By Christopher Monckton of Brenchley
Of government ministers it may be said that they seldom know how many beans make five. Frankly, numeracy is seldom their forte. Therefore, HM Government, for instance, has pietistically proclaimed time and time again at its daily press conferences that it will act solely on the basis of what the scientists say.
This species of abject abdication to the priests of the machine has long been evident in governments’ approach to the climate question. They have been readily fooled by totalitarian academics pushing an agenda that is both ideologically attractive and financially profitable to the academics.
Now that governments are habituated to the notion that man with beard wearing white coat with leaky Biros sticking out of front pocket him always right, yes indeed, goodness gracious me, they are easily led by the nose. So far, climate skeptics have generally failed to convince governments that they should not be so credulous, nor so completely in thrall to currently-fashionable academic political opinion masquerading as “scientific consensus”.
In Sweden, this childlike faith in scientists has been taken to the extreme. By law, ministers are denied any say in how to handle pandemics. The key decisions have been wholly delegated to the public health agency, which has decided that, though some precautions are to be taken, there will be no lockdown.
For those of us who would like the lockdowns to end in those countries where it is clear from our daily graphs that they are no longer needed, it would be welcome news if the Swedish experiment were to succeed. The next few weeks will make or break the no-lockdown policy, for Sweden’s first cases of infection were later than in most of the worst-affected European countries.
One consequence of innumerate governments’ abdication to radicalized scientists is that when the scientists cannot agree among themselves governments do not take decisions in time. In Britain, Ministers dithered for a fatal month after the first cases arrived. In the end, the Prime Minister took a command decision to lock the country down, based on a model from Imperial College, which predicted that in the absence of a lockdown some 500,000 of Her Majesty’s subjects might have been killed.
Already, more than 26,000 have been killed, for the Government is at last including the virus-related deaths outside as well as inside hospitals in its daily counts. On current trends, Britain will soon have the highest death toll in Europe.
How, then, to address the recurring problem of innumeracy among the classe politique? This question will become important as governments decide what to do about lockdowns.
The State of Georgia has taken the bull by the horns and has ended the lockdown altogether. For the United States, that decision – which went too far even for Mr Trump – will provide a useful point of comparison, just as Sweden does for Scandinavia (compared with which it is doing badly) and for Europe more widely (compared with which it is doing well).
Mean population density per square mile in Georgia is only 150 people, but the state has some 70 cities or towns with populations higher than the 1800 per square mile in Stockholm.
Most governments will keep control measures in place until the daily growth-rate in active cases has fallen below zero. But then what? Here is a simple piece Ministerial math: a neat device that allows Ministers to make a rough but not altogether valueless back-of-the-envelope estimate of how many deaths the Chinese virus will have caused in total by the end of the pandemic.
This useful trick arises from the fact that, where the cumulative mortality to day d – 1 is M, and if the mortality m on day d is declining by 1 / n, and if that rate of decline continues ad infinitum, total eventual deaths T to the end of the pandemic will simply be the sum of the cumulative mortality M to day d – 1 and the product of m and n. Formally,
Thus, if in the United States there were 2400 deaths on day d, and if each day thereafter the death toll were to decline by one-tenth, and if that rate of decline were to continue, there would be 24,000 deaths from day d to the end of the pandemic, in addition to the previous deaths M = 60,000 that had occurred before day d, for a total of 84,000 deaths.
Of course, one hopes that any rate of decline in deaths (it is not yet established in the U.S.) will itself decline. Therefore, it is helpful to give Ministers a ready-reckoner table showing how many deaths will occur from day d to the end of the pandemic for various values of n:
| Daily decline by | 1/100 | 1/50 | 1/40 | 1/30 | 1/20 | 1/15 | 1/12 | 1/10 |
| Rate of decline r | 0.99 | 0.98 | 0.975 | 0.967 | 0.95 | 0.933 | 0.917 | 0.9 |
| Multiplier n | 100 | 50 | 40 | 30 | 20 | 15 | 12 | 10 |
| Daily decline by | 1/9 | 1/8 | 1/7 | 1/6 | 1/5 | 1/4 | 1/3 | 1/2 |
| Rate of decline r | 0.889 | 0.875 | 0.857 | 0.833 | 0.8 | 0.75 | 0.667 | 0.5 |
| Multiplier n | 9 | 8 | 7 | 6 | 5 | 4 | 3 | 2 |
Then Ministers can apply the test to the daily death toll, averaged over 7 days using (2). Some statisticians prefer three-day averaging. Either way, Ministers can ask the statisticians what the mean rate of decline rd is, together with the day’s mortality rd, and can then look up the appropriate multiplier n, multiply the day’s death toll by it, add the cumulative mortality M up to the previous day, and Bob’s your uncle.
