About the current study situation on Covid-19, what we know better than in March and what we can expect
When the second wave comes, everything will be different. I'll take my conclusion, which should actually be at the end, first of all and will try to prove it in the following with arguments and links to scientific studies. Everyone is invited to come up with their own thoughts on this.
When the second wave comes, it becomes rather harmless where it was violent - and vice versa. In other words: Bergamo will not experience a second Armageddon, neither will Madrid, nor will the excess mortality of 20% or 60,000 deaths of the first half of the year be repeated in Great Britain.
But wherever the protective measures have so far been very lenient (excess mortality in Germany in the first half of the year: 0%), the race between winter and vaccine will be crucial. Unless the prevailing opinion in science makes a major U-turn, a full U-turn, and takes the media with it. And then we could face a second wave, wherever it may come from, in a more relaxed manner. But that would - in the long run - bring tears to the eyes of pension politicians.
Have I dropped enough bait? Because I'm afraid it will be long (but hopefully entertaining) and I won't skimp on criticism, not even self-criticism. Because I have burned my fingers on an almost unbelievable Covid 19 science crime story, for which I paid dearly. And which is still completely mysterious. But we'll get to that later.
Stefan Aust, once a very renowned journalist, has got his government and mask frustration off his chest in the "World". Among other things, his lamentation about the fact that the RKI does not provide figures on excess mortality in all corners of the globe free of charge as he would like (research should be the journalist's self-evident tool, shouldn't it?), he had an entrepreneur who found such data researched:
And it says: "In the other countries evaluated the death rates were also in the range of the long-term average - and almost all of them lower than in Germany".
All right, the obligatory Germany bashing, but how could a political journalist who is too comfortable digging through a few statistics have even the slightest idea why Portugal and Germany have a - with an 80-year life expectancy - "normal" mortality rate of 1.2% p.a. (100/80=1.2), while the USA, despite a lower life expectancy, is only around 0.9%? Because if this were due to life expectancy, would Americans have to live well over 100 years? Well, you take a better look at the birth rate and population growth and a few other dynamic factors, but that's too much to ask, I know. And by the way, Americans have a life expectancy of 2-3 years less than Germans, and they in turn have 2 years less than Italians, who unfortunately do not appear in Aust's splendid table.
But one can probably demand that even a political journalist can put two and two together and divide by four. Let's do that with the above table:
The four digits behind the decimal point are obtained by dividing four two-digit numbers each, they are not intended to feign accuracy beyond the two digits in the original table.
What was that again?
In the other countries evaluated, the death rates were also in the range of the long-term average.Stefan Aust
No, they weren't, they were all over it. Except in Germany and there very precisely in the middle.
Notabene: The four years also include the influenza epidemic of 2017/18, which was a severe outbreak due to the "wrong" vaccine.
I maintain: one can see very clearly here what a wrong policy like that of the clown in London does to a reasonably reasonable reaction. Of course we would have been even better off if homemade masks had been officially recommended. Because the fact that the flu wave this year has de facto failed (except for me, influenza A in January) is probably due to the masks, besides keeping distance etc., not least because the effectiveness of a simple mouth/nose protection has meanwhile been exemplarily proven. In the test, the turquoise mask, which is also worn in the operating theatre, came in 2nd place after the N95 mask.
And if you have ever seen one of the Plexiglas shields with a headband up close when worn with or without an additional mouthguard, you have been able to count the droplets directly in the first case. Well, from a purely mechanical point of view, it's actually a rush that one shouldn't have to explain to anyone that the mouthguard has two effects: large droplets are possibly atomized, if they can pass at all, and the horizontal speed decreases strongly. With a bigger distance, the horizontal speed of the person opposite arrives clearly less or not at all.
What we also know for sure is that the viral load during infection is crucial for its course. Actually, this should also be a rush, meaning that cause and effect are not so difficult to understand. In principle, our immune police are always "on patrol" and will deal with any unknown intruder as quickly as possible. However, there should always be a few intruders on patrol, otherwise the immune warriors will gladly attack their own people: The increase in allergy, hay fever and asthma sufferers due to - especially among children - obviously completely exaggerated hygiene in recent decades is no longer disputed.
As I said, intruders will be dealt with as quickly as possible. And "souvenir photos" are also taken, so that it is even easier to fight them next time, or if they want to get over a fence in larger numbers (the fence means skin or mucous membrane). But if the number of these hitherto unknown intruders is very large right from the start (i.e. large droplets with many viruses), then it doesn't work, the virus police are overloaded and have to call for reinforcements, the consequences are the annoying cold, the flu or even Covid-19. So it's clear what the mouthguard does: If it doesn't reach me, I won't be infected. And if instead of a lot, only little reaches me, it is much easier to end up well.
In this respect, it was simply incredibly stupid of Drosten as well as the government to negate the protective effect of masks just because you didn't have any - and that caused a very, very big loss of trust. One simply had to ask whether Mr Drosten would like to undergo an operation in which doctors and surgical assistants do not wear masks because they are of no use? I would have liked to hear him stammer.
