wuhan - coronavirus

[Pen]

7 minutes ago, square_25 said:

Right, that’s what I’m trying to express. It’s now clear that the risks of death are an order of magnitude bigger than the flu. It’s also clear that there are long-term effects we don’t fully understand. So then evidence of specific damage winds up concerning me. I am very well aware it may wind up overblown, but since I have to make decisions based on my perception of the risk, I don’t feel safe assuming they are actually overblown without evidence.

 

Based on my experience with my own relatives in health care, perception of risk also differs with specialty.  Dermatologist and psychiatrist (seeing medically less big deal aspects) have different views than cardiologist (seeing more severe damage aspects). They obviously see a different subset of patients. 

[EmseB]

6 minutes ago, square_25 said:

I mean, you can’t randomize studying the effects of a disease!! That’d be unethical... 

You can have control arms of healthy individuals though, right? Otherwise, where is the baseline? It can't be a doctor saying, "I've never seen this before."

For in vitro stuff, again, you can damage cells with a lot of otherwise innocuous substances in vitro and not be able to draw any conclusions. You can also do autopsies of very sick people and find very damaged organs. We have to have something to compare this to in order to make claims about covid in particular.

[Ausmumof3]

4 hours ago, Pen said:

Link? 

I heard an interview with a Dr from China a couple of months ago. (I can’t recall name, but that sounds familiar.) Probably same person, but different interview. Her English was not very good.  I don’t recall word “mutated” from what I had heard. 

  My recollection is that she said SARS2 was a laboratory virus, and one that was altered from normal bat virus. Her statement came from having worked in China.  Idk how reliable.  Personally, I do believe similar assertion by Luc Montagnier  based on study of the genome. I think what he says, that he is an old man and has nothing much to lose by speaking the truth is true. Further, Montagnier being French isn’t so much a part of the current US political climate.   I think a younger dissident wanting a place in a new country might have more reason to be untruthful, but I gave it more of a listen because it jived at least in part with what Montagnier had said.  It also had a small amount of support from the Australian researcher who, iirc, (at Flinders? I cant keep his name in my head) you had given links to, who said that SARS2 could have been out of a lab.

. Montagnier, iirc, had explained some about how a virus can be human altered such that ithe alteration does not look obviously unnatural .  It did have important implications as to effects on people and vaccines etc.   IIRC Dr. Montagnier suggested possible positive reason for the altered virus as being a search for an HIV vaccine.  

OTOH Dr Yan tended, iirc, to suggest nefariousness as reason for the altered virus such as biological/germ warfare research. 

 

I believe I have heard that laboratory induced mutation can be a way to alter virus (that doesn’t show up as manmade if WHO or CDC are looking at it) and maybe that’s where the word “mutate” came from in interview you heard? 

And Dr Luc Montagnier said that it could be expected to lose the HIV sequences fairly quickly? Maybe that type of change could lead to word “mutate”? 

 

 

 

 

The person I heard had family left behind and my understanding was that besides English being a problem, she was trying to avoid endangering them with what she said. 

If I can find interview you heard, I’ll listen and try to tell you what I understand from it. 

I can’t find the original link I saw but this has a link to it, I’m just not sure if it’s the full unedited version.

https://www.chroniclelive.co.uk/news/tv/coronavius-whistle-blower-loose-women-18918201.amp?__twitter_impression=true

nikolai petrovsky is the person in Australia and he’s also behind one of the vaccines being worked on here so I think pretty credible.  His idea is more that the virus has been grown in human cells and adapted to them for a while in a lab rather than modified because he says they are too perfectly adapted for infecting humans to have jumped directly from an animal source I think.

[Ausmumof3]

https://www.thetimes.co.uk/article/israel-becomes-first-nation-to-announce-a-second-coronavirus-lockdown-mbtfnwbrd
 

its looks like Israel is going into a second lockdown 

[Ausmumof3]

https://amp.france24.com/en/20200912-france-records-over-10-000-covid-19-cases-in-24-hours-for-first-time?__twitter_impression=true
 

10,000 cases in France in a single day.

