The CDC’s Fictional Flu Death Stats and Tamiflu’s Lethal Side Effects

“You don’t sell the drug, you sell the disease.”  

~ George Merck, founder of Merck

Flu season, or at least reporting on it, has reached a fever pitch … but the flu propaganda telling you it may be dangerous NOT to take Tamiflu and/or the flu vaccine may be a far greater risk to your health than the flu itself.

Take a look at this recent hysterical headline from the Daily Mail UK: “Flu virus has killed THOUSANDS in just ONE week with the death toll set to rise and Tamiflu shortages being reported across the country.” Sounds terrifying, right? They even went out of their way to capitalize THOUSANDS to make the point, presumably, that you or your loved ones could be the next casaulty.

According to the Daily Mail UK ‘report,’ “New CDC statistics show over 4,000 Americans died from the flu or pneumonia during the third week of January.”

Did you notice that despite their headline stating it was “flu virus” which “killed THOUSANDS,” they are referencing CDC statistics which clearly state that it was either the flu or pneumonia. Well, which one is it? Something doesn’t add up here.

The CDC Admits Their Flu Death Statistics Aren’t Based On Confirmed Influenza Cases

The CDC’s own resource page on the topic titled, “Estimating Seasonal Influenza-Associated Deaths in the United States,” clearly states both that, “Seasonal influenza-related deaths are deaths that occur in people for whom seasonal influenza infection was likely a contributor to the cause of death, but not necessarily the primary cause of death,” and even more succinctly: “CDC does not know exactly how many people die from seasonal flu each year.

So, what is the CDC’s magical formula through which it arrives at its flu death statistics?

The CDC has a far from lucid answer to this question under the subject heading, “What categories does CDC use to estimate flu-associated deaths?”, as follows:

“CDC uses two categories of underlying cause of death information listed on death certificates: pneumonia and influenza (P&I) causes and respiratory and circulatory (R&C) causes. CDC uses statistical models with records from these two categories to make estimates of influenza-associated mortality. CDC uses underlying R&C deaths (which include P&I deaths) as the primary outcome in its mortality modeling because R&C deaths provide an estimate of deaths that include secondary respiratory or cardiac complications that can follow influenza. R&C causes of death are more sensitive to describe flu-related deaths than underlying P&I deaths and more specific than deaths from all causes.”

Yes, you read that correctly. The CDC uses a fuzzy math-based statistical model which identifies influenza as the cause of death even when respiratory diseases like pneumonia, or circulatory causes like cardiac arrest, are officially reported to have been the cause of death. This is all the more suspect when  no virus testing is required to be performed in the majority of these cases. Absurdly, the CDC’s own resource page on pneumonia states that, “Viruses, bacteria, and fungi can all cause pneumonia.” Clearly, therefore, influenza alone can not be said to be the cause of all pneumonia deaths. You can see the same pseudoscientific process of arriving at annual flu death statistics exposed in the report below on Canada’s equally propaganda-driven health system:


Nor would the confirmed presence of influenza be sufficient to attribute the primary cause of death to the flu. Influenza, in fact, is a naturally occurring and often subclinical part of the human virome, detectable in human blood along with dozens of other viruses. Nor is influenza strictly ‘other,’ in the sense that its very infectious particle is comprised of host proteins and lipids. Learn more by reading: Why The Only Thing Influenza May Kill Is Germ Theory. Truth be told, we are only beginning to understand the role of viruses in mediating genotype-to-phenotype relationships within the immune system. And as Skip Virgin, PhD, explains brilliantly in a NIH lecture on the virome, many of the viruses we once thought were strictly harmful protect us against deadly bacterial infections and even cancer.

The CDC appears to be aware of the weaknesses of their approach, as evidenced by their feeling obligated to answer the following hypothetical question: “Why doesn’t CDC base its seasonal flu mortality estimates only on death certificates that specifically list influenza?” Their answer powerfully confirms their lack of interest in evidence-based confirmation of their flu death statistics:

“Seasonal influenza may lead to death from other causes, such as pneumonia, congestive heart failure, or chronic obstructive pulmonary disease. It has been recognized for many years that influenza is underreported on death certificates and patients aren’t always tested for seasonal influenza infection, particularly the elderly who are at greatest risk of seasonal influenza complications and death. Some deaths – particularly among the elderly – are associated with secondary complications of seasonal influenza (including bacterial pneumonias). Influenza virus infection may not be identified in many instances because influenza virus is only detectable for a short period of time and/or many people don’t seek medical care until after the first few days of acute illness. For these and other reasons, statistical modeling strategies have been used to estimate seasonal flu-related deaths for many decades. Only counting deaths where influenza was included on a death certificate would be a gross underestimation of seasonal influenza’s true impact.” [bold emphasis added]

As you can see above, they admit that “ Influenza virus infection may not be identified in many instances,” making it impossible to confirm that these are, indeed, flu-related deaths despite their being recording as such. In other words, this is NOT evidence-based whatsoever.

