Answer the question
FM1 - when have you not known me to reply directly?
Unfortunately you will find that your rhetorical style here - while it may sound impressive (it sort of hints that I'm evading questions) is not helpful.
You see, I am not certain precisely which question you want answering, and the question does not help. If you are more precise, giving all details, I'll be happy to oblige with a more precise answer - even though my answer may be "I'm not sure".
Such a rational person, love it. Less than 2 minutes.
Alex Belfield and the Voice of Reason
My favourite comedian /commentator/social critic
Former BBC radio host and now prolific YouTuber.
He's so loquacious I wouldn't be surprised if he's a descendant of William Shakespeare
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True, and most deaths in the 1918 pandemic were caused by bacterial pneumonia.
One of the fascinating things about COVID is how it is different from influenza - of any variety, or even common cold coronaviruses.
Here is a fairly recent metabolic analysis of what COVID does:
Untuned antiviral immunity in COVID-19 revealed by temporal type I/III interferon patterns and flu comparison
A central paradigm of immunity is that interferon (IFN)-mediated antiviral responses precede pro-inflammatory ones, optimizing host protection and minimizing collateral damage1,2. Here, we report that for coronavirus disease 2019 (COVID-19) this paradigm does not apply. By investigating temporal IFN and inflammatory cytokine patterns in 32 moderate-to-severe patients with COVID-19 hospitalized for pneumonia and longitudinally followed for the development of respiratory failure and death, we reveal that IFN-λ and type I IFN production were both diminished and delayed, induced only in a fraction of patients as they became critically ill. On the contrary, pro-inflammatory cytokines such as tumor necrosis factor (TNF), interleukin (IL)-6 and IL-8 were produced before IFNs in all patients and persisted for a prolonged time. This condition was reflected in blood transcriptomes wherein prominent IFN signatures were only seen in critically ill patients who also exhibited augmented inflammation. By comparison, in 16 patients with influenza (flu) hospitalized for pneumonia with similar clinicopathological characteristics to those of COVID-19 and 24 nonhospitalized patients with flu with milder symptoms, IFN-λ and type I IFN were robustly induced earlier, at higher levels and independently of disease severity, whereas pro-inflammatory cytokines were only acutely produced. Notably, higher IFN-λ concentrations in patients with COVID-19 correlated with lower viral load in bronchial aspirates and faster viral clearance and a higher IFN-λ to type I IFN ratio correlated with improved outcome for critically ill patients. Moreover, altered cytokine patterns in patients with COVID-19 correlated with longer hospitalization and higher incidence of critical disease and mortality compared to flu. These data point to an untuned antiviral response in COVID-19, contributing to persistent viral presence, hyperinflammation and respiratory failure.
There is quite a trail off this paper, but I can't say that I understand it!
"Where are the autopsies?"Viviane Fischer
At the beginning if the pandemic 2 x 100 autopsies have been made once in Italy next in Germany. All 200 cases - CoV-19 deaths, also the ones claimed being healthy - did show that all victims had at least one severe comorbidity. Most had 3.
So CoV-19 deaths are very rare. About 13% at most according NHS.
By investigating temporal IFN and inflammatory cytokine patterns in 32 moderate-to-severe patients with COVID-19 hospitalized for pneumonia and longitudinally followed for the development of respiratory failure and death, we reveal that IFN-λ and type I IFN production were both diminished and delayed, induced only in a fraction of patients
This is known since almost a year as the up-regulating is blocked by the ACE-2 virus lock. Also the follow-up story is known since a year, that this block caused an up-regulating of ACE-2 receptors, what opens even more doors to the virus.
So this post is a disparate try by THHuxleynew to gain/show some competence after one year ignoring all papers we linked..
Display MoreFM1 - when have you not known me to reply directly?
Unfortunately you will find that your rhetorical style here - while it may sound impressive (it sort of hints that I'm evading questions) is not helpful.
You see, I am not certain precisely which question you want answering, and the question does not help. If you are more precise, giving all details, I'll be happy to oblige with a more precise answer - even though my answer may be "I'm not sure".