Back to Aust, the numbers and his biased assessment:
The corona horror year 2020 - or at least the first half - is thus well behind the flu winters of 2017 and 2018, which have so far hardly been perceived as horror years.Stefan Aust
But clearly above the years 2016 and 2019, and in the annual average of 5 years exactly in the middle. And what would have happened without masks and lockdown, if it had just about reached the average now? Just look at the half-yearly statistics of Lombardy or England?
And another misleading sentence:
The average age is 81 years (median: 82 years).Stefan Aust
And that, we may assume from the tenor of the text, means that all of them must have already been in a state of suspended animation, so that without C-19 they would have died as soon as possible?
However, this is a big mistake, which can be made by almost anyone who has the life expectancy of 81 years in mind and compares it with such figures. I didn't get smart until I thought about it for the second time: Because anyone who has actually made it to this age has - from an actuarial point of view - 6-8 years to go, i.e. all of them and on average. This is shown by the DeStatis searched by Aust under loud moans and moans after only two clicks, if you let Google search for the following: [ life expectancy germany by age ] - destatis is the first link. And in the text snippet it also says: "Why is the attainable life expectancy in a mortality table at the age of 65 higher than at birth? Maybe Mr. Aust should have read that.
And if the median, i.e. quasi the watershed of equal numbers of people to the right and left of it, is higher with age (82) than the arithmetic average age (81), then this means? Yes, exactly: the sum of the "lost" years of the younger deceased is greater. For a dead 92-year-old, the counterpart must not have died at 72, as one could supposedly conclude from the median (92/82/72), but already at 70, as the arithmetic mean (92/81/70) shows us. 70 is certainly not the age at which people die, if the average life expectancy of a 70-year-old person is supposed to be somewhere between 16 years (65) and 8 years (80). Mr Aust has misappropriated all this.
And I do not like it when people so obviously mislead others by hiding known or easily researchable facts.
Intermediate result: C-19 is quite deadly if you mess up completely with the fight, like the British or Belgians. Unfortunately, the much-cited comparison with the "normal" flu, i.e. influenza, also fails. With influenza, we have experienced many waves of immunization, mostly at a younger age when one does not die from it. And there are vaccines, there is cross-immunity, all that. Covid-19 has hit people almost unprepared, apart from the potential pre-immunisation by corona rhinitis viruses, about which we still know too little.
The question is: What would have happened - apart from the public panic that images of stacked coffins cause - if it had been left running everywhere without a lockdown? Because the British half-baked lockdown was, just like the 400-year-old saying of Logau says, the greatest evil of all:
In Danger and in Deep Distress, the Middleway Spells Certain Death
Johnson managed both: the many excessive deaths and a massive economic slump on top of that. But the question is hypothetical, because Bergamo had to worry everyone, the pictures of military convoys transporting many coffins were just too haunting to be ignored.
There are very serious indications that in the Stockholm area 40% of the population may have had a Covid-19 infection by now - and I haven't read about it anywhere except here in Telepolis (thanks to Sebastian Rushworth and translator Uli Martin).
Researchers at the Karolingska Institute wanted to know how this relates to the course of the disease and the antibodies (very expected result: the more severe the more). But they did something very tricky: they did not only test for C-antibodies, but also for C-19-specific T-cells (these are the immune police officers with the "memory photos" on their lapels). And then came the very cleverest trick: they took blood samples from the blood donor center, in mid-May 2020. 2019 samples were also tested: Zero C-19 specific antibodies, zero C-19 specific T cells. May 2020: of 31 samples, 9 (=27%) had C-19 T cells, but only 4 (13%) also had C-19 antibodies. More than half of those who had definitely had an infection had not produced antibodies.
There are a few things to be clarified: Whoever donates blood signs that he/she is not aware of any infectious diseases was probably asymptomatic. And, quote RK: "Blood donations can be made by persons between the 18th and 70th birthday who meet certain health and legal criteria". So this is not a representative sample of people… It is unclear whether and in what direction the result is influenced.
A second one: This is about the city or region of Stockholm, and we know from New York and Madrid what population density has to do with the spread of the infection. So the result cannot simply be transferred to a whole, rather sparsely populated country. It is also clear that the 27% in May must have become considerably more, I have extrapolated this to 40% using my thumb.
Thirdly: As a single result, the chance of general validity would only be fifty-fity (maybe sixty/sixty, as Calli once said ;-). However, a probability of 95% can also be calculated for the fact that at least a quarter of C-19 T-cell carriers, i.e. those infected positively but without symptoms, do not produce antibodies. The 95% is the usual confidence limit in medical studies.
