Wrong, BBC, No ‘Climate Driven Millisecond Earth Rotation Crisis’ Exists
By Anthony Watts | ClimateRealism | May 29, 2026
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 Realism rebuttal 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.
Earth is not a precision quartz watch. It is a rotating, fluid planet with a molten core, dynamic oceans, shifting winds, and a gravitational partner in the Moon. Its spin rate fluctuates; it always has.
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.
The Gene Was Fake. The Body Believed it Anyway.
A fake DNA result and the uncomfortable truth about how much of your health your beliefs are quietly shaping
By Dr. Roger McFillin | Radically Genuine | May 31, 2026
In 2018, a team of researchers at Stanford ran an experiment that should have made bigger headlines than it did. They recruited a few hundred people under the cover story that they were studying the relationship between DNA and diet. They swabbed everyone’s cheeks, ran real genetic tests, and then sat each person down to deliver their results.
Here is the trick: the results were fake. Or rather, they were assigned at random, with no relationship to what the swabs actually showed. Some people were told they carried a high-risk version of a gene linked to poor exercise capacity, or to feeling hungry after meals. Others were told they carried the protective version. Then the researchers measured what happened to their bodies.
The people told they had the “bad” exercise gene performed measurably worse on a treadmill. Their lung function changed. They felt more exhausted, sooner, and they ran out of steam earlier, even when their real DNA said nothing of the sort. In the eating experiment, people told they had the “protective” satiety gene produced more of the hormone that signals fullness and reported feeling more satisfied after the same meal as everyone else.
The kicker, reported by the Stanford team, was this: the effect of what people believed about their genes was, in some measures, larger than the effect of the genes themselves.
Sit with that for a moment. A story about your DNA changed your DNA’s behavior more than your DNA did.
What if the steady drip of fear we live inside, the warnings about disease, the urgency of prevention, the dread of the next pandemic, is not only describing our health but quietly shaping it?
What if the constant push toward more checkups, more screening, more tests for things we would never otherwise have noticed slowly trains us to inhabit the identity of the perpetually sick?
And what if a belief, held tightly enough by enough people, does not stay politely inside the mind but reaches down into the body, the way it reached into the lungs of those runners on the treadmill, so that a culture convinced it is fragile and broken and doomed begins, quietly, to become exactly that?
These are questions, not verdicts. But they all circle the same suspect: an idea so familiar we have stopped noticing it is an idea at all. Genetic determinism, the belief that our genes are a sealed verdict, that disease is written into us at conception, that biology is destiny.
It is not a comforting story but a disempowering one, a marketable one, and above all a frightening one, because a person who believes in genetic determinism has surrendered their power before they ever thought to use it. But where our attention goes, our energy flows. And if that is true, then we are not the prisoners of this story at all. We are only beginning to understand the power we carry as conscious, creative beings. The story about genes, in most of the cases that matter most to us, is simply wrong.
The story we were sold
For the better part of three decades, we have been taught to think of the genome as a blueprint. When the Human Genome Project was completed in the early 2000s, the language around it was almost biblical: the “book of life,” the “code of codes,” the “instruction manual” for a human being. Newspapers ran a steady drumbeat of discovery: a gene “for” intelligence, a gene “for” depression, a gene “for” breast cancer, a gene “for” being unfaithful.
The blueprint metaphor is seductive because it is clean. A blueprint fully specifies a building. Hand it to any competent crew and you get the same house every time. If your genome is a blueprint, then your health, your temperament, your fate: these are simply the structure that gets built. Nothing to be done but watch it go up.
But here is the strange thing about a metaphor this powerful: we adopted it before the science was in. And as the science has come in over the last twenty years, it has steadily dismantled the very picture that sold it to us.
The conditions that fill our clinics and our anxieties (ADHD, heart disease, depression, type 2 diabetes, the common cancers) are not determined by one decisive gene but by hundreds or thousands of genetic variants, each nudging risk by a vanishingly small amount. There is no “gene for ADHD” or those other conditions mentioned. Instead, what exists is a faint pull spread across the whole genome, one that environment, behavior, and chance can tip in any direction.
This matters because of a word that gets badly misused: heritability. When you read that a condition is “80% heritable,” it is natural to hear “80% inevitable,” or “80% genetic in you, personally.” Neither is what the number means.
Heritability is a population statistic. It describes how much of the variation between people in a given environment can be statistically attributed to genetic differences. It says nothing about how fixed a trait is, and nothing about any individual.
The cleanest illustration is height, which is roughly 80% heritable. Yet average height in many countries rose by several inches over the twentieth century, far too fast for the gene pool to have changed. What changed was nutrition. A highly heritable trait moved dramatically because the environment moved. Heritable and changeable are not opposites. They were never opposites.
Then there is the discovery that should have ended the blueprint era on its own. When researchers ran large genome-wide studies hunting for the genes behind these heritable psychiatric and physical conditions, the genes mostly weren’t there, or rather, they were there in such tiny, scattered fragments of effect that they couldn’t add up to the heritability the twin studies had promised.
Geneticists named the gap politely: the “missing heritability problem.” The promised master genes for our most common diseases were searched for at enormous expense, and they did not show up. What showed up instead was complexity, contingency, and a genome that behaves far less like a verdict than we were told.
So why does the picture survive?
An idea this disempowering does not endure for decades on the strength of its evidence. It endures because it pays. Whole industries rest on the premise that you are broken in ways only they can manage. The determinism story feeds a steady pipeline of genetic tests, lifelong prescriptions, screening programs, and specialist referrals, each one justified by the conviction that your biology is a defect to be monitored rather than a system you can shape.
It underwrites diagnostic categories that expand a little wider every year and interventions that grow a little more expensive. You do not need to imagine a smoke-filled room or a coordinated conspiracy. You only need to notice the incentive: a story that keeps people anxious, dependent, and coming back is a story with deep-pocketed sponsors, and a person who feels capable and well is, on a great many balance sheets, a customer lost.
Planting a Seed
If the blueprint metaphor is broken, what replaces it?
Think of a seed instead. A seed is not the plant. It is a bundle of possibilities that only becomes something in contact with soil, water, light, and weather. Plant the seed in rich ground and it flourishes; plant it in drought and it withers; plant it in shade and it grows crooked toward whatever light it can reach. The seed sets the range of what is possible. The soil and the season decide what actually grows.
This is what the field of epigenetics has revealed about our DNA. Genes are not simply “on.” They are switched on and off, turned up and turned down, by chemical marks (methylation, histone modification) that respond continuously to what we eat, how we sleep, what we breathe, how stressed we are, and even how connected we feel to other people. The DNA is the seed. Everything around it, and everything we do to it, is the soil.
The evidence here is vivid. There is a famous strain of mouse, the agouti mouse, in which a mother’s diet during pregnancy determines whether her genetically identical pups are born yellow, fat, and disease-prone or brown, lean, and healthy. Same seed. The nutrition is the soil, and the soil decides which animal the seed becomes.
In humans, researchers studying people conceived during the Dutch “Hunger Winter” famine of 1944–45 found epigenetic and metabolic marks of that prenatal starvation still measurable decades later, alongside elevated rates of certain diseases. The famine ended in months. Its signature lasted a lifetime, written not into the genes but onto them.
The lesson is not that environment overrides genetics. It is subtler and more interesting: the genome is built to be responsive. Responsiveness is the point. We did not evolve sealed verdicts. We evolved seeds that read the ground they land in.
So how far does this reach?
If a fake gene can change a body, what can a strongly held belief do? We are used to treating the mind as a spectator to our health, watching from the stands while the real game plays out below in cells and chemistry. What if where we place our attention, and what we expect to be true, can move the body in ways we can actually measure?
You see this most clearly in two phenomena. With the placebo effect, the mere expectation of help is enough to move the body: pain eases, mood lifts, stress drains away, blood pressure settles. Belief shifts the body out of the clenched, defended state we might fairly call dis-ease, and into one of greater ease, the calm physiology in which the body’s own capacity to repair itself can do its work.
