#coronavirus Good news: the downtrend in Chinese-virus case-growth rates continues

By Christopher Monckton of Brenchley

The good news is that in most of the countries we are tracking the downtrend in the growth rates of both confirmed cases and deaths continues. It is important that people should see this at the moment, because in many countries record numbers of cases and deaths are being recorded, and these large figures tend to conceal the good news.

For instance, in the United States, where a passivist confidently told me only last week that there would be only 10,000 deaths in total, there have been 19,000 deaths already, of which more than 2000 occurred only yesterday.

Some commenters are still trying to maintain, in the teeth of the evidence, that the Chinese virus is no worse than the annual flu, and that no excess deaths compared with the same week in previous years are occurring or will occur.

Even though the cumulative-case growth rates continue to decline, offering real hope that healthcare systems will not, after all, be overrun, there will be many more cases and many more deaths before this is over: therefore, making comparisons now between last year’s and this year’s death rates, for instance, will make the Chinese virus falsely appear less harmful than it will prove to be. Cumulative-case growth rates must fall close to zero (and self-evidently not to less than zero, as nodding Homer carelessly wrote yesterday) before we can feel confident that the worst is over.

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Fig. 1. Mean compound daily growth rates in confirmed cases of COVID-19 infection for the world excluding China (red) and for several individual nations averaged over the successive seven-day periods ending on all dates from March 14 to April 10, 2020. A link to the high-definition PowerPoint slides is at the end of this posting.

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Fig. 2. Mean compound daily growth rates in reported COVID-19 deaths for the world excluding China (red) and for several individual nations averaged over the successive seven-day periods ending on all dates from March 23 to April 10, 2020.

The compound daily growth rate of total confirmed cases throughout the world excluding China and occupied Tibet, where the data have been widely and justifiably criticized as unreliable, is running at 6.6%, and the daily growth rate in deaths, a lagging indicator, at 8.7%.

If cases were to continue to grow at 6.6% compound every day for a month, the 1.7 million cases reported to date would exceed 12 million; for two months 80 million. Note that this is not a prediction, for it is very likely that governments will continue their control measures at least for another month or two.

On the other hand, it is very likely that true cases of infection exceed reported cases, perhaps by 1-3 orders of magnitude. Until antibody testing becomes possible, we shall not know for sure.

Happy Easter to one and all, and keep safe.

Original slides here.

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ren
April 11, 2020 11:08 pm

To the surprise of the scientists, the T cell became a prey to the coronavirus in their experiment. They found a unique structure in the virus’s spike protein that appeared to have triggered the fusion of a viral envelope and cell membrane when they came into contact.
The virus’s genes then entered the T cell and took it hostage, disabling its function of protecting humans.
https://www.scmp.com/news/china/society/article/3079443/coronavirus-could-target-immune-system-targeting-protective

Tim Bidie
April 11, 2020 11:24 pm

With no internationally consistent method for recording cause of death, numbers collated on various statistical websites are worthless:

‘…where massive screening has been performed in the whole population (eg, in South Korea and Switzerland), overall case fatality rates of less than 1% have been reported, because the denominator included many mild or asymptomatic cases.’

‘in areas with high infection rates, patients might be admitted to the ICU with, for example, severe trauma or acute brain injury, test positive for SARS-CoV-2 during the ICU stay, and eventually die because of the initial injury; these deaths will still be attributed to COVID-19 and included in the statistics. Similarly, some patients might have SARS-CoV-2 infection, but the actual contribution of the virus to the patient’s death might be minimal. For example, in a patient with metastatic cancer or terminal organ failure, is the viral infection or the patient’s underlying condition the cause of death? The actual role of SARS-CoV-2 infection in such deaths is particularly difficult to evaluate in countries where only one cause can be reported on a death certificate.’

‘Global numbers of deaths and case fatality rates provide only crude information.’

Understanding pathways to death in patients with COVID-19
The Lancet April 06, 2020

Reform of the NHS is urgently required (in a good way) to include the setting up of a fully independent National Health Authority similar to that of Sweden.

