The State of Affairs
(Download PDFs (German): Intro | Part 1 | Part 2 | Part 3)
Intro
Physicians' initiative urges widespread use of vitamin D against Covid-19
An initiative of more than 100 doctors and scientists summarizes the current study situation in an open letter and proposes to raise vitamin D levels in the population by giving out free vitamin D supplements, similar to what is already being implemented in England and Scotland for 2.5 million people from risk groups.
The letter, addressed to "all governments, health authorities, physicians and healthcare workers," can be viewed at. #VitaminDforAll and invokes current evidence on the impact of vitamin D on the immune response as well as fighting Covid-19 infection. The key action statement derived from this is to maintain vitamin D levels above 30 ng/ml (equivalent to 75 nmol/L) on a sustained basis across the population. This is to be achieved by the daily intake of approx. 4,000 IU (International Units, converted to 100 mcg) of vitamin D.
As the signatories of the letter have different opinions on the daily dosage, the letter was signed by each individual indicating his recommended dose as well as the dose he personally takes. The range of values given is from 2,000-10,000 IU. It is remarkable that none of the signatories mentions the value of 800 IU, which is currently recommended as the maximum dose by the German Nutrition Society (DGE). Since the DGE is of the opinion that a vitamin D deficiency is only present at levels below 20 ng/ml, the DGE with its recommendations not only lags behind the values from the above-mentioned initiative, but also behind those of the World Health Organization (WHO), which locates an optimal vitamin D level only in the range of 30-50 ng/ml, as reported by Telepolis already in April 2020 (Does vitamin D protect against Covid-19? Telepolis (heise.de)).
Infobox Vitamin D Supplementation:
The level of personal vitamin D can be determined from the blood serum. The blood sample can be taken by the family doctor and in some cases is covered by the health insurance. Otherwise, a co-payment of approx. 20-30 euros is charged. This means that in many cases the examination is more costly than the therapy, since vitamin D can be produced and stored so cheaply that a year's dose can be ordered on the Internet for 23.90 euros. In view of the low price and the fact that no product patents exist, one can guess why there has been little lobbying or subsidizing of more extensive studies to clarify the benefits of vitamin D supplements, at least on the part of the industry.
The topic of vitamin D supplementation is continuously discussed scientifically and the discourse is accompanied by Telepolis at regular intervals. This article attempts to summarize the current argumentation and expands it with current study results. A more detailed version of the article, in which the individual chapters are discussed in more detail, can be viewed here on the author's website. In the same place are also basic considerations on the infection fatality rate as well as on the treatment options for Covid-19 using Hydroxychloroquine.
Excerpt of the current study situation
Almost at the same time as the above-mentioned initiative, a working group from Italy, consisting of 61 physicians, has also compiled the current data situation. From the findings, the head of the working group, Prof. Giancarlo Isaia from the University of Turin, draws the conclusion that the vitamin D level should be kept permanently in a range of 40-50 ng/ml, especially in the risk groups, by daily vitamin D supplementation of approx. 4,000 IU, which is very close to the recommendation of #VitaminDforAll.
The "godfather" of vitamin D research, Michael Holick, who co-authored a study with data from over 190,000 patients who had contracted Corona. The result can be impressively illustrated with the curve shown below: The risk of becoming infected is more than twice as high for those with deficient D levels (<20 ng/ml) than for patients with (very) good D levels (>50 ng/ml). This curve shows the correlation:
The second example of a very comprehensive study of the same context comes from Israel, where an analysis of data on 4.6 million members of the Clalit Health Services (CHS) was carried out and the conclusion reached:
We compared 52,405 infected patients with 524,050 controls of the same sex, age, geographic region [...] to assess the relationship between baseline vitamin D levels[...] and positive Covid-19.[...]
In this large observational population study, we demonstrate a strong association between vitamin D deficiency and Covid-19 incidence. After adjustment for baseline characteristics and previous vitamin D levels, acquisition of liquid vitamin D products was associated with a reduced risk of Covid-19 infection.
In addition to these two examples, there are now a large number of studies on the relationship between vitamin D deficiency and severe courses of COVID-19, so many that it is best to resort to metastudies, i.e. summaries across many individual studies, in order to obtain an overview. One such meta-study has been published by Linda Benskin under the (translated) title "An overview of the risk and severity of COVID-19 in vitamin D deficiency", and in order to make it accessible to those less skilled in English, I had suggested the entire study be translated. With the help of DeepL this has been done, proofread by H.G. (MD/GP, France) and is now available here, with a link to the original, of course. Benskin writes:
Vitamin D deficiency increases [...] the activity of the X-chromosomal-linked "renin-angiotensin" system, making individuals with vitamin D deficiency (especially men) more susceptible to the fatal "cytokine storm" (dramatic overreaction of the immune system) in COVID-19. [...]
[...] the pattern of geographic distribution of COVID-19. [reflects] greater vitamin D deficiency in the (affected) population. Both in the US and globally, the mortality rate of COVID-19 parallels the rate of vitamin D deficiency.
[...]Although randomized controlled trial results will likely become available eventually, the current correlational and causal studies demonstrating an association between vitamin D deficiency and COVID-19 risks are already compelling enough to support action to address vitamin D deficiency.
The 141 author group, writing primarily on biological plausibility, explained in detail how vitamin D deficiency can explain every risk factor and complication of COVID-19, [...] COVID-19 was compared to dengue fever, where daily oral vitamin D supplements of 4000 IU for 10 days worked significantly better than 1000 IU to mitigate viral replication and regulate the "cytokine storm" (an immune system overreaction) responsible for the deaths.
Among the 47 original research studies summarized here, chart reviews found that serum vitamin D levels linearly predicted COVID-19 mortality rates (16 studies) and COVID-19 severity (8 studies). [...]
The literature review also found that prophylactic correction of possible vitamin D deficiency during the COVID-19 pandemic is extremely safe for patients. The widespread recommendation of 2000 IU of vitamin D daily for all populations with limited ability to make vitamin D from sunlight has virtually no potential for harm and is very likely to save many lives.
Incidentally, Anthony Fauci, immunologist and advisor to the US Trump and Biden administrations, has confirmed his personal supplementation of 6,000 IU vitamin D.
Official position (Germany)
According to the German Nutrition Society (DGE), healthy people who eat a varied diet do not need dietary supplements. And the WELT writes on 27 November 2020:
Vitamin D is absorbed not only through food but also through sunlight on the skin. In the crisis, it has often been recommended as a kind of miracle cure. The Federal Institute for Risk Assessment (BfR) emphasized in October that no studies are known according to which a vitamin D intake protects against a corona infection. Therefore, an additional intake is not necessary [...].
The consumer advice centre also rejects the idea and warns:
Vitamin D contributes to bone stability and tooth retention. It is also important for the immune system. A good supply situation can protect against acute respiratory infections, but does not protect against the Corona virus.
But the consumer watchdog believes:
Only in exceptional cases (e.g. when bedridden or fully veiled outdoors and older age) is an additional dietary supplement in consultation with the doctor advisable. [...] If taken regularly, do not take more than 20 mcg/day [equivalent to 800 IU].
Instead of a daily dose recommendation following the above-mentioned initiative, which is 5 times that amount, i.e. approx. 4,000 IU for a 70 kg person, then this from the consumer advice centre:
An overdose can lead to serious health problems such as nausea, headaches, reduced muscle tone and even kidney failure.
Vitamin D overdose
This ever-repeated warning occurs with inordinately excessive and long-term intake of vitamin D, combined with a deficiency of K2. According to studies this occurs after an intake of 50,000 IU daily for many months. However, it is common practice in hospitals to administer bolus doses of 300,000 units intramuscularly when D levels are low - of course, without any risk to patients, quite the opposite, as seen in studies above. But why then the urgent warning from the official side?
An overdose is not possible through the body's own production, but it is possible through the intake of high doses of Vitamin D, e.g. through certain food supplements. Such an overdose leads to increased calcium levels in the blood serum (hypercalcemia). The clinical symptoms associated with hypercalcemia in humans range from fatigue and muscle weakness to vomiting, constipation, cardiac arrhythmias and calcification of blood vessels. Persistent hypercalcemia can lead to kidney stones, renal calcification and ultimately to a decline in kidney function.
writes the BfR in its leaflet. Headline: "intake of high-dose food supplements is unnecessary". Here, 50 mcg D3 corresponding to 2,000 IU is already considered as high-dose.
However, all these horror stories only threaten us if there is too much calcium in the blood. This is the case when, thanks to vitamin D among other things, calcium is released from food but cannot be incorporated into the bones due to a vitamin K2 deficiency, but on the contrary calcium built up by osteoclasts is added. And this also happens with naturally produced vitamin D. This was already discovered in the 1990s with Israeli beach guards who spent all day in the sun and achieved natural vitamin D levels of 59 ng/ml. Largely nourished with beach junk food, they actually developed a conspicuous number of kidney stones.
In order to safely avoid hypercalcemia, one should (particularly if one supplements vitamin D) also supplement vitamin K2 to be on the safe side. As with iodine, vitamin B12, zinc and selenium, we tend to be nutritionally deficient anyway (refer to the study from the Netherlands below). And you can't take too much of it, as a lethal dose for K2 is unknown. More than 200 mcg / day is probably unnecessary, though.
However, the vast majority of vitamin D preparations prescribed by doctors have so far been without vitamin K2 - in any case a malpractice, because osteoporosis can only be cured if D and K2 are supplied. What the common family doctor does not know, because the medical associations do not know it, and the DGE and the BfR also not. Yes, it sounds almost unbelievable, but it is an unfortunate fact that while the effect of K2 has been elucidated for a long time, the vast majority of studies on D are done without K2. In the short term this is not problematic, but long term studies without K2 increase the rate of heart attacks, strokes, and unfortunately also osteoporosis. Which irritated the researchers and greatly shaped the overall predominantly negative reporting on vitamin D in recent decades.
And because of such studies, official warnings were issued against hypercalcemia caused by vitamin D, so that the common man is discouraged from buying and taking such things. But it gets even worse: Supposedly, we don't need any additional vitamin D at all.
Vitamin D deficiency
"Vitamin D supplements are much advertised - because every second German is said to be poorly supplied with the vitamin. But is that true?" writes the Hamburger Abendblatt on 28 November 2020. "Are we really so badly supplied with vitamin D in Germany? Do we need pills to change that? According to Helmut Schatz, board member of the German Society for Endocrinology, clearly no. "Many people talk about a vitamin D deficiency where there really isn't one."
[...] "Sure, less vitamin D is indeed synthesized in winter due to the lower UV-B radiation," says the director emeritus of the Bergmannsheil University Clinic in Bochum, "but a healthy person who regularly goes outside uncovered in summer stores enough vitamin D to get through the winter." And that, according to Schatz, without any pills at all .
Antje Gahl, spokeswoman for the German Society for Nutrition, agrees. [...]"But basically, the amount of vitamin D you take in between March and October is enough to get you through the winter. Of course, the level gradually decreases, Schatz also admits. "But some is there, still."
Regarding numbers and radiation physics: From an angle of incidence of 45°, the path through the atmosphere is so long that the short-wave UVB rays are reliably filtered away. This is the case when our shadow is longer than we are high. Only when it is shorter, i.e. the sun's position is greater than 45° (the red line below), only then is there UVB, and only then can D be synthesized.
At the sun's highest point, on 21 June, this is the case for a full 7 hours, between 8:30 and 15:30 (note: standard time). On the 20th of April and on the 23rd of August it is already from about 10 to 14 o'clock. But from mid-September until the end of March, the sun's position is less than 45° around the clock: de facto no UVB and no D anymore:
(By S.Wetzel, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=32947615, red line at approx. 43° from me, LB)
Professor Schatz again:
"Clearly, less vitamin D is indeed synthesized in winter due to lower UV-B radiation."
No, none at all. At least not in Bochum.
In Davos, perhaps, because the decisive one and a half kilometers higher and you bypass the thickest layer of air, the densest part of the UVB filter. And of course Thomas Mann's Zauberberg comes to mind, and the sunbaths against tuberculosis, and that you can get sunburnt in the Alps even in winter.
In Ischgl there were only two deaths among - according to antibody tests - at least 800 infected inhabitants, a very low IFR of 0.25%. And this although the virus droplets are supposed to fly longer and further in cold air.
Ischgl is located at 1377 meters above zero. In fact, initial data from the Andes suggest that mountain dwellers may be better able to withstand the pandemic: Peru, which has the most infections in the subcontinent after Brazil, has ten times fewer cases above 3000 meters than the plains. (Welt)
Again, to the key statement in the article:
"But basically, what you take in vitamin D from March to October is enough to get you through the winter." (Gahl, DGE)
Who actually determines how much is enough, how much is right? Well, for example the DGE, the German Society for Nutrition. The Federal Office for Risk Assessment (BfR) says the same thing: "Good" is everything above 20 ng/ml, 20 nanograms per millilitre of D3 (calcidiol) in the blood. "Undersupplied" is between 10 and 20 ng/ml, a deficiency is only to be recognized from 10 ng/ml.
The World Health Organization, however, has gone a bit further: below 20 ng/ml is already a deficiency (below 12 is generally considered a severe deficiency internationally), below 30 ng/ml is considered insufficient, and only more than 30 ng/ml is considered sufficient. (insufficient), only more than 30 ng/ml is considered sufficient. The RKI did a large study in 2016. The result is well known to the DGE and the BfR. On average, the D3 level of the population between 18 and 78 years and over the whole year is a meager 19 ng/ml. According to WHO criteria, we would have a deficiency all year round. In fact, the level fluctuates seasonally, ranging from about 24 in summer to a deficient 12 ng/ml in mid-March. In the older age groups, i.e. among senior citizens, it is mostly below 10 ng/ml in winter, values of 6 ng/ml but also 3 ng/ml in people over 70 are not uncommon. So the fracture of the neck of the femur is not really surprising. The reason? The skin of over 70-year-olds only produces 25-30% of the vitamin D that a 20-year-old produces.
The great mystery is the question of where the above values actually come from? One can research this for a long time, most likely it is "empirical values", average values from many laboratory measurements. The Bremen health department, for example, writes:
The laboratory findings show whether the supply status is sufficient (adequate), insufficient (suboptimal) or deficient. (adequate), insufficient (suboptimal) or deficient.
Many laboratories refer to levels below 20 ng/ml as mild vitamin D deficiency and levels below 12 ng/ml as severe deficiency.
However, this assessment is often considered outdated. In recent years, many scientific studies have shown that values of at least 30 ng/ml must be reached in order to avoid various health risks, and some even set the lower limit of an optimal supply at 40 ng/ml. According to the most common expert opinion of recent times, values in the range between 40 and 80 ng/ml would be considered optimal.
Bone experts call for blood levels of vitamin D to be at least 30 ng/ml, especially in people over the age of 60.
40-80 ng/ml are therefore the announcement, not half, not 20 ng/ml, as the DGE and the BfR repeatedly and still publish in contradiction to the "most frequently represented expert opinion of recent times". Where then did the old values come from? Well, if one takes young to middle-aged people in Central Europe as a yardstick, then, due to the low angle of sunlight, such average values must come out. And since these measurements were made on people who appear healthy, surely this must be sufficient?
Seasonality of the flu - and that of Corona
From the WELT comes this graphic, which was generated from DIVI intensive care register figures:
From the end of June into September, we see comparatively few C-19 cases in the intensive care units. However, the sheer numbers of infections after PCR tests had already risen steadily from week 28, i.e. mid-July, as this graph by Joachim Schappert shows:
This discrepancy is often explained by the decreasing average age of those tested, but this is simply not a sufficient factor. From the end of September, the ITS figures then rise considerably, and barely two weeks later the death figures follow them.
In the summer, therefore, despite increasing infections, the courses were predominantly mild, only very few severe and relatively constant throughout the summer. What could explain this striking seasonal pattern?
There are three main explanations given by virologists for this seasonality.
1) in the cold season, people tend to stay indoors and the risk of infection is therefore higher, the dry (heating) air dries out the mucous membranes and makes them more susceptible to infections.
