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COVID – why terminology really, really matters
428 Replies
4th September 2020
COVID – why terminology really, really matters
[And the consequences of getting it horribly wrong]
When is a case not a case?
Since the start of the COVID pandemic I have watched almost everyone get mission critical things wrong. In some ways this is not surprising. Medical terminology is horribly imprecise, and often poorly understood. In calmer times such things are only of interest to research geeks like me. Were they talking about CVD, or CHD?
However, right now, it really, really, matters. Specifically, with regards to the term COVID ‘cases.’
Every day we are informed of a worrying rise in COVID cases in country after country, region after region, city after city. Portugal, France, Leicester, Bolton. Panic, lockdown, quarantine. In France the number of reported cases is now as high as it was at the peak of the epidemic. Over 5,000, on the first of September.
But what does this actually mean? Just to keep the focus on France for a moment. On March 26th, just before their deaths peaked, there were 3,900 hundred ‘cases’. Fourteen days later, there were 1,400 deaths. So, using a widely accepted figure, which is a delay of around two weeks between diagnoses and death, 36% of cases died.
In stark contrast, on August 16th, there were 3,000 cases. Fourteen days later there were 26 deaths. Which means that, in March, 36% of ‘cases’ died. In August 0.8% of ‘cases’ died. This, in turn, means that COVID was 45 times as deadly in March, as it was in August?
This seems extremely unlikely. In fact, it is so unlikely that it is, in fact, complete rubbish. What we have is a combination of nonsense figures which, added together, create nonsense squared. Or nonsense to the power ten.
To start with, we have the mangling of the concept of a ‘case’.
Previously, in the world of infectious diseases, it has been accepted that a ‘case’ represents someone with symptoms, usually severe symptoms, usually severe enough to be admitted to hospital. Here, from Wikipedia…. yes, I know, but on this sort of stuff they are a good resource.
‘In epidemiology, a case fatality rate (CFR) — sometimes called case fatality risk or disease lethality — is the proportion of deaths from a certain disease compared to the total number of symptomatic people diagnosed with the disease.’ 1
Note the word symptomatic i.e. someone with symptoms.
However, now we stick a swab up someone’s nose, who feels completely well, or very mildly ill. We find that they have some COVID particles lodged up there, and we call them a case of COVID. Sigh, thud!
A symptomless, or even mildly symptomatic positive swab is not a case. Never, in recorded history, has this been true. However, now we have an almost unquestioned acceptance that a positive swab represents a case of COVID. This is then parroted on all the news channels as if it were gospel.
I note that, at last, some people are beginning to question how it can be that, whilst cases are going up and up, deaths are going down, and down.
This is even the case in Sweden, which seems to be the final bastion of people with functioning brains. However, even they seem surprised by this dichotomy. In the first two weeks of August they had 4,152 positive swabs. Yet, in the last two weeks of August, they had a mere 14 deaths (one a day, on average).
That represents 1 death for every 300 positive swabs or, as the mainstream media insists on calling them, positive ‘cases’. Which, currently, represent a case fatality rate of 0.33%. Just to compare that with something similar, the case fatality rate of swine flu (HIN1), was 0.5%. 2
Thus, lo and behold, COVID is a less severe infection than swine flu – the pandemic that never was. That’s what these figures appear to tell us. They tell us almost exactly the same in France where they ‘appear’ to have a current case fatality rate of 0.4%.
On the other hand, if you look at the figures from around the world, they are very different. As I write this there have been, according to the WHO, 25 million cases and 850,000 deaths. That is a case fatality rate of more than 3%. Ten times as high.
Why are these figures so all over the place? It is because we are using horribly inaccurate terminology. We are comparing apples with pomegranates to tell us how many bananas we have. Our experts are, essentially, talking gibberish, and the mainstream media is lapping it up. They are defining asymptomatic swabs as cases, and no-one is calling them out on it. Why?
Because… because they are frightened of looking stupid? Primarily, I believe, because they also have no idea what a case might actually be So, it all sounds quite reasonable to them.
The good news
However, moving on from that nonsense, there is some extremely good news buried in here. Which I am going to try and explain. It goes as follows.
At the start of the epidemic, the only people being tested were those who were being admitted to hospital, who were seriously ill. Many of them died. Which is why, in France, there was this very sharp, initial case fatality rate of 35%. In the UK the initial case fatality rate was I think 14%. Last time I looked at the UK figures, the case fatality was 5%, and falling fast.
This fall has occurred, and will occur everywhere in the World, because as you increase your testing, you pick up more and more people with less severe symptoms. People who are far less likely to die. The more you test, the more the case fatality rate falls.
It falls even more dramatically when you start to test people who have no symptoms at all. In fact, as you broaden your testing net, something else very important happens. You gradually move from looking at the case fatality rate to the infection fatality rate.
The infection fatality rate is the measure of how many people who are infected [even those without symptoms, or very mild symptoms] who then die. This is the critical figure to know because it gives you an accurate assessment of the total number of deaths you are likely to see.
IFR x population of a country x % of population infected = total number of deaths (total mortality)
So, where have we got to. Well, although the case fatality rate in the UK still currently stands at 5%, because it is dragged up by the 14% rate we had at the start. If we look at the more recent figures things have changed very dramatically.
In the first two weeks of August there were 13,996 positive swabs in the UK. In the second two weeks of August there were 129 deaths. If you consider every positive swab to be a case, this represents a case fatality rate of 0.9%. Around one fifteenth of that seen at the start.
I think you can clearly see a direction of travel here.
At the start on the pandemic we had a, brief, 35% fatality rate in France
It was 14% in the UK at the start
It now sits at 5% in the UK – over the whole pandemic
In August, in the UK, it was down to 0.9%
It is currently 0.47% in Germany
It is currently 0.4% in France
It is currently 0.33% in Sweden
It is falling, falling, everywhere. Where does it end up, this hybrid case/infection fatality rate? Remember, we are still only testing a fraction of the population, so we are missing the majority of people who have been infected, mainly those who do not have symptoms. Which means that these rates must fall further, as they always do in any pandemic.
To quote the Centre for Evidence Base Medicine on the matter:
‘In Swine flu, the IFR (infection fatality rate) ended up as 0.02%, fivefold less than the lowest estimate during the outbreak (the lowest estimate was 0.1% in the 1st ten weeks of the outbreak).’ 3
The best place to estimate where we may finally end up with COVID, is with the country that has tested the most people, per head of population. This is Iceland. To quote the Centre for Evidence Based Medicine once more:
‘In Iceland, where the most testing per capita has occurred, the IFR lies somewhere between 0.03% and 0.28%.’ 3
Sitting in the middle of 0.03% and 0.28% is 0.16%. As you can see, Iceland, having tested more people than anywhere else, has the lowest IFR of all. This is not a coincidence. This is an inevitable result of testing more people.
I am going to make a prediction that, in the end, we will end up with an IFR of somewhere around 0.1%. Which is about the same as severe flu pandemics we have had in the past. Remember that figure. It is one in a thousand.
