Where do you draw the line? C-19 or Mental Disorder caused by the NEWs and everyone else’s fears and panic.
Mass hysteria" redirects here, - Mass psychogenic illness** ( MPI ), also called mass sociogenic illness , mass psychogenic disorder , epidemic hysteria , or mass hysteria
I firmly believe that Boron infusions are the answer, due to many years spent studying Magical Thinking
If a little knowledge is dangerous, where is the man who has so much as to be out of danger?
-Thomas Henry Huxley
… because the mind is not an object like the body, it is a mistake to apply the predicate disease to it. … Although medicalization encompasses more than psychiatry, we must be clear about one thing: Psychiatry is medicalization through and through. Whatever aspect of psychiatry psychiatrists claim is not medicalization, is not medicalization only if it deals with proven disease, in which case it belongs to neurology, neuroanatomy, neurophysiology, neurochemistry, neuropharmacology, or neurosurgery, not psychiatry. Psychoanalysis is medicalization squared. It is important, in this connection, not to be fooled by lay analysis, clinical psychology, or social work. These and other nonmedical mental-health and counseling “professions” are medicalization cubed: as if to compensate for their lack of medical knowledge and qualifications, nonmedical mental-health “professionals” are even more deeply committed than psychiatrists to their claim of special expertise in the diagnosis and treatment of mental illnesses. … In short, medicalization is neither medicine nor science; it is a semantic-social strategy that benefits some persons and harms others.
Source: “The Therapeutic State - The Medicalization of Everyday Life”; Thomas Szasz (2007)
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(See Chapter 5, on Page 27):
“Diagnoses Are Not Diseases”,
“The Medicalization of Everyday Life - Selected Essays”;
Thomas Szasz (2007)
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(Nature, May 5, 2020):
(New York Times, May 7, 2020):
Well before shutdown orders, restaurant reservations were plummeting. Electricity usage, which falls when office buildings and factories empty out, was dropping, too. Public transit in many cities was in free fall. So was the number of air travel passengers passing through T.S.A. checkpoints. Such data, combined with opinion polling today, suggests that Americans who were turning off the economy on their own may not readily reopen it soon - even if officials say it’s OK to. …
… findings in the Nationscape surveys are remarkably consistent across different groups. Residents of states that have already reopened or plan to soon are about as wary of these activities as residents of states that remain locked down, a pattern also found in polling by The Washington Post and the University of Maryland. … Vast majorities … say they would not ride public transit, attend sporting events or go on a flight. Majorities of both say they wouldn’t send their children back to school, a prerequisite to resuming many economic activities. “Here’s this moment where almost everybody in the country agrees on a number of different things,” said Lynn Vavreck, a political scientist at U.C.L.A.
(Nature, May 8, 2020):
Blood thinners don’t reliably prevent clotting in people with COVID-19, and young people are dying of strokes caused by the blockages in the brain. … Researchers have also observed miniature clots in the body’s smallest vessels. … Why this clotting occurs is still a mystery. One possibility is that SARS-CoV-2 is directly attacking the endothelial cells that line the blood vessels. … The virus’s effects on the immune system could also affect clotting. … there could be other factors at play that aren’t specific to COVID-19. People with the disease who become hospitalized typically have a number of risk factors for clotting. They might be elderly or overweight, and could have high blood pressure or diabetes. They show up with high fevers and, because they’re seriously ill, have probably been immobilized. They might have a genetic predisposition to clotting, or be taking medications that increase the risk.
(MedicalExpress, May 8, 2020):
“Uncovering the potency and evasiveness of the COVID-19 virus”
SARS-CoV-2, the virus that causes COVID-19, is highly infectious. Curiously, in many patients, it triggers poor immune responses, which prolongs illness. This helps the virus spread widely, exacerbating the global pandemic. In a new study published in the “Proceedings of the National Academy of Sciences”, researchers at the University of Minnesota identified the biochemical mechanism that may explain how the virus infects people efficiently while evading their immune responses. …
… Specifically, the team of scientists investigated how the virus “unlocks” human cells using a surface spike protein as the “key.” They made three important findings:
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The full text of the referenced article (excerpt below): “Cell entry mechanisms of SARS-CoV-2”
SARS-CoV-2 spike binds to its receptor human ACE2 (hACE2) through its receptor-binding domain (RBD) and is proteolytically activated by human proteases. … Here we investigated receptor binding and protease activation of SARS-CoV-2 spike using biochemical and pseudovirus entry assays. Our findings have identified key cell entry mechanisms of SARS-CoV-2. First, SARS-CoV-2 RBD has higher hACE2 binding affinity than SARS-CoV RBD, supporting efficient cell entry. Second, paradoxically, the hACE2 binding affinity of the entire SARS-CoV-2 spike is comparable to or lower than that of SARS-CoV spike, suggesting that SARS-CoV-2 RBD, albeit more potent, is less exposed than SARS-CoV RBD. Third, unlike SARS-CoV, cell entry of SARS-CoV-2 is preactivated by proprotein convertase furin, reducing its dependence on target cell proteases for entry. The high hACE2 binding affinity of the RBD, furin preactivation of the spike, and hidden RBD in the spike potentially allow SARS-CoV-2 to maintain efficient cell entry while evading immune surveillance. These features may contribute to the wide spread of the virus. Intervention strategies must target both the potency of SARS-CoV-2 and its evasiveness.