[Ausmumof3]

https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2020.25.36.2001542

“In March 2020, we observed an outbreak of COVID-19 among a relatively homogenous group of 199 young (median age 21 years; 87% men) Swiss recruits. By comparing physical endurance before and in median 45 days after the outbreak, we found a significant decrease in predicted maximal aerobic capacity in COVID-19 convalescent but not in asymptomatically infected and SARS-CoV-2 naive recruits. This finding might be indicative of lung injury after apparently mild COVID-19 in young adults.”

and

“The median time between COVID-19 diagnosis and the fitness test was 45 days (range: 31–58 days), while the baseline test had been performed 3 months before the COVID-19 outbreak at the Armed Forces Base (Table)”

 

[Pen]

38 minutes ago, Ausmumof3 said:

I can’t find the original link I saw but this has a link to it, I’m just not sure if it’s the full unedited version.

https://www.chroniclelive.co.uk/news/tv/coronavius-whistle-blower-loose-women-18918201.amp?__twitter_impression=true

nikolai petrovsky is the person in Australia and he’s also behind one of the vaccines being worked on here so I think pretty credible.  His idea is more that the virus has been grown in human cells and adapted to them for a while in a lab rather than modified because he says they are too perfectly adapted for infecting humans to have jumped directly from an animal source I think.

 

I wish I could more easily understand Yan and that she would speak slower.

I found this which looks like a more full version:

https://youtu.be/7Lq3_rsBJ9w

 

I think “disappeared” means literally disappeared not just a work issue (sent to a forced labor /“re-education” camp, for example).  Don’t cross the red line was a Xi warning, iirc: https://www.ndtv.com/world-news/dont-cross-red-line-chinas-president-tough-message-in-hong-kong-1719214

 

(It has levels including discrediting the person, threats to family, etc.   afaik)

 

My posts are disappearing so I’ll try posting this now and doing more on a few minutes rather than trying to write more and have it vanished 

Edited September 12, 2020 by Pen

[Pen]

https://youtu.be/7Lq3_rsBJ9w

Around 5 minutes in, she is clearly saying it was laboratory modified and not a wet market etc accident type issue, that “wet market” explanation is a cover up.

 

I was listening for word “mutated” and didn’t hear that. I may listen again to see if I catch that. She gave the names of original coronaviruses that the lab had made modifications from (around 4 min in), but I couldn’t catch those.   

Maybe when paper comes out, it will be easier to follow in writing. 

 

Edited September 12, 2020 by Pen

[Corraleno]

45 minutes ago, EmseB said:

You can have control arms of healthy individuals though, right? Otherwise, where is the baseline? It can't be a doctor saying, "I've never seen this before."

For in vitro stuff, again, you can damage cells with a lot of otherwise innocuous substances in vitro and not be able to draw any conclusions. You can also do autopsies of very sick people and find very damaged organs. We have to have something to compare this to in order to make claims about covid in particular.

Well you can't really have "a control arm of healthy individuals" in a study that relies on chopping up heart tissue. If your argument is that maybe people who die of influenza also have the same pattern of heart damage that these researchers found (i.e., "distinguishing features of myofibrillar fragmentation in cardiomyocytes due to SARS-CoV-2 exposure are extremely precise, ordered disruption to the sarcomeric structure and complete dissolution of the cardiac contractile machinery"), then I suppose researchers could try to obtain post-mortem heart tissue from patients who died of influenza or other viruses and see how prevalent it is. But the possibility that this may occur with other viruses doesn't refute the theory that this is the mechanism by which Covid causes heart damage, which is the point of the research.

Edited September 12, 2020 by Corraleno

[EmseB]

10 minutes ago, square_25 said:

I had the strong impression other respiratory viruses didn’t directly attack other organs. Is that wrong?

I don't know why other viruses wouldn't, I guess. They manifest as respiratory viruses because that is where the most ace 2 receptor cells are, but we have them in other organs in our bodies (heart and kidneys and gi). I think of other viruses that cause cold symptoms but also a rash, etc. Or nausea with cold symptoms maybe? I could very well be wrong, but it seems like at least other coronaviruses would use the same mechanisms. I guess I've never thought that colds only impact the parts of the body where I'm directly experiencing symptoms.

[Corraleno]

13 minutes ago, square_25 said:

If I remember correctly, viruses like colds or flus cause heart inflammation without actually actively infecting those tissues. COVID seems like it actually does infect them.

But that’s my understanding and I’m not a doctor. I’d be grateful if someone who understood this better than me chimed in.

