OtherGround Forums OG doc. AMA on COVID-19

Edited: 4/30/20 10:07 AM
11/23/10
Posts: 243
Tomato Can -
Easters - 
Tomato Can - ACEP and AAEM released a joint statement condemning those 2 urgent care docs above, calling them reckless and their data biased:

https://www.acep.org/corona/COVID-19/covid-19-articles/acep-aaem-joint-statement-on-physician-misinformation/

So I'm seeing lots of doctors shit on these guys but so far nobody has said their data is incorrect.  What am I missing here? 


It is not that their data is incorrect, it is that they are making claims that are not supported by their data. They are either being intentionally misleading about the implications of their data, or they are morons.

Exactly. Their way of calculating fatality risk uses  a numerator/denominator that is irrelevant and their rates are thus misleading and impossible to interpret to something meaningful. At face value, that way of calculating fatality rates will make everything seem harmless - “millions of cases, small amount of deaths”, as they say.

Take the ongoing Ebola-outbreak in DR Congo for example, and use their method on data on the first year of the outbreak 2018-2019:

Population of 2,345,000. 110,000 suspected cases. Among those were 2060 confirmed cases, and 1390 deaths.

The doctors would extrapolate that 2060/110,000 * 2,345,000 = 43,915 people had been infected in the whole country. And they would then calculate an Ebola fatality rate of only 1390/43,915 = 3.17%.

No reason to be scared of Ebola, bro!

Edit: The misleading/underestimation effect of their method is actually more pronounced in COVID-19 compared to the Ebola example, because DR Congo have screened a high proportion of the population compared to the proportion of the US that has been tested for COVID-19.

4/30/20 9:03 AM
2/14/19
Posts: 321
NoNeed4aScreenName -
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the_shrike -
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Today's MedCram update - COVID-19 is really a lot worse than a flu, it's destroying blood vessel walls

Just watched that.  Frightening

Also mind boggling that there are people out there who are looking at this disease at this level.  Almost hard to believe.

 

Well prepare to have your mind boggled even more.  

This is still hypothetical level, stuff, but here he shows what could potentially be going on at a very low (detailed) level.  Basically the SAR-CoV-2 virus blocks angiotensin 1,7 from regulating the production of superoxides, which would be wreaking havoc on vessels.  

He starts off plainly saying COVID-19 is an endothelial disease.  

Son of a bitch. I could have hit this one on the head of the nail. THis is the shit I've been talking about. Seems like other researchers are taking the same stance 

 

 

A hypothesis for pathobiology and treatment of COVID?19: the centrality of ACE1/ACE2 imbalance

 

SARS viruses and Angiotensin action/signaling

Infection of cells by SARS viruses that bind ACE2 results in two effects: inhibition of ACE2 activity and

decrease of ACE2 expression in infected cells (Kuba et al., 2005; Haga et al., 2008; Glowacka et al.,

2010; Zhang et al., 2020). Indirect evidence for the latter response in COVID-19 is data showing

elevation in circulating ANG II with viral infection and increased circulating ANG II peptide with higher

viral loads (Liu et al., 2020b).

Our hypothesis is founded on the following ideas that derive from data in reports cited in ensuing

sections:

1. SARS viruses decrease ACE2 activity and expression.

2. The decrease in ACE activity creates an imbalance in signaling by ACE1 and ACE2 products

3. This imbalance increases ANG II/AGTR1 signaling and is superimposed on concurrent

pathology (e.g., chronic lung disease, cardiac remodeling in the lung and heart, respectively).

ANG II is a pivotal mediator of injury in both tissues; enhancement of its effects together with

signaling from comorbidities can increase severity of COVID-19.

4. In patients more susceptible to the damaging effects of ANG II, the decrease in ACE2 activity

by SARS viruses can unleash a cascade of injurious effects through a heightened imbalance in

the actions of the products of ACE1 versus ACE2.

5. The proposed imbalance in the signaling and actions of products of ACE1/ACE2 implies the

potential of pharmacological approaches that redress this imbalance via: a) decrease in ACE1

activity, b) blockade of AGTR1, and/or c) increase in ACE2-mediated signaling by affinity-

trapping the SARs virus, enhancement of ACE2 expression/activity, or d) by agonists for

receptors of ACE2-derived peptides

 

https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1111/bph.15082

 

That all sounds lot like what he goes through in the video.  You would understand it a lot better than I do. 

That's a review article that was just released on the 24th I believe. He's basically outlining what I have been saying is happening in the lungs. I think he's elaborating on the review.. I'm watching the med cram video now. I'm excited to see what he covers. I think that doctor is part of the journal team. THanks for the vid. 

 

It would be the same thing that is occuring the lungs but when ACE2 gets overwhelmed it no longer provides any type of protection to the lungs and then ARDS. 

 

I never bothered to bring in the free radical aspect of it (superoxide or any other ROS) but as free radicals increase you start to see lipid oxidation and protein carbynolation....

Do what’s the implication for people taking Ace inhibitors for blood pressure? Take them or not?

