Aletho News

The 12 Screenings That Manufacture the Patients They Claim to Find

An Essay on Threshold Manipulation, Overdiagnosis, Cascades, and the Markers That Aren’t What They Claim

Lies are Unbekoming | June 10, 2026

The Pattern Across the Programmes

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.

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.

The Great Cholesterol Con (2007) – Unbekoming

3. Blood Sugar — “Prediabetes”

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

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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

CT Scans: The Cancer Machine – Unbekoming

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Group C — The Cascade

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 Trap (2026) – Unbekoming

8. Prostate Biopsy

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

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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.

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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.

Interview with Jamie Andrews – Unbekoming

11. Antibody Tests

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

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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.

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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.

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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.

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References

1. 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.
2. 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.
3. 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.
4. 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.
5. 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.
6. Genuth S, Alberti KG, Bennett P, et al. Follow-up Report on the Diagnosis of Diabetes Mellitus. Diabetes Care. 2003;26(11):3160–3167.
7. 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.
8. 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.
9. 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.
10. 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.
11. 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.
12. 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.
13. Abramson JD, Rosenberg HG, Jewell N, Wright JM. Should people at low risk of cardiovascular disease take a statin? BMJ. 2013;347:f6123.
14. McCreight LJ, Bailey CJ, Pearson ER. Metformin and the gastrointestinal tract. Diabetologia. 2016;59(3):426–435.
15. Source materials on gestational diabetes thresholds and postpartum glucose surveillance from Medicalized Motherhood, including current ACOG and ADA screening protocols.
16. 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.
17. Gøtzsche PC, Jørgensen KJ. Screening for breast cancer with mammography. Cochrane Database of Systematic Reviews. 2013;6:CD001877.
18. 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.
19. 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.
20. Smith-Bindman R, Chu PW, Azman Firdaus H, et al. Projected lifetime cancer risks from current computed tomography imaging. JAMA Internal Medicine. 2025.
21. 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).
22. 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.
23. 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.
24. Ablin RJ. The Great Prostate Mistake. The New York Times. March 9, 2010.
25. 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.
26. 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.
27. Loeb S, Vellekoop A, Ahmed HU, et al. Systematic review of complications of prostate biopsy. European Urology. 2013;64(6):876–892.
28. 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.
29. Antimicrobial Resistance Collaborators. Global burden of bacterial antimicrobial resistance in 2019: a systematic analysis. The Lancet. 2022;399(10325):629–655.
30. 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.
31. 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.
32. 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.
33. 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.
34. 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.
35. 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.
36. 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.
37. 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.
38. 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.
39. Banks NT. AIDS, Opium, Diamonds, and Empire: The Deadly Virus of International Greed. iUniverse, 2010.
40. 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).
41. 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.
42. Goldgar D, Venne V, Conner T, Buys S. BRCA phenocopies or ascertainment bias? Journal of Medical Genetics. 2007;44(8):e86.
43. 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.
44. 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.
45. Association for Molecular Pathology v. Myriad Genetics, Inc., 569 U.S. 576 (2013).

June 14, 2026 - Posted by aletho | Corruption, Deception, Science and Pseudo-Science, Timeless or most popular