About a week ago, maybe a bit more, I downgraded my own guesstimate on COVID-19 “true” mortality rate from 0.8% to 0.75%
It looks like a good guess …
Australian scientists compared 13 studies and concluded that 0.75% is a good guess.
That means for every 133 infected, one will die …
If I calculate todays (Johns Hopkins) world COVID-19 mortality divided by confirmed cases (6.937%), the ratio of that divided by 0.75% is factor of ~5.25. I may have missed some of your methodology in deriving your ongoing estimates - but (in a simplistic sense), your estimate would seem to imply ~19% of all SARS-CoV-2 infections presently existing on the planet have been diagnosed (thus “confirmed”) ?
One thing that deserves mention is that the short-term (and even potentially permanent) effects upon one’s internal organs and nervous system from contracting the (disease state) “COVID-19” exceeds a simple “binary” dead or alive. The patients (already) most vulnerable (with cardiovascular, kidney, liver, pancreas, as well as lung conditions) can be irreversibly damaged/compromised. As well, people having the above listed chronic conditions and pre-existing disease-states are often immune-compromised, elongating recovery times, as well as likely making lasting and robust immunity to viral re-exposures less likely (actually “true” for all, as far as we presently know). This virus is notably cryptic, adaptive.
There seems to be little doubt that the treatment costs have/will severely strain the US for-profit system.
Reading published accounts of people who have recovered is always humbling and thought-provoking:
(Science Magazine, May 8, 2020):
“‘Finally, a virus got me.’ Scientist who fought Ebola and HIV reflects on facing death from COVID-19”
Well that seems quite a bit lower than what was being predicted previously.
Yes, I believe the “confirmed cases” numbers are useless. We simple haven’t tested enough.
A truly mind boggling number of infections are not recorded at all.
I originally played around with the numbers - South Korea was very useful to play around with. Pretty early on, I noticed that if I set the mortality rate to something high like 5% and calculated the number of infections, that number would be lower than the confirmed cases, which obviously makes no sense. I think initially my guesstimate was 1.5% and has slowly declined since, to 1.2% to 1% to 0.9% then 0.8% and then I settled a bit more than a week ago on 0.75% (also based on stuff I read).
Here is a graph of S. Korea with a mortality rate of 1.95%:
The dates are 22 days delayed, meaning that when a person died, they were infected 22 days earlier. In the beginning I read that the average time from infection to symptoms was 10 days, and a further 10 days to succumb to the disease. I’ve since adjusted it to 22 days. This number is also uncertain, as I don’t have much data on it - I know that in Denmark the intensive care patients are there very long before they either die or recover - up to 3 weeks.
This is the same graph with a mortality rate of 0.75%:
This looks much more reasonable and reveal that they only “found” about 1/3 of the infected people 22 days ago…
This is the same graph for the whole of the US:
Spain is starting to look better:
As is Italy:
France as well:
UK not so good:
General for the whole world:
Another number that is interesting to look at for predictions, is number of hospitalizations - but those numbers are hard to come by …
Depends on where you read, I think. A lot are actually talking about “Case Fatality Rates” which just uses the number of confirmed cases vs. dead - and as I mentioned, I don’t think we can use the confirmed cases number for much, because of how little we test…
300 Million years. Several hundred times the age of bozo erectus. We are “just another substrate”.
(Nature, May 4, 2020):
Estimates for the birth of the first coronavirus vary widely, from 10,000 years ago to 300 million years ago. Scientists are now aware of dozens of strains (3), seven of which infect humans. Among the four that cause common colds, two (OC43 and HKU1) came from rodents, and the other two (229E and NL63) from bats. The three that cause severe disease - SARS-CoV (the cause of SARS), Middle East respiratory syndrome MERS-CoV and SARS-CoV-2 - all came from bats. But scientists think there is usually an intermediary - an animal infected by the bats that carries the virus into humans. With SARS, the intermediary is thought to be civet cats, which are sold in live-animal markets in China.