Recently, my colleague RFK Jr. elaborated further on this gross misrepresentation of the truth in his article titled, “Caveat Emptor: Science vs. CDC on Scary Flu Shot Promotions,”:

“CDC’s strategy to use fear to ramp up flu vaccine sales ­­­­requires the agency to exaggerate both flu risks and vaccine efficacy. Pharmaceutical companies and public health officials vastly overstate flu cases and deaths in order to market influenza “as a threat of great proportions.” Simple fact-checking shows that since October 2017, only 14.7% of the almost 447,000 “flu” specimens tested by clinical laboratories working with CDC have tested positive for influenza. This proportion has remained relatively constant for the past two decades. According to the British Medical Journal’s Peter Doshi, “Even the ideal influenza vaccine…can only deal with a small part of the ‘flu’ problem because most ‘flu’ appears to have nothing to do with influenza.” Actual influenza deaths not only rank lower than the major killers such as heart disease and cancer but also are lower down in the mortality rankings than ulcers and hernias.”

The reality is that these frightening flu death statistics bandied about by the mainstream media and public health authorities as fact are not evidence-based in the least. Just like the CDC and media’s widespread misrepresentation of the flu vaccine as safe and effective, their facts and figures are not grounded in peer-reviewed, published research, as one would expect. But this is actually quite typical for the eminence-based, or cult of authority-based model of medicine and health policy that dominates the sociopolitical landscape today. Evidence has never really played a significant role in the CDC’s policies.

Tamiflu Caused Death Attributed To ‘The Flu’?

So, what happens when someone is treated for flu-like symptoms with Tamiflu and subsequently dies? Do you think the CDC accounts for the possibility that the drug or drugs used contributed to their deterioration or death or do they just blame ‘the flu’? This is an important question to ask, considering that Tamiflu’s lethality has been identified as a possible side effect in the medical literature. For instance:

“CONCLUSIONS: These data suggest Tamiflu use could induce sudden deterioration LEADING TO DEATH especially within 12 hours of prescription. These findings are consistent with sudden deaths observed in a series of animal toxicity studies, several reported case series and the results of prospective cohort studies. From “the precautionary principle” the potential harm of Tamiflu should be taken into account and further detailed studies should be conducted.” [capitalization emphasis added]”


“It is concluded that unchanged oseltamivir has various effects on the central nervous system (CNS) that may be related to clinical findings including hypothermia, abnormal behaviours including with fatal outcome, and SUDDEN DEATH” [capitalization emphasis added]”

Another, 2007 article published in the British Medical Journal addressed Oseltamivir’s Adverse Reactions as follows:

“…Thus adverse reactions to oseltamivir may be roughly classified into three groups: (a) sudden onset reactions related to central suppressive action of oseltamivir-P during cytokine storm, including sudden death, abnormal behaviours, and other sudden neuropsychiatric disorders; (b) late onset reactions such as pneumonia, sepsis, hyperglycaemia, and late onset neuropsychiatric disorders possibly related to inhibition of human cytosolic neuraminidase (sialidase) activity by oseltamivir carboxylate; and (c) allergic reactions and others…”

They listed the manner by which Tamiflu indices death as follows:

“…Of the total 80 deaths, 50 were sudden deaths or deaths from sudden cardiopulmonary arrest (18 in those <10 years old, 32 in those aged 20 or over)…”

Did you catch that? Heart and respiratory deaths — the very ‘causes of death’ attributed to flu by the CDC — were the most commonly reported cause of death from Tamiflu.

Again, what happens when a child, recently vaccinated with the flu vaccine, experiences symptoms of ‘the flu’ [technically over 200 different viruses can cause these symptoms, according to the Cochrane Summaries] and is immediately administered Tamiflu (which is the standard of care)? If a rapid decline in their condition is observed, or if that child dies, how would they differentiate the cause of death from vaccination and Tamiflu (and other co-administered interventions) or ‘the flu’? By default, the medical reporting system attributes the cause of death to the flu, with no differential technique employed to identify possible iatrogenic reactions produced by these presumably ‘life saving’ intervention. The same thing happens with chemotherapy-induced death in cancer patients. It’s standard practice to blame the victim and protect the guilty party, because without this sleight of hand, the business of medicine could not continue.

Amazingly, the toxicological data on Tamiflu makes it clear that one cannot distinguish Tamiflu-induced decline from flu-induced decline. Here’s an excerpt from the Toxnet monograph on Tamiflu under the subject heading Clinical Effects:

“Toxicity is commonly indistinguishable from the underlying influenza illness and the effects of other medications (eg, antihistamines, quinolones) with the potential to cause delirium.”

This is stated again in the document under the subject heading: “SEVERE TOXICITY”:

” In cases of severe toxicity, patients may very rarely develop neuropsychiatric illness including agitation, delirium, hallucinations, and psychosis. This appears to be common with high-dose therapy for critically ill patients with influenza, although whether the cause is directly due to oseltamivir toxicity or the underlying illness remains unclear.” [bold emphasis added]

Children appear to be uniquely susceptible to the toxicity of Tamiflu, and yet, in 2012, the FDA approved its use in children two months or younger. A clue to why they are more susceptible to harm is provided by an animal toxicity study, described as follows:

“LABORATORY ANIMALS: Acute Exposure/ In a 2-week study in unweaned rats, administration of a single dose of 1000 mg/kg oseltamivir phosphate to 7- day-old rats resulted in deaths associated with unusually high exposure to the prodrug. However, at 2000 mg/kg, there were no deaths or other significant effects in 14-day-old unweaned rats. Further follow-up investigations of the unexpected deaths of 7-day-old rats at 1000 mg/kg revealed that the concentrations of the prodrug in the brains were approximately 1500-fold those of the brains of adult rats administered the same oral dose of 1000 mg/kg, and those of the active metabolite were approximately 3-fold higher. Plasma levels of the prodrug were 10-fold higher in 7-day-old rats as compared with adult rats. These observations suggest that the levels of oseltamivir in the brains of rats decrease with increasing age and most likely reflect the maturation stage of the blood-brain barrier. No adverse effects occurred at 500 mg/kg/day administered to 7- to 21-day-old rats.” [bold emphasis added]

Source: [Physicians Desk Reference 60th ed, Thomson PDR, Montvale, NJ 2006., p. 2812] **PEER REVIEWED**

Did you catch that? Concentrations of the prodrug in the brains were approximately 1500-fold those of the brains of adult rats, presumably because their blood-brain barriers were not developed.

No wonder even the mainstream media can’t keep from reporting on the “odd side effects” of Tamiflu, particularly in children: USA Today:

Tamiflu may have odd side effects, particularly in children, experts say

As science begins to reveal the role of microbes in our own immunity, it is important to recognize the protest on the part of an establishment deeply invested in the role of routine pharmaceuticals in human health. They will use fear to provoke compliance with chemical interventions, ironically, capable of inducing exactly what they purport to protect you from. Hopefully this information will arm you with awareness and allow you to see media efforts for what they are – sales tactics.

FDA Approves Neurotoxic Flu Drug For Infants Less Than One

FDA Approves Neurotoxic Flu Drug For Infants Less Than One

Whereas the flu is self-limiting, the FDA’s capacity for bad decisions is not…

The recent decision by the FDA to approve the use of the antiviral drug Tamiflu for treating influenza in infants as young as two weeks old, belies an underlying trajectory within our regulatory agencies towards sheer insanity.

Tamiflu, known generically as oseltamivir, has already drawn international concern over its link with suicide deaths in children given the drug after its approval in 1999. In fact, in 2004, the Japanese pharmaceutical company Chugai added “abnormal behavior” as a possible side effect inside Tamiflu’s package.  The FDA also acknowledged in its April, 2012 “Pediatric Postmarket Adverse Event Review” of Tamiflu that “abnormal behavior, delirium, including symptoms such as hallucinations, agitation, anxiety, altered level of consciousness, confusion, nightmares, delusions” are possible side effects.[i]

Recent animal research on Tamiflu has found that the infant brain absorbs the drug more readily than the adult brain,[ii]  [iii]lending a possible explanation for why neuropsychiatric side effects have been observed disproportionately in younger patients.

The very mechanism of Tamiflu’s anti-influenza action may hold the key to its well-known neurotoxicity. Known as a neuromindase inhibitor, the drug inhibits the key enzyme within the flu virus that enables it to enter through the membrane of the host cell.  So fundamental is this enzyme that viruses are named after this antigenic characteristic. For instance,  the “N” in H1N1 flu virus is named for type 1 viral neuromindase.

Mammals, however, also have neurimindase enzymes, known as ‘sialidase homologs,’ with four variations identified within the human genome so far; NEU1,NEU2,NEU3 and NUE4.  These enzymes are important for neurological health. For example, the enzyme encoded by NEU3, is indispensable for the modulation of the ganglioside content of the lipid bilayer, which is found predominantly in the nervous system and constitutes 6% of all phospholipids in the brain.

It is therefore likely that neurimindase-targeted drugs like Tamiflu are simply not selective enough to inhibit only the enzymes associated with influenza viral infectivity. They likely also cross-react with those off-target neurimindase enzymes associated with proper neurological function within the host. This “cross reactivity” with self-structures may also explain why the offspring of pregnant women given Tamiflu have significantly elevated risk of birth defects (10.6%) relative to background rates (2-3%), according to a 2009 safety review by the European Medicines Agency.

Beyond the recognition of Tamiflu’s intrinsic toxicity, there are two additional problems with the use Tamiflu in infants:

  1. Infants do not yet have a sufficiently developed blood-brain barrier capable of keeping the chemical out of their rapidly developing brains
  2. Their detoxification systems are not sufficiently developed to remove the chemical rapidly enough to prevent harm

The FDA’s decision to include infants under one as treatable with Tamiflu is all the more disturbing when you consider that a 2010 study published in The Pediatric Infectious Disease Journal found that of 157 evaluable infants (mean age 6.3 months) treated for influenza with Tamiflu, complications due to the medication were found in the majority (54%) of the treated group.

According to the study

Complications were recorded in 84 patients (54%), the most serious of which were meningitis in 1 infant (1%), pneumonia in 9 (6%), and otitis media in 2 (1%).

Are meningitis, pneumonia and otitis media (ear infection) acceptable risks for treating influenza? Apparently for the FDA, it is.

How about death? Is that an acceptable risk of Tamiflu treatment for flu, a self-limiting disease?

