The study's authors propose two major mechanisms by which healthful plant-based diets might decrease the risk of chronic disease and premature death:

• Higher consumption of unprocessed plant foods may decrease the risk of obesity, low-grade inflammation, and impaired insulin sensitivity, all of which contribute to the development of both cardiovascular disease and cancer;
• Plant constituents including fibre (and, I would add, other microbiota-accessible carbohydrates, and polyphenols) may beneficially affect the composition and function of the gut microbiome, resulting in heightened production of health-promoting bacterial metabolites such as short-chain fatty acids and decreased production of harmful products such as secondary bile acids and trimethylamine-oxide, which may be associated with CVD and certain cancers, although further research in human populations is needed.

It's important to point out that the assemblages of highly-processed plant food components that are being heavily promoted by the Davos crowd and their acolytes have the exact opposite effect: they impair insulin sensitivity, cause inflammation, and trigger overeating and consequent weight gain.
The moral of the story is quite simple: if you want to maximise your chances of living a long, healthy life, eat more plant-derived foods in a state as close as possible to their natural form, and minimise your intake of highly processed plant-derived foods and animal foods. Your body will thank you for it, and your would-be overlords will be bummed that they've lost a customer for their sick-care business empire. That's a pretty damn good outcome, in my book.
​

Are psychedelic drugs the solution to the 'mental health crisis', or just the latest manifestation of our 'pill for every ill' delusion?


In a recent episode of the Stand Up Sits Down podcast, I shared my concerns about the resurgent interest in the use of psychedelic drugs for the treatment of various forms of psychological distress (discussion of this topic begins at around 58 minutes).

Before you all bombard me with hate mail and/or stories of your wonderful and life-altering experiences with psychedelics, let me make my position clear. As I stressed in the podcast, I am cautiously optimistic that the use of certain psychedelics may offer substantial benefit to certain people, when administered in the correct set (mindset) and setting (physical and social environment), and followed up with post-trip integration of the psychedelic experiences that is of sufficient duration, and delivered by ethical and skilled individuals.
That's a hell of a lot of preconditions that need to be met for a successful outcome, because there's a hell of a lot that can go wrong. For example:

• An ever-increasing number of people are reporting therapy abuse in the context of psychedelics.
• I have serious doubts that the conditions for beneficial use of psychedelics can be met by, for example, mail-order at-home ketamine programs (thinly-veiled advertorials for such programs notwithstanding).
• I have equally grave concerns about many of the versions of traditional psychedelic rituals that are now promoted to Western 'spiritual tourists', given that these rituals are, in essence, suggestibility techniques for inculcating culturally-sanctioned beliefs:

"Drawing on cross-cultural data analysis, Grob and Dobkin de Rios (1992); Dobkin de Rios and Stachalek (1999), and Dobkin de Rios et al. (2002) have suggested that hallucinogenic substances are used by many indigenous groups to create hypersuggestible states of consciousness, in order to promote fast-paced socialization for religious or pedagogical purposes, as enculturating adolescents during puberty rituals leaded [sic] by elders."

Psychedelics as Tools for Belief Transmission. Set, Setting, Suggestibility, and Persuasion in the Ritual Use of Hallucinogens
I am deeply suspicious of the motives underlying the aggressive proselytising and marketing of psychedelics by a slew of non-profits, universities, pharmaceutical companies and venture capitalists - including the Australian government's agency for scientific research, CSIRO.
My concerns are only heightened by the CIA's sordid history of use of these mind-altering substances in experiments conducted under the auspices of MK-Ultra, a long-running program of research into mind control.

But the bedrock of my concerns is this: The positioning of psychedelics as therapeutic agents for psychological conditions is just a continuation of the 'pill for every ill' mentality that has resulted in Australia, and other wealthy nations, becoming populations of chronic drug-takers. Consider these alarming statistics:

• According to a 2018 Roy Morgan poll, almost 90 per cent of Australians aged over 14 years (93 per cent of women and 85 per cent of men) had taken some form of medication in the last year.
• In the same year, when Australia's population stood at 25 180 200, 9 million people were taking at least one prescribed medicine every day, with 8 million taking two or more prescribed medicines in a week, and more than 2 million taking over-the-counter medicine daily.
• In 2020-21, the Australian government spent A$13.9 billion on medication subsidised by two schemes - the PBS and RPBS - which jointly underwrite almost all prescribed medicines (and some over-the-counter medicines and non-drug items), accounting for 81 per cent of the cost of PBS and RPBS medicines. This works out to A$541 spent per person. Consumers paid the remaining A$3.2 billion towards their PBS and RPBS prescriptions.
• Also in 2020-21, 4.5 million individuals (17.7 per cent of the Australian population) filled a prescription for a 'mental health-related medication', with an average of 9.4 prescriptions per patient; 73.1 per cent of these mental health-related prescriptions filled were for antidepressant medications. Females are one and a half times as likely to be prescribed a 'mental health-related medication' as males, and the percentage of people on such brain-altering drugs rises stepwise with age; an astounding 41 per cent of Australians aged over 85 are on prescription medications for a (purported) mental health condition:

What do we have to show for this profligate spending on pharmaceuticals? We're fatter, sicker and more miserable than ever before.
A sane but naive person would conclude that, if the 'health system' that we have isn't actually delivering healthier, happier people, then it is not working, and those running it should try a different approach.
A cynic, on the other hand, would observe that every system produces exactly the outcomes it was designed to produce. To the pharmaceutical-medical-industrial complex, production of permanently ill, chronically unhappy people is a feature, not a bug.
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And so, now that the 'serotonin deficiency'/'biochemical imbalance' hypothesis of depression has been comprehensively debunked, and the much-vaunted serotonin-modulating antidepressants are losing their sheen, the psychedelic-industrial complex is wheeling in the next miracle cure for human misery.
They even have a new version of the neurobabble that was used to sell us on selective serotonin reuptake inhibitors (SSRIs) and serotonin and norepinephrine reuptake inhibitors (SNRIs) as the salves for our suffering. As Dr Joanna Moncrieff (author of the devastating dismantling of the serotonin hypothesis that I referenced in my previous article, Has psychiatry finally reached its Apocalypse Now moment?) crisply observes:
"In an interview published in Nature, psychopharmacologist and psychedelic researcher, David Nutt, suggests that psychedelics ‘turn off parts of the brain that relate to depression’ and ‘reset the brain’s thinking processes’ via their actions on cortical 5-HT2A receptors. Others assert they enhance brain ‘connectivity’. The John Hopkins University website alleges they offer the promise of ‘precision medicine treatments tailored to the specific needs of individual patients’. All these claims are pure speculation."
Psychedelics—The New Psychiatric Craze
Forgive me if, like Joanna Moncrieff, I'm a little less than wildly enthusiastic about the latest panacea; I've seen this movie before. No doubt the busy-bee researchers who ploughed gazillions of taxpayer dollars into studies like the one that found that people whose antidepressant prescriptions were guided by pharmacogenomic testing weren't any less likely to be depressed after six months on their super-sciencey-selected drugs than people whose doctors just put them on whatever random happy pill they felt like dishing out that day, will happily pivot to burning up taxpayer dollars on studies that - eventually - find that pharmacogenomically-guided psychedelic prescriptions aren't any more effective than buying a pill from some shady dude at a rave. Because, as Will Hall incisively observes:
"Psychedelics—as weird, unpredictable, mind-shaking and life-altering as they can be—are still the same underground marketed drugs: they intoxicate you, get you high, and you come down."
Ending The Silence Around Psychedelic Therapy Abuse
What I find particularly irritating about the pro-psychedelic neurobabble is that the biological mechanisms by which these potent intoxicating agents are claimed to exert their 'curative' effects on psychological suffering, are also activated by a simple, safe, health-promoting intervention that doesn't put people at risk of therapy abuse or bad trips, and is known to be more effective than either medication or psychotherapy for relieving depression, anxiety and psychological distress. What is this secret wellness weapon, you ask? It's called exercise.
For example, last year Japanese researchers reported that the "rapid and sustained antidepressant-like actions of ketamine" are mediated by increased levels of insulin-like growth factor 1 (IGF-1) and brain-derived neurotrophic factor (BDNF) within the brain. They speculated that IGF-1 signalling in the medial prefrontal cortex of the brain might be crucial to the enhanced neuroplasticity (ability of the brain to rewire itself in response to experience) which is believed to induce the antidepressant effects of ketamine. The press release announcing the study breathlessly forecast a whole new line of drug development arising from this discovery (ka-ching!):
"The link between ketamine and IGF-1 presents a brand-new direction for future studies investigating antidepressants that target IGF-1 directly."

Using Ketamine to Find an Undiscovered Pathway in Depression
Y'know what else raises both IGF-1 and BDNF levels within the brain, and increases neuroplasticity? You guessed it: exercise. Added bonus: exercise does it without causing "dependence, hallucinations, and delusions". But what would be the fun in that? And more to the point, who would turn a profit from it?

A recently-published umbrella review of physical activity interventions found that exercise predictably reduces anxiety, depression and psychological distress, and furthermore, it is about 50 per cent more effective at doing so than either medication or cognitive behavioural therapy (CBT).

Higher intensity exercise programs of between six and 12 weeks duration were shown to be more effective than lower intensity exercise (such as moderate-paced walking, yoga and Pilates), but all forms of physical activity demonstrated beneficial effects on psychological function.
Furthermore, exercise enhances depressed people's ability to feel happy when good things happen to them - that is, it combats anhedonia, or reduced motivation or ability to experience pleasure, which is a hallmark of depression.
On the other hand, SSRI antidepressants reduce reinforcement sensitivity, causing emotional blunting (reduced ability to feel either happy or sad) in 40-60 per cent of patients taking these drugs.
This reduction in reinforcement sensitivity also causes reduced ability to reach orgasm even in non-depressed people. Sexual dysfunction is a widely-reported and exceptionally distressing adverse effect of SSRIs, which often persists long after people stop taking the drugs.