Complete reform of the World Health Organisation seems unlikely so WHO should have its funding removed, circumvented by a G20 international health committee as proposed by the house of commons foreign affairs committee.

ren
Reply to  Tim Bidie
April 12, 2020 12:53 am

Will homeless people who die on the streets of New York have a SARS-Cov-2 test?

ren
Reply to  Tim Bidie
April 12, 2020 1:03 am

Most Swedish cases are concentrated in the south of Sweden, in areas of larger human aggregates.

Fabio Capezzuoli
April 12, 2020 1:16 am

News about Wuhan coronavirus, some good some not so much.

South Korea reports that several patients tested negative returned positive. It is not clear what happened yet, but it doesn’t look good for the development of a vaccine or even collective immunity.
https://nypost.com/2020/04/07/51-recovered-coronavirus-patients-test-positive-again-in-south-korea/

Good news on treatment side from Italy instead (in Italian): autopsies showed that many patients died of multiple tromboembolism, not because respiratory failure. So trials of heparin as treatment is expected to start next week, while heparin is already used as preventative.
https://www.adnkronos.com/fatti/cronaca/2020/04/11/coronavirus-drago-tante-morti-per-tromboembolie-aifa-studio-eparina_F9JxZ20oXBZ0nG74cpTfIK.html

Now this can have important implications, because if the actual lethal mechanism is tromboembolism it means that a pharmacological treatment can drastically reduce the need for intubation and ventilation, which is the main health system bottleneck at this stage.

ren
Reply to  Fabio Capezzuoli
April 12, 2020 3:24 am

The increase in heme is the result of the breakdown of cells destroyed by the virus.

“Numerous cases of acute and chronic pulmonary conditions are accompanied by extravasation of erythrocytes to the lower respiratory tract (lung hemorrhage). These pathological events are frequently associated with marked leukocyte influx and an increase in inflammatory markers [1–7]. In cases of moderate to intense hemolysis that succeed hemorrhagic events, the scavenging of free heme by blood-derived hemopexin or albumin collapses, leading to the accumulation of free heme in the extracellular milieu [3]. It has been previously reported that high expression of haptoglobin, the major protein responsible for the removal of free hemoglobin, reduces tissue injury associated to blood exposure [1]. Accordingly, the induction of heme oxygenase-1 (HO-1) can promote cytoprotective responses in some models of lung injury [8–10]. This stress-inducible enzyme controls the deleterious effect of large amounts of free heme, catabolizing this porfirin in biliverdin, carbon monoxide, and free iron, which are addressed, both directly and indirectly, as cytoprotective agents [10]. These observations support the hypothesis that free heme may be involved in the onset and/or amplification of pulmonary inflammatory responses.”
https://www.hindawi.com/journals/mi/2013/946878/

Fabio Capezzuoli
Reply to  ren
April 12, 2020 4:40 am

I’d appreciate a statement of your point together with the citation.

ren
Reply to  Fabio Capezzuoli
April 12, 2020 8:24 am

Under oxidative stress however, some hemoproteins, e.g. hemoglobin, can release their heme prosthetic groups.[34][35] The non-protein-bound (free) heme produced in this manner becomes highly cytotoxic, most probably due to the iron atom contained within its protoporphyrin IX ring, which can act as a Fenton’s reagent to catalyze in an unfettered manner the production of free radicals.[36] It catalyzes the oxidation and aggregation of protein, the formation of cytotoxic lipid peroxide via lipid peroxidation and damages DNA through oxidative stress. Due to its lipophilic properties, it impairs lipid bilayers in organelles such as mitochondria and nuclei.[37] These properties of free heme can sensitize a variety of cell types to undergo programmed cell death in response to pro-inflammatory agonists, a deleterious effect that plays an important role in the pathogenesis of certain inflammatory diseases such as malaria[38] and sepsis.
https://en.wikipedia.org/wiki/Heme

Fabio Capezzuoli
Reply to  ren
April 13, 2020 12:55 am

I must ask you to state your position in concise terms, in clear relation to what I wrote in the first place.

Because long and very technical excerpts without any explanation only add to the background noise.