There is little to be said against this, except that it may explain the large number of infections, i.e. the respective "waves", but not the severity of the individual illness - just look for a flu with a severe course here in summer, because yes, viruses are also present in summer: "Between April 2009 and November 2015, rhinoviruses and adenoviruses were present throughout the year. Rhinoviruses were present most days of the year (84.7%), followed by adenovirus which was present on 52.3% of the days. RSV (36.4%), HMPV (32.8%) and IAV (32.7%) were present in around 1/3rd of the year." (from Nature.com)
2) viruses persisted longer in dry, cold air than in warm, humid climates
This is only partly true, because different viruses show different seasonal fluctuations, as the reef reporter reports: "In both hemispheres there is a clear flu season in the temperate climate zones, but sporadically the influenza viruses also appear in summer in some sick people. In tropical and subtropical regions, there is no classic flu season. There, people get sick with the flu all year round, usually there are outbreaks during or shortly after the rainy season."
3) and last-not-least the immune system of the people is also weaker in the respective winter.
Let's take a look at the course of the average vitamin D level in Germany over the year:
The vitamin D level in Germany, with a mean value of approx. 19 ng/ml (RKI) thus fluctuates between 12 ng/ml in March and 23 ng/ml at the end of August, which is twice the March minimum. And the flu season from December (15 ng/ml) to March (12 ng/ml) falls conspicuously in exactly this time of the minimum, while in October the D-level with 20 ng/ml is still 50% above the level of this minimum time.
If we turn our D curve upside down and compare it between mid-Apil, when the C-19 pandemic had really picked up steam, and into November, we see a fairly comparable trajectory: as vitamin D rises above 20 ng/ml, ITS numbers drop below 500, only to surpass 500 again and continue to rise sharply as it drops below the 20 ng/ml level in October.
The C-19 ITS numbers, since we are far from herd immunity, this is my prediction, will continue to follow the above curve D level curve exactly - in November this will become clearly visible and by spring 2021 this will become drastic unfortunately.
Unfortunately, there is a clear indication beyond the ITS figures: the IFR, i.e. the infection-fatality rate, is rising again. At the end of August, beginning of September, it was still at 0.32% in a 10-day interval (25.8./4.9.), then between 28.9. and 8.10. it had risen to 0.47%, which is almost 50% more deaths per infected person and this cannot be explained by a seasonal sensitivity of the virus and certainly not by the fact that less testing is now taking place. With the D-level curve, however, it can.
Media discourse and concluding remarks
It is impressive to see how the topic of vitamin D supplementation is gaining more and more shares in the media coverage, even if not fast enough. As one example of many, the article "Does Vitamin D Help Fight Coronavirus?" in SPEKTRUM is bemoaned in the D activist camp, but it is still a yes/no article, which I deal with in detail in the extended version of this article. Thereby also the study of the Dutch physicians of the Canisius-Wilhelmina-Hospital in Nijmegen is critically regarded, which among other things emphasizes the role of vitamin K, as well as an Indian study and a study from Brazil, each of which examined the influence of vitamin D supplements on Covid-19 infections. This reasoning seems more likely to confirm that vitamin D is a helpful treatment and effective - and that statistics can often be misleading if not treated mindfully. A "trial" on 1,000 hospitalized Covid-19 patients with (as suggested by many D activists around the world) with 300,000 IU bolus dose and 4,000-7,000 IU (plus 200 mcg K2) maintenance dose could very quickly show that with this the diseases usually end up mildly.
As long as there is no nationwide supply of effective and safe vaccines (see also "Would you get vaccinated against Corona?" at Telepolis) is secured, the supply of the population with vitamin D suggested by the above-mentioned doctors' initiative represents a simple, fast, harmless to health and cost-effective emergency and preventive measure against severe Covid-19 courses. The seasonal fluctuations in vitamin D levels further exacerbate the situation, as the seasonal low point of the immune response in Germany is not reached until March. The cost of vitamin D supplementation, in contrast to three more lockdown months, does not cause depressed families, frightened seniors, and overworked medical and nursing staff with the highest risk of death in their age group.
Acknowledgements:
Many thanks to Dr. René Greschert, RWTH Aachen, for the critical review and extension of the article.
Part I
The Lockdown, the Infection Fatality Rate and the Question of All Questions: Cui Bono
"Neither Taiwan nor South Korea nor Japan have experienced a hard lockdown," writes SPIEGEL in an worth reading article about the handling of Covid-19 in Asia. And the newspaper Welt asks "What is the secret of the Taiwan model?" and elaborates:
One of the first measures Taiwan took against the coronavirus was to close its borders. [...] In addition, the country sent all people who had been in contact with infected people into a two-week isolation. To this day, anyone coming from abroad must go into a 14-day quarantine [...]. In the quarantine the authorities monitor the location of those affected via their mobile phones. Anyone who leaves their location first receives a warning text message - and then, if they don't comply, a visit from the authorities.
350,000 people have been quarantined so far. Taiwan, with 23 million inhabitants, has just 607 "infections" (= positive PCR test for Covid-19) and only 7 people have died. The medical, but also the economic success of the measures, which seem harsh or even unreasonable to us, is obvious:
Moreover, in the second quarter, Taiwan's gross domestic product shrank by only 0.6 percent from a year earlier, compared with a 9.7 percent drop in Germany. (Welt)
Taiwan is considered a democracy, like Japan and South Korea. It is probably - the SPIEGEL article suggests - strongly related to the Asian culture that there are not only no protests against the described official requirements, but also that mere recommendations are followed quite voluntarily:
When Japan's government advised people to stay home and to close restaurants and bars, citizens complied - even without fines or surveillance.
Oshitani attributes the fact that people adhere to these guidelines to the strong social control in Japan. "Get on a subway in Japan. There, 99 percent of the people wear a mask," Oshitani says. The pressure is great, he says, to abide by the rules and not endanger others unnecessarily (ibid).
Island states such as Taiwan or New Zealand can close and monitor national borders relatively easily. This is not the case in Germany, especially when the population wants to go on holiday to the Mediterranean and the agricultural sector needs many harvest workers from other countries.
Moreover, people here have a different conception of individual freedom than in Taiwan, Japan or South Korea. A discussion about what is the better or worse model in terms of society as a whole or in terms of the happiness of the individual is not welcomed here. In a pandemic, however, the Asian "common good before selfishness" culture, which makes the acceptance of the strict measures described above possible in the first place, also has tangible advantages for very many people:
Millions of people there [meaning Japan, Taiwan, South Korea] have been able to move around largely freely for months. Cafés, restaurants and shops remained mostly open. (SPIEGEL)
There is no question that the necessary monitoring mechanisms would not have been accepted in Europe or even in the USA. Sweden has tried to use a strategy with maximum freedom and self-responsibility and must now - as already predicted in April harden them - the figures compared to the neighbouring countries appear to be simply too bad.
But what do the current figures really tell us about the state of play? The next tables show the IFR calculated from current Worldometer figures (24.11.20), the IFR, the Infection-Fatality-Rate, i.e. the number of deaths divided by the number of "cases", not to be confused with the CFR, the Case Fatality Rate, which is more rigidly defined, because only cases confirmed by clinical diagnosis count. For the Worldometer, however, laboratory-confirmed cases are sufficient, and in some cases only suspected cases:
Total Cases = reported total cumulative count of detected and laboratory [...] confirmed positive and sometimes - depending on the country reporting standards - also presumptive, suspect, or probable cases of detected infection.
Anything else would not make much sense either, because the majority of people under 50 do not develop any symptoms at all, and if they do, then with a 5-7 day delay, which would be too late for a timely calculation of R to which one wants to react. Without counting the cases of positive lab tests without a confirming clinical diagnosis, you couldn't do any meaningful screening, it would be hard to justify quarantining - way too late - and the RKI would have to make two different numbers suffice. Since flu is never tested without a reason, one has here at most a CFR, the ill patient with the confirming flu test, an IFR must be estimated with the help of e.g. excess mortality. In the case of C-19, however, even the PCR test - verified by a second measurement in case of doubt - is considered a "diagnosis", otherwise one could hardly justify such severe interventions in personal freedom as immediate quarantine. The RKI uses the term laboratory diagnostic confirmation here.
Why does the IFR not have to be estimated here by a dark figure to be added, as it is called in the definition? Because here, in contrast to the flu, there are very many de facto tests without a reason. This can be seen in the comparatively low percentage of positive versus negative tests. In Germany approx. 1.2 million people are tested weekly, and at present numbers circulate between 15,00 to 22,000 "new infections" per day, together about 11% of the test number. These are, of course, no longer travelers, but virtually all "contacts", apart from those who get tested on their own initiative because of symptoms. With such a high test surplus, a large deviation is rather unlikely.
Caveat: the figures for China are supposed to be based on real diseases, so would be a real CFR. They are not used here.
Any kind of e.g. false positive tests, by the way, would lower this IFR: 1/100 gives an IFR of 1%, but if 50% of the tests had been false positives, the correct IFR would then be 1/50 or 2/100, thus rising to 2%. The IFR of the above countries plus New Zealand looks like this:
Germany, on the other hand, ranks between South Korea and Japan, while Austria, Norway and Liechtenstein are better than the top-ranked Taiwan:
Countries with higher IFR...
...and low IFR:
One could now assume that it plays a role how many tests were performed in total. The easiest way to see this is as a percentage of the population, although the value can also rise to over 100% due to repeated tests, as in the case of the front-runner Luxembourg:
But Singapore also has a very high test rate compared to the rest of the world, while Burundi, the second best in terms of death rate, has a tiny test rate, which makes the calculated IFR seem a bit dubious:
Germany here only for comparison, which with place 36 of 180 is in the upper quarter. So you can see that the test rate nearly does not correlate at all with the IFR. Some examples from countries with higher, but in itself similar test rate:
One explanation for the extremely low lethality of Covid-19 in Singapore lies in the average age of those infected. Bernd Paysan, to whom I owe this reference, writes:
There [Singapore] the big wave from May onwards affected practically only closely packed migrant workers who are relatively young. And this outbreak was contained before it reached older people, thanks to the rigid measures.
and quotes Reuters:
About 95% of Singapore’s COVID-19 infections are among migrant workers, mostly in their 20s or 30s, living in cramped dormitories and employed in labour-intensive sectors such as construction and shipbuilding.
The fact that the lethality below the age of 50 is lower than that of influenza has been sufficiently documented by now.
If we look at a few countries with extremely high testing rates (only rich countries can afford this), we notice that all of them, except Iceland, are in more southern latitudes:
We know from the Icelanders, albeit anecdotally, that they consume cod liver oil on a fairly regular basis and of course eat a lot of cold water fish, both excellent sources of the immune-supporting vitamin D.
If you sort the whole table by lethality and omit about 5% at the top and bottom (8 out of 180 each), the IFR values range from 0.39% (Bahrain) to 5.29% (Liberia). But also from test rates significantly lower than 1% (Afghanistan) to 250% (Gibraltar).
But what does that mean in turn for the country in question? Did many or comparatively few people die?
The following tables show this in per thousand of the population:
So you can see that even the country-specific IFR or lethality of Covid-19 is not a measure of how much of a burden a country really has to take. For comparison, look at these three countries:
In Sweden, over 3 times more people have died in relation to the population than here, and over 9 times more than in Finland, with little difference in testing rates but a notable difference in lethality.
But "civilized" countries can do even worse:
One might now draw the conclusion that with death numbers in the >>promille range<< there is no reason for the sharp measures that have been taken almost everywhere in the world. After all, 1.25% of a population always die over the year (if the life expectancy is 80 years and the population development is static). However, this would be a mathematical fallacy. Nowhere the total population was or is infected, but only a small part. And how large this part is, results from population divided by positive tests, thus "cases":
E.g. between France and Singapore there is a difference to a factor of ~150! Between the Swedes and Taiwan the factor is even ~2000! Is that the price of freedom?
Australia has a high IFR (3.26%), but at the same time very few "cases" (0.11%). (0.11%), resulting in a very low number of deaths of 0.035 per thousand, relative to the total population. The state of Victoria still had a hard lockdown in September/October (beginning of spring there) with a curfew, 3 km zone for shopping, etc. - with hospitalization numbers that seemed almost ridiciulously low compared to those in Europe.
With a hundred times more "cases", i.e. 11% instead of 0.11%, the number of deaths would also have to increase a hundredfold, the per thousand value would grow to 3.5% per thousand or 0.35%. Another 6 times more, i.e. 66% infected, one would be at 2.1%, and that would be almost double the normal annual deaths - but in addition! Presumably such a rough calculation has prompted the politicians to take such harsh measures.
Why 66%? On the one hand, because it is easy to calculate in one's head (multiply by 100 and then multiply by 6), and on the other hand, because this is approximately the proclaimed limit of herd immunity - at least according to many researchers. Whether it is only 44% or 77% will probably forever remain in the dark, provided that the vaccines work, but it does not make a big difference for our calculation.
Let's recalculate this using the example of two countries with more than 100% tests each, i.e. more than one test per inhabitant:
With this test rate, compared to the cases found, one can assume with a clear conscience that there is hardly any room for an undetected number, neither through "false positives" nor through so-called "asymptomatics" who were not tested at all due to a lack of symptoms.
Iceland has one of the world's lowest IFRs (0.49%) and is on the lower end of the scale with 1.55% of "cases" rather in the lower range, both at least as far as the "first world" countries, resulting in a low number of deaths in relation to the total population of 0.076 per thousand. With e.g. 15.5% infected (cases), i.e. a factor of 10, this would result in 0.76 per mille and with 62% (15.5 x 4) then 3.04 per mille. A figure that would be just under a quarter of a standard total mortality of 1.25% (0.3x4=1.2), which would thus increase to 1.55%, but even this quarter would be clearly visible in the annual death statistics.
Luxembourg is with an IFR of 0.88% rather in the lower range in Europe, with the "cases" of 4.94%, however, almost at the top and has 0.4333 per thousand dead. With 49.4% "cases" (factor 10) this would be 0.433 per cent and with 64.2% "cases" (factor 1.33) then approx. 0.58% dead. Again, compared to total mortality, this is an increase of almost half, from 1.25% to 1.83%.
The figures for Germany: 1.13% "cases", 0.174 per thousand deaths, cases times 10 times 6 would then be 67.8% and 1.04% deaths, which would result in an increase in the mortality rate of 80% if these infections all occurred within one year.
Assuming that it takes 2/3 Covid-19 infected individuals for herd immunity, one can generate a list by increment to mortality if all these infections had occurred in a large wave within 12 months - and this list holds some surprises. Below is a selection from it. With a few exceptions, all countries with less than 20% testing have been eliminated, as have most very small countries; it would otherwise have been too long.
Surprises: two small European states, Andorra and San Marino are far apart: 0.8 vs. 2.0 percentage point increase to annual mortality of ~1.25%. UK at the top, with an extra 2.39%, while Hong Kong is in the middle at 1.25%. Sweden still ahead of Belgium and Spain - no one would have guessed. Finland worse than Germany, and Denmark better than Norway?
This shows the following: One should not be blinded by absolute figures, but even converted, relative ones, hold pitfalls. According to the number of deaths per inhabitant, Finland is not only much, much better off than Sweden, but also much better than Norway, but if you convert everything to the worst case, i.e. if no vaccine were available in time and no effective treatment or even prevention were found, if Covid-19 had to circulate like the Spanish flu until 2/3 of the population were once infected and then immune, then exactly this list results in additional mortality, in percentage points, which you would have to add to the normal total mortality of 1.25%. Above the 1.25%... (Hong Kong) there would already be a doubling, above 2.5% a tripling and even at 0.62% (Norway) an increase to one and a half times:
Of course, all this is just number crunching, thought experiments. But one can well deduce from this why it would not be expedient to let the infections "run", even if herd immunity would occur much earlier, perhaps already at 33%. That would halve the increases, but even that would still mean 50% more deaths for the Netherlands, for example - in the middle of the list above - calculated over one year. Even spread over three years, this would still be five times more than the worst flu wave of the last 20 years, and that for three years. To keep this going is certainly not an option.
