was delayed until a child was 24 months of age.”²² Japan’s overall infant mortality rate across all causes declined from 12.4 to 5.0 per 1,000 live births over the decade following the schedule change, a 60% improvement.²² The Task Force on Pertussis and Pertussis Immunization that produced the report concluded: “It is clear that delaying the initial vaccination until a child is 24 months, regardless of the type of vaccine, reduces most of the temporally associated severe adverse reactions.”²²
The Japanese experiment did not require a placebo group, randomization, or a controlled trial. It was a real-world intervention with a clear before-state and a clear after-state, with vaccination timing as the single variable change between them. The infant mortality decline cannot plausibly be attributed to anything else. The Japanese government delayed vaccination. Fewer babies died.
COVID lockdowns, 2020. During the early lockdown period of 2020, routine well-child visits were canceled or postponed across many jurisdictions, and childhood vaccination rates declined. An analysis comparing infant deaths in Oregon over the first six months of 2020 against the ten-year average documented a 42% drop in infant deaths during the period when lockdowns were in place and well-baby visits were canceled.²³ Similar patterns were documented elsewhere, alongside an unprecedented decline in premature births, which are themselves linked to vaccination during pregnancy.²⁴ The vaccine safety community had predicted, before the data became available, that the lockdowns would produce a once-in-a-generation natural experiment in reduced SIDS, because if vaccines are the cause, reduced vaccination should produce reduced deaths. The data confirmed the prediction.
Florida, 2021. In the year following the lockdown-driven decline in vaccination compliance, Florida’s childhood vaccination rate dropped from 93.4% to 79.3%. All-cause infant mortality under one year of age decreased by 8.93% during the same period, a reversal of the previous year’s trend.²⁵ The single largest variable that changed in Florida between 2020 and 2021 was vaccination compliance. The infant mortality figure moved in the direction the mechanism predicts.
International comparison. A 2011 study comparing infant mortality rates across the thirty-four nations with the lowest rates found a clear correlation between the number of required childhood vaccines and infant mortality.²⁶ The United States, with the largest childhood schedule among industrialized nations, also has among the highest infant mortality rates among industrialized nations.²⁷ A separate analysis comparing vaccine doses across developed nations found a strong association between dose counts and mortality rates.²⁸ Countries that vaccinate more, more often, earlier, lose more babies.
None of these experiments meets the design specifications of a randomized controlled trial. None of them needs to. Japan’s schedule change was real. The lockdowns were real. Florida’s compliance shift was real. The infant mortality figures are public record. Four independent natural experiments, three of them documented within the past five years, all moving in the direction the convergent mechanism predicts.
How the Category Has Mutated
The institutional response to the visible clustering pattern has been to mutate the category rather than investigate the relationship. The SIDS code was never the only container available. As the visibility of vaccine-induced infant death increased, the institutional pressure to disperse those deaths across multiple cause-of-death codes increased correspondingly.
In 1992, the American Academy of Pediatrics formally recommended that infants be placed supine rather than prone during sleep. The Back to Sleep campaign launched two years later, in 1994.²⁹ The campaign came eight years after the 1986 National Childhood Vaccine Injury Act, which had itself been passed in response to congressional hearings in which parents, including Donna Gary, linked DTP vaccination to infant deaths. The Back to Sleep campaign provided an alternative narrative: SIDS was caused by sleep position, not by what was injected into the infant before the sleep occurred.
The SIDS rate appeared to decline. Between 1992 and 2001, the post-neonatal SIDS rate dropped by an average annual rate of 8.6%.² This was presented as a vindication of the sleep-position hypothesis. The numbers told a different story when examined carefully. During the same period, the post-neonatal mortality rate from “suffocation in bed” (ICD-9 code E913.0) increased at an average annual rate of 11.2%.² Sudden, unexplained infant deaths that had been classified as SIDS before the campaign were now being classified as suffocation in bed. The deaths had not declined; the label on the certificate had changed.
The reclassification accelerated. From 1999 through 2015, the US SIDS rate declined 35.8% while infant deaths due to accidental suffocation increased 183.8%.² Approximately 90% of the apparent SIDS decline can be attributed to reclassification rather than reduction.² The category became more porous as institutional pressure to disperse the deaths intensified.
In 2012, the CDC introduced a new umbrella category: Sudden Unexpected Infant Death (SUID), which encompasses SIDS along with deaths attributed to suffocation and unknown causes.²⁹ The same year, the Back to Sleep campaign was rebranded as Safe to Sleep. The two institutional moves arrived together: a broader receiving category for the deaths, and a broader messaging framework for displacing their cause. Deaths that the SIDS code might have captured in isolation could now be distributed across three subcategories under the SUID umbrella, each of which can be reclassified independently as institutional preference dictates.
Safe to Sleep expanded the messaging beyond sleep position to a long list of parental responsibilities: avoidance of soft bedding, prohibitions on bed-sharing, recommendations on breastfeeding, pacifier use, smoke exposure, room temperature, swaddling. The messaging was directed disproportionately at African American communities, where SIDS rates are higher. A 2018 analysis of safe sleep public campaign messaging found that 60% of campaign messages used guilt-based framing, placing responsibility for the death on the parent’s behavior in the hours preceding it.²⁹ The campaign installed a moral framework. Parents who lost infants to sudden death were positioned within that framework as having failed it. The cause they had not been told about, the schedule they had complied with, did not appear in the framework anywhere.
In May 2025, the National Institutes of Health terminated the Safe to Sleep campaign.²⁹ The termination came after the 2020-2022 period documented a 12% rise in sudden infant deaths.²⁹ The campaign had operated in its two forms, Back to Sleep and Safe to Sleep, for over three decades without reducing SIDS deaths in any sustained way; the numbers showed reclassification rather than prevention. Its useful institutional life had ended.
The framework Safe to Sleep installed remained operational after the campaign itself was terminated. In June 2025, parents in Allentown, Pennsylvania were charged with felonies for placing their infants in unsafe sleep positions.³⁰ The Defender, reporting on similar cases, documented police charging parents with felonies after their babies died suddenly in their sleep, based on the parents’ alleged failure to follow supine sleeping guidance.³⁰ The guilt-based moral structure Safe to Sleep had installed in 2012 was now providing the legal basis for criminal prosecution in 2025. The criminalization of parents who have lost infants to deaths the system cannot explain has institutional precedent. Sally Clark, a British lawyer, was convicted in 1999 of murdering both of her infant sons, who had died unexpectedly weeks after receiving routine vaccinations. The conviction was overturned in 2003 after the statistical evidence underpinning the prosecution was discredited. She died of acute alcohol poisoning in 2007, in the aftermath.³¹ Her case is one documented historical instance. The June 2025 prosecutions are the contemporary instance of the same dynamic operating in real time.
The trajectory is consistent. Pre-1969, the deaths exist without a category to receive them. In 1969, the SIDS category is created. In 1979, the alternative cause-of-death code, vaccination, is removed from the ICD. In 1994, the Back to Sleep campaign provides a sleep-position narrative. From 1992 through 2025, deaths are reclassified into suffocation and unknown-cause codes as institutional preference shifts. In 2012, SUID broadens the receiving framework and Safe to Sleep broadens the messaging framework. In 2025, the campaign is terminated as its useful institutional life ends, and parents begin to be prosecuted under the framework the campaign installed.
At every stage, the institutional response has been to adjust the receiving infrastructure rather than investigate what is being received. The category mutates because the underlying deaths cannot stop. The schedule cannot be paused without admitting what it does, and the deaths cannot be officially named without admitting the cause. The mutation of the category is the visible trace of the institutional refusal to do either.
What SIDS Is
The official definition of SIDS describes a death that remains unexplained after thorough investigation. The definition is precise. What it describes is a death whose cause is structurally invisible to the investigation required to confirm the absence of explanation. The category exists to receive what the system cannot officially name.
The category did not exist before 1969. It was created in the same period that the childhood vaccination schedule expanded into the population of infants under one year of age. The 1979 ICD revision then eliminated the alternative cause-of-death code; the 1994 Back to Sleep campaign installed the sleep-position narrative; the 2012 SUID expansion broadened the receiving framework and the Safe to Sleep rebrand broadened the messaging framework alongside it. The 2025 campaign termination ended one phase of the construct, and the June 2025 felony prosecutions began another.
The mechanism is understood. Aluminum adjuvants reach the infant brainstem by macrophage transport and slow translocation. Microglia in the respiratory control region activate; excitotoxins release into the breathing center. The same aluminum, through electrostatic agglomeration, sludges the microcirculation supplying the same anatomical region, producing ischemia. Both pathways suppress the infant’s respiration and produce respiratory arrest. Neither leaves damage visible at the resolution the autopsy uses to look.
The infant who dies of SIDS dies of what was injected and what its body could not clear. The autopsy finds nothing because nothing visible was left to find; the death certificate names something else because the manual contains no code for what happened.
SIDS is the name the system gives to the deaths it has built itself not to see.
How to Explain It to a Six-Year-Old
Imagine grown-ups gave babies a medicine. Some of the babies got really sick after the medicine. A few of them died.
When the grown-ups looked at the babies, they couldn’t find anything wrong with them. The hurt inside was too tiny to see, like a scratch so small you’d need a special magnifying glass for ants to see it.
So the grown-ups said, “We don’t know what happened. It’s a mystery!” And they made up a special name for the mystery. The name was SIDS.
But here’s the thing. The grown-ups do know what happened. They’ve known for a long time. The medicine has something called aluminum in it. Aluminum is the same shiny stuff your sandwich wrap is made of. It’s okay on a sandwich. It’s not okay inside a baby.
The aluminum gets into the part of the brain that tells the baby to breathe. The brain stops working right. The baby stops breathing.
But the grown-ups don’t want to tell anyone, because lots of grown-ups get money from the medicine. So they keep calling it SIDS, the mystery.
When parents started to figure it out, the grown-ups changed the name. They called it “crib death.” Then “SIDS.” Then “SUID.” Now they say the babies suffocated, and sometimes the police take the mommies and daddies to jail, even though they didn’t do anything wrong.
Every time someone gets close to the truth, the grown-ups change the name.
The babies didn’t die from a mystery. They died from the medicine.
SIDS is the name grown-ups use when they don’t want to tell the truth about why a baby died.
References
Standard definition of Sudden Infant Death Syndrome as adopted by the Institute of Medicine and used by the CDC, the American Academy of Pediatrics, and the National Institute of Child Health and Human Development; cited in de Becker, G. (2022). Forbidden Facts.
Miller, N. Z. (2021). “Vaccines and Sudden Infant Death: An Analysis of the VAERS Database 1990–2019 and Review of the Medical Literature.” Toxicology Reports 8: 1324–1335. Historical context including the pre-1969 absence of the category and the post-1979 reclassification patterns.
National Center for Health Statistics, CDC; cited in Miller (2021).
International Classification of Diseases, 9th revision (1979); subsequent revisions ICD-10 and ICD-11; analysis in Miller (2021).
Valdes-Dapena, M. A. (1967). “Sudden and unexpected death in infancy: a review of the world literature 1954–1966.” Pediatrics 39(1): 123–138.
Torch, W. C. (1982). “Diphtheria-Pertussis-Tetanus (DPT) Immunization: A Potential Cause of Sudden Infant Death Syndrome.” Neurology 32(4). Conference abstract, American Academy of Neurology.
Health Resources and Services Administration, National Vaccine Injury Compensation Program statistical data, as of May 2021.
Miller, N. Z. (2021). Toxicology Reports 8: 1324–1335. Full statistical analysis including the day-by-day clustering, the 69-fold elevation on day two, and the p < 0.00001 significance.
Walker, A. M., et al. (1987). “Diphtheria-Tetanus-Pertussis Immunization and Sudden Infant Death Syndrome.” American Journal of Public Health 77(8): 945–951.
