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UK Govt Coronavirus Response: Sceptics Thread


sancho panza

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sancho panza
13 hours ago, Loki said:

Those comments are encouraging

I think tehre's beginning to be some real anger out there.

The more I see of Bozza the more uttterly out of his depth he looks.

Our political class are upper class twits on the whole with little idea of the real world.Can't believe I'm saying that like it's a surprise.

 

I think the anger will grow when it comes out what they did to care home residents and how they shifted covid patients to them knowingly.

via lockdown sceptics

Letter From Care Home Dated March 23rd

A reader has passed on the letter she received from her mother’s care home in Bagshot on March 23rd, the day the full lockdown was imposed.

This is with a great sadness I have to say that I have been informed by our Doctor today that NHS hospitals will not accept people over 70 years old if they have been tested positive with COVID 19, which means that these residents will be treated here, at Sunrise of Bagshot, and in case of deterioration they will go straight into palliative care. In these unprecedented times due to COVID-19 outbreak the NHS has no choice but to make tough decisions. I want to reassure you that we are doing everything possible to keep our residents safe and well protected.

At this moment we are working with Doctor to sign DNR forms for all of our residents. In order for us to complete this, I would ask you to send me a confirmation email if you agree for this to happen if your parent/loved one doesn’t have one.

If you have any questions or would like to discuss this with Doctor, please let me know and I will arrange telephone conversation.

Thank you for your understanding.

Horrendous. But at least this reader’s care home had the courtesy to consult her about the DNR form…

 

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Just now, sancho panza said:

I think tehre's beginning to be some real anger out there.

Still not enough.  My boomer parents (Sorry, but they are) will mostly agree with everything I say in a "Yes it's just dreadful" fashion then go and watch the BBC.  

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leonardratso

hehehe, boomers, got to love em.

The boomer-ish MIL last year clicked and started to see things for what they were, previously a BBC cheerleader, is now rabidly anti BBC and govt, this is an 80 year old woman - still all there mentally - calls out the reality TV BS for what it is as well regularly, Im really rather shocked at the change to be honest.

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My one person insubordination is going well.  I shopped in Tescos this morning and again no-one said anything about my lack of mask (6th shop without). 

I am slightly depressed that every other customer was masked up though.  I'm hoping my example will eventually be copied but they all seem to be very sheepish here.

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Noallegiance
5 hours ago, janch said:

My one person insubordination is going well.  I shopped in Tescos this morning and again no-one said anything about my lack of mask (6th shop without). 

I am slightly depressed that every other customer was masked up though.  I'm hoping my example will eventually be copied but they all seem to be very sheepish here.

Wish I had your balls. I'm currently going with a mask to avoid Gestapo treatment. Oh, and I need to feed my family.

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17 minutes ago, Noallegiance said:

Wish I had your balls. I'm currently going with a mask to avoid Gestapo treatment. Oh, and I need to feed my family.

There is no gestapo treatment. 

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  • 2 weeks later...

https://lockdownsceptics.org/2020/09/06/latest-news-126/

UK

The growth of the police state continues

Piers Corbyn solicitor has written to let us know that he was arrested again yesterday at an anti-lockdown rally in Sheffield.

Just to let you know that Piers Corbyn has been arrested and roughy handled by police in Sheffield today and was detained overnight while the police “gather evidence” that he is an organiser even though he was just a speaker.

We are starting to live in a Police State if this is how they treat a 73 year-old man for daring to speak at a peaceful political rally, in alleged breach of a Regulation that has never been debated in Parliament, for a non-imprisonable offence. To justify the arrest they claim it was done to out of necessity “for his own protection!” – a ludicrous assertion. It appears quite arbitrary, disproportionate and unnecessary, and conveniently prevents him speaking at the 12 noon rally today in Glasgow.

In my view it’s a shocking abuse of state power and should be utterly repellent to anybody who values the civil liberties that people in this country are meant to be proud of.

There was also an arrest of Kate Shemerani by police yesterday outside Downing Street, again for organising a political rally. Fortunately, she was released after her details were taken, but she also faces a £10,000 fine.

Will any single Member of Parliament from ANY Political Party be prepared to question what is being done on the streets of Britain when the Coronavirus Act is up for renewal on September 26th, to be debated for the very first time.

If not, what is our democracy worth?

A protestor who took part in the rally outside Downing Street yesterday confirms that the police made arrests.

Territorial Support Officers kettled our rally in Whitehall today and were quite brutal. Extinction Rebellion crew allowed free rein with no visible hassle. Not us. Kate Shemirani was collared and arrested for speaking on a megaphone.

You may think people like Piers Corbyn and Kate Shemerani are cranks, but why is their right to protest being curtailed while the police give BLM and XR protestors a free pass?

Stop Press: According to today’s Sunday Times, MPs are furious about XR’s blockade of printing plants on Friday night and are determined to stop similar protests in future. Boris has branded the blockades “completely unacceptable”.

 

In Australia

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Talking Monkey
13 hours ago, sancho panza said:

https://lockdownsceptics.org/2020/09/06/latest-news-126/

UK

The growth of the police state continues

Piers Corbyn solicitor has written to let us know that he was arrested again yesterday at an anti-lockdown rally in Sheffield.

Just to let you know that Piers Corbyn has been arrested and roughy handled by police in Sheffield today and was detained overnight while the police “gather evidence” that he is an organiser even though he was just a speaker.

We are starting to live in a Police State if this is how they treat a 73 year-old man for daring to speak at a peaceful political rally, in alleged breach of a Regulation that has never been debated in Parliament, for a non-imprisonable offence. To justify the arrest they claim it was done to out of necessity “for his own protection!” – a ludicrous assertion. It appears quite arbitrary, disproportionate and unnecessary, and conveniently prevents him speaking at the 12 noon rally today in Glasgow.

In my view it’s a shocking abuse of state power and should be utterly repellent to anybody who values the civil liberties that people in this country are meant to be proud of.

There was also an arrest of Kate Shemerani by police yesterday outside Downing Street, again for organising a political rally. Fortunately, she was released after her details were taken, but she also faces a £10,000 fine.

Will any single Member of Parliament from ANY Political Party be prepared to question what is being done on the streets of Britain when the Coronavirus Act is up for renewal on September 26th, to be debated for the very first time.

If not, what is our democracy worth?