Fair enough. In your opinion why did India see such a sudden drop in cases?
Of the "cheap and cheerful" drugs being trialed for outpatient treatment I am rather fond of metformin. It has quite a bit of carefully done but inherently low quality retrospective study support. It has (much better than Ivermectin) theoretical support, because of its known actions.
Here is a good quality multi-arm interventional study which would, if funded, surely provide some good evidence between the relative merits of Ivermectin and Metaformin. It is quadruply-masked and due to report in October.
They have only got Phase 1 funding (70 patients) not enough to get strong results unless any of the interventions are unusually effective.
At the beginning if the pandemic 2 x 100 autopsies have been made once in Italy next in Germany. All 200 cases - CoV-19 deaths, also the ones claimed being healthy - did show that all victims had at least one severe comorbidity. Most had 3.
So CoV-19 deaths are very rare. About 13% at most according NHS.
That is like saying that cancer deaths are rare because most cancer patients have co-morbidities (high blood pressure, diabetes, etc). Are you saying somone dying of cancer who has diabetes is not a cancer death?
Comorbidity was most prevalent in patients with lung cancer and least prevalent in Hodgkin lymphoma patients. Up to two-thirds of patients within each of the four cancer patient cohorts we studied had at least one comorbidity, and around half of the comorbid patients had multiple comorbidities. Our study highlighted common comorbid conditions among the cancer patient cohorts. In all four cohorts, the odds of having a comorbidity and the probability of multiple comorbidity were consistently highest in the most deprived cancer patients.
You can say it if it makes you happy
Fair enough. In your opinion why did India see such a sudden drop in cases?
https://www.ft.com/content/f0e…29-4195-a286-43b86f5661a3 (FT - May 26)
India’s new confirmed coronavirus infections are steadily declining because of regional lockdowns and increased levels of antibodies among the population, according to public health experts.
At least 150,000 people have died in the past two months as the country has been hit by a devastating second wave that overwhelmed health systems and caused acute shortages of medical supplies.
But India’s seven-day moving average of new daily infections has fallen to 237,000, down from a peak of 392,000 in early May. The country’s test positivity rate has also dropped to 9.4 per cent from a high of about 23 per cent earlier this month, although this is still well above the 5 per cent threshold the World Health Organization considers the benchmark for having a pandemic under control.
Bhramar Mukherjee, a professor of epidemiology at the University of Michigan, said the actual number of infections in the recent wave was probably 10-15 times higher than the official data. But she said the trend was clear, as people have retreated into their homes and avoided crowded places.
“The absolute numbers are all garbage, but the relative trends can still be picked up,” she said. “The true curve is much, much higher but it follows the same trajectory.”
“We still estimate that about 40 per cent of India is infected,” Mukherjee added. “It’s not enough to reach herd immunity but probably a lot of people right now have antibodies and those who do not are practising social distancing.”
India is still recording more than 4,000 deaths a day, close to its pandemic peak.
Although the spread of the virus is slowing down on a national level, there are still widespread regional variations. Rijo John, a health economist at the Rajagiri College of Social Sciences, said new cases are dropping sharply in densely populated areas such as Delhi and Maharashtra but infections in some other states were still on an upward trend.
The paucity of testing made it hard to gauge trends accurately in rural areas, he added.
“Your test positivity rate may look good on paper but that may not be the reality,” he said. “Most of our testing infrastructure is disproportionately concentrated in cities. Daily tests are now 2.2m a day, which is good, but how much of this is done in rural areas?”
Authorities now face the challenge of trying to ease restrictions and revive economic activity without contributing to a sharp rebound in cases.
and more recently:
Despite recorded infections steadily declining, experts fear the virus is spreading unchecked through India's rural areas - where the majority of its people live.
India is still second to the US in terms of total cases globally - with almost 29 million - but a lack of testing facilities and hospital capacity mean that figure is thought to be a vast underestimate.