GlaxoSmithKline (2012). “Confidential Clinical Study Final Report: Study 113808 (ROTA-075).” Made publicly available by Italian court order.
Zinka, B., Rauch, E., et al. (2006). “Unexplained cases of sudden infant death shortly after hexavalent vaccination.” Vaccine 24(31–32): 5779–5780.
D’Errico, S., Neri, M., et al. (2008). “Beta-tryptase and quantitative mast-cell increase in a sudden infant death following hexavalent immunization.” Forensic Science International 179(2–3): e25–29.
Ottaviani, G., Lavezze, A. M., Matturri, L. (2006). “Sudden infant death syndrome (SIDS) shortly after hexavalent vaccination: another pathology in suspected SIDS?” Virchows Archiv 448: 100–104.
National Vaccine Injury Compensation Program ruling, 2017; cited in Miller (2021) and Thomas, P. (2022). Vax Facts.
Thomas, P. (2022). Vax Facts. Handley, J. B. How to End the Autism Epidemic. Aluminum content data drawn from CDC Vaccine Information Statements and Mitkus, R. J., et al. (2011). “Updated aluminum pharmacokinetics following infant exposures through diet and vaccination.” Vaccine 29(51): 9538–9543.
Gherardi, R., et al. (2015). “Biopersistence and Brain Translocation of Aluminum Adjuvants of Vaccines.” Frontiers in Neurology 6: Article 4.
Mold, M., Umar, D., King, A., Exley, C. (2018). “Aluminium in brain tissue in autism.” Journal of Trace Elements in Medicine and Biology 46: 76–82.
Khan, Z., et al. (2013). “Slow CCL2-dependent translocation of biopersistent particles from muscle to brain.” BMC Medicine 11: 99.
Yao, Z., et al. (2015). Hepatitis B vaccination of postnatal rats modulating hippocampal synaptic plasticity and IL-6 elevation; cited in Handley, J. B. How to End the Autism Epidemic.
Hedley, K., et al. (2022). “Alterations in Brainstem Respiratory Centers following Peripheral Inflammation.” Journal of Neuroimmunology 369. Hoogland, I. C. M., et al. (2015). “Systemic inflammation and microglial activation: systematic review of animal experiments.” Journal of Neuroinflammation 12: 114.
Moulden, A. (2009). “What You Were Never Told About Vaccines.” Interview, VacTruth.com. BrainGuardMD.com archive. Analysis of the MASS framework, zeta potential, and microcirculation pathology.
Cherry, J. D., et al., Task Force on Pertussis and Pertussis Immunization. Pediatrics. Cited in Miller (2021) and Fraser, H. (2010). The Peanut Allergy Epidemic.
Snee, B., comment on A Midwestern Doctor (2022); Oregon infant death analysis comparing first six months of 2020 to the ten-year average.
A Midwestern Doctor. “The Century of Evidence That Vaccines Cause Sudden Infant Deaths.” MidwesternDoctor.com.
Florida Department of Health vaccination compliance data 2020–2021; CDC infant mortality data; analysis cited in A Midwestern Doctor (2022).
Miller, N. Z., Goldman, G. S. (2011). “Infant mortality rates regressed against number of vaccine doses routinely given: is there a biochemical or synergistic toxicity?” Human and Experimental Toxicology 30(9): 1420–1428.
CDC Childhood Immunization Schedule, comparative data 1983 and present; Thomas, P. (2022). Vax Facts; OECD infant mortality comparative data.
“Neonatal, Infant, and Under Age Five Vaccine Doses Routinely Given in Developed Nations and Their Association With Mortality Rates.” Cureus.
Children’s Health Defense (2025). “Media Slam NIH for Axing ‘Safe to Sleep’ Campaign — But Evidence Shows the Program Never Reduced SIDS Deaths.” American Academy of Pediatrics (1992). “Positioning and SIDS.” Pediatrics 89(6): 1120–1126. Salm Ward, T. C., Balfour, G. M. (2018). “Qualitative analysis of infant safe sleep public campaign messaging.” Pediatrics 43(2): 83–91.
The Defender (June 6, 2025). “Their Babies Died Suddenly in Their Sleep. Police Are Charging the Parents With Felonies for Not Placing Infants on Their Backs.” WFMZ Allentown, PA (June 6, 2025). “Parents accused of putting their infants in unsafe sleep positions charged with felonies.”
Sally Clark case (R v Clark, 2003 EWCA Crim 1020). Both sons died unexpectedly in infancy weeks after receiving routine UK childhood vaccinations; the conviction was overturned in 2003 after the statistical evidence presented by Sir Roy Meadow was discredited and previously withheld pathology evidence was disclosed.
A story broadcast and posted by WPLN, Louisville Public Media, claims Tennessee’s black bear population is being threatened by climate change. Data show this is false. Bear populations are growing along with improved conditions for black bears to flourish. The biggest threat to black bears is conflict with humans, which is being driven by population growth, both bears and humans, urban expansion into bear habitat, and poor garbage storage.
The problem with Eggers story is that its headline and lead sentence are woefully misleading. Most of the story’s details are pretty accurate. She notes that before large-scale European occupation and widespread forest clearing, black bears were common across Tennessee. After a sharp decline, bears populations have made a big comeback with an estimated 6,000 bears across the state.
Bear populations are doing so well, they are increasingly being seen in edge communities being developed in formerly wild areas and even in urban areas.
Black bear encounters with people are on the rise in Tennessee, and they are not always […] idyllic […]” writes Eggers. “Bears scrounge through trash, cars and sometimes even homes for an easy source of calories.
“The furry creatures arguably have the best noses in the animal kingdom, 300 times better than people,” Eggers continued. “The trend is, in part, driven by convenience for the bears. They are opportunistic feeders.”
So far, so good, but then the story begins to go off the rails. Eggers notes that rainfall from Hurricane Helene in 2024 caused flooding, knocking down a lot of trees, and then leapt to discuss a current drought in the Great Smoky Mountain national park. Yet neither of these events are historically unique or historically unusual. Flooding and drought, while never the norm, have been common throughout Tennessee’s history, and there is no evidence in the data that hurricanes, droughts, and floods have become more common or severe over time in Tennessee, or in general elsewhere in the United States, as detailed in various Climate at a Glance posts, here, here, and here, for example.
For Tennessee specifically, while rainfall amounts vary regionally across the state, data show no increasing trend in drought numbers or severity since 1895, but rather a modest increase in precipitation. (see the figure, below)
Temperatures in Tennessee have increased very modestly, about 0.5℉ over the past century. This is significantly below the national average rise in temperature and is likely due in large part to the Urban Heat Island effect from the growth of Tennessee’s large and midsized cities. In fact, Tennessee’s maximum high temperature was set and matched on two dates in 1930, more than 90 years of climate change ago.
Concerning forests, the data are clear that urban development and agriculture have replaced forests in some areas. But overall, the amount of forested lands has increased from lows set after initial European settlement, when many forests were cleared for small scale farming and grazing. In fact, forests cover approximately 52 percent of Tennessee, with rebounding coverage over the past 100 years. Natural forest coverage has doubled over the last century from 25 percent.
What’s more, connected forest cover and better precipitation has produced improved ecosystem conditions for bears, including increased animal and plant food sources, which largely explain Tennessee’s growing bear population.
Since modest warming over the past hasn’t made habitat and ecological conditions worse for bears in Tennessee, but rather has improved such conditions, contributing to a growing population, climate change can’t be “threatening” bear survival, as Eggers claims in her WPLN story.
Had Eggers not tried to drag climate change into her WPLN story about problems some Tennesseans are having with bears, she might have written a valuable and interesting story. She could have explained the dangers bears face due to urban expansion, some people’s propensity to think of bears as cute and feeding them, and poor garbage storage – all of which have led to problem bears and human/bear conflicts. Instead, she opened with a misleading, but perhaps attention-grabbing headline, and then wandered off the trail in an effort to feed the narrative popular with the media that “climate change causes everything bad.” In this case, that climate change is harming bears—despite clear evidence the black bear population is flourishing amid climate change. There is no trend or evidence, none at all, suggesting this will change in the foreseeable future.
Psychiatric drugs are the third leading cause of death in the developed world, after heart disease and cancer. The estimate comes from Peter Gøtzsche’s 2022 book Mental Health Survival Kit and Withdrawal from Psychiatric Drugs, and it is built from regulatory data the drug companies tried to keep buried. One drug alone — Zyprexa — was estimated to have killed 200,000 patients up to 2007. In a meta-analysis of placebo-controlled trials covering 5,000 elderly demented patients, one in 100 was dead within ten weeks on a psychosis pill; when Gøtzsche checked the underlying FDA data, the rate doubled, because around half of all deaths in psychiatric drug trials never reach publication. The TIPS study followed 281 first-episode psychosis patients with an average age of 29; within ten years, 12% of them were dead, and the authors mentioned the deaths only in a flowchart of patients lost to follow-up.
Gøtzsche is a specialist in internal medicine, co-founder of the Cochrane Collaboration in 1993, and author of more than 75 papers in the BMJ, the Lancet, JAMA, the Annals of Internal Medicine, and the New England Journal of Medicine. His scientific work has been cited over 150,000 times. He came to psychiatry from outside the speciality — his earlier books include Deadly Medicines and Organised Crime, which won the British Medical Association’s annual book award in 2014, and Deadly Psychiatry and Organised Denial. He was eventually expelled from the Cochrane Collaboration he had helped found, after the organisation’s leadership decided his criticism of the HPV vaccine and of psychiatric drugs threatened its institutional standing. The expulsion is documented in his 2019 book Death of a Whistleblower and Cochrane’s Moral Collapse. He continues his work through the Institute for Scientific Freedom in Copenhagen, which he founded the same year.
When the book appeared, Danish psychiatry professors were still telling patients in officially endorsed handbooks that depression is caused by a chemical imbalance corrected by depression pills — a claim the former director of the US National Institute of Mental Health, Steven Hyman, had already publicly disowned in 1996. A 2019 review of 39 popular health websites in 10 countries found 74% still made the same claim. The UK Royal College of Psychiatrists and the National Institute for Health and Care Excellence had spent five decades denying that the drugs were addictive — a denial precisely paralleling the 50-year delay before barbiturates were acknowledged as addictive, and the 30-year delay for benzodiazepines. The 2020 BBC programme that finally broke ranks still featured a voiceover assuring viewers that “although they are not addictive, they can lead to dependency issues.” Gøtzsche was writing into a profession actively defending the same lies it had told patients for half a century, while the patients themselves — surveyed as early as 1991 — had already concluded by a 78% margin that the drugs were addictive.
Gøtzsche is not a terrain practitioner. He is an evidence-based-medicine reformer working within mainstream pharmacology, but his findings converge with what Shelton documented a century earlier: drugs prescribed to suppress the body’s response to insult drive acute conditions toward chronic disease, and the harms of the suppression are then misread as evidence of progressing illness. The full summary unpacks the mechanism in detail — the cold-turkey trial design that converts withdrawal injury into apparent drug efficacy, the 12% greater dropout rate on drug than on placebo across 67,319 pages of clinical study reports that no researcher outside the companies had ever read, the 5 cm permanent height loss in children on stimulants at 16-year follow-up, the 79% rate of akathisia among mentally ill patients who attempted suicide, the contrast between drug-heavy Stockholm and the Open Dialogue model in Lappland where 19% versus 62% of first-episode psychosis patients ended up on disability five years later. The mother of one Danish patient killed by overdosed psychosis pills against her warnings was told the death was natural. Her daughter’s last words to her, before the lethal injection, were: Mom, won’t you tell the world how we’re treated?