It might if you’re healthy enough to take it. I hear that stuff can be brutal.
Maybe the Tigers got it from eating people in China?
(WARNING: GRAPHIC VIDEO)
I see that “The Beast” has wound it’s way deep within the cranial chambers. Truly, the “Pose-Truth Age”. 300 Million years in the making, the master epigenome executes its ineluctable substratic dance, silent in its indifference to our vanities and peeves. No neuron will be spared as Vlad’s radio-labeled tinctures slowly infuse into the deep dish, while the intrepid thin crusts reclaim the galaxy once again for farces of truth and justice, restored once again to its old glorious pizza prime. I am sure you might readily agree that conspirathism presents what seems likely the one and only way by which to mount a sufficiently anthropomorphic narrative so as to duly flatter and cater to our collective ontological incompetences.
Attack of the Killer Kittens cross-infected with Bat Scratch Fever seems to precisely explain everything:
(The Washington Post, May 10, 2020):
(USA Today, May 11, 2020):
“COVID-19 expert: Coronavirus will rage ‘until it infects everybody it possibly can’”
Dr. Michael Osterholm, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, said the initial wave of outbreaks in cities such as New York City, where one in five people have been infected, represent a fraction of the illness and death yet to come. “This damn virus is going to keep going until it infects everybody it possibly can,” Osterholm said Monday during a meeting with the USA TODAY Editorial Board. “It surely won’t slow down until it hits 60 to 70%” of the population, the number that would create herd immunity and halt the spread of the virus. Even if new cases begin to fade this summer, it might be an indicator that the new coronavirus is following a seasonal pattern similar to the flu. …
… If COVID-19 retreats only to return in the fall, the number of cases could peak and overwhelm hospitals that must deal with cases of flu and respiratory viruses. Furthermore, Asian nations such as South Korea and Singapore, lauded for strict controls and rapid testing to avoid damage during the first wave, might be vulnerable to a second wave of infections, he said. “It’s the big peak that’s really going to do us in,” he said. “As much pain, suffering, death and economic disruption we’ve had, there’s been 5 to 20% of the people infected, … That’s a long ways to get to 60 to 70%.” …
… Osterholm said only an effective vaccine can slow the virus before a large enough segment of the population becomes infected and develops some level of immunity. Even if a vaccine works, Osterholm said, it’s unknown whether it would be durable enough to confer long-lasting protection from SARS CoV-2, the virus that causes COVID-19. …
… Osterholm acknowledges that the nation “can’t lock down for 18 months” and said political and business leaders need to find a way to resume activities while adapting to a virus that won’t soon disappear. He doesn’t believe there has been enough of a frank assessment on the economic harm the virus will cause over coming months and its disruption to international supply chains. “We all have to confront the fact there’s not a magic bullet, short of a vaccine, that’s going to make this go away,” he said. “We’re going to be living with it. And we’re not having that discussion at all.”
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Osterholm is the author of more than 315 papers and abstracts, including 21 book chapters. …
He has received honorary doctorates from Luther College[19] and Des Moines University,[20] and is a member of the Institute of Medicine of the National Academy of Sciences.[6] His other honors are the Pumphandle Award from the Council of State and Territorial Epidemiologists; the Charles C. Shepard Science Award from the CDC; the Harvey W. Wiley Medal from the Food and Drug Administration; the Squibb Award from the Infectious Diseases Society of America; Distinguished University Teaching Professor, Environmental Health Sciences, School of Public Health, University of Minnesota; and the Wade Hampton Frost Leadership Award, American Public Health Association. He also has been the recipient of six major research awards from the National Institutes of Health and the CDC.
(The Conversation, May 11, 2020):
“Coronavirus: research reveals way to predict infection - without a test”
The problem is that most countries lack the resources to test and contact-trace enough people. But our app, which is called the COVID Symptom Study and is based on some 3.4 million users in the UK, US and Sweden logging symptoms daily, could help. In a new study, published in Nature Medicine, we show that this app can estimate whether someone has COVID-19 purely based on their symptoms - with a high degree of accuracy. …
… For our new study, which has been peer reviewed, we analysed data gathered from just under 2.5m people in the UK who had been regularly logging their health status in the app. Around a third had logged multiple symptoms associated with COVID-19. More than 15,000 people reported having had a test for coronavirus, with nearly 6,500 testing positive. …
… We investigated which symptoms known to be associated with COVID-19 were most likely to predict a positive test. Loss of taste and smell were particularly striking, with two thirds of users testing positive for coronavirus infection reporting them compared with just over a fifth of the participants who tested negative. … we created a mathematical model that can predict with nearly 80% accuracy whether an individual is likely to have COVID-19 based on their age, sex and a combination of four key symptoms: loss of smell or taste, severe or persistent cough, fatigue and skipping meals. …
… our results suggest that loss of taste or smell is a key early warning sign of COVID-19 infection. A loss of appetite and severe fatigue also outperformed the classical symptoms like cough and fever. … multiple symptoms occurring rapidly have a better prognosis than those coming on more slowly involving fatigue and chest symptoms. We are also finding many people with symptoms waxing and waning for over a month. …
… The COVID Symptom Study app is available to download from the Apple App Store and Google Play Store in the UK and USA as well as Sweden. Daily research updates and data which is shared with the NHS can be found here.