The country's health ministry said 2,427 new deaths were registered in the latest 24-hour period on Monday, taking the total to 349,186.
The India figures are very suspect - at least that is what their people think. Large towns get testing, and also have higher COVID surges due to more mixing. They benefit (a bit) from immunity of maybe 50% of population who have had COVID. That is not enough to stop delta alone, but it is enough to make looser lockdown work. And because of broken testing suystems no-one really knows what the real infection rate was. Maybe higher than this.
In the country there is much less data, deaths do not become cases because there is little testing.
So to answer your question, what i read from this (and i might be wrong, but it seems reasonable): India is so diverse, with different things happen in towns and country, and not enough testing even in towns to accurately track what is happening. While the above comments seem reasonable, and explain the "sharp reduction in cases" - lockdown aided by large amts of immunity - there is a lot of uncertainty in the figures. Like the UK case figures in our first wave which vastly underestimated cases due to lack of testing. But UK death figures are better even then - whereas in India death figures also cannot be trusted..
But India’s seven-day moving average of new daily infections has fallen to 237,000, down from a peak of 392,000 in early May.
Great again... The one day peek was 420'000 thousand now its 40'000 since a week. Are you able to spot your error...?
“We still estimate that about 40 per cent of India is infected,”
Which idiot paper to you cite here??? 40% of india is infected????
So Uttar Pradesh has <10 CoV-19 death since weeks. Do you think they cannot count deaths?
Causation: Cases did fall after all inhabitants got Ivermectin. Cases did fall much faster than after a lock-down, which now has been stopped weeks ago. Why do cases not go up again???
Brazil, Indonesia, Russia, South Africa, USA, UK,....currently have more deaths/mio than India... Why??? Even with 50% vaccinated
...
Display Morehttps://www.ft.com/content/f0e…29-4195-a286-43b86f5661a3 (FT - May 26)
India’s new confirmed coronavirus infections are steadily declining because of regional lockdowns and increased levels of antibodies among the population, according to public health experts.
At least 150,000 people have died in the past two months as the country has been hit by a devastating second wave that overwhelmed health systems and caused acute shortages of medical supplies.
But India’s seven-day moving average of new daily infections has fallen to 237,000, down from a peak of 392,000 in early May. The country’s test positivity rate has also dropped to 9.4 per cent from a high of about 23 per cent earlier this month, although this is still well above the 5 per cent threshold the World Health Organization considers the benchmark for having a pandemic under control.
Bhramar Mukherjee, a professor of epidemiology at the University of Michigan, said the actual number of infections in the recent wave was probably 10-15 times higher than the official data. But she said the trend was clear, as people have retreated into their homes and avoided crowded places.
“The absolute numbers are all garbage, but the relative trends can still be picked up,” she said. “The true curve is much, much higher but it follows the same trajectory.”
“We still estimate that about 40 per cent of India is infected,” Mukherjee added. “It’s not enough to reach herd immunity but probably a lot of people right now have antibodies and those who do not are practising social distancing.”
India is still recording more than 4,000 deaths a day, close to its pandemic peak.
Although the spread of the virus is slowing down on a national level, there are still widespread regional variations. Rijo John, a health economist at the Rajagiri College of Social Sciences, said new cases are dropping sharply in densely populated areas such as Delhi and Maharashtra but infections in some other states were still on an upward trend.
The paucity of testing made it hard to gauge trends accurately in rural areas, he added.
“Your test positivity rate may look good on paper but that may not be the reality,” he said. “Most of our testing infrastructure is disproportionately concentrated in cities. Daily tests are now 2.2m a day, which is good, but how much of this is done in rural areas?”
Authorities now face the challenge of trying to ease restrictions and revive economic activity without contributing to a sharp rebound in cases.
and more recently:
https://news.sky.com/story/cov…el-in-two-months-12326975
Despite recorded infections steadily declining, experts fear the virus is spreading unchecked through India's rural areas - where the majority of its people live.