30 Q&As
Question 1: What is the central claim about psychiatric drugs and mortality, and how does it compare to other causes of death?
Psychiatric drugs are the third leading cause of death in the developed world, after heart disease and cancer. The estimate is built from the best available evidence on placebo-controlled trials, regulatory data, and large cohort studies, and it implicates every major drug class used in mental health: depression pills, psychosis pills, lithium, antiepileptics used as “mood stabilizers,” and stimulants. Even the most cautious reading of the data forces the conclusion that these drugs kill hundreds of thousands of people every year and cripple millions, physically and mentally. One drug alone, Zyprexa, was estimated to have killed 200,000 patients up to 2007, most of whom should never have been treated with it.
Psychiatry occupies a unique position in medicine in this respect. There are no cardiology survivors or infectious-disease survivors, but there are psychiatric survivors — people who use that word to describe what they survived from their own treatment. In every other speciality, a patient who lives through serious illness is grateful for the doctor’s intervention. In psychiatry, doing what the doctor recommends may be what kills you. The patients who fight their way out of the system describe it as imprisonment, with a door in but not a door out, and many say it took 10 or 15 years before they realised that life is much better without the drugs.
Question 2: Why is the biological model of psychiatry — the idea that mental disorders arise from chemical imbalances corrected by drugs — considered scientifically bankrupt?
The biological model rests on three assumptions: that specific psychiatric diagnoses exist, that they result from specific brain changes, and that specific drugs correct those changes. Each assumption fails when examined. Diagnoses are made by checklist consensus rather than by any biological marker. The chemical imbalance hypothesis has been refuted repeatedly: mice genetically depleted of brain serotonin behave like other mice; tianeptine, which lowers serotonin, “works” for depression just as drugs that raise serotonin do; depression pills are tested on 214 unrelated diagnoses and seem to “work” for everything that has nothing to do with serotonin. The drugs do not correct an imbalance — they create one, as Steven Hyman, former director of the US National Institute of Mental Health, pointed out in 1996.
The collapse of the model has been hidden by relentless professional defence. When challenged, psychiatry’s spokesmen retreat — saying the chemical imbalance was always “a metaphor” or that they have “known for 20 years” the theory is too simple — only to reassert it in textbooks, patient handbooks, and consultations the moment the spotlight moves elsewhere. A 2019 survey of 39 popular websites in 10 countries found that 74% still attributed depression to a chemical imbalance or claimed depression pills could correct one. The myth survives not because it is supported by evidence but because it justifies lifelong prescribing, defends professional prestige, and protects an industry whose only motive is money.
Question 3: How did the chemical imbalance theory survive for decades despite the evidence against it, and what role did commercial interests play?
The recipe was simple. A drug was found to increase serotonin or lower dopamine, and a hypothesis was invented that patients must therefore be deficient in serotonin or producing too much dopamine. The hypothesis was rejected by every test — by genetic studies, by speed-of-onset studies, by the observation that drugs working in opposite directions both seem to “work” — but it was not abandoned, because abandoning it would mean abandoning the prescription. The 1992 Defeat Depression Campaign in the UK, run jointly by the Royal Colleges of Psychiatrists and General Practitioners, accepted donations from every major manufacturer of depression pills. The president of the Royal College of Psychiatrists, Robert Kendall, conceded that the companies’ major motive was to increase sales. There were no other motives.
The lay public was harder to convince than the doctors. A 1991 UK survey found 91% wanted counselling for depression, only 16% wanted pills, 78% considered them addictive, and 46% thought they worked. After the campaign, the figures had shifted only 5–10%. Patients drew their conclusions from their own experience and that of their relatives. The psychiatrists called this ignorance and prescribed “psychoeducation” — what is normally called brainwashing. The myth persists in 74% of major health websites, in psychiatric textbooks, in consultations where patients are told they have a chemical imbalance and need pills like a diabetic needs insulin. It persists because money, prestige, and guild interests demand that it persist, not because any scientific question is being asked.
Question 4: Why are psychiatric diagnoses described as neither specific nor reliable, and how does the DSM construct them?
Psychiatric diagnoses are made by checklist. A person with at least five of nine symptoms qualifies for major depression. The symptoms — sleep problems, appetite change, fatigue, difficulty concentrating, low mood — are common features of ordinary life, and the cut-off between five and four is decided by show of hands at committee meetings, not by any biological measurement. When psychiatrists are asked to diagnose the same patients independently, they disagree wildly. The American Psychiatric Association’s own reliability studies were so embarrassing that they were buried in short articles requiring detective work to locate. The largest study of 592 people produced poor agreement even after extensive training of the assessors.
The labels are social constructs, not natural kinds. You can have a dog or a car; you cannot have ADHD in the same sense. When a child fidgets and is called ADHD, then explained as fidgeting because she has ADHD, the reasoning is circular. The labels stick for life — affecting driver’s licences, custody decisions, adoption applications, insurance, and employment — and there is no court of appeal. Even when the diagnosing psychiatrist herself doubts the diagnosis, it cannot be removed. Filmmaker Anahi Testa Pedersen received the schizotypy diagnosis during acute distress over a divorce; eight years later, the system summoned her well-functioning daughter for examination because they assumed psychiatric disorders are inherited. The system makes diagnoses; it does not unmake them. The single best protection against this system is to avoid getting a diagnosis in the first place.
Question 5: What is meant by a “psychiatric career,” and how does prescribing one drug typically lead to additional diagnoses and a cocktail of further drugs?
A psychiatric career begins, most often, with a family doctor and a depression pill prescribed for some ordinary trouble — grief, divorce, work stress, sleeplessness. The patient is told the drug will fix a chemical imbalance. Then the drug produces its predictable effects. Depression pills make some people manic or psychotic, and when this happens the patient is now bipolar or has psychotic depression. A psychosis pill is added, then lithium, then an antiepileptic relabelled as a “mood stabilizer.” Each added drug brings new harms that overlap with the symptoms used to make new diagnoses. The harms are read as confirmation of progressing illness. The patient now collects diagnoses and medications in parallel, and there is no exit ramp.
The 21-year-old student described in the book illustrates the endpoint. She was discharged from a private hospital on diazepam, two depression pills, three psychosis pills, three antiepileptics, and lithium — eleven psychiatric drugs simultaneously, after 21 sessions of trans-cranial magnetic stimulation and 12 electroshocks. Stine Toft was given depression pills for stress, became manic from the drugs, was diagnosed bipolar, and spent 14 years on an escalating cocktail before realising the bipolar diagnosis was a misreading of drug-induced mania. Silje Marie Strandberg, bullied at 12, was prescribed Prozac at 16, lost herself, and was eventually medicated by 95 different doctors with 21 different psychiatric drugs over 10 years. The career pattern is not the exception — it is what the system produces by design.
Question 6: What does the term “medication spellbinding” describe, and why does it matter for patients trying to assess whether their drugs are helping?
Medication spellbinding describes the state in which a drug numbs a person’s capacity to evaluate the effect of the drug itself. The pills affect feelings, thoughts, and behaviour, and they affect the very faculty that would notice this. Patients lose the ability to see how much they have changed. They lose insight into their own emotional flatness, their cognitive slowing, their sexual numbness, their loss of interest in people and life. The main biasing effect is that patients underestimate the harms — sometimes catastrophically. A patient who can no longer feel music, who has stopped laughing, who no longer recognises herself, may report that the drug is “helping” because she can no longer feel the suffering it is causing.
This is why patient self-reporting on whether a drug is working is unreliable in exactly the wrong direction — it favours continuing the drug. It is also why withdrawal so often comes with a stunning return of basic experience: Stine Toft, in the bath during withdrawal, began crying because she could feel water on her body for the first time in years. The return of feeling is the return of the capacity to assess. Combination treatment with psychotherapy is undermined by spellbinding, because effective therapy requires a patient who can think, feel, and evaluate herself, and the drugs prevent exactly this. The patient on drugs is not in a position to know what the drugs have done to her until she comes off them.
Question 7: How are drug-induced harms — such as mania caused by depression pills or compulsive behaviour caused by stimulants — routinely misdiagnosed as new diseases?
The pattern is consistent across drug classes. A depression pill causes mania; the patient is diagnosed bipolar. A stimulant produces tics, twitches, and meaningless repetitive behaviour; the child is diagnosed with obsessive-compulsive disorder. A psychosis pill produces tardive dyskinesia; the movements are read as worsening of the underlying illness. The DSM-5 went as far as ruling that mania occurring during depression-pill treatment should be considered “true” bipolar disorder rather than drug-induced — a definitional sleight of hand that converts a side effect into a permanent diagnosis. There is considerable overlap between the harms of psychiatric drugs and the symptoms used to make psychiatric diagnoses, and the system reliably reads the harm as a new disease.
This is medical malpractice on a massive scale, and it is what produces psychiatric careers. A patient who would never have had mania in her life produces drug-induced mania, is now bipolar, and is now on lithium and an antiepileptic for the rest of her life. A child who would have grown out of fidgeting produces stimulant-induced obsessive behaviour, is now also diagnosed with OCD, and is now on additional drugs. Trials of ADHD drugs report psychosis or mania in 3% of treated children versus 1% on placebo — 30 times higher than the FDA’s own warning about “new psychotic or manic symptoms.” The harm is reliably catalogued as a disease that justifies further treatment, and the reverse arrow — that the treatment caused the harm — is rarely allowed to be drawn.
Question 8: What does the evidence show about whether depression pills work, and how do flaws in trial design create the appearance of an effect?
The smallest effect that can be perceived on the Hamilton Depression scale is 5 to 6 points. In flawed trials, depression pills produce about 2 points more than placebo. When the placebo contains atropine — which mimics the drug’s side effects so the blind cannot be broken — the difference shrinks to 1.3 points and disappears. Three of the 17 items on the Hamilton scale concern sleep, and a single shift on these can produce 6 points; an anxiety reduction can produce 8. Almost any substance with side effects can be made to “work” for depression by these mechanics, including stimulants. The question is not whether the patient feels something happening in her body — she does — but whether the change has any clinical relevance, and the answer is no.
The deeper problem is that no trial has ever measured whether depression pills return patients to a normal productive life. Over a thousand placebo-controlled trials have been conducted, and none uses the outcome the DSM itself defines as central — clinically significant impairment in social, occupational, or other functioning. When Gøtzsche’s group examined patient dropout rates across 73 trials covering 18,426 patients — reading 67,319 pages of clinical study reports that no one outside the companies had ever read before — they found 12% more patients dropped out on drug than on placebo. Patients voted with their feet. Even with broken blinding, even with cold-turkey placebos, even with rating scales that exaggerate small changes, the patients themselves prefer no drug. The reported “benefit” exists only on rating scales that the patients do not experience as benefit.
Question 9: Why is the cold-turkey placebo design in psychiatric drug trials considered fraudulent, and what does it mean for the published evidence base?
In a cold-turkey trial, patients already taking the drug are abruptly switched to placebo. They go into withdrawal — anxiety, agitation, insomnia, suicidal thoughts, the full constellation of abstinence symptoms that resemble the original condition. The trial then “finds” that patients on continued drug fare better than patients on placebo. What it has actually measured is the harm of sudden withdrawal, not any benefit of the drug. Virtually all psychiatric drug trials suffer from this design defect, and it pervades the evidence used to justify lifelong prescribing.
The mechanism is what produces the famous “relapse prevention” findings. Patients abruptly switched to placebo experience withdrawal-induced misery, restart the drug, feel relief from the abstinence, and the trial concludes the drug prevents relapse. As few as two patients are needed to produce one with withdrawal symptoms — the Number Needed to Harm is two. There cannot be a Number Needed to Treat below this, only the harm of forcing patients into acute withdrawal. The published literature is so saturated with this design that meta-analyses citing “established efficacy” are reading harm as benefit. When trials are conducted without cold turkey, the apparent effect collapses. The entire evidence base for long-term psychiatric drug use rests on a methodology that systematically converts withdrawal injury into evidence of drug benefit.