Now, quite different IFRs are being discussed in the circle of Corona skeptics, Ioannidis' 0.27% is just as much in the room as Streek's 0.37%. Ioannidis' preprint from the spring is now peer reviewed, but still receives strong criticism, some of it on matters of detail (incorrect figures, which epidemiologist Gideon Meyerowitz-Katz reported in several tweets), but above all it is criticized,
that Ioannidis had combined many relatively inferior studies that had a tendency to underestimate the respective IFR. Moreover, he had mostly adopted the low value as the median (DerStandard)
The very low IFR of Ioannidis is based, among other things, on the fact that inferior tests with a high false-positive rate were used in the cited studies. And this must of course lower the calculated IFR, while the actual IFR is much higher.
A very balanced and technically sound "critique" of Ioannidis comes from, among others, Ulrich Dirnagl, head of experimental neurology at Charité, in his blog "Insights of a science fool“.
And Streek now has a problem with his study. His number was calculated from the 7 known dead in Gangelt at the time and about 1,890 cases found using about 900 tests and then extrapolated to all of Gangelt. However, data up to the end of the study were taken into account - and everyone knows that the death curve lags behind the infection curve by an average of 14-18 days, sometimes cases are even added months later, when ventilation lasting several weeks ends fatally.
When the researchers submitted their article to the scientific journal "Nature Communications" on June 4, ten of the patients who had tested positive by the end of March had already died.
Thus, within five weeks after the end of the study, three infected study participants died, and in the months thereafter another six, of which only three were clearly attributed to the consequences of the C-19 infection (ibid.). However, this gives an IFR of 0.69%, which is not far from Luxembourg's (0.88%). There is further criticism of Streek's study, e.g. that only 19% of those allegedly infected had complained of loss of smell, but that this figure is generally a good three times higher, which would then give an IFR of about 2%, by no means unrealistic for the beginning of the "pandemic", when treatment protocols were still being sought.
The IFR picture around the world is very mixed, it is unclear for example why Botswana with a comparatively high test rate for Africa has such a low IFR:
Completely untreated and in the wild, Covid-19 is likely to develop an IFR of well over 2% or more. If good treatment options are available, an IFR of 1% is probably rarely too high, but often too low. Austria and Norway are just below this value, many European, but also Asian countries are often far above it (the total table with 180 countries from Afghanistan to Zimbabwe can be copied from the Worldometer, but I can also send it by mail as XLS or PDF including the columns I added).
It is understandable that governments do not want to accept a doubling of the normal death rate. However, relying nearly solely on the hope of vaccines, under the assumption that we have to remain more or less in lockdown until sufficient immunity is reached, could prove to be a serious mistake. This mistake will probably not be officially communicated in retrospect, though.
Who still confronts Drosten and Spahn today with their statements from spring that masks would not help with anything and who forces them to explain publicly why, against their better knowledge, they claimed the opposite of what they are urging us to do today? Not even Markus Lanz dares to do that.
"Against better knowledge" means in this case: the study situation was very, very thin, but just then a statement such as "Does not help" is at least as untrue as "Helps absolutely". And with the simple question: "Why does everyone in the operating room wear such masks if they don't help?" this lie could have been exposed very easily. Which would have been the task of the journalists - quite a few citizens have indeed raised the argument privately or in forum discussions, and the thought must also have occurred to one or the other cleverer journalist's head. So what is it that compels the capital city journalists to leave their critical spirit hanging in the cloakroom and not ask such an unpleasant question? Is it not even the duty of journalists to do so? Was it perhaps a desire not to undermine authorities they deem important for the public good - and their talk shows? In anticipatory obedience, but of course "for the greater good"?
But that's not a good deal. Because where do you stop, when is the lie big and heavy enough?
This also applies to the scenario we have chosen: masks plus more or less lockdown until the vaccines are available. It should be allowed to discuss alternatives without being either ignored or even denigrated as Corona deniers. No, it should even be required, and the fourth estate, in this case the science journalists, would have to lead the way - but they are not doing so.
If, for example, a certain treatment method could reduce the IFR and also the severe courses of disease by 2/3, as claimed and proven by studies, wouldn't it be right to at least examine this method in detail, without therefore renouncing vaccine research? And by exactly is meant: not only talk about the studies that fit into one's own preconceived opinion.
And if there were another, a preventive treatment that reduced the probability of infection by half and prevented severe courses altogether, wouldn't it be imperative, if only to avert economic damage, to discuss and test it without bias?
In the second part, I will discuss the current state of studies both pro and con of the two methods mentioned above, which in combination might have made the current lockdown obsolete. And I fear that the conclusions to be drawn are uncomfortable for mainstream science because, once all the evidence has been sifted through, the question of all questions will inevitably arise: Cui Bono?
LB/2020/11/29
Part II
The Hydroxychloroquine-Remdesivir Skirmish
The treatment options for Covid 19 patients have improved and the true IFR will decrease noticeably. Whereas in the spring 60% of all patients intubated on the ICU died, this figure has levelled off at 40% at present. Dexamethasone, a drug related to cortisone with anti-inflammatory effects, is now part of the standard protocol, and patients are also intubated later - for their own good. None of this means that the all-clear has been given.
In spring, when the world was still in Covid-19 shock, drugs were desperately sought to counter the exorbitant lethality of Corona. Although it was overestimated by a factor of 5-10 due to too few tests, in reality 1-1.5% remain. 10-20 times more than a severe flu epidemic, and thus socially unacceptable, as the pictures from Bergamo made impressively clear. And two hopefuls were hydroxychloroquine, the anti-malaria drug, and Remdesivir, a virus inhibitor.
The expensive Remdesivir - a treatment should cost $3000 - has, as of today, not fulfilled the expectations. And that is not so surprising. One has already experienced something similar with Tamiflu in the matter of swine flu. These antivirals inhibit the viruses from reproducing, but apparently for this to be effective they have to be applied immediately after infection. This is especially difficult with Covid-19 because symptoms usually don't appear until 5-7 days after infection - and by then it seems to be too late. However, it has only now become clear in autumn that Remdesivir cannot fulfil the hopes:
Pharmaceutical company Gilead disappointed: WHO advises against Corona drug Remdesivir
According to the World Health Organization, Remdesivir, the first Corona drug to be approved, should no longer be prescribed. Reason: Studies have cast doubt on its benefits - and the manufacturer, Gilead, is charging far too high a price.
(manager magazin on 20 Novemeber 2020)
At the same time, in spring, hydroxychloroquine was also a hope:
Wuhan - After French tropical medicine experts reported last week on successful healing trials with the antimalarial drug hydroxy-chloroquine in COVID-19 patients, a randomized study from China now also comes to positive results in medRxiv (2020; DOI: 10.1101/2020.03.22.20040758). The drug authorities consider widespread use to be premature and fear bottlenecks in approved indications.
A team led by Didier Raoult of Aix-Marseille University had used hydroxy-chloroquine in 20 patients who were mildly ill with COVID-19. After 10 days, 14 patients (70%) were virus-free, including all patients who had also received azithromycin. The study had only one historical comparison group, severely limiting its power. (Medical Journal April 2, 2020)
Hydroxychloroquine (HCQ), an anti-malarial drug, is comparatively cheap. If it could actually help, it would be the drug of choice, especially for poor countries. However, just like remdesivir, it doesn't seem to help once the infection is already full-blown and the patient needs to be hospitalized (a relatively recent study from October 2020 on this later). HCQ, the version of chloroquine with fewer side effects, must or should be prescribed at the latest after the appearance of the first symptoms (e.g. cough etc., see above: "mild symptoms"), if one follows this old study from 2005. At that time, the older brother of SARS-CoV-2 (Covid-19 is the disease the virus causes, the corona virus disease), namely SARS-CoV-1 appeared for the first time:
Chloroquine is a potent inhibitor of SARS coronavirus infection and spread
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2.
And HCQ should only be applied together with zinc:
Hydroxychloroquine inhibits the life stage of plasmodia in erythrocytes. It is less toxic to the retina than chloroquine.[3]
Chloroquine also acts as a zinc ionophore, causing increased intracellular zinc concentrations. Zinc, in turn, has an inhibitory effect on coronavirus RNA polymerase.[4][5] (Wikipedia)
And it must or should be discontinued at the latest when the patient's condition deteriorates significantly, when a cytokine storm threatens, because HCQ inhibits not only the ACE2 receptor but also autophagy, i.e. the ability of cells to clear away waste.
The TP commentator "aufdiedauer" wrote about it (obviously somewhat in rage ;-)
Yes, the "Institution" Lancet went for a swim and hasn't dried off yet afterwards. How junk science works - using HCQ as an example:
it is known since the beginning of April that it excellently works if you detect the infection as early as possible, preferably before symptoms appear. The correct dose is 2x 200 mg/day for 4-5 days, no longer. It is essential to take zinc with it.
Then hopefully, because it is immunomodulatory, it wards off a cytokine storm. This is an autoimmune overreaction, which is only triggered by the viruses, but not "implemented". The main danger for the at-risk group with CoV-2. At the same time, together with zinc, it has an antiviral effect, stops the viruses from multiplying. HCQ is not taken in any case when there has already been such a cytokine storm. Because the drug is no longer effective against autoimmune damage that has already been triggered. So that's been clear since early April. Using HCQ in patients with severe Covid 19 symptoms must be considered malpractice.
Now, when a plethora of large "studies" appear after early April administering HCQ to critically ill Covid-19 patients, there are only 2 options:
- the people who develop and conduct such studies are incredibly underqualified and do not know what they are doing because they are uninformed
- these are highly qualified professionals who want to demonstrate with intentionally false studies, junk science, at the expense of the patients, that HCQ does not work.
A treatment with HCQ costs 1.85 €, has proven itself -thousands of times. For Remsidivir $ 3800 were mentioned.
But what did he mean by "Lancet has gone down the drain"? And why has HCQ all but disappeared from the media? In fact, something very strange has been going on here. If you like you can google it all under "Lancet Gate" and research it, here are a few snippets from SPIEGEL from late May and early June:
23.05.2020 Study on controversial Covid 19 cure
Malaria drug increases mortality rate
Donald Trump is recommending hydroxychloroquine as a cure for Covid-19, and the British and Brazilian governments are also backing it. But the drug is not only ineffective, according to a study, but also dangerous. [...]
A research team from Harvard Medical School in Boston and the Heart Center at the University Hospital Zurich analyzed data from 96,000 patients in hundreds of hospitals worldwide for the study published in the journal "The Lancet".
According to this study, HCQ should double mortality. This led to the WHO recommending that all ongoing HCQ studies be suspended for the time being. Two weeks later it came to light that it had all been lies and fraud:
05.06.2020 Controversial hydroxychloroquine
Three authors retract results of corona study
A study on the drug hydroxychloroquine was published with data from a US company. Now the journal and three authors distance themselves from the results.
06/14/2020 Alleged Corona Database
US company Surgisphere provides a global patient database for trials - but it's apparently a massive hoax. Who is behind what is probably the biggest scientific scandal in the corona crisis?
[...] To invent a database with tens of thousands of patient data, to provide scientists with them, who then publish studies in renowned magazines whose basis is fantasy, would be a huge scandal. If the suspicion is confirmed, Sapan Desai would be at the centre of attention as one of the main suspects.
Desai, the boss of Surgisphere, must be - like the company itself - apparently of the windier sort, if one follows SPIEGEL. But also the English Wikipedia does not know much good to report about him. The scientific community had its scandal. And the consequences?
- The reputation of two renowned journals (Lancet and NEJM) has been quite damaged, the peer-review process thoroughly disavowed, far beyond the fundamental criticism that Ulrich Dirnagl, head of experimental neurology at the Charité explains in his science blog in detail.
- The main authors - burned
- And it was and remains a huge embarrassment for the "peers" involved, we'll see how many years it takes for them to dare to go public again
But one important question was never asked: What's the point? Cui bono? Why did Desai do it? After all, he dragged a relative into it, who in turn dragged a friend into it, and severely damaged their reputations.
It is unlikely that the elaborate generation of large amounts of raw data was only to satisfy an exaggerated need for prestige, because Desai knows the science business well enough not to know that he could quickly be exposed, having published science magazines himself.
In the original Press Release of the Brigham and Womens Hospital in Boston (see Press Release 5/22), it had still been said full-bodied:
Mehra and colleagues conducted their study using the Surgical Outcomes Collaborative database, an international registry comprised of de-identified data from 671 hospitals across six continents. The analysis included data on more than 96,000 patients hospitalized with COVID-19. This included almost 15,000 patients who had received the anti-malarial drug chloroquine or its analog hydroxyquinone
In the rather embarrassing retraction letter of Mandeep Mehra this passage can be found:
Dr. Desai, who served as a co-author and whose team maintained this observational database, conducted various analyses. [..] When discrepancies in the data started to arise, I and the remaining co-authors immediately asked for a re-analysis from Surgisphere and then proactively contracted Medical Technology & Practice Patterns Institute (MTPPI) to conduct an independent peer review. On June 3, MTPPI informed us that Surgisphere would not be able to transfer the data required to conduct this audit [..].
Allegedly because of legal implications etc., in the meantime it is clear that many of the allegedly cooperating hospitals do not even know Surgisphere, that the data cannot be correct because certain drugs do not even exist in the countries concerned and that the database probably only exists in the imagination of Sapan Desai. So it's a large-scale hoax. Mehra (Boston) and Ruschitzka (Zurich), the figureheads of the study, never saw the raw data? Only the evaluations that Desai did? Well, with this fraud he is scientifically "burned" for all times internationally and also economically ruined, at least in this sector.
But no one has yet tried to find a plausible motive for this fraud, such as a possible "trail of money." Because with what is known not only about Desai, but also his company... Surgisphere it's completely unclear how this company could have made money.
Sometimes the questions that aren't asked publicly are the ones that matter.
How does Desai buy his bread today, how does he live? From unemployment benefits? Or does he have a sponsor? What does he do and what does he say about his fraud? Why are none of the investigative magazines and newspapers investigating this question? Because the articles about Desai in the New York Times and in the English... Guardian only describe old familiar facts, and of course that Desai does not respond to inquiries:
Surgisphere's trendy website has been taken down. Dr. Desai, who gave several interviews before the studies were withdrawn, has gone silent. (NYT)
But nothing about the here and now, and you don't get the impression that anyone really bothered to find out what the point of it all was supposed to have been. Because after the 10/6/20 article, the Guardian hasn't written anything about Desai, and the NYT article is dated July 27, 2020. Since then, the matter has been as dead as a doornail. And it smells that way, unfortunately.
The three main authors (besides Sapan Desai) of this "retracted", i.e. withdrawn study are: Cardiac surgeons. Who have never worked together before or even written a paper together. One of them is even based on another continent, Prof. Ruschitzka at the University of Zurich. Another, Amid Patel, is, as he himself tweeted, "related to Dr. Desai by marriage".
But not only: Patel is also co-founder of "Triple gene". And "MRM reports personal fees from [...] Triple Gene." MRM is Mandeep Mehra, the star among the three aurors, a renowned cardiologist at Boston's Brigham and Womens Hospital, who thus receives money from Patel's company, from the man who in turn is related to Desai by marriage. It was Patel, then, who had introduced the most renowned of the three, Mandeep Mehra, to Desai. (sciencemag).
And there's one more little detail. Mehra, the cardiac surgeon who is suddenly doing a Covid-19 statistics study (anyone can do statistics in principle, but you wouldn't ask a cardiac surgeon first), was apparently invited as a key speaker to a Covid-19 conference in April, paid for by Gilead:
Coronavirus: Gilead and Seimc train more than 8,000 professionals
06/04/2020 Press releases
La Societat Espanyola de Malalties Infeccioses i Microbiologia Clínica (Seimc), amb el suport de Gilead, ha celebrat una sessió científica [..]
The Spanish Society of Infectious Diseases and Clinical Microbiology (Seimc), with the support of Gilead, held a scientific meeting led by some of the leading national and international experts and researchers [...]
The infectious disease and microbiology specialists who participated in the day are [...] Mandeep R. Mehra of the Division of Internal Medicine at Brigham and Women's Hospital and Harvard Medical School in Boston, USA; …
(Link from James Todaro to Twitter). Key speeches are usually well rewarded. The main sponsor of this conference was Gilead, the manufacturer of Veklury®, better known as: Remdesivir.