India is still second to the US in terms of total cases globally - with almost 29 million - but a lack of testing facilities and hospital capacity mean that figure is thought to be a vast underestimate.
The country's health ministry said 2,427 new deaths were registered in the latest 24-hour period on Monday, taking the total to 349,186.
The India figures are very suspect - at least that is what their people think. Large towns get testing, and also have higher COVID surges due to more mixing. They benefit (a bit) from immunity of maybe 50% of population who have had COVID. That is not enough to stop delta alone, but it is enough to make looser lockdown work. And because of broken testing suystems no-one really knows what the real infection rate was. Maybe higher than this.
In the country there is much less data, deaths do not become cases because there is little testing.
So to answer your question, what i read from this (and i might be wrong, but it seems reasonable): India is so diverse, with different things happen in towns and country, and not enough testing even in towns to accurately track what is happening. While the above comments seem reasonable, and explain the "sharp reduction in cases" - lockdown aided by large amts of immunity - there is a lot of uncertainty in the figures. Like the UK case figures in our first wave which vastly underestimated cases due to lack of testing. But UK death figures are better even then - whereas in India death figures also cannot be trusted..
Ok thanks, I'll get back to you on this but one more quick question, when do you sleep?
Hi FM1 - probably when you are still up?
vaccine vs natural immunity.
I've found a good reference to something useful I vaguely remembered. Now it is less vague.
So mRNA vaccines deliver antibodies that typically target more places in the RBD than natural immunity (not surprising) and therefore respond more broadly to variants, whereas natural immunity is more specific to one variant.
This data is experimental, but not real world - so treat it with caution. But it give grounds for some optimism.
These findings suggest that natural immunity and vaccine-generated immunity to SARS-CoV-2 will differ in how they recognize new viral variants. What’s more, antibodies acquired with the help of a vaccine may be more likely to target new SARS-CoV-2 variants potently, even when the variants carry new mutations in the RBD.
It’s not entirely clear why these differences in vaccine- and infection-elicited antibody responses exist. In both cases, RBD-directed antibodies are acquired from the immune system’s recognition and response to viral spike proteins. The Seattle team suggests these differences may arise because the vaccine presents the viral protein in slightly different conformations.
Also, it’s possible that mRNA delivery may change the way antigens are presented to the immune system, leading to differences in the antibodies that get produced. A third difference is that natural infection only exposes the body to the virus in the respiratory tract (unless the illness is very severe), while the vaccine is delivered to muscle, where the immune system may have an even better chance of seeing it and responding vigorously.
Whatever the underlying reasons turn out to be, it’s important to consider that humans are routinely infected and re-infected with other common coronaviruses, which are responsible for the common cold. It’s not at all unusual to catch a cold from seasonal coronaviruses year after year. That’s at least in part because those viruses tend to evolve to escape acquired immunity, much as SARS-CoV-2 is now in the process of doing.
The good news so far is that, unlike the situation for the common cold, we have now developed multiple COVID-19 vaccines. The evidence continues to suggest that acquired immunity from vaccines still offers substantial protection against the new variants now circulating around the globe.
The hope is that acquired immunity from the vaccines will indeed produce long-lasting protection against SARS-CoV-2 and bring an end to the pandemic. These new findings point encouragingly in that direction. They also serve as an important reminder to roll up your sleeve for the vaccine if you haven’t already done so, whether or not you’ve had COVID-19. Our best hope of winning this contest with the virus is to get as many people immunized now as possible. That will save lives, and reduce the likelihood of even more variants appearing that might evade protection from the current vaccines.
and
So mRNA vaccines deliver antibodies that typically target more places in the RBD than natural immunity
This is outraging nonsense and fake news generate by a reckless idiot. Pfizer targets a single protein and thus fails 2x more often than moderna that targets 2 proteins. T-Cell keep a much broader memory of all parts of the virus and are always better than the current dirt cheap RNA vaccines.
Such posting as above simply is spreading criminal and dangerous false information/FUD generated by ( as claimed by THH) state employee and FM/R/B/J member.
when do you sleep?