A protestor who took part in the rally outside Downing Street yesterday confirms that the police made arrests.

Territorial Support Officers kettled our rally in Whitehall today and were quite brutal. Extinction Rebellion crew allowed free rein with no visible hassle. Not us. Kate Shemirani was collared and arrested for speaking on a megaphone.

You may think people like Piers Corbyn and Kate Shemerani are cranks, but why is their right to protest being curtailed while the police give BLM and XR protestors a free pass?

Stop Press: According to today’s Sunday Times, MPs are furious about XR’s blockade of printing plants on Friday night and are determined to stop similar protests in future. Boris has branded the blockades “completely unacceptable”.

 

In Australia

its all getting very sinister the way opposition against the covid response is being throttled whilst XR and BLM can carry on. Added to which the absurdity that I can go into a fairly packed restaurant and have a meal but cannot go to my routine hospital appointment and have to have a phone consultation, the whole thing is nuts.

Are hospitals still very quiet SP, the health of the nation must have deteriorated a fair bit because of the lockdown/ lack of access to services 

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14 hours ago, sancho panza said:

Will any single Member of Parliament from ANY Political Party be prepared to question what is being done on the streets of Britain when the Coronavirus Act is up for renewal on September 26th, to be debated for the very first time.

Peter Hitchens column in the Mail on Sunday:

"The regulation used to fine Mr Corbyn - 5b of the Coronavirus Act - was hastily made  law the day before the demonstratoion was held.  It was introduced under an emergency procedure and was neither debated nor given even the most cursory scrutiny by any parliamntary process."

 

See also this about the Great Reset. We are being played:

https://www.zerohedge.com/geopolitical/covid-19-scamdemic-part-2-enabling-technocratic-parasite-class-great-reset

Edited by janch
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  • 2 weeks later...

Three eminent scientists go through the issues and explain why there will be no second wave, why PCR testing raises lots of false positives,why it's liekly we allready had 30% immunity,why kids don't get infected,why Ferguson's modelling was based on false premises etc etc

I weep at the sheer unbridled incompetence of this govt.

Looks like the scientific establishment is gearing up for a fight.

Hope they can get fegruson to publish his model for peer review.

 

 

https://lockdownsceptics.org/addressing-the-cv19-second-wave/

Paul Kirkham, Professor of cell Biology and Head of Respiratory Disease Research Group at Wolverhampton University

Dr Mike Yeadon, former CSO and VP, Allergy and Respiratory Research Head with Pfizer Global R&D and co-Founder of Ziarco Pharma Ltd

Barry Thomas, Epidemiologist

Screenshot-2020-09-08-at-02.25.34-1024x6

Contents

Executive Summary
Background
Mortality and critical care
A complete event of the pandemic
Epidemic outbreaks
Population susceptibility
Immunity threshold
The PCR Test
Expectations of a second wave
Spain and France
References

Executive Summary

Evidence presented in this paper indicates that the severe acute respiratory syndrome coronavirus 2 pandemic as an event in the UK is essentially complete, with ongoing and anticipated challenges well within the capacity of a normalised NHS to cope. The virus infection has passed through the bulk of the population as a result of wholly natural processes and evidence indicates that in the UK and other heavily infected European countries the spread of the virus has been all but halted by a substantial reduction in the susceptible population. This has occurred because the level of infection required to introduce enough immunity into the population to reduce the reproduction number (R) permanently below 1 occurred at markedly lower infection rates and loss of life than had been initially anticipated. The evidence presented in this paper indicates that there should be no expectation of a large scale ‘second wave’ with smaller localised outbreaks when the virus contacts pockets of previously uninfected populations.

Current mass testing using the PCR test is inappropriate in its current form. If it is to continue, then results and reporting should be refined to meet the gold standard of testing methodology to give clinicians improved information so that they are able to make appropriate clinical decisions. Positive tests should be confirmed by testing a second sample and all positive tests should be reported along with the Cycle Threshold (Ct) obtained during the test to aid assessment of a patient’s viral load.

It is recommended that a greater focus be placed on evidence-based medicine rather than highly sensitive theoretical modelling based on assumptions and unknowns. Current evidence allows for a greatly improved understanding of positive infectious patients and using the evidence to improve measurements and understanding can lead to sensitive measurements of active cases to give a more accurate warning of escalating cases and potential issues and outbreaks.

Background

Based upon guidance from NHS England, our primary and secondary care service across the country are currently following protocols to limit access to care due to the dangers of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2 or COVID-19) pandemic. Whilst work has begun to restore NHS services (the “restoration”), there remains a strong focus on preparing for a second wave as implied by the Imperial College epidemiological model designed by Professor Neil Ferguson and his team. While this model may have had some limited value when we were faced with a novel virus outbreak, the evidence that has emerged over recent months along with detailed analysis of previous outbreaks implies that the model that is still being followed is unreliable and not consistent with both previously measured systems and current evidence. This paper outlines the evidence and data we have gathered to support a change in focus to further expedite the return of both primary and secondary care to full capacity.

The COVID-19 pandemic has undoubtedly allowed for some very positive and rapid changes within NHS pathways, protocols and services which should be maintained. However, the current reduction in delivered primary care activity, referrals and elective care gives concern as to the degree of ‘collateral damage’ being caused in patients not receiving the diagnostic and ensuing care they should be receiving at the earliest possible stage of intervention. While there has been a very specific focus on the cancer and cardiology services, similar negative impacts can be seen across most services with, for example, neurological, dermatological and renal patients all presenting with more severe disease due to delays in receiving both diagnosis and treatment.

Mortality and Critical Care

National weekly mortality data is useful for looking at the effect of the COVID-19 pandemic. The past four years data were used for comparison purposes and to calculate upper and lower control limits (based on two standard deviations).

This shows that in the pandemic peak (April 17th to 30th) more than twice the number of seasonal average deaths occurred, with the number of deaths above the upper control limit from March 27th through to June 12th, totalling 44,895 excess deaths. Since June 26th the number of weekly deaths has now fallen so it is not only below the weekly average but has regularly dropped below the lower control limit, showing that we are now at the lowest number of weekly deaths recorded in many years.

weekly-all-cause-1024x451.png

Over the last three months since lockdown measures started easing on the May 10th there has been no increase in weekly deaths. On the contrary, these have continued to fall.