But: This is cloudy contact-guilt-suggestion. What you can't nail to the wall isn't a solid, in other words: Even if the whole story stinks to high heaven: It's not evidence against "Big Pharma" and unfortunately it is not evidence either that HCQ actually helps.
What of all this has stuck in people's minds? Hydroxychloroquine does nothing and is dangerous, even deadly. Oh yeah, there was a fake study on that too. And Trump, the lunatic, was always promoting it.
This then easily gives the false impression that all three pieces of information prove that one should not think anything of HCQ. But all three pieces of information do not prove anything. The fake study neither proves that HCQ is dangerous, nor the opposite or anything else, it was based on fictitious data. The reference to Trump is also useless to prove anything, because even if Trump has lied thousands of times, that is purely formal logic, not proof that every one of his statements is, was or must have been false. Definitely, though, HCQ treatment is out, despite positive studies. Press reports like this one attest to that:
24.11.2020 Berliner Zeitung:
The well-known antimalarial drug has also been used for a long time in the symptom treatment of autoimmune diseases such as rheumatoid arthritis or lupus. Hydroxychloroquine is available only on prescription and is sold under brand names such as Plaquenil or Quensyl. Its anti-inflammatory effects led to it coming into focus as a potential therapy soon after the outbreak of the Corona pandemic. However, it does little or nothing against Covid-19, as has been shown in a number of serious studies. The European Medicines Agency warns that the high-dose use of hydroxychloroquine for Covid-19, often in combination with antibiotics such as azithromycin, carries an increased risk of cardiac arrhythmias and cardiac arrest, as well as neuropsychiatric disorders.
The study linked to this is quite fresh, from October 8, and apparently not a fake this time:
CONCLUSIONS
Among patients hospitalized with Covid-19, those who received hydroxychloroquine did not have a lower incidence of death at 28 days than those who received usual care.
That doesn't sound good and the more precise data are even worse. Although the risk parameters such as ethnicity, high blood pressure, BMI, etc. the placebo group had overall more disadvantages, the HCQ group still showed worse results in all respects:
And then, in Table 1, to which little attention is paid at first because the data are largely referenced in the article, one finds what is perhaps the decisive clue:
On average, HCQ was administered only 9 days after the onset of symptoms. And more than ¾ of the patients already needed oxygen at this point, so the destruction of the lungs by cytokines and an overreaction of the patient's own immune system was already advanced, the immunomodulatory effect of HCQ would clearly come too late, also the intervention in the ACE2 system, which could dampen the docking of the virus at the ACE2 receptor, too late, as would the antiviral effect by transporting zinc into the cells, which would then help just as little as Remdesivir, because at this point it is rather not the virus but the overactive immune system that produces too many cytokines and thus causes the problems.
As the commentator "aufdiedauer" and also the Berliner Zeitung correctly noted, HCQ is a standard treatment for systemic lupus erythematosus (SLE, chronic inflammatory autoimmune disease affecting the skin and internal organs). as standard:
Anti-malarial drugs (chloroquine, hydroxychloroquine) are considered basic medication in SLE and should always be administered, provided there are no contraindications such as pathological changes in the cornea or retina of the eyes or allergic reactions.
However, chronic is not the same as acute, so in the case of an acute and severe immune reaction, it cannot be ruled out that the effect of HCQ is rather negative, after all, the drug has significant side effects. For the proactive effect by inhibiting the ACE2 receptor, through which the C-19 virus enters the cells, it is 9 days after the onset of symptoms, and thus a good 15 days after infection, simply too late, just as for the antiviral effect of zinc. Bad science? Bad science!
Of course, this does not prove anything, but the early French study, in which HCQ was administered with good success when symptoms occurred, is not refuted either. Nevertheless, the impression remains that the really cheap drug HCQ (hydroxychloroquine 200 mg film-coated tablets, basic price from: 0,58 € / 1 pc, Medizinfuchs) unfortunately cannot help.
However, from the international grapevine aka Twitter and co. one can gather that HCQ is definitely used in the poorer countries:
And the writer @gummibear737 wrote on July 16:
My Hydroxychloroquine Deep Dive - long thread
Gotta start with this chart many of you have seen by now. In early June after months of following articles, treatment protocols, declarations, etc. I was curious about how the countries lined up. For the most part, it's accurateIt's not perfect as HCQ was also used in Belgium and Spain and later in Italy, but the idea is that Western Europe as a whole never embraced the 'treat early and often' strategy. Mostly they tried it with sick patients, didn't work..moved on. They mainly followed the WHO position
And further down the thread, he links to a preprint of a study in mid-July that is now also peer reviewed:
Of 141 treated patients, 4 (2.8%) were hospitalised, which was significantly fewer (P < 0.001) compared with 58 (15.4%) of 377 untreated patients [odds ratio (OR) = 0.16, 95% confidence interval (CI) 0.06–0.5]. One patient (0.7%) in the treatment group died versus 13 patients (3.4%) in the untreated group (OR = 0.2, 95% CI 0.03–1.5; P = 0.12). No cardiac side effects were observed. Risk stratification-based treatment of COVID-19 outpatients as early as possible after symptom onset using triple therapy, including the combination of zinc with low-dose hydroxychloroquine, was associated with significantly fewer hospitalisations.
Yes, the sample is small again. But only 0.7% against 3.4%, that is a factor of 5 for deaths, only 2.8% hospitalized against 15.4%, again a factor of 5.5 - these are very impressive results. What seems to be decisive compared to the study quoted above is:
A median of 4 days [..] after the onset of symptoms, 141 patients [..] received a prescription for triple therapy for 5 days
That's 5 days earlier than in the above study, which found no positive effect. Just asking: if you suspected pneumonia... (coming) pneumonia, would one wait 5 days before giving antibiotics? Whereby the comparison is unfortunately very lame, because antibiotics would still be helpful then, with HCQ the matter could be much more complicated, just as described: immediately and only for 5 days, because after that it might be rather counterproductive. Gummibear737 lists in his thread a lot of data and facts and shows graphs, which are either all faked, or clearly prove that HCQ is effective and the negative studies were wrong. Last-not-least, he links to this website in August, a real meta-study of HCQ use worldwide:
Early treatment with hydroxychloroquine: a country-based analysis
Covid Analysis, August 5, 2020 (Version 35, November 14, 2020).
The unfortunately anonymous authors convey a professionally competent impression, write in an unagitated and factual manner and come to this conclusion:
Many countries have either included or rejected early treatment with HCQ, leading to a large study of 1.8 billion people in the treatment group and 663 million in the control group. [...] The treatment group has a 69.9% lower mortality rate.
The bibliography alone comprises 284 items, the country data, tables and graphs cover 69 screen pages, and the study, including all appendices, is over 150 screen pages long. You can see that experts were at work here. Why they started this non-profit project, who they are and why they want to remain anonymous, they explain in their FAQ. Let everyone make up their own mind about their seriousness and competence.
As an example, let us quote this small paragraph:
Zinc reduces SARS-CoV RNA-dependent RNA polymerase activity in vitro [te Velthuis], however it is difficult to obtain significant intracellular concentrations with zinc alone [Maret]. Combining it with a zinc ionophore such as HCQ increases cellular uptake, making it more likely to achieve effective intracellular concentrations [Xue]. Zinc deficiency varies and inclusion of zinc may be more or less important based on an individual's existing zinc level. Zinc consumption varies widely based on diet [NIH].
And an argument that seems obvious in view of the list of countries should be quickly refuted here:
The HCQ affine countries have predominantly in terms of their age distribution a real pyramid, so very many young people and few old people. The IFR or CFR is naturally lower here.
The website states: Age.
The COVID-19 IFR varies around four orders of magnitude depending on age. Since the proportion of older adults varies significantly between countries, this is likely to have a significant effect on the results [ Leffler ]. We approximate the relative risk based on age using the infection fatality rates provided in [ Verity ], and shown in Figure 3. Due to the distribution, simple adjustment based on the median age, the proportion of people over 65, or similar may not be very accurate. We obtained age demographics from [ United Nations ] which provides a breakdown within 5 year age groups. Using the 9 age groups provided by [ Verity ], we computed an age adjustment factor for each country to normalize the observed deaths to the predicted number of deaths if the country's age distribution matched that of the country with the oldest population. The age distributions and computed age factors are provided in Appendix 1. These adjustments are relatively significant as in [ Leffler].
Fortunately, the main statement of the authors can be checked on the basis of the Worldometer figures, as I had prepared them in Part I, namely to virtually calculate by how much the annual mortality would increase under the known country figures in the worst case, which is, for example, about 1.20% in our country. The whole thing of course "worst-case" calculated, i.e.: No vaccine and within 12 months 66% of the population is infected. Because if it were true that the mentioned countries with HCQ have a better "performance", this should show up clearly in the virtual mortality growth rates explained in part 1 - and it does:
On the green side, Algeria is missing, also missing from my Worldometers table for some unknown reason. And despite Turkey's comparatively poor factor, the result is still impressively clear.
So what do we have in terms of HCQ? In a clinical study with a negative result that is widely cited publicly: demonstrably "bad science".
The largest observational study with over two billion (involuntary) participants shows the effects it claims even when checked against the Worldometer figures. Whereby one should put the number "two billion" into perspective: One did not, of course, treat (or not treat) 2 billion infected people with HCQ; it is a subset of the world's population that, like all people, was and still is potentially exposed to the C-19 virus. Out of these countries with a total of 2.2 billion people, there were then - after the worldometer data without Algeria - 17.6 million "cases" with 397,000 deaths in the red group and 12.9 million "cases" with 202,000 deaths.
If you extrapolate the green result to the red 17.6 million, instead of 397,000 in the red group only 275,000 should have died, that would be 54% lower risk of death, the study itself calculates 69% less. But of course the Worldometer calculation is completely imprecise, it was only meant to test whether the direction was correct.
Did the authors perhaps choose the "green" countries based on this preference, i.e. low mortality rate, is this all "junk science" too? Unlikely - just scroll through the data appendix once. Anonymous authors without any reputational interest, moreover without any financial interest, who would benefit from such a site as fake news? Quote from the FAQ:
- Why should we trust @CovidAnalysis? There is no need to. We provide organization and analysis, but all sources are public and you can easily verify everything.
- Who funds this site? We have no funding, this is done in our spare time and we pay the web hosting fees personally (about $100 per month).
- Can we use your graphs? Yes. You can use any of our work free of charge.
Yes, I trust these people more than the authors of a study that already fails in design, because the administration of HCQ more than 9 days after the onset of symptoms and 3 days after hospitalization not only fails to have a positive effect, but must even be called contraindicated. Especially strange: if you plan and conduct such a study - why do you wait another 3 days in the hospital before administering the drug to the patient? In the retrospective case series study (see above) the HCQ therapy was applied even before hospitalization and already 4 days after the onset of symptoms. The authors - Roland Derwanda, Alexion Pharma Munich, Martin Scholz, Heinrich-Heine-University Düsseldorf and Vladimir Zelenkoc, Medical Group Practice, Monroe, NY - wrote:
Starting triple therapy as early as possible after symptom onset is critical for treatment success because SARS-CoV-2 viral load appears to peak at Days 5–6 after symptom onset [27], [28], [29] and severe cases progress to ARDS after only 8–9 days [30,31]. Early antiviral treatment is an established protocol to manage severe disease progression, as was shown [..] during the 2009 H1N1 influenza pandemic in Canada [32]. For patients at high risk for severe viral disease progression, it is recommended to start antiviral therapy as early as possible [33,34]. Early treatment might be also critically important to effectively reduce the SARS-CoV-2 viral load [5] and this underscores the role of early intervention by primary care physicians as reported herein.
But one of them works for Pharma, right? Under "competing interests" it says:
RD [..] and his engagement and contribution to this study and publication was private and independent from his employer (Alexion, Müchen, d.A); MS is/was at the time of writing External Senior Advisor for the company LEUKOCARE (Munich, Germany) and is/was Manging Director at Starts- and -Ups Consulting (Frankfurt, Germany); VZ is/was a general practitioner in New York State (USA).
Alexion does not manufacture hydroxy-chloroquine or azithromycin. LEUKOCARE is working(ed) with an Italian and Belgian company on an adenovirus-based COVID-19 vaccine development. There you have to see a conflicting interest rather the other way around: If someone, even though their own company is developing an expensive vaccine, is looking for an immediately available and inexpensive alternative - can there be more credibility than that? And under "Funding" it says simply and succinctly: None. No one has funded this study.
This is all a little different in the "negative" study with its obvious design flaw: In the RECOVERY Trial several drugs were tested under the highest authority (Oxford University). The Recovery Trial feeds on many different sources:
Supported by a grant [..] to the University of Oxford from UK Research and Innovation and the NIHR and by core funding provided by NIHR Oxford Biomedical Research Centre, Wellcome, the Bill and Melinda Gates Foundation, the Department for Internatio..... etc.
A lot of "funding." But there is apparently no "Conflict of interest" or "Competing interests" statement in the paper, and that seems odd. Is a large group of experts basically exempt from this? The RECOVERY Trial tested dexamethasone, hydroxychloroquine, lopinavir-ritonavir and other substances. For the limitations of the HCQ trial, see Wikipedia:
The trial did not address its use as prophylaxis or in patients with less severe SARS-CoV-2 infection managed in the community, though the RECOVERY Trial was specifically performed in the hospital context and another study by Oxford, the COPCOV trial, exists for the purpose of evaluating hydroxychloroquine as a prophylaxis.[32]
If you follow the given link (32), you will find: 40,000 participants, double-blind, randomized (RCT), everything your heart desires. Start: April 29, 2020. End? April 2021.
And the clinical trial? Was probably also started in April, on May 9 they lifted the age limit (18) and on June 5 they closed enrollment. But already on June 8 you can find this quote from one of the main authors:
"This is not a treatment for COVID-19. It doesn't work," Martin Landray, an Oxford University professor who is co-leading the RECOVERY trial, told reporters. "This result should change medical practice worldwide. We can now stop using a drug that is useless."
(China Daily Global Updated: 2020-06-08 10:37)
This statement is simply nonsense. It should have read, "9 days after symptom onset, treatment with HCQ, without zinc and without azithromycin, shows no significant effect." Generally stating, "It doesn't work. We can now stop using a drug that is useless" is a very brazen over-extension of what he could have said assuredly, and very unusual in the scientific establishment in such stridency.
When can we expect results from the prevention study? In April of next year? When vaccinations have probably already been given? A scoundrel who thinks evil of it.
I keep it with Heinz Erhard, play the prankster and think evil: Why do I need 40,000 participants? Everyone knows that even 2,000 participants produces any statistical certainty you want. The 2,000 would have been there within hours in the UK in April 2020. Even with the restriction that only a few hospitals participate, the plan was to enroll 40,000 in twelve months, but that's at least 3,333 per month, so you don't need three weeks for 2,000. You close the study in mid-May, wait another three weeks for the final results, you can announce the first results at the beginning of June, and you can publish the preprint at the end of June. This is how it was done in the clinical (late) intervention study. So why terminate the study with the only correct approach, i.e. the use of HCQ for prevention, in April 2021, when the progress of the pandemic can already be interrupted with vaccines according to all plans?
And in the clinical trial, which was much faster - they wait 3 days after admission in hospitalized patients before giving HCQ? Did they use azithromycin? No, they didn't:
Nor did it trial the use of HCQ in combination with azithromycin as has been suggested by some observational studies.[30] (Wikipedia)
Did they at least supplement zinc? The search for "zi" in the PDF results in 7 references, 6 of them A_zi_thromycin, one Bra_zi_l. With "zin" the search field turns red - no hit.
It even makes the rogue smile. Can renowned, highly paid, experienced clinicians make such rookie mistakes? Unintentionally? Quoting TP commentator "aufdiedauer" again:
- the people who develop and conduct such studies are incredibly underqualified and do not know what they are doing because they are uninformed
- these are highly qualified professionals who want to demonstrate with intentionally false studies, junk science, at the expense of the patients, that HCQ does not work.