Question 10: How are suicides, deaths, and serious harms hidden in published psychiatric drug research, and what did Gøtzsche’s group find when they read the unpublished clinical study reports?
Only about half of suicides and other deaths that occur in psychiatric drug trials are published. Deaths are wiped under the carpet — recoded as “unknown cause,” omitted before publication, attributed to the underlying disease rather than the drug. Companies report adverse events only above arbitrary thresholds — for instance, only if they occurred in at least 5% of patients — which conceals serious harms occurring at lower frequencies. In Lilly’s fluoxetine and duloxetine trials, only 2 of 20 suicide attempts and only 3 of 17 akathisia events were documented in the public summaries. Akathisia was recoded as “hyperkinesia” in three sertraline trials. Sexual dysfunction in women was coded as “Female Genital Disorder,” with the blame implicitly placed on the patient.
Gøtzsche’s group obtained 71 clinical study reports from European and UK regulators — 67,319 pages, around seven metres if stacked — and read them all. They were the first researchers outside the companies ever to do so. They found 12% more dropouts on drug than on placebo. They found that 9 of 15 study reports contained selectively reported quality-of-life data, and 24 of 26 corresponding publications did. Quality-of-life data were sometimes measured in 11 trials but reported in only 5. Two-thirds of trials had at least one primary outcome that was changed, introduced, or omitted after the data were seen, and 86% of trialists denied this when asked. The published evidence base for psychiatric drugs is not what the trials actually showed; it is what the companies decided patients and doctors would be allowed to see.
Question 11: What does the evidence show about the deadliness of psychosis pills, both in elderly demented patients and in young people with first-episode psychosis?
In a meta-analysis of placebo-controlled trials in 5,000 elderly demented patients, 3.5% had died after only ten weeks on olanzapine, risperidone, quetiapine, or aripiprazole, compared with 2.3% on placebo. One patient killed per 100 in ten weeks. When Gøtzsche checked the FDA’s underlying data — because around half of deaths in psychiatric trials go missing — the rates rose to 4.5% versus 2.6%. Two patients killed per 100 in ten weeks. A Finnish cohort study of 70,718 community-dwellers newly diagnosed with Alzheimer’s disease found that psychosis pills killed 4 to 5 patients per year compared with patients not treated, and 57% more if the patients received more than one psychosis pill. There is no other drug, given to patients who do not need it, with a death rate this high.
For young people with schizophrenia, the picture is no better. The TIPS study followed 281 patients with first-episode psychosis whose average age at entry was 29. Within 10 years, 31 of them — 12% — were dead. The authors took no interest in the deaths, mentioning them only in a flowchart of patients lost to follow-up. They focused on symptom scores. When Gøtzsche wrote asking what the patients had died of, the response came months later, in a separate paper, with the death numbers changed and the causes still not given. The patients with schizophrenia have a lifespan 15 years shorter than the rest of the population. Psychiatry blames patient lifestyles. The drugs cause weight gain, hypertension, diabetes, cardiovascular sudden death, pneumonia from sedation and inactivity, and irreversible brain damage. The roadblocks against finding out why young people on these drugs die are guarded by the psychiatric guild itself.
Question 12: What is akathisia, why is it dangerous, and how is it concealed in clinical trials?
Akathisia is a horrible feeling of inner restlessness — a Greek word meaning inability to sit still. The patient may pace endlessly, fidget, wring her hands, or sit motionless while experiencing unbearable inner torment, rage, dissociation, and delusional ideation. In one study, 79% of mentally ill patients who attempted suicide suffered from akathisia. Half of all fights at a psychiatric ward in another study were related to akathisia. Moderate to high doses of haloperidol made half the patients markedly more aggressive — sometimes to the point of wanting to kill their psychiatrists. Akathisia is one of the most direct mechanisms by which psychiatric drugs cause suicide, violence, and homicide.
In clinical trials, akathisia is systematically miscoded. In three sertraline trials, it was recorded as “hyperkinesia.” In paroxetine trials, not a single case was found, which is implausible given the clinical reality of these drugs. Lilly’s summary reports for fluoxetine and duloxetine documented only 3 of 15 akathisia events. The harm appears in product information for psychosis pills like Zyprexa as “extreme inner anxiety and restlessness,” but the language obscures what is happening. A patient who kills herself on a depression pill is rarely connected back to the akathisia that drove her there, because the akathisia was either not recorded or was recorded under a different name. The harm is real, it is common, it is lethal, and it is hidden.
Question 13: What is tardive dyskinesia, how common is it among long-term users of psychosis pills, and why did psychiatry take 20 years to recognise it as drug-caused?
Tardive dyskinesia is an involuntary movement disorder — uncontrollable grimacing, lip-smacking, tongue-thrusting, jerking of the limbs and trunk. It develops in 4 to 5% of patients on psychosis pills per year, which means most patients in long-term treatment will eventually develop it. In 1984, FDA scientist Poul Leber extrapolated the data and concluded that, over a lifetime, all patients on psychosis pills might develop the condition. It is often irreversible, and it is masked by ongoing treatment — the drug that causes it also conceals it, so stopping the drug both reveals and may permanently expose the damage. Around half of patients in the TIPS study who remained on psychosis pills 10 years after first-episode psychosis would have developed it.
Psychiatry took 20 years to acknowledge that tardive dyskinesia was iatrogenic — caused by the doctor’s own treatment. Even after acknowledgement, the denial continued. Three years after Leber’s extrapolation, the president of the American Psychiatric Association told an Oprah Winfrey audience that tardive dyskinesia was not a serious or frequent problem. Forced treatment with these drugs continues to be ordered by psychiatric tribunals even when patients have already developed akathisia or tardive dyskinesia from prior treatment. In one of 30 forced-treatment cases reviewed by Gøtzsche’s group, an expert confirmed the patient had developed akathisia on aripiprazole and on the same page recommended forced treatment with the same drug. The drugs that produce permanent brain damage continue to be prescribed, often against the patient’s will, by a system that does not allow the harm to register as evidence.
Question 14: How do depression pills affect sexual function, why is the harm often permanent, and how do drug companies and doctors deflect blame onto the patients?
Half of patients with previously normal sex lives experience disruption or destruction of sexual function on depression pills. In one carefully conducted study of 1,022 patients, 57% reported decreased libido, 57% delayed orgasm, 46% no orgasm, 31% erectile dysfunction or decreased lubrication. In unpublished Phase 1 trials with healthy volunteers, over half experienced severe sexual dysfunction, and in some cases it persisted after the drug was stopped. The numbness can become permanent — post-SSRI sexual dysfunction, in which patients report being unable to feel chili paste rubbed into their genitals. Some patients kill themselves when they discover the damage is permanent. An Australian child psychiatrist told Gøtzsche he knew three teenagers who attempted suicide because they could not get an erection the first time they tried to have sex.
The Prozac package insert lists decreased libido at 4% — barely above placebo — while the actual rate is around 57%. The deflection mechanism is built into the language of the labelling itself: “changes in sexual desire, sexual performance, and sexual satisfaction often occur as manifestations of a psychiatric disorder.” The blame is placed on the patient’s depression, not the drug. SmithKline Beecham coded female anorgasmia as “Female Genital Disorder.” Doctors tell patients the problem is psychosomatic, prescribe psychosis pills on top, refuse to believe the complaints, or — in one documented exchange — tell the patient she has a choice between losing orgasms and “going mad.” Meanwhile, the same pharmacological action is repackaged and sold as Priligy for premature ejaculation. The drug industry knows exactly what these compounds do to sexual function. The denial is a marketing decision, not a scientific uncertainty.
Question 15: What is known about lithium’s actual benefits and harms, and why is the claim that it prevents suicide unreliable?
Lithium is a highly toxic metal with a narrow therapeutic window — toxicity occurs at doses close to therapeutic concentrations, so serum levels must be constantly monitored. It can cause irreversible brain damage, kidney damage, cardiovascular harm, ataxia, tremor, drowsiness, and a long list of other serious effects. Many other drugs alter lithium’s serum level, making safe co-prescription extremely difficult. Like most psychiatric drugs, it sedates and incapacitates rather than treats. The studies that claim lithium prevents suicide rest on a tiny number of trials — when Gøtzsche and a Swedish psychiatrist excluded the cold-turkey trials and looked only at the four remaining studies, the data were too unreliable to draw any conclusion, and the trials were poorly blinded because lithium’s side effects are pronounced.
The 2013 review most often cited as evidence that lithium prevents suicide noted six suicides in the trials, all on placebo. The reviewers themselves cautioned that just one or two moderately sized trials with neutral or negative results could materially change the finding, and selective reporting of deaths in old psychiatric drug trials is the rule rather than the exception. Around half of all deaths in psychiatric drug trials are missing from publication. Trials that titrate patients up to “the most appropriate dose” before randomising half to placebo are measuring abrupt withdrawal harm, not suicide prevention. The case for lithium is built on selectively reported old data, broken blinding, and cold-turkey designs. It is not a drug that should be recommended to anyone.
Question 16: How are antiepileptic drugs used in psychiatry, and why are they harmful when prescribed for mood rather than for seizures?
Antiepileptics double the risk of suicide. Their effect in psychiatry is to numb and sedate — what Gøtzsche calls a chemical straitjacket — and they are prescribed for almost everything, particularly for what is called mania. Anything that knocks a patient down will appear to “work” for mania, but the drugs do not cure or stabilise mood; they suppress emotional responsiveness. They can also do the opposite of what is claimed: antiepileptics can themselves induce mania, which then produces a new diagnosis and a new layer of drugs. One in 14 patients on gabapentin develops ataxia — loss of voluntary muscle coordination. The marketing label of “mood stabilizer” was coined without anyone clarifying what it means. The category includes antiepileptics, lithium, and even psychosis pills like asenapine — a flexible commercial term, not a pharmacological class.
The trial evidence is fraudulent. Lamotrigine reached the market with two positive published trials; seven large negative trials were buried. Two positive trials are all the FDA requires, and the agency treats negative results as “failed trials” rather than as evidence the drug does not work. Cochrane reviews of methylphenidate and ADHD-related antiepileptics performed by attentive researchers found every single trial at high risk of bias. The British drug agency’s own document recorded the rate of aggression on methylphenidate as 1.2% on page 61 and 11.9% on page 63 — same population, same follow-up, same document. Antiepileptics drive psychiatric careers forward by adding harms, requiring further drugs, and making it almost impossible for the patient to function or to come off. They should not be used for mental health issues.
Question 17: Why is ADHD described as a social construct rather than a real disease, and what does the long-term evidence show about stimulant medications in children?
ADHD is a label, not an entity. The reasoning that constructs it is circular: a child fidgets and is diagnosed with ADHD; the child fidgets because she has ADHD. The label cannot be observed in nature like an elephant. The diagnostic checklist consists of behaviours common to ordinary childhood, and the cut-off is decided by committee. When a diagnosis was needed for children who sat too still, ADD was invented; the drug industry’s logical endpoint is a diagnosis for everyone in the middle, so that no one escapes treatment. The drugs used are stimulants — methylphenidate, amphetamine, and amphetamine derivatives — pharmacologically equivalent to crystal methamphetamine. The WHO classifies amphetamine-type stimulants as a public health danger when bought on the street, and says nothing about the same compounds prescribed at similar population-wide rates.