However, another study has been added, which has achieved the same result by other means:
Jena Corona Study: Half of infected people have not developed antibodies
"We were surprised that half of the infected persons, in whom the virus had been detected six weeks earlier, had no antibody titres, although we had looked for it with six different tests", explained the head of the study, Professor Matthias Pletz […].MDR
Having two such different studies at such different locations with practically identical results greatly increases the reliability of the results. The Jena scientists will now also test for C-19 T cells, as Prof. Pletz wrote to me: "The specific T cells are currently being measured in Prof. Kamradt's laboratory (cc). We have the funding for this for the time being."
So what can we conclude from these results, and what figures should we expect to see? I asked a Swedish friend where I could get numbers from, and she gave me the link to this current statistic (translated with Google):
This week (week 37, LB)
Cases of illness / 100,000 inhabitants: 11
Cases of illness: 251
Intensive care: 4
cases of illness / 100,000 inhabitants: 967
cases of illness: 22,979
intensive care cases: 926
And she wrote: "On the left you can set the week and the region. The first thing that comes up is the information that 3900 samples turned out too inaccurately positive, although the virus count was probably too low. […] According to the news here, they also suspect that the number of those who are more or less immune in Stockholm is 40% or more, I heard somewhere. There they are, my 40% ;-)
From the cases of disease / 100,000 p.e. (926) and the total (22,979), the number of inhabitants is 2,376,318, which is the Stockholm region. If we assume 40% immunized people (950,527), this would result in an IFR (infected death rate) of 0.25%, and that would actually be very good news. Because the "official" figures mentioned above (cases of illness: 22,979, deaths: 2,397) would result in a CFR (case-death rate) of over 10%. But the Swedes have always tested far too little, and then such horror numbers come out.
However, if Stockholm is said to have had 27% infected people by mid-May and the first case was located on 25 February, then the initial spread rate of R=3 must be corrected upwards: With (less than) 12 weeks we get with R=3: 1/3/9/27/81/243/729/2187/6561/19.683/59.049/177.147 and that would be only a fraction of the above estimated number of 950.000 infected people - and moreover the corresponding weakening by already immunized people is missing.
With R=4 there will be 4 million without the weakening of R by those already immunized. Taking into account the weakening, one easily reaches 950,000, but R=4 at the beginning results in a herd immunity limit of 75%, not only 66% (Hi = 1-1/R).
And if we don't assume that the IFR has been driven up by an increased spread in senior citizens' circles, but that the infection has been "racing" all the time, especially through the young population (thank you for that, Franziska ;-), but mostly just "quiet", then it remains the case that if the almost doubling of the number of people necessary for herd immunity occurs, several more people have to die. How many? We will see.
According to the above table, Sweden has shown an excess mortality rate of 0.0325% per half year and has 5,800 deaths. 41% of these, according to the above figure, are in the Stockholm region, which however has only 23% of the population. The 5,800 deaths throughout Sweden thus represent a population of approximately 5.6 million with an immunity rate of 40%. Extrapolated to 10 Mio and almost doubled (40%=>75%) we would have to reckon with about 19.000 excess deaths in Sweden - without vaccine. In a country where 273 road deaths per year are already so much too many that there is serious debate about reducing the already low speed limit.
If this figure (i.e. the "real" IFR) were also valid for us, it would demand 150,000 "fatalities" until herd immunity is achieved. Here too: without vaccine. For comparison: So many people "normally" die in two months, but here in addition. Calculated for exactly one year: 15% more. Instead of 100 deaths, fifteen more: 115. Everyone can classify this as they like. If it's your own beloved grandmother who gets it, you will judge it differently than if it's the hated hereditary uncle. And if you belong to the risk group yourself because of asthma or the like, probably differently. Not considered here: improved treatment methods, for example with dexamethasone. Also not included here: by wearing a mask, many mild infections with a low viral load, which nevertheless lead to immunisation.
At the end of March I compiled statistics based on the then known figures for Bergamo (120,000 inhabitants). Quote:
Even with a high lethality rate of 3.7% (as in Hubei) due to the overburdening of the health system, 30% of the population must have become infected to date, at peak time on 5 March almost 1,500 per day, because otherwise the reported death toll cannot be reproduced. "Every day, more than a hundred more Covid-19 patients come to the emergency room" was reported in the SPIEGEL on 27 March - with ~10% severe courses, this fits quite well with this report from last week, with a delay of 10-14 days from infection to respiratory distress.
A total of about 36,000 p.e. would now already be infected instead of the 5,200 reported last week, an unreported figure of factor 7 (700%). Assuming a lethality rate of only 2.5% (Tab Bergamo-2), the similar number of deaths would mean that about 45% of the population (55,000 people) would be infected, with a peak of 2155 on 6 March and an estimated number of unreported cases of more than 12, which is not plausible.
I would like to take back the last sentence ;-) - at least I have already accepted 7x more infected people than were reported. And until today it is not quite clear how an IFR of 0.25% should fit into this. Meanwhile it is assumed that there are 35% to almost 60% infected people in Bergamo. But with an IFR of 0.25, a maximum of 200 people would have died of Corona - and there were far more.