Tertium non datur, I'm afraid. But I'm not sure which of the two options to choose:
The Oxford luminaries are in truth dim sparkles, completely overwhelmed with more than one agent and a well-known treatment protocol?
Or they designed both studies, the short intervention study and the extra overlong prevention study so that there was no way they could be successful (in time)?
The first option is about as likely as hitting seven in the lottery. But that leaves option 2 and you have to ask: Why are they doing this? Cui Bono? Is there any plausible motive for Surgisphere's fraud, or for Oxford's apparently deliberately mis-designed studies? Occam's razor Says:
Of several sufficient possible explanations for one and the same state of affairs, the simplest theory is preferable to all others.
And the simplest would be: money? So would you find what you were looking for if you dug deeper into the web of sponsors? Do you just have to follow the money trail? And why does nobody do that?
Oh, yes, some do. It's just pretty little is known, unfortunately. Those who consider FranceSoir (the former Resistance newspaper) a trustworthy source can learn quite astonishing things. Not only are the two authors of the Oxford RECOVERY HCQ study, Horby and Landray, strangely misinformed about some things (one claims, for example, that they use HCQ according to the medication for amoebic dysentery, which is definitely bunk, because that is treated with hydroxy-quinoline, and not: -chloroquine - well, you can get that mixed up, can't you? Especially if you want to see the dosage ;-), they also don't know their own treatment protocol etc.), but above all they deny that Remdesivir would be tested in the context of RECOVERY. FranceSoir writes:
The Remdesivir has been included in the Recovery test since 26 May by decision of the authorities (MHRA) and Recovery as of 27 May 2020. This was presented to investigators in a document dated June 2. The program allows the addition of a drug to bring the best of science during the trial. In the interview on 5 June 2020, Professor Landray told us:
Remdesivir was never included in the ReCoveRy trial.
The aforementioned authority MHRA - the "Medicines and Healthcare products Regulatory Agency" - will be mentioned later, so here's a short diversion:
ERGO, another research centre run by Prof Horby, has received 14 million pounds from Astra Zeneca and Zuckerberg, the founder of Facebook.
ERGO, "run by Horby", is the Epidemic diseases Research Group Oxford. And Horby one of the two lead authors of the HCQ study above. And AstraZeneca, as is well known, is developing a Covid-19 vaccine. And Handelsblatt writes on June 7, 2020:
This deal could turn the pharmaceutical industry upside down: According to a media report Astra-Zeneca approached Gilead for a merger.
The British company's portfolio, which is strongly focused on cancer, respiratory and cardiovascular drugs, would be complemented by Gilead's top-selling antiviral drugs. The US group is by far the leading supplier in this field [...]. Gilead's attempt to gain a foothold in the oncology sector, on the other hand, has so far proved less successful. On the other hand, with its active ingredient Remdesivir, Gilead currently has the only drug that has shown at least some, if not yet a resounding, effect against Covid-19.
As I said, as of June 7. So do we get to choose? Remdesivir or vaccine, as long as its from AstraGileZenecAd? ;-)
Landray, the other author of the above study is, among other things, "Acting Director of the Big Data Institute."
Funding for the Big Data Institute comes from the Li Ka-shing Foundation, a Chinese philanthropist, and the Robertson Foundation, the founder of hedge fund Tiger, which was one of Gilead's largest shareholders.
And lastly, the aforementioned MHRA which is supposed to control the whole thing. Are there any "connections"? Unfortunately, there are:
Among Board members, Anne Toni Rodgers and Amanda Calvert declare conflicts of interest with AstraZeneca, which has just announced a proposed merger with Gilead. AstraZeneca has also just signed a contract with several other countries to sell 2 or 3 billion euros worth of vaccine doses to European countries.
The two ladies are "shareholders" of Astra-Zeneca.
So, is this still "cloudy contact guilt suggestion"? Or do we not have massive conflicts of interest on the part of those involved here? Would Messrs. Hornby and Landray have been allowed to conduct a fair scientific study under these circumstances on a substance that would be in direct competition with Remdesivir or a vaccine? Is anyone still wondering about the crazy study design on HCQ? Where are our investigative media to grill these two gentlemen properly, where are the science journalists to debunk this FakeNews?
To be clear again: there are a whole series of small HCQ studies with positive results. There is the country comparison corrected for all risk factors (age, comobidities etc.) with 30 million "cases" and 600,000 "fatalities", which shows a significantly lower mortality for patients treated with HCQ. And there are two negative studies: the one by Mehra, Desai et.al., which was a pure invention, but was published in the most important research journals, Lancet and NEJM, and made it into the world press with the news that HCQ doubles mortality, a lie of the purest water, and the Oxford RECOVERY-HCQ study, so obviously designed to ensure that the drug would not only cause no benefit, but also as much predictable harm as possible, that one would be ashamed not to speak of intent here. And the manufacturers of a competing product (Remdesivir) or a vaccine are lurking in the background with many interconnections to the actors.
Anyone who draws certain conclusions from this will be accused of indulging in conspiracy theories. Very well.
But one thing should be emphasized once again: the fact that the use of not inconsiderable means and the acceptance of possibly also legal consequences, but certainly of extreme damage to the reputation of authors and specialist magazines was attempted to force Hydroxy-Chloroquine out of the market in the off-label application against C-19, only proves that there must have been a massive interest in not allowing a very inexpensive drug to prevail. And the fact that hydroxy chloroquine is actually so relatively cheap, the 5x2 tablets would be available for less than 10 euros, is mainly due to the fact that as a malaria drug it is a 3rd world drug. Cynically spoken: We will not let the market for expensive antiviral drugs and vaccines go to ruin.
However, it does not prove that HCQ would actually be effective; suspicion alone would be sufficient for the above actions.
Only the smaller studies cited and, if applicable, the country overview prove efficacy. This would have been sufficient reason for a real large prevention study, i.e. HCQ + zinc immediately after a positive test result and not longer than 5 days, prophylactically in all infected persons with at least one risk factor (BMI>30, hypertension, diabetes, age >60). Verum versus placebo, 1000 subjects each. But no one will tackle that now that the vaccine is coming soon.
Well, then they were successful, Messrs Horby and Landray, Mehra and Ruschitzka. You have to wish them that it was at least financially worthwhile - and that it will never be uncovered.
Something very similar took place with a bearer of hope, which only parts of the stupid people wanted to see as such, and also a few twisted research amateurs, and which you have to talk these people out of by hook or by crook. Until one has to admit it slice by slice at some point. Like e.g. today in the WELT. But not too fast, and only in homeopathic doses, best only when we are through with the vaccination, because then one will not be able to test the whole thing, and we can take our time with the truth: how many people have died completely in vain. More on that in the third part.
LB, 11/30/2020
Part III
D3 - The Ignored Immune System Booster
"Treatment options for Covid 19 patients appear to have improved," we learned in Part II, even though the hopeful option of mitigating severe cases of by prevention with hydrochloroquine and zinc, and perhaps avoiding fatal cases, was shot down on target by one miserably designed (too little, too late, RECOVERY Oxford) and one genuine fake trial (Lancet-Surgisphere scandal). In both cases there is reason to suspect monetary interest and in some countries the off-label use of hydrochloroquine has now been made more difficult because of these fake studies, such as in the U.S., where in June the exemption was revoked so that doctors are now personally liable if they prescribe it, which is the end of the line given the litigation culture in the US. The rationale is exactly the same as the Surgisphere fake data study results: ineffectiveness and serious side effects (heart problems).
A very similar pattern emerges when one takes a closer look at what is probably the best known and most controversial "food supplement vitamin D3". Here in Germany they don't want to know anything about it, and the fact that the well known Mr. Fauci, the Drosten of the USA, himself swallows 6,000 units per day, doesn't interest anyone here. Because, as one will find always and everywhere:
According to the German Nutrition Society (DGE), healthy people who eat a varied diet do not need dietary supplements.
And the Welt writes on November 27, 2020:
Vitamin D is absorbed not only through food but also through sunlight on the skin. In the crisis, it has often been recommended as a kind of miracle cure. The Federal Institute for Risk Assessment (BfR) emphasized in October that no studies are known according to which a vitamin D intake protects against a corona infection. Therefore, an additional intake is not necessary [...].
The consumer advice centre also rejects the idea and warns:
Vitamin D contributes to bone stability and tooth retention. It is also important for the immune system. A good supply situation can protect against acute respiratory infections, but does not protect against the corona virus.
The "godfather" of vitamin D research, the discoverer, Michael Holick, co-authored a study with data from over 190,000 patients who had contracted Covid-19. The result: the risk of becoming infected is more than twice as high for those with deficient D levels (<20 ng/ml) as for patients with (very) good D levels (>50 ng/ml). This curve shows the correlation:
And in Israel, an analysis of the data of 4.6 million members of the Clalit Health Services (CHS):
We compared 52,405 infected patients with 524,050 controls of the same sex, age, geographic region [...] to assess the relationship between baseline vitamin D levels[...] and positive Covid-19.[...]
In this large observational population study, we demonstrate a strong association between vitamin D deficiency and Covid-19 incidence. After adjustment for baseline characteristics and previous vitamin D levels, acquisition of liquid vitamin D products was associated with a reduced risk of Covid-19 infection.
But, the consumer watchdog believes:
Only in exceptional cases (e.g. bedridden or fully veiled outdoors and older age) is an additional dietary supplement in consultation with the doctor advisable. [..]
This is exactly what the above study shows: the results in population groups "Arab" and "Ultra Orthodox" are particularly striking, because here the full-face veil is not the exception. Nevertheless, the average values for vitamin D in Israel are apparently 20% higher than ours (23:19 ng/ml). And again the VZ:
Do not take more than 20 µg/day if taken regularly.
That would be only 800 units, a value that an uncovered body in June at noon already produces in 2 minutes of sun exposure, and in 20 minutes about 10,0000-15,000 IU, then the biochemistry will be regulated down. So the 10,000 IU should not be unhealthy.
Instead of a reasonable daily dose recommendation, which as we will see is at least 6 times that, so about 5,000 IU for a 70 kg person, then this from the VZ:
An overdose can lead to serious health problems such as nausea, headaches, reduced muscle tone and even kidney failure.
But this warning, repeated over and over, only occurs with inordinately excessive and long-term intake, combined with a deficiency of K2. And we're talking about 50,000 units a day for many, many months. And of absolute isolated cases, because if you google, you keep coming across the same quotes and case histories. In hospitals, bolus doses of 300,000 units are also administered intramuscularly when D levels are low - of course without any risk to the patient, quite the opposite, as can be seen from studies such as these.
There are now a large number of studies on the association of Vit D deficiency and severe courses of Covid-19, so many that it is best to look at metastudies, summaries across many individual studies, to get an overview.
Such a meta-study has been published by Linda Benskin under the title "An overview of the risk and severity of COVID-19 in vitamin D deficiency", and in order to make it accessible to those less familiar with English, I had suggested to have it translated. With the help of DeepL this has been done, proofread by H.G. (MD/GP, France) and is now available available here, of course with a link to the original. Benskin writes
Vitamin D deficiency increases [...] the activity of the X-chromosomal-linked "renin-angiotensin" system, making individuals with vitamin D deficiency (especially men) more susceptible to the fatal "cytokine storm" (dramatic overreaction of the immune system) in COVID-19. [...]
[...] the pattern of geographic distribution of COVID-19. [reflects] greater vitamin D deficiency in the (affected) population. Both in the US and globally, the mortality rate of COVID-19 parallels the rate of vitamin D deficiency.
[...]Although randomized controlled trial results will likely become available eventually, the current correlational and causal studies demonstrating an association between vitamin D deficiency and COVID-19 risks are already compelling enough to support action to address vitamin D deficiency.
The 141 author group, writing primarily on biological plausibility, explained in detail how vitamin D deficiency can explain every risk factor and complication of COVID-19, [...] COVID-19 was compared to dengue fever, where daily oral vitamin D supplements of 4000 IU for 10 days worked significantly better than 1000 IU to mitigate viral replication and regulate the "cytokine storm" (an immune system overreaction) responsible for the deaths.
Among the 47 original research studies summarized here, chart reviews found that serum vitamin D levels linearly predicted COVID-19 mortality rates (16 studies) and COVID-19 severity (8 studies). [...]
The literature review also found that prophylactic correction of possible vitamin D deficiency during the COVID-19 pandemic is extremely safe for patients. The widespread recommendation of 2000 IU of vitamin D daily for all populations with limited ability to make vitamin D from sunlight has virtually no potential for harm and is very likely to save many lives.
And that's what three directors of the Iranian Hospital Dubai believe. It is well known that people in Dubai only choose the best of the best because they can afford it. And that Iran has excellent doctors and a very long medical tradition, we know not only since the Medicus. So the existence of an Iranian hospital in Dubai, despite possible political-religious differences, is certainly no coincidence.
In the July/August issue of the Journal of Contemporary Medicine appeared. following letter to the editors (note in {curly brackets} by the author):
Recommended role of vitamin D supplementation in the severity of COVID-19.
Parviz Afshar, Director of Iran Hospital Dubai, Dubai, UAE
Mohammad Ghaffaripour, Director of Intensive Care, Iranian Hospital Dubai, Dubai, UAE
Hamid Sajjadi, Director of Neuro-Ophthalmology, Iranian Hospital Dubai, Dubai, UAE
Vitamin D, a prehormone, regulates and/or influences several functions such as immune, coagulation, cardiovascular, central nervous system, inflammation, cancer rates, deep vein thrombosis, sleep apnea, and respiratory tract infections (RTI) {RTI= respiratory tract irritation, respiratory tract infection}).[1-8]
The role of vitamin D in reducing RTI is excellent, as shown in a meta-analysis.[2] Our first reference is a paper with over 150 references on RTI reduction in patients with a vitamin D level >40 ng / ml compared to <20 ng / ml.[1] {The association between} Vit D levels and Covid severity was well established in a recent study.[9] The two major causes of COVID-19 severity requiring ventilators and possibly leading to death are:
Cytokine storm and complement dysfunction, ending in a death spiral of respirator and drowning in fluids.[2-6]
2. hypercoagulation state that ends with multiple diseases of the peripheral system, such as cardiomyopathy or encephalopathy.[7,8]
Vitamin D plays an important role in both processes.[2-9] From 2010 to 2020, over 5,000 patients in the Department of Neuro-Ophthalmology had their Vit D levels checked. 66% had a deficiency (<20 ng / ml), the prevalence changed to 83% when <30 ng / ml was selected, and 93% when <35 ng / ml was set as deficient. Between 2010 and 2012, after patients discontinued vitamin D after reaching normal levels, Vit D deficiency recurred in all cases at 4-month follow-up.
Table 1 shows the proposed limits accepted by most endocrine societies.
Vit D deficiency is multifactorial and endemic worldwide. An attack on {a reduction of} Vitamin D can be caused by artificial colors and flavors in processed foods, soft drinks, lack of sun exposure, etc., chronic diseases such as diabetes, hypertension, chronic kidney disease, obesity, and more. Heat (avoiding sun exposure) and skin color (less UV effect for vitamin D with darker skin) cause Vit-D deficiency. African countries have higher Vit D deficiency than Scandinavian nations. With insufficient sun exposure and constant poisoning of vitamin D by food additives and chronic diseases, lifelong vitamin D supplementation is a must for urban dwellers.
We have seen few good Vit D levels (> 40 ng / ml without vitamin D supplement) only in patients who live in rural areas and consume the food from their own farms including milk and no soft drinks. The majority of people who consume processed foods become Vit D deficient. In this group, many doctors stop supplementation when vitamin D reaches normal levels, and this almost always leads to a recurrence of Vit D deficiency. In the Department of Neuro-Ophthalmology, we have been using 70-100 IU of vitamin D3/kg/day since 2010 for maintenance {4,900-7,000 IU per day at 70 kg}. We used 70 IU/kg/day in patients with normal eye exams and 100 IU/kg/day in retinal and optic neuropathy patients.