And of course, exercise has an immense number of positive 'side effects' on many of the pathophysiological hallmarks of depression and anxiety. To name just a few:

• Exercise reduces visceral adipose tissue, the deep belly fat that is associated with heightened risk of depression.
• Exercise reduces inflammation, while depressed people have elevated levels of inflammatory chemicals both in their brains, and throughout their bodies.
• Exercise helps to overcome insulin resistance; insulin resistance is strongly associated with increased risk of developing major depressive disorder.
• As mentioned previously, exercise increases secretion of IGF-1 and BDNF, both of which rapidly exert antidepressant effects.

Now, it may turn out that psychedelics are safer and more effective than SSRIs, SNRIs, and all the previous drugs that have been proffered as solutions to the pain of life. They may not cause emotional blunting, or sexual dysfunction, or bone fractures, or terrible withdrawal symptoms (although as Joanna Moncrieff points out, the early promise that psychedelics would 'cure' depression in just one to two sessions has not panned out, with many people converting to long-term users).
But even if they do prove superior to other psychoactive medications, my question will be:
"Are they better than exercise?"

That is, can any drug be more effective at improving mood, enhancing your ability to feel happy, and boosting your sense of self-efficacy, all while making you physically healthier and reducing your need for other pharmaceuticals (such as drugs for high blood pressure, diabetes and high cholesterol), than exercise? Because if it doesn't work better across the board than exercise, then by definition it's an inferior treatment and I would question whether it should be publicly funded.
Whatever the benefits of psychedelics may be, I would take a lot of convincing that, at least in the current economic and social context, they're not feeding into the 'pill for every ill' mentality that has generated our thoroughly dysfunctional not-health-care system.


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https://robynchuter.substack.com/p/psychedelics-panacea-or-psychiatrys

​In Part 1 of this miniseries, I summarised three studies that suggest that adolescents are not at risk of neurocognitive or psychological symptoms of ‘long COVID’; and that the major risk factors for developing ‘long COVID’ are being physically unwell (including being overweight) and experiencing psychological distress before contracting SARS-CoV-2 infection.

Let's continue exploring the medical literature on long COVID. First up, a study comparing outcomes of COVID and non-COVID respiratory illness:
Study #4: Association of Initial SARS-CoV-2 Test Positivity With Patient-Reported Well-being 3 Months After a Symptomatic IllnessTop-line summary: People who had a non-COVID respiratory illness were more likely to still be unwell three months later, than people who had COVID-19.

​The long version:

This US study was a planned interim analysis of an ongoing multicentre prospective longitudinal registry study (the Innovative Support for Patients With SARS-CoV-2 Infections Registry [INSPIRE]) - seriously, who comes up with this stuff? - which was set up specifically to assess long-term outcomes of adults with COVID-19, and to compare them to contemporary controls comprising adults who had similar symptoms but tested negative for SARS-CoV-2 on either a PCR or antigen test.
The subjects of this study were the first 1000 participants who completed baseline and 3-month follow-up surveys which used the Patient-Reported Outcomes Measurement Information System (PROMIS-29) - again with the dinky acronyms - to assess their physical function, anxiety, depression, fatigue, social participation, sleep disturbance, and pain interference, and the PROMIS Short Form–Cognitive Function 8a scale to assess cognitive function.

Just over 72 per cent of participants tested positive to SARS-CoV-2 (for what that's worth) while 28 per cent tested negative. (Remember, all participants presented for medical attention with similar symptoms.) Although the rate of moderate to severe impairments across any PROMIS domain were quite similar at baseline (64.7 per cent in the COVID-19–positive group vs 67.4% in the COVID-19–negative group, hinting at just how sick the average American is), the two groups were quite heterogeneous; those who tested negative tended to be older, of non-white race, unmarried, poorer, unemployed, and publicly rather than privately insured, to have been tested for SARS-CoV-2 in an emergency department, and to have moderate or severe asthma, hypertension or diabetes. In other words, those who were not diagnosed with COVID-19 were in worse shape overall at the beginning of the study. Unsurprisingly then, at baseline they were more anxious, depressed, and reported more pain than the COVID-positive group.

Nonetheless, those who tested positive for SARS-CoV-2 reported more symptoms at baseline and were more likely to have been hospitalised for their symptomatic illness. In fact, 10.8 per cent of those who tested positive were hospitalised vs only 1.5 per cent of those who tested negative.
Three months later, almost 40 per cent of people with test-confirmed COVID-19 reported moderate to severe impairments across any PROMIS domain... but so did 53.5 per cent of COVID-19-negative patients. 22 per cent of participants with test-confirmed COVID-19 were moderately to severely anxious or depressed, compared to 27 per cent of participants with a non-COVID illness.
​
The following chart illustrates the health trajectory of both groups; the 50th percentile line indicates population norms for each metric:

The authors of the study point out the obvious weakness in many other studies that have reported high rates of postviral symptoms - no control group - and also underline the difficulty of distinguishing between genuine postviral symptoms, the effects of delayed or inadequate medical care, and the societal upheaval inflicted by 'public health' policies:
"Although other studies21-24 have found that those who recover from acute SARS-CoV-2 infection are at increased risk of an array of mental health disorders during the subsequent year, participants in the current cohort experienced similar rates of depressive symptoms at baseline and follow-up regardless of initial COVID-19 status. The presence and persistence of poor mental health among nearly 1 in 4 participants (21.9% of the COVID-19–positive group and 27.3% of the COVID-19–negative group) may reflect a more general pandemic exposure, which participants in both groups experienced. The inclusion of a control group of participants who were exposed to the pandemic yet tested negative and the use of validated scores with prepandemic population norms were important to identifying broader pandemic impacts which may have had consequences for observed changes in well-being. For instance, similarity in observed changes in both groups may be reflective of the experience of being ill during a pandemic when access to care was hampered by pandemic restrictions, potentially slowing recovery regardless of the cause of the underlying infection. These broader pandemic societal impacts therefore call for increased attention to mental health services irrespective of SARS-CoV-2 infection status."
Association of Initial SARS-CoV-2 Test Positivity With Patient-Reported Well-being 3 Months After a Symptomatic Illness

Implications of this study:Poor physical and mental health are shockingly common in the US, and other industrialised nations. People who were already in bad shape before getting acutely ill with a respiratory illness may continue to suffer poor health afterwards, but if anything, those who had a non-COVID illness may do even worse. The brouhaha about long COVID obscures the damage done to people's well-being by non-evidence-based pandemic policies.


Next, a study on postviral symptoms after a mild case of COVID-19:
Study #5: Long covid outcomes at one year after mild SARS-CoV-2 infection: nationwide cohort studyTopline summary: People who experience mild symptoms of COVID-19 have a heightened risk of a small number of conditions, most of which are resolved within a year from diagnosis.
​
The long version:This study analysed electronic health records from Maccabi Healthcare Services (MHS), the second largest health maintenance organisation in Israel, which covers a quarter of the Israeli population. The database includes longitudinal data for all COVID-19 diagnoses (counted as a positive PCR test, an extremely problematic diagnostic criterion) and their aftermath, along with detailed demographic information, diagnoses of other conditions, medication prescriptions and pathology test results. The study subjects were all those who were PCR tested for SARS-CoV-2 at least once (comprising 76 per cent of MHS’ members, or over 1.9 million Israelis) but not admitted to hospital with COVID-19 during the 30 days after infection. Patients who tested positive were matched with test-negative patients by age, sex and vaccination status.
Of all the health outcomes studied, only abnormalities in smell and taste (anosmia and dysgeusia), concentration and memory impairment, breathing difficulties (dyspnoea), weakness, palpitations, streptococcal tonsillitis, and dizziness were significantly more common in people who tested positive for SARS-CoV-2 infection (dots to the right of the vertical line in Figure 2 below), and almost all had completely resolved within 12 months of infection (Figure 3):

Fig 4 Monthly risk of significant reported outcomes in unvaccinated infected patients. Hazard ratios (with 95% confidence intervals) for reported health outcomes that were significantly different for unvaccinated people infected with SARS-CoV-2 compared with matched uninfected people. Monthly risk of reported outcomes was evaluated longitudinally during early and late periods; from Long covid outcomes at one year after mild SARS-CoV-2 infection: nationwide cohort study

​The authors stressed that persistent breathing difficulties are common after any respiratory illness, and are no more likely to occur after COVID than after non-COVID disease:
​
"Dyspnoea emerged as the most frequently reported respiratory symptom in patients with mild covid-19, lasting a year from diagnosis and resulting in increased numbers of prescriptions for related drugs. Nevertheless, the risk of receiving a prescription for a pulmonary diagnosis was independent of SARS-CoV-2 infection, indicating that the pulmonary outcomes following mild covid-19 are not severe and do not need increased drug treatment."
Long covid outcomes at one year after mild SARS-CoV-2 infection: nationwide cohort study
The study also compared health outcomes in people who tested positive to SARS-CoV-2 after getting an mRNA transfection agent ("COVID vaccine") vs those who were not injected. Only people who tested positive at least 14 days after their second injection were counted as "vaccinated". Research indicates that people have a higher risk of becoming infected in the two weeks after their first shot, yet anyone whose positive test result occurred in this time period was lumped into the 'unvaccinated' category. Notwithstanding this diagnostic sleight-of-hand, only breathing difficulties and hair loss were reported significantly more commonly in unvaccinated COVID patients, while impaired concentration and memory occurred significantly more commonly in the vaccinated.