Another useful measure of disease impact is the Adult Critical Care Bed Occupancy which showed a peak in bed demand between April 7th and 23rd with the number of patients occupying critical care beds significantly higher than our national baseline capacity. However, by the end of May the occupancy had dropped back to pre-COVID-19 levels, well below the national baseline capacity and has shown no statistical change since.

beds-1024x326.png

Restrictions have been progressively eased across the country for over three months. A continuation of the virus would be expected to manifest itself as an increase in both Critical Care bed occupancy and national All-Causes Mortality statistics. This has not been the case in either critical indicator.

A Complete Event of the Pandemic

There are very good reasons to believe that the population of the UK and of many heavily infected countries have arrived at a position where the prevalence of the virus is low and probably falling further because the reproduction number (R) has been below 1 for several months. We understand the term ‘herd immunity’ can raise hackles in some quarters of the media. However, it might be more acceptably expressed by stating that the proportion remaining of the population who are susceptible to the virus has fallen sufficiently far that a sustained and growing outbreak of disease is no longer supported. This end state is not at all new or, in our view, controversial. It is how mammals – specifically jawed vertebrates – learned to live with the thousands of viruses that infect every living organism on the planet, not just us, but even plants, fungi and bacteria.

We are of the view that a continued focus primarily on the virus flows from responding to what we are concerned is a seriously flawed transmission model. We are told that only seven per cent of the population have antibodies to the virus and it is implied that this represents the proportion of the population who have so far been infected. The model assumes that we started with 100% susceptibility, because the virus is new, therefore the virus hasn’t gone away and must sooner or later return. This is the basis of all the second wave fears we hear about.

However, we do not believe the model is correct and our assertions and inferences are based upon recently published science, some in highly eminent journals and some by researchers in pre-review online servers which have this year become crucial in keeping pace with emerging science.

While published data on deaths ‘with’ COVID-19 is dependent on testing regimes and therefore liable to inaccuracy due to missing information – for example undetected asymptomatic patients – the data does allow a sound approximation of the flow of the outbreak. Inspecting the daily COVID-19 deaths vs. time curve for the UK we see a Gompertz-type curve (Rypdal and Rypdal, 2020) which are typical of natural, biological phenomena, well documented in biomedical scientific papers over the last 40 years. Note the lack of discontinuities in the curve, suggesting no effective interventions have interrupted its development.

gompertz-death.png

Epidemic Outbreaks

The Gompertz-type plot seen above, which is formed by a single surge in activity, often followed by smaller minor upturns as the disease reaches new populations is typical of previous virus outbreaks that have been well documented, none of which have demonstrated a significant second wave even though control methods were used to prevent the spread of disease in each case.

For example, below we see in the MERS CoV outbreak of 2015 what appears to be a significant double wave. However, it is actually multiple single waves affecting geographically distinct populations at different times as the disease spreads. In this case the first major peak was seen in Saudi Arabia with a second peak some months later in the Republic of Korea. Analysed individually, each area followed a typical single event Gompertz curve.

mers-cov.png sk-mers.png

Similarly, when we look at the SARS outbreak of 2003 the initial identification of an apparent double wave when looking at world wide data is actually multiple single events or waves in disparate locations each following the typical Gompertz-type curve.

2003-sars.png guandong-1024x388.png

Population Susceptibility

It is now established that at least 30% of our population already had immunological recognition of this new virus, before it even arrived (Le Bert et al, 2020; Braun et al, 2020; Grifoni et al, 2020). COVID-19 is new, but coronaviruses are not. There are at least four well characterised family members (229E, NL63, OC43 and HKU1) which are endemic and cause some of the common colds we experience, especially in winter. They all have striking sequence similarity to the new coronavirus. A major component our immune systems is the group of white blood cells called T-cells whose job it is to memorise a short piece of whatever virus we were infected with so the right cell types can multiply rapidly and protect us if we get a related infection. Responses to COVID-19 have been shown in dozens of blood samples taken from donors before the new virus arrived. The most recent paper by Mateus et al (2020) was published in the journal Science in August and supports the previous findings of Le Bert et al (2020). Importantly, only Mateus performed detailed epitope mapping and found that epitopes present in each of the known endemic coronaviruses share sequence homology or close similarity to those in the new virus. Prior to this, three other groups including immunologists in Germany, Sweden and the USA each independently published similar findings (refs as above and discussed in Sewell, 2020). These papers showed this pre-immunity is geographically widespread and prevalent within each population studied, but it was only the Mateus paper that gave us the understanding as to why and how. It had previously been suggested that pre-pandemic immune responses in circulating T-cells might have occurred following exposure to one or more of the endemic coronaviruses. Mateus, by using parts of these endemic coronaviruses which also exist within COVID-19 confirmed this.

We understand that objections might be raised about the clinical correlates of this T-cell recognition. While that is a fair challenge, it would be unreasonable to dismiss it and assume is has no relevance. This is because this is how T-cell memory works (for example, Ling et al, 2020 show that convalescent COVID-19 patients analogously display exactly these T-cell responses) and more importantly because we have solid evidence in the case of SARS that those expressing T-cell recognition of that coronavirus were resistant to it. In a study of 23 people who survived SARS in 2003, every single one had memory T-cells that recognised the SARS virus 17 years later. (Le Bert et al, 2020). The T-cell response was consistent with measurements taken after vaccination with approved vaccines for other viruses. As important, these T-cell responses also develop even in recovering patients infected with the new virus but who were asymptomatic (Sekine et al, 2020).

In conclusion, we believe it is reasonable to take from this body of work that those displaying vigorous T-cell responses to this family of coronaviruses are resistant to or immune from infection. They are distinct from the others in the population who do not have these T-cell responses and are therefore susceptible to a new virus.

Immunity Threshold

Transmission models, such as the one used by the Imperial team, are highly sensitive to the input parameters they are based on and we argue that a modification of the current model should be applied with, at most, 70% initial population susceptibility. This is a conservative value since current literature finds that between 20% and 50% of the population display this pre-pandemic T-cell responsiveness, meaning we could adopt an initially susceptible population value from 80% to 50%. The lower the real initial susceptibility, the more secure we are in our contention that a herd immunity threshold (HIT) has been reached.