The long-term evidence is grim. The US MTA trial randomised 579 children and followed them for 3, 6, 8, and 16 years. After 16 years, those who consistently took their pills were 5 cm shorter than those who took very little. Children developed tics, twitches, obsessive-compulsive behaviour, apathy, depression — more than half in some studies. Animal studies confirm reproductive harm persisting after the drugs are stopped. The compulsive behaviour at school is often misread as improvement: a child who copies everything from the board without learning anything is judged to be focusing well. Children on these drugs have suddenly dropped dead in classrooms. Stimulants increase the risk of violence. The short-term effect of getting children to sit still disappears quickly; the long-term effects on developing brains can only be guessed at. The drugs do not protect against crime, delinquency, or substance abuse, contrary to what psychiatrists testify in parliamentary hearings — if anything, they do the opposite.
Question 18: What is the truth about benzodiazepine and depression-pill addiction, and why did it take 30 to 50 years for the authorities to acknowledge it?
Benzodiazepines were marketed as the safer alternative to the addictive barbiturates. Barbital came on the market in 1903; it took 50 years before barbiturates were officially recognised as addictive. Benzodiazepine dependence was documented in 1961 and described in the British Medical Journal in 1964. Sixteen years later, the UK Committee on the Review of Medicines published a systematic review estimating that only 28 people had become dependent between 1960 and 1977. The actual number was millions. The Medicines Control Agency finally wrote to doctors about the problem in 1988 — nearly 30 years after the dependence was first documented. Then SSRIs replaced benzodiazepines as the safer alternative, and the cycle began again. Imipramine dependence had been described in 1971 in just six healthy volunteers. Authorities denied SSRI addiction for another 50 years.
The denial is now performative rather than substantive. Authorities use words like “discontinuation symptoms” and “dependency issues” to avoid saying addiction. Professors of psychiatry argue patients are not dependent because they do not crave higher doses — a definition that would exonerate every smoker who maintained a constant pack-per-day for 40 years. A 2020 BBC programme reported that the UK mental health charity Mind was directing people to street drug charities to help them withdraw from depression pills, while the voiceover insisted the drugs are not addictive. Gøtzsche’s systematic review found that withdrawal symptoms are described in similar terms for benzodiazepines and SSRIs, and 37 of 42 identified symptoms are very similar across the two drug classes. The patients have known the drugs are addictive for at least 30 years; lay people surveyed in 1991 already considered them so by a 78% margin. The institutions that refuse to call it what it is are protecting prescribing rights, not patients.
Question 19: What does the evidence show about electroshock, and why does its mechanism of action raise serious ethical concerns?
Electroshock works by causing brain damage. The effect, when there is one, does not last beyond the treatment period — which is why patients receive long series of shocks rather than one dramatic intervention. If electroshock genuinely cured anything, repetition would not be needed. Most patients who receive ECT experience memory loss, often severe and often permanent. Leading psychiatrists deny this, despite well-documented evidence in the medical literature. About 1 in 1,000 patients dies from electroshock. Many more suffer serious irreversible cognitive damage. One patient described in the book could not remember the name of the Danish capital after her treatments — she had been sexually abused as a child, given a psychiatric diagnosis she never met the criteria for, and electroshocked into permanent brain injury.
The mechanism is the ethical problem. A treatment whose therapeutic effect is brain damage, whose effect requires endless repetition, whose memory destruction is denied by the practitioners who administer it, and which can be enforced upon patients against their will — including patients who have not consented — is a treatment no humane medical system should retain. Some patients say it has helped them. Some patients say morphine has helped them. Anecdotes do not establish efficacy; they establish what the patient experienced. There is no reliable evidence that electroshock saves lives, and there is reliable evidence that it kills some patients and brain-damages many others. The fact that it can still be enforced on unwilling patients in democratic countries is one of the markers of how far psychiatry stands outside ordinary medical ethics.
Question 20: Why is the Number Needed to Treat (NNT) considered bogus when applied to psychiatric drugs?
The Number Needed to Treat tells you how many patients must take a drug for one to benefit. It is meaningful only when there is a real benefit to count. In psychiatry, the trial methodology is so corrupted that the apparent benefits are artefacts. The cut-off for “improvement” can be moved until the data confess what marketing wants. NNT calculations rest on rating-scale changes that patients themselves do not experience as meaningful — the 2-point difference on the Hamilton scale that drug companies celebrate is invisible to the person taking the pill. NNT also ignores harms entirely, treating drugs as if their possible benefits existed in a vacuum.
In a depression-pill trial, only two patients on cold-turkey placebo are needed to produce one with withdrawal symptoms — the Number Needed to Harm is two. Twelve per cent more patients drop out on drug than on placebo, giving a Number Needed to Harm of about eight on dropout alone. The Number Needed to Harm for sexual dysfunction is below two. There is no Number Needed to Treat in psychiatry that survives once harms are placed alongside the apparent benefits. The UK psychiatrists who claimed depression pills had an NNT of three for preventing recurrence were measuring nothing more than the cold-turkey withdrawal harm in their placebo group. The NNT framework, as applied to psychiatric drugs, exists to produce numbers that flatter prescribing. It does not exist as a legitimate measurement of benefit.
Question 21: How have medical journals, mainstream media, and Boards of Health acted to suppress critical information about psychiatric drugs and children’s suicides?
The censorship is comprehensive. Major psychiatric journals declined to publish or even discuss any of 13 to 14 pivotal studies on whether depression pills worsen long-term outcomes or cause persistent sexual dysfunction. Editor-in-chief positions in psychiatric journals are often held by people on drug industry payroll. When the British Medical Journal devoted an issue to conflicts of interest in 2004, the drug industry threatened to withdraw advertising; Annals of Internal Medicine lost an estimated 1 to 1.5 million dollars in advertising after publishing a study critical of industry practice. Giovanni Fava found it so impossible to publish results his peers disliked that he founded his own journal. Mainstream newspapers — Svenska Dagbladet, Dagens Nyheter, La Vanguardia — have killed interviews with Gøtzsche. A Dagens Nyheter editor told the journalist directly that explaining the suicide risk to readers would be too dangerous. National TV documentaries are routinely sanitised in editing, with the hardest material removed and a voiceover inserted assuring viewers that “many people are helped by psychiatric drugs.”
Boards of Health have been similarly unresponsive. Gøtzsche alerted the Boards of Health in the Nordic countries, New Zealand, Australia, and the UK to the fact that two simple interventions — the Danish Board’s reminder to GPs, and his own public warnings — had nearly halved Danish children’s depression-pill prescriptions between 2010 and 2016. He noted that depression pills double the risk of suicide in randomised trials and urged action. He received no replies, late replies, or what he considered bullshit. The Finnish Ministry replied after five months that “increased suicidal thoughts have been connected with SSRIs in some studies.” The Swedish Drug Agency’s 2016 treatment recommendations contained no information at all about suicidality under side effects, while the Swedish package insert for fluoxetine listed suicidal behaviour as a common side effect in children. New Zealand had the highest teenage suicide rate in the world — twice Sweden’s, four times Denmark’s — and a 78% rise in adolescent depression-pill prescriptions between 2008 and 2016. The Director of Mental Health, when asked to make the drugs unlawful in children, said only that some children were so depressed the drugs should be tried.
Question 22: What does the contrast between Stockholm and Lappland reveal about whether psychosis can be treated without drugs, and what is the Open Dialogue model?
In Lappland, the Open Dialogue Family and Network Approach treats first-episode psychosis at home, involving the patient’s social network, beginning within 24 hours of contact. In Stockholm, the standard biomedical approach prevails. The patient populations were closely comparable. In Stockholm, 93% of first-episode patients were treated with psychosis pills, 33% in Lappland. Five years later, ongoing drug use was 75% in Stockholm versus 17% in Lappland. Sixty-two per cent in Stockholm versus 19% in Lappland were on disability allowance or sick leave. Hospital bed use was 110 days versus 31 days on average. The differences are not subtle. They are the difference between a system that produces chronic disability and one that produces recovery.
The contrast is not a randomised trial, but the magnitude of the effect makes the result impossible to dismiss. The Lappland team waits, listens, involves family, and keeps drugs to a minimum. At a London psychosis ward, staff waited about two weeks before starting medication on newly admitted patients; most chose only small doses or none, suggesting it was respect, time, and shelter that helped, not the drugs. The Norwegian Akershus University Hospital has operated without rapid tranquillisation regimens. Iceland has not used chains, belts, or physical restraints since 1932. Italy’s Mental Health Law treats danger as a police matter, not a justification for forced drugging. The evidence that psychiatric care without drug coercion is not only possible but produces dramatically better outcomes is not hidden. It is ignored, because acknowledging it would dismantle the prescribing model that defines the profession.
Question 23: What does the evidence show about psychotherapy compared with depression pills, particularly in the long term and for suicide prevention?
Psychotherapy halves the risk of a new suicide attempt in people acutely admitted after a suicide attempt. The finding came from Gøtzsche’s meta-analysis with his daughter, focused on cognitive behavioural therapy because most trials used it, but emotion regulation therapy and dialectical behaviour therapy show similar effects. Across the broader literature, psychotherapy outperforms pharmacotherapy in the long run — the longer the trial follow-up, the clearer the advantage. The effect of psychotherapy is enduring because it teaches patients adaptive emotion regulation: how to handle feelings, thoughts, and behaviour in ways that strengthen them. Drugs do the opposite. They impose maladaptive emotion regulation by numbing, blunting, and disconnecting. The patient on drugs does not learn to handle her life; her capacity to feel her life is suppressed.
Combination therapy of drugs and psychotherapy is poorly supported. Effective psychotherapy requires a patient who can think and feel, and medication spellbinding prevents both. Trials comparing the two are not effectively blinded, and the dominant biomedical assumption among psychiatrists biases their assessments toward drugs. Short-term comparisons are misleading; only follow-up of a year or more reveals what the treatment is actually doing. Trauma and severe stress underlie most psychiatric symptoms, and these conditions tend to self-heal if the patient is given time and humane support. The healing leaves the patient stronger and better equipped for future trouble. Drugs prevent this by numbing the very experience the healing requires. They also provide doctors with an excuse not to engage — a patient on a drug needs less of the doctor’s presence than a patient being listened to.
Question 24: Why does the book argue that most psychiatric symptoms are responses to trauma and severe stress rather than brain disorders?
When psychiatrists fail to take careful patient histories — and they often do — they miss the trauma that produced the symptoms. A current episode of distress diagnosed as depression frequently began as anxiety years earlier when the patient was a teenager. Stine Toft’s “bipolar” diagnosis followed depression-pill-induced mania during a difficult period of her life. The patient permanently brain-damaged by electroshock had been sexually abused as a child and had no psychiatric disorder. The patient who was told she had to choose between orgasms and “going mad” had also been sexually abused as a child. Trauma drives most of what arrives at the psychiatric clinic, and the clinic responds with a checklist that produces a diagnosis, a prescription, and a career.
A meta-analysis of studies on childhood adversity found it markedly increases the risk of psychosis. The same applies to cumulative traumas across the lifespan. Acute conditions — psychoses, depressions — are typically related to trauma and tend to self-heal if treated with patience. The healing process teaches the patient something useful and builds self-confidence. Drugs interrupt this. They numb feelings, prevent learning, and convert what should be a temporary crisis into a chronic medication-dependent state. The biopsychosocial model has been replaced by a bio-bio-bio model that ignores the social and psychological dimensions. The result is that the experiences that produced the patient’s distress — abuse, bereavement, divorce, unemployment, isolation, the wrong marriage, the bullying boss — are reframed as evidence of brain malfunction. The trauma is buried under the drug.
Question 25: What practical steps make safe withdrawal from psychiatric drugs possible, and what role do tapering strips and hyperbolic tapering play?