In 2011, the International Journal of Vaccine Risk and Safety in Medicine published an article titled, “Oseltamivir and early deterioration leading to death: a proportional mortality study for 2009A/H1N1 influenza,” described 119 reports of Tamiflu-induced death. According to the study:  “of 119 deaths after Tamiflu was prescribed, 38 deteriorated within 12 hours (28 within 6 hours).”

The study concluded:

These data suggest Tamiflu use could induce sudden deterioration leading to death especially within 12 hours of prescription. These findings are consistent with sudden deaths observed in a series of animal toxicity studies, several reported case series and the results of prospective cohort studies. From “the precautionary principle” the potential harm of Tamiflu should be taken into account and further detailed studies should be conducted.

So, how did the FDA justify its decision to consider Tamiflu safe in infants under one year? Did it use controlled, randomized, placebo-controlled trials to ascertain safety?  Of course not. Testing drugs on infants is unethical, and no parent in their right mind would enroll their newborn in such a trial. Lacking definitive evidence of safety, the FDA’s expanded approval in children younger than one year was based on extrapolation of data from previous results in adults and older children.[iv]  This, of course, is inappropriate as it denies the aforementioned differences in the susceptibility to drug toxicity and neurotoxicity between infants and older individuals.  It also avoids proper consideration of the studies in the biomedical literature indicating its potential for severe, if not life-threatening toxicity to infants, children and adults alike.

Another concern, not addressed in the FDA announcement, is that as of Dec. 15th, 2010, the World Health Organization has acknowledged that, based on over 300 tested worldwide samples of the 2009 pandemic H1N1 flu, resistance to Tamiflu is growing.[v]  Therefore, treating an infant with Tamiflu-resistant influenza would not only do nothing to combat the infection, but would poison that child and further disable their natural immune response.

The clear winner in the FDA’s decision will be the bottom line of Roche, the manufacturer of this patented chemical.  How much longer can the FDA continue to expect those subject to its regulatory decisions to maintain the illusion that it is interested in the public welfare?

We must remember that infants do not get sick from the flu as a result of Tamiflu deficiency, or flu vaccine deficiency for that matter.  They do get sick from the immune-disrupting effects of synthetic chemicals completely foreign to human physiology (such as Tamiflu), and lack of vital hormone modulating compounds that result from adequate sunlight exposure (vitamin D3), and good nutrition.

For additional information on this topic view our research on natural anti-influenza agents.


Tamiflu and Abnormal Behavior

It’s a particularly nasty flu season, right – what should we do??

Last week, a student in my daughter’s elementary school died. An apparently healthy, active, and vital 10-year old child suddenly departed. Despite an initial announcement of “cause unknown,” the administrators followed up with a suddenly clear pronouncement that he died “from the flu.” Looking beyond the fact that now even school administrators feel entitled to give clinical advice (“if you haven’t yet received your flu shot, please do”), I was interested to see that this child’s flu vaccine status was not mentioned. I wondered if he had received the flu shot or taken Tamiflu – especially since both have been associated with sudden death in the pediatric population. 1

It’s a “deadly” flu season, and the pharmaceutically-funded media would have you believe that you must head on over to CVS and get your flu shot to make it through the year. And if the flu shot doesn’t work – even the CDC estimates its effectiveness around 39%2 – well then, just head to your doctor and get treated with Tamiflu!

But is it really that simple? Is it possible that we are bumping up against the glass ceiling of the Simple Solution for Sickness? Many of us are rolling our eyes at the “10% off your shopping order!” flu shot incentives, and our sniffles don’t send us running to the doctor for antibiotics “just in case.” As our own memories tell a different story from the scary stories on TV (wait…the chicken pox and the flu are deadly? Mom, Dad…didn’t you both have Measles and live to tell the tale?), we are becoming less and less susceptible to fabricated lore. We are harder to scare into action. We are beginning to accept that the magic pill is a fantasy, and that this crisis of confidence in our medical system is no small hurdle to overcome. It is an initiation into a new belief system.

I believe that this initiation begins with information and understanding. This understanding leads to informed choices. These empowered choices lead to a new experience of trust in your bodyand in the natural world.

Let’s bring this back to earth with an example. Let’s look at the Simple Solution for the flu: Tamiflu.

Conventional medicine tells us that you can pull one thread of the spider web without impacting the whole design. So, is it possible that Tamiflu can enter your system, kill those nasty flu germs, and quietly exit without harming any innocents?

What is Tamiflu, and how does it work?

Tamiflu (oseltamivir) is prescription medication that is FDA-approved for anyone 2 weeks of age and older.3 It is designed to prevent the influenza virus from replicating and invading other cells. The pharmaceutical company that developed Tamiflu, Roche (also called Hoffmann–LaRoche), claims that Tamiflu can protect against getting the flu and reduce the severity of flu symptoms. Roche cites studies like a 1999 article in JAMA, in which authors write that Tamiflu “…provided significant antiviral, biochemical, and clinical effects in experimental human influenza virus infection. Prophylactic administration either once or twice daily completely protected against viral recovery in the upper respiratory tract and against infection-associated respiratory tract illness.” 4

Well that sounds good, right? In 1999, Roche presented this study, along with two clinical trials involving 1,358 patients,5 to an FDA committee of medical advisors – but the committee declined to approve Tamiflu due to a lack of convincing data.