However, our concerns with the Imperial model are not limited solely to T-cell memory mediated reduction in initial susceptibility. This is because there are factors other than T-cell mechanisms which alter a person’s susceptibility to the virus. We now know that children, especially young children, appear harder to infect and/or they are less affected by the virus. To do us harm, viruses need to get inside our cells. To do that, they exploit as ‘grappling hooks’ receptors on the outside of those cells – in the case of the new virus, and at high speed, scientists determined it is an enzyme called ACE2. It turns out that the levels of ACE2 are highest in adults and much lower in children, becoming progressively lower the younger they are (Lingappan et al, 2020). That is a fortunate finding indeed, and goes some way in explaining why children have been relatively spared. In addition, other groups have shown that infectivity is significantly reduced in individuals with the O-blood group (Wu et al, 2020; Ellinghaus et al, 2020). There are approximately eight million children aged 0-10 in the UK and 12.7 million aged 0-15. These cohorts represent approximately 11.9% and 19% of the UK population, respectively

Taking this into account it is, in total, at least 35%, and likely to be significantly more of the population who are resistant or immune to the virus, meaning that they will neither get ill nor participate significantly in viral transmission (Lee, 2020). This is crucial to understanding where we are with respect to the epidemic in the UK and the potential for a second wave of infections.

The proportion of the population that need to be resistant to an infection, in order to stop it spreading, depends on the proportion who were originally susceptible and the initial reproduction number, or R0. If 100% truly were susceptible, then epidemiology suggests that 65% would have to be infected for the herd immunity threshold to be reached, given the initial estimates of R0. That would have resulted in very many more deaths than have been measured. But if, as we are now reasonably sure, a much lower initial percentage was susceptible, it takes far fewer people to catch the virus before there are too few susceptible people remaining within the population for the virus to be able to find the next person to infect.

Recent seroprevalence studies, which measure the proportion of the population displaying antibodies to the novel virus, are widely assumed to show the proportion of the population which has been infected. However, the observation that, for example, only 17% of Londoners have antibodies is not the same as saying only 17% have been infected (though the media often wrongly assumes it does). It is important to appreciate that much of the early serological studies were conducted on hospitalised patients who, by definition, are the most ill cohort. In such patients the majority do seroconvert (eg Theel et al, 2020). In mildly symptomatic and asymptomatic patients, a lower proportion seroconvert (Long et al, 2020). This is because the antibody system is but one of several tools our immunology has to defend us. There have been a number of papers illustrating this important principle. Long et al (2020) find that almost half of previously infected individuals are no longer seropositive a few months later. Gallais (2020) shows that none of the familial contacts of those testing positive to SARS-CoV-2 went onto to develop antibodies.

A reasonable hypothesis is that the lower intensity of immunological challenges tends to rely less on the generation of antibodies and more on innate and cellular responses. This means that a factor of two-fold and possibly higher would need to be applied to population serology data in order to better approximate the infected population. If 7% is the mean for UK, then perhaps 14-21% of the population has actually been infected (which would imply, very approximately, 9-14 million people infected). The authors recognise that the exact number in this example is speculative, but conversations with immunologists indicate that this principle is widely accepted as reasonable for community infection where viral load varies widely and contrasts markedly with seroconversion after vaccination, where the goal is close to 100%.

Interestingly, this question of what percentage of the population have been infected can be approached using a different methodology. Numerous estimates have been made of the infection fatality ratio (IFR) for this new virus. Naturally, it varies depending on the population under study as well as the methodology used and, accordingly, researchers have arrived at a wide range of estimates for IFR. The Centre for Evidence-Based Medicine has done much work in this area and their current estimate is 0.1-0.4% (Oke and Heneghan, 2020). Let us take a midpoint value, especially as for months the US CDC displayed a value for IFR of 0.26% on their website. This implies that for every death from COVID-19, there were a preceding 100/0.26 or ~400 infections. The UK has suffered approximately 42,000 such deaths which, to a first approximation using IFR, implies 16.8million infections, or 25% of the population having been infected.

Consequently, two different and independent analytical approaches provide estimates that are at least in the same range for total population having been infected (overlapping at approximately 20%), and this is crucial in the argument put forward here. Other, theoretical epidemiological studies show that, with the extent of prior immunity that we can now reasonably assume to be the case, only 15-25% of the population being infected is sufficient to bring the spread of the virus to a halt (Lourenco, 2020; Gomez et al, 2020). Importantly, we emphasise there are additional schools of epidemiological work which show that variation in likelihood of becoming infected itself can greatly reduce the so-called herd immunity threshold and that this can be reached at even lower proportions of the population having been infected (e.g. Aguas, 2020).

We saw early on in the pandemic that the number of daily deaths rapidly soar and at that time did we not know where and when it would stop rising. It has been evidenced previously that the most easily infected people got infected earliest (see Gomez et al, 2020). Humans vary hugely, not only in our responses to viruses, but also in the ease or difficulty the virus experiences as it tries to invade us. The most susceptible were those already elderly and/or ill, some very ill, and so we saw very high death rates initially. Once that super-susceptible group were removed from the pool of susceptible individuals by the virus, it began a slower march through everyone else, slowing all the time, as the remaining population’s susceptibility fell continually towards the herd immunity threshold. That is where our evidence indicates we are now and why the virus is disappearing from the environment.

It is important to see this document in light of information available elsewhere in the world. It has widely been observed that in all heavily infected countries in Europe and several of the US states likewise, that the shape of the daily deaths vs. time curves is similar to ours in the UK. Many of these curves are not just similar, but almost super imposable. Italy, France, Spain, Sweden and the UK, for example (OWID, 2020). The shape of the deaths vs. time curve implies a natural process and not one resulting mainly from human interventions, given the widely varying non-pharmaceutical interventions in those countries. Taking this and applying it more widely, the very strong similarities of UK data with that of nearby countries which employed different responses yields another conclusion – that none of the interventions altered the broad course of the pandemic event. Further, it is reasonable to conclude that the pandemic event has ended in those countries, too. Famously, Sweden has adopted an almost laissez faire approach, with qualified advice given, but no generalised lockdowns. Yet its profile and that of the UK’s is very similar. The officials in Sweden appear to be of the view that their population has closely approached or in some places reached what they term herd immunity, with R persistently lower than 1.