Its dark twin, the nocebo effect, is the body worsening in response to the expectation of harm. Patients warned of a drug’s side effects get those side effects more often, even on sugar pills. Expectation is not a passive lens through which we view our health. It is an active input into it.
And consider the most powerful nocebo of all: the prognosis. Two doctors can hold the exact same statistic and hand a patient two entirely different futures. One says, “Ninety percent of people with this disease are dead within five years.” The other says, “One in ten people with this disease recover, and we are going to do everything those people did.” The facts are identical. The arithmetic is identical. But which sentence would you want spoken over your body? Which one leaves a door open, and which one quietly walks you toward its conclusion?
The question cuts deeper when the prophecy is inherited. If your mother died of breast cancer, or your father of heart disease, the medical system can begin to treat you as a smaller, earlier version of them: a case history waiting to repeat itself, marked from your first appointment as the one who is next. At what point does being watched as a fate begin to summon it? At what point does a family history, handed to you as a verdict instead of a probability, become a script you never agreed to perform?
Now return to the Stanford experiment with this in mind. When people were told they carried a high-risk gene, their bodies began, in part, to enact the prophecy. That is the nocebo effect aimed squarely at our deepest story about ourselves: the story of our own DNA. And it points to the most unsettling possibility in this whole essay: that genetic determinism is not only a flawed scientific theory. It may be a self-fulfilling one. Tell a person they are doomed by their biology, and you have just added a risk factor.
Self Fulfilling Prophecies
Here is the part I find genuinely unsettling, and it is the heart of this argument.
A prophecy does not need to be true to come true. It only needs to be believed with enough authority that the believer begins, without noticing, to arrange the world around it. And our culture has no prophecy more authoritative than the one stamped with the word genetic. Tell people their depression, their weight, their heart, their cancer was written into them before birth, and you have not merely described their future. You have begun to build it.
Watch how the loop closes. A person told they are genetically doomed turns their attention toward the threat, and attention is not passive. It is the most powerful filter the brain owns, the thing that decides what is real enough to act on.
Fixed on the fear, the body settles into the physiology of fear: chronic stress, vigilance, inflammation, the very biochemical soil in which disease grows best. The behaviors that would protect them start to feel pointless, so they quietly fall away. Every twinge becomes evidence. Every symptom is a confirmation. In time the prophecy delivers what it promised, and everyone nods knowingly: the genes, of course. This is the dark engine beneath the Stanford treadmill. Those runners did not fake their exhaustion. A belief reached into their lungs and made it true.
Now hold that loop in your mind and run it backwards, because the same machinery turns both ways. This is what people are reaching for, often clumsily, when they talk about being conscious creators.
Strip away the mysticism and a hard, almost mechanical truth is left standing: where attention goes, energy flows, and where energy flows, biology tends to follow. Not because thoughts are magic, but because attention decides what you notice, what you fear, what you feed, and what you repeatedly do. And what you repeatedly do, across months and years, is precisely what lays down the epigenetic marks and builds the body you have to live in.
So if the genome is a seed, you are not the seed. You are the one tending the ground. You did not choose what you were handed, and no amount of will turns a drought into rain. But the soil is made of things you touch every single day: what you eat, how you sleep, who you let close, what you rehearse in your mind, the story you accept about who you are and what you are doomed to become.
A gardener cannot command a seed. A gardener can absolutely decide what grows. To be a conscious creator is nothing more mystical than that, and nothing less powerful: to stop being the passive ground your inheritance falls into, and to start, deliberately, attending to what you want to take root.
You are not only the seed. You are the soil, the season, and the hand that tends the ground.
So tend it.
And be careful what you let take root. Attention is the gardener’s most powerful tool, and almost everything competing for yours has an interest in keeping you afraid. The headline built to alarm you. The endless forecasting of the next catastrophe. The tired paradigm that profits whenever you believe you are broken, powerless, and next in line. None of it is neutral, and fear is among the fastest-growing things you can plant. Give it your attention and it will spread until it crowds out everything else.
You do not have to fight every frightening thought. You only have to stop watering it. Turn your attention, again and again, toward what you actually want to grow: the proof that you are capable, the people who steady you, the ordinary daily acts that tell your body it is safe. This is not denial and it is not wishful thinking. It is the most practical thing you can do, because where your attention goes your energy flows, and your biology, patiently, follows.
You were handed a seed. What grows from it is still, in most of the ways that matter, yours to decide.
AWAKEN.
Immune bootcamp: Training your body to fight cancer, superbugs & more
The HighWire with Del Bigtree | May 28, 2026
New research from Trinity College Dublin shows that “training” immune cells with interferon gamma, rather than vaccinating, can supercharge the body’s ability to kill drug-resistant superbugs like MRSA and tuberculosis. Meanwhile, studies on bee venom and gut microbiota are challenging 50 years of cancer orthodoxy, as scientists increasingly look to nature to do what chemotherapy can’t.
Wrong, Sky News, Human-Caused Climate Change Isn’t to Blame for the Alaskan Megatsunami
By Linnea Lueken | Climate Realism | May 18, 2026
Sky News claims that a recent Alaskan tsunami was caused by a climate change-induced landslide. This claim is speculative at best, since it is difficult to say whether the particular tidewater glacier is retreating because of warming or other factors that impact glacial movement. Climate change and glacial retreat have always occurred, but media overuse of the former term conflates natural shifts with supposed human-caused change. This has made it difficult, if not impossible, to discuss natural hazards.
The Sky News article, “Alaskan megatsunami bigger than Empire State Building triggered by climate change,” tries to convince people that using fossil fuels is causing megatsunamis. Sky News writes “[t]he wave at the Tracy Arm Fjord in the Tongass National Forest was triggered by a rock landslide which was driven by climate change,” and the “climate change” link goes to a list of Sky News articles connecting natural phenomena to human use of fossil fuels. This is not true. Recent warming is not all human-driven, except locally in the case of the urban heat island effect.
The amount of warming that humans contribute by industry and other activities releasing carbon dioxide is a question of ongoing debate. It’s true that industrialization has increased the amount of carbon dioxide in the atmosphere, but ice core data show that carbon dioxide was gradually rising even before that, most likely due to outgassing from the oceans as the world warmed after the end of the Little Ice Age, as discussed in Climate at a Glance: Natural vs. Human Contributions to Greenhouse Gases and Global Average Temperatures. Human contributions to greenhouse-gas related warming are very small, probably around 0.28 percent, because the vast majority of the greenhouse effect comes from water vapor, not carbon dioxide.
Modern warming is likewise not unprecedented. In fact, global average temperatures are still lower today than there were during the Holocene Climate Optimum.
In the case of this tsunami, glacial retreat is said to have destabilized a section of the fjord walls and a massive landslide resulted, which caused the second-tallest tsunami wave on record (that is to say, that we are aware of) at 1,578 feet high. The record is still held by the 1958 Lituya Bay landslide-caused tsunami, which was an incredible 1,720 feet high. No one was blaming climate change back then.
Gradual retreat of glacier ice can destabilize valley walls like those of the Tracy Arm fjord, but whether climate change (human or otherwise) is the main cause of this specific glacial retreat is unknown.
NASA reports that moderate rainfall was a contributing factor to destabilizing the slope, as is the case with many landslides.
Tidewater glaciers like the South Sawyer Glacier undergo hundred-plus-year-long retreat and advance cycles, and are unique in that they lose ice primarily through calving, or breaking off massive chunks, rather than gradual melting. It is notable that tidewater glaciers are not as sensitive to climate during their retreat and advance cycles as other kinds of glaciers are. Calving is impacted by water depth (which changes as the ice retreats or advances), along with other physical conditions like mass imbalances. Today, there are tidewater glaciers in Alaska that have advanced, not retreated, amid the modest warming of the past century. The Johns Hopkins Glacier is one of them; it has advanced a mile since 1948. It is unclear how global climate change could be causing one tidewater glacier to collapse while others, in the same climatic region, are expanding.