Let’s dive a bit deeper to see if the data are indeed unconvincing (the full-text of this article is free!). This study involved 117 young adults (median age was 21), split into several groups that ranged from 11 to 64 subjects. Any scientist or statistician will immediately warn you that those group sizes (called sample sizes) are too small to draw statistically significant conclusions. With that in mind, let’s continue unpacking this study…

To measure the prophylactic effects of Tamiflu, researchers gave 12 people a placebo pill, and they gave 21 people various doses of Tamiflu before they stuck influenza virus into their noses. Flu-like symptoms were measured after viral inoculation, and people who had received Tamiflu were rated to exhibit lower symptom scores. From this experiment (based on a paltry 33 subjects), researchers concluded that Tamiflu indeed protects against getting the flu.

Next, to determine if Tamiflu reduced the severity of flu symptoms, researchers infected 80 people with the influenza virus (again in their noses). They gave Tamiflu to 56 people and a placebo to the rest. Then, researchers washed out people’s noses and measured the number of virus particles in their mucus. They reported that Tamiflu treatment reduced the number of viral copies in people’s nasal passages.

Quantifying the number of viral particles in people’s noses – after the flu virus was stuck into people’s noses – does not tell us anything about how the flu virus is spreading throughout the body. Anyway, for whatever reasons (you can use your imagination), FDA administrators overruled the medical expert committee’s suggestion and approved Tamiflu in October 1999. 6 But the FDA hedged a bit and required the drugmaker to issue the following statement:

“Tamiflu has not been proven to have a positive impact on the potential consequences (such as hospitalizations, mortality, or economic impact) of seasonal, avian, or pandemic influenza.” 7

Since its FDA approval, clinical trials touting the effectiveness of Tamiflu have been published – though a look at the authors and footnotes of these studies may give you pause. For example, Penelope Ward, MD has authored dozens of scientific studies that support Tamiflu,8 including the 1999 JAMA study we just deconstructed, a 2001 JAMA study with similar methods and conclusions,9 study of Tamiflu a mechanistic study of Tamiflu,10 and an oft-cited 1999 study in the New England Journal of Medicine (NEJM) entitled ‘Use of the Selective Oral Neuraminidase Inhibitor Oseltamivir to Prevent Influenza’ – and she served as the Head of Clinical Development for Hoffman-LaRoche.11 Actually, let’s look at the footnote of the 1999 NEJM study:12


Overall, it appears that all the studies that support the efficacy of Tamiflu are funded by the pharmaceutical companies that stand to profit from its sales.

Fortunately, a group of unbiased medical experts at the US Cochrane Center13 re-analyzed data from 20 clinical trials like these, reporting their results in a 2009 BMJ article. Their meta-analysis showed that there was no significant evidence that Tamiflu reduced influenza symptoms or complications – the only possible positive association was that Tamiflu might decrease the length of time people exhibited symptoms by a few hours.14 Further, the reanalysis found that Tamiflu increased nausea.

As an interesting aside, Cochrane Center researchers noted that it took years-long concerted efforts to obtain clinical data from drugmakers.15 Along these lines, investigative articles published in The Atlantic in 200916 and 201317 suggest that political and financial motivations (to the tune of billions of dollars) underpin this Tamiflu delusion.

So where does this leave us? Perhaps Tamiflu doesn’t work that well, but is there any harm in taking it anyway, just to be safe?

Is Tamiflu safe?

A 2007 scientific report18 suggests that Tamiflu is in fact exceedingly dangerous. In the 6 years that Tamiflu was marketed in Japan, the Japanese Ministry of Health Labour and Welfare received 1377 reports of adverse reactions. Approximately half of these reactions were serious neuropsychiatric cases, including delirium, convulsions, and encephalitis. Eighty deaths were reported, though only 71 were considered to be directly related to Tamiflu. Two of the most alarming deaths were suicides by 14-year-old teens on Tamiflu.19

As such, Japanese authorities advised against Tamiflu for adolescents, and the National Institute for Health and Clinical Excellence (the UK’s version of the FDA) recommends against Tamiflu as a preventative strategy in healthy people.20 Yet, American agencies like the CDC and FDA continue to push Tamiflu in spite of its documented side effects of hallucinations.21

Several recent news stories have highlighted these side effects of Tamiflu. For example, on January 15, 2018 a 6-year-old Texan girl took Tamiflu, hallucinated, and tried to jump out of a window22. About a week later, another Texan child, this time a two-year-old boy, suffered from hallucinations that caused him to repeatedly slap his mother.23

In a news article from January 24, 2018, the mother of a five-year-old girl who experienced severe hallucinations and seizure-like symptoms stated, “The flu is bad, it’s horrible, you feel helpless your child’s sick…I would take that a hundred times over the reaction she had to the Tamiflu.”24Perhaps most telling is an article in Time entitled ‘Tamiflu Made My Kid Hallucinate. I Think the Flu is Preferable to Delirium.’25

Very sadly, a 6-year old girl named Emily Muth from North Carolina died this week – three days after being given Tamiflu.26 According to her mother, Emily suffered from labored breathing (a known side effect of Tamiflu) right before her tragic passing.