It may surprise you to know that I am not the only person to have made this exact same prediction. On the 28th February, yes that far back, the New England Journal of Medicine published a report by the National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD (A.S.F., H.C.L.); and the Centers for Disease Control and Prevention, Atlanta. 4
In this paper ‘Covid-19 — Navigating the Uncharted’ they stated the following:
‘On the basis of a case definition requiring a diagnosis of pneumonia, the currently reported case fatality rate is approximately 2%. In another article in the Journal, Guan et al. report mortality of 1.4% among 1099 patients with laboratory-confirmed Covid-19; these patients had a wide spectrum of disease severity. If one assumes that the number of asymptomatic or minimally symptomatic cases is several times as high as the number of reported cases, the case fatality rate (my underline) may be considerably less than 1%. This suggests that the overall clinical consequences of Covid-19 may ultimately be more akin to those of a severe seasonal influenza.’
A case fatality rate considerably less than 1%. Their words, not mine. As they also added, ‘the overall clinical consequences of Covid-19 may ultimately be more akin to those of a severe seasonal influenza.’
At this point, you may well be asking. Why the hell did we lockdown if COVID was believed to be no more serious than influenza? Right from the start by the most influential infectious disease organisations in the World.
It is because of the mad mathematical modellers. The academic epidemiologists. Neil Ferguson, and others of his ilk. When they were guessing (sorry estimating, sorry modelling) the impact of COVID they used a figure of approximately one per cent as the infection fatality rate. Not the case fatality rate. In so doing, they overestimated the likely impact of COVID by, at the very least, ten-fold.
How could this possibly have happened?
When they put their carefully constructed model together on the 16th of March, if they had been reading the research, they must have been aware that they were looking at a maximum case fatality rate of just over 1% in China, right at the start, where the figures are always at their highest.
Which means that, unless COVID was going to turn out nearly 100% fatal, we could never get anywhere near 1%, for the infection fatality rate. Even Ebola only kills 50%.
But they went with it, they went with 1%. Actually, Imperial College reduced it slightly to 0.9%, for reasons that are opaque.
From this, all else flowed.
If the INFECTION fatality rate truly were 0.9%, and 80% of the population of the UK became infected, there would have been/could have been, around 500,000 deaths.
0.9% x 80% x 67million = 482,000
LOCKDOWN
However, if the case fatality rate is around 1%, then the infection fatality rate will be about one tenth of this, maybe less. So, we would see around 50,000 deaths, about the same as was seen in previous bad flu pandemics.
DO NOT LOCKDOWN
What Imperial College London did was to use a model that overestimated the infection fatality rate by a factor of ten.
We now know, as the IFR rates of various countries falls and falls, that the Imperial College estimated IFR was completely wrong. The UK, for example, has seen 42,000 deaths so far, which is 0.074% of population. The US has seen about 200,000 deaths 0.053%. Sweden, which did not lockdown down, has seen about 6,000 deaths, which is an infection fatality rate of 0.06%. All three countries are opening up and opening up. Whilst the ‘cases’ are rising and rising, the deaths continue to fall. They are, to all intents and purposes, flatlining.
In Iceland it is around 0.16% and falling. In other words…
Stop panicking – it’s over
Whilst everyone is panicking about the ever-increasing number of cases, we should be celebrating them. They are demonstrating, very clearly, that COVID is far, far, less deadly then was feared. The Infection Fatality Rate is most likely going to end up around 0.1%, not 1%.
So yes, it does seem that ‘the overall clinical consequences of Covid-19 may ultimately be more akin to those of a severe seasonal influenza.’
Wise words, wise words indeed. Words that were written by one Anthony S Fauci on the 28th of February 2020. If you haven’t heard of him, look him up.
Critically though, eleven days after this, he rather blotted his copybook, because he went on to say this “The flu has a mortality rate of 0.1 percent. This (COVID) has a mortality rate of 10 times that. That’s the reason I want to emphasize we have to stay ahead of the game in preventing this.” 5
The mortality rate Dr Fauci? Could it possibly be that he failed to understand that there is no such thing as a mortality rate? Did he mean the case fatality rate, or the infection fatality rate? If he meant the Infection mortality rate of influenza, he was pretty much bang on. If he meant the case fatality rate, he was wrong by a factor of ten.
The reality is that, no matter what Fauci went on to say, severe influenza has a case fatality rate of 1%, and so does COVID. They also have approximately the same infection fatality fate of 0.1%.
It seems that Dr Fauci just got mixed up with the terminology. Because in his Journal article eleven days earlier, he did state… ‘This suggests that the overall clinical consequences of Covid-19 may ultimately be more akin to those of a severe seasonal influenza… [and here is the kicker at the end] (which has a case fatality rate of approximately 0.1%).’
You see, he did say the case fatality rate of influenza was approximately 0.1%. Wrong, wrong, wrong, wrong… wrong.
Oh dear, oh dear, oh dear. With influenza, Dr Fauci, the CDC, his co-authors, the National Institute of Allergy and Infectious Diseases and the National Institutes of Health and the New England Journal of Medicine got case fatality rate and infection fatality rate mixed up with influenza. Easy mistake to make. Could have done it myself. But didn’t.
You want to know where Imperial College London really got their 1% infection fatality rate figure from? It seems clear that they got it from Anthony S Fauci and the New England Journal of Medicine. The highest impact journal in the world – which should have the highest impact proof-readers in the world. But clearly does not.
Imperial College then used this wrong NEJM influenza case fatality rate 0.1%. It seems that they then compared this 0.1% figure to the reported COVID case fatality rate, estimated to be 1% and multiplied the impact of COVID by ten – as you would. As you probably should.
So, we got Lockdown. The US used the Fauci figure and got locked down. The world used that figure and got locked down.
That figure just happens to be ten times too high.
I know it is going to be virtually impossible to walk the world back from having made such a ridiculous, stupid, mistake. There are so many reputations at stake. The entire egg production of the world will be required to supply enough yolk to cover appropriate faces.
Of course, it will be denied, absolutely, vehemently, angrily, that anyone got anything wrong. It will be denied that a simple error, a mix up between case fatality and infection fatality led to this. It will even more forcefully stated that COVID remains a deadly killer disease and that all Governments around the world have done exactly the right thing. The actions were right, the models were correct. We all did the RIGHT thing. Only those who are stupid, or incompetent cannot see it.
When wrong, shout louder, get angry, double-down, attack your critics in any way possible. Accuse them of being anti-vaxx, or something of the sort. Dig for the dirt. ‘How to succeed in politics 101, page one, paragraph one.’
However, just have a look, at the figures. Tell me where they are wrong – if you can. The truth is that this particular Emperor has no clothes on and is, currently, standing bollock naked, right in front of you. Hard to believe, but true.