Implications of this study:The risk of 'long COVID' was one of the sticks used to beat people who resisted getting an experimental injection into submission. People who knew they were at negligible risk of suffering a severe case of COVID-19 were told that they should still get vaccinated to reduce the chances of developing long COVID. But people who have a mild case of COVID have about the same risk of suffering prolonged postviral symptoms as they would after any other viral respiratory disease, and vaccination makes little to no difference in that risk.


Next, let's look at whether COVID 'vaccines' prevent long COVID:
Study #6: The effectiveness of coronavirus disease 2019 (COVID-19) vaccine in the prevention of post–COVID-19 conditions: A systematic literature review and meta-analysisTopline summary: COVID 'vaccines' reduce the absolute risk of developing long COVID by a clinically insignificant 1.5 per cent.

The long version:This 'study of studies' analysed data from ten studies on the efficacy of COVID vaccines in reducing long COVID symptoms. The definitions of 'long COVID' used in each of these studies were all over the map, ranging from symptoms lasting more than three weeks to symptoms continuing for over six months post-infection. One study did not report the duration of symptoms defined as 'long COVID' at all.

Four of the studies evaluated vaccine effectiveness in preventing 'long COVID' among those who received the COVID-19 vaccine only after having COVID-19, three studies evaluated vaccine effectiveness for post–COVID-19 conditions among those who were vaccinated before having COVID-19, two looked at vaccine effectiveness among those who were vaccinated both before and after COVID-19, and one did not specify the timing of the vaccine in relation to having COVID-19.
Five studies found no benefit of COVID-19 vaccination in reducing post–COVID-19 condition symptoms while four showed a protective effect, and one did not report any statistical analysis of effectiveness.
The meta-analysis of the six studies which evaluated post–COVID-19 conditions among those who received at least one dose of a COVID-19 vaccine before or after having COVID-19 found that
"The pooled prevalence of post–COVID-19 conditions was 39.1% among those who were unvaccinated and 37.6% among those who received at least 1 dose."

The effectiveness of coronavirus disease 2019 (COVID-19) vaccine in the prevention of post–COVID-19 conditions: A systematic literature review and meta-analysis
That's a 1.5 per cent reduction in absolute risk, for the mathematically challenged. Wow, that's impressive.
All the studies included in the review and meta-analysis were observational rather than randomised, which the authors admit introduces multiple biases (including the 'healthy user bias', which Mathew Crawford has written about extensively, and which probably accounts for the entirety of observed vaccine efficacy).
Furthermore, the authors were not able to perform any analyses about possible adverse events after vaccination as only one of the included studies reported possible vaccine adverse events.
​
Implications of this study:People who were sold on the idea of taking a COVID jab to prevent long COVID have been sold a bill of goods. With a 1 in 800 risk of suffering a serious adverse reaction to a COVID 'vaccine', any benefit of these injections in preventing long COVID (which is most likely an artefact of the healthy user bias in any case) pales into insignificance.
And finally, what protects people against developing long COVID?
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Study #7: Adherence to Healthy Lifestyle Prior to Infection and Risk of Post–COVID-19 ConditionTopline summary: People who follow healthy lifestyle practices have a reduced risk of long COVID, and the more healthy lifestyle practices, the lower the risk.
The long version:This study enrolled participants in the long-running Nurses’ Health Study II cohort. Participants were assessed for their adherence to six healthy lifestyle habits:

• Healthy body mass index (BMI of 18.5-24.9);
• Never smoking;
• At least 150 minutes per week of moderate to vigorous physical activity;
• Moderate alcohol intake (5 to 15 g/d);
• High diet quality (upper 40 per cent of Alternate Healthy Eating Index–2010 score); and
• Adequate sleep (7 to 9 h/d).

Among those who had tested positive to SARS-CoV-2 with either an antibody, antigen, or PCR test, there was a stepwise decrease in the risk of post-COVID conditions, defined as symptoms lasting for longer than four weeks after a bout of COVID, with increasing number of healthy lifestyle factors:

The authors calculated the relative risk of developing long COVID in participants with the most vs the fewest healthy lifestyle factors, and also the population attributable risk percentage (PAR). PAR is an estimate of the proportion of long COVID in this cohort that hypothetically would not have occurred if there was truly a causal relationship between healthy lifestyle factors and long COVID, and all participants were in the low-risk group:
"Compared with women who did not adhere to any healthy lifestyle factors, those having 5 or 6 factors had a 49% lower risk of PCC [post-COVID conditions]... Assuming a causal relationship, the PAR for healthy lifestyle was 36.0% (95% CI, 14.1%-52.7%)."

Adherence to Healthy Lifestyle Prior to Infection and Risk of Post–COVID-19 Condition
In plain English, 36 per cent of long COVID symptoms would not have occurred if all participants had adhered to five or six healthy lifestyle factors.
Being overweight and getting inadequate sleep turned out to be the strongest risk factors; the PAR overweight/obesity was 10.3 per cent (i.e. roughly one in ten participants who had postviral symptoms would not have had them if they were a healthy weight) while the PAR for inadequate sleep was 6.6 per cent.
The authors propose three biological mechanisms linking unhealthy lifestyle factors with an increased risk of long COVID:

1. Chronic inflammation: Each of the six unhealthy lifestyle factors that they examined has previously been shown to be associated with chronic inflammation, while sustained systemic inflammation has been implicated in the development of post-COVID conditions.
2. Dysregulation of adaptive autoimmunity: Unhealthy lifestyle factors derange immune function, and dysregulated adaptive autoimmunity has been found in individuals with long COVID.
3. Blood clotting abnormalities: These are seen in people with obesity, smoking, physical inactivity, and excessive alcohol intake, and pathophysiological changes in blood clotting have been observed in people with long COVID.

Implications of this study:In Part 1 of this miniseries, we saw that fat, sick people were more likely to develop long COVID. This study provides evidence of the corollary: people who take care of their health are less likely to suffer from postviral symptoms, and the more healthy lifestyle behaviours an individual practises, the lower their risk.
Summing upThe 'long COVID' bugaboo is just one thunderclap in what Professor Mark Crispin Miller has labelled an "ever-rolling thunder of Big Lies". Postviral syndromes do occur, and they definitely do cause distressing and life-limiting symptoms in a minority of people. However, 'long COVID' is no more common nor severe than postviral syndromes after other infections; it's not prevented by COVID 'vaccines'; and the strongest protective factors are the healthy lifestyle behaviours that reduce the risk of every other chronic condition.
​
If governments had invested our taxpayers' dollars into making sure that everyone had access to healthy, fresh food instead of issuing stay-at-home orders that drove up reliance on home-delivered food; encouraged exercise rather than closing gyms, parks, beaches and playgrounds; and issued calm, accurate messages about risk rather than ginning up fear and anxiety which drove many people to booze, smoke and binge on junk food and Netflix, we would not only have avoided a large percentage of long COVID cases; we would have had a healthier population overall.
But then, those would be the actions of a government that actually served the interests of its people rather than its corporate masters, wouldn't it?

What is 'long COVID', who's really at risk of developing it, and why?

​Back in November 2021, I wrote an article called The “long COVID” PSYOP, about the weaponisation of the syndrome of persistent postviral symptoms after SARS-CoV-2 infection, aka 'postacute sequelae of SARS-CoV-2' (PASC), aka 'long-haul COVID', aka 'long COVID'. In that article, I stressed that postviral syndromes do genuinely occur after a wide variety of viral infections, but that the threat of 'long COVID' had been blown out of all proportion to its actual prevalence and severity. I also contended that one of the principle motivations for doing so was to terrorise people into accepting an experimental vaccine which they were (falsely) promised would protect them against this bogeyman.


​Since then, numerous articles have been published on long COVID which only confirm my thesis from 16 months ago.
Over the next few posts, I'm going to walk you through some of these studies. Let's get started with a study that set out to discover whether teenagers are at risk of detrimental psychological and cognitive outcomes of COVID-19:

Study #1: Comparison of mental health outcomes in seropositive and seronegative adolescents during the COVID19 pandemicTop-line summary: There was no difference in the prevalence of neurocognitive, general pain and mood symptoms in adolescents who had been infected with SARS-CoV-2 vs those who had not.
The long version:In this study, 1560 German high school students underwent regular blood tests for antibodies to SARS-CoV-2, indicating that they had been exposed to the virus (with or without developing symptoms of infection). The adolescents also responded to a 12 question long COVID survey which asked them if they had experienced any of the following symptoms in the previous seven days: difficulty concentrating, memory loss, listlessness, headache, abdominal pain, muscle or joint pain, reduced physical capacity, insomnia, or changes in mood (happy/sad/angry/tense).
Rather worryingly, each of these symptoms was reported by at least one-third of the students in the previous seven days... but there was no statistically significant difference between reporting rates in kids who had been exposed to SARS-CoV-2 vs those who hadn't, with one strange and inexplicable exception: those who had been infected were significantly less likely to report having experienced sad mood (indicated by the asterisk in the figure below). Go figure.

Female students reported a consistently higher prevalence of neurocognitive, pain and mood symptoms compared to male students, in keeping with a large body of research showing that a mental health 'gender gap' opens up in adolescence and persists through adulthood, with females having significantly higher prevalence of common mental health disorders than males (particularly in countries with the greatest commitment to gender equality, paradoxically enough).
​
There was no difference in the prevalence of long COVID symptoms in adolescents who already knew they had had a SARS-CoV-2 infection vs those who were found to have antibodies to the virus but didn't report being diagnosed with infection.
The authors pointed out that previous studies that had found a high prevalence of symptoms attributed to long COVID in children and adolescents, had no uninfected control group. Furthermore, they suggested that their results indicated that many, if not most, of these symptoms were likely caused or exacerbated by the impact of public health policies such as school closures and (anti)social distancing on the well-being of young people.
Implications of this study:The threat of a tsunami of long COVID in children and adolescents has not materialised. Ill-considered, poorly-targeted, non-evidence-based pandemic policies have had a far more negative impact on young people's well-being than COVID-19 itself.