The truth will probably be somewhere in the middle and we must also accept that the IFR varies from country to country and region to region. There are reasons for this, but more about that later.
Marginal note: Under this problem, namely that an IFR cannot be determined exactly, in addition under different circumstances (weather, population density, immune status of the population, skin colour, geographical latitude etc.) highly volatile, all mathematical models have to suffer, even much more demanding ones than my rather hand-knitted ones, thus also as complex as those listed in the Telepolis article by Mohr und Püschel. This is not to be understood as a criticism, only as an indication of where modeling and the algorithms on which it is based have their natural limits.
In some regions and countries, infection rates are rising again, there are travel warnings, quarantine is imposed, etc.pp., but CFR, i.e. death rates for confirmed C-19 infections, are not or hardly rising. Some, especially politicians and the leading media, warn of the rising infection numbers, such as the "Welt" on September 9th under the title "What's going wrong in Spain, France and Italy" and the alarmist lead story:
The three southern countries were Europe's focal points during the first Corona wave. Now the number of infections is rising sharply again. Why are EU members threatened by the second crisis?The World
The others point their fingers at the low death figures, which the "Welt" incidentally provides in the same article, see their fundamental doubts about the government and leading media confirmed and Wodarg and Bakhdi justified - there would be a simple explanation that both could agree on:
In the beginning, the tests were not only expensive, but also rare. Only those who showed clear symptoms were tested. Then they were followed up. I did not find any reliable statements about how many days lie between the initial infection of the spreader and the test of a contact person, and I have to roughly estimate this: after 7 days of symptoms, but infectious from day 1. Then test result: + 2 days? Then contact tracing and ordering the test … I would not be surprised if 11-14 days could have passed between infection of the contact persons and the test smear. But if a person with a very good immune status clears the virus successfully and therefore quickly, can the smear, which would have been clear on the 1st or 2nd day, find enough virus material after 12 or 14 days to be positive? I think: No.
Today, however, tests are being carried out without any reason, e.g. for those returning from a trip. Those who were infected just yesterday or three days ago could/must have a positive result. So this is where all those who are currently "actively" infected are caught, and that is something completely different from testing only on an occasional basis, because this way all symptom-free C-19 carriers are eliminated, who never even thought that they could have infected others, who in turn only notice when they have symptoms. Etc.pp.
In this respect, it is very easy to understand that today's figures are not at all comparable with those of March and must also be higher. As a result, both CFR and IFR quotas must fall. As already mentioned, the "Welt" also provides figures for the excitement article, e.g. from France: "According to the Ministry of Health on Tuesday evening, 38 patients died in the previous 24 hours. In France, statistically, 2,235 people reach the end of their lives every day. 38 is 1.7%, far from the 1,100-1200 who died of C-19 in the first three days of April.
And to Italy:
Indeed, despite the increasing numbers, the situation in Italy is comparatively well under control and differs greatly from the corona outbreak in spring. […] Experts suspect that this is mainly due to the fact that the infected people are younger this time and therefore have an easier course of the disease. In addition, holiday returnees from some regions were tested extensively and thus many asymptomatic corona infected people were identified who probably went unnoticed during the first outbreak. […] Within seven days 256 people died. At the wedding in spring, the figure was just under 1000 - per day.The World
256/7=36, thus the same situation as in France.
However, with all the good news on the IFR and CFR front, we should beware of equating Covid-19 with a severe flu. The medical consequences of a C-19 infection can be far more serious, as the German Association of Pathologists explained in a study:
"I was not surprised that Covid-19 was the bringer of death for the majority of patients," says pathologist Friemann, who himself autopsied twelve corona deaths. "But what I saw in the lungs was unexpectedly radical. In some cases the walls of the alveoli were completely destroyed in a way that I have rarely experienced," writes "Der Spiegel" in a detailed report on the 154 autopsies that 26 institutes affiliated with the association had performed. "The results are clear: 'In more than three-quarters of the autopsies, Covid-19 disease was documented as a major or sole fatal disease', according to the presentation of the results.
Whoever has studied this article carefully, and then still thinks that all measures against C-19 were exaggerated, can probably not be helped.
If 57% of the people in Bergamo have actually already suffered a C-19 infection, it is quite clear that there is not much room for a second wave. Conversely, where the virus has not yet spread, it could strike. Take us, for example. And the timing is predictable. December, January, February.
Not only the flu waves, but also history gives a hint: There is a strong presumption that the Russian flu of 1889 ff. was not a "flu" at all, but was caused by a cattle coronavirus rampant between 1870-1890, which spread to humans during the mass slaughter of animals dying of a mysterious lung disease (sic!). For there are also reports from that time which claim that the symptoms are so very different from those of influenza, but instead very similar to those of today, e.g. the loss of the sense of smell and taste. This was also described in Telepolis (Did Covid-19 have a historical predecessor? ), so I will spare myself further details, just this much:
After the first wave in 1889/1890 there was a second (spring 1891), a third (January/February 1892) and a fourth (December 1893 to January 1894).FAZ
Of course this is not very exhilarating. What's interesting is the seasonality, the concentration on winter.