Because there are a lot of factors that influence tidewater glacier cycles, and some Alaskan glaciers’ advances are unaffected by recent modest warming, it is unclear whether to blame climate change – natural or otherwise—for the recent megatsunami, and even more specious for Sky News to blame human activity for it by extension.
The Biggest Breast Cancer Advance in the Last Twenty Years
By Alan Cassels | Brownstone Institute | May 17, 2026
In medicine, we love a good heroic story. A patient suffers a serious disease. A drug company produces a brilliant new drug which proves to be beneficial. Lives are saved. Everyone is happy. Another battle won in the war on disease. Science marches triumphantly forward.
But sometimes the real story is less heroic and far more awkward. And the major “advance” comes not from a new drug, but from the opposite: because patients stopped swallowing a drug that never should have been so widely used in the first place.
That is almost certainly the case of breast cancer in North America in the early 2000s.
The pivotal moment came in the summer of 2002 when a major randomized trial, called the Women’s Health Initiative (WHI) was published, aiming to answer a question which physicians had long pondered: was long-term use of hormone replacement therapy, typically prescribed for women going through menopause, good for the heart?
Up to that point, hormone therapy had been marketed as a kind of fountain-of-youth elixir for menopausal women. Promising to protect the heart, keep bones strong, preserve youthfulness, and generally smooth out biological inconveniences of aging, women were prescribed these drugs and stayed on them for years, sometimes for decades. At that time, there was considerable debate about long-term effects, with some experts claiming the heart protective-effects of hormones were so pronounced that even studying the issue was a waste of time.
Launched in 1997, the WHI enrolled more than 16,000 post-menopausal women to test the effects of combined estrogen-progestin. Another arm tested the effects of estrogen alone in 10,000 women who had undergone a hysterectomy. The larger trial was terminated three years earlier than originally planned, once the findings showed an increased risk of breast cancer, heart disease, stroke, and blood clots among participants. The smaller trial was also halted a year earlier than planned due to increased risk of stroke.
That was the day that the music died for hormone therapy.
Or at least we thought.
Within months women stopped taking and physicians stopped prescribing hormone therapy. The everyday use of this class of drugs fell dramatically, by roughly half within a year.
And then something remarkable happened.
Breast cancer incidence in the United States dropped. Some say that the rates had been in decline for several years, but the drop was significant, falling by roughly six to seven percent in 2003. It was one of the sharpest year-to-year declines ever observed. The drop was especially pronounced among women over 50 and in estrogen-receptor positive tumors, precisely the cancers most likely to be stimulated by hormones.
This wasn’t a subtle statistical wiggle. For epidemiologists, this was the sort of signal that almost never happens so cleanly in real life. Usually population health trends are messy, tangled up in dozens of possible explanations. There are long latency periods with cancer yet here a cause and effect appeared almost choreographed.
Drug exposure goes down. Disease incidence goes down, Just like that. Overnight, by stopping a drug we probably saw the most important advance in the fight against breast cancer in the last half century. But….
HRT Revisited
But today? Memories are short, and for many obstetricians, women’s health advocates, and even health reporters, it seems like the lessons from the WHI are being rewritten. The known and proven harmful effects of hormones on women’s health are undergoing a massive rewrite which is stimulating a resurgence in HRT.
This new Hormone Replacement Therapy conversation lately is captured in such articles as this piece from PBS; “How a Decades Old Study Gave Hormone Therapy a Bad Reputation,” which calls the WHI a “flawed” study. Other major media outlets like the New York Times, the Washington Post and TIME Magazine are eagerly celebrating the renewed interest in menopause, emphasizing that women’s health concerns are never adequately dealt with, and that HRT needs a second look.
The media attention was amped last year up when the FDA convened an Expert Panel on Menopause and Hormone Replacement Therapy for Women. That meeting led to the removal of the boxed warnings in November 2025 even though the labels still warn of the risk of uterine and endometrial cancer associated with estrogen-only HRT, which is typically prescribed to people who have had their uterus removed through a hysterectomy.
A lot of the hullabaloo over the removal of the FDA’s Black Box Warning on Hormone Therapy relied on a strange mix of both revisionism (the science has changed) and egalitarianism (women needed “more choice”). For the media, this was an easy sell.
The rationale used by the FDA committee and hormone aficionados everywhere was that the science has been fully reinterpreted, and “corrected.” Let’s be clear what has happened: there has been new “analyses” of the effects of hormones, but no new original research showing that the previous safety concerns are exaggerated.
Much of the renewed support for HRT uses the ‘window of opportunity’ argument that suggests that it is safe if a 50-year-old woman takes hormones, but in her 60’s it’s unsafe. Can we really accept that the effects of these drugs on women would be dramatically different at some sort of arbitrary age-related cutoff? That’s the line we are expected to believe.
But look at how that argument is easily confounded. If the drugs show a reduced harm in younger women that’s mostly because, for any disease, younger age usually means lower disease burden. The revisionists discredit the WHI even though there were thousands of women in their 50’s in that trial, and many of them were among those harmed.
A distinction needs to be made here, where one has to examine the exact reason why one is taking hormones. Is it to control menopausal symptoms (especially hot flashes, vaginal dryness) or to prevent diseases of aging (breast cancer, heart disease, dementia)?
The WHI study was aimed at determining the long-term, post-menopausal effects of the drug, and hence it was looking at the second question. As to the first question, hormones are undoubtedly effective for treating menopausal symptoms.
Symptomatic treatment is therefore behind the major push for the drugs these days. One doctor friend of mine told me that “every menopausal woman he knows is taking hormones,” implying that this was both right and natural. Another friend, who is turning 60 this year, just recently told me over coffee she’s been on the drugs for ten years and has no plans for stopping them, as she remembers how bad the sleeplessness and brain fog were when she was in menopause. This was a head-scratcher to me, left me wondering why her doctor isn’t concerned about the recent post-black box warning recommendations that if menopausal women are going to take hormones they should do so in the lowest dose possible, for the shortest period of time possible.
The message here: take these drugs, but not for long, and not in high doses. That’s the pharmaceutical equivalent of someone shouting “Danger!”
What pharmaceutical companies do best is not develop drugs, but develop drug markets and you see this on full display in the current menopausal makeover. With a highly malleable clientele, who have both money and motivation, the key obstacle is convincing prescribers that these women urgently need chemical assistance to get through this tough life transition, and that prescribing hormones is one way to fight back against the manosphere. Were it only so easy…
Revising the HRT market depends on the usual tactics: some high-octane marketing including funding pro-HRT “studies,” selectively publishing data that emphasize HRT’s benefits and downplay the harms, funding direct-to-consumer advertising campaigns wrapped in the justice angle, while sponsoring guideline panels and medical education for your and my doctors. By paying off key opinion leaders, and getting social media influencers slurping on the HRT taps the media serves up this revival as a “feel-good” story of female emancipation.
Let’s face it, menopause in 2026 is the sort of uplifting health story that the mainstream media has leaped on with uncommon gusto. In Canada, our public broadcaster, CBC, finds the subject so compelling it runs its own series (Small Achievable Goals) about menopause, organizes noontime Menopause Month call-in shows to dive into the many ‘equity’ issues related to menopause (like why are Canadian women paying out of pocket for menopause care from private practitioners?) and produces a litany of programs that are mostly repetitive recitations over the need to counter the “stigma” caused by menopause. We get it. Menopause is clearly not fun for many women and employers who don’t make concessions for suffering women need to be brought into the 21st century.
The punchline, however, always seems the same: Women are not being taken seriously when it comes to menopause and they’re mad as hell. And no one should stand in their way of getting full access to menopausal treatments, especially those prescribed medications produced by the biggest drug companies in the world. We have a term for this: Pinkwashing. In other words, taking corporate business objectives and painting them in a feminine way in order to show how much you care.