Emily Muth

Unfortunately, Tamiflu is neither safe nor effective. I hope that presenting the terrible experiences of the children and families mentioned in this article will serve as a warning to prevent more tragedies.

Fighting won’t win this fight

When you understand that the preschool analogy of foreign invaders (germs) fighting your inner soldiers (immune system) has been rendered obsolete by our awareness of the microbiome(including the virome!), and the poetic reality that we are made up of the very organisms we thought that we were fighting…well, then pharmaceutical medicine seems something like cutting off your nose to spite your face.

This is when you can graduate to a deeper sense that illness is purposeful, that the body recalibrates through fever, and that we are simply here to support the body’s innate wisdom…the less fear, the better.

There are many evidence-based tools for supporting your body’s detoxification process including vitamins A and D, herbs like ginseng, elderberry, and ginger, and food-derived compounds like AHCC and beta glucan, and, my favorite in this case, homeopathy (Oscillococcinum).27 Take the cue to stop, rest, and just be – while your body does its wise work.

This Flu Season, Don’t Forget About Tamiflu

Despite recent controversies about its effectiveness, clinicians should not forget about using the antiviral, oseltamivir (Tamiflu), to help shorten the course of influenza among patients during the coming flu season. In this exclusive MedPage Today video, Arnold Monto, MD, of the University of Michigan School of Public Health in Ann Arbor, discusses how antivirals may be more important than ever this flu season — both in adult and pediatric populations — with an influenza vaccine that may not be as effective.

Following is a transcript of his remarks:

What’s happening is that we are about to have an influenza outbreak, or it’s already starting. We know that this influenza outbreak in the U.S. is mainly H3N2, which is the one that’s the most severe in terms of causing severe morbidity and mortality.

We also know that the vaccine doesn’t work as well against this kind of influenza, and what we really need to remember is that we should be using Tamiflu as the one licensed antiviral that we have which is commonly available. We have others that are a little harder to get a hold of, but they will shorten the duration of illness and prevent complications. We should not hesitate to use what we’ve got because these drugs are not super drugs.

We know that we need better antivirals, and there are new ones in the pipeline, but they are not currently available. The CDC is very strong in their recommendation in certain risk groups that the antivirals — mainly oseltamivir, Tamiflu — be used in the appropriate situations.

I think the CDC has spoken — as have various other organizations like the Infectious Diseases Society, pediatric groups — [about] appropriate use of antivirals, and we need to remember to use them during the coming flu season because we expect the vaccine to work, but not as well as we would like.

There has been controversy between two journals in terms of how they view Tamiflu, which is very strange because we are all science-based and we should really go on the evidence.

We published an article in Lancet looking at the clinical trials of Tamiflu, and we are now about to publish a paper in Clinical and Infectious Diseases that looks at the effect of Tamiflu in pediatrics. We find that it not only shortens the duration of influenza, but also prevents complications [like] otitis media, which is an important complication that occurs after a case of influenza.

It’s a scandal drug trial results are still being withheld.

The Commons public accounts committee’s report into the government’s handling of the UK’s £424m stockpile of the influenza drug Tamiflu, published last week, was damning. But starting from this narrow remit, the committee also stumbled – with palpable amazement – into a far wider problem.

Several different types of statin pills tablets, UK

Nobody can give you a fully informed view on the benefits of any treatment, let alone Tamiflu, because the results of clinical trials are being routinely and legally withheld from doctors, researchers and patients. As the committee pointed out, government agencies around the world disagree on whether Tamiflu reduces your chances of pneumonia and death, but we can have no idea who is right, because we can’t see the evidence. Astonishingly, in withholding this information for five years, Tamiflu’s makers, Roche, have broken no law – and it is only an accident of history that this drug has become the poster child for change.

The first study on the problem of missing results was published in 1986. A 2010 review article by the NHS’s own research body summarises the results of a dozen more studies on the same subject: this found that, overall, the chances of a completed trial being published are roughly 50%. This undermines our ability to make informed decisions on everything from surgical techniques to drugs and devices. Unsurprisingly, trials with positive results are twice as likely to be published as those with negative results, so the evidence we do see is potentially biased. Large studies from the past two years, chasing up results from huge registries of completed trials, report similar results. Information isn’t just passively left unpublished: it is actively withheld when requested by researchers.

Doctors like me cannot possibly make informed decisions about which treatment is best when the information we rely on has been distorted in this way. The problem is endemic, has a serious impact on public health, and has been well documented for over two decades. How can this have been allowed to happen?

It’s tempting to fall back on crude fairytales of evil corporations, and there is no doubt that industry has lobbied hard against change. Secret internal memos, leaked in 2013, showed the US and EU industry representative bodies discussing their “advocacy strategy” against transparency, including a plan to “mobilise” the patient representative groups the industry often generously funds.

But the real scandal lies with the very people we expect to protect us. It seems some civil servants at medicines regulators still wish for a quiet life, where they can ruminate on secret data behind closed doors, with no or limited academic or public scrutiny over their decisions. This is particularly dangerous when you consider that some of the biggest medical scandals of the past few years – problems with the evidence for Vioxx, Avandia and Tamiflu, for example – were only spotted by independent researchers and academics, often after a long fight for access to information on clinical trials.

