What Is Tamiflu?

An Essay on Neuraminidase, Sialidosis, and a Drug That Attacks the Patient

Author’s Note

Two registers operate in what follows. The establishment frame: a viral disease called influenza, caused by a virus carrying a surface enzyme called neuraminidase, treated with a drug called Tamiflu that inhibits that enzyme. The terrain frame: a seasonal illness that medicine attributes to a virus, a drug that inhibits an enzyme present throughout the human body, and a harm profile that follows from what the drug actually does rather than from what it was sold to do.

When this essay quotes Roche, the CDC, the World Health Organization, or peer-reviewed virology, the establishment frame is operating. When this essay states what the drug does to the patient, the terrain frame is operating. Both are present because the establishment’s own evidence, in its package inserts, its trial data, and its biochemistry, collapses the establishment’s own claims.

The central finding is straightforward. Neuraminidase is not a viral property. It is a family of four human enzymes performing essential metabolic and signaling functions in every major organ. The disease caused by deficiency of one of these enzymes is severe, progressive, and well documented. Tamiflu inhibits the enzyme family. The harms Roche acknowledges in its own product information are what the mechanism predicts.

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The Disease Called Sialidosis

A young person, somewhere between the ages of twelve and twenty-five, develops difficulty walking. Vision dims. Reading becomes harder. An ophthalmologist examines the back of the eye and finds a bright red spot at the center of the macula, surrounded by a pale halo of lipid-laden retinal ganglion cells. The patient develops myoclonus, sudden involuntary muscle jerks that worsen with movement, interrupt walking, and make eating difficult. Seizures follow. Cerebellar ataxia. Tremor in the legs. Peripheral neuropathy. The body’s capacity to move, see, and coordinate deteriorates progressively.

This is sialidosis type I, also called cherry-red spot myoclonus syndrome.¹

In its more severe form, sialidosis type II, the disease begins in infancy or before birth. Hydrops fetalis. Ascites in the fetal abdomen. Coarse facial features. Skeletal dysplasia. Enlarged liver and spleen. Sensorineural hearing loss. Gingival hyperplasia. Macroglossia. Intellectual disability. The congenital form typically results in stillbirth or death within the first two years of life. The juvenile form, beginning after age two, features progressive psychomotor regression, myoclonic seizures, macular cherry-red spots, and dark-red cutaneous vascular lesions.²

The disease arises from deficient NEU1 function. Mainstream genetics identifies the cause as mutations in a single gene on chromosome 6p21.3 that codes for the enzyme.³ When NEU1 cannot perform its work, sialylated glycoconjugates accumulate in lysosomes throughout the body. The accumulation poisons the nervous system, the skeletal system, the visceral organs, the eyes. Patients with the infantile form rarely survive past their second decade. Patients with the milder adult form are progressively disabled by myoclonus and visual loss.

NEU1 is one of four neuraminidases in the human body.

Tamiflu is a neuraminidase inhibitor.

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What Neuraminidase Does

The human body contains four neuraminidase enzymes, named NEU1, NEU2, NEU3, and NEU4.⁴ Each performs essential functions in cellular signaling, metabolic regulation, tissue maintenance, and neurological development.

NEU1 is ubiquitous. The kidney, the pancreas, the skeletal muscle, the liver, the lungs, the placenta, and the brain all express it at high levels. Within the cell, NEU1 lives in the lysosome, the structure that breaks down and recycles cellular waste. There it removes a specific sugar called sialic acid from proteins and fats that the lysosome is processing. NEU1 also moves to the outside of the cell, where it regulates the receptors the body uses to detect bacterial substances. One of these, called Toll-like receptor 4, governs the inflammatory response.⁵ NEU1 works with two partner proteins to form the receptor complex that assembles elastic fibers, the protein networks that give skin, lungs, arteries, and cartilage their flexibility and resilience.⁶ NEU1 also processes the LDL receptor and participates in the liver’s lipid metabolism. It is the main enzyme that processes monocytes as they mature into the macrophages that clean up cellular debris.⁷

NEU2 works in the cytoplasm, the cell’s interior fluid, helping muscle cells mature and processing the body’s complex sugar-bearing proteins and fats.