I would like to thank Ronald B Brown for pointing out this catastrophic error, in his article ‘Public health lessons learned from biases in coronavirus mortality overestimation.’ 6
I had not spotted it. He did. All credit is his. I am simply drawing your attention to what has simply been – probably the biggest single mistake that has ever been made in the history of the world.
1:
https://en.wikipedia.org/wiki/Case_fatality_rate
2:
https://www.thelancet.com/journals/lani ... %C2%B75%25.
3:
https://www.cebm.net/covid-19/global-co ... ity-rates/
4:
https://www.nejm.org/doi/full/10.1056/nejme2002387
5:
https://reason.com/2020/03/11/covid-19- ... ony-fauci/
6:
https://www.cambridge.org/core/journals ... BB28DCC6E9
This entry was posted in COVID-19 on September 4, 2020.
COVID – What have we learned?
344 Replies
25th August 2020
We have learned that people who are asymptomatic can, cannot, can, cannot, can, cannot, can… spread the virus.
That the accuracy of PCR antigen testing is brilliant, useless, brilliant, useless, brilliant, useless.
That false positive tests are impossible, common, impossible, common, impossible, common.
That facemasks are useless, necessary, useless, necessary, useless… absolutely necessary.
We also know that some people are, are not, are, are not are, naturally immune. In addition, we know that having had COVID means that you can, cannot, can, cannot, can cannot – maybe you can, frankly who knows, get it again. I think Kurt Vonnegut Junior put it best:
“We do, doodley do, doodley do, doodely do,
What we must, muddily must, muddily must, muddily must;
Muddily do, muddily do, muddily do, muddily do,
Until we bust, bodily bust, bodily bust, bodily bust.”
I like to think I have some expertise in reading medical research papers, then trying to work out what they really mean, rather than what they say they mean. I even gritted my teeth and wrote the book “Doctoring Data” in order to help people understand the endless games and manipulations that are played with research studies.
I analysed the power of money to distort research findings, in ways such that black can be magically turned into white.
Of course, distortion is not just driven by money. This is only one of the factors that lays its heavy hand upon research. There are many others. The immense power of an idea to set thoughts in concrete, previous public statements made and fearing loss of authority if you change your mind. Status, power, political games, etc.
Just to look at an example of actions not (obviously) driven by money. On the back of COVID, Bill Gates seems determined to be remembered as the man who vaccinated the world. It will be his enduring legacy. He probably knows that his Microsoft empire will simply be a sub-paragraph in an MBA hypothesis in a hundred years. On the other hand, worldwide vaccination will secure him a place in history.
Although I understand many of the forces at work to distort research, and how the manipulates are carried out, when it comes to COVID I have almost given up. Almost everyone seems to have an agenda, twisting and turning meaning this way and that.
In many cases, the end result seems to be a determined effort to inflate the mortality figures, or paint COVID as the evillest virus ever. I suspect the vaccine manufacturers have a major role to play in this.
Just to give one reasonably well-known example of this. In England, if you ever had a positive test for COVID, and then died, you were added to the COVID death statistics. Whatever killed you, however long after you had a positive test you died of COVID.
This has recently been changed. Primarily because it was so patently ridiculous that even Matt Hancock (UK health secretary) was no longer able to confirm that this was absolutely the correct thing to do. Although it seems he had no idea it was happening in the first place.
Despite this change, we still have the situation in the UK, where you can never, officially recover from COVID – which is equally mad. Once you’ve got it, you’ve got it. I suspect this will be quietly changed at some point – maybe it has been, and I didn’t notice.
On the other hand, other very strange things took place, in the opposite direction. Right at the start of the pandemic, the UK Govt changed COVID to an infection no longer considered of high consequence
As of 19 March 2020, COVID-19 is no longer considered to be a high consequence infectious disease (HCID) in the UK.1
Yes, the 19th of March. The UK went into lockdown on the 16th of March [Error, this should be the 23rd march], and three days later COVID was no longer a high consequence disease. The only disease in history which has required lockdown, including the obliteration of many basic human rights, and the trashing of the entire economy. Yet it is not a disease of high consequence?
This happened virtually unremarked. Very quietly, you could almost say sneakily. What on earth went on here? My guess is this was done to stop healthcare workers suing the NHS if they contracted COVID at work – as almost no medical staff had adequate PPE. There may be other reasons, but I struggle to think what they may be.
Wherever you looked there was confusion, and statistical manipulation, and then we moved onto the hydroxychloroquine saga. At the very start of the pandemic I wrote a blog suggesting hydroxychloroquine could be helpful. This was based on earlier research demonstrating this drug could hamper viral entry into cells and, once within the cell, could impede viral entry into the nucleus. I even tried to get my trust to stockpile some of the drug – no chance there. Hydroxy-what?
Little did I know the massive storm that would erupt around this drug. A drug that has been around for decades. It is available over the counter in many countries and is, I think, the most widely used drug in India. It is primarily an anti-malarial drug – as it helps to prevent entry of the malaria parasite into cells and can hamper it breaking down haemoglobin, thus destroying red blood cells.
It is also used as an anti-inflammatory in diseases such as rheumatoid arthritis and systemic lupus erythematosus (SLE), where it is extraordinarily safe (in the correct doses). It has been looked at as a possible anti-viral for many years. Earlier this year, I was reading various papers about it. Such as this one ‘Effects of chloroquine on viral infections: an old drug against today’s diseases.’
Chloroquine is a 9-aminoquinoline known since 1934. Apart from its well-known antimalarial effects, the drug has interesting biochemical properties that might be applied against some viral infections. Chloroquine exerts direct antiviral effects, inhibiting pH-dependent steps of the replication of several viruses including members of the flaviviruses, retroviruses, and coronaviruses. Its best-studied effects are those against HIV replication, which are being tested in clinical trials. Moreover, chloroquine has immunomodulatory effects, suppressing the production/release of tumour necrosis factor α and interleukin 6, which mediate the inflammatory complications of several viral diseases’.2
[Chloroquine and hydroxychloroquine are essentially the same drug, when it comes to efficacy/activity, but hydroxychloroquine has less side-effects. ‘Hydroxy’ means an OH group has been added to the basic compound]
I have to say I didn’t bother to read anything from 2020. It was clear that commercial interests were already heavily contaminating this area.
Which meant that, in order to get a handle on untainted data, I went back to calmer research papers from another era. Anyway, having read around the area, it seemed that hydroxychloroquine might do some good. It was certainly pretty safe, and we had nothing else at the time. Thus, I recommended that it might be used.
Then, the distorting engine was switched to full power. Driven by two main fuel types. Type one was money. Companies with anti-viral agents, such as remdesivir, did not want a ‘cheap as chips’ drug being used. No sirree, they wanted massively expensive (and almost entirely useless) anti-virals to be used instead.
This resulted in a study published in the Lancet, no less, slamming hydroxychloroquine through the floor. It turns out the study was almost entirely fabricated, by researchers strongly associated with various companies who, surprise, surprise, make anti-virals.