After supplementation, all patients had a Vit D level> 40 ng / ml with some between 60 and 89 and none above 90 in the last 9 years. In a subset of over 500 patients on continuous 1-8 year treatment/follow-up, we did not see even one case of toxicity. Since the onset of COVID-19, we have had 21 patients with Vit D levels> 40 ng / ml. (including 2 healthcare workers and several with chronic conditions such as diabetes, hypertension, and obesity) who were regularly screened for ocular disease and who told us they had COVID-19. However, the length of hospital stay was less than 4 days for all of them. This finding prompted us to recommend this dosage for all other hospitalized cases.
Subsequently, we started vitamin D supplementation as a routine treatment in all SARS-CoV-2 and COVID-19 patients (SARS-CoV-2 with typical signs and symptoms requiring admission) at Iranian Red-Crescent Hospital from early June 2020. A dramatic and complete resolution of ICU admissions was observed in Dubai hospital in the last 8 weeks. We cannot overemphasize the role of vitamin D in controlling all infectious diseases, especially COVID-19. We had no patients with initial vitamin D levels of> 40 who required more than 2-3 days of hospitalization, with no cytokine storm, hypercoagulation or complement deregulation occurring. Prior to this change, we had several deaths in COVID-19 patients on ventilators.
Our vitamin D supplementation (in addition to required therapies such as chloroquine, remdesivir, or others) was:
1. 300,000 IU, IM {intramuscular] Vitamin D3 once, followed by:
2. 100 IU / kg / day. {that is 7,000 IU per day for a 70 kg adult}.
3. we know that a bolus injection is not enough and the patient must continue daily dosing to maintain. This regime is very safe and far from toxic.
4. hydroxychloroquine is also known to decrease Vit D levels.
5. switch to oral vitamin D3 one week after IM dosing in hospitalized patients,
6. if the patient recovers in a shorter time, he is discharged with the daily dosage and the Vit D level is checked in 3 months BUT 6 days after the last dosage.
Since vitamin D3 is fat soluble, increasing its level definitely depends on weight. Therefore, in many studies with uniform doses, it is difficult to increase the level of Vit D in obese patients. This may be the main cause of cytokine storm and death in young healthy obese individuals. Although a daily dose of 70-100 ng / ml / kg is preferred, the 50,000 IU capsule vitamin D3 supplement is widely used We recommend individuals between 50 and 100 kg take 50,000 IU of vitamin D3 weekly {approximately 7,000 IU/day} to protect against cytokine storm and hypercoagulation syndromes from COVID-19 and other respiratory viruses. [...]
Based on recently available scientific evidence and numerous new functions of this prehormone, we would like to suggest that the value for an ordinary Vit D level should be changed to 40-100 ng / ml and below 40 should be considered deficient.
References:
1. MDPI
2. BMJ
3. NCBI
4. VitaminDwiki.com
5. EuropePMC
6. JSTage
7. MDPI
8. NCBI
9. NCBI
10. Merck Manuals
And, of course, this is not the only study in the literature, but in its wording and with the facts cited, it is perhaps one of the most forceful.
And nevertheless one presents with us the population again and again the message: One does not need, does not help, is dangerous. Like virologist Drosten, asked about vitamin C and D:
So taking any kind of things, any kind of vitamins, there may be scientific evidence for that here and there, but that's not my field of research, I'm not familiar with that at all, (NDR-Podcast, April 3, 2020).
That Germany's leading virologist claims to know nothing about the crucial role that vitmain D plays in the immune system is almost unbelievable. Already in 2009 W. Klein writes in his PhD thesis:
[...] that about 500 of the 2500 human genes are under the control of 1,25(OH)2D3. Furthermore, it could be shown that many cells of the immune system, such as macrophages, dendritic cells, as well as B and T lymphocytes, possess a vitamin D binding receptor and can also produce 1,25(OH) 2D3 themselves {from Vit-D3 in the blood, LB}. Thus, on the one hand, 1,25(OH)2D3 promotes the differentiation of monocytes into macrophages and their phagocytosis rate, and on the other hand, it promotes the activity of lysosomal enzymes, e.g. cathelicidin, in macrophages, which have a crucial role in bacterial and viral defense. Cathelicidin is a peptide that is capable of destroying many pathogens, such as Mycobacterium tuberculosis. Thus, in the presence of vitamin D deficiency, monocytes or macrophages are unable to adequately stimulate the innate immune system. This may also be the reason why African Americans, who often suffer from a vitamin D deficiency due to their strong pigmentation and the associated reduced vitamin D photosynthesis in the skin, are more susceptible to contracting tuberculosis and show a much more aggressive course after infection has occurred.In another study 29 , which was intended to show the relationship between vitamin D supplementation and influenza, 30 µg of vitamin D was administered daily to one group and a placebo to the other between December 2008 and March 2009. The risk of contracting influenza A in the group with sufficient vitamin D levels was reduced by 61% compared to the placebo group.
The fact that Drosten is allowed to say eleven years later that he knows nothing about it and is even praised for this "honesty" is only understandable in times in which Boris Johnson and Donald Trump are revered by the people for their clownesque acts, it seems that it is no longer the truth that counts, but the chutzpah, because the truth includes that a top virologist should of course know what defensive weapons our body has at its disposal. For this realization one needs neither nature nor study: If not all die from the virus, but only some, then nature must have given our body defense strategies. To simply not be interested in this as an expert is ignorance of the worst kind.
But where does the seemingly Babylonian confusion of language regarding vitamin D come from?
This already starts with the terminology. D is not a "vitamin" at all, but a secosteroid hormone. The precursor, the prohormone cholecalciferol, is formed in the skin with the ultraviolet of sunlight, more precisely the UVB component of 7-dehydrocholesterol, a derivative of cholesterol. UVA radiation produces melanin, makes brown, the more energetic UVB produces cholecalciferol and later sunburn). In the liver it is converted to calcidiol, also calcifediol, in this form it floats in the blood and is stored in fat cells; this is also what is measured as D3 in the lab and prescribed as a drug or you can buy as a supplement. And from this, the active hormone calcitriol( 1,25(OH)2D3) is synthesized in the kidneys, but also in many cells of the body.
Unfortunately, all forms are often simply called D3, in fact only the calcidiol, which we measure in the blood and which is then written as D3 on the laboratory report, and theoretically still the active calcitriol, which can actually be applied intravenously as a drug in very severe deficiency or high demand. Confusingly, there is also a "sister molecule", D2, which is found in plants, and can also be utilized by the body, but less efficiently. It also, just like the amounts of D3 in food, hardly plays a role (an exception proves the rule).
"The physiologically active form of the D vitamins is calcitriol, which acts as a protein inducer, immune system modulator, and in calcium absorption in the intestine" (Wiki).
And that's where the problems start, because you can see that three completely different functions are attributed to D3 here. The last one, the regulation of calcium-phosphate metabolism has of course to do with our skeleton. The terrible effects of D deficiency are what's known as bone softening, known as rickets in children and osteomalacia in adults, and osteoporosis, susceptibility to cooking fractures. Rickets was the most feared and the elderly will remember the daily obligatory spoonful of cod liver oil in winter that they had to swallow as children:
The excellent efficacy of cod liver oil against rickets was discovered by German scientists in 1824, about two years after it became known that sunlight, in the form of the then popular sun cures, could also be used to prevent or treat this disease. (Wiki)
The reason is the high D3 content in Lebertan, after all 1,100 I.U. per tablespoon. - d here we are with the confusion of units. I.U. means international units, if instead it says IU without dots, these are "internatiol units", the same in green. And then there is the weight unit mcg, microgram, also often written with a Greek 'mü:' as µg, which are millionths of a gram. One µg of D3 corresponds to 40 IU (I leave out the dots), 20 µg are for example 800 IU, a very common tablet size and most frequently mentioned daily dose for children and osteoporotic seniors (remember the above indication of 4,900-7,000 IU / day, which the Iranian doctors permanently recommend to their Dubai patients).
The body regulates the calcium level in the blood very finely, among other things by taking 20 grams of approx. 1 kg of calcium into, around or out of the bones per day. The osteoclasts break down the calcium, the osteoblasts build it in, and D ensures that as much calcium as possible is provided from the diet.
Again from Wolfgang Klein's PhD thesis:
At a 25(OH)D level of 40 ng/ml, the greatest bone density was measured, whereas at a level of less than 30ng/ml, there was a significant decrease in intestinal calcium absorption and an increase in parathyroid hormone, which led to a decrease in bone density.
The incorporation into the bones, however, depends decisively on a substance that is completely unknown to most doctors. And without talking about it in detail, you will not understand the Babylonian language confusion of the scientists, most of whom apparently do not even understand anything about D - like the virologist Drosten quoted above.
But now ask your family doctor what "K2" is. Nineteen out of twenty doctors will answer, "A peak in the Himalayas?" or "the second highest mountain in the world?". But if it's a doctor who specializes in naturopathy, she's quite likely to say, "You mean vitamin K2"?
Yes, K2, like "bone" or "coagulation", i.e. blood clotting. In fact, vitamin K was discovered in the 1930s in connection with internal blood clotting, also called coagulation, hence the name vitamin K. Only later was it discovered that there are several variants of K:
Vitamin K is found in the blood as K1 (phylloquinone from green leafy vegetables) and K2. K2 is produced in humans by enzymatic conversion of K1. In addition, K2 is absorbed as a bacterial metabolite with fermented foods. (IMD)
Vitamin K1 (and K2) primarily regulate blood clotting, which closes wounds in internal injuries (as opposed to external injuries, where oxygen-based blood clotting kicks in). Lots of K1 is in greens, such as spinach. But you have to take a good portion of it, because K1 also has to be converted into bone-active K2, and the conversion is not very efficient. And without sufficient K2, the osteoblasts are unable to incorporate the calcium into the bones, while the osteoclasts happily continue to build it up. Our ancestors ate a lot of greens in the form of leaves, so vitamin K/K2 deficiency was unknown.
But the bone-active K2 is also available from other sources, bacteria produce it, and lactic pickled vegetables such as sauerkraut contain a lot of it. Whether it survives the pasteurization process that store-bought sauerkraut must go through? Unclear. But K2 is also found in animal products, meat, butter and milk. However, these products have to come from grazing animals that mainly eat grass, because corn and soy scrap hardly contain K1 and without K1 there is no K2 in cattle.
So now you know a lot about K2, but why only you need to know? Because like a sword of Damocles hangs over the "food supplement D" the saying: "Caution, can also be dangerous, kidney stones, heart attack, stroke, even kidney failure threaten!
An overdose is not possible through the body's own production, but it is possible through the intake of high doses of vitamin D, e.g. through certain food supplements. Such an overdose leads to increased calcium levels in the blood serum (hypercalcemia).
The clinical symptoms associated with hypercalcemia in humans range from fatigue and muscle weakness to vomiting, constipation, cardiac arrhythmias and vascular calcification, among others. Persistent hypercalcemia can lead to kidney stones, renal calcification and ultimately to a decline in kidney function.
writes the BfR in its Fact sheet. Under the headline that the "intake of high-dose food supplements is unnecessary". Here, 50 mcg D3 corresponding to 2,000 IU is already considered high-dose.
However, all these horror stories only threaten us if there is too much calcium in the blood. This is the case when, thanks to vitamin D among other things, calcium is released from food but cannot be built into the bones due to a K2 deficiency, but on the contrary calcium built up by osteoclasts is added. And this also happens with naturally produced vitamin D, as was already discovered in the nineties with Israeli beach guards, who, all day in the sun and natural D levels of 59 ng/ml, but largely nourished beach-junkfoood, actually developed a strikingly large number of kidney stones.
In order to safely avoid hypercalcemia, one should, especially if one supplements D, take vitamin K2 to be on the safe side, of which we, like iodine, B12, zinc and selenium have a nutritional deficiency anyway (see study from NL below). And you cannot take too much of it, a lethal dose for K2 is unknown, but more than 200 mcg / day are probably superfluous.
Most of the vitmaion D preparations prescribed by doctors have so far been without vitamin K2 - in any case a malpractice, because osteoporosis can only be cured by adding D and K2. Which many common family doctor do not know, because the medical associations do not know it, and the DGE and the BfR also do not. Yes, it sounds almost unbelievable, but it is an unfortunate fact that while the effects of K2 have been elucidated for a long time, the vast majority of studies on vitamin D are done without K2. In the short term this is not problematic, but in long-term studies without K2 increase the rate of heart attacks, strokes and unfortunately also of osteoporosis. Which irritated researchers and has greatly shaped the overall predominantly negative coverage of vitamin D in recent decades. As in Part II: Junk science.
And due to such bad studies also officially before the hypercalcemia by Vitmian D warned, so that the common humans are to be kept from it to buy and take such a thing, but it goes still worse: Supposedly we need no additional Vitmain D at all:
"Vitamin D supplements are much advertised - because every second German is said to be poorly supplied with the vitamin. But is that true?" writes the Hamburger Abendblatt on November 28, 2020."Are we really so badly supplied with vitamin D in Germany? Do we need pills to change that? According to Helmut Schatz, board member of the German Society for Endocrinology, clearly no. "Many people talk about a vitamin D deficiency where there really isn't one."
[...] "Sure, less vitamin D is indeed synthesized in winter due to the lower UV-B radiation," says the director emeritus of the Bergmannsheil University Clinic in Bochum, "but a healthy person who regularly goes outside uncovered in summer stores enough vitamin D to get through the winter." And that, according to Schatz, without any pills at all .
Antje Gahl, spokeswoman for the German Society for Nutrition, agrees. [...]"But basically, the amount of vitamin D you take in between March and October is enough to get you through the winter. Of course, the level gradually decreases, Schatz also admits. "But there's a little bit there."
Let's start with the appeasing "there's a little left". If you ride your bike regularly, is there enough air left in a half flat tire to ride up a curb without damaging the rim? Because: "a little bit of air is still there"?
Does this get you through the winter? Is it enough to inflate the tyre only every six months, but then a little more firmly, as a sort of reserve? No, that's not enough to cushion a sharp curb at the end of half the year - that would be a fat flu in February. But even worse: only with natural means (sun) you cannot inflate the tyre (body) so tightly that the air supply (D-supply) lasts for half a year without a severe shortage (half or rather three-quarters flat) occurring. Because Mother Nature has built us a three-month storage, not 6 months, of which later still.
Regarding numbers and radiation physics: From an angle of incidence of 45°, the path through the atmosphere is so long that the short-wave UVB rays are reliably filtered away. This is the case when our shadow is longer than we are high. Only when it is shorter, i.e. the sun's position is greater than 45° (the red line below), only then is there UVB, and only then can vitamin D be synthesized.
At the solar zenith, on June 21, this is the case between a full 7 hours, between 8:30 and 15:30 (attention: standard time). On the 20th of April and on the 23rd of August it is already from about 10 to 14 o'clock. But from mid-September until the end of March, the sun's position is less than 45° around the clock: de facto no UVB and no D anymore:
(By S.Wetzel, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=32947615, red line at approx. 43° from me, LB)
Professor Schatz again:
"Clearly, less vitamin D is indeed synthesized in winter due to lower UV-B radiation."
No, none at all. At least not in Bochum.
In Davos, perhaps, as it is decisive one and a half kilometres higher and thus bypasses the thickest layer of air, the densest part of the UVB filter. And of course Thomas Mann's Zauberberg comes to mind, and the sunbaths against tuberculosis, and that you can get sunburnt in the Alps even in winter.
In Ischgl there were only two deaths among - according to antibody tests - at least 800 infected inhabitants, a very low IFR of 0.25%. And this although the virus droplets are supposed to fly longer and further in cold air.
Ischgl is at 1377 meters above zero. In fact, initial data from the Andes suggest that mountain dwellers may be better able to withstand the pandemic: Peru, which has the most infections in the subcontinent after Brazil, has ten times fewer cases above 3000 meters than in the plains. (Welt)
Let's return to the key statement in the article:
"But basically, the amount of vitamin D you take in from March to October is enough to get you through the winter." (Gahl, DGE)
But if you catch a bad flu, so the curb is high and sharp, and your tire is almost flat, what about "getting through the winter"?
And who actually determines how much is enough, how much is right? Well, for example the DGE, the German Society for Nutrition. The Federal Office for Risk Assessment (BfR) says the same thing: "Good" is everything above 20 ng/ml, 20 nanograms per millilitre of D3 (calcidiol) in the blood. "Undersupplied" is between 10 and 20 ng/ml, a deficiency is only to be recognized from 10 ng/ml.