Study #2: Associations of Depression, Anxiety, Worry, Perceived Stress, and Loneliness Prior to Infection With Risk of Post–COVID-19 ConditionsTop-line summary: People who were already experiencing psychological distress before experiencing a SARS-CoV-2 infection are more likely to report symptoms of 'long COVID'.

The long version:This study recruited nearly 55 000 participants, who were already enrolled in one of three large, long-running and predominantly female cohort studies: the Nurses’ Health Study II, Nurses’ Health Study 3, and the Growing Up Today Study. The average age of participants was 57.5 years, and nearly two in five (38 per cent) were employed in health care.
Participants were eligible to participate if they had no evidence of SARS-CoV-2 infection in April 2020. They answered a questionnaire to assess their levels of depression, anxiety, worry about COVID-19, perceived stress, and loneliness at baseline, and were then followed up with periodic surveys on their psychological function, COVID-19-related symptoms, degree of life impairment and any positive SARS-CoV-2 test results, until November 2021.
Fascinatingly, during 19 months of follow-up, while a supposedly highly-contagious respiratory virus was supposedly wreaking havoc on the world, only six per cent of participants reported a positive result on a SARS-CoV-2 antibody, antigen, or polymerase chain reaction test. Remember, 38 per cent of participants were actively employed as health care workers during the study, and presumably many of them were directly involved with the care of patients diagnosed with COVID-19, and most or all would have undergone regular testing. Yet 94 per cent of participants didn't get infected.
Of participants who did report a positive SARS-CoV-2 test result during the follow-up period, 44 per cent reported post–COVID-19 conditions. Of these, 87 per cent said their symptoms lasted two months or longer, and 56 per cent reported at least occasional daily life impairment related to post–COVID-19 conditions.


Get the appThe most common symptoms were fatigue (56 per cent), smell or taste problems (44.6 per cent), shortness of breath (25.5 per cent), confusion/disorientation/brain fog (24.5 per cent), and memory issues (21.8 per cent).
After adjustment for demographic factors, all the types of psychological distress assessed at baseline were significantly associated with an increased risk of post–COVID-19 conditions:

• Participants who had probable depression at baseline had a 39 per cent higher risk of long COVID symptoms;
• For probable anxiety, the risk was 47 per cent higher;
• Those who were very worried about COVID-19 had a 43 per cent higher risk;
• Those who perceived their stress level to be the highest had a 50 per cent higher risk than those with the lowest perceived stress;
• Those who reported feeling lonely some of the time or often were at 35 per cent higher risk;
• Participants with two or more types of distress had a 54 per cent higher risk of reporting long COVID symptoms than those with none.

And here's something really interesting: psychological distress was a stronger predictor of long COVID symptoms than established risk factors for developing severe COVID-19 (which is a known predictor of long COVID risk) including age, obesity and diabetes. In fact, older participants were at lower risk of developing long COVID than younger participants.
Check out this forest plot, which depicts the magnitude of various risk factors for predicting long COVID (the further the coloured symbol is to the right of the vertical line, the higher the risk; symbols to the left of the line indicate reduced risk):

Another interesting finding was that the only long COVID symptoms that tended to be more common in participants who were not psychologically distressed at baseline were the symptoms most characteristic of COVID-19 itself: persistent cough, and problems with taste and smell:


​

It was the more nonspecific symptoms - such as fatigue, brain fog, mood changes - that were more likely to be reported in participants with pre-infection psychological distress.

So does that mean that the persistent symptoms reported by psychologically distressed people are 'all in their heads'? No, say the researchers. Here's their proposed mechanism that links a perturbed mind to long COVID symptoms:

"Inflammation and immune dysregulation may link psychological distress with post–COVID-19 conditions. Distress is associated with chronic systemic inflammation, resulting in sustained production of proinflammatory cytokines and reactive oxygen species.19-23 Inflammatory cytokines have been proposed as possible causes of respiratory, neurological, cardiovascular, muscular, and gastrointestinal long-term COVID-19 symptoms.51-53 In addition, stress activates the hypothalamic-pituitary-adrenal axis, which can lead to chronic immune suppression. Immunosuppressive conditions have been found to be associated with risk of persistent symptoms after COVID-19,12 but findings were not conclusive.13,54,55 Furthermore, autoantibodies have been associated with both mental health conditions and post–COVID-19 conditions.14,56 In the central nervous system, mental health disorders are associated with chronic low-grade inflammation and microglia activation, which may cause cognitive impairment and long-term fatigue.57 Hypometabolism in the frontal lobe and cerebellum, a pathopsychological change associated with major depression, has also been implicated in post–COVID-19 fatigue.58-60"

Associations of Depression, Anxiety, Worry, Perceived Stress, and Loneliness Prior to Infection With Risk of Post–COVID-19 Conditions
In other words, there are measurable disturbances in the physiology of people who are suffering from psychological distress, and these disturbances have profound and multifactorial effects on the ability of these people to fight off infection and recover from its effects.
(I’ve discussed the link between inflammation and impaired psychological and physical functioning in several previous articles, including Inflammation: why you’re fat, sick, tired, depressed and in pain… and what to do about it, Rumination inflammation and Hearts, minds and bodies on fire: Loneliness, social isolation, inflammation and COVID-19.)
Implications of this study:People presenting with long COVID should be assessed for psychological distress, and the treatment plan must include comprehensive and effective strategies for addressing it.
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Study #3: Long-lasting Symptoms After an Acute COVID-19 Infection and Factors Associated With Their ResolutionTop-line summary: The factors most strongly associated with having long COVID are those most strongly associated with having any chronic disease: obesity, older age, and being anxious or depressed.
The long version:This study involved over 53 000 participants in three French population-based cohorts, who were surveyed about persistent COVID-19 symptoms, defined as "symptoms occurring during the acute infection and lasting 2 or more months".
Of those who were infected by SARS-CoV-2 during the first wave of COVID-19 in France (confirmed by antibody testing), fully one third reported no symptoms of COVID-19 whatsoever. Of those who did report acute symptoms, 90 per cent were fully recovered within 12 months, and 92 per cent after 18 months.
The persistent symptoms that were least likely to resolve were memory loss, sleep disorders, joint pain, heart palpitations, loss of taste or smell and attention or concentration disorders:

In other words, being already in a state of poor physical and/or mental health made participants less likely to recover from a viral respiratory illness. What a surprise.
Implications of this study:Fat, sick people are more likely to become seriously ill when they contract a respiratory illness (as I explained in my previous article When Two Pandemics Collide: How obesity affects COVID-19) and more likely to have a delayed or incomplete recovery. That's because they're fat and sick. If our 'health authorities' were genuinely interested in reducing the burden of 'long COVID' they would be pivoting our disease care system to a true health care system focused on preventing chronic illness and treating it with evidence-based lifestyle medicine programs, rather than squandering taxpayers' dollars on an ever-growing arsenal of pharmaceuticals.
Stay tuned for Part 2 of this series!

https://robynchuter.substack.com/p/long-covid-truth-lies-and-propaganda
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Go back and read that quote one more time, out loud, so you can really take in its significance. The whooping cough vaccine that all Australian children are exhorted to receive five doses of within their first five years of life, with compliance enforced through substantial financial penalties and (for many) the threat of exclusion from the benefits of preschool education,

• Does not prevent colonisation of the child's airways with Bordetella pertussis;
• Does not prevent a vaccinated child from passing B. pertussis to any other individual; and
• Does not have any community benefit in the form of herd immunity.

The only benefit that it offers is reduced risk of developing the clinical manifestation of B. pertussis colonisation, which is pertussis, or whooping cough. This is a selfish benefit in the sense that it only offers advantages to the vaccine recipient, rather than to the community.
​
In fact, if - as vaccine advocates claim - acellular pertussis vaccines prevent recipients from developing clinical manifestations of infection (at least for a limited time), then vaccinated children pose a greater hazard to the community because they could become 'silent spreaders', whereas unvaccinated children's symptoms alert their parents to seek medical attention (including diagnostic tests), and to keep their sick kids isolated at home until they're no longer infectious.

Nonetheless, parents who opt for other methods of protecting their children against serious pertussis illness besides vaccination are punished for their choices, even though those choices have no consequences for the health of others given that both unvaccinated and vaccinated children can contract and spread B. pertussis.
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Why doesn't the acellular pertussis vaccine prevent infection with, or spread of, B. pertussis? It's our old friend, mucosal immunity:
"Studies that have compared immune responses after natural B. pertussis infection and the administration of both wPVs [whole-cell pertussis vaccines, which have been replaced by acellular pertussis vaccines in the developed world but are still used in developing countries - more on that later] and aPVs have clearly shown that the immune stimulation evoked by aPVs is different from that due to natural infection and wPVs (49–51). Natural infection evokes both mucosal and systemic immune responses, while aPVs induce only a systemic immune response. As B. pertussis is a mucosal pathogen and only exceptionally causes infection outside the respiratory tract, this difference is of particular importance in pertussis control. Mucosal immunity is essential to prevent colonization and transmission of B. pertussis organisms. Consequently, preventive measures such as aPVs that do not induce a valid mucosal response can prevent disease but cannot avoid infection and transmission. Animal studies have shown that natural infection is associated with a strong secretory IgA response in both the upper and lower airways and induction of resident memory T cells (TRM) (52, 53)... Natural infection was associated with the most persistent protection against nasal colonization and this correlated with potent induction of nasal tissue TRM cells. These animal data suggest that the lack of mucosal immune response after aPV administration might explain its lower efficacy when compared to wPVs and the shorter duration of protection compared to both wPV vaccination and natural infection." [emphasis added]