The other fuel type was the hybrid money/vaccine. If hydroxychloroquine (plus zinc and azithromycin) works, then there was great concern this would lower uptake of any vaccine that was developed. In addition, it would not be possible to impose emergency vaccine laws, which would make the manufacture of any vaccine far quicker and easier.
Such laws, in the US, are known as Emergency Use Authorisation (EUA). If enacted, these laws mean that a vaccine does not have to be tested for safety and efficacy before use. Just whack it out there, untested. Also, there is no possibility of suing a vaccine manufacturer if it turns out the vaccine caused serious problems.
In the US, UK, and several other countries, complete legal protection against vaccine damage is already enshrined in the law, so nothing changes here.
However, there is still a requirement to carry out at least some research on efficacy and safety. The EUA would remove this barrier. Just get it out there, no questions asked, none possible.
Depending on your view of the ethical standards of those companies manufacturing such vaccines, you would either welcome this move, or feel deeply disturbed. I would be in the latter camp. No way I am taking an active medication that has not been tested for either safety or efficacy.
Whatever camp you are in, there are vast fortunes to be made from developing the first vaccine for COVID-19. If all barriers to immediate uptake are removed, we have a goldrush on our hands. No need to prove your vaccine works, no need to demonstrate it is safe, no chance of being sued. Billions of dollars to be made. What could possibly go wrong?
Which takes us back to that pesky drug, hydroxychloroquine. Does it work, does it not? It seems we will never be allowed to know. Recently the Food and Drug Administration in the US, removed authorisation for its use. Even in a hospital, such as he Henry Ford in Detroit, that appeared to be getting impressive results:
‘”The U.S. Food and Drug Administration informed us that it would not grant our request for an emergency use authorization for hydroxychloroquine for a segment of COVID-19 patients meeting very specific criteria,” said Dr. Adnan Munkarah, Henry Ford’s executive vice president and chief clinical officer, in a statement’ 3
All other trials around the world have also being stopped by the National Institutes of Health, the World Health Orhanisation and the UK health authorities.
This, remember, is a drug that has been taken by, literally, billions of people. It is considered safe enough to buy over the counter, yet now it is so dangerous that it cannot even be used for research purposes. Of course, you can still take it if you have rheumatoid arthritis, SLE, malaria – or suchlike – where it remains perfectly safe and is also known to reduce inflammation (a major problem with COVID).
At a stroke discussion, or research, has become virtually impossible, as noted by the Henry Ford hospital in Detroit.
‘Last week, Henry Ford issued an open letter about its study, saying, “the political climate that has persisted has made any objective discussion about this drug impossible.”
The health system said in the letter that it will no longer comment outside the medical community on the use of hydroxychloroquine to treat novel coronavirus.’
So, what have we learned? We have learned that medical science is not a pure thing – not in the slightest. We have also learned that the world of research has not come together to conquer COVID, it has split apart.
Those wanting to make money, have distorted and damaged research for their own ends. Those who want to vaccinate the world, forever, have seen a door open to the promised land. Those who wanted lockdown, are inflating the numbers of those killed. Democrats in the US are using COVID as a stick to beat Donald Trump. It is all a bloody horrible mess.
It is said that the first casualty of war is the truth. Never has this been more certain that with COVID. In this case, first we killed the truth, then we killed science, then we beat inconvenient facts to death with a club. It is all extraordinarily depressing.
1:
https://www.gov.uk/guidance/high-conseq ... f-covid-19
2:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7128816/
3:
https://eu.freep.com/story/news/health/ ... 360940001/
This entry was posted in Conflicts of Interest, COVID-19 on August 25, 2020.
How bad is COVID really? (A Swedish doctor’s perspective)
676 Replies
7th August 2020
A doctor working in Sweden as an emergency care physician contacted me to discuss all things COVID-19. He has also written a blog, which can be seen here.
I asked if I could reproduce it on my blog as I felt it was a fascinating persepctive on what was happening in Sweden. It is also incredibly well written, in English, for someone who is Swedish. Most humbled. I hope you enjoy it.
Ok, I want to preface this article by stating that it is entirely anecdotal and based on my experience working as a doctor in the emergency room of one of the big hospitals in Stockholm, Sweden, and of living as a citizen in Sweden.
As many people know, Sweden is perhaps the country that has taken the most relaxed attitude of any towards the COVID pandemic. Unlike other countries, Sweden never went in to complete lockdown. Non-essential businesses have remained open, people have continues to go to cafés and restaurants, children have remained in school, and very few people have bothered with face masks in public.
COVID hit Stockholm like a storm in mid-March. One day I was seeing people with appendicitis and kidney stones, the usual things you see in the emergency room. The next day all those patients were gone and the only thing coming in to the hospital was COVID. Practically everyone who was tested had COVID, regardless of what the presenting symptom was. People came in with a nose bleed and they had COVID. They came in with stomach pain and they had COVID.
Then, after a few months, all the COVID patients disappeared. It is now four months since the start of the pandemic, and I haven’t seen a single COVID patient in over a month. When I do test someone because they have a cough or a fever, the test invariably comes back negative.
At the peak three months back, a hundred people were dying a day of COVID in Sweden, a country with a population of ten million. We are now down to around five people dying per day in the whole country, and that number continues to drop. Since people generally die around three weeks after infection, that means virtually no-one is getting infected any more.
If we assume around 0.5 percent of those infected die (which I think is very generous, more on that later), then that means that three weeks back 1,000 people were getting infected per day in the whole country, which works out to a daily risk per person of getting infected of 1 in 10,000, which is miniscule. And remember, the risk of dying is at the very most 1 in 200 if you actually do get infected. And that was three weeks ago. Basically,COVID is in all practical senses over and done with in Sweden.
After four months. In total COVID has killed under 6,000 people in a country of ten million. A country with an annual death rate of around 100,000 people. Considering that 70% of those who have died of COVID are over 80 years old, quite a few of those 6,000 would have died this year anyway. That makes covid a mere blip in terms of its effect on mortality.
That is why it is nonsensical to compare covid to other major pandemics, like the 1918 pandemic that killed tens of millions of people. COVID will never even come close to those numbers. And yet many countries have shut down their entire economies, stopped children going to school, and made large portions of their population unemployed in order to deal with this disease.
The media have been proclaiming that only a small percentage of the population have antibodies, and therefore it is impossible that herd immunity has developed. Well, if herd immunity hasn’t developed, where are all the sick people? Why has the rate of infection dropped so precipitously? Considering that most people in Sweden are leading their lives normally now, not socially distancing, not wearing masks, there should still be high rates of infection.
The reason we test for antibodies is because it is easy and cheap. Antibodies are in fact not the body’s main defence against virus infections. T-cells are. But T-cells are harder to measure than antibodies, so we don’t really do it clinically. It is quite possible to have T-cells that are specific for covid and thereby make you immune to the disease, without having any antibodies.
Personally, I think this is what has happened. Everybody who works in the emergency room where I work has had the antibody test. Very few actually have antibodies. This is in spite of being exposed to huge numbers of infected people, including at the beginning of the pandemic, before we realized how widespread COVID was, when no-one was wearing protective equipment.