Safe withdrawal requires slow, individualised dose reduction over months, sometimes more than a year. The patient must be in charge of the pace, and a support person must follow her closely because the danger signals — irritability, restlessness, suicidal thoughts — may not be visible to the patient herself. Withdrawal can be the worst experience of a person’s life, and the patient must be ready for it; she should not start when overworked or stressed. The drugs must never be stopped abruptly. Withdrawal reactions can include severe emotional and physical symptoms that can be dangerous and lead to suicide, violence, and homicide. Tapering takes longer than most patients expect — six months or more is often required, and venlafaxine in particular can be exceptionally difficult.
Tapering strips, developed in the Netherlands by Peter Groot and Jim van Os, are pre-prepared series of progressively smaller doses. Each strip covers 28 days, and patients can use one or more to regulate the pace. Of 895 patients on depression pills who used the strips, 71% were off their drug after a median of 56 days. Of 810 venlafaxine patients starting at 37.5 mg, 90% tapered off in three months or less. The strips work because they remove the obstacle the drug companies created — limited dose strengths that make small reductions impossible. Splitting tablets, opening capsules and dissolving them in water, switching to liquid forms, ordering split fragments by size — all are improvisations forced on patients because regulators allowed companies to bring drugs to market without providing the strengths needed to come off them safely. Dutch insurers refuse to reimburse the strips because “there is no evidence in the literature” that slow withdrawal is needed. The system that hooked the patients refuses to pay for the way out.
Question 26: How can patients distinguish between withdrawal symptoms and a return of the original condition, and why does the difference matter?
Withdrawal symptoms emerge quickly after a dose reduction and resolve within hours of restoring the dose. The original condition, if it returns at all, returns gradually and does not respond instantly to the previous dose. This is the practical test, and it matters because doctors routinely tell patients suffering withdrawal that their disease has come back, that they need lifelong drugs, that they have proven they cannot manage without medication. The patient, terrified by withdrawal symptoms she has been told are her illness, restarts the drug, feels better within hours, and concludes her psychiatrist was right. The cycle locks her in. The same misreading drives the cold-turkey trial findings used to justify long-term prescribing — withdrawal misery is read as relapse, restoration of the drug as evidence of effect.
The withdrawal-symptom list overlaps almost perfectly with the symptoms used to make psychiatric diagnoses. Anxiety, agitation, insomnia, low mood, irritability, suicidal thoughts, dissociation, racing thoughts — all are common withdrawal effects, and all are also the criteria for depression, anxiety disorder, bipolar, and other diagnoses. The withdrawal-induced state can be more severe than the original condition that prompted the prescription. A patient who never had suicidal thoughts before drugs may become suicidal during withdrawal. This is not relapse; it is iatrogenic harm. The single most important piece of information a patient withdrawing from a psychiatric drug can have is the knowledge that what she is experiencing is the drug leaving her body, not her old self returning. Without that knowledge, she will give up and the system will claim her as proof its drugs are necessary.
Question 27: What does Anders Sørensen’s work with 30 consecutive patients show about what successful withdrawal requires?
Anders Sørensen, a psychologist working with Gøtzsche, took on 30 consecutive patients who contacted them for help. He set no limits — any drug, any diagnosis, any duration of use, any prior failed attempts. About half had been on drugs for 15 years or more. Most had tried to withdraw before without success. He worked with them in his spare time, without pay, mentoring most of them through to becoming drug-free. The protocol involved three questionnaires — one before tapering began, one after becoming drug-free, and a quality-of-life measure six months later. Patients had his mobile number and could call any time. Group gatherings four times a year let them share experiences. Once a year, an information evening for patients and relatives explained the basics of withdrawal, because relatives often resist the patient’s choice and undermine the process.
The work shows what successful withdrawal requires: time, individual pacing, peer support, family involvement, education about what the drugs have done and what the body is doing as it recovers, and a clinician who is genuinely committed to getting the patient off rather than keeping her on. A separate study of 250 adults who tried to come off psychiatric drugs found only 54% met their goal, and 54% rated their withdrawal symptoms as severe. Self-education and contact with others who had succeeded were rated more helpful than doctors — only 45% rated doctors as helpful, 16% withdrew against medical advice, and 27% did not tell the doctor or stopped seeing one. The Danish Research Ethics Committee killed Sørensen’s formal trial by demanding a psychiatrist take responsibility for safety — a psychiatrist from a department where two patients had recently been killed by overdosing was on the committee. Sørensen and Gøtzsche proceeded with the work outside the research framework. The patients were withdrawn anyway. The system that approved the drugs would not approve the means of escape from them.
Question 28: Why is forced psychiatric treatment described as a violation of human rights, and what do the appeals processes reveal about the system’s accountability?
Forced psychiatric treatment violates the United Nations Convention on the Rights of Persons with Disabilities, which virtually every country has ratified. It is the only sector of society where the law is systematically broken with no consequence. Italy and Iceland show coercion is not necessary. Akershus University Hospital in Norway operates without rapid tranquillisation. With proper de-escalation training and adequate alternatives — 24-hour refuges, sufficient staffing, time, and respect — coercion can be eliminated. The danger criterion used to justify forced drugging is not even consistent across jurisdictions: in Italy it is treated as a police matter, not a medical one. The argument that psychiatry cannot practice without coercion is empirically false.
The appeals system in countries that retain forced treatment is a sham. Gøtzsche’s group studied 30 consecutive cases from Denmark’s Psychiatric Appeals Board and found the law had been violated in every single one. All 30 patients were forced to take psychosis pills they did not want, even though less dangerous alternatives like benzodiazepines could have been used. In all 21 cases with information on prior drug effects, psychiatrists claimed the drugs had worked well, while none of the patients agreed. The harms of prior medication played no role in the decisions, including in seven patients with suspected akathisia or tardive dyskinesia. Five patients expressed fear of dying from forced treatment. Patients’ diagnoses were doubtful in nine cases. The catch-22: a patient who disagrees with her diagnosis is said to lack insight, which itself proves illness. The psychiatrists are investigators and judges; the appeal boards consist of the same people or their close colleagues; the patients have been declared insane and so their testimony does not count. Gøtzsche compares this to the Soviet Gulag and Nazi concentration camps, where the deaths of those held by the state were also recorded as natural deaths and the appeals were also sham. The comparison is uncomfortable. It is also accurate.
Question 29: What patient stories — Stine Toft, Luise, Silje Marie Strandberg, David Stofkooper — illustrate about what psychiatry routinely does to people?
Stine Toft entered psychiatry stressed by life troubles, was given depression pills, became manic from the pills, was diagnosed bipolar, and spent 14 years on an escalating cocktail of drugs — through a withdrawal she described as crazier than the medicated state, including periods when her body felt crooked and her hand would not release a stick during a game. She emerged with her sense of life returned, started a coaching practice, and now helps other patients withdraw. Her family, told repeatedly that she was sick and needed her pills, no longer sees her. The bipolar diagnosis is glued to her permanently. Her driver’s licence must be renewed every two years to prove she is not sick. Luise, killed by Danish psychiatrists with overdosed psychosis pills against her and her mother’s protest, told her mother before she died: “I shall be next.” Her death was recorded as natural. Her mother, Dorrit Cato Christensen, wrote a book about it; every year, on the anniversary, around 20 relatives of psychiatric patients killed in the same way demonstrate at the hospital.
Silje Marie Strandberg was bullied at 12, admitted at 16, given Prozac for moderate depression. She started cutting herself, became suicidal, was given a psychosis pill, then saw a hooded figure ordering her into a river. Over the next decade she received 21 different psychiatric drugs from 95 different doctors, was put in belts 195 times, was electroshocked, was diagnosed with schizoaffective disorder. A single caregiver who saw the girl behind the diagnoses brought her back. The book she planned to write was cancelled by her publisher when her story turned from a “psychiatric success” into a critique of psychiatry. David Stofkooper, a 23-year-old Dutch student with a flourishing social life, consulted a psychiatrist for repetitive thoughts, was given sertraline, became suicidal within two weeks. The dose was increased. He became zombified, with no libido, no emotions, no personality. Cold-turkey withdrawal followed. He never recovered the capacity to feel. He killed himself, leaving a note: “You present them with a problem that is created by the treatment you got from them, and as a reaction, get blamed yourself.” He had read Gøtzsche’s book — too late. Each story shows the same pattern: a patient enters with ordinary trouble, the drugs produce harm, the harm is read as worse illness, the dose escalates, life is destroyed. The pattern is not the exception. It is the system functioning as designed.
Question 30: What is the proposed plan for dismantling psychiatry as it currently exists, and why does the book argue that collective action is the only realistic path?
The proposal is direct: disband psychiatry as a medical specialty. In an evidence-based healthcare system, interventions that do more harm than good are not used. During a transition period, psychologists opposed to psychiatric drugs should head psychiatric departments. Existing psychiatrists should be re-educated as psychologists, or retire. The focus should shift to helping patients withdraw, not maintain them on drugs. Mandatory courses on withdrawal for all mental-health workers. A 24-hour helpline. Free tapering strips for patients. Apologies from psychiatric associations for the lies told about the chemical imbalance and about pills protecting against suicide. DSM-5 and ICD-11 discarded entirely. All treatment voluntary. Forced treatment unlawful. Psychiatric drugs available only for tapering, for permanent brain damage that cannot be tapered, and for narrowly defined medical situations like alcoholic delirium and surgical sedation. No financial conflicts of interest with manufacturers permitted for anyone working in mental health. The diagnosis-based gating of social benefits abolished, since it creates an incentive to label rather than help. The very words psychiatry, psychiatric disorder, and psychiatric drugs replaced with mental health, depression pills, psychosis pills, and speed on prescription — language that names what these things actually are.
The reform will not happen through professional self-correction. The leadership has too much invested in the lies, the industry has too much money tied to continued prescribing, and politicians have too much use for a profession that exerts tighter social control over difficult populations than the criminal justice system would allow. The only force that can move the system is collective public action — an unstoppable revolution of patients, relatives, and the few psychiatrists willing to defect. Slavery lasted thousands of years as an officially accepted norm. The Nazis came to power because too few protested early enough. People accept almost anything if they get used to it, no matter how unfair, harmful, or unethical. One worker striking is fired. Everybody walking out forces negotiation. The book is written so that those who recognise what is happening can become part of the resistance — the way Gøtzsche’s grandfather was part of the Danish resistance against Nazi occupation, taking real personal risk, and saving people who would otherwise have been killed by a system that called its killings natural deaths.
Analogy
Imagine a town where the firefighters are paid by the gallon of water sprayed, not by the fires extinguished. After a few decades, you would notice some odd patterns. Houses burning more often than they used to. Firefighters arriving at small kitchen fires and flooding the entire neighbourhood. Families who once had a smoke alarm now living with industrial sprinkler systems running permanently. Children of fire victims being preemptively flooded to prevent fires they have not had. When residents notice the houses are deteriorating from constant water damage, they are told their wood has a chemical imbalance that requires lifelong saturation. When mould develops from the damp, it is called a new disease — different from fires, but equally requiring water. When residents try to turn the sprinklers off, they discover the wood has rotted around the pipes; pulling the pipes out collapses the walls. They are told this proves they needed the water all along.
The firefighter chief insists the town has never been safer. The town’s newspapers are partly funded by the water company. The fire academy teaches new recruits that water is the answer to fires, mould, dry rot, termites, and unhappiness. When a new firefighter notices the houses without sprinklers in the next town are doing better than the houses with them, she is told she does not understand fire science. When a senior fireman publishes data showing water is the third leading cause of structural collapse after earthquakes and hurricanes, he is expelled from the firefighters’ association. When residents form support groups to slowly dry their houses out, the residents’ association refuses to help, and the regulator demands a licensed firefighter take responsibility for any drying — even though it was the firefighters who flooded the houses in the first place. The flood does not stop because the fires require it. The flood continues because the water is sold by the gallon, and stopping it would empty the company’s accounts and the chief’s pension.