Reply to  Fabio Capezzuoli
April 14, 2020 11:30 am

I can think of a possibility that is as yet compatible with what has been regarded to be the case.
It is related to the extended length of time that patients with this form of viral pneumonia are spending with the condition and awaiting resolution.
It may be that the unusual thromboemoli are a result of being intubated and suffering from the pulmonary symptoms is outside what has previously been seen, and is simply a consequence of a prolonger period of pneumonia symptoms plus cytokine storm like damage.
Treating with blood thinners may resolve such a question.
If it simply a result of the length of time, blood thinners may not be expected to be of much help, but if indeed the blood thinners are associated with more rapid recovery and/or an improved odds of favorable outcome, this would tend to lend support to the idea there is some novel effect on the blood from this virus.

Ian
April 12, 2020 2:11 am

Monckton of Brenchley

You are quite right to highlight the danger of being a passivist with a virus that is ballpark 10 x more lethal than seasonal flu and maybe twice or more transmissible.

The early stages of any transmissible disease looks exponential, but due to the pool of people catching it and thereby gaining immunity it can’t be. The proper form is an S shaped function, an example of which is the Gompertz curve.

https://en.wikipedia.org/wiki/Gompertz_function

An example of it being used in Wuhan is here.

https://arxiv.org/pdf/2003.05447.pdf

This has the benefit of being able to forward project the end state of the disease to a certain level of accuracy once the disease has passed up to the midpoint.

Here’s the daily UK data that I’ve fitted using the Gompertz curve for both total cases (blue) and deaths (red)

comment image

And the daily changes for the same.

comment image

This suggests we are about the peak of the UK total cases as the function begins to slow and reach its upper value.

You can get the function in this software, which won’t cost an arm or a leg, and allows multiple nonlinear functions to be fit to data .

https://www.curveexpert.net/products/curveexpert-professional/

richard
April 12, 2020 2:12 am

“Dr John Ioannidis from Stanford University estimates a death rate between 0.025% and 0.65%. Another study, from Japan, found the death rate to be between 0.04 and 0.12.”

Tim Bidie
April 12, 2020 2:44 am

All of the arguments around Covid 19 will no doubt be aired exhaustively during the U.S. Presidential election and there will be nowhere to hide.

The only numbers within OECD nations that actually bear international comparison will be overall death rates from all causes. Will they be noticeably higher this year or plumb normal compared to other years? I know where my money is.

In Britain, Public Health England is responsible for infectious diseases and preparations for national medical emergencies. For that organisation, there is really is nowhere to hide. It cannot claim that hospital intensive care units likelihood of being overwhelmed was due to any shortage of funding since it has only been allocating 25% of its budget towards protection from infectious diseases over the previous two years.

As for the coverage of the Covid 19 outbreak, the words of the German author and journalist on medical matters of over 25 years experience, Harald Wiesendanger, bear repetition:

‘How a profession that is supposed to control the powerful as an independent, critical, impartial Fourth Estate can succumb as quickly as lightning to the same collective hysteria as its audience, almost unanimously, and give itself over to court reporting, government propaganda and expert deification: It’s incomprehensible to me, it disgusts me, I’ve had enough of it, I dissociate myself from this unworthy performance with complete shame.’

David
April 12, 2020 2:46 am

This remarkable, highly qualified doctor is pioneering a cure for the Wuhan Virus that really works.
This is not some crazy fad – this is worth watching

John Finn
April 12, 2020 2:46 am

“Dr John Ioannidis from Stanford University estimates a death rate between 0.025% and 0.65%. Another study, from Japan, found the death rate to be between 0.04 and 0.12.”

Ioannidis was merely guessing. He speculated that it might be 0.3% and that 1% of Americans might get the virus. From this he estimated that deaths from coronavirus might be 10,000. Just a few days later, and with the pandemic still in its infancy, his basic ball park figure was comfortably surpassed.

He hasn’t got a clue.

David
April 12, 2020 2:47 am
Hokey Schtick
April 12, 2020 3:05 am

I have no clue about anything, but my point is this. I used to find Monckton of Brenchley’s overwrought wrestling with the english language to be an amusing rhetorical flourish. Now I find his garbageous word salad and intemperate profusional spoutings to be annoying as all heck. Put a sock in it, my Lord, or talk normal like everyone else. Now is not the time for this verbal wiggywaggimany.