I don't know about the direct infection thing, but my understanding (although I could be wrong) is that what makes that research significant is that the damage they found is structural, and it's permanent. People can recover from the inflammation of myocarditis, but when the muscle fibers in your heart are severed, there's nothing the body can do to repair that, so it represents a permanent loss of function. Since the only patients whose tissue they had access to are already dead, they can't know for sure if the same type of damage (if not the extent of the damage) may also occur in milder cases, but they seemed to feel that it was significant that only one of the three patients had been diagnosed with myocarditis. But obviously we need more research in this area.

[EmseB]

36 minutes ago, Corraleno said:

Well you can't really have "a control arm of healthy individuals" in a study that relies on chopping up heart tissue. If your argument is that maybe people who die of influenza also have the same pattern of heart damage that these researchers found (i.e., "distinguishing features of myofibrillar fragmentation in cardiomyocytes due to SARS-CoV-2 exposure are extremely precise, ordered disruption to the sarcomeric structure and complete dissolution of the cardiac contractile machinery"), then I suppose researchers could try to obtain post-mortem heart tissue from patients who died of influenza or other viruses and see how prevalent it is. But the possibility that this may occur with other viruses doesn't refute the theory that this is the mechanism by which Covid causes heart damage, which is the point of the research.

You can examine people who have died of other things, though. And again, if you're only examining people who have gotten so sick so as to have died from covid, a)you already have quite a selection bias right there that is necessarily going to involve maybe sepsis and multi-organ failure, and b) you need to control for people with prior heart issues really well, especially since we know that prior disease means people are more likely to die of covid.

These are not my pet theories or kookiness, it's stuff I've seen experts bring to the forefront about these particular papers and subsequent headlines.

[Ausmumof3]

https://www.statnews.com/2020/09/12/astrazeneca-covid19-vaccine-trial-resumes-uk/
 

astra Zeneca trial is recommencing.

[Lanny]

On 9/11/2020 at 2:35 AM, EmseB said:

I am reading of anti-lockdown protests and government retaliation in Colombia. Hoping @Lanny is okay.

 

Hello and thank you for thinking about us! We are doing great. 🙂    I am not sure if these protests have anything to do with the COVID-19 lockdown. We have been in Quarantine for 6 months, but they are beginning to ease that now and we now have a few Domestic airline flights operating.  I believe the protests are (supposedly from what I've read) protesting someone who died after rough treatment from the National Police (Policia Nacional) in Bogota. Normally the protests are infrequent and we have no idea why they are protesting, other than they just want to disrupt traffic and do vandalism.  We live in Cali, in S.W. Colombia.   We have anti-riot Police here in Colombia. Their acronym is ESMAD.  They are very tough and I wouldn't want to have a problem with one of them.  🙂    Or, any of the regular Police.  In 25+ years, I have never had a problem with the Police here.  🙂

[EmseB]

15 minutes ago, square_25 said:

Yeah, and hopefully those comparisons will be done. I don’t think you’re being kooky, I just think we both don’t know enough to make intelligent deductions from the data. 

Well, I think I can read other people making intelligent deductions from the data. That's what helps me understand most of it, to be honest.

I do think public health decisions are being driven by these preprints, and by people who are not dissecting the studies or thinking about them with a critical eye on the science. And amplified in the media by like 1000%. And causing people to feel freaked out perhaps unnecessarily, or at least without complete information for people like you and me.

I am honestly really concerned about the sheer volume of unvetted data being published and consumed as sensationalist headlines AND the vetted data is letting stuff like the Surgisphere debacle just slide right by.

[Corraleno]

5 minutes ago, EmseB said:

You can examine people who have died of other things, though. And again, if you're only examining people who have gotten so sick so as to have died from covid, a)you already have quite a selection bias right there that is necessarily going to involve maybe sepsis and multi-organ failure, and b) you need to control for people with prior heart issues really well, especially since we know that prior disease means people are more likely to die of covid.

These are not my pet theories or kookiness, it's stuff I've seen experts bring to the forefront about these particular papers and subsequent headlines.

Did you read the actual paper we're talking about? Your comments make it sound like they just found some generic heart damage that could just as easily have been caused by lots of other things, or could have been due to pre-existing health conditions. The damage the UCSF team found in both the in vitro samples and the autopsy samples is VERY specific:

"“Widespread myofibrillar disruption throughout the cytoplasm, which manifested as a unique pattern of very specific periodic cleavage of myofibrils into individual sarcomeric units of identical size but without any alignment. <snip> The striking consistency and periodicity of this fragmentation suggests it is the product of cleavage by a specific protease…” and then they go on to describe the mechanism by which they believe this may be caused by a specific SARS-CoV-2 protease.