4/30/20 10:06 AM
2/4/09
Posts: 11182
Bot -
NoNeed4aScreenName -
Trust -
NoNeed4aScreenName - 
Trust -
EFM - 
the_shrike -
Trust -

Today's MedCram update - COVID-19 is really a lot worse than a flu, it's destroying blood vessel walls

Just watched that.  Frightening

Also mind boggling that there are people out there who are looking at this disease at this level.  Almost hard to believe.

 

Well prepare to have your mind boggled even more.  

This is still hypothetical level, stuff, but here he shows what could potentially be going on at a very low (detailed) level.  Basically the SAR-CoV-2 virus blocks angiotensin 1,7 from regulating the production of superoxides, which would be wreaking havoc on vessels.  

He starts off plainly saying COVID-19 is an endothelial disease.  

Son of a bitch. I could have hit this one on the head of the nail. THis is the shit I've been talking about. Seems like other researchers are taking the same stance 

 

 

A hypothesis for pathobiology and treatment of COVID?19: the centrality of ACE1/ACE2 imbalance

 

SARS viruses and Angiotensin action/signaling

Infection of cells by SARS viruses that bind ACE2 results in two effects: inhibition of ACE2 activity and

decrease of ACE2 expression in infected cells (Kuba et al., 2005; Haga et al., 2008; Glowacka et al.,

2010; Zhang et al., 2020). Indirect evidence for the latter response in COVID-19 is data showing

elevation in circulating ANG II with viral infection and increased circulating ANG II peptide with higher

viral loads (Liu et al., 2020b).

Our hypothesis is founded on the following ideas that derive from data in reports cited in ensuing

sections:

1. SARS viruses decrease ACE2 activity and expression.

2. The decrease in ACE activity creates an imbalance in signaling by ACE1 and ACE2 products

3. This imbalance increases ANG II/AGTR1 signaling and is superimposed on concurrent

pathology (e.g., chronic lung disease, cardiac remodeling in the lung and heart, respectively).

ANG II is a pivotal mediator of injury in both tissues; enhancement of its effects together with

signaling from comorbidities can increase severity of COVID-19.

4. In patients more susceptible to the damaging effects of ANG II, the decrease in ACE2 activity

by SARS viruses can unleash a cascade of injurious effects through a heightened imbalance in

the actions of the products of ACE1 versus ACE2.

5. The proposed imbalance in the signaling and actions of products of ACE1/ACE2 implies the

potential of pharmacological approaches that redress this imbalance via: a) decrease in ACE1

activity, b) blockade of AGTR1, and/or c) increase in ACE2-mediated signaling by affinity-

trapping the SARs virus, enhancement of ACE2 expression/activity, or d) by agonists for

receptors of ACE2-derived peptides

 

https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1111/bph.15082

 

That all sounds lot like what he goes through in the video.  You would understand it a lot better than I do. 

That's a review article that was just released on the 24th I believe. He's basically outlining what I have been saying is happening in the lungs. I think he's elaborating on the review.. I'm watching the med cram video now. I'm excited to see what he covers. I think that doctor is part of the journal team. THanks for the vid. 

 

It would be the same thing that is occuring the lungs but when ACE2 gets overwhelmed it no longer provides any type of protection to the lungs and then ARDS. 

 

I never bothered to bring in the free radical aspect of it (superoxide or any other ROS) but as free radicals increase you start to see lipid oxidation and protein carbynolation....

Do what’s the implication for people taking Ace inhibitors for blood pressure? Take them or not?

I'm speculating on the underlying mechanism of the disease. 

 

I'm in no way qualified to offer medical advice. If the doctors are saying to stay on it, i would follow their advice. 

4/30/20 10:28 AM
12/1/12
Posts: 2445
prof -
turducken - 

 

Can a doctor comment on this video?  It's one of those things where someone with legit credentials is talking in a confident manner that sounds authoritative, but as a layman you have no idea if whether what is being said is accurate or not




Jebus! That video and the comment section seem to be a conspiritard clusterfuck. Like bees to honey.

Sadly a lot of this thread is exactly those people posting these kinds of videos, "curious" if they are factual.

4/30/20 10:29 AM
12/1/12
Posts: 2446
avnersch -
mataleo1 -
Believe in the Power of One - 

Also, are there tests in the US or not? Can you clear that up at all? I know they fucked the first kit up, but is there something better?

How close to a vaccine? 

Thank you!


I'm in NYC and we do have access to tests for patients considered at risk and those with typical symptoms.

Some teams already claim they have a vaccine but it still takes testing (pharmacokinetics, safety, immunogenic responses, etc...). I'd say we're about 6 months away to having vaccines available to large populations.

Not sure how you came up with the 6 months. This is completely unrealistic. Even if everything is perfect it takes 12-18 months. For some viruses we have never been able to develop vaccines like HIV, Herpes, and non of the Coronoaviruses. 

Wanted to note that the group in Oxford talking about a Sept. vaccine just partnered with AstraZeneca so the claim has more credibility now.