I am not denying that COVID is awful for the people who do get really sick or for the families of the people who die, just as it is awful for the families of people who die of cancer, or influenza, or an opioid overdose. But the size of the response in most of the world (not including Sweden) has been totally disproportionate to the size of the threat.
Sweden ripped the metaphorical band-aid off quickly and got the epidemic over and done with in a short amount of time, while the rest of the world has chosen to try to peel the band-aid off slowly. At present that means Sweden has one of the highest total death rates in the world. But COVID is over in Sweden. People have gone back to their normal lives and barely anyone is getting infected any more.
I am willing to bet that the countries that have shut down completely will see rates spike when they open up. If that is the case, then there won’t have been any point in shutting down in the first place, because all those countries are going to end up with the same number of dead at the end of the day anyway. Shutting down completely in order to decrease the total number of deaths only makes sense if you are willing to stay shut down until a vaccine is available. That could take years. No country is willing to wait that long.
COVID has at present killed less than 6000 in Sweden. It is very unlikely that the number of dead will go above 7,000. An average influenza year in Sweden, 700 people die of influenza. Does that mean COVID is ten times worse than influenza? No, because influenza has been around for centuries while COVID is completely new.
In an average influenza year most people already have some level of immunity because they’ve been infected with a similar strain previously, or because they’re vaccinated. So it is quite possible, in fact likely, that the case fatality rate for COVID is the same as for influenza, or only slightly higher, and the entire difference we have seen is due to the complete lack of any immunity in the population at the start of this pandemic.
This conclusion makes sense of the Swedish fatality numbers – if we’ve reached a point where there is hardly any active infection going on any more in Sweden, in spite of the fact that there is barely any social distancing happening, then that means at least 50% of the population has been infected already and have developed immunity, which is five million people.
This number is perfectly reasonable if we assume a reproductive number for the virus of two: If each person infects two new, with a five day period between being infected and infecting others, and you start out with just one infected person in the country, then you will reach a point where several million are infected in just four months. If only 6000 are dead out of five million infected, that works out to a case fatality rate of 0.12 percent, roughly the same as regular old influenza, which no-one is the least bit frightened of, and which we don’t shut down our societies for.
This entry was posted in COVID-19 on August 7, 2020.
Cholesterol lowering has no impact
161 Replies
5th August 2020
This article was first published on RT.com on the 4th of August, and it can be seen here
In the midst of the COVID-19 epidemic almost every other medical condition has been shoved onto the side-lines. However, in the UK last year, heart attacks and strokes (CVD) killed well over one hundred thousand people – at least twice as many as have died from COVID-19.
CVD will kill just as many this year. Which makes it significantly more important than COVID-19, even if no-one is paying much attention to it right now. So, it is good to see that research goes on, and papers are still being published.
One of the most significant, and of great interest to me personally, was a critical examination of the benefits of lowering cholesterol. This was published on the fourth of August. The paper was called ‘Hit or miss: the new cholesterol targets,’ and it came out in Evidence Based Medicine, one of the key titles that sits under the umbrella of British Medical Journal publishing
It was carefully worded, as all clinical papers are, but a key section of the press release was as follows: “Setting targets for ‘bad’ (LDL) cholesterol levels to ward off heart disease and death in those at risk might seem intuitive, but decades of research have failed to show any consistent benefit for this approach, reveals an analysis of the available data, published online in BMJ Evidence Based Medicine.”
What is being said here is the following. Everyone thinks that lowering LDL, a.k.a. ‘bad cholesterol is considered the single most important way to reduce the risk of heart disease and strokes. However, “decades of research have failed to show any consistent benefit for this approach.”
Surely this flies in the face of almost all the advice we have been bombarded with for the last fifty years, or so? Cholesterol – by which we really mean low density lipoprotein (LDL) – is a killer and must be lowered. This is the whole point of statins, the single most widely prescribed type of drug in the history of medicine. Drugs that have racked up sales of nearly one trillion dollars since their launch.
Now, newer, and far more expensive LDL lowering medications are available, riding on the success of statins. They are injectable, rather than a tablet, and the cost is far higher. In the US, you are looking at around $5,000 per year. In the UK, one of these drugs Repatha, costs the NHS just over £4,000 per year. These drugs are known as PCSK9-inhibitors.
These are eye-watering costs. It is estimated that around seven million people in the UK take statins currently. If everyone converted to a PCSK9-inhibitor, this would cost the NHS twenty-eight billion pounds a year. Not far off the entire defence budget.
But do these drugs work, does lowering LDL work? Surely it does, surely it must. The answer is, not necessarily. Yes, statins have been found to reduce the risk of cardiovascular disease, not by a massive amount, but the effect exists. At least in some studies, if not all.
However, many other drugs also reduce the risk of cardiovascular disease without having any
effect on LDL levels, e.g. aspirin. A number of researchers have long argued that the benefits of statins are mainly due to “off-target” effects. By which they mean that, yes, statins lower LDL, but they also have effects on many other things and it is the “other things” that provide the benefit.
For example, statins have been found to have quite strong anti-coagulant (anti blood clotting) effects. Same as aspirin, as highlighted in the 2013 paper, ‘Anticoagulant effects of statins and their clinical implications.’ It states: “There is evidence indicating that statins… may produce several cholesterol-independent antithrombotic [anti-coagulant] effects.”
So, it has always remained possible that the main benefit of statins was NOT due to their impact on lowering LDL BUT because of something else that they do.
In this recent study, the authors decided to examine this possibility. So they gathered together all the LDL lowering trials – at least those big enough, and long enough to count – and try to establish whether the amount that the LDL was lowered, matched the reduction, if any, in cardiovascular disease. The technical term for this is “dose-response”.
Or, to put this another way, if the LDL hypothesis is correct, the greater the LDL lowering, the greater the benefit on CVD should be. What did they find? Here are the key findings – from the press release:
“Their analysis showed that over three quarters of all the trials reported no positive impact on the risk of death and nearly half reported no positive impact on risk of future cardiovascular disease.
And the amount of LDL cholesterol reduction achieved didn’t correspond to the size of the resulting benefits, with even very small changes in LDL cholesterol sometimes associated with larger reductions in risk of death or cardiovascular ‘events,’ and vice versa.
“Thirteen of the clinical trials met the LDL cholesterol reduction target, but only one reported a positive impact on risk of death…
“Considering that dozens of [randomised controlled trials] of LDL-cholesterol reduction have failed to demonstrate a consistent benefit, we should question the validity of this theory.”
And they conclude: “In most fields of science the existence of contradictory evidence usually leads to a paradigm shift or modification of the theory in question, but in this case the contradictory evidence has been largely ignored, simply because it doesn’t fit the prevailing paradigm.”
In short, what they found was that there was absolutely no correlation between the amount that LDL was lowered and the resulting benefit on CVD. In fact, the benefit was inverse i.e. the less the LDL was lowered, the greater the benefit.