pops-deaths-1024x547.png

The PCR Test

The PCR test for the virus is good enough to confirm infection in someone with symptoms. “Is it flu or is it COVID-19?” is a question easily answered. What it is very poor at, however, is what is being asked of it now, namely estimating the percentage of people who are currently infectious in the community. We do not know exactly what the false positive rate is, but it is widely believed to be greater than the actual, remaining prevalence of the virus (Heneghan, 2020), which is around 1:2000, or 0.05%. (ONS prevalence survey Aug 14th 2020). The result of continuing to use this test alone on a massive widescale screening program is inevitably to generate a high proportion of false positives. The problem of using any assay to conduct surveillance on a low prevalence virus with a PCR test has been widely discussed (Heneghan, 2020). Under present parameters, even accepting an unlikely 0.1% False Positive rate and a prevalence of 0.1%, more than half of the positives are likely to be false, potentially all of them. It is the opinion of the authors that the false positive rate is higher and the prevalence lower than this. Consequently, it is impossible for the positives to be much other than false. A recent letter to the British Medical Journal (Healy, 2020) exemplifies the extent of harm that actually arose in a setting in which all but one of the positives ended up being false positives. This resulted not only in considerable time and money wasted by surgeries, but also other medical issues being delayed. It is not rational and may even be dangerous to use these results to drive policy. Note that recent so-called ’spikes’ were never accompanied or followed by people getting ill, going to hospital and dying in elevated numbers. Consequently, it is possible that most of the positives from mass testing are either false positives or ‘cold positives’ (fragments of real virus which are not intact and incapable of replication or of causing disease or infecting others) and therefore begs the question of whether mass testing of patients without symptoms is in fact helpful or misleading? It may be of relevance to note that, on August 24th the US CDC changed its guidance on when PCR testing is appropriate. They now recommend not testing people with no symptoms who are not contacts in a contact-tracing activity.

There are practical alternatives to mass testing. For example, calls to the NHS111 service captures all reports of what is termed ‘influenza-like illness’. Change in this parameter is likely to be a much more sensitive measure of the presence of increasing prevalence of SARS-CoV-2 infection than flawed PCR testing without modifications. Obviously, and perhaps it has already happened, there is the potential for emerging influenza to complicate the picture. A modification to the strategy involving PCR testing which would easily resolve any uncertainty is this: every positive test result is followed up as quickly as possible, ideally within 24 hours of the positive result, and every one is retested. If this is done, almost all the false positives will be removed. We predict there would be few genuine positive results remaining. But even here, it is important to recall what it is that the PCR test measures, and it is simply the presence of partial RNA sequences present in the intact virus. This means that even a true positive does not necessarily indicate the presence of viable virus. In limited studies to date, many researchers have shown that some subjects remain PCR-positive long after the ability to culture virus from swabs has disappeared. We term this a ‘cold positive’ (to distinguish it from a ‘hot positive’, someone actually infected with intact virus). The key point about ‘cold positives’ is that they are not ill, not symptomatic, not going to become symptomatic and, furthermore, are unable to infect others. As each PCR test that is carried out returns the Cycle Threshold (Ct) used to obtain a positive result, it is important that this Ct is reported with every positive result. The Ct gives strong evidence of the viral load and aids clinicians in determining if a patient has a “hot” infectious positive result or a “cold” non-infectious positive result. Gniazdowski et al (2020) studied 161 positive PCR test samples with a Ct value below 23 that yielded 91.5% of virus isolates and the study showed a strong correlation between recovery of SARS-CoV-2 infectious virus on cell culture and Ct values. Ct values above 30 returned negative cultures in all except one case.

ct-value-1024x660.png

Expectations of a Second Wave

Daily deaths from and with COVID-19 have almost ceased, having fallen over 99% from peak. All the numbers monitored carefully fall like this, too: the numbers being hospitalised, numbers in hospital, number in intensive care – all are falling in synchrony from the April peak. Viral evidence historically tells us that you don’t generally get infected by the exact same virus twice, certainly not within a short period of time. It’d be a poor immune system which lets that happen and we’d probably not have made it as a species into the 21st century if that’s how it worked. So there’s an expectation of some duration of immunity. It needs studying, but our experience and evidence for coronaviruses (Le Bert et al, 2020) suggests that if you have memory T-cells, durability can be very long lasting. This study showed that people still had robust T-cell responses in 2020, 17 years after the first SARS outbreak back in 2003. The concerns people have expressed about falling antibody levels underscores a lack of knowledge about acquired immunity. It is not efficient nor required for immunity to maintain high levels of antibodies to everything to which you are immune. Instead, cellular memory enables very rapid re-generation of antibodies upon re-encounter with the antigen, if that is required to defend the host. Alternatively, innate and cellular memory responses can be sufficient.

The NHS currently remains ‘COVID-19 ready’ in preparation for an expected second wave, a highly unlikely scenario based upon an initial model with highly sensitive input variables that we already know to be inaccurate. The evidence we’ve presented leads us to believe there is unlikely to be a second wave and that while there have been apparent multi-‘wave’ respiratory viruses in the past, notably 1918-20, in many cases it became clear that this was either different populations being infected at different times or in some cases multiple different organisms involved. There is no biological principle that leads us to expect a second wave based on the accumulation of data over the past six months. Instead, it is likely there will be local, small and self-limiting mini-outbreaks as areas previously unexposed come into contact with the virus.

Spain and France

So what is happening in terms of second wave concerns in France and Spain? As the rate of hospitalisations, ICU utilisation and the daily death rate from COVID-19 all decayed steadily, it appears that several but not all countries have greatly expanded their testing capacity in the broader population of people who are not showing any symptoms of infection. We contend that the many claims in the media for outbreaks, spikes and second waves are all artefacts of amplified rates of testing. It should be noted that illness, hospitalisations and deaths have not reversed in any clear and sustained manner. Specifically, careful examination of the weekly all-causes mortality data in France is completely clear. Six weeks into an apparent surge of cases, the number of deaths remain completely flat and normal, in all age bands (as of mid-August when this document was written).

fr-cases-1024x650.png fr-deaths.png es-cases-1024x663.png es-deaths-1024x641.png uk-cases.png uk-tests.png uk-deaths.png

References

Aguas, et al (2020). Herd immunity thresholds for SARS-CoV-2 estimated from unfolding epidemics. medRxIV https://doi.org/10.1101/2020.07.23.20160762.