You don’t have to do a systematic review of the mainstream media’s menopause mongering, but even a quick global survey of the main English language outlets can identify some dominant themes. Even though millions of women stopped HRT in 2002, and breast-cancer incidence dropped significantly, not a single story in 2026, as far as I can tell, mentions this fact. It’s curious. Even though most epidemiologists who have examined these data say that all the evidence points towards HRT promoting breast-tumor growth.
The remake of HRT has certainly paid off. Overall HRT demand in North America has grown, driven by what the experts call “increased menopause awareness, guideline updates, and reduced stigma.” Data from insurance claims and health systems show hormone therapy use is steadily rising again after years of decline. Its use among women aged 45–65 increased about 20% between 2020 and 2023. This pink trend is occurring alongside a surge in menopause clinics, telehealth menopause services, and the growing pervasiveness of influencer physicians and social-media menopause advocates.
The HRT market in North America has grown steadily too, worth about $5 billion per year, dominated by drugs like Premarin (branded conjugated estrogens) made by Pfizer. Without any generic competition in the US until late 2025 Pfizer has been able to dominate the market, selling more than $100 million worth of Premarin in 2022 alone. Prempro (conjugated estrogens + medroxyprogesterone,) has been generically available since 2006 or so and has many other generic companies dominating the market due to much lower pricing.
Let’s recap.
Medicine has a long history of embracing interventions that appear beneficial at first glance, only to discover later that the harms outweigh the benefits. Hormone therapy for menopause became a textbook example. The dramatic changes in practice left us with one of the clearest natural experiments in modern epidemiology.
The Women’s Health Initiative revealed a risk.
Millions of women stopped taking the drug.
Breast cancer rates fell.
If you were designing a demonstration of how pharmaceutical exposure can shape population health, you could hardly script it better.
The lesson is not that all drugs are bad or that medical progress is an illusion. It’s that sometimes the most powerful intervention in medicine is restraint.
Before we celebrate the next pharmaceutical breakthrough it might be worth remembering that one of the biggest declines in a major, frequently fatal disease in modern history happened for a very simple reason: Millions of women stopped taking a pill.
Some clinicians and public-health researchers (myself among them) would argue that the media narrative minimizes known and proven downsides of these drugs, often trivializing or ignoring serious harms, including risks of stroke, blood clots, gallbladder disease, and increased breast cancer risk.
The swinging pendulum is now carving its frightful arc from fear and danger towards promotional enthusiasm, and women who are supposed to be beneficiaries of these changes will only suffer further.
Alan Cassels is a Brownstone Fellow and a drug policy researcher and author who has written extensively about disease mongering. He is the author of four books, including The ABCs of Disease Mongering: An Epidemic in 26 Letters.
EBM: Evidence-Biased Medicine
An Essay on the Machinery That Decides What Counts as Knowing
Lies are Unbekoming | May 16, 2026
The 1992 Inversion
In November 1992, the Journal of the American Medical Association published a paper titled “Evidence-Based Medicine: A New Approach to Teaching the Practice of Medicine.”¹ The authors, the Evidence-Based Medicine Working Group at McMaster University, led by Gordon Guyatt, announced a paradigm shift. The first paragraph named what was being replaced: “intuition, unsystematic clinical experience, and pathophysiologic rationale.”¹ The replacement was a hierarchy in which the randomised controlled trial sat at the top and clinical observation sat near the bottom.
The paper was not modest. It described its proposal in Kuhnian terms and predicted that the old approach — the physician’s accumulated judgement, the recognition of patterns across thousands of patients, the reasoning from mechanism and first principles — would be superseded.¹ Within a decade, the framework had been adopted across major medical journals, accreditation bodies, and clinical guideline organisations. In a 2007 BMJ poll of more than 11,000 readers asked to name the most important medical milestones since 1840, the sanitary revolution placed first, antibiotics second, anaesthesia third; evidence-based medicine appeared on the shortlist of fifteen.²
What was elevated to the top of the hierarchy was the one form of evidence pharmaceutical companies could afford to manufacture at scale. What was demoted to the bottom was everything they could not control. This was not the discovery of how medicine should be practised. It was the redefinition of what counted as knowing. The framework called itself evidence-based. What it actually was, was evidence-biased — a hierarchy in which what counted as evidence was determined, first, by who could afford to produce it.
The essay examines what that redefinition did, who it served, and the cost in lives.
Explain It to a Six-Year-Old
For a long time, children have learned about the world in many ways. Some things they see with their own eyes. Some things they hear from grandparents who have lived a long time. Some things they figure out by thinking carefully. Some things they know because they have tried them and watched what happened. All of these are ways of knowing.
One day, the school makes a new rule. From now on, the only things that count as knowing are things that have been seen in a special room, by a man with a clipboard, who writes down what he saw. Hearing from grandparents does not count anymore. Trying things and watching what happens does not count. Thinking carefully does not count. The teacher tells the children, “Those were just stories. Real knowing happens in the special room.”
The special room is very expensive. Only one company can afford to rent it. The company pays the man with the clipboard. The company decides what gets looked at in the room and what does not. Apples never go in the room. Sunlight never goes in the room. Grandmothers’ soup never goes in the room. So the school says, “We do not know if apples are good. We do not know if sunlight is good. We do not know if grandmothers’ soup is good. Nobody has seen them in the room.”
The company sells biscuits. The biscuits go in the room every day. The man with the clipboard writes down that the biscuits are good. The teacher tells the children, “We know the biscuits are good, because we saw them in the room.”
Some children eat the biscuits and get tummy aches. They tell the teacher. The teacher says, “Tummy aches have not been seen in the room. We do not know that the biscuits cause tummy aches.” When a doctor visits and says she has seen many children with tummy aches after eating biscuits, the teacher says the doctor is only telling stories. Stories do not count.
Years pass. The children eat more biscuits and fewer apples. Many of them are sick. The company is very rich. The teacher still says the only real knowing is the knowing that happens in the special room.
That is what happened to medicine in 1992.
What Sits at the Top of the Hierarchy
The EBM hierarchy of evidence places systematic reviews of randomised controlled trials at the apex. Beneath them sit individual RCTs, then cohort studies, then case-control studies, then case series, then expert opinion and clinical experience at the bottom.³
The framework is presented as neutral. It is not.
A randomised controlled trial of a pharmaceutical product costs between twenty and three hundred million dollars to conduct.⁴ The trial requires regulatory approval, site recruitment, statistical infrastructure, monitoring, data management, and publication support. The entities capable of funding such trials are, in practice, three: pharmaceutical companies, the National Institutes of Health, and a small number of large foundations whose priorities track institutional medicine. The pharmaceutical industry funds the majority of clinical research in the United States and a higher proportion of late-phase trials of new products.⁵
A trial of a whole food, a traditional practice, a non-patentable substance, a low-cost generic, or a non-pharmaceutical intervention almost never reaches the funding threshold the hierarchy requires. Substances and practices that produce no return on investment do not generate the evidence the framework recognises, and so they sit at the bottom of the hierarchy or fall off it entirely.
The hierarchy then performs a second move. When a question has not been studied at the top tier, the framework declares “insufficient evidence” or “no evidence of benefit.” Absence is treated as a finding. The reader is led to conclude that the unstudied intervention does not work, when what has actually been established is that no one has been willing to pay for the kind of study the framework demands.
The streetlight effect — searching for keys under the lamp because that is where the light is — is not a flaw of the framework. It describes how the framework operates by design. The hierarchy of evidence is a hierarchy of who can afford to generate evidence.
The Trials at the Top Are Built by the Sponsor
The architecture of the modern pharmaceutical trial is the second mechanism. The sponsor — the company that owns the product — controls the design.
The sponsor selects the primary endpoint. A trial of an antidepressant can be designed to measure a small change on a subjective rating scale at week six, rather than functional recovery at one year. A trial of a statin can be designed to measure relative risk reduction in cardiovascular events, rather than all-cause mortality. A trial of a cancer drug can be designed to measure progression-free survival — the time until the tumour grows on a scan — rather than overall survival.⁶ The endpoint determines what answer the trial is permitted to give.