The medical profession, until recently, has been supine. In 2012 the medical royal colleges, societies and even the Department of Health signed up to a bizarre set of documents – apparently orchestrated by industry – claiming there is a “robust regulatory framework” ensuring access to trial results. Not only does this give false reassurance on a vitally important matter of public safety, but the signatories refused to answer even the simplest questions about how they came to sign such peculiar statements.

Now, all that has changed. Some 130 patient groups, representing more than 100 million patients, have signed up to All Trials, a campaign I co-founded with the BMJ and other groups a year ago. Others supporting the campaign include Nice, the Medical Research Council and GlaxoSmithKline one of the biggest drug companies in the world.

The final frontier is delay and denialism at the Medicines and Healthcare Products Regulatory Agency, the Department of Health and the government. David Cameron, when asked about missing trial results and Tamiflu, at prime minister’s questions, explained that he took this problem seriously, and suggested new EU legislation will fix it. This is untrue. New EU legislation – which the industry have been lobbying desperately against – only requires better sharing for trials starting after 2014. Even if it passes, this will do nothing to improve the evidence base for the decisions made in clinics around the world today. The overwhelming majority of treatments prescribed by doctors right now – the everyday drugs for blood pressure, cholesterol, ulcers and more that are taken by millions – all came on the market over the past two decades, not the past seven days. That is the era of evidence that patients need.

Government should ride the wave we have created, and act. There has been more progress on trials transparency in the past 12 months than in the past 25 years. Proposals from industry and regulators are riddled with loopholes so huge they exempt the vast majority of trials on the medicines we use today: but these loopholes are finally being called out.The net is tightening for those who belittle this problem, or pretend it has been fixed, and it’s almost painful to see how easy it was for patients and doctors to have such an impact. We should have acted sooner, but we have an unprecedented opportunity for change. Anyone undermining the case for transparency will find themselves on the wrong side of patients and the wrong side of history. Medicine relies on evidence: future generations will look back on us tolerating withheld results in the same way we look back on medieval blood-letting.

What does Tamiflu do, and how will we know?

Jonathan Nguyen-Van-Tam, virologist and researcher from the University of Nottingham, told a group of triallists and virologists last week “we must remember why we’re here—because of the controversies. The clinical world doesn’t believe that Tamiflu works. We should assess whether the regulatory approval/product insert for Tamiflu is valid.”

That group, the MUltiparty Group for Advice on Science (MUGAS) was at a workshop in Brussels on 18 June organised by the European Scientific Working group on Influenza (ESWI) and supported by an unrestricted grant from Roche. Led by several of the original Tamiflu regulatory triallists, the workshop heard plenty of evidence to challenge current claims about Tamiflu’s effects. MUGAS decided to plan and conduct individual participant data (IPD) meta-analyses of the randomised trial data—and observational data. That’s quite a remarkable turnaround, given the strength of claims made by some of the same people over the past decade.

BMJ readers will already be very familiar with growing concerns about oseltamivir’s effectiveness. Earlier this year Professor Harlan Krumholz and co-authors concluded in an editorial in the BMJ that “Despite government claims, we should acknowledge the uncertainty surrounding oseltamivir’s effectiveness and the gaps in publicly available evidence. On the basis of the available data, at best the drug shortens symptoms by about a day when used within the first two days of symptoms, but it has no effect on hospital admissions. In addition, trial data from which to draw conclusions about complications and transmission of flu are lacking.”

WHO made particularly firm claims about oseltamivir in August 2009 during the swine flu (H1N1) pandemic. WHO then stated that, “The guidelines represent the consensus reached by an international panel of experts who reviewed all available studies on the safety and effectiveness of these drugs…Evidence reviewed by the panel indicates that oseltamivir, when properly prescribed, can significantly reduce the risk of pneumonia (a leading cause of death for both pandemic and seasonal influenza) and the need for hospitalization.”

That expert panel advising WHO was anonymous: all its members had signed a confidentiality agreement. But at least one member was identified later as Professor Arnold Monto of the University of Michigan, who coauthored several trials of neuraminidase inhibitors back in the 1990s. The same Professor Monto is one of the four convenors of MUGAS, along with Professor Ab Osterhaus (of Erasmus MC University in Rotterdam, a scientific advisor to Roche, another oseltamivir triallist), Professor Menno de Jong (of Academic Medical Center Amsterdam, virologist and researcher) and Professor Rich Whitley (of University of Alabama at Birmingham, professor of pediatric infectious diseases and an adviser on flu to the Obama administration).

Barry Clinch, Principal Clinical Scientist at F. Hoffmann-La Roche, presented at the MUGAS workshop an overview of all studies in the company’s oseltamivir research programme. His slides showed that in all, 18,928 patients had taken part in trials, observational studies of treatment, and studies of prophylaxis; around 11,500 of them treated with oral oseltamivir. Randomised controlled trials (RCTs) had included 4799 adults and 1368 children and, along with some open label studies, a total of 8078 patients had taken part. All but one of the 12 RCTs took place in the late 1990s. Roche’s lab researchers had also done experimental flu studies and clinical pharmacology studies.