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Referenced Article (Frontiers in Microbiology, April 11, 2018):
“Bats, Coronaviruses, and Deforestation:
Toward the Emergence of Novel Infectious Diseases?”
Coronaviruses (CoV) were for a long time associated with several major veterinary diseases such as avian infectious coronavirus, calf diarrhea, winter dysentery, respiratory infections (BRD-BCoV) in cattle, SDCV, PEDV, SECD in swine and dog, intestinal disease or Feline Infectious Peritonitis (Saif, 2014), and the human mild and common cold. However, SARS emerged in 2002 in China and spread across 29 other countries with a 10% death rate. More recently, the MERS-CoV outbreak in Saudi Arabia in 2012 displayed a death rate of 38%. The emergence of these two events of highly pathogenic CoVs shed light on the threat posed by coronaviruses to humans. Bats are hosting many viruses (Calisher et al., 2006) and in particular coronaviruses, which represent 31% of their virome (Chen et al., 2014). Furthermore, bats display a remarkable resistance to viruses (Omatsu et al., 2007; Storm et al., 2018). The risk of emergence of a novel bat-CoV disease can therefore be envisioned. …
… The biological problem of viral emergence has not fundamentally changed, however the probability of occurrence of the risk is increasing owing to environmental change and higher environmental pressure. … the emergence of a disease is impossible to predict. It is an accidental process, i.e., the occurrence of an extremely low probability event resulting from a stochastic combination of low probability independent events. If the exact time and nature of the emergence of a disease cannot be predicted, the increased probability of encounter and occurrence of an emergence-leading chain of events yielded by anthropized environments must be considered seriously. …
… Major human infections by bat-borne viruses have been documented quite recently, although they might have occurred earlier in history. CoVs were mostly associated with veterinary diseases, with livestock and pets acting as intermediate carriers for transfer to humans. … the emergence of a novel pathogen within the immune-naive human population. In such a case, the risk of large epidemics is very high along with high mortality. Once adapted to humans, CoVs may evolve to develop a more efficient intra-species mode of transmission. During SARS outbreaks in Toronto and Taiwan, certain persons were very efficient at transmitting SARS-CoV and were named “Superspreaders” (McDonald et al., 2004). A total of 83.2% of the transmission events were epidemiologically linked to five “superspreaders,” all of whom had pneumonia diagnosed at the first medical consultation. …
… the problem of bat-borne viruses is not restricted to CoVs. Among the 60 viral species reported to be associated with bats, 59 are RNA viruses which might possibly be responsible for emerging and re-emerging infectious diseases in humans (Brook and Dobson, 2015). However, bats are not necessarily involved in primary infection of humans. The main risk for emergence of diseases is directly linked to the development of anthropized environments and their attractiveness for different bat species. …
… A recent phylogenetic study has provided strong evidence that viruses isolated from bats in China are clustering by geographical location rather than by bat species, suggesting that high contact rates among specific bat species favor the spread of CoVs (Lin et al., 2017). It is believed that most CoVs, if not all, are also circulating in different mammal species originating from ancestral bat CoVs. Notably, only a small minority of the estimated 1,240 bat species has been tested for CoVs. It is likely that many more CoVs could be discovered in bats. Although 31% of bat-borne viruses are CoVs (Calisher et al., 2006), only 6% of all CoV sequences in GenBank are from bat CoVs.
Even though the direct transmission of bat CoVs to humans has not been evidenced yet, the creation of conditions for more frequent encounters between bat CoVs, domestic animals and humans poses a significant threat for the future (Chan et al., 2013). … The emergence of a disease is an accidental process and it is therefore impossible to predict the scenarios and dynamics of emerging infectious disease events. The attractive effect on bats of anthropized environments is a major risk factor in the emergence of novel bat-borne diseases in both humans and animals.