Pertussis Prevention: Reasons for Resurgence, and Differences in the Current Acellular Pertussis Vaccines
Hmmm, are you feeling that déjà vu-ey kind of feeling?
Natural immunity vs vaccine-induced immunityInfection with B. pertussis generates protection against another episode of whooping cough which can last for more than 30 years in some people, although 10 per cent of individuals lose protection within 10 years after infection. Importantly, natural immunity acquired from infection also prevents colonisation with, and transmission of, the bacteria to other people.
Whole-cell pertussis vaccines provide similar or slightly reduced duration of protection against clinical disease, and also against colonisation and transmission.
But acellular pertussis vaccines - again, this is the only type of pertussis vaccine used in Australia - protect against pertussis disease for a relatively brief period and as noted previously, do not prevent colonisation or transmission. Furthermore, the lousy performance of acellular pertussis vaccines isn't improved by tweaking the composition of the vaccine, altering the timing between shots, or adding booster doses:

"The duration of immunity after immunization with aPVs appears to be shorter [than either natural immunity or whole-cell pertussis vaccine-induced immunity], independent of the schedule used, the numbers, and concentrations of antigens included in each vaccine and the methods used to prepare the vaccines. Reports also suggested that pertussis occurred significantly earlier in subjects fully vaccinated with aPV than in those given wPV (41–43). Clark et al. (41) in 2012 reported that children who were fully immunized during infancy with an aPV had pertussis more often in the first years of school, while those given a wPV were at higher risk later, mainly during adolescence. Similar differences were demonstrated by Vickers et al. (43), who found that children who had received an aPV during infancy were already at risk of pertussis within the first 4 years of life, whereas those vaccinated with wPV did not contract pertussis until 5–9 years. Finally, Klein et al. (44) demonstrated that most of the pertussis cases diagnosed in adolescents during an outbreak were seen in individuals fully immunized during infancy with an aPV, rather than in those who had received wPV. Individuals receiving only aPV had five times higher odds of pertussis disease than those receiving wPV (OR 5.63, 95% CI 2.55–12.46). When aPV effectiveness (VE) was measured over time, its effectiveness was lower than that expected after wPV or natural infection (44). Early waning of immunity was reported regardless of the schedule used for immunization (44).

The addition of booster doses of aPV to prolong protection was also assessed. Although there was transient protection afforded by additional booster doses, the protection waned rapidly. A meta-analysis of 11 studies (45) that measured long-term immunity to pertussis after three or five doses of diphtheria-tetanus-aP (DTaP), according to the schedules used in many European countries and in the USA, respectively, did not reveal a significant difference between the annual odds of pertussis for the three or five dose regimens."

Pertussis Prevention: Reasons for Resurgence, and Differences in the Current Acellular Pertussis Vaccines
In fact, booster doses may backfire by inducing an increase in the production of IgG4 antibodies, which induce tolerance to B. pertussis rather than an appropriate immune system response, especially in children who received a primary course of acellular rather than whole-cell pertussis vaccine in infancy:

"The administration of aPV booster doses at 4 and 9 years of age was associated with an increase in the production of IgG4, regardless of the type of vaccine used for priming, but was significantly higher in aPV-primed children (66). IgG4 antibodies are unable to activate the complement system and lead to a suboptimal inflammatory response with impaired phagocytosis and antimicrobial defense, another potential mechanism for the lower efficacy of aPVs compared to wPVs (67). Moreover, the evidence that production of IgG4 after immunization with aPV increases with each dose seems to indicate that the protection offered by aPVs tends to be as shorter with each subsequent boosters (68, 69)."
Pertussis Prevention: Reasons for Resurgence, and Differences in the Current Acellular Pertussis Vaccines
Hang on a minute, what's that funny feeling I'm getting?

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In a nutshell, not only do acellular pertussis vaccines offer limited personal benefit - protection against whooping cough - and zero community benefit - protection against infection and transmission - but they may even be a net harm in both cases, in that they permanently alter the immune response to Bordetella pertussis through the IgG4 class switching mechanism, and turn vaccinated people into potential silent spreaders, increasing the circulation of the bacteria in the general population:
"Lack of mucosal immune responses after aPV administration favor infection, persistent colonization, and transmission of the pathogen."
Pertussis Prevention: Reasons for Resurgence, and Differences in the Current Acellular Pertussis Vaccines
Why don't we go back to using the whole-cell pertussis vaccine?Good question. If it's nearly as good as natural immunity at preventing reinfection, albeit with a reduced duration of protection, and that benefit comes with a reduced risk of suffering pertussis disease, isn't that the best of both worlds?
If only life were that simple.
The reason that rich countries like Australia replaced whole-cell pertussis vaccines with acellular vaccines is that although pertussis case rates dropped after the whole-cell pertussis vaccines were added to the paediatric schedule, these vaccines were associated with a high rate of serious side effects, including:

• Protracted crying and screaming (often described by parents as "inconsolable");
• Shock or shock-like state, collapse, and hypotonic, hyporesponsive episodes (HHE); and
• High fever and febrile convulsions.

Many parents reported onset of seizure disorders, developmental delays and death of their infants in close temporal proximity to them receiving the whole-cell pertussis vaccine. Vaccine manufacturers faced such an onslaught of lawsuits that many stopped producing the vaccine.
Widespread parent refusal of the whole-cell pertussis vaccine, while frustrating to public health authorities with their single-minded focus on disease elimination, was perfectly understandable: the death rate from pertussis had already declined by 90 per cent in wealthy, industrialised countries before mass vaccination campaigns began in the 1940s, due to increasing natural resistance, better living standards and the advent of antibiotic treatment of pertussis-associated pneumonia and bronchitis, and effective treatments for maintaining fluid balance in very young infants.
With whooping cough's incidence having long since decoupled from its mortality, as awareness of the dangers of the whole-cell pertussis vaccine mushroomed, many parents were no longer willing to subject their healthy children to a vaccine which had even a remote chance of severely injuring or killing them, in order to prevent a disease which, although distressing (especially in very young infants), was now highly treatable and rarely deadly.
But public health policymakers, concerned that whooping cough incidence would rebound if vaccine refusal continued to grow, pushed for the development of "a less reactive vaccine... based on isolated B. pertussis components that induced protective immune responses with fewer local and systemic reactions." These so-called acellular vaccines demonstrated "comparable short-term protection to the most effective wPVs with fewer local and systemic reactions" in clinical trials, and began supplanting whole-cell pertussis vaccines in most industrialised countries from the late 1980s (although Japan had already replaced the whole-cell pertussis vaccine with its home-grown acellular pertussis vaccine in 1981).
For a few years, it looked like the ideal solution to the pertussis problem had been found: a new class of vaccines that seemed to work as well as the old ones at taming whooping cough, but without the public-confidence-destroying side-effects. However, the triumph was short-lived:
"After over a decade of use, a rise in pertussis incidence was demonstrated in several industrialized countries, including Australia and the United States (18–22)."
Pertussis Prevention: Reasons for Resurgence, and Differences in the Current Acellular Pertussis Vaccines
And that's how we got to where we are today: pertussis remains the second most frequently notified vaccine preventable disease in Australia despite 95 per cent compliance with the childhood vaccination schedule, and frank admission by 'the experts' (in the privacy of their academic journals) that even if we repeatedly vaccinated every man, woman and child in this country, we cannot, and will not, eradicate whooping cough with the vaccines we're using.
Meanwhile, in developing countries, whole-cell pertussis vaccines continue to be used because they are considerably cheaper than the acellular versions. According to extensive research led by Drs Peter Aaby and Christine Stabell-Benn, their use (in the form of the diphtheria-pertussis-tetanus, or DPT vaccine) is associated with more than double the risk of death in children in the small and desperately poor African country of Guinea-Bissau, with girls being particularly at risk. Their conclusion is chilling:
"Although having better nutritional status and being protected against three infections, 6–35 months old DTP-vaccinated children tended to have higher mortality than DTP-unvaccinated children. All studies of the introduction of DTP have found increased overall mortality." [emphasis mine]
Evidence of Increase in Mortality After the Introduction of Diphtheria–Tetanus–Pertussis Vaccine to Children Aged 6–35 Months in Guinea-Bissau: A Time for Reflection?
So no, returning to the use of whole-cell pertussis vaccines is definitely not the answer.


The vaccine true believers hold fast to the notion that all we have to do to solve these problems is to develop better acellular pertussis vaccines. (Of course they do. Check out the Conflict of Interest notice on the WAidid/EVASG report:)
​

Pertussis Prevention: Reasons for Resurgence, and Differences in the Current Acellular Pertussis VaccinesBut, to quote that great Australian sage, Darryl Kerrigan, they're dreaming.
The dance between humans and pathogens has been going on since our species emerged, with the resultant "biological arms race" shaping the evolution of both we humans, and the microbes that seek to colonise us.
It is the height of hubris to believe that whooping cough, or any other infectious disease, can be conquered with more and better vaccines. As the pertussis vaccine saga has amply demonstrated, every move the vaccine developers make is met with a counter-move; it's fair to say that our ancient, wily adversary, Bordetella pertussis, now has them in checkmate.
But we don't have to play this no-win game. The dramatic decline in infectious disease mortality that preceded the introduction of vaccines not just for whooping cough, but for all other infectious diseases, occurred because of dramatic changes in human living conditions that improved overall health.
Instead of myopically focusing on 'fighting disease'; we need to build health, through human-appropriate nutrition; adequate physical activity, rest and sleep; meaningful and nurturing relationships; time spent outdoors, in nature; and a sense of purpose in life. None of these building-blocks of health turn a profit for Big Pharma or provide a paycheck for a so-called healthcare worker, but they're the most important investments you can make in yourself and your family.

https://robynchuter.substack.com/p/deja-vu-all-over-again-the-whooping
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Do vaccines increase or decrease the number of children who die in the first year of life? Two researchers set out to answer this question. You'll never guess what happened next.