This is a hugely important finding that really ought to be shouted from the rooftops. I admit I have a horse in the race, having long argued that LDL has nothing to do with heart disease (and being roundly condemned for doing so). So, it is nice to have my thoughts so powerfully supported in a peer-reviewed, high impact journal.
For the average person on this street, what this research means is that you should stop worrying about your LDL levels, and obsessively trying to get them down with drugs or diet. Tucked away in the paper was this significant finding:
“Moreover, consider that the Minnesota Coronary Experiment, a 4-year long RCT [randomised controlled trial] of a low-fat diet involving 9423 subjects, actually reported an increase in mortality and cardiovascular events despite a 13% reduction in total cholesterol.”
Cholesterol (LDL) went down, CVD went up. We really are wasting a colossal amount of money. And causing avoidable death?
This entry was posted in Cardiovascular Disease, Cholesterol & Statins on August 5, 2020.
COVID fear
741 Replies
25th July 2020
This was first published on RT.com
https://www.rt.com/op-ed/495421-inflate ... ity-rates/
Why the scaremongering about COVID?
This week we were told that, in the UK at least, anyone who had a positive COVID test who then died – of anything – would be recorded as dying of COVID. No matter when they die.
Which means that someone could have been tested positive in March, with no symptoms of COVID at all, who then died in July. They would be recorded, in the official figures, as dying of COVID. Even if the were hit by a bus.
Even more weird is the fact that there does not seem to be any time limit to this. So, you could test positive in March 2020, then die in March 2040, and still be recorded as dying of COVID. I doubt this will happen, but it could.
To be honest I have known something very strange has been going on with the UK data for some time. In that, the UK has not provided any figures on how many people have recovered from COVID. In almost all countries, figures are provided on the total number of cased, the total number of deaths, the number of active cases and the number who have recovered.
In the US for example, there have been just over three and a half million cases, a hundred and forty thousand deaths and one point seven million people have officially recovered. In the UK, there have been nearly three hundred thousand cases, forty-five thousand deaths – and no recorded recoveries.
In short, in the UK, you cannot ever recover from COVID. Once you’ve got it, that’s it, you’ve got it. This anomaly has been reported on before. Here for instance, from the Guardian in June.
‘Britain is an outlier internationally in not reporting the number of people who have recovered from Covid-19 alongside statistics on deaths and numbers of identified cases.’ 1
Why would anyone want to do this? You would think the Government would be pulling out all the stops to decrease the number of recorded COVID deaths. Especially as the UK is sitting in a pretty dismal place on the international comparison charts. Why deliberately inflate your figures.
However, it is not just the UK that is hyping up COVID deaths. A reader of my blog sent me an analysis of the WHO advice on death certification, which seems accurate. In his analysis:
If you die of anything and they suspect you might have it, with no tests and perhaps just because everyone else is assumed to have it, then COVID-19 goes on the death certificate as primary cause of death. Broadly speaking… unless the patient dies of something that is sudden and cannot be a long-term comorbidity.
If you have the same symptoms as flu or pneumonia you must be put down as COVID19 and not due to an influenza type illness.
Any certificates that are in any way erroneous with regard to the above must be recoded to conform.
Any COVID-19 codes that are wrong should not be fixed in any circumstances
To me looks like a recipe for systematic over inflation of death counts, designed to disallow or circumvent clinical judgement 2.
In the US Dr Scott Jensen, who is a physician, and a member of the Minnesota senate, has been notified by the board of medical practice in Minnesota that he is being investigated for public statements he has made.
Essentially, he is being accused of spreading misinformation about the completion of death certificates, and the overestimation of deaths from COVID-19. Also, that he has been comparing COVID-19 to influenza, in terms of how serious it is. This is considered ‘reckless advice’.
For pointing out the over-reporting of COVID-19 deaths and daring to claim that COVID-19 is no worse than a bad flu season, he could be struck off the medical register. You can see Dr Jensen discussing this YouTube 3.
So, it seems that, around the world the same things are being seen. A seemingly coordinated attempt to vastly over-inflate the number of deaths caused by COVID-19, and to drive home how deadly it is.
For example, a few days ago, a new story hit the headlines in the UK, warning of hundreds of thousands of deaths this winter.
‘The UK could see about 120,000 new coronavirus deaths in a second wave of infections this winter, scientists say.
Asked to model a “reasonable” worst-case scenario, they suggest a range between 24,500 and 251,000 of virus-related deaths in hospitals alone, peaking in January and February.’ 4
Where did this come from? It was a model, using exactly the same assumptions as that created by Prof Neil Ferguson from Imperial College London in March. The one that warned of five hundred thousand deaths in the UK. Only out by a factor of ten. Probably far more, because many of the deaths recorded as due to COVID have been, simply, wrong.
How certain was their prediction of 120,000 deaths? Professor Stephen Holgate, who chaired the report then said. ‘This is not a prediction – but it is a possibility.’ A possibility… Perhaps it should be published in the Journal of possibility-based medicine. A journal where you simply make up facts, then see how many people run around in sheer terror.
What is now happening is extremely disturbing. COVID has certainly been a serious disease, but the flu epidemics of 1957 and 1967 were just as bad, if not worse, with regard to total fatalities. They were both over a million, and COVID has a long way to go to match that 5
In addition, in those epidemics far more younger people died. With COVID, if you are under fifteen, the chance of dying of COVID is around one in two million, which is three times less than the chance of being struck by lightning 6.
Across Europe, the excess in deaths has simply disappeared 7. There is no increased mortality anywhere to be seen. Whilst we are told about outbreaks of COVID deaths in various cities, the rate of new infection in these ‘outbreaks’ is less than one in a thousand. Which is not really an outbreak at all.
Despite this, mask wearing is to be mandatory. When COVID-19 took off, no-one was wearing a mask in my unit, unless they were helping a patient, and there was no social distancing between staff. Now the trust has decreed masks must be worn at all time, and social distancing is being ruthlessly enforced. A bell now rings, and we must wipe of all surfaces in front of us…
The reality is that COVID-19 has all but gone in the UK and Europe. The slow, but inexorable rise in deaths in the UK is being driven by the fact that anyone who has ever had a positive COVID-19 test, who dies, is recorded as dying of COVID.
Yet, as COVID-19 disappears, mask wearing and social distancing is being enforced as never before, and the prospect of a deadly second wave is being waved like a black shroud, with warnings of hundreds of thousands of deaths to come.
A biomedical scientist in the UK sent me an e-mail two days ago, about the testing they had done.
‘In the week 9th – 16th July we carried out 2800 PCR tests (across three different platforms: mainly on the Hologic Panther, but some on the Cepheid GeneXpert and Biomerieux BioFire) and had only 4 positives. These 4 positives were all patients who had previously tested positive. We had NO new cases, and after checking back a few weeks, the only positives we have had have been from repeat swabs from these same 4 patients – they were almost acting like QC samples to ensure that our tests were actually working properly!’