Fluvoxamine appears to have some beneficial effects on insomnia
no effect on ivermectin -aversion
it actually is top of the list for antiCovid efficacy..
Merck's ersatz ivermectin is pretty high..
however for lack of side effects its pretty hard to beat IVM/VitD/Zn
Remdesivir is pretty bad for both..efficacy and side effects
Amazing, especially for us in LENR, accused of fraud, and having overved fraud by MIT and incompetence by Caltech since long...
Meanwhile on XAV19 by Xenothera
Funding by EU
trials are continuing
It is polyclonal antibodies, more evident to viral evasion.
The trial is in process, recruitment completed in may... It's slow...
The company report positive advance, emergency allowanc...
Medical nationalism is a reality, but trial are not the problem... it works, it is just slow, too shoortly slowly funded, and under publicized by foreign media...
anyway it is not magic, it save many patients, but not all.
Sadly as too common on French companies, few article in english
English speaking media talk more of REGN-COV2 (Regeneron), a mix of two monoclonal antibodies.
mazing, especially for us in LENR,
not amazing for https://ivmmeta.com/
Elgazzar paper removed from metaanalysis
This is outraging nonsense and fake news generate by a reckless idiot. Pfizer targets a single protein and thus fails 2x more often than moderna that targets 2 proteins. T-Cell keep a much broader memory of all parts of the virus and are always better than the current dirt cheap RNA vaccines.
Such posting as above simply is spreading criminal and dangerous false information/FUD generated by ( as claimed by THH) state employee and FM/R/B/J member.
I understand that you consider yourself more of an expert on disease and virus genetics than the authors of this (well referenced - so at least they have read a decent amount and added links to it) paper.
Perhaps you could comment specifically on which bit of their analysis of the new experimental data they have obtained that you don't like?
I agree it is a bit surprising - and not certain. Pretty well nothing in medicine is certain. But we are all open to new evidence. Aren't we?
As for T-cell memory being broader that is true. And T-cell immunity is not addressed here. What evidence do you have on the relative strength of natural and vaccine-induced T-cell immunity to COVID?
This looks quite encouraging (Pfizer). They cannot directly say whether vaccines induce higher T-cell response than natural infection because they performed testing only on vaccinated individuals. But they can indirectly say this, as below. As always in medicine it is not conclusive. You might speculate that natural infection delivers better response in the lung and throat tissues where it is most needed in initial COVID infection.
linked paper: https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3812375
Key findings from the PITCH study:
Have your never-ending pandemic: just don’t call it an emergency
Dr. Ron Brown – Opinion Editorial
July 15, 2021
As capacity crowds gathered to watch the mid-summer Major League Baseball All-Star game, we were reminded that the summer respite from the COVID-19 pandemic is surely welcome. But as Broadway gears up productions for reopening, storm clouds are beginning to form on the distant horizon. The long-term forecast this coming fall and winter calls for increasing chance of variants, vaccines, and lockdowns. Australia and other nations in the southern hemisphere have already witnessed the return of the pandemic scourge during their current winter season, which is predicted to head our way next. But there is a simple way to evade collateral damage as the nth wave of the pandemic howls over us like gales in a hurricane: just cease calling it an emergency.
The COVID-19 pandemic was declared an emergency by World Health Organization on March 11, 2020 when the WHO Director-General said, “I remind all countries that we are calling on you to activate and scale up your emergency response mechanisms.” WHO Director-General’s opening remarks at the media briefing on COVID-19 – 11 March 2020.
Emergency response mechanisms include granting authoritative powers to local officials to implement and enforce lockdowns and other mitigation measures. In general, legislatures have willingly conceded this power to the executive branch of governments to facilitate an emergency response. But who (not WHO) gets to determine what is an emergency? At the urging of their constituents, it’s time for legislators to take an active role and declare, “Not so fast!” You can have your never-ending pandemic, but just don’t call it an emergency.