Back in April 2022, I wrote two articles about the impact that the COVID-19 ‘vaccine’ debacle has had on the confidence of the general public and the medical profession in vaccines in general. In the first of those articles, Why you need to stop saying “I’m not an antivaxxer, but…”, I mentioned the 8.93 per cent decline in Florida’s infant mortality rate that coincided with a marked drop in the percentage of children who were fully compliant with the CDC-recommended childhood vaccination schedule. Specifically, there was a 14.1 percentage point drop in children aged 24 to 35 months in the state who were ‘up to date’ with their shots, from 93.4 per cent in 2020 to 79.3 per cent in 2021, and a 5.8 percentage point drop in 1-2 year olds, from 73 per cent in 2020 to 67.2 per cent in 2021.

Huh. But aren’t vaccines supposed to reduce the number of infant deaths by protecting tiny babies with immature immune systems against dangerous infectious diseases? Well, that’s the theory. As I mentioned in that previous article, according to John and Sonia McKinlay’s exhaustive analysis of US data, medical interventions for infectious diseases (including vaccines, antibiotics and diphtheria toxoid) accounted for a measly 3.5 per cent of the steep reduction in total mortality that occurred between 1900 and 1973 in that country; most of that reduction was due to the dramatic decline in deaths from infectious disease. The vast bulk of the decline in infectious disease mortality was directly attributable to ‘old fashioned’ public health interventions including provision of clean water and uncontaminated food, sanitation, and improved housing standards.
And that brings me to three studies which grapple with the important question, ‘Do childhood vaccines help or hinder the attempt to reduce infant mortality?’ Reading and dissecting these studies is an object lesson in how science should and should not be conducted, and the types of statistical sleights-of-hand that researchers can use to torture the data until it confesses, even to crimes that were never committed.

These studies essentially constitute a debate between two teams of researchers, one calling vaccine orthodoxy into question, and the other staunchly defending it. Let’s step through these, in the order in which they were written:
Study #1: ‘Infant mortality rates regressed against number of vaccine doses routinely given: Is there a biochemical or synergistic toxicity?’This study, published in the journal Human & Experimental Toxicology in 2011, was coauthored by Neil Miller and Gary Goldman. You might remember Goldman from my previous article, Backlash: How the vaccine pushers turned true believers into vaccine sceptics – Part 2. In 2002, he quit his job as a research analyst when his employer, the Los Angeles County Department of Health Services, refused to publish his discovery that their paediatric chickenpox vaccination campaign was associated with a dramatic increase in the incidence of shingles in both children and adults. This agency then collaborated with the CDC in a lengthy harassment campaign to try to prevent Goldman from publishing his findings independently.
Rather than being intimidated into silence, Goldman’s bruising experiences prompted him to become curious about the safety and efficacy of vaccines in general.

In collaboration with Miller, Goldman conducted a linear regression analysis on the relationship between infant mortality rates in 34 highly developed countries, and the number of vaccine doses on the immunisation schedules in those countries.

• Infant mortality rate (IMR) is the number of deaths of children under 1 year of age, per 1000 live births.
• Linear regression is a statistical technique used for modelling the relationship between two factors, known as variables. In simple terms, it’s the first step that needs to be taken in the process of ascertaining whether a correlation between two variables is due to causation rather than coincidence.
• ​
  

The 34 countries selected for this analysis were the US – which, at 26 vaccine doses for infants aged less than 1 year (as of 2011), has both the most intense vaccination schedule and the highest per capita spend on health care in the world – and the 33 countries that have a lower IMR than the jabbed-to-the-eyeballs leader of the free world.


Importantly, most of the nations included in this study had coverage rates in the 90–99 per cent range for the most commonly recommended vaccines – DTaP, polio, hepatitis B, and Hib (when these vaccines were included in the schedule), minimising the impact of any potential confounding effect of variability in coverage rates. Remember this – its importance will become evident when we discuss Study #2.
Here are the 34 countries with the lowest infant mortality rates in the world, as of 2009:

​

(Does it strike you as odd that Cuba has a lower IMR than the wealthy country that has maintained an embargo on it since 1962, crippling its economic development and hindering its access to medical supplies?)
And here are the number of vaccine doses on each nation’s vaccination schedule, as of 2008-2009:

From Infant mortality rates regressed against number of vaccine doses routinely given: Is there a biochemical or synergistic toxicity?After performing an initial exploratory analysis which indicated that there was indeed a relationship between the number of vaccine doses and IMR, Goldman and Miller then compared average IMRs between groups of nations whose vaccination schedules specified 12-14, 15-17, 18-20, 21-23 and 24-26 doses of vaccines before the age of 12 months. They produced the following chart, which indicates a statistically significant difference in IMRs between countries that give 12–14 vaccine doses and (a) those giving 21–23 doses (61 per cent higher infant mortality rate) and (b) those giving 24–26 doses (83 per cent higher IMR):


​

(For those unfamiliar with statistics, ‘r‘, or Pearson’s coefficient, represents the strength of association between two variables – in this case, number of vaccine doses and infant mortality rate. The value of r is always between +1 and –1. The closer to +1 r is, the stronger the positive association between the variables. The p value, or probability value, is a statistical measurement used to validate a hypothesis against observed data. The lower the p value (i.e. the smaller the number), the greater the statistical significance of the observed difference; or, in layman’s terms, the less likely it is that the result is due to simple random chance rather than a true association.)

In the discussion section of their paper, Goldman and Miller point out that many developing nations have extremely high vaccine coverage rates yet their IMRs continue to be appalling, and emphasise that no amount of vaccines will compensate for the absence of foundational public health measures:
“For example, Gambia requires its infants to receive 22 vaccine doses during infancy and has a 91%–97% national vaccine coverage rate, yet its IMR [infant mortality rate] is 68.8. Mongolia requires 22 vaccine doses during infancy, has a 95%–98% coverage rate, and an IMR of 39.9.8,9 These examples appear to confirm that IMRs will remain high in nations that cannot provide clean water, proper nutrition, improved sanitation, and better access to health care. As developing nations improve in all of these areas a critical threshold will eventually be reached where further reductions of the infant mortality rate will be difficult to achieve because most of the susceptible infants that could have been saved from these causes would have been saved. Further reductions of the IMR must then be achieved in areas outside of these domains. As developing nations ascend to higher socio-economic living standards, a closer inspection of all factors contributing to infant deaths must be made.”

Infant mortality rates regressed against number of vaccine doses routinely given: Is there a biochemical or synergistic toxicity?
They go on to discuss the introduction of ‘sudden infant death syndrome’ to medical nomenclature in 1969, after national immunisation campaigns were initiated in the US in the 1960s, and its rapid rise to become the leading cause of postneonatal mortality by 1980. They speculate that overvaccination may impose a toxic burden on infants’ health, and call for rich nations with high vaccine doses and relatively high IMRs to “take a closer look at their infant death tables to determine if some fatalities are possibly related to vaccines though reclassified as other causes”.
The response to this study by academics and policy-makers was deafening silence, until late in September 2021, when a professor from Brigham Young University, Elizabeth Bailey, and several of her students, produced an as-yet-unpublished paper which accused Goldman and Miller of “inappropriate data exclusion and other statistical flaws”. Which brings us to…
Study #2: ‘Infant Vaccination Does Not Predict Increased Infant Mortality Rate: Correcting Past Misinformation’This paper was first uploaded to the pre-print server medRxiv in September 2021. It has since undergone three revisions without yet being accepted for publication in any peer-reviewed journal.
It is a sign of the extraordinary times that we live in, that in the very title of their paper, the authors denigrate Goldman and Miller’s peer-reviewed, published study as “misinformation”. This is not how scientists behave when they wish to challenge each others’ views.

But as we shall see, this is not primarily a scientific paper, but a propaganda piece that explicitly aims to reduce the general ‘vaccine hesitancy’ that “has intensified due to the rapid development and distribution of the COVID-19 vaccine” – by which I presume they mean that the public has finally twigged to the fact that the inadequately-tested, rushed-to-market COVID-19 ‘vaccines’ are neither safe nor effective, and are wondering whether their asleep-at-the-wheel regulatory agencies have been similarly lax with all the other vaccines that are pumped into them, and their children. (Hint: they have been.)
The authors begin their paper with the stock trope that vaccines are “viewed as one of the greatest public health successes of all time”. As examples of that success, they cite smallpox, poliomyelitis, measles, rubella, tetanus, diphtheria, Haemophilus influenzae type b and unspecified “others”. Yet the McKinlay paper cited above concluded that medical measures made little to no impact on deaths from measles, diphtheria, smallpox and poliomyelitis in the twentieth century; the CDC acknowledges that tetanus mortality had already markedly decreased before routine vaccination began; rubella mortality was already negligible before a vaccine was developed (although this usually benign disease can wreak havoc on the developing foetus when contracted during pregnancy); and implementation of Haemophilus influenzae type b (Hib) vaccination has resulted in an increase in infections caused by non-vaccine preventable strains, and antibiotic-resistant strains of the bacteria.
The authors then go on to claim that “addressing vaccine hesitancy by increasing public confidence in vaccine safety has the potential to positively impact public health and save lives”. To reiterate my earlier point, the contention that vaccines have, do, or will “save lives” is called into question by the McKinlay paper. Furthermore, the net public health impact of vaccination has never been assessed, as this would require a comparative longitudinal study of the overall health of vaccinated vs unvaccinated groups within the same population, and the CDC admits that it has not conducted such a study, nor does it hold any record of such a study.