Take Italy. The most recent daily death toll was 323. Seven days previously it was 437. Therefore, the rate of decline was (323/437)1/7, or 0.96. If that rate were to continue, there would be somewhere between 20 and 30 times 323 deaths. Call it 24 times. Therefore, there would be 24 x 323, or 7750 deaths, still to come, plus the 27,350 deaths that have already occurred, bringing the final total to about 35,000. That figure will be a maximum if the rate of decline falls below 0.96, as it almost certainly will.
None of this works unless the daily rate of change in deaths is a decline. In the United States, that is not yet the case, but one hopes it soon will be, since the daily rate of change in active cases has reached zero for the first time.
Fig. 1. Mean compound daily growth rates in estimated active cases of COVID-19 for the world excluding China (red) and for several individual nations averaged over the successive seven-day periods ending on all dates from April 1 to April 29, 2020.
Fig. 2. Mean compound daily growth rates in cumulative 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 April 8 to April 26, 2020.
Ø High-definition Figures 1 and 2 are here.
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Wexelman BA, Eden E, Rose KM. Survey of New York City Resident Physicians on Cause-of-Death Reporting, 2010. Prev Chronic Dis 2013;10:120288.
https://www.cdc.gov/pcd/issues/2013/12_0288.htm
Conclusion
Most resident physicians believed the current cause-of-death reporting system is inaccurate, often knowingly documenting incorrect causes. The system should be improved to allow reporting of more causes, and residents should receive better training on completing death certificates.
Christopher
You made the remark, “… just as Sweden does for Scandinavia (compared with which it is doing badly) …” One has to remember that this is not just a problem for Scandinavia. It is a global pandemic. On that basis, Sweden is not doing so badly. The compound growth rate of deaths in Sweden is noticeably better than Ireland and Canada, and marginally better than the US, as shown in your charts. It would be my judgement that the differences between strict lockdowns, and voluntary social distancing, is not statistically significant. We certainly aren’t dealing with an order of magnitude difference in the global rates. What differences there are might easily be attributed to differences in definitions of “Death by,” general health of the populations (as comorbidity has been shown to be critical), and cultural willingness to cooperate with social distancing guidelines.
The single most amazing thing about this farce is that Boris Johnson acted on advice from Neil Ferguson and Imperial College, London. Imperial College has extensive form for alarmism, including giving advice on foot and mouth disease that led to the unnecessary culling of six million healthy animals, and giving advice which led to the UK’s government’s estimate that the Swine Flu epidemic, in ‘a reasonable worst case scenario’ could lead to 65,000 deaths – in the end the disease killed 457 people.
See Professor Thrusfield on Imperial Colleges’s flawed research with regard to foot and mout, and his feelings of deja vu when he read their projection with regard to Covid19. https://www.telegraph.co.uk/news/2020/03/28/neil-ferguson-scientist-convinced-boris-johnson-uk-coronavirus-lockdown-criticised/
The Spectator summarised some of Imperial Colleges failings here – it is fairly fully referenced, but I assure you that where sources are lacking, it is very easy to fill the gaps by doing one’s own research. https://www.spectator.co.uk/article/six-questions-that-neil-ferguson-should-be-asked
As for their latest wild projections, a number of epidemiologists have expressed surprise at the “unqualified acceptance of the Imperial model”, such as Prof. Sunetra Gupta of Oxford University, who led a study which concluded that the virus is far less lethal than claimed by the College. https://www.ft.com/content/5ff6469a-6dd8-11ea-89df-41bea055720b
One analysis concluded that Imperial College had exaggerated the risk of Covid19 131 times. https://www.youtube.com/watch?v=7sRxb5VJ5R0&feature=youtu.be
UKGov: ‘As of 9am on 30 April, 687,369 tests completed, of whom 171,253 tested positive.’ = Roughly 24% infection rate.
Population of UK: 65 million = 16 million positive cases in UK. 26,000 deaths.
This equates to 0.16% chance of death ‘associated with COVID-19’.