The sponsor selects the comparator. A new drug compared against placebo where an effective comparator already exists tends to win. A new drug compared against an existing drug at the wrong dose, or in the wrong patient population, tends to win. The comparator becomes a design choice rather than a scientific reference.
The sponsor selects the population. Trials that approve drugs exclude the elderly, the polypharmacy patients, the pregnant, those with comorbid conditions, those with abnormal laboratory values, and those with histories of the very adverse events being assessed. The drug is then prescribed to the population that was excluded. The VIGOR trial of Vioxx excluded patients with significant cardiovascular risk; the drug was marketed and prescribed to a population dominated by such patients.⁷
The sponsor selects the duration. A trial of six weeks tells you nothing about a drug that will be taken for life. A trial of two years tells you nothing about lifetime cancer risk. Sponsors routinely halt trials early “for benefit” once a favourable interim result is reached, eliminating the longer follow-up that would have permitted assessment of late-emerging harms; the JUPITER statin trial discussed later was stopped at a median of 1.9 years rather than completing its planned four-year duration.⁸
The sponsor controls the data. Investigators at trial sites send data to the sponsor. The sponsor’s statisticians analyse it. The sponsor’s medical writers produce the manuscript. The 2017 Cochrane systematic review by Lundh and colleagues, examining 75 studies across multiple drug classes, found industry-sponsored research produces conclusions more favourable to the sponsor’s product than independently funded research of the same questions, with the effect persisting after adjustment for methodological quality.⁹ A 2003 BMJ analysis by Lexchin and colleagues found that industry-funded trials of new drugs produced results favourable to the sponsor’s product at roughly four times the rate of independently funded trials.¹⁰
The RCT does not measure efficacy. It measures what its sponsor designed it to measure.
What Happens to the Trials That Find Harm
The third mechanism concerns what happens to the data the sponsor would prefer not to publish.
In 2008, Erick Turner and colleagues at the Department of Veterans Affairs published an analysis in the New England Journal of Medicine of all FDA-registered trials of antidepressants conducted between 1987 and 2004 — 74 trials covering 12 drugs. The FDA records, obtained under freedom of information requests, showed 38 trials with positive results and 36 trials with negative or questionable results. Of the 38 positive trials, 37 were published. Of the 36 negative trials, 22 were not published at all, and 11 were published in a way that conveyed a positive outcome.¹¹ The published literature on antidepressants showed positive findings in 94% of trials. The actual data showed 51%.
This is publication bias as a system, not as accident. The same pattern has been documented for COX-2 inhibitors, antipsychotics, neuraminidase inhibitors, and statins.¹² Trials that find harm are buried. Trials that find benefit are amplified.
A second layer operates below publication. Ghostwriting — the practice of pharmaceutical companies producing manuscripts and recruiting academic authors to attach their names — has been documented across multiple drug classes. Internal Merck documents released in the Vioxx litigation showed company employees drafting clinical trial papers and review articles, then recruiting academic physicians to be listed as authors; in the litigation review by Ross and colleagues, the company author was frequently the first or last name on the draft before the academic name replaced it.¹³ Wyeth’s hormone replacement therapy promotion was supported by at least 26 ghostwritten papers published in the medical literature between 1998 and 2005, identified through documents released in litigation and analysed by Adriane Fugh-Berman.¹⁴
A third layer operates at the journals themselves. When a pharmaceutical company publishes a favourable trial in a major medical journal, it routinely purchases tens or hundreds of thousands of reprints of that article from the journal — reprints distributed to physicians by sales representatives as the academic credential for the product. Richard Smith, former editor of the BMJ, described medical journals in 2005 as “an extension of the marketing arm of pharmaceutical companies,” noting that reprint orders for industry-favourable studies can generate revenues sufficient to constitute a substantial share of a major journal’s income.¹⁵ The journals at the top of the EBM hierarchy depend financially on the companies whose products they evaluate.
The reader of the medical literature encounters what appears to be the considered opinion of an academic physician. The reader does not see the company writer who drafted the manuscript or the company statistician who selected the data presented.
“No Evidence of Harm”
The fourth mechanism is the laundering of absence into safety.
When a harm signal appears in post-marketing data, the framework processes it in stages. The harm is not yet established because no RCT has been designed to test for it. The harm cannot be established because the RCT that would test for it has not been conducted. The harm has not been confirmed because the studies that exist were not powered to detect it. The correlation between exposure and harm is not causation, because the gold-standard trial has not been performed. By the time the gold-standard trial is performed, if it ever is, the drug has been on the market for a decade and the harm is too widespread to deny.
Each stage uses the framework’s own standards to keep the product on the market. Each stage requires the evidence that the framework’s funding structure ensures will not be generated.
The phrase “no evidence of harm” does work the reader rarely notices. It does not mean studies were conducted and harm was not found. It usually means that studies sufficient to detect the harm were not conducted. The phrase converts absence into safety. The asymmetry is structural: “no evidence of benefit” is treated as a finding against an unfunded substance, while “no evidence of harm” is treated as a finding in favour of a marketed product.
The framework is unfalsifiable for the things it protects and fatal for the things it does not.
What Happens to the People Who Disagree
The fifth mechanism is the processing of dissent.
A clinician who observes a pattern of harm in patients and reports it is reasoning from unsystematic clinical experience — the bottom of the hierarchy. The observation is dismissed as anecdotal. A researcher who publishes findings unfavourable to a major product class is subjected to coordinated response: methodological critique, accusations of conflict of interest, retraction campaigns, ridicule in the trade press, and loss of funding. A physician who treats outside guideline-driven protocols is referred to the medical board. A patient who reports the harm is told the condition is unrelated, idiopathic, or psychological.
Peter Gøtzsche, co-founder of the Cochrane Collaboration and author of multiple Cochrane reviews unfavourable to the pharmaceutical industry, was expelled from the Cochrane governing board in 2018 after publishing critical analyses of mammography screening, psychiatric drug regulation, and antidepressant suicidality.¹⁶ The expulsion processed dissent.
John Ioannidis, professor of medicine at Stanford and one of the most cited scientists in medical literature, published “Why Most Published Research Findings Are False” in PLoS Medicine in 2005, demonstrating from within the establishment that the statistical and structural assumptions of the published evidence base were unreliable.¹⁷ The paper was met with hostility from those it implicated and quietly absorbed by those it embarrassed. The framework continued unchanged.
David Healy, a psychiatrist and historian of antidepressants whose research had exposed the suicidality signal in SSRI trial data, was offered the chair of the Mood and Anxiety Disorders Programme at the University of Toronto’s Centre for Addiction and Mental Health in 2000. After a public lecture in which he discussed Prozac-induced suicidality, the appointment was withdrawn. The Centre received substantial funding from Eli Lilly, the manufacturer of Prozac.¹⁸ Nancy Olivieri, a haematologist at the University of Toronto, reported safety concerns about deferiprone, a thalassaemia drug manufactured by Apotex, after observing harm in her clinical trial. Apotex threatened legal action; the university, which was at the time negotiating a substantial donation from Apotex, did not defend her academic freedom.¹⁹ Both cases preceded the EBM apparatus’s deployment against later dissenters; both established the template.
The framework does not produce truth and then defend it against error. The framework produces orthodoxy and then defends it against observation.
Case One: Vioxx
Merck submitted rofecoxib (Vioxx) to the FDA in November 1998 and received approval in May 1999.²⁰ The drug was a COX-2 inhibitor — a new class of anti-inflammatory marketed as gentler on the stomach than older drugs. Before its withdrawal, more than 80 million people worldwide had been prescribed Vioxx.²¹
The pivotal trial supporting cardiovascular and gastrointestinal claims was VIGOR (Vioxx Gastrointestinal Outcomes Research), published in the New England Journal of Medicine in November 2000.²² The trial compared Vioxx against naproxen in 8,076 rheumatoid arthritis patients. The publication reported that Vioxx caused fewer serious gastrointestinal events than naproxen. The published paper also reported that patients on Vioxx had four times the rate of myocardial infarction; further analysis presented to the FDA Arthritis Advisory Committee in February 2001 determined the rate to be fivefold.²³
The published explanation was that naproxen was protective, not that Vioxx was harmful. The cardioprotective effect of naproxen had not been established at this magnitude before VIGOR and was not established afterwards.²⁴ The interpretation served the sponsor.