NEU3 sits at the cell’s outer membrane in specialized signaling zones, where it processes gangliosides, which are sugar-bearing fat molecules. NEU3 regulates how cells stick together, how nerve cells form, and how the body responds to insulin.

NEU4 works in three locations: the lysosome, the outer membrane of the mitochondria where cellular energy is produced, and the endoplasmic reticulum where proteins are folded and finished. NEU4 processes the long sugar chains on the molecules that hold nerve cells together, and regulates how nerve fibers grow in the developing brain.

These enzymes control the sialylation state of every major cellular system. Inflammation, cholesterol uptake, elastic fiber assembly, cell adhesion, cell motility, and receptor activation all depend on them. The catalytic site of NEU1 is the same site that, when defective, produces sialidosis with its cherry-red spot, myoclonus, skeletal dysplasia, and early death.

Tamiflu binds that site.

In vitro studies have documented that neuraminidase inhibitors, including oseltamivir, inhibit human NEU enzymes in addition to whatever the establishment has assigned to influenza.⁸ Laboratory antibodies raised against microbial neuraminidases cross-react with human NEU3, the plasma membrane isoform that regulates neuronal signaling.⁹ The synthetic substrates used in research assays to measure “viral” neuraminidase activity, such as 4-methylumbelliferyl-α-D-N-acetylneuraminic acid, are also cleaved by human NEU1 and NEU3.¹⁰ The biochemical distinction between viral and human neuraminidase, on which the drug’s selectivity claim rests, fails at the catalytic site, at the substrate level, and at the antigenic level.

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The Mechanism Claim Examined

The drug’s mechanism rests on a story. Influenza virus, the account runs, carries on its surface a tetrameric glycoprotein called neuraminidase, which cleaves sialic acid residues from host cell receptors. Without this cleavage, newly assembled virus particles cannot detach from the cell and cannot spread. Inhibit the enzyme, the establishment claims, and the virus is trapped at the cell surface.

The 1918 “Spanish flu” virus is the foundational reference for influenza neuraminidase structure. Jeffery Taubenberger and colleagues sequenced its neuraminidase gene from formalin-fixed lung tissue and from a frozen Alaskan lung preserved in permafrost.¹¹ Tumpey and colleagues reconstructed the entire 1918 virus through reverse genetics in 2005, assembling it from plasmid sequences in cell culture.¹² No 1918 virus was isolated from a patient. The genome was assembled from sequences taken from tissue, then rebuilt as infectious virus in a laboratory by inserting the sequences into cells. The mechanism on which Tamiflu rests was designed against a virus reconstructed from sequence after the patients had been dead for eight decades.

This is the establishment’s evidence on its own terms. The drug was designed to inhibit a viral enzyme characterized by reverse genetic reconstruction, against a virus that no living person has provided as a purified specimen. The drug, in the human body, inhibits the human enzymes whose deficiency causes sialidosis.

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Roche’s Own Document

The Australian Product Information for Tamiflu, last revised by Roche on 22 August 2023, is a public document. It lists the adverse reactions observed in post-marketing experience under the heading “Adverse Effects (Undesirable Effects).”¹³

Hypersensitivity reactions are listed first: allergic skin reactions including dermatitis, rash, eczema and urticaria, erythema multiforme, anaphylactic and anaphylactoid reactions, face edema, Stevens-Johnson syndrome, and toxic epidermal necrolysis. Toxic epidermal necrolysis is a condition in which the skin separates from the body in sheets. Mortality is high, commonly cited at 25 to 50 percent.

Hepatitis and elevated liver enzymes appear under hepatobiliary disorders.

Convulsions and delirium appear under psychiatric and nervous system disorders. Within the delirium category Roche names altered consciousness, confusion, abnormal behavior, delusions, hallucinations, agitation, anxiety, and nightmares. Roche acknowledges that some of these events “resulted in a fatal outcome.”¹⁴

Gastrointestinal bleeding appears, with hemorrhagic colitis specified.

Thrombocytopenia appears under blood and lymphatic system disorders. Visual disturbances appear under eye disorders.

The consumer leaflet, also distributed by Roche, lists nausea, vomiting, headache, stomach pain, and diarrhea as the more common effects and characterizes them as “mostly mild.” Patients receive the leaflet. They do not, as a rule, receive the prescriber’s document.