Eliza
April 12, 2020 3:11 am

So in Sweden deaths are spiking at ~800 as of today and next 3 days or so then watch the peak go down sharply as it continues to rise in countries in lockdown for months! Many more will die over time because of this lockdown. The “flattening of the curve”will simply prolong death and misery. Well done Swedes for being smart!Looks like Denmark and Norway are agreeing as they are opening schools tomorrow like Sweden

John Finn
Reply to  Eliza
April 12, 2020 4:29 am

Denmark & Norway believe they have the virus under control.

Eliza
April 12, 2020 3:13 am
Eliza
April 12, 2020 3:21 am

Re Sweden should be peaked at TOTAL deaths to date of 800 so NOT 800 per day! my bad. 800/150 = 5 per day average since Jan 2020.

A C Osborn
Reply to  Eliza
April 12, 2020 7:08 am

You cannot compare Sweden with a population density of 25 people per sqaure Km to any other country unless they also have a similar density.
The whole of Sweden almost fits in New York City whose density is 10,194 per square Km.
Get that, 400 times higher and Manahatten is 25,846, 1000 times higher.
Plus they did quite a bit of controlling without an actual lockdown, like
Travel restrictions
Cancelling meetings, seminars, festivals, sports meetings et.
The majority of cases & deaths were in Stockholm.
Why you think that Sweden’s 88 deaths per million is somehow better than the USAs 62 per million I don’t know?

ren
April 12, 2020 4:01 am

Boris Johnson has said he owes his life to the NHS staff treating him for coronavirus.

In a statement released by No 10, the prime minister, 55, thanked medics at St Thomas’ Hospital in London, where he continues to recover after spending three nights in intensive care.

It comes as UK deaths from the virus are expected to pass 10,000 on Sunday.

On Saturday, the UK recorded 917 new coronavirus deaths, taking total hospital deaths to 9,875.
https://www.bbc.com/news/uk-52258980

richard
Reply to  ren
April 12, 2020 2:55 pm

Ren ,

how many died “with” Corona vs “of|” Corona?

for illustration-

“Last week, Connecticut’s Governor Ned Lamont used the tragic and accidental death of a 6-week old infant to spin a narrative that newborns were susceptible to dying from Covid-19.

In a press conference, he feigned upset by stating, “Probably the youngest person ever to die of COVID has died here in Connecticut,” This is a falsehood. Governor Lamont told a lie that caused not only inspired mass hysteria but also targeted the most vulnerable members of our society: mothers and infants.

CALL FOR LAMONT’S RESIGNATION TODAY
While the infant in question did indeed test positive from COVID-19, its death was not caused by the virus. Police officers that were called to the scene were informed that the infant tragically lost its life due to having been accidentally smothered by its caretaker. It was only after the infant had passed that the hospital tested and found that the child was also positive for COVID-19.

In essence, it was not the virus that claimed this child’s life, but rather a tragic accident at home. Rather than include these details or any details that would have allowed mothers to rest easy, Governor Lamont saw an opportunity to shock and drive fear into the homes of families all over the world”

April 12, 2020 5:18 am

I have a suspicion, based on anecdotal evidence, that the virus was present in the UK back in January and may have been present as far back as October 2019.
The evidence I have are people presenting to an Urgent Care Centre with low grade fever (37.5< T < 38.0) and a persistent cough. The temperature would not raise any alarm bells as it doesn't score on NEWS2 or paediatric scoring tools. Other observations were within normal range.
Those with comorbidities seemed to fair worse. This is not just my experience but several of my colleagues noticed the same trend. Of course any person who was particularly vulnerable and who died at that time from a respiratory disease would not and could not have been tested for Sars2 virus.

Tim Bidie
Reply to  John
April 12, 2020 6:56 am

I also believe that.

Figures for England & Wales from the Office of National Statistics of deaths this year from all causes (the only figures of any use) show that deaths are, currently, well down on the five year average (by about 10% representing 14,000 fewer deaths) although March was about 200 deaths over the five year average. For comparison, the first week in January was also 200 deaths over the five year average.

This is all excellent news and the country should be delighted………

Tim Bidie
Reply to  Tim Bidie
April 12, 2020 7:43 am

That should read ‘well down on 2018 figures (by about 10%……….’

But only about 4,000 fewer deaths so far this year than the five previous years average.