Back in March 2020, no one knew much about the risks of COVID-19 infection as well as the collateral damage from severe mitigation measures. Going forward, the now known risks and benefits of lockdowns and other mitigation measures need to be openly debated by elected legislators. There is no longer an excuse to continue to grant unconditional executive power to authorities to declare an emergency response for what was once a novel disease with unknown lethality and prevalence.
Yes, there is still plenty more to learn about COVID-19, but certainly whether or not we are past the emergency phase is worthy of public debate. In the meantime, the public has a right to continue to vaccinate and treat themselves with Ivermectin as much as they like, pandemic or no pandemic, emergency or not.
Ah, the good old days, when we had pandemics without people even noticing them! You may not notice an ambulance coming down the street with its lights and siren turned off, but during an emergency, those flashing lights and sirens are designed to attract your attention. It’s time to turn off the sirens and flashing lights of the COVID-19 pandemic.
Bioethics of Experimental COVID Vaccine Deployment under EUA: It’s time we stop and look at what’s going down
Robert W Malone, MD, MS1
I provide this brief essay for the TrialSite community because you are involved or at least interested in human subject clinical research. By way of background, please understand that I am a vaccine specialist and advocate, as well as the original inventor of the mRNA vaccine (and DNA vaccine) core platform technology. But I also have extensive training in bioethics from the University of Maryland, Walter Reed Army Institute of Research, and Harvard Medical School, and advanced clinical development and regulatory affairs are core competencies for me.
Before examining the bioethical foundations of current policy and practice which underpin experimental COVID vaccine deployment in many in many western nations, allow me to begin by sharing some “real world” first-hand evidence.
I was on a call with a Canadian primary care physician last week for a couple of hours. He related the story of the six (in his mind) highly unusual clinical cases of post-vaccination adverse events that he has personally observed in his practice involving vaccination of his patients with the Pfizer mRNA vaccine product. Keep in mind that it was Canadian physicians – acting of their own accord – who filed the FOIA to gain access to the Pfizer vaccine IND (see https://trialsitenews.com/did-…-of-mrna-clinical-trials/).
What was most alarming to me was that my clinical primary practice physician colleague told me that each of these cases were reported as per the proper channels in Canada, and each was summarily determined to not be vaccine related by the authorities without significant investigation. Furthermore, he reported to me that any practicing physician in Canada who goes public with concerns about vaccine safety is subjected to a storm of derision from academic physicians and potential termination of employment (state-controlled socialized medicine) and loss of license to practice.
This is one face of censorship in the time of COVID (see https://www.embopress.org/doi/full/10.15252/embr.202051420). But what are official public health leaders afraid of? Why is it necessary to suppress discussion and full disclosure of information concerning mRNA reactogenicity and safety risks? Let’s analyze the vaccine-related adverse event data rigorously. Is there information or patterns that can be found, such as the recent finding of the cardiomyopathy signals, or the latent virus reactivation signals? We should be enlisting the best biostatistics and machine learning experts to examine these data, and the results should- no must- be made available to the public promptly. Please follow along and take a moment to examine the underlying bioethics of this situation with me.
I believe that adult citizens must be allowed free will, the freedom to choose. This is particularly true in the case of clinical research. These mRNA and recombinant adenovirus vaccine products remain experimental at this time. Furthermore, we are supposed to be doing rigorous, fact-based science and medicine. If rigorous and transparent evaluation of vaccine reactogenicity and treatment-emergent post-vaccination adverse events is not done, we (the public health, clinical research and vaccine developer communities) play right into the hands of anti-vaxxer memes and validate many of their arguments. The suppression of information, discussion, and outright censorship concerning these current COVID vaccines which are based on gene therapy technologies cast a bad light on the entire vaccine enterprise. It is my opinion that the adult public can handle information and open discussion. Furthermore, we must fully disclose any and all risks associated with these experimental research products.