Interim conclusion: Without a vaccine, in order to avoid or at least mitigate a second wave wherever the virus has not yet raged, the known protective measures must remain in force if we do not want to gamble everything away, because then the effort would really not have been worthwhile.
Since the day before yesterday, I have been pelted by many who know of my involvement in C-19, but especially in vitamin D, even here in Telepolis (Does vitamin D protect against Covid-19?), with a study that is actually haunting the fringe media:
"Vitamin D status could influence the risk of infection," writes zm-online, for example:
The retrospective cohort study at an urban academic medical center in Chicago, USA, included 489 patients with 25-hydroxycholecalciferol or 1,25-dihydroxycholecalciferol levels measured within one year before being tested for SARS-CoV-2 from March 3 to April 10, 2020. […]
In the multivariate analysis, a positive test was associated with increasing age up to the age of 50 years and probably deficient vitamin D status. The predicted infection rates in the vitamin deficiency group were 21.6 percent (95 percent CI, 14.0 percent - 29.2 percent) compared to 12.2 percent (95 percent CI, 8.9 percent - 15.4 percent) in the adequate group.
A similar study was conducted a little more precisely and with similar results several weeks ago from Israel, almost 7,000 test persons and current D-tests. It was slightly absurd that the best protection against corona was the presence of dementia. This is of course medically nonsense, sociologically it makes sense: the best cared for risk group.
Both studies, however, suffer from one fundamental question: Does vitamin D protect against infection? Or does it protect against the consequences? I'm leaning towards the latter: A good immune status clears the virus more quickly and thus shortens the time window in which the infection can be detected by PCR test. As a result, on any given test day, I get fewer active PCR tests from people with a better immune status, which is usually associated with a higher D-level, because the active time windows overlap less among the test subjects, precisely because they are shorter.
From China came the news of the atypical pneumonia, about which a young doctor had exchanged information with colleagues, who then had to row back under political pressure and unfortunately died himself of Covid-19 a little later, just 34 years old. From today's perspective, I would say: much too high a viral load due to the constant work in the intensive care unit, as is well known, the loss rate among doctors and nursing staff is alarmingly high. And, of course, work-related… …but I'm getting ahead of myself.
At the end of March, the Focus report on a study in which 54 of 191 patients had died came from China. And all 54 had developed sepsis, 38 even suffered septic shock. Now I wanted to know whether vitamin D, which had helped me to get through influenza A quickly in January, would also be effective against sepsis. So I googled it: [ Sepsis Vitamin D ] Score.
An Iranian study that examined the occurrence of sepsis in patients after surgery, with regard to their acute vitamin D levels. The results were conclusive. I distributed this study by email, with the suggestion to initially measure the vitamin D level in C-19 patients and later correlate it with the course of the disease, to Drosten, Wendtner (Schwabinger Klinikum), Spiegel, Focus, Die Welt, all media that also offer "health" or medical sites. No reaction, nowhere. And then I sat down and wrote the first article about it. The impressive table I had generated from the data of the Iranian study, here again:
vitamin D level
Vit D < 20 ng/ml
Vit D 20-30 ng/ml
Vit D > 30 ng/ml
66,2 +/- 14,6
65,3 +/- 14,3
53,7 +/- 17,3
"The Relationship of Serum Vitamin D Level With the Outcome in Surgical Intensive Care Unit Patients":
Note: 1st and 2nd group are almost the same age (~65/66), but the third group is only 54, but with a very wide range, 36-70 years. Despite this limitation of comparability: We see from little too much vitamin D in each case a halving of the duration of stay in the ICU (24/12/6), in sepsis the effect is even greater (~36/~18/~3), this already smells strongly of causality, especially since the effect of vitamin D on the immune system is sufficiently known. And it fatally coincides with what we know about the dying, especially of old, previously ill seniors and their correspondingly low vitamin D levels.
The reactions to the article were manageable. The experts ignored it, as hardly to be expected. Who would believe an Iranian study. Only the Spiegel had picked it up - apparently in response to my e-mail - but only to evaluate it in an article that was supposed to make us believe that vitamin D plays no role in C-19. Whoever eats a balanced and healthy diet… (I can't hear that saying anymore ;-)
I have commented on this in the above article. And in the same article I listed many more studies that suggest a connection between the course of infectious diseases, but also of Covid-19, and vitamin D status, even intervention studies with bolus doses in people who already have the disease. None of this has been reported in the press. When I read this today, I have to say that it is nothing new in the West. I begged Hinz and Kunz to do D-tests on C-19s, I would pay for them. No reply. Instead, great silence. I had the impression of walking into a wall.