 

Braun, et al. (2020). Presence of SARS-CoV-2 reactive T cells in COVID-19 patients and healthy donors. medRxIV https://doi.org/10.1101/2020.04.17.20061440

 

Ellinghaus et al. (2020) Genomewide Association Study of Severe Covid-19 with Respiratory Failure. New Eng. J Med. DOI: 10.1056/NEJMoa2020283

 

Gallais, (2020). Intrafamilial exposure to SARS-CoV-2 induces cellular responses without seroconversion. medRxIV https://doi.org/10.1101/2020.06.21.20132449.

 

Gomez et al. (2020). Individual variation in susceptibility or exposure to SARS-CoV-2 lowers the herd immunity threshold. MedRxIV https://doi.org/10.1101/2020.04.27.20081893

 

Grifoni et al. (2020. Targets of T Cell Responses to SARS-CoV-2Coronavirus in Humans with COVID-19Disease and Unexposed Individuals. Cell 181, 1489–1501. https://doi.org/10.1016/j.cell.2020.05.015ll

 

Healy, B (2020). Covid-19 testing, low prevalence and the impact of false positives. Brit Med J. 2020;369:m1808.

 

Long, et al. (2020). Clinical and immunological assessments of asymptomatic SARS-CoV-2 infections. Nature Med 26, 1200-04.

 

Heneghan (2020). How many Covid diagnoses are false positives? The Spectator, July 20 2020.

 

Le Bert et al (2020) SARS-Cov-2 specific T cell immunity in cases of Covid19 and SARS and uninfected controls. Nature. Doi 10.1038/s41586-020-2550-z

 

Lee & Raszka (2020). COVID-19 transmission and children: the child is not to blame. Pediatrics, e2020004879 DOI: 10.1542/peds.2020-004879.

 

Ling, et al (2020). Detection of SARS-CoV-2-Specific Humoral and Cellular Immunity in COVID-19 Convalescent Individuals. Immunity 52(6), 971-77.

 

Lingappan et al (2020). Understanding the age divide in COVID-19: why are children overwhelmingly spared? Am. J. Physiol (Lung Cell Molec. Physiol) https://doi.org/10.1152/ajplung.00183.2020

 

Lourenco et al (2020). The impact of host resistance on cumulative mortality and the threshold of herd immunity for SARS-CoV-2. MedRxIV https://doi.org/10.1101/2020.07.15.20154294

 

Mateus et al (2020) Selective and cross-reactive SARS-CoV-2 T cell epitopes in unexposed humans. Science. DOI: 10.1126/science.abd3871

 

Oke& Heneghan (2020). Global Covid-19 Case Fatality Rates. https://www.cebm.net/covid-19/global-covid-19-case-fatality-rates/

June 9 2020 update.

 

ONS coronavirus survey (Aug 14 2020). https://www.ons.gov.uk/peoplepopulationandcommunity/healthandsocialcare/conditionsanddiseases/bulletins/coronaviruscovid19infectionsurveypilot/latest

 

OWID (our world in data: display UK, Sweden & France, confirmed daily deaths, log plot per million) https://ourworldindata.org/coronavirus-data-explorer?yScale=log&zoomToSelection=true&time=2020-03-02..latest&deathsMetric=true&interval=smoothed&aligned=true&perCapita=true&smoothing=7&country=TWN~GBR~SWE~FRA&pickerMetric=location&pickerSort=asc

 

Rypdal & Rypdal (2020) A parsimonious description and cross-country analysis of COVID-19 epidemic curves. https://arxiv.org/pdf/2008.02475.pdf

 

Sekine et al. (2020). bioRxiv preprint doi: https://doi.org/10.1101/2020.06.29.174888.

 

Sewell, H. (2020). BMJ 2020;370:m3018.

 

Theel et al (2020). The Role of Antibody Testing for SARS-CoV-2: Is There One? J. Clin Microbiol, 28(8), 1-7.

 

Wu et al (2020) Association between ABO blood groups and COVID-19 infection, severity and demise: A systematic review and meta-analysis. Infection , Genetics and Evolution. Doi 10.1016/j.meegid.2020.104485

 

Wood (2020). Did COVID-19 infections decline before UK lockdown? https://arxiv.org/pdf/2005.02090.pdf

 

Gniazdowski V, Morris P, Wohl S et al. Repeat COVID-19 molecular testing: correlation with recovery of infectious virus, molecular assay cycle thresholds, and analytical sensitivity. medRxiv 2020.08.05.20168963; doi: https://doi.org/10.1101/2020.08.05.20168963

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Is it incompetence or are they being bribed?

https://www.armstrongeconomics.com/world-news/corruption/belarusian-president-claims-imf-world-bank-offered-him-a-bribe-to-impose-covid-restrictions/?utm_source=Newsletter&utm_medium=Email&utm_campaign=RSS

Belarusian President Aleksandr Lukashenko said last month via Belarusian Telegraph Agency, BelTA., that World Bank and IMF offered him a bribe of $940 million USD in the form of “Covid Relief Aid.” In exchange for $940 million USD, the World Bank and IMF demanded that the President of Belarus:

• imposed “extreme lockdown on his people”
• force them to wear face masks
• impose very strict curfews
• impose a police state
• crash the economy

Ivor Cummins re-tweeted this; https://www.technocracy.news/world-economic-forums-techno-totalitarian-roadmap/

As the days go by these conspiracy theories seem to make more and more sense!

Edited by Viceroy
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https://lockdownsceptics.org/covid-19-parliamentary-brief

Whilst my note on the false positive rate (FPR) made its way into the corridors of power, the Health Department’s response was at once dismissive but innumerate. Fortunately, not all parliamentarians are so easily fobbed off and one has asked me to prepare a brief, which is why the following is not in the usual format.

It appears that the number of amplification cycles used in PCR tests, whether there is any quality control, the false positive rate (for both Pillar 1 and Pillar 2) and the incidence of the disease are all state secrets. However, what is clear is that none of those wielding the controls understand the maths.

Both Secretary of State, Matt Hancock (who says the FPR is “under 1%”) and Baroness Harding’s chief medical advisor, Dr Susan Hopkins (definitely less than 1-in-100 and more likely 1-in-1000) believe the FPR is so low as to result in what Hancock calls a “very small proportion of false positives”.

In fact, even a FPR as fancifully low as 0.1% (and there is a mass of evidence to suggest it is 10-20x higher than that) would mean that 4 out of 5 positives were false.