Internal Merck documents released in subsequent litigation showed company awareness of the cardiovascular signal predating VIGOR’s publication. Internal communications discussed how to manage the signal; the published trial reports did not communicate what the internal analyses had described.²⁵ Merck withdrew Vioxx in September 2004 after the APPROVe trial, designed to assess Vioxx’s effects on colorectal polyps, demonstrated a doubling of cardiovascular events.²⁶ FDA epidemiologist David Graham testified before the Senate Finance Committee that Vioxx had caused an estimated 88,000 to 139,000 excess heart attacks, of which 30 to 40 percent were fatal.²⁷ The lower bound was approximately 26,000 American deaths.
The trial that approved the drug satisfied every requirement of evidence-based medicine. It was randomised. It was controlled. It was published in the most prestigious medical journal in the world. It supported guideline recommendations and reimbursement decisions. The framework that produced it found nothing wrong with it.
The harm was visible in the data. The harm was known to the sponsor. The harm was published in a form that obscured its meaning. The framework continued to recommend the drug for almost five years. When the drug was withdrawn, the framework was not.
Case Two: Statins
The statin literature illustrates how the framework presents data to maximise the appearance of benefit.
Statins reduce LDL cholesterol. Whether they reduce all-cause mortality in primary prevention — in patients without established cardiovascular disease — has been contested in the literature for two decades.²⁸ The framework has resolved the contest in favour of mass prescription.
The presentational device is relative risk reduction. A statin trial reports that the drug reduces cardiovascular events by some percentage. The figure is technically accurate. What it conceals is the absolute risk reduction — the actual difference in event rates between the treated group and the untreated group.
In the JUPITER trial of rosuvastatin (2008), patients on the drug had a 1.6% rate of major cardiovascular events over 1.9 years. Patients on placebo had a 2.8% rate.²⁹ The relative risk reduction was 44%. The absolute risk reduction was 1.2%. The number needed to treat — the number of patients who must take the drug for one to avoid an event — was approximately 95 over two years. The other ninety-four took the drug and received no cardiovascular benefit from it.
The framework permits the relative figure to be reported in the headlines, the abstract, the press release, the guideline recommendation, and the prescribing conversation. The absolute figure appears, if at all, in the body of the paper. The patient is told the drug reduces heart attack risk by 44%. The patient is not told the drug reduces their personal two-year risk from 2.8% to 1.6%.
Adverse effects are processed through related machinery. Many statin trials use a run-in period — patients are given the drug before randomisation, and those who experience adverse effects are excluded before the trial begins.³⁰ Trials then report low rates of muscle pain, cognitive impairment, and new-onset diabetes. Surveys of statin users in real clinical practice — without the run-in selection — find muscle symptoms in 10 to 25 percent of patients, against trial-reported rates in the low single digits.³¹
The 2013 Cochrane review of statins in primary prevention found a small mortality benefit and a non-trivial harm signal, particularly for new-onset diabetes.³² The framework’s response was not to question primary prevention prescribing. It was to expand it. The 2013 ACC/AHA cholesterol guidelines lowered the threshold for statin prescription and added an estimated 13 million Americans to the eligible population.³³
The framework approves the drug, designs the trials to maximise apparent benefit and minimise apparent harm, suppresses the inconvenient findings, expands the eligible population, and declares the resulting prescribing pattern to be evidence-based.
Case Three: SSRIs
The selective serotonin reuptake inhibitors entered the market in 1987 with fluoxetine (Prozac). They were marketed on the basis of a “chemical imbalance” theory of depression — the claim that depressed patients had low serotonin and the drugs corrected the deficiency.³⁴ The theory was never demonstrated. A 2022 systematic umbrella review by Joanna Moncrieff and colleagues, published in Molecular Psychiatry, concluded that the evidence does not support the hypothesis that depression is caused by reduced serotonin activity or concentrations.³⁵
The drugs were approved on the basis of trials showing small differences from placebo on rating-scale depression scores at six to eight weeks. The Turner analysis cited earlier in this essay found that the published literature substantially overstated the actual trial outcomes; when unpublished trials were included, the apparent efficacy fell substantially, with roughly half the trials having failed to demonstrate benefit.¹¹ A 2008 meta-analysis by Irving Kirsch and colleagues using FDA data found that the difference between SSRIs and placebo on depression rating scales fell below the threshold for clinical significance for all but the most severely depressed patients.³⁶
The harms followed the framework’s standard sequence.
Sexual dysfunction was acknowledged in trial reports at rates of 2 to 16 percent, well below the 50 to 70 percent rates documented in subsequent clinical surveys.³⁷ Post-SSRI sexual dysfunction — persistent sexual dysfunction continuing after discontinuation — was denied for two decades. The European Medicines Agency added a warning label in 2019.³⁸ Patients reporting the syndrome had been told for two decades it was not a recognised condition.
Suicidality in children and adolescents was visible in the trial data from the early 1990s. The published literature did not communicate the signal. A 2004 FDA review of pediatric trials confirmed it, and the FDA added a black box warning in October 2004.³⁹ A 2016 BMJ analysis by Tarang Sharma, Peter Gøtzsche and colleagues, using clinical study reports rather than published papers, found the suicidality signal in adults as well — and found systematic misclassification of suicide attempts as “emotional lability” in the original trial reports.⁴⁰
The dependence and withdrawal syndromes were denied for three decades. SSRI manufacturers and prescribing guidelines characterised the discontinuation syndrome as a mild, transient phenomenon affecting a small minority of patients. A 2019 systematic review by James Davies and John Read found 56% of patients experience withdrawal effects when attempting to discontinue, with 46% of those affected describing the experience as severe.⁴¹ The UK Royal College of Psychiatrists revised its position later that year, acknowledging that withdrawal could be severe and prolonged.⁴² The acknowledgement came thirty-two years after the first SSRI was approved.
Around one in eight American adults now takes an antidepressant.⁴³ The framework that approved them functioned exactly as designed.
Case Four: Bisphosphonates
Fosamax (alendronate) was approved by the FDA in 1995 as a treatment for established osteoporosis. The market was small. In 1995, the number of American women with documented osteoporosis was a fraction of what the drug’s commercial prospects required.
The framework supplied the market. In 1994, a World Health Organization study group convened in Rome, financed by the pharmaceutical industry, produced arbitrary diagnostic cutoffs based on bone mineral density measured against the average of a healthy thirty-year-old white woman.⁴⁴ Bone density between one and 2.5 standard deviations below this reference was named “osteopenia.” Bone density more than 2.5 standard deviations below was named “osteoporosis.” The categories were statistical cutoffs imposed on a normally distributed biological variable; they were not derived from outcome data on who actually fractured. Anna Tosteson, a member of the original WHO group, later said the categories had been intended as population research tools, not individual diagnoses; the chair of the meeting, John Kanis, said the same.⁴⁵ A subsequent 1999 WHO panel on osteoporosis cost analysis included eleven members, eight of them employed by pharmaceutical manufacturers.⁴⁶
Merck did the rest. The company established the Bone Measurement Institute, a nonprofit that lobbied for insurance coverage of bone density testing and underwrote the placement of scanners in physician offices across the United States.⁴⁷ In 1997, the FDA cleared a lower 5 mg dose of Fosamax specifically for women with osteopenia. Approximately thirty percent of postmenopausal women now had a “disease” requiring early intervention.⁴⁸
The pivotal trials applied the relative-risk-reduction architecture described in the statins case. The Fracture Intervention Trial reported a 47% relative reduction in hip fracture and a 52% relative reduction in radiographic vertebral fracture in women with established osteoporosis.⁴⁹ The trial enrolled high-risk women in whom even modest relative reductions translated into modest absolute differences. It did not study the population in which the drug was subsequently prescribed in greatest numbers — women with osteopenia, who carried substantially lower baseline fracture risk. The framework approved the prescribing pattern anyway.