The World Health Organization, however, has gone a bit further: Below 20 ng/ml is already a deficiency (below 12 is generally considered a severe deficiency internationally), below 30 ng/ml is considered insufficient, and only more than 30 ng/ml is considered sufficient. (insufficient), only more than 30 ng/ml is considered sufficient. The RKI did a large study in 2016. The result is well known to the DGE and the BfR. On average, the D3 level of the population between 18 and 78 years and over the whole year is a meager 19 ng/ml. According to WHO criteria, we would have a deficiency all year round. In fact, the level fluctuates seasonally, ranging from about 24 in summer to a deficient 12 ng/ml in mid-March. In the older age groups, i.e. among senior citizens, it is mostly below 10 ng/ml in winter, values of 6 ng/ml but also 3 ng/ml in people over 70 are not uncommon. So the fracture of the neck of the femur is not really surprising. The reason? The skin of over 70-year-olds only produces 25-30% of the vitamin D that a 20-year-old produces.
The great mystery is the question of where the above values actually come from? One can research this for a long time, most likely it is "experience values", average values from many laboratory measurements. The health department Bremen e.g. writes:
The laboratory findings show whether the supply status is sufficient (adequate), insufficient (suboptimal) or deficient. (adequate), insufficient (suboptimal) or deficient.
Many laboratories refer to levels below 20 ng/ml as mild vitamin D deficiency and levels below 12 ng/ml as severe deficiency.
However, this assessment is often considered outdated. In recent years, many scientific studies have shown that values of at least 30 ng/ml must be reached in order to avoid various health risks, and some even set the lower limit of an optimal supply at 40 ng/ml. According to the most common expert opinion of recent times, values in the range between 40 and 80 ng/ml would be considered optimal.
Bone experts call for blood levels of vitamin D to be at least 30 ng/ml, especially in people over the age of 60.
40-80 ng/ml are therefore the announcement, not half, not 20 ng/ml, as the DGE and the BfR repeatedly and still publish in contradiction to the "most frequently represented expert opinion of recent times". Where then did the old values come from? Well, if one takes young to middle-aged people in Central Europe as a yardstick, then, due to the low angle of sunlight, such average values must come out. And since these measurements were made on people who appear healthy, surely this must be sufficient?
No, it doesn't have to. If we were "normally supplied", then there should be no osteoporosis and no rickets. Without D-supplementation, however, there is, so the prescription of D-tablets for the youngest is part of the preventive care at the pediatrician. But why should children, who like to play outside, who are already in the baby basket "Why should they have a deficiency that adults should no longer have? That's like asking why everyone wears a mask in the operating room - if it supposedly doesn't help at all?
And if that still doesn't convince you: Why are all pregnant women automatically prescribed vitamin B12 and not just vegans? If we were all sufficiently supplied with it, then also the pregnant women? Why should nature afford such a deficiency with such serious consequences, especially in the case of reproduction, which is so important? Well, of course it didn't, evolution is not stupid, and our ancestors did not know any B12 deficiency - it is solely a consequence of our modern lifestyle, and by no means the only one.
And as the Iranian doctors had said above: they had some patients with D levels above 40 ng/ml, but these were farmers living off their own produce and not consuming soft drinks. So 40+x is the natural D level then, anything less a result of processed foods and too little sun? And a real deficiency?
Example iodine. According to the DGE, the desired intake for adults is 180-200 mcg daily, but daily intake averaged only 120 mcg in 2003-2006. Or 2014-2017 apparently only at 90 mcg, because the use of iodized salt in bread and rolls has decreased to 2%. At least that's what the German Federal Ministry of Food and Agriculture writes here. And further:
About 30 percent of adults and 44 percent of children and adolescents have an iodine intake below the estimated mean requirement and are thus at increased risk of iodine deficiency.
Nevertheless, the DGE proclaims unabashed:
According to the German Nutrition Society (DGE), healthy people who eat a varied diet do not need dietary supplements.
Ah yes. So almost half of all children are either ill or do not eat a varied diet, or both? No. Germany, Austria and Switzerland have always been iodine deficient areas, our soils have been washed out for millions of years, that is the simple truth. Why do you think salt has been iodized in Switzerland since 1925? Because, especially in mountain villages, the ubiquitous Iodine deficiency bad consequences, the goitre, the goiter was widespread and there was at least one case of cretinism in every village. These serious consequences no longer exist since the iodization of table salt. Which, by the way, was already decreed in the GDR in the 50s and only "allowed" (not prescribed!) in the FRG in 1985. And so one believes then, everything is now in order, also on HealthInformation.com, carried by an institute in the government order, we find the saying:
If you eat a balanced and varied diet, you get all the nutrients your body needs. Taking additional vitamins and minerals is then unnecessary.
So you see, there are real trivialisers at work here. Because on the other hand, nobody seriously wants to claim that we have 80,000 thyroid operations a year, i.e. that every 12th person has a thyroid operation in the course of their life, and that this has absolutely nothing to do with iodine deficiency, when iodine deficiency, as we know, leads to goitre, to goiter?
So there is plenty of reason to distrust the constantly repeated statement that we do NOT need supplements. Because what, pray tell, is the iodine in salt? What the B12 for the pregnant women, what the vitamin D for the little ones and the seniors? And the athletes, don't they all take magnesium voluntarily? Why, when they are healthy and eat a varied and balanced diet - which is what most active athletes do?
Where we once came from, people still live essentially as they did 50,000 years ago, the Maasai and Hadza in the savannah of northern Tanzania. They have a very dark skin colour, which protects them from Sunburn and skin cancer protection. The steep angle of sunlight provides high UVB radiation year-round, so despite their dark skin, they have a vitamin D3 level of 46 ng/ml on average. Our siblings from 6 million years ago, who are still our closest relatives genetically, the chimpanzees in central Africa, have black fur but our white skin underneath. And despite the leafy canopy and fur, they have enough for 48 ng/ml, although the amount of dietary D2 may play a role.
In any case, a D3 level of about 50 ng/ml seems to be considered sufficient by nature, because one thing nature never does: too much, if it costs energy. Because when it comes to saving energy, Mother Nature is the master par excellence. Why? Because the greatest killer, and this is still true today, is insufficient food, hunger; it kills more creatures than any disease and has always been the greatest threat to humans as well. So that's why we want to feed all the time, crave sweets, which then end up right on our hips... - a survival stock for a drought that could come at any time.
For humans it had to apply: everyday injuries and infections were not allowed to endanger the preservation of the group. So please, as much immune system as necessary, but no more, so that enough energy remains to build up fat stores for times of hunger. The three month store? Is for the rainy season, because there's no UVB when there's cloud cover. And then 45 ng/ml quickly becomes only 35 ng/ml, and that must be enough for a flu without vaccination, because - listen and be amazed - even while the virus droplets should fly so much better in the damp, cold air, which is why our flu season is in winter: At the equator there is only one flu season, and that is the rainy season. Humid? Yes. Cold? No way.
Ah, anyway, the seasonality of the flu - and Corona's. Welt provides this graph, generated from DIVI intensive care registry numbers:
We see comparatively very few C-19 cases in ICUs from late June into September. However, the sheer numbers of infections (determined by PCR test) had been steadily increasing from week 28, i.e. mid-July, as this graph from Joachim Schappert shows:
This discrepancy is often explained by the decreasing average age of those tested, but this is simply not a sufficient factor. From the end of September, the ITS figures then rise considerably, and barely two weeks later the death figures follow them.
In the summer, therefore, despite increasing infections, the courses were predominantly mild, only very few severe and relatively constant throughout the summer. What could explain this striking seasonal pattern?
We know similar seasonal courses from other respiratory infectious diseases (RTI), rhinovirus rhinitis or influenza. - know the summer cold and the summer flu, but they are not really taken seriously, because there are usually only a few cases and the course remains undramatic in contrast to the winter. This is also hardly statistically recorded or tested on a regular basis, but it is very likely that random tests for influenza viruses still produce relevant results in summer, but remain undetected thanks to largely mild symptoms. And we know that this seasonality exists in the southern hemisphere with a mirror-image offset of half a year, and that the closer one gets to the equator, the noticeably weaker it becomes in terms of incidence, but also in terms of seasonal fluctuations:
Fig. 1 The seasonal and latitudinal distribution of outbreaks of type A influenza in the world, 1964–1975, summarized from the Weekly Epidemiological Record of the World Health Organization into major zones (Source)
On this seasonality virologists generally provide three explanations.
… in the cold season, people tend to stay indoors and the risk of infection is therefore higher, the dry (heating) air dries out the mucous membranes and makes them more susceptible to infections.
There is little to be said against this, except that it may explain the large number of infections, i.e. the respective "waves", but not the severity of the individual illnesses - just look for a flu with a severe course here in summer, because yes, viruses are also present in summer: "Between April 2009 and November 2015, rhinoviruses and adenoviruses were present throughout the year. Rhinoviruses were present most days of the year (84.7%), followed by adenovirus which was present on 52.3% of the days. RSV (36.4%), HMPV (32.8%) and IAV (32.7%) were present in around 1/3rd of the year." (from Nature.com)
… the viruses lasted longer in dry cold air than in warm humid climate
This is only partially true, as different viruses show different seasonal variations. These figures show the course of viral infections in Edinburgh, Scotland:
IAV/IBV: influenza A and B viruses, HMPV: human metapneumovirus, RSV: respiratory syncytial virus (Please note the different scale of virus incidence, HPMV (red), the meta-pneumonia virus comes to max. 1.7, the flu (influenza A, ochre) on the other hand comes to over 5 in January, i.e. three times, LB)
With the exception of RSV, which peaks in December, all three others culminate between mid-January and mid-March.
This leaves rhinoviruses and adenoviruses, which also have different seasonality and even lower incidence:
The authors remark:
Following logistic regression adenovirus, influenza viruses A, B, RSV and HMPV preferred low temperatures; RSV and influenza A virus preferred a narrow “humidity-range” [..].
We see the strongest progression and the one that is most highly correlated with temperature in influenza A and B, the common flu. And the Riffreporter reports:
In both hemispheres, there is a distinct flu season in the temperate climate zones, but the influenza viruses also appear sporadically in the summer in some people who fall ill. In tropical and subtropical regions, there is no classic flu season. There, people fall ill with influenza all year round, and there are usually outbreaks during or shortly after the rainy season.
Influenza viruses therefore never disappear completely. Around the equator it is always seasonal, the flu wave on the southern half of the earth starts half a year later than ours.
3) and last-not-least the immune system of humans is also weaker in the respective winter.
That also seems to be only half the truth, because melatonin is released more in winter, and that has effects. Again the Riffreporter:
However, studies on animals clearly showed: "Via melatonin, which controls the day-night rhythm, the length of the day affects the hormonal situation and thus also the immune system," says the immunologist.
Immune cells themselves and also the thymus gland, an important maturation organ for a group of defence cells, carry receptors on their cell surface to which melatonin can dock. In animals that have had their pineal gland removed, the thymus does not form properly and the immune defenses are severely weakened.
[...] The bottom line is that most studies show a rather immune-boosting effect of melatonin, which is an "immune boosting" effect during the darker months of the year. In a world where living things are exposed to increasing light pollution, the loss of nighttime could contribute to a chronic weakening of organisms' immune defenses, making them more susceptible to infections and immune system derailments.
So that adds up to a lot. But that's not all. On the website of the well-known pharmaceutical company Pfizer, you can read:
They (a team of researchers from the University of Cambridge) found that more genes for the production of pro-inflammatory substances are activated in winter than in summer. And there is a reason for this: because these substances increase the immune system's readiness to defend itself and protect the body from invaders such as bacteria or viruses. We particularly need this in the cold season, as many factors favour infectious diseases at this time of year:
Our body produces less vitamin D in the cold season, which has a positive influence on the immune system. However, vitamin D is only produced when enough sunlight reaches our skin. In autumn and winter the days become shorter and so we are exposed to less sun during these seasons.
When analyzing the gene activity, the researchers made another exciting discovery: The pro-inflammatory genes were particularly active in participants from European countries from October to December, but less so in the summer. In Australia, the same pattern of increased activity of these particular genes was found, but shifted by 6 months. This reflects the temporal difference in the seasons, as summer and winter are shifted by 6 months in the northern and southern hemispheres, respectively: It's summer in Australia when it's winter here, and vice versa.
However, these genes do not seem to be influenced only by summer and winter. At the equator - where there is not much difference between the seasons - these genes are especially active during the rainy season. At this time, people in these latitudes are more exposed to pathogens because they love the humid weather.
Remains to be added: Flu season is cold in our country. But the rainy season is the only time at the equator where there is little or no UVB radiation due to cloud cover and thus the vitamin D level drops.
So as far as the immune system is concerned, on the one hand we have the melatonin effect, in other words: the shorter length of the day should actually increase the melatonin level and strengthen the immune defence, but this is counteracted by our way of life (artificial light). And that which could protect us from this, which undoubtedly improves the immune defence, the presence of vitamin D, is declared a minor matter, as best it can be. Yes, one should always walk diligently, and that would be enough.
However, in zones where the annual temperature is comparatively high and fluctuates little, i.e. at the equator, there should be no pronounced summer/winter seasonality, and this is exactly what can be seen on relevant graphs (see above). However there is a "bump", an excess in the infection figures, and this - with some delay - during the 2-3 month rainy season.
Let's keep this in mind and look at the course of the vitamin D level over the year:
The vitamin D level in Germany, with a mean value of approx. 19 ng/ml (RKI) thus fluctuates between 12 ng/ml in March and 23 ng/ml at the end of August, which is twice the March minimum. And the flu season from December (15 ng/ml) to March (12 ng/ml) falls conspicuously in exactly this time of the minimum, while in October the D-level with 20 ng/ml is still 50% above the level of this minimum time.
How does this fit in with the rainy season in Africa? Well, UVB radiation is reliably blocked by clouds, the formation of vitamin D is thus just as little possible as in our latitudes in winter, the D store begins to empty. That and what vitamin D has to do exactly with the general "immune status", everyone can read in Wikipedia.
If we turn our D curve upside down and compare it between mid-April, when the C-19 pandemic really took off, and into November, we see an extremely parallel progression: With the rise to over 20 ng/ml Vit D, the ITS numbers drop below 500, only to exceed 500 again and continue to rise sharply with the drop below the 20 ng/ml limit in October.
Yes, correlation is not causation. But it also doesn't prove the opposite, that correlation is purely coincidental and there is no causality.
If we compare Stockholm with Bergamo, for example, it is striking that with 2.3 million inhabitants in the Stockholm region there were around 2,500 deaths, including, as we know, many, many elderly people in homes. In Bergamo we count at least 600 deaths out of a population of 120,000, but extrapolated to Stockholm that would be over 11,000 deaths, four times as many. Half of it may be explained by the fact that Bergamo is far more heavily infested, at 50% and more, while in Stockholm they talk about 40% - the other half of the Bergamo death rate would thus be unexplained.
But another difference is known, albeit a rather counterintuitive one: the Italian seniors had a vitamin D level of about 9 ng/ml at the beginning of the outbreak in March, but the Swedish ones of 19 ng/ml - the Iranian professors had reported exactly the same in their "letter" mentioned above.
Reasons for this could be that seniors in the south tend to avoid the sun, and seniors in Sweden not only eat a lot of fatty fish, but also take D-preparations or have them administered in the retirement homes, because, as a private mail from Sweden tells me, this is cheaper than antibiotics.
Yes, correlation is not causation. But when I find two highly different correlations (flu seasonality and D levels, senior D levels I/SWE and death rates) with the same reference....
No, three, because the flu seasonality due to the rainy season, which brings the vitamin D synthesis to a standstill due to cloud cover, would be added...
