Although rare, a statistically significant association between BNT162b2 vaccination and myo/pericarditis and AKI was observed. While the association between BNT162b2 and myo/pericarditis has been confirmed internationally, further research is required to understand the association of AKI. BNT162b2 was not found to be associated with most of the AESIs investigated, providing reassurances around the safety of the vaccine.
Published 20 December 2010
If peer review was a drug it would never be allowed onto the market,’ says Drummond Rennie, deputy editor of the Journal Of the American Medical Association and intellectual father of the international congresses of peer review that have been held every four years since 1989. Peer review would not get onto the market because we have no convincing evidence of its benefits but a lot of evidence of its flaws.
Yet, to my continuing surprise, almost no scientists know anything about the evidence on peer review. It is a process that is central to science – deciding which grant proposals will be funded, which papers will be published, who will be promoted, and who will receive a Nobel prize. We might thus expect that scientists, people who are trained to believe nothing until presented with evidence, would want to know all the evidence available on this important process. Yet not only do scientists know little about the evidence on peer review but most continue to believe in peer review, thinking it essential for the progress of science. Ironically, a faith based rather than an evidence based process lies at the heart of science.
Epidemiological literature on the health risks associated with non-optimal temperature has mostly reported average estimates across large areas or specific population groups. However, the heterogeneous distribution of drivers of vulnerability can result in local differences in health risks associated with heat and cold. We aimed to analyse the association between ambient air temperature and all-cause mortality across England and Wales and characterise small scale patterns in temperature-related mortality risks and impacts.
See commentary from The Daily Sceptic: Eighty Times More Excess Deaths Associated With Cold Each Year than Heat
The present coronavirus crisis caused a major worldwide disruption which has not been experienced for decades. The lockdown-based crisis management was implemented by nearly all the countries, and studies confirming lockdown effectiveness can be found alongside the studies questioning it. In this work, we performed a narrative review of the works studying the above effectiveness, as well as the historic experience of previous pandemics and risk-benefit analysis based on the connection of health and wealth. Our aim was to learn lessons and analyze ways to improve the management of similar events in the future. The comparative analysis of different countries showed that the assumption of lockdowns’ effectiveness cannot be supported by evidence—neither regarding the present COVID-19 pandemic, nor regarding the 1918–1920 Spanish Flu and other less-severe pandemics in the past. The price tag of lockdowns in terms of public health is high: by using the known connection between health and wealth, we estimate that lockdowns may claim 20 times more life years than they save. It is suggested therefore that a thorough cost-benefit analysis should be performed before imposing any lockdown for either COVID-19 or any future pandemic.
While our understanding of viral transmission mechanisms leads to the assumption that lockdowns may be an effective pandemic management tool, this assumption cannot be supported by the evidence-based analysis of the present COVID-19 pandemic, as well as of the 1918–1920 H1N1 influenza type-A pandemic (the Spanish Flu) and numerous less-severe pandemics in the past. The price tag of lockdowns in terms of public health is high: we estimate that, even if somewhat effective in preventing death caused by infection, lockdowns may claim 20 times more life than they save. It is suggested therefore that a thorough cost-benefit analysis should be performed before imposing any lockdown in the future.
So it is curious that since the Covid pandemic began, this hugely influential figure has been at the heart of the scientific establishment’s efforts to stifle debate on the origins of the virus that emerged in Wuhan.
The Oxford, Edinburgh and London-educated infectious diseases expert has claimed scientists ‘know’ Covid was not created in a lab, suggested such an idea was a ‘conspiracy theory’ and insisted that ‘evidence’ indicates it spilled over naturally from animals.
Now, The Mail on Sunday can reveal that emails from America’s top infectious disease chief, Anthony Fauci, show how Farrar played a key role behind the scenes in marshalling top scientists’ response to concerns over the virus’s origins, even demanding secrecy on their discussions.
Crucially, he was a central figure behind two landmark statements published by leading science journals that helped to silence dissident views, arguing against the plausibility of ‘any type of laboratory-based scenario’.
Science journals have encouraged and enforced a false Covid narrative
Bear in mind that in the heat of this pandemic, papers printed in important journals were peer-reviewed within 10 weeks; one rattled through the process in just nine days for Nature. But, like Petrovsky, I have heard similar stories from many other frustrated experts who confronted the conventional wisdom that this lethal virus was a natural spillover event. Some could not even get letters published, let alone challenge those key papers promoting the Chinese perspective which have since turned out to be flawed or wrong.