In this context, the adult public are basically research subjects that are not being required to sign informed consent due to EUA waiver. But that does not mean that they do not deserve the full disclosure of risks that one would normally require in an informed consent document for a clinical trial. And now some national authorities are calling on the deployment of EUA vaccines to adolescents and the young, which by definition are not able to directly provide informed consent to participate in clinical research – written or otherwise.
The key point here is that what is being done by suppressing open disclosure and debate concerning the profile of adverse events associated with these vaccines violates fundamental bioethical principles for clinical research. This goes back to the Geneva convention and the Helsinki declaration. See https://www.wma.net/policies-p…involving-human-subjects/. There must be informed consent for experimentation on human subjects. The human subjects – you, me, and the citizens of these countries – must be informed of risks. As a community, we have already had a discussion and made our decision – we cannot compel prisoners, military recruits, or any other population of humans to participate in a clinical research study. For example, see the Belmont report, which provided the rationale for US federal law Code of Federal Regulations 45 CFR 46 (subpart A), referred to as “The Federal Policy for the Protection of Human Subjects” (also known as the “Common Rule”).
Quoting from the Belmont Report:
“Informed Consent. — Respect for persons requires that subjects, to the degree that they are capable, be given the opportunity to choose what shall or shall not happen to them. This opportunity is provided when adequate standards for informed consent are satisfied.
While the importance of informed consent is unquestioned, controversy prevails over the nature and possibility of an informed consent. Nonetheless, there is widespread agreement that the consent process can be analyzed as containing three elements: information, comprehension and voluntariness.”
Information, comprehension, and voluntariness. To my eyes, it appears that in many regions public health leadership has stepped over the line and is now violating the bedrock principles which form the foundation upon which the ethics of clinical research are built. I believe that this must stop. We must have transparent public disclosure of risks – in a broad sense – associated with these experimental vaccines. It is either that, or the entire modern bioethical structure which supports human subjects research will have to be re-thought.
I really think we need to
“stop, children, what’s that sound – everybody look what’s going down”
(For What it’s Worth, Buffalo Springfield)
Furthermore, as these vaccines are not yet market authorized (licensed), coercion of human subjects to participate in medical experimentation is specifically forbidden. Therefore, public health policies which meet generally accepted criteria for coercion to participate in clinical research are forbidden.
For example, if I were to propose a clinical trial involving children and entice participation by giving out ice cream to those willing to participate, any institutional human subjects safety board (IRB) in the United States would reject that protocol. If I were to propose a clinical research protocol wherein the population of a geographic region would lose personal liberties unless 70% of the population participated in my study, once again, that protocol would be rejected by any US IRB based on coercion of subject participation. No coercion to participate in the study is allowed. In human subject clinical research, in most countries of the world this is considered a bright line that cannot be crossed. So, now we are told to waive that requirement without even so much as open public discussion being allowed?
In conclusion, I hope that you will join me; stop to take a moment and consider for yourself what is going on. The logic seems clear to me. 1) An unlicensed medical product deployed under emergency use authorization (EUA) remains an experimental product under clinical research development. 2) EUA authorized by national authorities basically grants a short-term right to administer the research product to human subjects without written informed consent. 3) The Geneva Convention, the Helsinki declaration, and the entire structure which supports ethical human subjects research requires that research subjects be fully informed of risks and must consent to participation without coercion. Has that bright line been crossed? If so, what actions are to be taken? I look forward to learning from your thoughts and conclusions.
Patients with long COVID have reported more than 200 symptoms affecting 10 organ systems, according to a new study.
Researchers surveyed 3,762 people from 56 countries who joined the Body Politic online COVID-19 support group and reported coronavirus-like symptoms between December 2019 and May 2020.
In total they reported 203 different symptoms, with 66 identified for the whole seven-month period.
The most common were fatigue, post-exertional malaise (worsening of symptoms after physical or mental exertion), and cognitive dysfunction - often referred to as brain fog.
Among the other symptoms identified were visual hallucinations, itchy skin, menstrual cycle changes, sexual dysfunction, bladder control issues, diarrhoea, heart palpitations and tinnitus.