Whereby it would have been a clever trick of Mother Nature, if the approximate range of the vitamin D storage - we are talking about 2-3 months - also corresponded to the duration of the rainy season. If, yes, if the D level had previously been the 45-50 ng/ml usual down there with a traditional way of life (Massai, Hadza, chimpanzees), because then it would drop by about 1/3 in the three months before the sun can replenish, so it would still amount to >30 ng/ml, which the WHO considers to be the lower limit for a "sufficient, adequate" supply (>30: sufficient, <30 insufficient, <20 deficient).
I, for one, know why I keep my family and myself at a D level that the average person in East Africa has: twice the average maximum here, which is 48 ng/ml and above. Just like Massai & Hadza in East Africa and the chimpanzees in the Central African jungle. But for me, summer and winter, all year round, with no "rainy season" break. Caveat: never without K2!
Because: the C-19 ITS numbers, since we are far from herd immunity, that is my prediction, will continue to follow exactly the above curve D level curve - in November this will become clearly visible (I wrote at the end of October) and the next spring will be even more drastic.
Unfortunately, there is a clear indication beyond the ITS figures: the IFR, i.e. the infection-fatality rate, is rising again. At the end of August, beginning of September, it was still at 0.32% in a 10-day interval (25.8./4.9.), then between 28.9. and 8.10. it had unfortunately risen to 0.47%, which is almost 50% more deaths per infected person and this cannot be explained by a seasonal sensitivity of the virus and certainly not by the fact that less testing is now taking place. With the D-level curve, however, it can.
Slowly, however, the penny seems to drop even for andernrots. The article quoted in the following excerpts "Does vitamin D help against the coronavirus?" in the SPEKTRUM is mourned in the camp of the D-activists, but it is at least a yes/against article. Stupid only again that the author and/or the quoted professor cannot differentiate again times between good and bad studies. And of course they have to add the inevitable warning about overdoses at the end. But one after the other:
From a nutritional medicine point of view, it is [...] "quite correct to claim" that a severe vitamin D deficiency increases the risk of a viral infection - also with Sars-CoV-2 - and of a severe course, says Martin Smollich, pharmacist from the Institute for Nutritional Medicine at the University Hospital Lübeck.
However, it becomes problematic if one deduces from this that a high-dose vitamin D administration could reduce the risk of death in the case of an existing Covid-19 disease. Current studies are repeatedly used for this purpose. But: "None of them proves a clear benefit," says Smollich.
The following two paragraphs even summarize our knowledge of vitamin D (which Mr. Drosten obviously does not have) in an excellent popular scientific way:
Vitamin D is an ancient survival molecule that is photosynthesized by all life forms on Earth - by phytoplankton in the ocean as well as by mammals and humans, writes Antonio Vella of the University of Verona in a review paper. Vitamin D is actually not a vitamin, but a hormone. It does not necessarily have to be ingested with food, which is actually considered a characteristic of a vitamin, but can be synthesized by the body itself in the skin under sunlight. Vitamin D influences the activity of several hundred genes in the body. "Among other things, it regulates the immune system in quite a number of places and is of central importance in ensuring that the defence responds to a threat in a balanced manner," Martin Smollich explains. On the one hand, the immune defense must be "sharp" enough to fight off intruders, but on the other hand it must not overreact and thereby damage the body's own tissue.
Among other things, vitamin D influences immune cells of the innate immune defense, such as macrophages and dendritic cells. These immune players decide early on during the defence reactions where the journey is headed. They assess how threatening the situation is and ensure an appropriate response. The active form of vitamin D, for example, inhibits the maturation and immunostimulatory effects of the dendritic cells and thus makes the immune response more "tolerant". According to researchers, a vitamin D deficiency could therefore increase the risk of the dreaded cytokine storm, an overreaction of the immune system that gets out of hand and is life-threatening in some patients.
"In some patients" can also be rephrased: in de facto all Covid-19 deaths. Because Chinese researchers had already determined this in February: of 191 Covid-19 patients, 54 had died, all 54 had suffered sepsis (blood poisoning) and 38 a cytokine storm. Now individual studies are cited and weighed:
However, if one looks at concrete studies on this, one comes across contradictory data. For example, a study by Dutch doctors from the Canisius-Wilhelmina Hospital in Nijmegen found no correlation between vitamin D status and disease severity in 135 patients hospitalized for Covid-19.
Makes you wonder if anyone the study really looked at it? No? Just read the abstract again? For one thing, the authors say they could not find a connection with vitamin D, but they could find a connection with vitamin K (in another study).
We recently proposed vitamin K status as such a modulator [1] based on the strong association between vitamin K insufficiency and poor outcome in a cohort of COVID-19 patients [2].
and the article doesn't mention that at all. Maybe also because you can read in the fine print that the main author, but also all the others (except one) have a conflict of interest regarding vitamin K:
RJ discloses application of a patent on vitamin K in COVID-19. RJ, JW and ASMD have a scientific collaboration with Kappa Bioscience AS, a manufacturer of vitamin K2 (MK-7). JMWO and RJ are owners of Desmosine.com. HD declares no competing interests.
And this statement needs to be looked at more closely:
We found no difference in vitamin D status between those with good and poor outcome (defined as intubation and/or death).
If you look at the table with the patient data,
then it is noticeable that the group with the "poor outcome" clearly predominates in 4 of 5 risk factors, the patients are 8 years older, are 78% versus 61% male, have ¼ more diabetics and half more heart disease. That a difference in D-level can no longer come through in such "sorting" is perfectly clear, oranges are being compared to apples here. By the way, contrary to the generalized statement, there is a difference in D-level between the two groups, namely 37.7 vs. 45 nanonmol/L. You have to divide that by 2.5 to get the more familiar measure ng/ml: 15 ng/ml in the "poor outcome" group and 18 ng/ml in the younger group. Not a lot in either group and explainable by the age difference alone. And it plays into the same direction as all the other risk factors in favor of the "good" group. But one thing is clear: sorting like this reliably prevents you from getting a result by D level. The correct thing to do would have been: Sort by D level, and adjust for the known risk factors of age, sex, and pre-existing conditions. The authors have omitted to do this, although this is absolutely standard and every statistics program is capable of this multifactorial evaluation.
Nevertheless, the authors have earned a great merit by pointing out the possibly decisive role of vitamin K with regard to "elastic fiber degradation" by calcination. For scientists and interested laymen in this respect a "must-read".
After mentioning a Indian study, which believes to come to a definite conclusion,
Of the 91 study participants whose Sars-CoV-2 infection was asymptomatic, only one third had a vitamin D deficiency. In contrast, almost all, namely 61 of the 63 infected persons who had to be admitted to the intensive care unit for treatment, had a vitamin D deficiency.
Professor Smollich then writes more broadly:
The significance of such studies is very limited, says Martin Smollich. In most cases, it is unknown what the vitamin status of the patients was before their hospital stay. It is therefore not known whether the vitamin D deficiency is the cause or the consequence of severe Covid-19. After all, the level of vitamin D can drop sharply, especially in the case of severe immune reactions, which are common for a severe Covid-19 disease.
After all, this argument is also countered in the article itself:
In 80 patients with confirmed Covid-19, old vitamin D values were researched that had been determined during medical examinations up to three months before the disease. A pre-existing vitamin D deficiency significantly increased the risk of severe disease after infection with Sars-CoV-2.
The study literally states (translated):
Results: We included 80 patients, of whom 31 (39%) presented the endpoint. Vit D deficiency tended to predict an increased risk of developing severe COVID-19 after adjusting for age, sex, obesity, heart disease, and kidney disease [OR 3.2 (95% CI: 0.9-11.4), p = 0.07].
An odds ratio (OR) of 3.2 is extraordinarily high, it means that the risk of group B (14 ng/ml) to end up in the ICU was more than 3 times higher than in group A with 28 ng/ml - and that after correction for all important risk factors. Here you can see how it is done correctly and the Dutch authors should perhaps have their raw data evaluated by the Spanish.
And now Ms Gebhard comes directly to the "group of vitamin D advocates":
On the other hand, it is a completely different question whether it is possible to influence the course of the disease favourably with a high dose of vitamin D - and this when the child has already fallen into the well. That the vitamin is suitable for therapy is currently advocated by a sometimes more, sometimes less vociferous group of vitamin D proponents. [...] One study from Brazil puts a big damper on the high expectations for vitamin D. A team from the University of São Paulo had administered a single dose of 200,000 International Units of vitamin D3 to 120 patients with severe Covid-19 in a double-blinded study, while 120 other sufferers received a placebo. Patients with pre-existing conditions such as hypertension or diabetes were equally represented in both study groups, according to the researchers led by Rosa Maria Rodrigues Pereia.
The last sentence is a falsehood. Equal means equal, but as in the Dutch study, although the groups were supposedly randomized, they were strangely more unequal than one might have expected from pure dice rolling.
Central statement of the study:
Among hospitalized patients with severe COVID-19, a single dose of 200,000 IU of vitamin D3 supplementation was safe and increased 25-hydroxyvitamin D levels, but did not reduce hospital length of stay or any other clinically relevant outcomes vs placebo. Thus, this trial does not support the use of vitamin D3 supplementation as an adjuvant treatment of patients with COVID-19.
The placebo group had better scores in more than one category of known Covid 19 risk factors. (see Table 1 in the PDF). The factors shown below are calculated in comparison to D3 = 1. Less than 1 means less risk, but cannot be used directly as a multiplier or divisor. For example, "age" is a risk of death that increases disproportionately compared to Influenca. While Covid-19 has a much lower risk for young people compared to influenza, the risk of death is said to be the same at age 50, but 80 to 200 times more deadly in patients over 80 and over 90.
The estimated age-specific IFRs are very low for children and younger adults but increase progressively to 0.4% at age 55, 1.3% at age65, 4.2% at age 75, and 14% at age 85.
(here factor 35 between 55 and 85, the normal flu mortality is 0.1%, if this is the value for 50-year-olds, this results in a factor of 140 to the 85-year-olds)
This would mean an increase in risk by at least a factor of 3 per year of life. Thus, even a minimal age difference - in this case approx. 1 year - can have a greater influence on the statistics. Other known risk factors are also predominantly on the side of the D3 group. If three main factors (hypertension, diabetes II, and COPD) are 33% more prevalent in the D3 group (3:4 or worse), it is difficult to explain how randomization across more than 200 patients should lead to such an unbalanced result.
Placebo group: ~ 1 year younger
(0.98), less overweight (31/37, 0.84), less obesity
(58/63, 0.92), less hypertension (58/68, 0.74), less diabetes II (35/49, 0.71), less COPD (5/7, 0.71%), less asthma (7/8, 0.88), no chronic kidney disease (0/2, 0.0) , less rheumatic disease (10/13, 0.77).
Thus, although the D3 group had a significantly higher risk of disease, especially for the known risk factors of hypertension, COPD, and diabetes, all of which were less than 75% compared to the D3 group = 100%, the following table does show some differences between the conditions of the D3 treatment group and placebo:
Oxygen supplementation |
No. (%) D3 |
No. (%) Placebo |
|---|---|---|
No oxygen therapy |
16 (13.3) |
9 (7.5) |
Oxygen therapy |
86 (71.7) |
97 (80.8) |
Non-invasive ventilation |
18 (15.0) |
14 (11.7) |
The numbers do not add up to 100% of each group (16 + 86 = 102, 9 + 97 = 106), but again: compared to D3 = 100%, only 56% of the placebo group managed without oxygen therapy and only 77% were able to avoid non-invasive ventilation; the group clearly disadvantaged by risk factors was significantly better in all respects. Not clinically relevant looks different.
The central message of the study is based on the following values:
Category |
114 Patients D3 200K IE |
118 Patients Placebo |
|---|---|---|
Age (120/120) |
56.8 (±14.2) |
55.8 (±15.0) |
Death/Mortality |
8 (7,0%) |
6 (5,1%) |
Adm. to ICU |
18 (15,8%) |
25 (21,2%) |
mech. Ventilation |
8 (7,0%) |
18 (14,4%) |
With the exception of mortality (8/6: 1.25), the D3 group-although much more at risk overall-had a lower risk of being sent to the ICU (0.72) and only a 0.44-fold risk of being mechanically ventilated compared with placebo (normalized to 1.0).
Thus the affirmative statement:
This study does not support the use of vitamin D3 supplementation as adjuvant treatment for patients with COVID-19.
clearly not supported by the data.
Given the disadvantages of the D3 group, it is highly unlikely that the much better performance in terms of oxygen therapy required is merely coincidental.
An oral single dose of D3, even if administered in peanut oil, also seems to be an inadequate treatment according to the current state of research. On the one hand, the initial bolus dose is usually administered intramuscularly, and on the other hand, in addition to vitamin K2 - which is needed to regulate calcium levels and to down-regulate blood clotting - the co-factors needed for high-dose D3 treatment are missing: selenium, zinc and magnesium, without which D3 cannot have an adequate effect.
But there is still a statistical puzzle to solve: supposedly there was no difference in the length of hospital stay.
The bias in at least nine risk factors, all of which are unfavorable to the D3 treatment group, some of them strongly unfavorable, has a very, very low statistical probability, even though some of the factors are not completely independent of each other (hypertension correlates with diabetes II, etc.). Nevertheless, the mean length of stay was practically the same with 7 days each and almost identical standard deviation, which was one of the main statements in the abstract.
The explanation for this can be seen in a simple thought experiment:
If risk factors are equally distributed (or statistically corrected) for all patients with the same disease, those subjects treated with "helpful therapy" should show better scores on clinical paranmeters than placebo. Otherwise, therapy or treatment would be of little value.
Therefore, in the case of Covid-19, the length of stay in the hospital/ICU should be shorter if therapy is helpful.
However, there is one case where this is not true: if treated patients experience improvement, when they die it means that they have survived longer in the ICU, just as a cancer patient survives longer with the help of chemotherapy. Meanwhile, patients with initially the same health condition but untreated would die faster.
This leads to a strange artifact. While untreated patients who do not die have longer stays in hospital than treated patients, this is reversed in the case of death, untreated the time to death becomes shorter. As I said, assuming that the therapy is helpful. This can easily lead to the fact that the average length of stay of the two groups, i.e. once shorter+longer, once longer+shorter, is on average the same.
Example: in both groups 10% deaths each with a duration of 10 days (placebo) and 20 days (D3). The other 90% in each case would then have to be discharged after 6.66 days (placebo) in order to arrive at an average duration of 7 days. (placebo), but after only 5.55 days under treatment and here despite the higher risk factors. You can play with the numbers, the result will always be the same.
And that this was very likely exactly the case is shown by the much better values of the D3 treatment group in terms of oxygen treatment times and cases. Since D3 counteracts these risk factors, this explains why the untreated patients had to be ventilated far more often. And this despite the fact that they had a better start - due to the unevenly distributed risk factors. If the authors had separated the respective length of stay, it would have been quickly noticed that the deaths in the placebo group occurred after a shorter time than in the D3 group.
In fact, the authors could have seen this for themselves because they created a graph using Kaplan Meier curves. Normally, the Kaplan-Maier estimator is used to estimate a chance of survival based on patients dying after a period x. Here it was used to plot the length of stay of patients to the defined endpoint. But in reality, there were two endpoints here: hospital discharge and patient death. This is definitely the misuse of a statistic.
So this reasoning seems to rather confirm that D3 is a helpful treatment and efficient - and that statistics can often be misleading if not treated mindfully.
Concluding remarks
A test for vitamin D of 2,000 "infected" would have cost 40,000 €, three weeks later it would have been clear whether there is the connection claimed by some scientists. A "trial" on 1,000 hospitalized Covid-19 patients with - as suggested by the Iranians mentioned above and many D-activists around the world - 300,000 IU bolus dose and 5,000-7,000 IU (plus 200 mcg K2) maintenance dose would have shown very quickly that the diseases usually end smoothly. And if one had started immediately with a mild (200 mg) hydroxychloroquine+zinc treatment before hospitalisation, already at the first symptoms such as cough, and then increased this to the usual 2x200 mg for a maximum of 5 days after a positive test result, then many hospitalisations would probably not have occurred at all.
With D3 tests paid for by the insurance companies and clear information to the population about the necessary supplementation, the population could have been brought up to the required D3 level of 50 ng/ml over the summer - and the second wave would have been so much milder than the first that a lockdown would not have been necessary.
LB, 6.12.2020