4/30/20 11:00 AM
4/27/14
Posts: 24036

Interesting interview in Die Welt wiith German pathologists running the autopsies on COVID-19 patients: https://www.welt.de/wissenschaft/plus207550727/Pathologen-zu-Corona-Wichtig-welche-Vorerkrankungen-vorliegen.html. For those who don't speak German, here is the summary:

DIE WELT has a long (and for me enlightening!) interview with two pathologists at the U. Of Hannover medical school, one of them a lung pathology professor. They perform numerous autopsies on patients deceased from COVID19. Normally they spend 5% of their time doing autopsies and 95% analyzing tissue samples from living patients, mostly for suspected tumors or to help establish optimal cancer treatment plans for confirmed tumors. Nowadays — mostly COVID19 dead. Below follows a mixture of paraphrased summaries and (in quotation marks) hand-corrected machine translations from the original German.

The pathologists broadly hint that invasive respiration (“ventilators”) does more harm than good, and exposes the patients to all sorts of secondary infections [by antibiotic-resistant “hospital bugs”].
Primary infection is via nose and throat. 80% of cases are mild [and get better without treatment]. Of the remaining 20%, one-third end up in intensive care with severe lung involvement.

“Jonigk: Blood clotting occurs in the lung [capillaries], which are in the walls of the lung alveoli that serve to absorb oxygen and remove CO2. The damage causes protein to escape from the blood into the alveoli. Oxygen must somehow be transported from the air we breathe into the capillary network. That’s how we breathe. Anything that lengthens that route ensures that the patient can no longer supply himself with sufficient oxygen. It’s like playing soccer when you’ve skinned your knee: First a brown-red crust of protein and blood develops. We have a similar situation in the air bubbles. And breathing through them is massively difficult. The patient has a feeling of breathlessness, too little oxygen gets into the organism. It is more likely to be secondary to an inflammatory reaction. A downward spiral begins, which ends in a so-called shock lung. The lung and with it the patient fight for their lives.[…]”
Q: [which pre-existing conditions?]

A: “Older people with previous damage to the lungs. Patients who are dependent on medication that diminishes the immune system. And smokers, for example. Or people who live in an area with high particulate matter pollution and therefore already have pre-damaged lungs. So they are already not well before that. If an acute infection such as SARS-CoV-2 is then added, this can be enough to put the already sick patient’s life in danger.”
“ pneumonia is a bacterial infection with purulent sputum. The pus is yellow because it is made up of fatty granulocytes. Their task is to fight the enemy, the pathogen, in the body. But SARS-CoV-2 is a virus. It attacks cells directly and reprograms them. After an initial unspecific reaction, the response to this infection consists of specific T-lymphocytes, a subtype of white blood cells. These can recognize and attack virus-infected cells. We now have a large number of lymphocytes in the basic structure of the lung, which collect in the walls of the alveoli and develop their inflammatory activity there.”

Q: [what about other organs?]
“Up to 25 percent of intensive care patients have disorders of liver and kidney functions. In addition, blood coagulation often appears to be permanently disturbed. Small, local blood clots form at many sites because the inflammatory cells beat around to destroy the virus-infected cells, which include vascular cells. No matter where this occurs, it always has considerable consequences for the organ — strokes occur and sometimes extremities have to be amputated. In many organs, the occlusion of a blood vessel can be compensated. But if you have many occlusions, the blood does not flow properly, organ damage occurs, inflammatory cells do not get where they actually want to go, and the heart is also put under strain.”

Q: [is this just a COVID19-thing?]
“When you have a nasty cold with a fever, there’s always the recommendation: “Don’t go to the gym.” The basic idea behind this is that any virus can, in principle, infect any organ. Normally you have a resting heart rate of 65 or 70, but if you want to be a tough guy and go to the gym and treadmill and give it all you’ve got, you have a pulse of 150, so your heart is pumping properly. The chance of the virus infecting the heart suddenly increases dramatically. When you are infected, the body fights most viral infections with lymphocytes that go to the heart muscles and kill the infected cells. And this heart muscle inflammation is the most common reason for heart transplants in people under the age of 25.”

 
4/30/20 11:00 AM
4/27/14
Posts: 24037
“At the moment when [the blood flow in] small vessels in the lungs is disturbed, the heart has to apply increased pressure to pump the blood through the lungs at all. This places an enormous strain on the right ventricle, which is normally only responsible for a low pressure. If the pressure requirements increase, it is quickly overtaxed, resulting in acute right heart failure. The left ventricle does not pump the blood into the lungs, but into the rest of the organism. It is capable of producing a pressure four to ten times greater than the pulmonary circulation. Regardless of whether it is caused by Covid or some other infection: as soon as the pressure in the pulmonary circulation is increased and the right heart is put under pressure, the patient can quickly die. […] So when the lungs are infected, the right heart has to run at full throttle for 1.5–2 weeks and is stressed far beyond normal levels. A young, fit person is more likely to cope with this than someone who already has a previous injury. But the virus is apparently also able to damage the heart itself. And the blood clots can of course also appear in vessels in the heart. So you have a heart that is pumping strongly, and suddenly the blood supply to the heart itself goes down. Then you have two hard strains, which can already be too much for the damaged heart.”
Q: [what about pre-existing conditions?]