Question still remains, of course, whether *anyone* has ever died of COVID-19
Old friend T= M+ m e raised to the power( negative r n)…. Serology study from NYC estimated covid 19 prevalence of 25%. Extrapolated to USA population= 330 million x .25 = 80,000,000 infected . 80,000,000 x .001( virulence of seasonal flu) = 80 , 000 deaths .Average number of deaths per year to Syncytial virus -approximately 15,000 . Tens of thousands of deaths per year in USA are attributed to pneumonias , without causative agent ID . This year ,many who will die of(or with) covid 19 , if not for this corona virus, would otherwise likely die with a diagnoses , placing them in one of the two latter groups. The number of deaths in the USA, attributed to pneumonic infections, may by years end , not differ significantly from past years.
“Old friend T= M+ m e raised to the power( negative r n)…. Serology study from NYC estimated covid 19 prevalence of 25%. Extrapolated to USA population= 330 million x .25 = 80,000,000 infected . 80,000,000 x .001( virulence of seasonal flu) = 80 , 000 deaths .Average number of deaths per year to Syncytial virus -approximately 15,000 . Tens of thousands of deaths per year in USA are attributed to pneumonias , without causative agent ID . This year ,many who will die of(or with) covid 19 , if not for this corona virus, would otherwise likely die with a diagnoses , placing them in one of the two latter groups. The number of deaths in the USA, attributed to pneumonic infections, may by years end , not differ significantly from past years.”
Nice dream, but there is no evidence any of these numbers apply to covid.
‘This year ,many who will die of(or with) covid 19 , if not for this corona virus, would otherwise likely die with a diagnoses”
this is a counterfactual with zero evidence.
you might as well say “if frogs had wings they would not bump their ass when they jump”
Most governments will keep control measures in place until the daily growth-rate in active cases has fallen below zero.
Politely and humbly, I must point out that a growth rate cannot fall below zero. Growth may be fast, it may be slow, it may even stop, i.e. equal zero. But a growth rate cannot be negative. That would entail a negative number of active cases on a particular day, which cannot occur.
Politely, without rancor or prejudice, I must point out that the cumulative (total cases or deaths or hospitalizations) growth curve is S-shaped, always positive, and always trending upwards.
The first derivative or incremental slope of cumulative growth is the growth rate (cases or deaths or hospitalizations per day). The growth rate increases, peaks, and declines in a shape like a camel’s hump, but it is always positive or zero (no new cases etc. on that day).
The second derivative (the incremental slope of the growth rate, i.e. the daily change in the rate) is acceleration. Acceleration may be negative, in which case it is called deceleration. Acceleration falls through zero and assumes negative values (becomes deceleration) at the peak of the growth rate curve.
Politely, without accusation or imprecation, I must point out that none of these curves is linear. They are all non-linear. Assuming linearity is an incorrect assumption vis a vis curves.
Humbly and without casting disparagement, I think it would be nice if these mathematical truisms were reflected in the discussion.
Might want to try a hot water soak with Epsom salts, or a bandage soaked in povidone for a while.
Mike, I think Christopher is talking about the growth rate in active cases. If the number of people reported as recovered on a day is greater than the number of new cases, then the growth in the number of active cases is negative. Of course, in those countries that seem unable to count recovered cases (the UK and the Netherlands, for example) this rate can never go below zero, so you are correct that the growth rate of number of cases can never go negative in those countries.
Well, best as I can tell, I am currently suffering from Chicom #19 toe rot. Toe #2 on right foot is red and inflamed and has been for ten days. Too bad all the local walk in clinics are shut down to treat all the non existent Chicom #19 ventilator patients.
Guess I will wait for June 1 when the normal health care system will start it’s sclerotic warm-up to treat normal people. Maybe I can get a swab up the nose. Yay!
Worldometers shows the daily change in new cases and deaths has been constant for the past month in Sweden.
This means the increase in new cases is linear in Sweden, not exponential as predicted.
And since hospital survival much beyond 30 days in ICU is unlikely due to the damage done by mechanical lifesaving. Sweden should be reaching its peak patient load about now.
Everyone seems to forget the reason for isolation was to prevent hospital overload. Unless there is a change in the rate of daily new cases, it appears Sweden has achieved that without shutting down the economy.
The main treatment should be a reduction of angiotensin II, because it is the main proinflammatory factor in Covid-19 disease. Therefore, deterioration of the patient’s condition often occurs after 10 days, despite the production of antibodies.
https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/angiotensin-converting-enzyme-2
What about patients taking ACEI/ARBs for hypertension? These act along the same pathway. Hypertension is a top conorbiditiy. Should patients on ARCI/ARBs switch to alternate medication and then hunker down until your ACE2 receptors normalize.