Not that researchers would not answer a layperson on principle. Even Nobel Prize winners do that. Only when I started on vitamin D, I was immediately ghosted. Then came the studies from Southeast Asia, and in early May I learned about them.
Big ballyhoo in the vitamin D activist community. This very loose and very colourful group has perhaps one, two dozen members worldwide at most, and all agree that the ubiquitous relative lack of vitamin D has a decisive influence on general health. And is completely ignored by the medical profession, science and politics. And since there are no real conspiracy theorists among them, everyone is frustrated and confused.
Yes, Big Pharma pays for practically all research studies and would not be interested in a cheap drug that could significantly reduce the incidence of practically all diseases. Doctors also prefer to cure with drugs rather than remedy deficiencies. If you cannot believe this, I will give a prominent example here. Iodine, we know, is essential. When iodine deficiency occurs, the thyroid gland freaks out, either it enlarges to form a goiter or it gets lumps. The iodine deficiency and its very extreme consequences, namely cretinism, were recognised by a Swiss doctor in 1925 and alleviated by the iodination of common salt. How bad the cretinism was before, especially in the mountain villages, can be read in the Wikipedia.
Is iodine deficiency still a problem today? Yes. According to the DGE, we consume 120 mcg on average, but according to the DGE we actually need 200 mcg. Does this lead to anything? Do the family doctors test for iodine? Do they prescribe iodine? Not that I know of (and exceptions confirm the rule). Well, then it can't be that bad, can it?
Let me give you another number: 80,000 thyroid operations a year. And after that, the patient has to take thyroid hormones every day. And that's one in 12 of us. So if the severe deficiency as it existed in past centuries led to goiter and cretinism, then the slight but decades-long deficiency should have nothing to do with this horrendous number of thyroid operations?
I'm sorry, I don't buy that. Nature knows no thresholds, not even at LD50, which is a dose of poison. LD50 means: lethal dose 50%, meaning: half die, the other half survive. Of course there are doses that are absolutely and always lethal, but as soon as the value falls below 100%, we have gradations. And they are always individual, because we are all different. We can of course live with the fact that only one in 12 of us has thyroid surgery. And the other 11 can somehow manage iodine deficiency. But if we were all adequately supplied with iodine, would there still be thyroid surgery? Cretinism, which was an individual destiny, was finally defeated, it was only a question of the dose.
Back to the D: So now finally studies that had done exactly what the D activist community had so urgently demanded: to match the relative D level and the course of the disease. And three of them. Each of which confirmed the general suspicion: D deficiency leads to more severe courses of disease, a high D level "protects" against a lethal outcome. The studies were referenced on all relevant D-websites, and in fact, they did get some press coverage. Well, if you call "In-Franken.de" the press.
In the meantime I had contacted the author of the most important study, the one from Indonesia. As well as others from all over the world, as I learned later. I had questions about the raw data, he had questions about statistics. According to my wishes, his statistician created new, more meaningful evaluations with SPSS, Bernd Glauner created the appropriate curve from it. Together we wrote a Telepolis article: "7 Cent or Lockdown". The title should signalize what a daily dose of vitamin D per capita costs and why this could make the lockdown unnecessary. We are translating the article into English. We wrote to the Chancellor and the Prime Ministers. And 200 newspapers and magazines. The vitamin D essentials linked in them, practically a shortened 7_cent article, went around the world, were downloaded 96,000 times and we received mail from all over the world.
In the meantime the main author and doctor had succumbed to a heart attack. So sad. I continued with the statistician. And at some point I demanded the raw data. And I got it. And they were weird. What you hadn't seen in the aggregated data, now you could see. Unmistakable abnormalities. Not just runaways, but real weirdness. Why hadn't they seen this? Why had they left the raw data to me? A mystery.
Meanwhile one must assume that the data, which is definitely taken from a larger set, which I got some time later, is part of an even larger data set. If they were handmade, the oddities, the obvious gaps would not exist. And by now it seems to be clear that the author mentioned, with whom I have exchanged hundreds of emails, does not exist at all, that someone else has written these and other studies, under a false name. Only the cui bono is completely unexplained. Why would someone do such a thing? Just hoping to collect donations from vitamin D maniacs? Because there were such donations, and I am not the only one who donated after nobody in Germany wanted my money for D-tests. I don't want to speculate any further here, and the whole thing is far more complicated and confused. Bizarre is what an English activist called it. Anyway, all three trials are dead, withdrawn. So is our fine article. A bitter story.