That is psychiatry. The drugs are the water. The patients are the houses. The fires are ordinary human distress — grief, anxiety, sleeplessness, the bullying boss, the wrong marriage, the bereaved child — that almost always pass on their own with time, support, and the body’s own capacity to heal. The flood is what does the lasting damage. The book is the senior fireman explaining, with the data the company tried to hide, exactly how the system works and how to dry your house out before the walls collapse.
The One-Minute Elevator Explanation
You know how we are told that depression and anxiety are caused by chemical imbalances in the brain, and that psychiatric drugs correct them like insulin corrects diabetes? The drugs do not correct an imbalance. They create one. The chemical imbalance theory was disowned by the former director of the US National Institute of Mental Health in 1996, but 74% of major health websites still tell patients otherwise — because the lie is what justifies the prescription, and the prescription is worth tens of billions a year. Psychiatric drugs are the third leading cause of death after heart disease and cancer.
Think about that. One drug — Zyprexa — killed an estimated 200,000 patients up to 2007. In trials of 5,000 elderly demented patients, one in fifty was killed in just ten weeks on a psychosis pill. In a study of 281 first-episode psychosis patients with an average age of 29, 12% were dead within ten years — and the authors mentioned the deaths only in a flowchart of “patients lost to follow-up.”
So what happened when the trials kept showing the drugs barely worked? They redesigned the trials. They put the placebo group through cold-turkey withdrawal, mistook the withdrawal misery for relapse, and called the original drug “preventive.” Then they buried half the suicides, miscoded akathisia as “hyperkinesia,” recorded female anorgasmia as “Female Genital Disorder,” and changed primary outcomes after seeing the data — in two-thirds of trials.
The depression-pill effect on the Hamilton scale is 2 points. The smallest perceptible difference is 5 to 6. Fifty-seven per cent of patients with previously normal sex lives have it destroyed. Children on stimulants are 5 cm shorter at 16-year follow-up. Forty-one percent of Danish children stopped getting depression pills after one persistent critic kept publishing the data — and other countries’ Boards of Health refused to act, while New Zealand teenagers killed themselves at four times Denmark’s rate.
The brutal reality: psychiatry runs on the same lie barbiturate makers ran on for 50 years and benzodiazepine makers ran on for 30. It is the medical equivalent of the asbestos industry insisting the lung problems are caused by the patients’ anxiety about asbestos, and the entire profession is too invested in lifelong prescribing to admit the obvious truth.
[Elevator dings]
Want to know more? Look up the chemical imbalance myth Steven Hyman 1996 and Open Dialogue Lappland Stockholm psychosis. The evidence is hiding in the patient files, in the FDA’s own data, and in 67,319 pages of clinical study reports that no researcher outside the drug companies had ever read until Gøtzsche’s group read them.
12-Point Summary
1. Psychiatric drugs are the third leading cause of death. Built from regulatory data, large cohort studies, and unpublished clinical study reports, the estimate places psychiatric drugs behind only heart disease and cancer in lethality. One drug, Zyprexa, was estimated to have killed 200,000 patients up to 2007. In a meta-analysis of placebo-controlled trials in 5,000 elderly demented patients, 1 in 100 was dead within 10 weeks; FDA data revised the rate to 1 in 50. A Finnish cohort of 70,718 Alzheimer patients showed psychosis pills killed 4 to 5 patients per year compared with the untreated, with a 57% increased death risk on multiple psychosis pills. Patients labelled schizophrenic die 15 years earlier than the general population — and the drugs, not the patients’ lifestyles, account for much of the gap.
2. The chemical imbalance theory was always a marketing device, not a scientific finding. Steven Hyman, former director of the US National Institute of Mental Health, publicly disowned it in 1996. Mice genetically depleted of brain serotonin behave normally. Tianeptine, which lowers serotonin, “works” for depression as well as drugs that raise it. Depression pills “work” for 214 unrelated conditions. The drugs do not correct an imbalance — they create one, which is why patients struggle to come off them. A 2019 review of 39 popular health websites in 10 countries found 74% still attributed depression to a chemical imbalance, because abandoning the lie would mean abandoning the prescription.
3. Psychiatric diagnoses are checklist consensus, not biological categories. Major depression is declared when a patient has 5 of 9 common symptoms decided by show of hands at committee meetings. Reliability studies were so embarrassing that the American Psychiatric Association buried them. Diagnoses stick for life — affecting driver’s licences, custody, adoption, employment — with no court of appeal, even when the diagnosing clinician herself doubts the label. The schizotypy test for personality disorder is so broad that most psychiatrists would test positive. The single best protection against the system is to avoid getting a diagnosis in the first place.
4. The “psychiatric career” is the system functioning as designed. A patient enters with ordinary trouble, receives a depression pill, becomes manic from the drug, is rediagnosed bipolar, receives lithium and an antiepileptic, develops further harms read as new diseases, and accumulates diagnoses and drugs in parallel. The 21-year-old student described in the book left a private hospital on 11 simultaneous psychiatric drugs after 21 sessions of trans-cranial magnetic stimulation and 12 electroshocks. Silje Marie Strandberg received 21 different psychiatric drugs from 95 different doctors over 10 years, beginning at age 16 with Prozac for moderate depression. Drug harms and diagnostic symptoms overlap so completely that the harm reliably becomes the next diagnosis.
5. The trial methodology converts withdrawal injury into apparent drug efficacy. Virtually all psychiatric drug trials randomise patients already on the drug to abrupt placebo — cold turkey — which produces withdrawal misery indistinguishable from relapse. The trial then “finds” the drug prevents relapse. As few as two patients are needed to produce one with withdrawal symptoms, so the Number Needed to Harm is two; there cannot be a Number Needed to Treat below this. The depression-pill effect on the Hamilton scale is about 2 points; the smallest perceptible effect is 5 to 6. With atropine in the placebo to mimic side effects and preserve the blind, the effect collapses to 1.3 points and disappears.
6. Around half the deaths in psychiatric drug trials never reach publication. Suicides are recoded, omitted, or attributed to the underlying disease. Adverse events are reported only above arbitrary thresholds. Akathisia is miscoded as “hyperkinesia.” Female anorgasmia is recorded as “Female Genital Disorder,” with the blame placed on the patient. In two-thirds of trials, primary outcomes were changed, introduced, or omitted after data were seen, and 86% of trialists denied this when asked. Gøtzsche’s group read 67,319 pages of clinical study reports — material no researcher outside the companies had ever read — and found systematic selective reporting in 24 of 26 publications and 12% greater dropout on drug than on placebo.
7. Akathisia and tardive dyskinesia are common and often hidden. Akathisia — unbearable inner restlessness — afflicted 79% of mentally ill patients in one study who attempted suicide. Half of all fights at a psychiatric ward in another study were related to it. Half the patients on moderate-to-high haloperidol became markedly more aggressive, sometimes wanting to kill their psychiatrists. Tardive dyskinesia — irreversible involuntary movements — develops in 4 to 5% of patients on psychosis pills per year. FDA scientist Poul Leber extrapolated in 1984 that all patients on long-term psychosis pills might eventually develop it. Three years later, the president of the American Psychiatric Association told an Oprah Winfrey audience it was not a serious problem.
8. Sexual dysfunction is widespread, often permanent, and routinely deflected onto patients. Around 57% of patients with previously normal sex lives experience disruption on depression pills. In unpublished Phase 1 trials with healthy volunteers, over half developed severe sexual dysfunction, sometimes persisting after the drug was stopped. Some patients describe being unable to feel chili paste rubbed into their genitals. Some kill themselves on discovering the damage is permanent. The Prozac package insert lists decreased libido at 4%; the actual rate is 57%. The same compounds are repackaged and sold as Priligy for premature ejaculation. The denial is a marketing decision, not a scientific uncertainty.
9. Children are harmed at an industrial scale. ADHD is a social construct, not a biological entity. Stimulants are pharmacologically equivalent to crystal methamphetamine. The 16-year US MTA trial follow-up found children who consistently took their pills were 5 cm shorter than those who took very little. More than half of children on stimulants develop depression and obsessive-compulsive behaviour. Some have suddenly dropped dead in classrooms. The British drug agency’s own document recorded aggression on methylphenidate as 1.2% on page 61 and 11.9% on page 63 of the same report. After Gøtzsche’s persistent public warnings, Danish children’s depression-pill prescriptions fell 41% between 2010 and 2016. New Zealand, where prescriptions rose 78%, has the highest teenage suicide rate in the world — twice Sweden’s, four times Denmark’s.
10. Psychiatry without coercion and drugs produces dramatically better outcomes. In Lappland, the Open Dialogue model treats first-episode psychosis at home with the patient’s social network beginning within 24 hours. In Stockholm, standard biomedical care prevails. Five years later, 17% versus 75% of patients remained on psychosis pills; 19% versus 62% were on disability or sick leave; hospital bed use averaged 31 versus 110 days. Akershus University Hospital in Norway operates without rapid tranquillisation. Iceland has not used physical restraints since 1932. Italy treats danger as a police matter, not a justification for forced drugging. Psychotherapy halves the risk of a new suicide attempt in patients admitted after a suicide attempt. Trauma and severe stress underlie most psychiatric symptoms and tend to self-heal with time and humane support.
11. Safe withdrawal is possible but requires patient-led, slow, individualised tapering. Drugs must never be stopped abruptly; withdrawal can produce suicidal, violent, and homicidal states. Hyperbolic tapering — 10% reductions of the previous dose, slowing as the dose lowers — over months or longer is required. Tapering strips, developed in the Netherlands, allow 71% of depression-pill patients to taper off after a median of 56 days. Withdrawal symptoms emerge quickly after dose reductions and resolve within hours of restoring the dose; relapse, if it occurs at all, returns gradually. Distinguishing the two is essential, because doctors routinely tell patients in withdrawal that their illness has returned, locking them back onto the drug. Anders Sørensen withdrew most of 30 consecutive patients in his unpaid spare time. The Danish Research Ethics Committee killed his formal trial, while the same committee included a psychiatrist from a department that had killed two patients with overdosed psychosis pills.
12. The book proposes dismantling psychiatry as a medical specialty. The 15-point plan: disband psychiatry; re-educate psychiatrists as psychologists; mandate withdrawal training; provide free tapering strips; require psychiatric associations to apologise; abolish DSM-5 and ICD-11; make all treatment voluntary; outlaw forced treatment; restrict drugs to tapering, brain-damaged patients who cannot taper, and narrow medical situations like alcoholic delirium; ban financial conflicts of interest; remove diagnosis-based gating of social benefits; and replace stigmatising language — psychiatry, psychiatric drugs, antidepressants — with neutral terms like depression pills, psychosis pills, and speed on prescription. Reform will not come from the profession. It requires collective public action — the comparison Gøtzsche draws is to slavery and Nazi acquiescence: people accept almost anything if they get used to it, and few protest a sick system because it might be uncomfortable. His grandfather was in the Danish resistance against Nazi occupation. He sees the work the same way.
The Golden Nugget
The single most profound idea in the book — and the one fewest people will know — is that the entire long-term efficacy case for psychiatric drugs rests on cold-turkey trial design that mistakes withdrawal injury for relapse, and the system has made this methodology the standard precisely because it converts harm into apparent benefit.
This is not a peripheral methodological complaint. It is the structural reason psychiatry’s evidence base says one thing while patients’ lived experience says the opposite. Take a patient who has been on a depression pill for years. Randomise her to abrupt placebo. Within days she experiences anxiety, agitation, insomnia, suicidal thoughts, racing thoughts, dizziness, irritability — a constellation that looks identical to severe depression and anxiety. Restart her drug, and within hours the abstinence symptoms resolve. The trial concludes the drug “prevented relapse.” What it actually measured was the harm of forcing her into acute withdrawal. As few as two patients are needed to produce one with withdrawal symptoms. The Number Needed to Harm is two. There cannot be a Number Needed to Treat that survives this.