1% false positive rate does NOT mean 1% of positives are false

Transcript, Matt Hancock TalkRadio interview with Julia Hartley-Brewer, 8.42am Fri 18th Sept

JHB: “What is the FPR on the testing we’re doing in the community?

MH: Under 1%.

JHB: It’s under 1%. Even around under 1%… do you know the exact rate?

MH: It’s um.. well, under 1% means that for all the positive cases the likelihood of one being a false positive is very small. 

JHB: I understand what under 1% means. But do you have the exact figure for what it is?

MH: We do. We do. I don’t have it in my head. I know that the specificity is what it’s called of the PCR test is over 99%… But Julia, I can see the thrust of the questions and what I can tell you is that we take into account, of course we do, the issue of the very small proportion of false positives (my bold).

If incidence is < the FPR, most positives are false

The Secretary of State for Health, Matt Hancock, seems to think that a false positive rate (FPR) of 1% means that 1% of positives are false but what it actually means is that 1% of all negatives will test positive. If the incidence is lower than the FPR, more than half of all positives are false. Hancock is dangerously and complacently unaware that when incidence is low, up to 99% of all ‘cases’ might be false positives. This relationship is illustrated by the matrix below (FPR down the left-hand side and incidence along the top).

Matrix: % of ‘cases’ that are false positive

fpr-matrix-1024x293.png

Results from a pilot survey of 35,000 people by ONS ‘academic partners’ found household incidence peaked on 26 April at 0.32% (right-hand column above) before ‘stabilising’ at 0.08% (centre column) by the end of the study period on 28th June. However, after that, NHS daily ‘estimated admissions’ fell another 80% from 246 on 28th June, to < 50 by late August, which implies that incidence declined to 0.016%, a level that renders 98-99% the 1,200+ daily ‘cases’ reported at that time ‘false’ (see matrix above).

worked-example-fpr-1024x299.png

Positives are not ‘cases’

By 1st September, UK ‘cases’ had risen 2.5x from the 8th July low, yet hospitalisations (incidence) were down by three quarters. Which is the signal and which the noise? In April we were getting 5,000 cases a day from less than 20,000 tests (25%). Today we are getting 4,400 ‘cases’ from 235,000 tests (1.9%) 70% of which are being analysed by people who weren’t even doing this job in April.

The signal and the noise

The very low level of NHS diagnoses (only about 37 a day by early September) compared to the large number of Pillar 2 tests suggests that > 90% of Pillar 2 tests are taken by people who are asymptomatic (demand is now 4x capacity). So, since 28th June, only 6.5% (3,638) out of 56,047 ‘cases’ during July and August were confirmed by NHS England diagnoses. If most Pillar 2 subjects are asymptomatic, then their selection is close to random and the consistent 2% Pillar 2 positivity is indicative of the underlying FPR (making the Pillar 2 FPR up to 200x higher than the 0.1% that ONS assumes for NHS-lab Pillar 1) and explains the huge discrepancy between positives (top), which are almost back to April highs and the hard data on hospitalisations (middle) and deaths (bottom), which are barely off the floor. The plan to increase tests to 10m per day will guarantee that all tests are effectively random (i.e. asymptomatic), so we will keep finding ever more ‘cases’, no matter the incidence.

signal-noise-1024x837.png

Amplification: why the analytical FPR is ~1%, not 0.1%

PHE consultant Dr Susan Hopkins provided Baroness Dido Harding with a “rapid off my head (sic) response that could be used” clearly intended to dismiss the warnings about false positives out of hand, rather than invite further informative discussion. Hopkins confirmed a “population prevalence < 0.02%” whilst insisting that all serological tests (Pillars 1, 2 and 4) had FPRs that are “definitely less than 1 in 100 and… more likely 1 in 1000.” Yet she did not seem to understand the mathematical implications. With 0.02% incidence, a FPR of “1 in 1000” means 83% of positives are false, whilst “1 in 100” means 98% would be. Does H3 (Hancock, Harding and Hopkins) seriously not know this?

Amplifying the inaccuracy

However, there is very little chance that the FPR is as low as 1-in-1000 for two important reasons. The first is that the cycle threshold (Ct) used to establish the original ONS 0.1% FPR must have been far lower than the Ct in use today. Fear that the false negative rate (FNR) is higher than the FPR has led to the increased amplification of swab samples far beyond the accurate limit of 24 Ct or even the conventional PCR max of 30 Ct (i.e. 2 to the power of 30 = 1 billion DNA copies). Amplification increases sensitivity (fewer false negatives) but also the specificity (more false positives) until, ultimately, all (negative) samples would test positive.

The relationship between Ct (amplification) and accuracy (measured here by the successful isolation of live virus in cell culture) is shown in the chart below. The accuracy of the test falls away sharply above 24 Ct (17 million copies) and > 33 Ct (8.5bn copies) zero live cultures can be obtained in vitro (i.e. in the absence of any functional immune system) suggesting no viable virus and zero chance of a human with a functioning immune system being either infected or infectious. Yet pillar 2 PCR assays are amplified all the way up to 42-45 Ct (35 trillion copies), 2 million times more than the Ct 24 accurate (> 90%) live virus detection cut-off point and 30,000x the maximum ‘safe’ limit used by experienced lab researchers. The pillar 2 use of very high Ct amplification is also why previously infected but recovered cases are also (wrongly) testing ‘positive’, sometimes weeks later.

amplification-v-accuracy-1024x620.png

Operational FPR is always much higher than analytical FPR

The second reason why the FPR will be substantially above the ONS best-case, 1-in-1000 is because even if we went back to reduced amplification to bring the analytical FPR back down to 0.1%, there is nothing that can be done to control the pillar 2 ‘operational’ FPR.

Analytical vs operational FPR

RT-PCR equipment is sensitive, requires delicate handling and inaccurate enough to be marked ‘not for diagnostic use’. Unlike the experienced NHS labs which carry out < 30% of tests (pillar 1), 70%+ of tests are carried out in the private sector by the Lighthouse Labs network (pillar 2) which was assembled from scratch in May and is run by Deloitte. Most machines were co-opted from universities (on the promise of replacement upgrades later) by labs unfamiliar with the hardware, often without the supporting software instructions, to be run by inexperienced teams, using emergency approved testing kits (now numbering more than 500), synthetically validated and provided by new suppliers of unproven, not to say dubious, quality.