Two thousand eight hundred tests and none positive. This scientist contacted other laboratories, and they were seeing the same things. ‘I have contacted a couple of nearby NHS Pathology Labs and they reported the same findings as us: zero or near zero new cases for several weeks.’
What on earth is going on?
1:
https://www.theguardian.com/world/2020/ ... d-19-cases
2:
https://www.who.int/classifications/icd ... VID-19.pdf
3:
https://www.youtube.com/watch?v=KpGeRFK0tao
4:
https://www.bbc.co.uk/news/health-53392148
5:
https://www.webmd.com/cold-and-flu/what ... utbreaks#3.
6:
https://www.ons.gov.uk/peoplepopulation ... injune2020
7:
https://www.euromomo.eu/graphs-and-maps ... by-country
This entry was posted in COVID-19 on July 25, 2020.
Replies to the vitamin D article by the guest contributor
309 Replies
11th July 2020
Having published the guest article by ‘Bob’ there have been a lot of comments. I have not replied, as it was not my article. However, Bob has put together a kind of generic reply to people’s posts which I think may be useful and informative.
Hello Everybody – I wrote the article and have read your comments. First, I want to thank Dr. Kendrick for publishing my thoughts in his esteemed blog. I started following Dr. Kendrick’s blog around 2015 and am a devoted reader. My favorite single post is the one titled “Salt Is Good for You.”
I was introduced to the wonderful world of Vitamin D in 2010 when a physician directed me to the Vitamin D Council website, now defunct. John Cannell’s articles on influenza, and on autism, were compelling for me. I started taking 5000 IU per day in December 2010 (at age 60) and I noticed that I no longer got colds or influenza in the winter. Before 2010 I would get one or two colds every winter, with the usual sore-throat – head cold – chest congestion sequence. Since then I have had exactly 5 colds, all very mild. I now take a higher dose but I think people should look at the advice provided in the Grassrootshealth article and make up their own minds as to appropriate dose.
My article sketches out a theory that yields a series of hypotheses which can be tested. Thus, one notes a general pattern, and scratches one’s head over exceptions. Hence my discussion of Ecuador and South America.
I propose that an underlying difference in susceptibility to coronavirus arises from the fact that the New World was epidemiologically isolated from the rest of the world until about 500 years ago. Before then the indigenous populations of the New World and the Old World were exposed to and therefore developed adaptive mechanisms to ward off different groups of pathogens.
This is illustrated by the well-known susceptibility of New World populations to Old World pathogens like measles and smallpox. The higher death rates in many South American countries suggests that the indigenous New World genome has not yet fully adapted to Old World coronaviruses. Thanks, Terry Wright, for the Guayaquil reference.
Thank you, John Stone, for the reference to the Stadler article observing that there is a significant level of immunity to Covid19 already present in the population. We had another clue to this fact early in the pandemic with outbreaks on two ships, the cruise ship Diamond Princess, and the US aircraft carrier Theodore Roosevelt. Both occurred before people took protective measures, and it can be argued that the close quarters of shipboard life are ideal for the transmission of the disease. On both ships, everybody was tested for Covid19. Results were remarkably similar. On both ships, 17 percent of the people tested positive for the virus, and of those, 50 percent were asymptomatic. It looks like 83 percent of the shipboard populations were immune to the virus. Why?
Several of you have pointed out that death rates from various countries are inconsistent with the sunshine theory. First, do not confuse cases with deaths. Case totals are the creatures of testing programs, which vary from place to place. Deaths are a much harder statistic.
That said, country-specific factors come into play. In comments, Andrew Larwood and Simon C pointed out Finland’s vitamin D supplementation program would reduce deaths. Their death rate per million is 59, which seems very low for a country in the winter at such a high latitude. Now I know why. Another factor may be fatty fish, a dietary source of Vitamin D, which is consumed in quantity in Scandinavia. Håkan, your comment about Sweden is relevant.
Many people attribute the higher rate of Covid19 deaths to the lack of a lockdown. However, an equally good case can be made that the dark-skinned immigrant population in Sweden is more deficient in vitamin D and thus more susceptible to the illness. See this article by Dr. David Grimes where he notes that 1 percent of the Swedish population may be responsible for 40 percent of deaths:
http://www.drdavidgrimes.com/2020/04/vi ... rtant.html and this one:
https://www.bmj.com/content/368/bmj.m1101/rr-10 If you have read Dr. Kendrick’s last blog post, “Distorting science in the COVID pandemic,” you would know that the very low death rate (7 per million) in Morocco may be due to their use of hydroxychloroquine to treat sick patients.
Does implementation of hydroxychloroquine treatment explain the abrupt decline of coronavirus deaths in the UAE on May 12?
https://www.palmerfoundation.com.au/pre ... -benefits/ If you look at the death rate graphs for a number of Muslim countries, there is a distinct uptick in cases at the end of May. Does this have something to do with Ramadan, which was April 23 to May 23 this year?
David Bailey, your comment is spot-on. Look at the seasonality of acute myocardial infarction. In the higher latitudes one gets daily doses of sunshine in the summer, but not in the winter, and it is the dailiness of the dose that is key to protection of the endothelium. This is also why randomized clinical trials of vitamin D tend not to show a strong protective effect against CVD, because most do not use a daily dose, rather, dose intervals are weekly or longer (and the dose is usually too small and the duration of the trial too short).
Thank you all for your comments.
This entry was posted in Dr Malcolm Kendrick on July 11, 2020.
Here is a Coronavirus puzzle for you to ponder – A guest article
323 Replies
9th July 2020
A guest article
I was sent this piece on Vitamin D and COVID by a reader of this blog. I thought it was very good and asked them if they minded me posting it. They said fine, but they wish to remain anonymous. Not everyone likes the glare of publicity – with all the attending Trolling and insults that inevitably follow [you should read my in-box sometime].
Season, Latitude, and COVID-19 Severity
Here is a coronavirus puzzle for you to ponder. For context, let’s look at how many people have died of COVID-19 in the USA (as of mid-June). Websites give different totals, but it’s around 120,000, or about 360 per million of population. So how many died in Australia? 102. How many died in New Zealand? 22. In both countries, the death rate is 4 per million. That is an extraordinary contrast!
Wouldn’t public health officials like to know the cause of this difference? Are the Antipodeans that much better at hand-washing and social distancing than the people of New York, Italy or Great Britain? Do they share a highly-effective cure kept secret from the rest of the world? Or is there another reason for the disparity?
Unlike the USA and other countries where the disease has taken a huge toll, the coronavirus arrived in Australia and New Zealand in mid-summer. Most of the inhabitants of these two countries are descendants of pale-skinned British settlers (and convicts in the case of Australia). Yet at the same time the death rate in Great Britain, the homeland of their ancestors, is over 600 per million.
This suggests that sunshine, and, specifically, the sunshine vitamin, are responsible for the difference. If you look at the death rates throughout the world, it becomes apparent that countries in the southern hemisphere fared much better than countries north of the equator.