“There is the old saying: A healthy patient is only a patient who has not been examined well enough. For example, high blood pressure is a disease of old age. In Germany, this will be about 35 percent of the total population. Up to now, mainly elderly people in Germany have died of Covid-19, which means that most Covid-19 deaths have had hypertension. Us being Germans, we also drink a lot of alcohol, so many citizens are overweight and have a fatty liver. The patient over 60 who has no previous illness – statistically there are only few. The important thing is not that there are pre-existing conditions, but which ones. And in what context do these have an influence on the probability of survival in the case of Covid-19 disease? It’s not enough to say, “This patient had something.” Rather, the previous illnesses must be systematically uncovered in relation to the population.”
“You have to separate whether someone died of, or with, a Covid-19 infection. It’s already affecting statistics. As far as we know, in Italy a corona test was carried out on every person who died and everyone who was found to have the virus was considered to have died of corona. In the case of pre-existing conditions, a distinction must also be made between diseases that generally shorten life expectancy and diseases that specifically increase the risk of corona infection and possible complications. This is somewhat muddled in the public discussion.”

Q: [brain involvement]
A [paraphrased]: we cannot conclusively rule out direct virus involvement, but the brain is so sensitive to disturbances in blood flow that blood clots quickly lead to headaches, then strokes.
[Paraphrased] “Overall, we know a lot about what happens at the cellular level with the virus, but relatively little about what happens at the organ level. Cell cultures can only tell you so much. So here is where autopsies come in.”

Translation at https://spinstrangenesscharm.wordpress.com/2020/04/29/covid19-update-yom-haatzmaut-edition-coronahotels-for-mild-cases-in-israel-pathology-professor-discusses-what-can-be-learned-about-covid19-from-autopsies/, which also has a story about how Israel is repurposing hotels into facilities for mild COVID-19, run by the IDF, cases to free up hospital space.

4/30/20 12:26 PM
1/1/01
Posts: 65688
used2wrestle - 
prof -
turducken - 

 

Can a doctor comment on this video?  It's one of those things where someone with legit credentials is talking in a confident manner that sounds authoritative, but as a layman you have no idea if whether what is being said is accurate or not




Jebus! That video and the comment section seem to be a conspiritard clusterfuck. Like bees to honey.

Sadly a lot of this thread is exactly those people posting these kinds of videos, "curious" if they are factual.


"Modern medicine is the leading cause of death."

GTFO with that shit.

I also find it really funny that their own website is misspelled for the entire fucking video.
4/30/20 1:37 PM
4/1/11
Posts: 2250
The Stewed Owl -

Interesting interview in Die Welt wiith German pathologists running the autopsies on COVID-19 patients: https://www.welt.de/wissenschaft/plus207550727/Pathologen-zu-Corona-Wichtig-welche-Vorerkrankungen-vorliegen.html. For those who don't speak German, here is the summary:

DIE WELT has a long (and for me enlightening!) interview with two pathologists at the U. Of Hannover medical school, one of them a lung pathology professor. They perform numerous autopsies on patients deceased from COVID19. Normally they spend 5% of their time doing autopsies and 95% analyzing tissue samples from living patients, mostly for suspected tumors or to help establish optimal cancer treatment plans for confirmed tumors. Nowadays — mostly COVID19 dead. Below follows a mixture of paraphrased summaries and (in quotation marks) hand-corrected machine translations from the original German.

The pathologists broadly hint that invasive respiration (“ventilators”) does more harm than good, and exposes the patients to all sorts of secondary infections [by antibiotic-resistant “hospital bugs”].
Primary infection is via nose and throat. 80% of cases are mild [and get better without treatment]. Of the remaining 20%, one-third end up in intensive care with severe lung involvement.

“Jonigk: Blood clotting occurs in the lung [capillaries], which are in the walls of the lung alveoli that serve to absorb oxygen and remove CO2. The damage causes protein to escape from the blood into the alveoli. Oxygen must somehow be transported from the air we breathe into the capillary network. That’s how we breathe. Anything that lengthens that route ensures that the patient can no longer supply himself with sufficient oxygen. It’s like playing soccer when you’ve skinned your knee: First a brown-red crust of protein and blood develops. We have a similar situation in the air bubbles. And breathing through them is massively difficult. The patient has a feeling of breathlessness, too little oxygen gets into the organism. It is more likely to be secondary to an inflammatory reaction. A downward spiral begins, which ends in a so-called shock lung. The lung and with it the patient fight for their lives.[…]”
Q: [which pre-existing conditions?]

A: “Older people with previous damage to the lungs. Patients who are dependent on medication that diminishes the immune system. And smokers, for example. Or people who live in an area with high particulate matter pollution and therefore already have pre-damaged lungs. So they are already not well before that. If an acute infection such as SARS-CoV-2 is then added, this can be enough to put the already sick patient’s life in danger.”
“ pneumonia is a bacterial infection with purulent sputum. The pus is yellow because it is made up of fatty granulocytes. Their task is to fight the enemy, the pathogen, in the body. But SARS-CoV-2 is a virus. It attacks cells directly and reprograms them. After an initial unspecific reaction, the response to this infection consists of specific T-lymphocytes, a subtype of white blood cells. These can recognize and attack virus-infected cells. We now have a large number of lymphocytes in the basic structure of the lung, which collect in the walls of the alveoli and develop their inflammatory activity there.”