The drug’s mechanism of action determined what would follow. Bisphosphonates concentrate in bone and disable osteoclasts, the cells responsible for clearing old bone and allowing new bone to be laid down in response to mechanical load. Blocking the clearing side of the remodeling cycle while leaving the building side unopposed produces bones that are denser by measurement and more brittle by behaviour — old bone that should have been replaced accumulates as highly mineralised, structurally compromised material. The scan reads higher. The bone breaks more easily.
The harm signal emerged after the prescribing pattern was established. Reports of atypical femoral fractures — spontaneous breaks in the shaft of the thighbone, occurring with little or no trauma — appeared in the orthopaedic literature from 2007.⁵⁰ The drug marketed to prevent fractures was producing a different category of fracture in long-term users. The FDA issued a safety warning in October 2010 but did not retract the prescribing recommendation; osteonecrosis of the jaw was added as a separate documented harm.⁵¹ A 2011 JAMA study reported significantly elevated risk of subtrochanteric and femoral shaft fractures in long-term bisphosphonate users.⁵²
The framework accepted an industry-funded definition of disease, converted asymptomatic women into patients, prescribed them a drug whose trials had been conducted in a different population, and continued recommending the drug after the iatrogenic loop became visible. Nothing in this sequence required new science. It required only the framework’s willingness to treat industry-supplied definitions as medical knowledge, industry-funded trials of one population as evidence about another, and a metric the drug improved (density on the scan) as a proxy for the outcome the drug worsened (the strength of the bone under stress).
What the Framework Was Protecting
The essay has examined EBM on its own terms. By its own stated standards, the framework does not produce reliable knowledge, does not protect patients, does not exclude bias, and does not distinguish truth from manufactured evidence. Every claim it makes for itself can be inverted with examples from its own literature.
A deeper question remains.
EBM is the epistemological enforcement layer for a particular model of medicine. That model holds that the body is a malfunctioning machine, that illness is caused by external invaders or internal genetic defects, that the response to illness is the introduction of a patented chemical or biological product, that the practitioner’s task is to match product to diagnosis, and that the evidence required to justify the product is the kind of trial pharmaceutical companies are equipped to manufacture.
The framework’s structural bias against whole foods, traditional practices, low-cost interventions, and reasoning from mechanism is not incidental to this model. The pharmaceutical paradigm requires the bias to function. A framework that recognised the body’s intrinsic capacity for self-regulation and repair, that attended to the actual sources of damage — toxic exposure, nutritional depletion, electromagnetic burden, psychological strain — and that treated the practitioner’s task as the removal of obstacles rather than the introduction of products, would not need RCTs at the top of its hierarchy because it would not be generating products to be tested. It would be observing what the body does when the obstacles are removed.
EBM is not science being corrupted by industry. EBM is the epistemological form industry required. It was designed in the 1990s, codified in the 2000s, and operated at civilisational scale in the 2020s. The framework has done what its architecture predicted.
This is what political economist Toby Rogers, in testimony before the United States Senate in 2025, named epistemic capture — the colonisation of knowledge production itself rather than the regulation of its products.⁵³ When an industry captures regulation, it controls decisions. When an industry captures epistemology, it controls what is allowed to count as a fact. EBM is epistemic capture’s operating system in medicine. The same investment funds that hold major positions in the pharmaceutical companies whose products the framework evaluates also hold major positions in the publishers of the journals that perform the evaluation; the producer and the certifier of medical knowledge share their owners.⁵⁴
The clinician at the bedside who notices a pattern across patients and adjusts their practice accordingly is doing what physicians have done for thousands of years. The framework calls this anecdote and ranks it at the bottom of the hierarchy. The patient who recovers from a chronic condition through dietary change, sunlight, sleep, and the removal of pharmaceutical exposures is doing something the framework cannot measure, because the framework was not designed to measure it. The traditional practitioner whose people have used a plant for fifteen generations is reasoning from a form of evidence the framework excludes by definition.
What the framework calls evidence is what industry can pay for. What the framework calls anecdote is what the body actually does.
The 1992 paper announced a paradigm shift. The shift was real. The direction was not what the paper claimed. Medicine did not move from intuition to evidence. It moved from the physician’s accumulated judgement to the industry’s manufactured documentation. The hierarchy of evidence is the hierarchy of who paid for the study. Evidence-based medicine, examined as machinery, is evidence-biased medicine — biased structurally, by what gets funded; biased methodologically, by what gets measured; biased editorially, by what gets published; biased financially, by who owns the journals; biased institutionally, by what gets recommended after the harm has been documented. The bias is the framework.
The document is publicly available. The signatures are on it. The date is November 1992. Whatever the framework was sold as, the framework is what its architecture produced. What its architecture produced is in the medical journals, in the prescribing patterns, in the disability statistics, and in the cemeteries. It is also in the minds of two generations of doctors and patients who no longer believe their own observations count.
References
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- Petersen M. “Hormones and Bones: How the Drug Companies Made Aging Into a Disease.” New York Times, November 16, 2003. See also Heaney RP et al. and consensus development conference: “Diagnosis, Prophylaxis, and Treatment of Osteoporosis.” American Journal of Medicine 94, no. 6 (June 1993): 646–650, and Kanis JA, WHO Study Group. “Assessment of Fracture Risk and Its Application to Screening for Postmenopausal Osteoporosis: Report of a WHO Study Group.” WHO Technical Report Series 843. Geneva: World Health Organization, 1994.
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- Moynihan R. “Osteoporosis and the Marketing of a Disease.” Therapeutics Initiative Workshop, University of British Columbia, October 2006. Fosamax sales figures: Merck Annual Reports, 1996–2005.
- Black DM, Cummings SR, Karpf DB, et al. “Randomised Trial of Effect of Alendronate on Risk of Fracture in Women with Existing Vertebral Fractures.” The Lancet 348, no. 9041 (December 1996): 1535–1541. See also Black DM, Thompson DE, Bauer DC, et al. “Fracture Risk Reduction with Alendronate in Women with Osteoporosis: The Fracture Intervention Trial.” Journal of Clinical Endocrinology & Metabolism 85, no. 11 (November 2000): 4118–4124.
- Neviaser AS, Lane JM, Lenart BA, Edobor-Osula F, Lorich DG. “Low-Energy Femoral Shaft Fractures Associated with Alendronate Use.” Journal of Orthopaedic Trauma 22, no. 5 (May 2008): 346–350. Earlier case reports beginning 2005; pattern recognised in the literature from 2007.
- US Food and Drug Administration. “Safety Update for Osteoporosis Drugs, Bisphosphonates, and Atypical Fractures.” FDA Drug Safety Communication, October 13, 2010.
- Park-Wyllie LY, Mamdani MM, Juurlink DN, et al. “Bisphosphonate Use and the Risk of Subtrochanteric or Femoral Shaft Fractures in Older Women.” JAMA 305, no. 8 (February 2011): 783–789. See also Dell RM, Adams AL, Greene DF, et al. “Incidence of Atypical Nontraumatic Diaphyseal Fractures of the Femur.” Journal of Bone and Mineral Research 27, no. 12 (December 2012): 2544–2550.
- Rogers T. Testimony before the United States Senate Committee on Homeland Security and Governmental Affairs, September 10, 2025. See also Rogers T. “Big Pharma’s Epistemic Capture of Medical Research.” uTobian (Substack), September 2025.