Since then, the D-activists have been waiting for someone to take pity on them and make such a D-study. Instead, Dr. Mercola in the USA is covered with unsubstantiated accusations of a consumer association, David Grimes' eBook on corona and vitamin D is rejected by amazon and Kobe for undisclosed reasons, YouTube has already blocked videos on this topic several times, it all feels strange. Clinic directors who "secretly" supply their C-19 patients with high doses of vitamin D, who had written to us themselves, suddenly no longer answer when asked for results …
Sometime in July I had an idea. The blood testing laboratories in Germany are, besides several private ones, organized in three chains. Shouldn't it be possible to do such an ex-post study with their data? Just see if you have a D value from C-19s sometime before? Tedious, but in the end only database queries. How long are the data kept? The phone call with my laboratory had a funny result: It would be much easier if I didn't know that the samples would be frozen? And it would be possible to determine the D-mirror at any time afterwards. How then, so simple? Yes, that simple. See Jena, where they are now testing for C-specific T cells, just like the Swedes did. Why not also on D, please? No reply. Well, maybe they do.
So if it's that simple, and I, the layman, came up with it, what reason can there be that nobody takes the 4,000 or 5,000 euros in hand and does 200 D-tests of blood samples from corona patients? And correlated with the course of the disease? Especially if I would even pay for it? After all, it is not possible that I, as a layman, would be smarter than all the experts, who of course know that too.
So it would be very easy to silence those annoying vitamin D screamers, and it wouldn't even cost much. But one thing I have learned in the meantime. Silence when things get sticky, but no lying. Not even in Southeast Asia, where a lot of things were faked, only the data most probably not. Their origin is probably neither Indonesia, nor the Philippines, because of a certain peculiarity they could come from the American continent. Enough wild speculation, there are better things to report, and in the next few days and weeks you can judge for yourself whether the wall of silence on vitamin D really exists.
Linda Benskin has written a fantastic review study on the subject, and, as she is currently emailing, this has now been finally published: "A Basic Review of the Preliminary Evidence That COVID-19 Risk and Severity Is Increased in Vitamin D Deficiency".
If, after the 300 references, you still doubt that a healthy vitamin D level could significantly lower IFR and CFR rates, I would counter with a second study announced months ago and published over a week ago. Double-blind, randomized, bolus doses of vitamin D - with clear results.
The Spanish study was published by Reina Sofía University Hospital, Córdoba, in the Journal of Steroid Biochemistry and Molecular Biology on August 29. I sent it to the usual suspects on September 3. To this day, it has not appeared anywhere, oh, that's not quite true: it is mentioned in "meinbezirk.at", Lower Austria edition. Big press, right? No matter. Dr. Peter Meyer's article about it is so good that I want to quote him here:
In Spain, a very careful placebo-controlled and randomized study has now been conducted. […]
76 patients with acute respiratory tract infections confirmed by X-ray examinations were randomly divided into two groups. 50 patients received the best treatment with vitamin D, the 26 in the control group only the best treatment but without vitamin D. […]
The group of 50 received 0.532 mg of calcifediol orally on admission and 0.266 mg each on days 3 and 7 and weekly thereafter. In this group, one person received intensive care, but of the 26 in the control group, 13 and 50 percent, respectively.
Of the vitamin D group, all survived and were discharged without complications. In the group without vitamin D there were two deaths, which is also a comparatively good result.Peter Meyer
Note: 2 out of 26 without vitamin D result in a death rate of 7.6%. Compared to 0% of those with vitamin D. And the one of the 50 with D who had to go to intensive care is only 2%. Compared to 50% of the group without D.
Vitamin D reduces the cytokine storm, it regulates the renin-angiotensin system (RAS) and it modulates the activity of neutrophils. It also protects the lungs and prevents fluid accumulation, stimulates the repair of epithelial cells and reduces any increased coagulation of the blood. It therefore has a positive effect on almost all risk factors of Covid-19.
[…] Higher levels of vitamin D are needed to reduce the excessive reaction of the immune system. This is exactly the problem that leads to severe courses of Covid-19. The immune system does not regulate in time and the cytokine or bradykinin storm destroys parts of the lungs or other organs.Peter Meyer
I might add: The "best treatment" (for both groups) was the administration of hydrochloroquine and azithromycin. There is a new study about the latter, just published in The Lancet, which states
In patients with severe COVID-19, adding azithromycin to standard of care treatment (which included hydroxychloroquine) did not improve clinical outcomes.
In plain English: Nothing helps. We've known about hydrochloroquine for quite some time, but nobody believes in it anymore except Trump.
So now we have it together: if we don't want to wait for the vaccine and if we don't want a second wave, especially in places where C-19 has not been very widespread, then we would have to take vitamin D as a preventive measure. Because it not only "protects" us from getting infected (let's say: from getting infected noticeably and with consequences), but obviously also from a severe course of the disease. But how much - and why are so many studies not much clearer?
We humans are not the same, that's a rush. Otherwise we would all be the same size. But our height is distributed according to a wonderful mathematical function, the Gauss or bell curve, because it looks like a bell. Sometimes a little to the left or right, but Gauss. And this Gauss curve is the blueprint for almost everything that has more than a few dozen influencing factors. Whether we throw the dice or shoot the bow and arrow, whether we are more or less healthy or sick, how fast or slow we drive on the motorway, everything can be depicted in Gauss curves. If you examine data, first look to see if they are at least a bit Gaussian. If not, you need a really good reason.