Clinch confirmed that investigators were told to always report admissions to hospital during the Roche trials, but warned that “caution should be exercised in interpreting results on hospitalisation.” This is because there were such low event rates: for example in trial WV15671 just 1 of 201 participants was hospitalised. The main intention to treat analyses in the 12 Roche RCTs (for all patients enrolled with flu-like illness and who had at least 1 dose of trial medication) failed to find statistically significant evidence that hospitalisation rates were reduced by oseltamivir when compared against placebo. For the ITTI population (the subset with flu confirmed by culture or >4 fold rise in antibody titre) the overall P value was 0.06 but this was grossly underpowered.

Presenting the key oseltamivir trials that yielded data on flu complications, Clinch explained that a standard case report form was used to collected data on “Secondary illness.” “We didn’t ask physicians to actively look for complications,” he said. “They simply reported them if they thought patients had, for example, sinusitis, otitis media, bronchitis, pneumonia or other chest infections.” Clinicians could also say if patients needed antibiotics or X rays—thereby implying that there might be some secondary illness—but there was no requirement to confirm diagnoses without anything more than a clinical diagnosis. “To be honest, we weren’t that stringent at the time,” acknowledged Clinch. (And, of course, at that time Roche was testing oseltamivir primarily as another antiviral for seasonal flu, not as a lifesaver in a pandemic.) Only two trial protocols required reporting of clinically diagnosed complications (coded as bronchitis, pneumonia, lower respiratory tract complication, or antibiotic prescription occurring >48h after start of treatment with oseltamivir) as a formal secondary endpoint: those among older and at risk participants. Statistical analyses of these outcomes were exploratory, said Clinch.

The ensuing questions and discussion among the MUGAS review board members (some of whom co-authored some of the trials in question) confirmed that “secondary illness” was indeed only a clinical diagnosis, that in most of the trials its reporting was ad hoc, and that Roche does not know the extent of any missing data. Decisions to give antibiotics were made for nonspecified clinical reasons, and, as someone pointed out, antibiotic usage rates will have varied a lot from site to site because of geographical variations in prescribing behaviour.

However, some of the MUGAS virologists said we know from Roche’s original observational studies and from subsequent case series from the H1N1 pandemic that oseltamivir does reduce complications. Do we? Not yet, although Professor Van Tam’s group has conducted a systematic review and IPD meta-analysis of published andunpublished observational study data during the H1N1 pandemic that will be submitted soon for publication. This study was sponsored by Roche but Professor Van Tam said the data agreement gives Roche no access to the data. The authors plan, however, to share the data with other investigators on request.

When asked what proportion of the original Roche oseltamivir research programme had results in the public domain, Clinch said “about 90% in one form or another.” Virologist Fred Hayden, co-author of several Roche trials, asked: “the contentious area is the 8-10 unpublished trials done some time ago. Are there any plans to publish those?” Clinch replied “it’s a good question…we’d like MUGAS to discuss that. Roche has no objection to that.” Professor Osterhaus said that MUGAS wants to analyse the IPD from those trials and to publish the resulting papers in peer reviewed journals.

So, of course, does the Cochrane Acute Respiratory Infections Group, which has been struggling for years to get the unpublished trial data from Roche. That data release has now begun, and the Cochrane group is poring over the partly redacted Clinical Study Reports right now.

So it’s from famine to feast, with two different groups working towards meta-analyses of the unpublished patient-level data on the effects of oseltamivir in flu. Will they come to the same conclusions?

Source: BMJ

H7N9 Seems to Readily Develop Resistance to Neuraminidase Inhibitors.

The novel influenza A virus H7N9 has shown a “concerning” ability to develop resistance to neuraminidase inhibitors such as Tamiflu (oseltamivir) and Relenza (zanamivir), according to a Lancet study.

Researchers studied 14 patients admitted to a Shanghai hospital with H7N9 influenza. In tracking patients’ viral loads, they noted that two showed persistently high loads after starting neuraminidase inhibitors. Both had also received steroid treatment. A mutation in the virus’s neuraminidase gene was associated with persistent high viral loads and poor clinical outcome.

The researchers wonder what, if any, role the steroid therapy had in the emergence of resistance. They advise early treatment with neuraminidase inhibitors.

Meanwhile, China has reported no new H7N9 cases for 2 weeks. The case count now stands at 131, with 32 deaths.

Source: Lancet

Basis for Clinical Approval of Influenza Drugs Relenza and Tamiflu Questioned .

Patients may ask about a widely reported call from the Cochrane Collaboration for full disclosure of information about clinical studies leading to the approval of the neuraminidase inhibitors oseltamivir (Tamiflu) and zanamivir (Relenza) used to treat influenza.

The reviewers point out that data on oseltamivir from 8 trials of a 10-trial meta-analysis remain unpublished and were not available either from the studies’ authors or the manufacturer. That meta-analysis “has been the sole publication” cited by the CDC in support of its treatment guidelines.

On the basis of drug company data submitted to government agencies, the reviewers estimate that 60% of patient data from oseltamivir’s phase III trials “have never been published.” Using such “regulatory information” rather than published journal studies, the reviewers estimate that oseltamivir showed “no evidence of effect” on hospitalization rates; there was not enough information available to assess the drug’s effects on complications or viral transmission.

Source: Cochrane Library.