Q: [what about other organs?]
“Up to 25 percent of intensive care patients have disorders of liver and kidney functions. In addition, blood coagulation often appears to be permanently disturbed. Small, local blood clots form at many sites because the inflammatory cells beat around to destroy the virus-infected cells, which include vascular cells. No matter where this occurs, it always has considerable consequences for the organ — strokes occur and sometimes extremities have to be amputated. In many organs, the occlusion of a blood vessel can be compensated. But if you have many occlusions, the blood does not flow properly, organ damage occurs, inflammatory cells do not get where they actually want to go, and the heart is also put under strain.”

Q: [is this just a COVID19-thing?]
“When you have a nasty cold with a fever, there’s always the recommendation: “Don’t go to the gym.” The basic idea behind this is that any virus can, in principle, infect any organ. Normally you have a resting heart rate of 65 or 70, but if you want to be a tough guy and go to the gym and treadmill and give it all you’ve got, you have a pulse of 150, so your heart is pumping properly. The chance of the virus infecting the heart suddenly increases dramatically. When you are infected, the body fights most viral infections with lymphocytes that go to the heart muscles and kill the infected cells. And this heart muscle inflammation is the most common reason for heart transplants in people under the age of 25.”

 

Ltr

4/30/20 2:09 PM
1/1/01
Posts: 11822
This part from Stewed Owl's post alarmed me:

-----------------------

“When you have a nasty cold with a fever, there’s always the recommendation: “Don’t go to the gym.” The basic idea behind this is that any virus can, in principle, infect any organ. Normally you have a resting heart rate of 65 or 70, but if you want to be a tough guy and go to the gym and treadmill and give it all you’ve got, you have a pulse of 150, so your heart is pumping properly. The chance of the virus infecting the heart suddenly increases dramatically. When you are infected, the body fights most viral infections with lymphocytes that go to the heart muscles and kill the infected cells. And this heart muscle inflammation is the most common reason for heart transplants in people under the age of 25.”

------------------------


My layman's brain is saying: Hold on, if that's the case, maybe my daily exercising is more danger than help.

Like many I'm trying to stay in shape (I'm 56, no chronic health problems, BMI of 22), and that includes getting my heart rate up at some point every day. Sometimes it's jogging, often I'll also throw in some sprints or running up and down stairs to get the heart rate up. Part of it is for feeling and being fit, part for health, stave off things like hypertension, diabetes and other things that can come with getting too lazy with age.

Anyway, if that article is correct, stressing your heart while being infected with a virus can actually lead to "dramatic" increase in the possibility of the virus infecting the heart!

Well, if one is often asymptomatic for a while with COVID before symptoms show (or even are having an asymptomatic course of the disease), that suggests I may be out there running up some stairs stressing my heart while not knowing I have the virus, and hence increasing my risk of complications.

Can someone help me here? I need some 'splainin'....
4/30/20 4:20 PM
2/27/11
Posts: 11280
prof - This part from Stewed Owl's post alarmed me:

-----------------------

“When you have a nasty cold with a fever, there’s always the recommendation: “Don’t go to the gym.” The basic idea behind this is that any virus can, in principle, infect any organ. Normally you have a resting heart rate of 65 or 70, but if you want to be a tough guy and go to the gym and treadmill and give it all you’ve got, you have a pulse of 150, so your heart is pumping properly. The chance of the virus infecting the heart suddenly increases dramatically. When you are infected, the body fights most viral infections with lymphocytes that go to the heart muscles and kill the infected cells. And this heart muscle inflammation is the most common reason for heart transplants in people under the age of 25.”

------------------------


My layman's brain is saying: Hold on, if that's the case, maybe my daily exercising is more danger than help.

Like many I'm trying to stay in shape (I'm 56, no chronic health problems, BMI of 22), and that includes getting my heart rate up at some point every day. Sometimes it's jogging, often I'll also throw in some sprints or running up and down stairs to get the heart rate up. Part of it is for feeling and being fit, part for health, stave off things like hypertension, diabetes and other things that can come with getting too lazy with age.

Anyway, if that article is correct, stressing your heart while being infected with a virus can actually lead to "dramatic" increase in the possibility of the virus infecting the heart!

Well, if one is often asymptomatic for a while with COVID before symptoms show (or even are having an asymptomatic course of the disease), that suggests I may be out there running up some stairs stressing my heart while not knowing I have the virus, and hence increasing my risk of complications.

Can someone help me here? I need some 'splainin'....

Yeah i wonder the same.

Im in the same boat.

 

4/30/20 4:22 PM
4/27/14
Posts: 24039

Ditto, wondering about cardio as a risk factor.

Edited: 4/30/20 4:37 PM
11/23/10
Posts: 245
prof - This part from Stewed Owl's post alarmed me:

-----------------------

“When you have a nasty cold with a fever, there’s always the recommendation: “Don’t go to the gym.” The basic idea behind this is that any virus can, in principle, infect any organ. Normally you have a resting heart rate of 65 or 70, but if you want to be a tough guy and go to the gym and treadmill and give it all you’ve got, you have a pulse of 150, so your heart is pumping properly. The chance of the virus infecting the heart suddenly increases dramatically. When you are infected, the body fights most viral infections with lymphocytes that go to the heart muscles and kill the infected cells. And this heart muscle inflammation is the most common reason for heart transplants in people under the age of 25.”

------------------------


My layman's brain is saying: Hold on, if that's the case, maybe my daily exercising is more danger than help.