This isn't just edema or inflammation or generic myocarditis, this is a very specific and "unique" pattern of damage, which the lead researcher said he had never ever seen before in a decade of research on myocytes, and it was found in both the in vitro samples (which obviously did not have any pre-existing health conditions) as well as in all three patients who died. 

If you have read specific criticism of the UCSF paper (not the German paper, I've seen plenty of criticism of that), I would be grateful if you would link it, because I would very much like to read it.

 

[EmseB]

15 minutes ago, Corraleno said:

Did you read the actual paper we're talking about? Your comments make it sound like they just found some generic heart damage that could just as easily have been caused by lots of other things, or could have been due to pre-existing health conditions. The damage the UCSF team found in both the in vitro samples and the autopsy samples is VERY specific:

"“Widespread myofibrillar disruption throughout the cytoplasm, which manifested as a unique pattern of very specific periodic cleavage of myofibrils into individual sarcomeric units of identical size but without any alignment. <snip> The striking consistency and periodicity of this fragmentation suggests it is the product of cleavage by a specific protease…” and then they go on to describe the mechanism by which they believe this may be caused by a specific SARS-CoV-2 protease.

This isn't just edema or inflammation or generic myocarditis, this is a very specific and "unique" pattern of damage, which the lead researcher said he had never ever seen before in a decade of research on myocytes, and it was found in both the in vitro samples (which obviously did not have any pre-existing health conditions) as well as in all three patients who died. 

If you have read specific criticism of the UCSF paper (not the German paper, I've seen plenty of criticism of that), I would be grateful if you would link it, because I would very much like to read it.

 

Unrelated, but did you notice that the one you linked has already been corrected/amended in some way? There's a red box towards the top with a link to a newer version. I don't know exactly what's changed other than the first line of the abstract (c&p below) so I'm looking at that and hunting the links for you that I saw a few days ago.

"COVID-19 causes cardiac dysfunction in up to 50% of patients,"

Vs.

"Although COVID-19 causes cardiac dysfunction in up to 25% of patients"

[EmseB]

Just now, square_25 said:

But papers are also making deductions from the data. There's no reason that the more concerned people publishing the papers have to be wrong, and the people who are less concerned have to be right. It's just different interpretations of the data, and there's currently no consensus. That means it's worthwhile paying attention to both sides. 

 

I mean... that's science for you. People always do release preprints -- that's how things work in most sciences, including in math. It's just that mainstream media has much more interest in them now. 

If one is an intelligent consumer of science, then one does sees the corrections. I agree that it's a problem that the media jumps on the sensational paper and not on the 10 papers that then show no effect, but that's always been the case. Hence the coverage of the "chocolate prolongs your life for 10 years, scientists say!!" and not much coverage of the "...actually, not if you do proper statistical analysis it doesn't." 

I don't know that public health decisions ARE being driven by these preprints all that much. Do you mean the decision to pause sports? Because otherwise, I'd say that if anything, our public health decisions have been way too far behind the data -- too inertial, not too reactive. In my opinion, it should have been obvious from the data not to open restaurants and to mandate masking and to worry about air conditioning... people were too slow. 

Well, I disagree with just about all of this when it comes to the how's and whys but my eyes are crossing on my phone.

If someone is publishing something that is an objective misrepresentation of the data, or overstating risk of severe illness, and the math is very obviously wrong, or a database is falsified or WHATEVER the issue that is a huge problem if we even react a little bit. For instance, pausing sports, whether we want it to or not, causes millions of dollars to be lost in jobs, scholarships lost, etc. And you will get no argument from me on that score if we're talking about saving tens or dozens of lives due to heart damage from covid. But my feeling after reading is there is much greater risk to football players from things like TBI rather than covid and we don't stop them playing football (maybe we should!).

Anyway, I am not talking about a simple disagreement on evaluation of accurate data. I am talking about disagreement on the validity of the data and research itself.

[Corraleno]

11 minutes ago, EmseB said:

Unrelated, but did you notice that the one you linked has already been corrected/amended in some way? There's a red box towards the top with a link to a newer version. I don't know exactly what's changed other than the first line of the abstract (c&p below) so I'm looking at that and hunting the links for you that I saw a few days ago.