The current medical advice on this subject, to leave well enough alone seems to ignore the hypertension risk.
The ACE enzyme converts angiotensin I into angiotensin II, so you should think about drugs that inhibit ACE activity.
Angiotensin-converting enzyme (ACE) inhibitors
ACE inhibitors are commonly prescribed to treat high blood pressure, heart problems and other conditions. Find out how they work and their potential side effects.
By Mayo Clinic Staff
Angiotensin-converting enzyme (ACE) inhibitors help relax your veins and arteries to lower your blood pressure. ACE inhibitors prevent an enzyme in your body from producing angiotensin II, a substance that narrows your blood vessels. This narrowing can cause high blood pressure and force your heart to work harder. Angiotensin II also releases hormones that raise your blood pressure.
https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/in-depth/ace-inhibitors/art-20047480
Other substances that dilate blood vessels should also be considered, e.g. nitric oxide.
These medications can help with Covid-19 disease.
The problem I have is that ACE inhibitors are the most common first line treatment for hypertension. And hypertension is a strong predictor of a bad outcome with coronaviris. Which contradicts the notion that ace inhibitors are going to help.
I have more and more difficulties to read and understand you, this for 2 reasons:
1. You keep mentionning the 500,000 deaths from the IC when it has been criticised and even reviewed down by Prof Ferguson.
2. You consider that we have the correct number of deaths due to the Coronavirus (not even “with”) when we all know that figures is false with the consequence that it is exagerated (probably to defend their policy).
The Imperial College forecast of ½million deaths has been reduced to 50,000. That tells me that the first “estimate” was a guess, and that the second “estimate” was also a guess. The track record of Prof Ferguson’s guesswork is that previous guesses, like the first one for Covid19, were grossly exaggerated.
Having cried wolf too many times before, we should ignore his work and seek advice from others better able to guess what may or may not happen. In the real world if you have been given duff advice by an “expert” a few times, you are very unwise to rely on any future advice from same expert.
The Imperial College forecast of ½million deaths has been reduced to 50,000.
No it hasn’t. The original ½million figure related to deaths if no mitigating action were taken. Ferguson has not changed that projection. Lower figures relate to different intervention strategies.
The Imperial College projection for the current UK lockdown has been pretty much spot on. It accurately predicted the peak number of ICU beds required and the date of the peak.
It’s complete nonsense to suggest this model is – or has been – wrong.
“It’s complete nonsense to suggest this model is – or has been – wrong.”
I agree. Yet we have countless people here and on the broadcast airways saying just that. They are seeing what they want to see, not what is there. A trap humans fall into very readily when they want a certain outcome, unfortunately.
195 countries with corona.
out of 234, 000 deaths , 206,086,000 took place in 11 countries. Most of them 1st world countries.
40 countries have had no deaths.
hmmm, who would have thought it was a rich country’s virus.
Those numbers do not match up with sites I have seen of total deaths by country.
And it seems a stretch to call Brazil and Iran rich countries.
At least a few countries where we know a lot of deaths are occurring are not having those deaths show up in official counts.
Easy to understand why…poor countries do not keep track of deaths and are less diligent about statistics and record keeping, in general.
Also, this is a new disease, and much of the initial wave is tightly correlated with how many people travel around, and in particular to specific other countries, but then also within a country. Because first the virus had to go from where it was to a particular new country, and then be spread around the new country, for an infection to disperse rapidly and efficiently.
The places that got it first have it worst, because everyone in the whole world became aware of a new virus killing people, and many took steps to limit transmission.
In places with little money and few roads and few means of rapid transit, fewer people are able to or have the means of travel.
Plus…five months ago, a few people in one city had this virus, so anything one can say about where it is now and how many have been sickened is hardly likely to be the last word on it.
Six weeks ago people were talking about how only a few old people in a nursing home in Washington had anything to worry about.
“most of them 1st world”
I used Worldometer.
The lower the population density the lower the Ro value. An isolated magically infected individual with no opportunity to spread the virus will not start an epidemic.
High density population, Japan – 435
Dear Christopher Monckton of Brenchley,
All these figures are meaningless in the face of reality! You have no image of the mountain of infection that precedes your lagged so called “death rates”.