Like many I'm trying to stay in shape (I'm 56, no chronic health problems, BMI of 22), and that includes getting my heart rate up at some point every day. Sometimes it's jogging, often I'll also throw in some sprints or running up and down stairs to get the heart rate up. Part of it is for feeling and being fit, part for health, stave off things like hypertension, diabetes and other things that can come with getting too lazy with age.

Anyway, if that article is correct, stressing your heart while being infected with a virus can actually lead to "dramatic" increase in the possibility of the virus infecting the heart!

Well, if one is often asymptomatic for a while with COVID before symptoms show (or even are having an asymptomatic course of the disease), that suggests I may be out there running up some stairs stressing my heart while not knowing I have the virus, and hence increasing my risk of complications.

Can someone help me here? I need some 'splainin'....

Don’t stress it, you’re doing the right thing. That statement is not well-documented by evidence. The rest of Stewed Owl’s post is on-point, but that part irked me a little.

It’s a two-part question:

1: Risk of getting infected: There is not a great quality of evidence behind it, but physical exercise seems to lower the risk of getting upper respiratory tract infections in the average person. Long-term/very strenious exercise in athletes seems to increase the risk.

2: Risk of harm if infected: Even less evidence, but in an animal study from the 1980’ies, prolonged/strenious physical activity in mice infected with influenza or coxsackie-virus (another common upper respiratory tract virus) increased mortality. There’s never been a similar study made in humans as far as I know  (and good luck getting one approved by a scientific ethics committee).

I would not worry. If anything you’re reducing your risk of getting the infection in the first place. If you get infected anyway, I think your body will make you rest as needed when you feel sick.

Edit: Physically preconditioned/fit people and animals in studies do better than the rest in most types of infection, so that would be another argument for keeping up the physical activity.

4/30/20 4:55 PM
1/1/01
Posts: 11825
Job Security - 
prof - This part from Stewed Owl's post alarmed me:

-----------------------

“When you have a nasty cold with a fever, there’s always the recommendation: “Don’t go to the gym.” The basic idea behind this is that any virus can, in principle, infect any organ. Normally you have a resting heart rate of 65 or 70, but if you want to be a tough guy and go to the gym and treadmill and give it all you’ve got, you have a pulse of 150, so your heart is pumping properly. The chance of the virus infecting the heart suddenly increases dramatically. When you are infected, the body fights most viral infections with lymphocytes that go to the heart muscles and kill the infected cells. And this heart muscle inflammation is the most common reason for heart transplants in people under the age of 25.”

------------------------


My layman's brain is saying: Hold on, if that's the case, maybe my daily exercising is more danger than help.

Like many I'm trying to stay in shape (I'm 56, no chronic health problems, BMI of 22), and that includes getting my heart rate up at some point every day. Sometimes it's jogging, often I'll also throw in some sprints or running up and down stairs to get the heart rate up. Part of it is for feeling and being fit, part for health, stave off things like hypertension, diabetes and other things that can come with getting too lazy with age.

Anyway, if that article is correct, stressing your heart while being infected with a virus can actually lead to "dramatic" increase in the possibility of the virus infecting the heart!

Well, if one is often asymptomatic for a while with COVID before symptoms show (or even are having an asymptomatic course of the disease), that suggests I may be out there running up some stairs stressing my heart while not knowing I have the virus, and hence increasing my risk of complications.

Can someone help me here? I need some 'splainin'....

Don’t stress it, you’re doing the right thing. That statement is not well-documented by evidence. The rest of Stewed Owl’s post is on-point, but that part irked me a little.

It’s a two-part question:

1: Risk of getting infected: There is not a great quality of evidence behind it, but physical exercise seems to lower the risk of getting upper respiratory tract infections in the average person. Long-term/very strenious exercise in athletes seems to increase the risk.

2: Risk of harm if infected: Even less evidence, but in an animal study from the 1980’ies, prolonged/strenious physical activity in mice infected with influenza or coxsackie-virus (another common upper respiratory tract virus) increased mortality. There’s never been a similar study made in humans as far as I know  (and good luck getting one approved by a scientific ethics committee).

I would not worry. If anything you’re reducing your risk of getting the infection in the first place. If you get infected anyway, I think your body will make you rest as needed when you feel sick.

Edit: Physically preconditioned/fit people and animals in studies do better than the rest in most types of infection, so that would be another argument for keeping up the physical activity.



Many thanks!
4/30/20 9:58 PM
2/4/09
Posts: 11194

Clinical trial guys. Does this significantly change the primary outcomes of the study?

 

5/1/20 4:16 AM
11/23/10
Posts: 246
NoNeed4aScreenName -

Clinical trial guys. Does this significantly change the primary outcomes of the study?

 

As much as I dislike Didier, and as much as he’s the last person in the world entitled to criticize a scientific study for lack of transparency - he’s got a point here. Mata has more experience with RCTs than I, but here’s my take until he’s back:

It is a big difference to omit death as an outcome. It’s the most clinically important outcome, and it is also a competing risk to the other chosen outcomes, so you have to take it into account in the analysis of those tol. Still, they’re registering deaths, and will be analyzing and reporting on those as well, so it’s ultimately of less importance, more a question of formality and semantics.