The harms catalog reads as a portrait of NEU function compromised across the body. Elastic fiber assembly disrupted produces skin manifestations, which include the dermatologic reactions Roche lists at the head of its hypersensitivity section. Hepatic NEU1 inhibition disrupts cholesterol regulation and produces the hepatitis Roche acknowledges. Inhibition of NEU1 at Toll-like receptor 4 disrupts the regulated inflammatory response and predicts the anaphylactic spectrum Roche lists. Inhibition of NEU3 at the plasma membrane disrupts ganglioside signaling in neurons and predicts the convulsions, the delirium, the abnormal behavior, the hallucinations. NEU4 inhibition in lysosomal and mitochondrial compartments disrupts the metabolic functions that sialidosis type II disrupts more profoundly, predicting the gastrointestinal damage, the liver dysfunction, the thrombocytopenia.

Roche does not call this a category of mechanism-predicted harm. The package insert presents these effects as unexpected. The mechanism predicts them.

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The Cochrane Battle

In 2009, during the H1N1 panic, the United Kingdom government asked the Cochrane Collaboration to update its assessment of neuraminidase inhibitors. The Cochrane reviewers, led by Tom Jefferson and Peter Doshi, examined the evidence base. They found that the central claim, that Tamiflu reduces complications, hospitalizations, and mortality, rested on a 2003 meta-analysis by Kaiser and colleagues, funded by Roche, which pooled data from ten clinical trials. Eight of the ten trials had never been published.¹⁵

The reviewers asked Roche for the underlying data. Roche offered to provide it on condition that the reviewers sign a confidentiality agreement which would itself be kept secret. The reviewers declined.

Between 2009 and 2013, the British Medical Journal, under editor Fiona Godlee, campaigned for full clinical study report release.¹⁶ The campaign treated Roche’s withholding of the data as an admission. The campaign succeeded. In 2013, Roche released 83 clinical study reports covering more than 24,000 patients. In April 2014, Cochrane published the re-analysis.¹⁷

The findings collapsed Tamiflu’s clinical case.

In adults, oseltamivir reduced the time to first alleviation of symptoms by 16.8 hours. Seven days to 6.3 days. In healthy children, 29 hours. In asthmatic children, no statistically significant benefit at all. No reduction in hospitalizations. No reduction in pneumonia when pneumonia was defined by radiologic confirmation rather than self-report. No reduction in serious complications. No reduction in transmission. No reduction in mortality.

The harms were substantial. For every 28 adults given Tamiflu, one was made nauseous by the drug who would not have been on placebo. For every 22, one was made to vomit. Headaches and renal events followed. A statistically significant dose-response relationship in psychiatric events. A five percent absolute reduction in antibody titer increase, indicating that the drug suppresses what the establishment calls the immune response.

The trial design itself was compromised. The placebo capsules contained dehydrocholic acid, a synthetic bile acid that can induce diarrhea, abdominal cramping, and nausea.¹⁸ By including a gastrointestinal irritant in the control arm, the trials artificially inflated the rate of gastrointestinal harm in the placebo group and made Tamiflu appear better tolerated than it is. The primary endpoint, “time to alleviation of all symptoms,” was a composite measure requiring all seven symptoms to score as none or mild for at least 24 hours, a construction that maximized the appearance of benefit. Outcome definitions changed mid-trial. The presentation window was extended from 36 hours to 48 hours to enable enrollment, diluting any apparent treatment effect by including patients further from symptom onset.

Roche’s response was to commission its own analysis. In 2015, Dobson and colleagues published an industry-funded individual-patient-data meta-analysis in The Lancet reporting a 17.8-hour symptom reduction, essentially identical to Cochrane’s 16.8 hours, but claiming fewer lower-respiratory complications requiring antibiotics and fewer hospital admissions in the infected population.¹⁹ The Cochrane reviewers’ response was that both recovered endpoints rest on clinician judgment, the decision to prescribe antibiotics and the decision to admit a patient. Both are vulnerable to ascertainment bias in an unblinded post-hoc analysis. The Dobson reanalysis recovered as positive findings precisely the two endpoints Cochrane had flagged as unreliable when constructed from clinician decisions rather than radiologic confirmation or actual hospitalization records. The disagreement is not over the symptom reduction figure, on which the analyses converge, but over whether complication and admission data filtered through clinician judgment can carry the weight of policy.