If you have no idea how many have been infected because you are only testing the symptomatic and you are only testing them for active infection then you are not only driving blind you a deliberately blindfolding yourself and taking your hands off the wheel!
Without knowing how many have been infected already the figures you keep listing week after week are the sheerest form of propaganda. And given the disaster to the health system this has created and the consequent loss of real lives* this disgusting misinformation is culpably murderous!
You know that testing only the sick will bias the death rate but given that the data itself is heavily and admittedly contaminated by co-morbidities it is grossly irresponsible and completely unscientific, let alone enumerate to continue to propagate it!
What we do need, is wide spread antibody testing combined with rigorous data collection. This should have been done at the earliest date and those results should have driven our response. This still isn’t being done and in my country it has been legislated against!
Using the less reliable PCR testing of only the sick is the surest way to sex-up the figures and scare the population into accepting the most draconian restrictions to life and liberty and the most enormous totalitarian overreach the world has ever seen!
It isn’t a coincidence that the global integrated financial system had already begun to collapse in September 2019. Our government introduced a bill to limit cash that year which will allow – with the stoke of a pen – to make it illegal to withdraw cash from a bank and at the same time – coincidentally – that the banks want to introduce negative interest rates! Make no mistake we are in a world wide financial armageddon right now and it will lead to uncountable deaths.
*400 new cancers go undetected every week in the UK while screening services have been shut down and you can add another 2300 people that are not being diagnosed for cancer by their local doctor every week. Not to mention the number one killers heart disease and stroke and the uncountable knock on effect this shut down, slow down and crumble down of the health system will achieve!
I did mean innumerate above but typing inumerate – with one “n” – auto corrects to enumerate. It is Freudian though because I was thinking of long lists!
I’m not illiterate or innumerate but I do suffer from dysgraphia which means I have some difficulty with written language!*
It has been a constant source of pain throughout my entire life. I still have trouble with the symbols “b” and “d” and have to use a mental trick to get them right to this very… bay! 😉
*Although I touch type and have a good vocabulary; if that makes any sense at all!
We only can work with the numbers we have we all know that.
That one day we will have better numbers is an other question, for a retrospect.
206,086
The average life expectancy in Germany is approximately 79 years. The average age of the dead with corona is around 80 years. If, in the worst case, 50% of the population are infected without a lock down until a vaccine is available (approx. 1 year), around 20% more old people will die than on average with a death rate of 0.5%. However, if smoking were banned instead of a lockdown, life expectancy would increase by a total of 2 years due to the smoking ban (in Germany 23% smokers, shortening
life expectancy per smoker approx. 8 years).
and the vaccine will probably not work on the 80 year olds.
The flu vaccine was largely ineffective in the elderly, in the UK. This years was adjuvanted to provoke a better immune response:
“For those aged 65 and over, there are three vaccines that JCVI advisedare equally suitable for use. The adjuvanted trivalent influenza vaccine (aTIV)continues to be recommended for this age group asit is likely to bea more effective vaccine than the standard dose non-adjuvanted trivalent and egg-based quadrivalent-influenza”
https://www.england.nhs.uk/wp-content/uploads/2019/03/annual-national-flu-programme-2019-to-2020-1.pdf
SARS-CoV-2 is not the flu. In many biological f***ing ways. It’s tiring to point this out again and again
A lot of vaccines are working perfectly fine and in the elderly as well.
yep, the flu kills the young, Corona doesn’t.
The measles kill the young, Corona doesn’t.
Equally meaningless statement.
COVID deaths are treated as being infinitely more important than heart attacks, cancer, strokes, third world starvation etc. Even when 90% of the fatalities are to 75+ age group.
There are easy measures to most likely never die form SARS-CoV-2.
What are the easy measures to most likely never die from heart attacks, cancer, strokes?
We are putting a lot research money into those and third world starvation is multi-factorial and not solved by all the money in the world alone e.g. Rwanda.
https://en.wikipedia.org/wiki/Economy_of_Rwanda
Let’s hope so-
25,898 Communicable disease deaths today.
Easy? — you mean like wearing face masks that you CONSTANTLY touch, pull down about your neck, fail to wash or sanitize between uses, and wear for hours on end rather than the two-hour recommended limit PER … CLEAN … PROPERLY HANDLED … mask?