Not sure I can agree with conclusion
More Vaccinated People Are Dying of COVID in England Than Unvaccinated – Here’s Why
Health
More Vaccinated People Are Dying of COVID in England Than Unvaccinated – Here’s Why
By Christian Yates, University of Bath on Jul 15, 2021
COVID Vaccine Success
More vaccinated people are dying of COVID than unvaccinated people, according to a recent report from Public Health England (PHE). The report shows that 163 of the 257 people (63.4%) who died within 28 days of a positive COVID test between February 1 and June 21, had received at least one dose of the vaccine. At first glance, this may seem alarming, but it is exactly as would be expected.
Here’s a simple thought experiment: imagine everyone is now fully vaccinated with COVID vaccines – which are excellent but can’t save all lives. Some people who get infected with COVID will still die. All of these people will be fully vaccinated – 100%. That doesn’t mean vaccines aren’t effective at reducing death.
The risk of dying from COVID doubles roughly every seven years older a patient is. The 35-year difference between a 35-year-old and a 70-year-old means the risk of death between the two patients has doubled five times – equivalently it has increased by a factor of 32. An unvaccinated 70-year-old might be 32 times more likely to die of COVID than an unvaccinated 35-year-old. This dramatic variation of the risk profile with age means that even excellent vaccines don’t reduce the risk of death for older people to below the risk for some younger demographics.
PHE data suggests that being double vaccinated reduces the risk of being hospitalized with the now-dominant delta variant by around 96%. Even conservatively assuming the vaccines are no more effective at preventing death than hospitalization (actually they are likely to be more effective at preventing death) this means the risk of death for double vaccinated people has been cut to less than one-twentieth of the value for unvaccinated people with the same underlying risk profile.
However, the 20-fold decrease in risk afforded by the vaccine isn’t enough to offset the 32-fold increase in underlying risk of death of an 70-year-old over a 35-year-old. Given the same risk of infection, we would still expect to see more double-vaccinated 70-year-olds die from COVID than unvaccinated 35-year-olds. There are caveats to that simple calculation. The risk of infection is not the same for all age groups. Currently, infections are highest in the youngest and lower in older age groups.
One way to imagine the risk is as a rain of differently sized ball bearings falling from the sky, where the ball bearings are the people that get infected with COVID. For simplicity’s sake, let’s assume there are roughly equal numbers of ball bearings in each age group. In each age category, there is also a variation in the size of the balls. The balls representing the older groups are smaller, representing a higher risk of death.
Now imagine there’s a sieve that catches many of the balls. Most people who get COVID will not die (most balls get caught in the sieve). But some of the smaller balls fall through. The older you are, the more likely you are to fall through the holes. The balls that make it through the first sieve are hugely skewed towards older age ranges, represented by the smaller ball bearings. Before COVID vaccines came along, the people that fell through the holes represented the people who would die of COVID. The risk was massively skewed towards older people.
Vaccination provides a second sieve underneath the first, to prevent people from dying. This time, because we haven’t vaccinated everyone, it’s the holes in the sieve that are of different sizes. For older people who’ve had both doses, the holes are smaller, so many ball-bearings are stopped. The vaccines will save many of those who would previously have died.
For younger people the holes in the vaccine sieve are currently bigger as they are less likely to have received both doses and so more likely to fall through the sieve.
If all the filtering were just done by the second sieve (with no skew in risk of death by age, represented by the first sieve), then we might expect younger unvaccinated people to account for a larger proportion of the deaths. But it isn’t. The first sieve is so hugely biased towards older people that even with vaccination, more of them slip through the second sieve than the younger unvaccinated people. Given the UK’s vaccination strategy (vaccinate older, more vulnerable people first), you would expect high proportions of the people who die from COVID to have been vaccinated. And that is exactly what we see in the data.
The fact that more vaccinated people are dying than unvaccinated people does nothing to undermine vaccine safety or effectiveness. In fact, it’s exactly what we’d expect from the excellent vaccines, which have already saved tens of thousands of lives.