Finally, the authors get down to the real purpose of the paper: discrediting Goldman and Miller’s study. They seem to be particularly bothered that “this manuscript is in the top 5% of all research outputs since its publication, being shared extensively on social media with tens of thousands of likes and re-shares” (perhaps especially since they can’t even manage to get their own paper published in a peer-reviewed journal after nearly a year and a half, let alone shared widely).
Their chief criticism is that Goldman and Miller cherry-picked data, selecting only 34 countries out of a dataset that included 185 countries. In addition, they accused Goldman and Miller of relying on vaccine schedules rather than data on actual vaccine doses administered.
They conclude that the chief determinant of IMR is actually the Human Development Index, and that, in complete contradiction to Goldman and Miller’s conclusions, “fewer vaccine doses in the schedule were predictive of higher infant mortality rate.”

How did Goldman and Miller respond to this critique of their paper? Let’s turn to…
Study #3: ‘Reaffirming a Positive Correlation Between Number of Vaccine Doses and Infant Mortality Rates: A Response to Critics’Published in the peer-reviewed journal Cureus on 2 February 2023, this paper examines the claims made in Study #2, and reanalyses the data from the original study published in 2011.
As always, I urge you to read the paper (and the other two referenced above) for yourself, but here’s my quick-and-dirty summary:

• Indiscriminately combining developing and developed nations with varying rates of vaccination and vast socioeconomic disparities, as the critics did for their reanalysis, introduces multiple confounding variables that were not present in the original analysis, which was confined to economically developed countries. It is not appropriate to group together for analysis countries as socioeconomically disparate as Belgium (IMR = 4.44) and Angola (IMR = 180.21), just because they both specify 22 vaccine doses in the first year of life. Likewise, it is not appropriate to group Chad, which has a coverage rate of 10 per cent for three doses of the hepatitis B vaccine, with economically developed countries that have greater than 90 per cent coverage, and not adjust for confounding.
• Despite these confounding variables, there was still a small but statistically significant correlation between total vaccine doses and IMRs in the reanalysis (r = 0.16 for the dataset of 185 countries, compared to r = 0.7 for the 30 countries with the lowest IMRs).
• The critics’ claim that the Human Development Index (HDI) – rather than number of vaccination doses – predicts IMR, is not justified, because of a number of well-known errors of misclassification in the HDI.
• There are significant flaws in the critics’ linear regression analysis of IMR as a function of percentage vaccination rates, which essentially invalidate their findings.
• The critics failed to count doses of vaccines accurately for several countries, because they relied on UNICEF data rather than cross-checking with each country’s published vaccination schedule. In the case of Indonesia, this resulted in the critics counting just seven vaccine doses, while the true number of doses administered is 18. They also reported only seven infant vaccine doses for Australia when the true value is 24.
• The critics excluded six countries from their analysis without explanation, and included five countries that should have been excluded because they have so few births, that their IMR is unstable.
• Goldman and Miller invited an independent statistician to conduct an odds ratio analysis on the original dataset, controlling for 11 different variables (including low birth weight, child poverty, and breast feeding), which confirmed their original findings of a strong correlation between vaccine doses and IMR.
• There were still statistically significant correlations between number of vaccine doses and IMR when they expanded their original analysis from the top 30 to the 46 nations with the best IMRs. After this point, there is too much heterogeneity between the socioeconomic conditions of nations for a consistent relationship between vaccine doses and IMR to be apparent.
• Replicating their original 2011 study using updated 2019 data corroborated the trend they found in the first paper, namely that the more vaccine doses, the higher the IMR.

Goldman and Miller summarised their response to the critics in the following table:

Table 1: Data characteristics and linear regression analysis outcomes of original Miller-Goldman study and the reanalysis by Nysetvold et al. aWhen the residuals are not normally distributed, the hypothesis is that they are not from a random dataset. The amount of residual error in the model is inconsistent across the full range of observed data. bThe model is sensitive to these outliers that represent poor quality data from Third World nations with the highest IMRs. This has the effect of changing the magnitude of the correlation coefficient and altering both the slope and y-intercept of the best-fit line.  cThe linear regression analysis of Nysetvold et al. is irredeemably confounded due to varying vaccination rates and socioeconomic disparities between developed and Third World nations that have the effect of attenuating the significant positive correlation between IMR and number of vaccine doses that was found among nations with top-ranked IMRs.

It gets even worse. In the supplementary material for the paper, Goldman and Miller reveal that in earlier versions of their critics’ paper, the authors made several libellous statements that were so egregious that
“an attorney contacted a faculty chairman to inform the Bailey team that their article sets a poor example to students that libel is acceptable, and suggested that they remove their malicious and false statements prior to going forward with publication. Although this language was adjusted in later versions, it served to reveal author bias and demonstrated a misunderstanding and misuse of basic scientific methodologies.”
The original version of the paper also made false claims about the funding source for Goldman and Miller’s paper, and, despite claiming that they used an “identical dataset” for IMRs as that which was used in Study #1, they in fact used a different dataset retrieved from an alternate resource containing less recent IMR data; as one example, “the IMR for Sierra Leone in the CIA dataset that we used is 81.86 but the Bailey team has it listed as 154.43 and used this figure in their analyses.”
But yeah, apart from all that, it was quality work.
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Goldman and Miller go on to discuss the biological plausibility of an association between infant vaccination and sudden infant death, citing:

• The abrupt disappearance of the category ‘sudden [infant] death’ in Japan when Japanese authorities raised the age of pertussis (whooping cough) vaccination from three months to two years;
• A 1987 study which found that infants died at a rate more than seven times greater than expected in the period zero to three days following DTP vaccination when compared to the period beginning 30 days post-vaccination;
• A 2021 analysis by Miller of Vaccine Adverse Event Reporting System (VAERS) data which found that 58 per cent of the 2605 infant deaths reported to VAERS from 1990 to 2019 occurred within three days post-vaccination, and 78 per cent occurred within seven days post-vaccination;
• Compensation has been paid to parents of children who died after receiving vaccines, with acknowledgement that vaccines drive the production of cytokines which can interfere with the brain’s ability to regulate breathing, resulting in the abrupt cessation of breathing that characterises sudden infant death syndrome.

They concluded that
“A positive correlation between the number of vaccine doses and IMRs is detectable in the most highly developed nations but attenuated in the background noise of nations with heterogeneous socioeconomic variables that contribute to high rates of infant mortality, such as malnutrition, poverty, and substandard health care.”

Reaffirming a Positive Correlation Between Number of Vaccine Doses and Infant Mortality Rates: A Response to Critics
Why does this matter?The significance of this tale of three papers goes way beyond a somewhat entertaining spat between two teams of data nerds. (“Cop this regression analysis straight in your goolies! Right back at you with a devastating odds ratio analysis to your solar plexus!”)

The salient difference between Goldman and Miller, and Elizabeth Bailey and her coauthors, is that the former are independent researchers while the latter are attached to an educational institution. As evolutionary biologists Heather Heying and Bret Weinstein frequently point out in their Dark Horse podcast, universities have been entirely captured by an entity that might be described as the medical-academic-pharmaceutical-industrial complex. Their apparatchiks, like Elizabeth Bailey, perform something that has the cosmetic appearance of science but is definitively not science, in the sense of conforming to the scientific method and the attitude of radical scepticism that underpins it.

If you recall Gary Goldman’s story, which I recounted in Backlash: How the vaccine pushers turned true believers into vaccine sceptics – Part 2, he took a job as a research analyst with the LA County Health Department having never questioned the safety or effectiveness of vaccines. However, when the data that he was analysing indicated that chickenpox vaccination was leading to significant harm in the form of increased incidence of shingles, Goldman followed those data where they led, even though this meant revising his entire belief system (not to mention losing his job and suffering significant harassment by his former employer).
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The lesson of the last three years of COVIDiocy has been that only a tiny minority of scientists display this level of integrity and commitment to uncovering the truth and disseminating it to the public. And when they do so, they are vehemently opposed by the majority, who have, through some strange quirk of human psychology, assumed the interests of the medical-academic-pharmaceutical-industrial complex as their own.
Substacker El Gato Malo (the Bad Cat) frequently writes of the politicisation of science and the need to open data to public scrutiny and crowd-source its analysis through a genuine peer review system. This is the way of the future. Open the books. Free the data. Question everything.

https://robynchuter.substack.com/

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Molnupiravir causes transmissible mutations in SARS-CoV-2

​Ok, so I told you masks don’t work to prevent respiratory virus infection and transmission, and now the latest Cochrane review has confirmed that they don’t work.

Aaaaand, I told you that neither influenza vaccines nor COVID-19 vaccines prevent infection with, or transmission of, the viruses associated with them, and now Dr Anthony ‘I Am the Science’ Fauci himself has confirmed that neither they, nor any other vaccines for respiratory diseases caused by viruses that replicate predominantly in the respiratory mucosa, prevent infection or transmission.
Let’s try for three for three.

I told you back in May 2022 that Merck’s antiviral drug molnupiravir (sold under the brand name Lagevrio) generated mutated versions of SARS-CoV-2 that were shed in recipients’ nose and throat secretions, and could potentially lead to new, transmissible variants of unknown virulence. Our fearless drug regulator, the Therapeutic Goods Administration (TGA), airily dismissed the significance of this finding on the say-so of an unnamed ‘independent expert’:

“The likelihood of mutations resulting in a more virulent strain of SARS-CoV-2 from treatment with molnupiravir over the long-term has not been assessed. It is less likely, but unproven, that virus mutation induced by molnupiravir will increase virulence of SARS-CoV-2.”
​
Australian Public Assessment Report for Molnupiravir, p. 39
As a result of the TGA’s provisional approval of molnupiravir, over 380 000 prescriptions for this twenty year old drug which has never been used before due to concerns about its mutagenicity, had been issued in Australia by December 2022. Australian health authorities are still heavily pushing its use despite evidence of higher death rates in people treated with molnupiravir compared to placebo, and despite the National Clinical Evidence Taskforce in the UK recommending against it:

In summary, mutations consistent with molnupiravir’s known mechanism of action, and of the same types that were found in the nasopharyngeal secretions of people who took the drug in a clinical trial, have shown up in global sequencing databases, since molnupiravir began to be prescribed, in the countries which are using it, in the age group for which it is approved, and in patterns which indicate that it is generating transmissible variants with high mutation rates.