As for easy with respect to heart attacks, cancer, strokes, … well, a really easy thing to do, in theory, is push away from food, after a certain ingested amount, in order to avoid overeating that leads to obesity. And what’s easier than putting one foot in front of the other for a couple of miles every day, in order to maintain some sort of physical fitness?
Or simply choosing water to drink, instead of Mountain Dew?
Easy in theory and reality in practice are two entirely different things. What I am seeing with the mask-wearing pod people is a failure to truly understand chain of contamination, as they walk about PRETENDING that they are doing something … “simple”, where they are actually “simply” fooling themselves.
Can you name one vaccine that is useful, in your country?
@Robert Kernodle
What are you talking about? As if what you describe would apply for all people. Nonsense. Typical reductio ad absurdum. And even if you are working in job like that you could change it if you are afraid you would not be able to act accordingly.
For the real easy measure: social distancing? Heard of that? Technically, it doesn’t get any easier as a method than that.
“As for easy with respect to heart attacks, cancer, strokes…”
That’s the bad thing: you can do all the tings you listed but still die of any of those. And you can do none of those and die at the age of 120 by total organ failure. It’s unfair world we live in.
But if you don’t catch SARS-CoV-2 you can’t die prematurely from it. That’s the difference.
@niceguy
“Can you name one vaccine that is useful, in your country?”
The vaccine against streptococcus pneumoniae is very famous at the moment to prevent secondary infections in context of SARS-CoV-2.
Life expectancy in Germany is ~81 years by 2017.
You have to look at the median not the average. A couple of 90+y old will push your average.
What is the most reliable measure of the outcome of COVID-19. We cannot rely on death statistics.
I think we should use excess deaths as the best measure.
One interesting thing with excess deaths is that many countries get a negative number. Lockdown contributes to less deaths of other causes. And very few with other diseases die from a medical system that has some shortcomings.
How many beans make five? 2 + 2.
Obama’s wife- “we urge you to stay at home”. In the meantime her husband goes off playing golf- https://www.youtube.com/watch?v=UJgRk1p8ktY
All animals are created equal. Some are more equal than others.
We know Cov-2 binds to the ACE2 enzyme, which stops functioning in the lungs. This causes narrowing of the blood vessels in the lungs and pneumonia in completely healthy people.
The ACE2 enzyme is an extremely important enzyme that regulates the level of angiotensin II in the body by reducing angiotensin II to angiotensin (1-7), which has the opposite effect (dilates the blood vessels). Excess angiotensin II wreaks havoc on the body.
Antiviral drugs are effective in the first phase of treatment, however, in the second phase, inactivation of ACE2 by the virus causes an increase in angiotensin II, which is a very strong and fast-acting hormone. Despite the fact that the antibodies work, there are changes in the lungs.
A prophylactic dose of 4000 vitamin D units appears to be indicated.
The effects of vitamin D on the renin-angiotensin system:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3999581/
‘Compared with vitamin D-sufficient individuals, those with vitamin D deficiency and insufficiency had greater plasma angiotensin II levels’
https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/angiotensin-converting-enzyme-2
The ACE enzyme converts angiotensin I into angiotensin II, so you should think about drugs that inhibit ACE activity.
Angiotensin-converting enzyme (ACE) inhibitors
ACE inhibitors are commonly prescribed to treat high blood pressure, heart problems and other conditions. Find out how they work and their potential side effects.
By Mayo Clinic Staff
Angiotensin-converting enzyme (ACE) inhibitors help relax your veins and arteries to lower your blood pressure. ACE inhibitors prevent an enzyme in your body from producing angiotensin II, a substance that narrows your blood vessels. This narrowing can cause high blood pressure and force your heart to work harder. Angiotensin II also releases hormones that raise your blood pressure.
https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/in-depth/ace-inhibitors/art-20047480
Other substances that dilate blood vessels should also be considered, e.g. nitric oxide.
These medications can help with Covid-19 disease.