The Cochrane reviewers concluded that the modest clinical benefit was outweighed by the documented harms and recommended urgent revision of stockpiling policies.

The United Kingdom Public Accounts Committee, examining the £424 million the Department of Health had spent stockpiling Tamiflu between 2006 and 2013, concluded that the decision was based on “judgment rather than evidence.”²⁰ Of that stockpile, £74 million had to be written off due to inadequate storage records. In 2017, the World Health Organization downgraded oseltamivir from its core list of essential medicines to the complementary list. The Expert Committee cited evidence that had “lowered earlier estimates of the magnitude of effect.”²¹

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Japan and the Children Who Jumped

Japan was the world’s largest consumer of Tamiflu per capita. The drug was prescribed routinely to children and adolescents during the winter months throughout the early 2000s.

In February 2007, a 16-year-old girl in Aichi died after a fall on 16 February. Eleven days later, on 27 February, a 14-year-old boy in Sendai fell to his death the day after taking Tamiflu. Both had been prescribed oseltamivir for symptoms doctors had labeled influenza.²²

The Japanese Ministry of Health, Labour and Welfare issued an emergency safety communication in March 2007, restricting Tamiflu prescription in patients aged 10 to 19. By May 2007, the Ministry had recorded 1,377 adverse event reports since the drug’s 2001 approval. Of these, 567 were serious neuropsychiatric cases, 211 featured severe abnormal behavior, and between 71 and 80 had ended in death. Fifty deaths occurred suddenly during sleep or as cardiopulmonary arrest. Eight were accidental deaths following abnormal behavior, of which five involved teenagers.²³

In 2011, Rokuro Hama and colleagues published a comparative mortality study of the 2009 H1N1 deaths in Japan in the International Journal of Risk and Safety in Medicine.²⁴ Of 162 deaths analyzed, 119 occurred after Tamiflu prescription. Of those 119, 38 deteriorated and died within twelve hours of the first dose. Twenty-eight died within six hours. Of the fifteen patients who had received zanamivir, an inhaled neuraminidase inhibitor, none deteriorated within twelve hours. The pooled odds ratio for sudden deterioration leading to death within twelve hours was 5.88, with a confidence interval excluding chance. Hama’s design is comparative rather than randomized and cannot by itself establish causation. The comparator gives the finding its weight: the patients who died fast were the patients who received the systemic neuraminidase inhibitor.

The mechanism is consistent with what the biochemistry predicts. Oseltamivir phosphate, the unmetabolized parent compound, crosses the blood-brain barrier. The barrier is less mature in children and adolescents and becomes more permeable during systemic inflammation. In the brain, oseltamivir phosphate inhibits nicotinic acetylcholine receptors involved in respiratory drive and hypothermia regulation, and it inhibits human monoamine oxidase-A, altering monoaminergic neurotransmission in ways that drive hyper-excitatory behavior. NEU3 inhibition at the plasma membrane of neurons disrupts ganglioside signaling. NEU4 inhibition disrupts neurite regulation. The drug acts on the neurological machinery of children at the moment that machinery is most vulnerable to disruption.

Roche denied causation. The Ministry, in 2018, lifted the adolescent restriction after a review concluded that abnormal behavior rates did not differ significantly between oseltamivir and other neuraminidase inhibitors. Roche presented the lifting as exoneration. The finding it actually reports is class-wide neurological toxicity rather than oseltamivir-specific harm. The entire neuraminidase inhibitor class produces neurological effects because the entire class inhibits human cellular machinery.

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The Commercial Failure That Became a Blockbuster

Tamiflu was developed by Gilead Sciences and licensed to Roche in 1996.²⁵ Donald Rumsfeld chaired the Gilead board from January 1997 until early 2001, when he became Secretary of Defense under President George W. Bush. On entering the administration, he held Gilead stock valued at between five and twenty-five million dollars.²⁶

The drug performed poorly through its first years on the market. Between 1999 and 2002, Roche sold only 5.5 million treatment courses worldwide.²⁷ The mechanism produced modest symptom reduction at high cost and substantial adverse effects. Doctors prescribed it sparingly. In June 2005, Gilead served Roche notice of termination, alleging material breach of contract for inadequate marketing.²⁸