Prjindigo
April 12, 2020 6:14 am

Since the primary vector was fast-shipped Chinese manufactured products shipped directly from China it’s no wonder there was a drastic downturn in the increase in cases.

It *isn’t* “sars-2” by the way because SARS is Sudden Acute Respiratory Syndrome and you can get that from bear spray, caustic vapors, alcohol inhalation and medications… *and* Covid-19 is genetically dissimilar.

richard
April 12, 2020 7:25 am

Boris Johnson out of Hospital. There were some alarmists had him at deaths door a few days ago. Such a miracle that he is at home to enjoy Easter. What a sudden, speedy recovery!!

ren
April 12, 2020 8:52 am

Without ACE2 acting as a guardian to inactivate the ligands of B1, the lung environment is prone for local vascular leakage leading to angioedema. Angioedema is likely a feature already early in disease, and might explain the typical CT scans and the feeling of people that they drown. In some patients, this is followed by a clinical worsening of disease around day 9 due to the formation antibodies directed against the spike (S)-antigen of the corona-virus that binds to ACE2 that could contribute to disease by enhancement of local immune cell influx and proinflammatory cytokines leading to damage.
https://www.preprints.org/manuscript/202004.0023/v1

Lee
April 12, 2020 2:57 pm

There is still plenty of reason to remain alarmed about coronavirus. World-wide the epidemic continues to grow:
http://www.gmxanalytics.com/pages/world.htm
and most countries still show either a linear or exponential growth rate.
http://www.gmxanalytics.com (click on any country). One of the few exceptions is Italy (and China if you believe their numbers),
which is clearly and definitely subsiding.
http://www.gmxanalytics.com/pages/Italy.htm
This continues to be a worrisome epidemic.

richard
April 12, 2020 3:04 pm

Japan, a densely packed country of 126 million people has had 108 deaths.

We are still waiting to hear from the grandiosely titled, Lord , how many died “with” Corona as opposed to died “of” Corona.

Alas! I fear we will wait in vain.

ak in vt
April 12, 2020 7:37 pm

Unfortunately, Mr MONKTON of BRENCHLEY and all agreeing with him misunderstand the whole point of why the lockdown is wrong:

LIVING UNDER LOCKDOWN IS NOT LIVING. We are NOT living in order that we may live: HUH?

The scarf lady (whose name I refuse to repeat) is already talking about how “they” know how we can combat the next pandemic as this lockdown has proven we can beat it. I have heard her twice, the most recent on Friday the 10th of April’s press conference with the president on covid-19. Give me a break!

AK

Roger A
April 13, 2020 12:25 pm

It has been said that the virus first appeared in the UK as early as September2019
Transported by Chinese students returning to UK universities from summer holidays in their home country.
This may explain the pre Xmas surge in fatalities and equally, the lower than average deaths experienced late Jan to mid March – Probably because the C19 virus led to the earlier pre Xmas demise of many terminally ill patients who ordinarily would have lived for a few more months as would have been the case if C19 were absent.
But if the virus had continued in full strength from September, then surely the disparity between pre and post Xmas death rates would not be as pronounced as they are.
For example, if the virus had maintained its strength from Sept to the present then the post Xmas death rate would still cause the demise of the less ill, leading to many more deaths post Xmas but not necessarily as high as the pre Xmas figures.
The sharp dip over Xmas is due to under reporting over the holiday period.
Now, come late March, the All Cause Mortality (ACM) as recorded by the Office of National Statistics (ONS) is rising again.
What could be the reason?
Revisiting the situation we could say that C19 is weaker than alluded to in the scenario above.
It started in September, killed of all the terminally ill sooner than would ordinarily be the case and faded.
So,
A] Virus began Sept and faded relatively quickly, then,
B] End of February UK students, et al, returning from half term Skiing holiday In Northern Italy (or the Far East) introduced a new wave of C19 infections.
Acknowledging that the worst case scenario is around 26 days from infection to death.
Then surely it is logical? To assume? That the surge in death rate late March stems from infections contracted late February, as per B above rather than a continuation of the September 2019 wave.
In which case we could say that infection waves may be short lived?
I understand that may be too simplistic an opinion but if close to the mark it is good news.

April 14, 2020 11:03 am
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