Operational (real world) FPR is always going to be far higher than the analytical (ideal world) FPR; but especially when handled by inexperienced operators, using unfamiliar equipment, under stressful conditions (pillar 2 tests have risen from zero to 173,000/day in less than 5 months) due to:

  1. contamination of ‘clean room’ test kits during manufacture & distribution
  2. contamination of equipment or reagents during sampling
  3. ‘aerosolization’ can cause sample cross-contamination during swab extraction
  4. cross-reaction with other genetic material during DNA amplification
  5. contamination of the DNA target

The ‘expected’ FPR

Consequently, to believe in an operational FPR as low as 0.1% flies in the face of all previous experience. A review of 35 previous EQAs of RT-PCR RNA assays with negative samples, for 13 separate pre-Covid-19 viruses, found that the median FPR was 2.5% (25x higher than the ONS’ wishful-thinking) with an interquartile range of 1.2-4.0% (12x-40x higher).

Five ways to find the FPR

Ironically, it would be quite easy to establish what the pillar 2 FPR was, using any one of five different approaches, though government seems unwilling to provide the data.

  1. Simplest would be to re-test all positives, preferably twice and in different labs to the ones producing the initial result. The proportion of positives corroborated will give you a rough estimate of the FPR.
  2. You could seed definite negatives (eg. saline) in the test kits at the manufacturing stage and see how many came back positive.
  3. You could test positives for viral protein.
  4. The Sanger Institute could report what proportion of ‘positives’ they are able to gene sequence (according to Hopkins this will be published shortly but if it doesn’t include the number of invalid and/or unviable, then these results will be useless.
  5. Culture the samples to detect what Hopkins calls “live or viable virus.” Once again, unless this is published data and includes the relevant Ct amplification necessary, compared to that used in pillar 2 positive tests, such results will be uninformative (see Ct chart above).

The ‘second wave’

The idea behind lockdown was to ease the ‘burden’ on the NHS but as at 17th September 2020 there were 1,081 diagnosed COVID-19 patients in hospital, significantly less than one patient for each of the UK’s 1,257 hospitals. The woeful state of statistical understanding underpinning the Government’s dependence on positive pillar 2 tests notwithstanding, what are we to make of the September surge in positive tests? Unless corroborated by hard data, like NHS diagnoses, hospital admissions and, with a 2-week lag, deaths then we should consider the possibility that the surge in positives may be due to contamination (a ‘lab crash’ in the parlance). The shortage of available test kits will have put pressure on distributors to release kits that had been held back as sub-standard. Rumours of contaminated supplies, especially vials, are now widespread.

Perspective

The number of healthy people below the age of 60 that have died is only in the 300s, whilst all those that have died within 28 days of symptom-onset is closer to 37,000. The number that die in a bad flu year (eg. 2017-18) is about 25,000 more than in a good year (e.g. the last two winters). Thus the ‘dry tinder’ theory, as explained by Dr Ivor Cummins and viewed > 1.1m times, means that total UK Covid-19 deaths (i.e. not from old age) could realistically be as low as 12,000 (sub-0.02% of the population).

Appendix: Theory of models

theory-of-models-1024x663.png

 

 

 

 

 

Tory MP's starting to realsie the damage Bozza has done.

 

Edited by sancho panza
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This turned out to be less interesting than I expected. I was wondering how far through this thing we might be, assuming that Sweden won't have a significant "second wave", and it seemed that the sensible thing to plot would be the number of deaths as a proportion of the vulnerable population, which I took to be those over 65. The argument being that this should plateau out at about the same percentage for every population, even though places like Somalia don't really have old people, and in Italy you can't step out of the door without tripping over zimmer frames. Anyway, here's what it looks like. I surmise that Somalian data is rubbish (who would have thought?) and China is lying (gosh!). If the original idea holds any water at all, then the Netherlands, Japan, India, Poland and Russia still have a long way to go, and the UK and Italy are basically through it. South Africa and the USA seem to be heading for significantly higher plateaux (I was surprised how young the US population is); for the USA, that might be a high prevalence of what can medically be termed "fat bastards", and for South Africa, I just don't know ... but it looks bad for them. Linear scales on the left, log scales on the right.

 

 

covid19_stats.png

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Slightly tighter spread if you try to correct for obesity, using the naive approximation that age and obesity are uncorrelated. The USA is no longer an outlier, but India becomes one: they seem to be more susceptible than you would expect (or, alternatively, they are the future, and even Sweden still has a lot of deaths to come).

 

covid19_stats_v3.png

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4 hours ago, janch said:

A warning from a German guy about the true purpose behind what's happening with CV-19.  I keep an open mind:

https://www.armstrongeconomics.com/international-news/disease/parliamentary-advisor-to-the-german-bundestag-has-come-out-warn-the-people/

Article is in German but trsnslation is at the end

The start of the article had a bit of an "I am a Nigerian prince..." air about it, but I think the author is voicing possible, albeit unlikely, claims for the response to CV19 being coordinated to achieve economic and political aims (a conspiracy in the literal sense).

I think that, being a German, he is very (perhaps hyper-) sensitive to how bureaucracy can slide quickly into tyrany. During the second war, it was a principal weapon of oppression and part of the "banality of evil" behind the holocaust. It doesn't help that his worst fears about the state stripping its people of their freedoms are already coming true in China.

His main idea is that the principal movers are private financial institutions, who are trying to ensnare governments into deregulation and other political ends by trapping them in debt. On the surface, that sounds unlikely (and more so because governments seem to be monetizing debt rather than accepting large loans from private banks). What makes it slightly frightening though, is that this is exactly the modus operandi used by first world countries against the third world (see "Diary of an economic hit-man"), so it is not quite impossible that it might be used against first world countries by supra-national organizations.

His point that many of the top jobs in the supra-nationals are occupied by people from Goldman Sachs etc. is valid, I think. The idea that they want to destroy the middle classes sounds ridiculous, as they/we have been the source of the wealth of nations for a hundred and fifty years. What makes it worryingly (almost) possible though, is that, as he says, the middle classes may no longer be needed if automation continues apace.

So, I would say it's a loopy article, and (as Spy would remark) much too tin-foil-hatted. However, it's close enough to the truth to make a good halloween story if you have very boring teen-aged children.

... Or maybe it's real.

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