The implication runs through everything. The “relapse prevention” data used to justify lifelong prescribing — measuring withdrawal harm. The clinical “experience” of psychiatrists watching patients deteriorate when they try to come off — withdrawal harm. The patients themselves becoming convinced they cannot live without their pills — withdrawal harm. The professors of psychiatry confidently telling audiences of 600 people “Who would take insulin from a diabetic?” — staking the analogy on a body of evidence that, when stripped of cold-turkey design, shows the drugs do not work and cannot be safely stopped because the system never developed a way to stop them. The methodology was not chosen for scientific reasons. It was chosen because it produces the answer the industry needs, and once the methodology became standard, the whole edifice of long-term psychiatric prescribing — covering hundreds of millions of patients globally, generating tens of billions of dollars annually, defining the profession’s identity — became dependent on a study design that systematically converts iatrogenic injury into evidence of therapeutic benefit. The patients have been hooked for decades on drugs whose continued necessity was demonstrated by the suffering of their own withdrawal.
The British Broadcasting Corporation (BBC) Science Focus article “Something ‘unprecedented’ is now happening to Earth’s rotation, scientists say” claims that climate change is causing an “unprecedented” slowing of Earth’s rotation by 1.33 milliseconds per century, something not seen in 3.6 million years. This is false. The data show that millisecond-scale variations in Earth’s length of day are routine, naturally occurring, and both technologically and biologically insignificant.
The BBC sensationalizes the issue as something extraordinary, stating that today’s rate of change is “unequivocally” unlike anything in millions of years. But Earth’s rotation has never been constant. As explained in the Climate Realismrebuttal to Euronews on the same topic, seasonal atmospheric mass redistribution alone produces annual variations of 0.5 to 1 millisecond. Interannual ENSO shifts add another ±0.3 to 0.5 milliseconds. Decadal core-mantle coupling produces swings of 3 to 4 milliseconds. These are measured, observed phenomena, not model projections.
In that context, 1.33 milliseconds per century is not planetary destabilization. It is background noise, certainly nothing that would be noticed by even the most sensitive ecosystem or living being.
The BBC emphasizes that melting ice shifts mass toward the equator, comparing it to a spinning skater extending their arms. That physics analogy is correct in principle. What is incorrect is the implication that this is some new geophysical regime. Earth’s length of day has fluctuated throughout recorded history due to tidal friction from the Moon, atmospheric angular momentum exchange, ocean circulation, and core dynamics. The long-term tidal braking trend alone is about +1.7 to +1.8 milliseconds per century based on 2,500 years of eclipse records, a rate comparable to or larger than the BBC’s headline number.
Even more inconvenient for the narrative is the recent acceleration of Earth’s rotation. As noted in the Climate Realism piece, June 29, 2022 was the shortest day ever recorded in the atomic timekeeping era, about 1.59 milliseconds shorter than 86,400 seconds. If climate change were producing a simple, monotonic slowdown, we would not be seeing record-setting shorter days in the same decade.
The BBC also attempts to inflate the significance of the change by invoking dramatic metaphors. One researcher is quoted comparing the energy involved to a catastrophic earthquake, saying: “The change in the Earth’s rotational energy is equivalent to a magnitude 9.0 earthquake.” This is nothing but irresponsible doom mongering. The comparison is not about destructive force, as the article admits, but about abstract energy equivalence. It is an analogy designed to impress, not to inform. No cities are shaking. No ecosystems are collapsing. No lifeform on Earth can feel a thousandth of a second difference.
Let’s put the number in perspective. One millisecond is 0.001 seconds. A 1.33 millisecond change represents approximately 0.000015 percent of a 24-hour day. Human circadian rhythms are tuned to roughly 24 hours, not to thousandths of a second. There is no plausible biological mechanism by which such a tiny change could affect human health, animal behavior, or plant life. It is physiologically undetectable. Even if the rate of change were accurate, consistent, and sustained, it would take approximately 75,188 years for the day to lengthen by exactly one full second.
Technologically, the “crisis” BBC claims is even more absurd. Modern systems already handle irregular rotation through leap seconds. Since 1972, 27 leap seconds have been added to Coordinated Universal Time to synchronize atomic clocks with Earth’s spin. Discussions are underway about possibly implementing a negative leap second because of recent acceleration. GPS, spacecraft navigation, financial trading platforms, and astronomical observatories continuously ingest Earth orientation parameters from the International Earth Rotation and Reference Systems Service and adjust automatically. They already deal with corrections far larger than 1 millisecond.
Society adjusts clocks by one hour every year for daylight saving time in many regions. That is 3.6 million times larger than the 1.33 millisecond change being described. Leap years add a full day. Compared to those routine adjustments, this isn’t even a rounding error.
The BBC article goes further, suggesting that by 2100 climate change could outpace even the Moon’s gravitational influence on day length. That projection is model-dependent and scenario-driven. It assumes the now discredited and removed RCP8.5 high-emissions pathways and continued ice loss at rates embedded in climate models. It is not an observed reality. It is a modeled extrapolation.
And even if that projection were accurate, we are still talking about millisecond-scale shifts. The practical consequences remain limited to timekeeping adjustments that modern civilization already manages with ease. There is no crisis as the infinitesimal change in the Earth’s rotation has and can have no plausible impact on ecosystems or living beings.
The most telling line in the BBC piece is the assertion that “human influence on the Earth system has become so profound that we are now changing the very way our Earth spins.” That statement is designed to provoke awe and alarm. It is also technically trivial. Humans also change Earth’s mass distribution through groundwater extraction, reservoir construction, mining, and urbanization. These processes are measurable, they are not existential.
In the end, the BBC’s hyped 1.33 millisecond per century change to the Earth’s length of rotation, even if true, represents trivial geophysical adjustment. One that is not biologically meaningful, technologically disruptive, and not outside the envelope of natural variability observed over decades and centuries.
Framing a millisecond-scale variation as “unprecedented” planetary destabilization represents a a textbook example of taking a measurable but trivial geophysical adjustment and inflating it into a symbolic crisis. It is a giant nothingburger. An attempt to scare people with a story that is not scary in the least.
Japan has achieved dramatic long-term declines in childhood tooth decay — despite never implementing nationwide water fluoridation and only recently recommending fluoridated toothpaste, according to a new study in BMC Public Health.
The research, by Yoshihisa Yamashita, D.D.S, Ph.D., of Kyushu Dental University, describes Japan’s experience as a “natural social experiment” that could reshape how public health experts address preventing dental cavities at the population level.
Unlike many other high-income countries, Japan has historically limited fluoride exposure during childhood — which makes the country a “unique and underexplored case.”
Using decades of national dental survey data, the study found that average rates of tooth decay among Japanese 12-year-olds fell steadily over roughly 40 years.
Levels dropped from a peak national Decayed, Missing, and Filled Teeth (DMFT) index score of 4.75 in 1984 to just 0.53 in 2023 — “well below levels historically reported in populations exposed to systemic fluoride through community water fluoridation,” according to the study. DMFT is the standard international measure of decayed, missing and filled teeth.
“This trajectory unfolded in the absence of nationwide community water fluoridation,” the paper states. High-fluoride toothpaste was not widely available in Japan until 2017 and was not officially recommended for school-aged children until 2023, according to the study.
Dr. Griffin Cole, conference chairman of the International Academy of Oral Medicine and Toxicology, said the study’s method of using national dental records across an entire population, rather than measuring fluoride exposure among a small group, provided important evidence on oral health.
“By examining real-world outcomes, Yamashita’s analysis provides strong evidence of what we already know: Oral health can improve through nutrition, behavior and broader public health measures, rather than adding fluoride chemicals to our water supplies,” he said.
The findings are the latest to challenge long-standing assumptions promoted by organizations such as the Centers for Disease Control and Prevention (CDC) and the American Dental Association that systemic fluoride exposure through community water fluoridation explains large-scale reductions in tooth decay.
Decades-old study by U.S. researchers still used to justify fluoridation?
The study compared modern Japanese cavity rates with historic U.S. data collected by early fluoride researcher and dentist H. Trendley Dean in the 1930s and 1940s, and later consolidated by F.J. McClure.
Despite a small study size and issues with collection bias, Dean’s research formed the scientific foundation for North American fluoridation policies by showing lower cavity rates in four communities with naturally fluoridated water supplies.
But according to the new study, Japan’s current cavity rate is substantially lower than the minimum levels observed in Dean’s high-fluoride communities — even though Japan’s drinking water contains effectively no added fluoride.
Yamashita said it was also notable that Japan has only recently introduced high-fluoride toothpaste. Most toothpaste previously available contained less than 1,000 parts per million (ppm).
Popular children’s toothpaste brands in the U.S., including kids’ Crest and Colgate, contain about 1,100 ppm.
The paper argues that broader social and behavioral changes likely play a major role in reducing tooth decay.
The author suggested several possible contributing factors, including:
A long-term decline in sugar consumption and shifts in dietary habits.
Changes in childhood feeding and parenting practices, including reductions in prolonged bottle feeding.
Universal access to dental care through Japan’s national health insurance system.
Improved oral hygiene awareness and preventive behaviors as a result of greater healthcare access.
Fluoride ‘not a magic bullet for controlling tooth decay’
Japan’s per-capita sugar consumption has declined by more than 30% since the 1970s, according to national statistics cited in the paper.
However, the author noted that cavity rates continued falling even after sugar intake stabilized, suggesting that multiple factors likely worked together over time.
Dr. Hardy Limeback, professor emeritus in the Faculty of Dentistry at the University of Toronto, told The Defender that a 1996 Japanese study found even lower tooth decay rates in Japan during World War II, when sugar supplies were scarce and rationing took place.
“The effects of total fluoride did not seem to have much effect on the caries rates in Japan in the 20th century,” Limeback said. “In that country, increasing fluoride exposures by means other than fluoridation did not appear to be ‘one of the top 10 public health procedures of the 20th century,’ as claimed for fluoridation by the CDC in America.”
“Fluoride is not a magic bullet for controlling dental decay,” Limeback added. “Limiting sugar intake is.”
Countries should look beyond fluoride for dental health solutions
The study arrives amid renewed international discussion about fluoride safety.
Following a landmark 2024 judgment that found fluoride at current levels recommended for water fluoridation in the U.S. posed an “unreasonable risk” to children’s health, communities and states across the country stopped adding fluoride to their water.
The ruling also mandated that the U.S. Environmental Protection Agency (EPA) regulate it.
Yamashita argued for a “broader multicausal approach” to oral health policy.
“Substantial and sustained reductions in dental caries can be achieved through multicausal pathways,” the paper concludes, “even in the absence of universal water fluoridation.”
Yamashita said countries seeking to reduce tooth decay should consider not only fluoride-based strategies, but also policies addressing diet, early childhood environments, access to care and wider social determinants of health.
He also suggested that a bias toward fluoride has posed a barrier to understanding the multicausal approach that can improve dental health.
“This analysis highlights insights that have long remained unrecognized — not because the evidence was unavailable, but because prevailing frameworks shaped what researchers expected to see,” Yamashita wrote.
When the House of Commons was debating how much to increase the time limit for detention without trial the question of torture came up. Officially this was limited to the nice considerations of whether it was all right to send people to places where torture is used and whether Britain can use information collected by the use of torture in other countries. This discussion gave an impression of democratic Britain as the home of civilised behaviour where the very idea of torture is repugnant to our legislators – unlike, say, the US with its secret CIA jails… In reality, the British state has a long history of using and developing a whole range of torture techniques. … continue
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