Then the bird flu panic arrived. The World Health Organization recommended Tamiflu for individuals exposed to H5N1. The Bush administration announced a national pandemic preparedness plan that included a stockpile of Tamiflu. National governments followed. Roche’s Tamiflu sales in 2004 were $258 million. In 2005, they were $1.2 billion, with approximately half attributed to government stockpile purchases.²⁹

Gilead’s royalty revenue quadrupled in 2004 and quadrupled again in 2005. The Gilead share price rose from approximately $35 to $57 during the panic. Fortune magazine estimated that Rumsfeld’s Gilead holdings appreciated by between $2.5 million and $15.5 million.³⁰ George Shultz, former Secretary of State and a member of the Gilead board, sold more than $7 million of Gilead stock starting in early 2005.

The November 2005 dispute settlement between Gilead and Roche restructured the royalty at 14 to 22 percent of net sales, blended to approximately 18 to 19 percent for 2005, with Roche paying Gilead $62.5 million in retroactive royalties. The drug that doctors could not prescribe in 2002 became, through the bird flu panic and the swine flu panic that followed, the highest-grossing antiviral in history.

Through 2017, Roche reported more than $18 billion in cumulative oseltamivir revenue.³² After that point Roche stopped breaking the drug out as a separate line item, folding it into aggregate antiviral revenue. The UK government's 2008 business case for its stockpile assumed Tamiflu would deliver a 40 to 50 percent reduction in influenza complications and mortality, an assumption that appeared nowhere in the published evidence base because the published evidence base was incomplete.

Worldwide stockpiling reached more than 220 million treatment courses at a cost of approximately $6.9 billion, as documented in the Centers for Disease Control’s own Emerging Infectious Diseases journal.³¹ Most of the stockpile expired unused. The United Kingdom wrote off £74 million. The United States extended shelf lives through controlled stability testing, postponing rather than eliminating the loss. The clinical evidence, when Roche was finally forced to release it, showed seventeen hours of symptom reduction.

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What Flu Actually Is

In the terrain frame, what medicine calls influenza is the body’s response to a seasonal pattern of insults. Cold exposure depletes vitality. Nutritional shifts occur as fresh food becomes scarce. Indoor air pollutants accumulate from winter heating. Sunlight reduces. Holiday stress accumulates. Electromagnetic exposure increases as people spend more time indoors with devices. The toxic burden carried from autumn into winter reaches a threshold at which acute cleansing becomes necessary.

The body’s response is unified across these insults. Fever accelerates metabolic clearing. Mucus traps and expels irritants from the respiratory tract. Cough drives material out of the lungs. Fatigue enforces the rest the body requires to detoxify. Appetite suppression diverts energy from digestion to cleansing. The whole pattern, which medicine calls influenza, is the body doing what the body does when its accumulated burden reaches the threshold.

When multiple people in the same household or workplace become ill at the same time, the explanation is shared environment: the same toxic burden, the same seasonal conditions, the same exposures, not transmission of an invisible agent. Daniel Roytas documented the failed contagion experiments comprehensively in Can You Catch a Cold? Researchers tried for decades to demonstrate person-to-person transmission of influenza. They failed. The work has been ignored by the establishment, not refuted.

Tamiflu, in this context, interrupts the cleansing. The neuraminidase enzymes participate in inflammation regulation, in lysosomal recycling of cellular waste, in the desialylation of monocytes maturing into the macrophages that clear debris, in the receptor signaling that coordinates the body’s response. Tamiflu inhibits them. It suppresses what the establishment calls the immune response by five percent on the trial’s own measure. It produces, in its harm profile, the portrait of cellular machinery compromised across the body. The patient who would have cleansed in five to seven days with rest and water and minimal interference instead receives a drug that shortens that period by seventeen hours and adds to the toxic burden the body was attempting to clear.

The drug works against healing. It does not assist the body’s response. It interrupts the body’s response by poisoning the machinery the response runs on.

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Chemotherapy, and the Pattern

Chemotherapy was built on the postulate that cancer cells divide rapidly and normal cells do not. The drugs were designed to poison rapidly dividing cells. But the bone marrow, the gastrointestinal lining, the hair follicles, the lymphocytes, and the reproductive tissues also divide rapidly. The drug cannot distinguish. The toxicity profile of chemotherapy, which includes bone marrow suppression, mouth ulcers, gut destruction, hair loss, infertility, and secondary cancers, is not a side effect of the mechanism. It is the mechanism, applied to its full biological substrate.