The rest of the changes to the outcome are probably of less importance. It’s probably a question of adapting the 8-level ordinal outcome to a binomial model because they had issues with variance and/or statistical power. They probably had little-to-no data available before the trial to make accurate calculations of statistical power, so perhaps it is to be expected that they had to change it along the way. Still, it’s so far into the study that they changed it, that it’s susceptible to being an opportunistic choice. They must have had enough results in by that point to see which outcome yielded which result.

One thing to note though: This is a bonanza just like with tamiflu and swine flu, but crazier. The study investigators weren’t ready to make these preliminary results public. I can’t remember authorities ever disclosing preliminary results like this before. The study is still ongoing, the conclusions may change, and you can’t make valid preliminary conclusions like this unless you had a plan for it at the start.

TLDR: It’s very good news and seems to show that remdesivir is probably more potent against COVID-19 than tamiflu is against influenza. It’s premature to draw any conclusions until the investigators finish the study and report it in detail in a few weeks.

5/1/20 9:43 AM
2/4/09
Posts: 11195
Job Security -
NoNeed4aScreenName -

Clinical trial guys. Does this significantly change the primary outcomes of the study?

 

As much as I dislike Didier, and as much as he’s the last person in the world entitled to criticize a scientific study for lack of transparency - he’s got a point here. Mata has more experience with RCTs than I, but here’s my take until he’s back:

It is a big difference to omit death as an outcome. It’s the most clinically important outcome, and it is also a competing risk to the other chosen outcomes, so you have to take it into account in the analysis of those tol. Still, they’re registering deaths, and will be analyzing and reporting on those as well, so it’s ultimately of less importance, more a question of formality and semantics.

The rest of the changes to the outcome are probably of less importance. It’s probably a question of adapting the 8-level ordinal outcome to a binomial model because they had issues with variance and/or statistical power. They probably had little-to-no data available before the trial to make accurate calculations of statistical power, so perhaps it is to be expected that they had to change it along the way. Still, it’s so far into the study that they changed it, that it’s susceptible to being an opportunistic choice. They must have had enough results in by that point to see which outcome yielded which result.

One thing to note though: This is a bonanza just like with tamiflu and swine flu, but crazier. The study investigators weren’t ready to make these preliminary results public. I can’t remember authorities ever disclosing preliminary results like this before. The study is still ongoing, the conclusions may change, and you can’t make valid preliminary conclusions like this unless you had a plan for it at the start.

TLDR: It’s very good news and seems to show that remdesivir is probably more potent against COVID-19 than tamiflu is against influenza. It’s premature to draw any conclusions until the investigators finish the study and report it in detail in a few weeks.

It doesn't seem like this is much better than HCQ butbthe media really is touting this one. 

 

Could it be sue to patent and price. I think its bullshit. Neither seem to be super great

5/1/20 12:11 PM
1/13/10
Posts: 47795

My older cousin and his wife were on Facebook all day yesterday posting articles and memes downplaying this pandemic. They believe it’s a government hoax and not as bad as the media etc are making it out to be. He mentions that it’s a business, and hospitals are getting paid more if doctors write down a patient being Covid or deemed Ventilator necessary. 
 

https://amp.usatoday.com/amp/3000638001

5/1/20 1:43 PM
11/23/10
Posts: 248
NoNeed4aScreenName -
Job Security -
NoNeed4aScreenName -

Clinical trial guys. Does this significantly change the primary outcomes of the study?

 

As much as I dislike Didier, and as much as he’s the last person in the world entitled to criticize a scientific study for lack of transparency - he’s got a point here. Mata has more experience with RCTs than I, but here’s my take until he’s back:

It is a big difference to omit death as an outcome. It’s the most clinically important outcome, and it is also a competing risk to the other chosen outcomes, so you have to take it into account in the analysis of those tol. Still, they’re registering deaths, and will be analyzing and reporting on those as well, so it’s ultimately of less importance, more a question of formality and semantics.

The rest of the changes to the outcome are probably of less importance. It’s probably a question of adapting the 8-level ordinal outcome to a binomial model because they had issues with variance and/or statistical power. They probably had little-to-no data available before the trial to make accurate calculations of statistical power, so perhaps it is to be expected that they had to change it along the way. Still, it’s so far into the study that they changed it, that it’s susceptible to being an opportunistic choice. They must have had enough results in by that point to see which outcome yielded which result.

One thing to note though: This is a bonanza just like with tamiflu and swine flu, but crazier. The study investigators weren’t ready to make these preliminary results public. I can’t remember authorities ever disclosing preliminary results like this before. The study is still ongoing, the conclusions may change, and you can’t make valid preliminary conclusions like this unless you had a plan for it at the start.

TLDR: It’s very good news and seems to show that remdesivir is probably more potent against COVID-19 than tamiflu is against influenza. It’s premature to draw any conclusions until the investigators finish the study and report it in detail in a few weeks.

It doesn't seem like this is much better than HCQ butbthe media really is touting this one. 

 

Could it be sue to patent and price. I think its bullshit. Neither seem to be super great

If the preliminary results hold, then - as opposed to the HCQ-studies - this study actually examines the type of patients we want to treat (it is restricted to severe cases with long stays in hospital). So whereas we know nothing about the effect of HCQ in practice, remdesivir has that going for it.