- Bazin X. Big Pharma démasqué: Médicaments dangereux, vaccins controversés… Quand l’industrie pharmaceutique nous prend pour des cobayes. Trédaniel, 2022. Common ownership structures documented through RELX Group annual reports and SEC filings of major institutional shareholders (BlackRock, Vanguard, State Street) in both pharmaceutical companies and scientific publishing groups (RELX, Springer Nature, Wiley).
Hantavirus, the WHO, and the Conflicts in Weighing Mortality
By David Bell | Brownstone Institute | May 13, 2026
Yesterday, almost 2,000 people, mostly young children, died of malaria because they could not access effective and relatively cheap treatment quickly enough. About 4,000 people died of tuberculosis (TB), including many young adults leaving orphans. This happens every day. Progress in reducing these numbers is stalling, as partly due to the continuing economic damage from the Covid-19 response.
In the past two weeks three tourists unfortunately died among about 150 passengers and crew on a cruise ship MV Hondius off the west coast of the African continent where most of those malaria and TB deaths occurred. The Hondius had a hantavirus outbreak, known to have infected less than 10 people but including at least two of those that died.
The World Health Organization (WHO) estimates that 10,000 to 100,000 hantavirus cases occur every year, spread across the Americas, Europe, Africa, and Asia. The current media coverage and WHO news conferences therefore concern about one-thousandth of the cases expected this year. The United States averages about 30 – they simply have not been newsworthy.
Hantavirus is transmitted from mice and rats through their feces, urine, saliva, or their bite. The Andean variety, which occurred on the cruise ship, can also sometimes transmit from a sick infected person. However, as the low number of cases on the ship demonstrates, the risk of human-human transmission is not great. It is, however, a nasty virus, with reported mortality around 15% of cases and sometimes significantly higher.
So, among the 170,000 average deaths in the world each day, and thousands from the WHO’s traditional focus diseases, why the excitement over Hantavirus? Why the pictures of hazmat-suited emergency response crews and desperate contact tracing, when we don’t usually notice? Why is the Director-General of the entire WHO spending so much time on this, when diseases of poverty are rising and basics such as nutrition funding are falling? A fascinating question.
The WHO wants the United States and Argentina to rejoin, and WHO DG Tedros Ghebreyesus has raised this in his hantavirus briefings. Multilateral cooperation in global health has demonstrably helped in addressing malaria and TB in the past, but reliance on detached and homogenous WHO recommendations for Covid worked out really badly. The WHO is wisely claiming the MV Hondius is not heralding a pandemic, but nonetheless are making all the mileage they can from the fear created around this epidemiologically irrelevant event.
Just two weeks ago, African nations also rejected (again) a pathogen-sharing requirement for the WHO’s new Pandemic Agreement (treaty). This would require them to implement surveillance at their expense and provide data on pathogens to the WHO, which will then provide it to large Pharma companies to produce vaccines that the WHO will recommend and market.
Malaria and TB deaths should increase further through this process because the WHO wants over $10 billion from donor countries diverted to its pandemic agenda, and $20 billion spent by low- and middle-income countries to support it (the world spends about $3.5 billion on malaria each year). While malaria, TB, HIV, nutrition, and improving access to primary care clinics may be a greater priority for such countries, false charges of putting the world at risk by failing to sign the WHO’s Pandemic Agreement may eventually prove too much to withstand.
A further potential influence is conflict of interest, though its impact on the current situation is unclear. The WHO’s largest donor is now the Gates Foundation, a private operation directed by Bill Gates with a strong history of investment in the mRNA vaccine company Moderna. Moderna is working on a hantavirus mRNA vaccine, which is surprising from an investment perspective as the market seems small. How would a viable commercial market be ensured for a vaccine for such an obscure disease? This viable market requires large swathes of the population to be convinced that they are at far higher risk than they actually are, or coerced into taking it. In the United States the risk is about 1 case per 10 million people per year, with perhaps 1 per million to 1 per 100,000 globally.
A direct connection between Moderna’s market problem and the current hysteria does not need to be made. The point is that the WHO is now an organization in which its largest funder also has large, vested interests in the sales of specific health products. Through specified funding, the funder also determines which activities the WHO will undertake.
The WHO’s second largest funder over 2024-2025 was Gavi, a public private parentship for vaccines, again involving Gates and Pharma companies. Public-private partnerships, which the WHO has itself essentially become, are intrinsically designed around vested or conflicted interest – the justification for private companies expending resources is gain for their investors.
No sane approach would allow vested commercial private interests to determine global health policy. Pharma’s job is to maximize profit, while the WHO’s job is to maximize health and health equity. One of these must be failing.
A vast global health industry has been built in which private investors determine priorities, taxpayers foot most of the bill, and populations have become markets. As this plays out, public health messaging becomes increasingly incoherent and detached from reality until several cases of hantavirus among tourists on a cruise ship, out of up to 100,000 expected this year, appear as an international crisis.
The result is not just fear and confusion, but a massive institutional failure that allows huge numbers of children to die disregarded while public health workers don hazmat suits as media celebrities. We need to ask why. There is a path for an organization such as the WHO to act in an ethical, proportionate manner that serves humanity rather than parasitizing it. The hantavirus roadshow can be an impetus for change, but not to further enrich and empower those promoting it. We need to, as citizens and as a public health community, insist that institutions such as the WHO do better, or insist on replacing them with something better.
David Bell, Senior Scholar at Brownstone Institute, is a public health physician and biotech consultant in global health. David is a former medical officer and scientist at the World Health Organization (WHO), Programme Head for malaria and febrile diseases at the Foundation for Innovative New Diagnostics (FIND) in Geneva, Switzerland, and Director of Global Health Technologies at Intellectual Ventures Global Good Fund in Bellevue, WA, USA.
46 IPCC Scientists Break Rank, Publicly Challenge Long-Standing Dogmatic Climate Claims
Cracks in the facade of global climate science get wider as a significant group of experts chooses to break rank
By P Gosselin | No Tricks Zone | May 5, 2026
According to a recent report by the German online TKP, a movement is gaining momentum within the scientific community that threatens to dismantle the official IPCC narrative from the inside out. This rebellion is led by 46 scientists, many of whom have direct experience working with the Intergovernmental Panel on Climate Change, who are now publicly challenging the foundational claims that have dictated global policy for decades.
The heart of their argument lies in the fundamental failure of current climate models.
These prestigious researchers – among them Dr. Robert Balling, Dr. Lucka Bogataj, Dr. John Christy and Dr. Judith Curry – contend that the IPCC has relied on simulations that are heavily biased toward human-induced CO2 while systematically ignoring or downplaying natural variables. By prioritizing political consensus over raw data, these models have consistently overestimated global warming, creating a gap between alarmist predictions and the actual temperature trends observed over the last several years.
The scientists suggest that the “climate emergency” is less a scientific reality and more an ideological construct designed to drive the Net Zero agenda.
Power natural factors ignorerd by IPCC
Furthermore, this group highlights the critical role of natural drivers that are often missing from the mainstream conversation. They point to solar activity, atmospheric water vapor, and complex cloud cycles as the true drivers of Earth’s climate. By looking back at historical periods like the Medieval Warm Period, they argue that the planet’s current warming is well within the bounds of natural variability and is not the unprecedented catastrophe it is often portrayed to be.
Culture of scientific suppression
Perhaps most concerning is the article’s depiction of a scientific community under pressure. The rebelling scientists describe a culture of suppression where dissenting opinions are sidelined through the loss of funding, career gatekeeping, and media blackouts. This internal collapse suggests that the “science is settled” mantra is no longer sustainable.
Dogmna coming to an end
As these 46 voices come forward, they signal a shift toward a more skeptical, data-driven approach that prioritizes objective reality over the prevailing political narrative, suggesting that the era of unquestioned climate dogma may be coming to an end.
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Study Buried For Four Years Shows Crime Lab DNA Testing Is Severely Flawed
By Tim Cushing – TechDirt – September 27, 2018
DNA is supposed to be the gold standard of evidence. Supposedly so distinct it would be impossible to convict the wrong person, yet DNA evidence has been given far more credit than it’s earned. … continue
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