Severe Acute Respiratory Syndrome (SARS)
Mei-Shang Ho, in Tropical Infectious Diseases (Third Edition), 2011
Pathogenesis and Immunity
Tissue tropism of SARS-CoV is stipulated by a specific receptor-facilitated process; angiotensin converting enzyme 2 (ACE2) has been identified as the cellular receptor that binds directly to the viral S protein. ACE2 is expressed in alveolar epithelial cells and in surface enterocytes of the small intestine, both of which are the primary target cells of SARS-CoV infection. ACE2, which acts as a negative regulator of the local renin–angiotensin system and is down-regulated by viral infection, can protect the lung against external damage in experimental animal models. In addition, the S protein of SARS-CoV can also bind to C-type lectins, i.e., CD209 (also known as dendritic cell-specific intercellular adhesion molecule-grabbing nonintegrin, or DC-SIGN) and CD209L, and gain access to cell entry. Although SARS-CoV particles and genomic sequence are detected in a large number of circulating lymphocytes, monocytes, and lymphoid tissues during the early phase of infection, no virus has been found in dendritic cells. Viremia, with or without cell association, occurs early in the clinical course, thus contributing to the spread of virus to organs other than the site of entry.
The intestinal tract is an important extrapulmonary site of viral replication; specimens taken by colonoscopy or at necropsy reveal evidence of active viral replication within both the small and large intestinal mucosa but with minimal pathological changes,and SARS-CoV RNA may be detected by reverse transcriptase polymerase chain reaction (RT-PCR) from gastrointestinal specimens for up to 10 weeks after onset.53 In an autopsy series of 18 patients who died between days 14 and 62, epithelial cells of the digestive tracts of all patients were virally infected but displayed only mild inflammatory changes.49 The most obvious lesion in the digestive tract is depletion of the submucosal lymphoid tissues. The minimal pathology in the gastrointestinal tract contrasts sharply with the diffuse alveolar damage in the lung, while both organs serve as primary sites of viral replication. Thus, the pathogenesis must involve tissue-specific host responses, which are most likely intensified during week 2 of illness when pulmonary function worsens with concomitant decreasing viral load in the airways (Fig. 59.3). Clinical studies of cytokines during the acute phase suggest that activation of Th1 cell-mediated immunity and an excessive innate inflammatory response, rather than direct damage from uncontrolled virus growth, are responsible for the pathogenic process in severe cases who survive through week.
A protracted clinical course was intensified by slower and prolonged convalescence due to complications of pulmonary fibrosis occurring in week 3 in some patients. Results of high-resolution computed tomographic scans in follow-up of SARS patients corroborate this observation, with a strong correlation between bilateral fibrotic lung changes and clinical severity.
Viral Load and Mortality
Viral shedding in the nasopharynx, measured by quantitative RT-PCR, peaks on day 10 (Fig. 59.3).32 However, analysis of 265 laboratory-confirmed SARS patients in Taiwan demonstrates that, on any given day of the clinical course, SARS-CoV shedding in the nasopharynx varies widely from individual to individual, ranging from below the detection limit to as high as 108 RNA copies/mL; male patients and elderly patients are more likely to have detectable virus shedding, suggesting that individual host differences.
https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/angiotensin-converting-enzyme-2
“Thus, the pathogenesis must involve tissue-specific host responses, which are most likely intensified during week 2 of illness when pulmonary function worsens with concomitant decreasing viral load in the airways (Fig. 59.3). Clinical studies of cytokines during the acute phase suggest that activation of Th1 cell-mediated immunity and an excessive innate inflammatory response, rather than direct damage from uncontrolled virus growth, are responsible for the pathogenic process in severe cases who survive through week.”
May 1 (GMT)
Updates
6201 new cases and 739 new deaths in the United Kingdom
Let the bells ring and the banners fly.
This civilization changing and it is happening because of covid-19 and because Trump is not a politician.
We have the first of the jump up and down civilization and complete industry changing medical breakthrough.
We could have a Star Trek like solution, or Covid, by September.
Trump has given $500 million, to a company that has breakthrough disruptive technology, uses a virus like entity to enter some of the human cells to create a synthetic copy of the virus’s spike protein.
This is not a ‘vaccine’. This is an engineered microbiological entity that is smart and only does what we want.
What was stopping the use of microbiological entities to ‘fix’/change the body rather than dumb chemicals or dead viruses was….
The body’s immune system.
What changed to enable engineered ‘virus’ like entities to do our bidding…
….was the development of software that can emulate any virus or virus like entity in a computer and emulates the bioactive response of the human body.
This complex software evolves the microbiological entity, in the computer, to enable it to defeat the human immune system, to enable it to enter a person’s body to do very, very specific tasks.
https://www.cnn.com/2020/05/01/us/coronavirus-moderna-vaccine-invs/index.html
Moderna, Inc. — originally called Moderna Therapeutics — was founded on a big idea that would disrupt the pharmaceutical industry.