Tamiflu was built on the postulate that influenza virus has a neuraminidase enzyme essential for its replication, and human cells do not. The four human neuraminidases sit at the lysosome, the plasma membrane, the mitochondrion, and the endoplasmic reticulum. They regulate cellular signaling, inflammation, cholesterol metabolism, elastic fiber assembly, neuronal function. The drug cannot distinguish. The toxicity profile of Tamiflu, which includes Stevens-Johnson syndrome, toxic epidermal necrolysis, hepatitis, convulsions, delirium, hallucinations, hemorrhagic colitis, thrombocytopenia, anaphylaxis, and sudden death, is not a side effect of the mechanism. It is the mechanism, applied to its full biological substrate.

The convergence is not accidental. NEU1 and NEU3 are elevated in many cancers, and sialic acid metabolism is now a recognized target in oncology research. Cancer researchers have begun investigating oseltamivir as a potential cancer drug, with studies in pancreatic, breast, ovarian, and prostate cancer models. The molecular target Tamiflu was sold as hitting in a virus is the same target that matters in human cancer biology. The establishment has noticed the off-target effect. The proposal is to monetize it in oncology rather than admit it explains the harm profile in flu patients. The drug works on human cellular machinery. The flu indication and the cancer indication are the same drug doing the same thing to the same human enzymes, sold for two different diseases.

The pattern repeats across the pharmaceutical formulary. Statins inhibit HMG-CoA reductase, an enzyme essential to the body’s production of cholesterol, coenzyme Q10, dolichols, and the protein prenylation that controls cellular signaling. The harm profile, which includes muscle damage, cognitive decline, hepatic injury, and metabolic disruption, follows. SSRIs inhibit a serotonin transporter present in the gut, the platelets, and the brain. The harm profile follows. Antibiotics devastate the bacterial communities the body depends on for digestion, nutrient absorption, and metabolic regulation. The harm profile follows.

The category error is the same in every case. A drug is designed against a biological process assumed to be unique to the disease agent. The process is not unique. The drug attacks the human equivalent. The harms are predicted by the mechanism. The package insert documents what the drug does to the patient. The marketing documents what the drug was sold to do. The two documents describe two different actions of the same molecule.

Tamiflu attacks the patient. The neuraminidase it inhibits is the patient’s neuraminidase. The disease it produces, in mild and severe forms, is the disease that neuraminidase deficiency causes when nature produces it through mutation. Hepatitis. Neurological damage. Skeletal effects. Cellular signaling disruption. Sudden death in the vulnerable. The drug is dose-limited iatrogenic sialidosis, sold as flu prevention, stockpiled by governments at a cost of $6.9 billion, downgraded from the World Health Organization’s core essential medicines list, and still prescribed to children at the first sign of fever.

Roche wrote the package insert. Every harm it documents is what neuraminidase inhibition predicts. The marketing tells a different story. The patient gets the marketing.

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Explain It To A 6 Year Old

Inside every cell in your body there is a tiny worker called neuraminidase. This worker has lots of jobs. It helps your skin stretch. It helps your liver clean your blood. It helps your brain send messages. It helps your body know when something is wrong so it can fix it. There are four different kinds of these workers, and they live in every part of your body.

A long time ago, some scientists thought that flu was caused by a tiny invader that had its own neuraminidase worker. They made a medicine called Tamiflu to stop that worker. But the medicine cannot tell the difference between the invader’s worker and your worker. So when you take the medicine, it stops your workers too.

Some children who took Tamiflu started seeing things that were not there. A few of them died very quickly. The medicine was supposed to make flu shorter. When doctors looked at all the studies, the medicine made flu only about seventeen hours shorter, and people got sicker from the medicine than they would have from just resting.

Governments bought millions of these pills. Most of them were thrown away because nobody used them. The man who used to run the company that invented the medicine became much richer when the governments bought them.

Flu is something your body knows how to heal on its own. The medicine made the healing harder. What your body needs is simple. Rest. Water. Food when you want it. A medicine that stops the workers inside your cells does not give you any of that.

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