In all medical studies there are cases that mock the suspected theory. Take life-shortening smoking and Helmut Schmidt. Take the drinking, smoking, overweight, no-sports Churchill. Or the healthy athlete who dies far too soon. That's exactly what "Gauss-spread" means, with outliers on both sides, but the mass of results in the middle of the bell. And we see this in almost all medical studies, also in connection with vitamin D.
80% of multimorbid seniors have a pronounced vitamin D deficiency, but 20% do not have one either. 80% of healthy seniors of almost the same age have a "good" D level, but 20% are deficient and still healthy. So says the Federal Office for Risk Assessment (BfR) in a paper published in 2011. How can this be explained?
In 2016, Professor Carsten Carlberg, a researcher at the University of Kuopio in Finland, has published a groundbreaking study: "The concept of the personal vitamin D response index".
Carlberg tested volunteers for gene activity after they had been given bolus doses of vitamin D and came to the conclusion
Humans can be differentiated into high-, mid- and low-responders with respect to vitamin D by measuring vitamin D-sensitive molecular parameters, such as changes in epigenetic status and the respective transcription of genes of mobile immune cells from blood or the level of proteins or metabolites in serum. Therefore, we suggest that the need for vitamin D supplementation be measured by an individual's personal vitamin D response index to vitamin D status rather than by absolute vitamin D status alone.
This sounds as complicated as the experimental procedure was, but it says the following: Since vitamin D is involved in over 700 synthesis processes for proteins and enzymes, many of which are directly or indirectly related to our immune system, the question is how a person's individual genome responds to vitamin D. Carlberg has measured this and found between 33% and 87.5% "activations". If you take his measurements, the result is - surprisingly - a wonderful Gaussian curve.
And this explains why there are healthy people with relatively low D levels and sick people with relatively "high" D levels. The rigid limits of DGE (<10 ng/ml: deficiency, <20ng/ml: inadequate, 20-30 ng/ml: good), but also the higher limits of WHO (<20, <30, >=30) are appropriate for some people, but not for all. Apart from the fact that Mother Nature gave us much more in the cradle of mankind (this is also stated in Carlberg's study), namely 45 ng/ml on average. With a range of 24-68 ng/ml, as I have found elsewhere.
It is therefore possible to survive a C-19 infection unharmed with (low) 20 ng/ml because you are one of the high responders. Or you may have a severe course because you are one of the low-responders.
By the way, the seniors in Stockholm have on average 19 ng/ml, those in Bergamo only 9 ng/ml. This could explain a good part of the much higher IFR in Bergamo, even if the values seem implausible at first. Of course there is much less sunshine in Sweden, but people eat a lot of fish and, as I was told, a lot of vitamin D is distributed in the old people's homes, because it is cheaper than antibiotics. Vitamin D is also sold in pharmacies, and there is said to have been a shortage of it in mid-March. And the Italian senior citizens rather avoid the midday sun, but in the afternoon the UVB index decreases very much, and in the shade you still get brown from the longer-wave UVA, but UVB does not reach the shade. Moreover, in Lombardy there is a high fine dust pollution and air pollution, which reliably slows down UVB radiation. But without UVB there is no vitamin D - unless you eat fish or cod-liver oil for rickets, but that is something only those over 60 years of age who had to take it as children still know.
Conclusion: The essentially important effect of vitamin D on our immune system can no longer be denied. After the Spanish study, a change in thinking is finally needed. The majority of the population shows a - confirmed by the RKI - vitamin D deficiency, promoted by our indoor lifestyle and: sun cream with protection factor 30. If this is the case, only supplementation helps. It is time to rewrite the age-old narrative of the supposedly dangerous vitamin D. With 45-50 ng/ml - and that means an intake of about 5,000 IU per day and not the ridiculous 800 IU that is still considered the gold standard - all other people would be well provided for, except for the absolute low responders who rather need 70-80 ng/ml. And it doesn't hurt the high responders; a light that has already been switched on cannot be switched on again. Even the WHO sees the limit for "adverse effects" only at well over 120 ng/ml. Only one thing I always mention: not without K2!
To reach levels of this magnitude through supplementation, the average adult would not need to consume the 800 I.U. (20 mcg) D3 usually prescribed by the DGE/doctors, but 4,000-5,000 I.U. per day. However, this is generally not recommended without additional vitamin K2.
K2 is only present in food in very small quantities. However, an imbalance between D and K2 inevitably leads to hypercalcemia. K2 ensures the correct distribution of calcium. Without K2, a high D level releases additional calcium from the bones and aggravates osteoporosis, despite additional calcium intake. Unfortunately, this has been proven by many studies, which also had to document other consequences of hypercalcemia: in addition to kidney stones, increased calcium plaque and subsequently heart attacks and strokes, and in the case of very severe hypercalcemia, kidney damage up to failure. Therefore: Vitamin D never without corresponding vitamin K2.