In theory, an mRNA vaccine enables scientists to plug a small piece of the coronavirus’s genetic code into a human cell to create a synthetic copy of the virus’s spike protein.
That’s the part of SARS-CoV-2 that resembles a plastic bristle on a hairbrush, and which attaches to human cells.
Because it is just a small portion of the virus, the synthetically created spike protein can’t infect a person. And partly because there is no need to manipulate a virus in the lab, the process is faster.
The coronavirus spike-protein lookalike would then be produced by the body’s own cells. If all goes well, the body then counterattacks the “invader” — the synthetic antigen created by a person’s own cell — with antibodies.
The technology “teaches the human body to recognize the virus by teaching the body to make snippets of the virus on its own,” said Zaks, Moderna’s chief medical officer.
On January 11, Chinese researchers released the genetic sequence of SARS-CoV-2, a 30,000-character string of the letters a, u, g and c.
Largely because of the ongoing cooperation between Moderna and NIH, the process of designing the mRNA for delivery was lightning fast. Indeed, it took just 42 days, as Bancel told Trump.
Its vision is to harness a new technology that synthesizes messenger RNA, or mRNA — essentially an instruction manual in every living cell for creating protein — to prompt the human body to make its own medicine. The hope has been to find “transformative” treatments for heart disease, metabolic and genetic diseases, kidney failure, even cancer.
On March 3 — the day after the roundtable — the FDA green-lit Moderna’s product for trial, making it the first vaccine candidate to advance to the first phase of a clinical study, in which an as-yet unapproved vaccine is injected into the arms of a small group of 45 human volunteers.
Moderna’s unproven but potentially paradigm-shattering technology has garnered enthusiastic press: Moderna was ranked No. 1 on the CNBC Disrupter 50 list in 2015 for its goal to help “the human body make the medicine it needs to cure a disease,” putting it in company with eventually the likes of Airbnb, Lyft and WeWork. More recently, it was praised in an op-ed by Bill Gates — whose namesake foundation has given millions to Moderna — though his piece didn’t mention the company by name.
A German company is trying the same approach. Problem:
As promising as this approach sounds it has never successfully done before.
At the moment I hope the Chinese company that used just inactivated virus to generate a vaccine that proved to work in monkeys is successful. The same approach works very well for polio and hepA+B.
The production method they used can be easily copied in many facilities around the world so production of tens of millions vaccination units could be ramped up very fast. Even facilities for veterinarian vaccines use the same procedure and could be reassigned.
No chance to contain this virus when things like this happen. Every sailor on board tested. Everyone quarantined for two weeks or more. 162 sailors who tested negative more than two weeks ago and then were quarantined for two weeks. Ready to go back on board and tested again and found positive with no symptoms. As best as I can find over 50% of positives from over a month long ordeal remain asymptomatic. 1 death and last update I could find 4-8 hospitalization out of 1154 infections to date. 25% of crew infected so far. https://www.sandiegouniontribune.com/news/military/story/2020-04-30/coronavirus-cases-surge-on-carrier-uss-theodore-roosevelt-destroyer-uss-kidd
A couple of days ago I wrote:
“Actually Willis has also been recommending Gompertz curves, which I have been using to good effect, and with those, instead of multiplying the deaths before peak by 2, you multiply by e = 2.718281828.”
and LM replied:
“Certainly the epidemic or S or sigmoid or logistic or Gompertz curve, which has been discussed both by my good friend Willis Eschenbach and also by me, is of particular value when studying an epidemic that will pass right through the population at a more or less uniform reproduction rate. That does not apply to the current pandemic, which is why studying the case-growth and death-growth rates is more likely to produce reliable answers.”
The thing is, I have been successfully applying Gompertz curves to UK hospital death data for several weeks, coming out with projections of 30-35k total by the end. Here is a recent graph (if moderators could tell me how to get it to display inline I’d be most grateful – the Test page didn’t help):
Rather than using a general error minimizer, I choose 3 points, marked by triangles, through which to fit the curve. I do this by eliminating 2 variables in y = c exp(-b exp(-at)) and then solving the 3rd by binary search, then recovering the other 2 variables.
Those 3 dates were March 27th, April 5th, April 14th, and 17 days later the data had strayed only a small amount below the curve.
So whatever high level theory there might be as to whether Gompertz should, or should not, fit, it seems to do remarkably well. Thanks again Willis, for introducing those curves to me.
Rich.
MofB: I have read all of your pieces. Why so little said here about HCQ?