Actually, the division between countries with high death rates and low death rates is about the 37th parallel north. According to Wikipedia, the 37th parallel is the dividing line between greater than average and less than average sun exposure.
So it appears that people living south of the equator, and south of the 37th parallel north, experienced, in general, higher levels of sun exposure and lower death rates from the coronavirus than those in the northern hemisphere north of the of the 37th parallel.
This explains the very low death rates observed in Africa. Many experts have forecast that the coronavirus would take a heavy toll in Africa because of poor healthcare infrastructure in much of the continent. Yet this has not happened. For example, death rates in Ghana, Nigeria, Kenya, Ivory Coast, Togo, South Sudan, Niger and Burkina Faso are between 2 and 3 per million.
Virtually all of the continent is south of the 37th parallel north and sub-Saharan Africa is close to the Equator. It could be argued that the low death rate is an artifact of poor record keeping, but reasonably good data about another virus, Ebola, reached world attention, so high death rates from coronavirus would likely be evident.
The same is true in the Far East. Indonesia, Malaysia, Singapore and Sri Lanka are near the equator and have coronavirus death rates per million of 8, 4, 4, and 0.5. But this pattern breaks down when one looks at that most equatorial of nations, Ecuador.
Here the reported coronavirus death rate is about 223 per million. Other major countries of the South American continent, Brazil, Peru, Chile and Bolivia, have per million death rates of 208, 208, 176, and 54, which is quite a contrast to those seen in Africa and Southeast Asia. The disparity may arise from a greater susceptibility to the coronavirus among people with indigenous ancestry.
Support for this idea comes from the death rates in Argentina and Uruguay, which are 19 and 7, per million, respectively. Unlike the rest of South America, the populations of these two countries are very largely of European ancestry, mostly Spanish and Italian. Remember that while it was summer in Argentina and Uruguay, at the same time it was winter in Spain and Italy, where COVID-19 death tolls per million were 580 and 571, respectively.
This analysis supports the idea that the virulence of the coronavirus, as measured by death rate, varies inversely with sun exposure. Where the coronavirus struck during the summertime, in the southern hemisphere, death rates were very low, in very marked contrast to countries in the higher latitudes of the Northern Hemisphere, where the coronavirus struck in mid-winter. The cause proposed to explain this disparity is Vitamin D levels in the respective populations. How does that work?
Vitamin D3 is created in the skin by the ultraviolet light in sunlight. Before the advent of dietary supplements, sunlight was the only significant source of Vitamin D3. Fatty fish is a natural dietary source. Vitamin D3 is transformed inside the body to calcidiol, 25(OH)D3, which is not a vitamin, but a hormone.
Calcidiol has a half-life in the body of 2 to 3 weeks, so serum levels decline if they are not continually replenished by sun exposure or dietary supplements. Winters in the higher latitudes diminish sun exposure due to shorter days, lower sun angle (if the sun is lower than 45 degrees in the sky, little UV light makes it through the atmosphere), and the need to bundle up or stay indoors in cold weather.
About 15 years ago it was discovered that Vitamin D is critical to the proper function of the innate immune system. Broadly, there are two kinds of immunity – innate and acquired. The body acquires immunity when it creates antibodies in response to infection by a specific pathogen. This is the principal behind vaccines – to trigger the creation of antibodies.
However, the body also has an innate immune system that responds to the wide range of pathogens to which it is exposed every day. Recently it has been demonstrated that the innate immune system is the body’s principal defense against another viral disease – influenza. The annual wintertime outbreaks of influenza are triggered by declining levels of serum vitamin D in the host population. That is why influenza doesn’t occur in the summer and is very uncommon in the tropics.
For in-depth discussion of innate immunity, Vitamin D3 and influenza, read the paper in Virology Journal titled “On the Epidemiology of Influenza” by John Cannell, et. al., and his earlier paper “Epidemic Influenza and Vitamin D” published in the journal Epidemiology and Infection. Open access full text of both articles can be found on the internet on PubMed.
However, the COVID-19 coronavirus is not influenza, so the role of innate immunity and Vitamin D in the incidence and virulence of this disease must be established. Given the very recent emergence of COVID-19, it is understandable that not very much research on the role of Vitamin D has been published.
However, one key paper has come out, which has been summarized in the website Grassroothealth.net/blog/first-data-published-covid-19-severity-vitamin-d-levels/. The data are observational and the population of patients was 212, but the results are statistically significant. People with adequate levels of serum Vitamin D in their blood experienced mild bouts of COVID-19, while those with inadequate levels suffered ordinary, severe or critical cases. The chart in the article illustrates these data.
The results of this study are exactly consistent with the idea that sun exposure is inversely correlated with the virulence of COVID-19. When serum levels of Vitamin D are high, the disease is mild. When they are low, the disease is severe. Which then leads one to ask what are the specific effects of Vitamin D that reduce the severity of COVID-19 infection?
There are at least two. Severe cases can be complicated by what is called a “cytokine storm.” This is a severe over-reaction of the immune system that can be fatal. Vitamin D is known to prevent this condition (see the above-referenced articles by John Cannell). A second effect is related to the recent discovery that COVID-19 attacks blood vessels, in particular, the endothelium, which is the internal lining of vessels, causing widespread clotting1.
Research published in 2015 showed that Vitamin D3, in the form that is created in the skin by UV light or taken as a dietary supplement, has a direct, protective effect on the endothelium 2 Because Vitamin D3 lasts in the body only a day or so before it is processed into calcidiol, one needs a daily dose of sunshine or supplement to maintain the protective effect on blood vessels. It should be underscored that sunscreen blocks UV rays from reaching the skin and therefore diminishes the formation of Vitamin D. The skin pigment melanin is a natural sun screen and has a similar effect.
What does this mean for people who want to protect themselves from the malign effects of COVID-19? Vitamin D3 is not some untested off-label prescription drug or sketchy supplement: it is an essential hormone naturally produced in the human body by sunlight on the skin.
With enough sun, one’s body makes all that is necessary to counteract the virus. But modern lifestyles can make it impossible for many people to get sufficient daily sun exposure in the summer, and during Minnesota winters it is physically impossible because the sun is too low in the sky, not to mention that it is too cold to take off your clothes.
Therefore, one needs a program of supplementation with Vitamin D3, which is readily available over the counter. The question, of course, is how much. Grassrootshealth has devoted considerable study to finding the answer, a good discussion of which can be found here 3 The coronavirus statistics I used are from the site Worldometers 4
1:
https://www.sciencetimes.com/articles/2 ... rything.ht.
2:
https://journals.plos.org/plosone/artic ... ne.0140370.
3:
https://www.grassrootshealth.net/blog/c ... tions-low/
3::
www.worldometers.info/coronavirus/#countries.
This entry was posted in COVID-19 on July 9, 2020.
Distorting science in the COVID pandemic
352 Replies
https://drmalcolmkendrick.org/