The time-to-recovery measure of effect is somewhat similar to the effect measure that was able to show an effect of tamiflu against influenza (no effect has been shown of tamiflu on mortality afaik)  but remdesivir seems to shorten it by half a week, where tamiflu only shortened it by about 24 hours iirc (and only if treatment was initiatied shortly after symptom onset). So even if it’s a bullshit measure, it’s better bullshit than tamiflu.

And the old primary outcome (including deaths) is still going to be analyzed in the planned fashion, according to their protocol, just as a secondary outcome. In the end, not much has changed except the formalities, but I think they should have stuck to their guns and kept it as a primary outcome for sake of consistency. It’s just weird and unnecessary to switch them around. I don’t understand it at all - they will get an absurdly high impact even if they technically  only report a significant secondary outcome effect. It’s not like they have to inflate their results to get published. And even as a secondary outcome it would surely create enough equipoise that remdesivir would become the standard of care, similarly to what happened with tamiflu. Strange times.

5/1/20 4:19 PM
12/1/12
Posts: 2449

Remdesivir approved.

Obviously it's not a cure but it's better than nothing and at least based on a randomized dataset. Very sad how HCQ become a political debate and through this, fauci was labelled a science denier and the BARDA guy got reassigned.

5/1/20 7:06 PM
9/8/02
Posts: 26079
Buddy of mine is a police officer here in California. The city tested 200 officers this week. Of the 200, only one officer had anti-bodies, everyone else negative. This officer never knew he was even sick. These guys ride in cars together, cough in the same space, interact with the public, some even live in bunks at the station during the week. One person infected.

There were 3 officers in particular that were REALLY sick earlier in the year, and everyone in the dept joked they probably had Corona Virus...all three negative. They had a bad flu.
Edited: 5/2/20 4:04 AM
11/23/10
Posts: 250
jcblass - Buddy of mine is a police officer here in California. The city tested 200 officers this week. Of the 200, only one officer had anti-bodies, everyone else negative. This officer never knew he was even sick. These guys ride in cars together, cough in the same space, interact with the public, some even live in bunks at the station during the week. One person infected.

There were 3 officers in particular that were REALLY sick earlier in the year, and everyone in the dept joked they probably had Corona Virus...all three negative. They had a bad flu.

TBH I’m starting to question if antibody testing of COVID-19 is even useful on a population level in the current state. So many different test kits around, many of them not good enough to be reliable, and wildly differing estimates from survey to survey, even when accounting for the expected test inaccuracies. And the mounting evidence of weak antibody responses in mild/non-hospitalized cases.

A study of 5500 blood donors here in Denmark in the last week yielded a positive rate of 1.9%. An earlier test of blood donors in our capital region a months ago found a 2.5% positivity rate. So the estimated ratio of diagnosed vs. undiagnosed COVID-19 cases went from x30-80 to x12-29. In the last month, we’ve started opening up, and since reopening R increased from 0.6 to 0.9 according to estimates. Either spreading has been massively haulted while testing has increased, or the tests aren’t accurate at all for making these estimates.

5/2/20 9:12 AM
11/24/09
Posts: 2371

the dr hasn't been here in a few days i hope all is well

then again it may just be because you guys hijacked this thread 

5/2/20 10:18 AM
12/1/12
Posts: 2450
akbar87 -

the dr hasn't been here in a few days i hope all is well

then again it may just be because you guys hijacked this thread 

I was thinking the exact same thing. He's usually very responsive.

5/2/20 10:19 AM
1/1/01
Posts: 27136
Job Security -
NoNeed4aScreenName -

Clinical trial guys. Does this significantly change the primary outcomes of the study?

 

As much as I dislike Didier, and as much as he’s the last person in the world entitled to criticize a scientific study for lack of transparency - he’s got a point here. Mata has more experience with RCTs than I, but here’s my take until he’s back:

It is a big difference to omit death as an outcome. It’s the most clinically important outcome, and it is also a competing risk to the other chosen outcomes, so you have to take it into account in the analysis of those tol. Still, they’re registering deaths, and will be analyzing and reporting on those as well, so it’s ultimately of less importance, more a question of formality and semantics.

The rest of the changes to the outcome are probably of less importance. It’s probably a question of adapting the 8-level ordinal outcome to a binomial model because they had issues with variance and/or statistical power. They probably had little-to-no data available before the trial to make accurate calculations of statistical power, so perhaps it is to be expected that they had to change it along the way. Still, it’s so far into the study that they changed it, that it’s susceptible to being an opportunistic choice. They must have had enough results in by that point to see which outcome yielded which result.

One thing to note though: This is a bonanza just like with tamiflu and swine flu, but crazier. The study investigators weren’t ready to make these preliminary results public. I can’t remember authorities ever disclosing preliminary results like this before. The study is still ongoing, the conclusions may change, and you can’t make valid preliminary conclusions like this unless you had a plan for it at the start.

TLDR: It’s very good news and seems to show that remdesivir is probably more potent against COVID-19 than tamiflu is against influenza. It’s premature to draw any conclusions until the investigators finish the study and report it in detail in a few weeks.

thanks!