When it comes to the implication of their findings, the study authors take a cautious approach. They point out that they have not proved that the use of molnupiravir is driving the mutations that they identified, nor that these mutations are intrinsically more dangerous or transmissible. They call for “public health authorities in countries showing these patterns [to] perform investigations to determine if these sequences or clusters can indeed be directly linked back to use of molnupiravir.”
However, as coauthor Theo Sanderson, a computational biologist at the Francis Crick Institute in London, stressed,
“I would say that our work closes down the possibility that these [molnupiravir-mutated] viruses can never be transmitted.”
COVID drug drives viral mutations — and now some want to halt its use

Rustem Ismagilov, a quantitative bioscientist at the California Institute of Technology in Pasadena who was not involved in the study, stressed that it “underscores the need to quickly measure any risk that molnupiravir poses in terms of sparking new variants, and to weigh them against the drug’s benefits”, adding
“If we are playing Russian roulette, we’d better know our odds.”
COVID drug drives viral mutations — and now some want to halt its use

All I can say is, good luck with that one. I’d lay odds on hell freezing over before any study on the adverse effects of molnupiravir secures funding.

Given molnupiravir’s lack of clinical benefit, the unanswered questions about its capacity to trigger cancer, and these latest findings that point to the strong possibility that it is driving variants with high mutation rates, any sane health authority would drop it like a hot brick. But the TGA continues to insist that it “meet[s] the high safety, efficacy and quality standards required for use in Australia.” One wonders how bad a drug has to be to not meet those standards. (Or perhaps the disqualifying criteria are actual safety and effectiveness, as with hydroxychloroquine and ivermectin.)


Get the appWhat can we ordinary folk do in the face of the complete regulatory capture that is driving unsafe, ineffective and inadequately tested products into the mouths and arms of Australians?

• If you have elderly relatives or friends, share this article with them so that they are forewarned and forearmed to ‘just say no’ to any doctor who recommends that they take molnupiravir.
• If you are the guardian of a person living in an aged care facility, put the facility on notice that your relative is not to be given molnupiravir.
• Print this article out and take it to your local GP or community pharmacist. Ask them if they’re prescribing or dispensing molnupiravir/Lagevrio and if so, do they know that it is ineffective and that the UK’s National Clinical Evidence Taskforce has recommended against its use?
• Phone or email your MP and request that they ask a question on notice about the TGA’s continued recommendation of this drug in the face of overwhelming evidence of its lack of safety and efficacy, and its disendorsement by the UK’s National Clinical Evidence Taskforce.
• Share this article on social media.

And thank you for slogging through the technical bits in this article, and making it all the way to the end! Together, we are learning our way forward.

Empowered! is a reader-supported publication. Paid subscriptions help me to continue this work. All readership is greatly appreciated. Please share this post widely.
​https://robynchuter.substack.com/

Vaccine-induced antibodies don't confer immunity against viruses that replicate primarily in respiratory mucosa - like influenza and SARS-CoV-2. Says who? Says Anthony Fauci.

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In last week's post, I told you that masks don't work to prevent viral respiratory illness. Not for source control, not for infection protection, not when worn in a healthcare setting by properly-trained professionals. They Just Don't Work.
Previously, I told you that influenza vaccines don't prevent infection with, or transmission of, influenza virus, here, and here. I also told you that COVID-19 'vaccines' don't prevent infection with, or transmission of, SARS-CoV-2 here, here, and here, and here, and I explained why here.
In a nutshell, all the injected flu vaccines and all the COVID-19 'vaccines' currently on the market induce production of antibodies that travel in the blood (immunoglobulin G [IgG] and circulating immunoglobulin A [IgA]), but SARS-CoV-2 replicates in the mucous membranes that line our airways (the respiratory mucosa), not in the blood. The type of antibody that is required to stop this respiratory mucosal replication is secretory IgA (sIgA). None of the COVID-19 vaccines induce production of sIgA, and neither IgG nor circulating IgA can reach the respiratory mucosa.
Here's the illustration of sIgA production and activity that I included in my previous article, Why COVID-19 “vaccines” will never end the pandemic which was published on 20 December 2021:


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https://www.youtube.com/watch?v=vT-BO3y8szQ&embeds_euri=https%3A%2F%2Frobynchuter.substack.com%2F&feature=emb_logo


(Just as an aside, there’s a fascinating rabbit-hole you could go down regarding Zangen Pharmaceuticals, the drug company that The Big Bang Theory's Bernadette and Penny work for. For starters, there’s the name, which is shared with an Iron Cross-decorated Nazi general. And then there’s Bernadette’s disarmingly ingenuous revelations of Zangen’s involvement in mutating viruses to cross the species barrier, crossing Ebola with a common cold virus, and conducting unethical human experimentation. Is this merely dark humour, is it a confession, or is it predictive programming?)
But enough about The Big Bang Theory. Let’s run through ‘This Week in I Told You So’.
‘I Informed You Thusly’#1: Masks Don’t WorkI told you that there is no reliable scientific evidence that face masks stop or even reduce the transmission of respiratory viruses, on multiple occasions. Ian Miller produced so many charts showing that neither cloth masks, nor N95s reduce case or death rates, no matter how high the compliance rates, that eventually he literally wrote the book on it. Paul Alexander compiled over 170 studies and articles demonstrating the ineffectiveness of masks for preventing respiratory virus transmission and illness, as well as the harms of masking.


And now, the latest Cochrane Review on Physical interventions to interrupt or reduce the spread of respiratory viruses has confirmed what every previous Cochrane Review on the subject had found: masks don’t work when worn in the community. ‘In the community’ means outside of a healthcare setting – that is, people conducting their ordinary business, with no access to fit testing, and neither training in proper donning and doffing procedures nor the capacity to follow them. It’s also very likely that N95/P2 respirators don’t work, even when worn by properly-trained health care workers in settings that support correct use.
(For those not familiar with Cochrane, it is the pre-eminent organisation for assessing the evidence base for medical and public health practice. Cochrane’s integrity and independence has been compromised in the last few years by its acceptance of donations from the Bill and Melinda Gates Foundation, which ultimately led to the expulsion of one of its prominent members, Peter Gøtzsche.
Hence, Cochrane reviews are not as reliable as they used to be. It’s important to check the authorship of each review. The lead author of the mask review is Tom Jefferson, a stalwart defender of scientific integrity. Investigative journalists Maryanne Demasi and Paul Thacker have recently conducted interviews with Tom Jefferson, which are well worth reading as companion pieces to this post. Jefferson makes a particularly interesting revelation in the Demasi interview: the Cochrane organisation held up the publication of the previous update to this ongoing review, which was due to be published in early 2020, for seven months, in which time mask mandates had been imposed all over the world despite a total lack of evidence for their efficacy.)
Here are the chief findings of the Cochrane review:
1. Masks don’t work to reduce symptoms of respiratory illness:
“Wearing masks in the community probably makes little or no difference to the outcome of influenza‐like illness (ILI)/COVID‐19 like illness compared to not wearing masks (risk ratio (RR) 0.95, 95% confidence interval (CI) 0.84 to 1.09; 9 trials, 276,917 participants; moderate‐certainty evidence.”
Physical interventions to interrupt or reduce the spread of respiratory viruses
(Note that while the risk ratio of 0.95 suggests that mask wearing may reduce symptoms of respiratory illness by 5 per cent, the confidence interval includes 0, meaning that there is a good chance that there is is no difference between wearing and not wearing a mask.)


2. Masks don’t work to reduce lab-confirmed flu or COVID:
“Wearing masks in the community probably makes little or no difference to the outcome of laboratory‐confirmed influenza/SARS‐CoV‐2 compared to not wearing masks (RR 1.01, 95% CI 0.72 to 1.42; 6 trials, 13,919 participants; moderate‐certainty evidence).”
Physical interventions to interrupt or reduce the spread of respiratory viruses
(Once again, the confidence interval includes zero.)
3. N95/P2 respirators don’t appear to work any better than cloth or surgical masks when it comes to preventing illness symptoms. There’s a slight signal of benefit, but the studies are too poorly-designed and reported to have confidence in them, and their results were all over the map:
“We are very uncertain on the effects of N95/P2 respirators compared with medical/surgical masks on the outcome of clinical respiratory illness (RR 0.70, 95% CI 0.45 to 1.10; 3 trials, 7779 participants; very low‐certainty evidence). N95/P2 respirators compared with medical/surgical masks may be effective for ILI (RR 0.82, 95% CI 0.66 to 1.03; 5 trials, 8407 participants; low‐certainty evidence). Evidence is limited by imprecision and heterogeneity for these subjective outcomes.”
Physical interventions to interrupt or reduce the spread of respiratory viruses
4. N95/P2 respirators don’t work any better than cloth masks when it comes to preventing influenza, whether in the general public or healthcare workers:
“The use of a N95/P2 respirators compared to medical/surgical masks probably makes little or no difference for the objective and more precise outcome of laboratory‐confirmed influenza infection (RR 1.10, 95% CI 0.90 to 1.34; 5 trials, 8407 participants; moderate‐certainty evidence). Restricting pooling to healthcare workers made no difference to the overall findings.”
Physical interventions to interrupt or reduce the spread of respiratory viruses
In short, masks don’t work. And I told you so.
Sneak preview of Part 2 of this miniseries: Teflon Tony Fauci admits that COVID and flu vaccines don’t work, and he knew along why they don’t. Stay tuned :).


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By: Robyn Chuter 
https://robynchuter.substack.com/p/i-informed-you-thusly-part-1