Only now is acceptance emerging that the science establishment colluded to dismiss the lab leak hypothesis as a conspiracy theory, assisted by prominent experts with clear conflicts of interest, patsy politicians and a pathetic media that mostly failed to do its job. And yet, at the heart of this scandal lie some of the world’s most influential science journals. These should provide a forum for pulsating debate as experts explore and test theories, especially on something as contentious and fascinating as the possible origins of a global pandemic. Instead, some have played a central role in shutting down discussion and discrediting alternative views on the origins, with disastrous consequences for our understanding of events.
Levels of antibodies in the blood of vaccinated people that are able to recognise and fight the new SARS-CoV-2 Delta variant first discovered in India (B.1.617.2) are on average lower than those against previously circulating variants in the UK, according to new laboratory data from the Francis Crick Institute and the National Institute for Health Research (NIHR) UCLH Biomedical Research Centre, published today (Thursday) as a Research letter in The Lancet.
The results also show that levels of these antibodies are lower with increasing age and that levels decline over time, providing additional evidence in support of plans to deliver a vaccination boost to vulnerable people in the Autumn.
In the case of single-dose recipients, our data show that NAbTs are significantly lower against B.1.617.2 and B.1.351 VOCs relative to B.1.1.7, implying that although a single dose might still afford considerably more protection than no vaccination, single-dose recipients are likely to be less protected against these SARS-CoV-2 variants. These data therefore suggest that the benefits of delaying the second dose, in terms of wider population coverage and increased individual NAbTs after the second dose,7 must now be weighed against decreased efficacy in the short-term, in the context of the spread of B.1.617.2. Worldwide, our data highlight the ongoing need to increase vaccine supply to allow all countries to extend second-dose protection as quickly as possible.
In the longer term, we note that both increased age and time since the second dose of BNT162b2 significantly correlate with decreased NAb activity against B.1.617.2 and B.1.351—both of which are also characteristic of the population in the UK at highest risk of severe COVID-19 (ie, older and vaccinated earlier), independent of other existing factors such as compromised immune status or comorbidity, or geographic-specific responses to vaccination.
“It is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgment of trusted physicians or authoritative medical guidelines. I take no pleasure in this conclusion, which I reached slowly and reluctantly over my two decades as editor of The New England Journal of Medicine”.
More recently, Richard Horton, editor of The Lancet, wrote that “The case against science is straightforward: much of the scientific literature, perhaps half, may simply be untrue. Afflicted by studies with small sample sizes, tiny effects, invalid exploratory analyses, and flagrant conflicts of interest, together with an obsession for pursuing fashionable trends of dubious importance, science has taken a turn towards darkness”.
“Those errors are when introducing people of more than one hundred years, it has happened that they are figurative as that those deceased have 1 year, or 2, or 3 instead of 101, 102 or 103 “, considers one of them,” Pere Soler, pediatrician of the Infectious Pathology and Pediatric Immunodeficiencies unit of the Vall d’Hebron hospital explains.
Amid the dire Covid warnings, one crucial fact has been largely ignored: Cases are down 77% over the past six weeks. If a medication slashed cases by 77%, we’d call it a miracle pill. Why is the number of cases plummeting much faster than experts predicted?
In large part because natural immunity from prior infection is far more common than can be measured by testing. Testing has been capturing only from 10% to 25% of infections, depending on when during the pandemic someone got the virus. Applying a time-weighted case capture average of 1 in 6.5 to the cumulative 28 million confirmed cases would mean about 55% of Americans have natural immunity.
…explained only by natural immunity. Behavior didn’t suddenly improve over the holidays; Americans traveled more over Christmas than they had since March. Vaccines also don’t explain the steep decline in January. Vaccination rates were low and they take weeks to kick in.
Most people infected with SARS-CoV-2 are contagious for 4–8 days.7 Specimens are generally not found to contain culture-positive (potentially contagious) virus beyond day 9 after the onset of symptoms, with most transmission occurring before day 5. This timing fits with the observed patterns of virus transmission (usually 2 days before to 5 days after symptom onset), which led public health agencies to recommend a 10-day isolation period. The short window of transmissibility contrasts with a median 22–33 days of PCR positivity (longer with severe infections and somewhat shorter among asymptomatic individuals). This suggests that 50–75% of the time an individual is PCR positive, they are likely to be post-infectious.
Ivor Cummins aka the Fat Emperor – gives James the lowdown on why you can’t trust anything our governments tell us about Covid-19. If you want the facts on Coronavirus – how deadly is it? do lockdowns and masks work? how does it compare with previous pandemics? – you’ve come to the right place
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The UK’s pandemic response relies too heavily on scientists and other government appointees with worrying competing interests, including shareholdings in companies that manufacture covid-19 diagnostic tests, treatments, and vaccines. Government appointees are able to ignore or cherry pick science—another form of misuse—and indulge in anti-competitive practices that favour their own products and those of friends and associates.
COVID-19 is not a pandemic. It is a syndemic. The syndemic nature of the threat we face means that a more nuanced approach is needed if we are to protect the health of our communities.
A syndemic is not merely a comorbidity. Syndemics are characterised by biological and social interactions between conditions and states, interactions that increase a person’s susceptibility to harm or worsen their health outcomes. In the case of COVID-19, attacking NCDs will be a prerequisite for successful containment.
What accounts for Sweden’s high Covid death rate among the Nordics? One factor could be Sweden’s lighter lockdown. But we suggest 15 other possible factors. Most significant are: (1) the “dry-tinder” situation in Sweden (we suggest that this factor alone accounts for 25 to 50% of Sweden’s Covid death toll); (2) Stockholm’s larger population; (3) Sweden’s higher immigrant population; (4) in Sweden immigrants probably more often work in the elderly care system; (5) Sweden has a greater proportion of people in elderly care; (6) Stockholm’s “sport-break” was a week later than the other three capital cities; (7) Stockholm’s system of elderly care collects especially vulnerable people in nursing homes. Other possible factors are: (8) the Swedish elderly and health care system may have done less to try to cure elderly Covid patients; (9) Sweden may have been relatively understocked in protective equipment and sanitizers; (10) Sweden may have been slower to separate Covid patients in nursing homes; (11) Sweden may have been slower to implement staff testing and changes in protocols and equipage; (12) Sweden elderly care workers may have done more cross-facility work; (13) Sweden might have larger nursing homes; (14) Stockholmers might travel more to the Alpine regions; (15) Sweden might be quicker to count a death “a Covid death.” We give evidence for these other 15 possible factors. It is plausible that Sweden’s lighter lockdown accounts for but a small part of Sweden’s higher Covid death rate.
Review of autopsy reports enabled the determination of the relative contributions of undiagnosed COVID-19 and lockdown restrictions on deaths. Of the 67 autopsies done at our hospital during the first 2 months of lockdown, only two autopsies identified COVID-19 that was undiagnosed before death. More frequently, reduced access to health-care systems associated with lockdown was identified as a probable contributory factor (six cases) or possible contributory factor (eight cases) to death. These causes included potentially preventable out-of-hospital deaths such as acute myocardial infarction and diabetic ketoacidosis, in which patients contacted the health services by telephone and were advised to self-isolate at home rather than attending hospital. Direct reference to financial or work pressures caused by COVID-19 was identified in three of ten cases of suicide.
Lockdowns may reduce the peak of transmission and recovery rates but not the number of critical cases or overall mortality.
Lastly, government actions such as border closures, full lockdowns, and a high rate of COVID-19 testing were not associated with statistically significant reductions in the number of critical cases or overall mortality.
…full lockdowns and early border closures may lessen the peak of transmission, and thus prevent health system overcapacity, which would facilitate increased recovery rates.
Note: Coughing and large droplets are note the issue beause breathing exhales more virus in fine aerosols than coughing. Finer aerosols bypass masks and nose to the lungs. Since masks nebulise particles, the solution is ventilation, not face masks.
The global pandemic of COVID-19, caused by severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]) has been associated with infections and deaths among health-care workers. There have been conflicting recommendations from health authorities on the use of masks or respirators to protect health-care workers. When I first reviewed personal respiratory protection against tuberculosis for health-care workers more than 20 years ago, there was very little information on infectious aerosols. Since then, colleagues in various disciplines have provided a wealth of data. The purpose of this Viewpoint is to review the scientific literature on the aerosols generated by individuals with respiratory infections, and to discuss how these data inform the optimal use of masks, respirators, and other infection-control measures to protect health-care workers from those aerosols. This is not a review of the literature on the use of surgical masks or respirators, as several have been done already.
Increasing COVID-19 caseloads were associated with countries with higher obesity (adjusted rate ratio [RR]=1.06; 95%CI: 1.01–1.11), median population age (RR=1.10; 95%CI: 1.05–1.15) and longer time to border closures from the first reported case (RR=1.04; 95%CI: 1.01–1.08). Increased mortality per million was significantly associated with higher obesity prevalence (RR=1.12; 95%CI: 1.06–1.19) and per capita gross domestic product (GDP) (RR=1.03; 95%CI: 1.00–1.06). Reduced income dispersion reduced mortality (RR=0.88; 95%CI: 0.83–0.93) and the number of critical cases (RR=0.92; 95% CI: 0.87–0.97). Rapid border closures, full lockdowns, and wide-spread testing were not associated with COVID-19 mortality per million people. However, full lockdowns (RR=2.47: 95%CI: 1.08–5.64) and reduced country vulnerability to biological threats (i.e. high scores on the global health security scale for risk environment) (RR=1.55; 95%CI: 1.13–2.12) were significantly associated with increased patient recovery rates.