"COVID-19 causes cardiac dysfunction in up to 50% of patients,"

Vs.

"Although COVID-19 causes cardiac dysfunction in up to 25% of patients"

They changed that because the reference they originally cited for that statistic was the German study, which was later amended. But that is just general background info that is not tied to their own study. I haven't compared every word of the first and second versions, but from what I have looked at, they have not seen changes to their own results.

[EmseB]

@Corraleno, this was the original critique of the original link you posted. There is more cardiology twitter discussion of more issues with the paper itself.

Second tweet of his just for fun:

 

[EmseB]

6 minutes ago, square_25 said:

@EmseB -- you gotta give me at least a bit of credit for knowing how things work in academia, lol. I'm married to a mathematician, and both my dad and my first stepdad are professors who publish papers all the time. (I've proofread both of their papers and inserted the articles "a" and "the" where appropriate, because as Russian speakers, they can't manage them, lol.) Oh, and I have a math Ph.D, so I'm really no stranger to academia. So I do happen to know how the publishing process works for the sciences. 

I can give you credit! I have however read many academic types very concerned about the way science is being done and published wrt covid.

[Corraleno]

10 minutes ago, EmseB said:

For instance, pausing sports, whether we want it to or not, causes millions of dollars to be lost in jobs, scholarships lost, etc. And you will get no argument from me on that score if we're talking about saving tens or dozens of lives due to heart damage from covid. But my feeling after reading is there is much greater risk to football players from things like TBI rather than covid and we don't stop them playing football (maybe we should!).

Personally I do believe that unless football can be modified to significantly reduce or eliminate the risk of TBI, then it should be stopped, so I find this argument really uncompelling — lots of college football players may get brain injuries, so if a dozen or so drop dead on the field because of undiagnosed myocarditis, that's a reasonable price to pay so that other people can make money? 

I happen to have a kid who's one of the top athletes in his sport (international medalist, medaled at the last Olympic qualifier, was on the Olympic selection list, etc.) and if he tests positive this year he has already decided he will sit out the season rather than take on the risks associated with strenuous training with possibly undiagnosed heart damage.

[EmseB]

15 minutes ago, square_25 said:

Well, yeah, the Surgisphere thing was awful. That was bad science and should have been caught and ugh.

As for the math being obviously wrong, I gotta tell you -- medical researchers are often not that good at math and mess it up all the darn time. They don't have a background in statistics and often just run the numbers in their software, which can lead to ridiculous numbers they don't catch because they don't know what the numbers are supposed to be. That's not always evidence of ill intent -- it's as often evidence of rushing. 

We've already had athletes die from heart attacks, no? And there's plenty of evidence of people with serious heart irregularities that are not just in these new preprints. If it was just ONE big paper that had tons of mistakes, I'd agree with you. 

I am not suggesting ill intent, but sloppiness in the interest of being firstor publishing the most or just fatigue in trying times. Why do I believe they were sloppy with one set of data and not another, or not their conclusions?

Bolded -- you mean generally or because of covid? Because I know it does happen. I have a kid with benign PVCs and every cardiologist he sees says they are not an issue. I still worry he is going to get a virus (or even not get a virus) and be one of the news stories you hear about of random very healthy athletes having a cardiac event during sports and dying.

And again, I don't know about plenty of evidence vs. a baseline of normal or even normal in the course of other viruses. That was my original post today, that these exact issues were seen after and during the common cold.

[Corraleno]

6 minutes ago, EmseB said:

@Corraleno, this was the original critique of the original link you posted. There is more cardiology twitter discussion of more issues with the paper itself.

What am I missing? He doesn't address any of the actual research, he just criticizes a few of the references they cite for background info. The only criticism I have seen of the UCSF research is people, who haven't read it, dismissing it by saying "well, you can introduce all kinds of stuff in a test tube that will damage a heart, but that doesn't mean it happens in people." But this unusual pattern of damage did happen in people — the same pattern they found in vitro.

[EmseB]

7 minutes ago, square_25 said:

 

See, this doesn't make me feel a lot of trust, because it's incredibly dismissive. Namely, he doesn't even engage with the topics -- he just criticizes the things they are citing?? 

 

 

Lol, okay, I gotta actually do something in the forum. He's explaining why he doesn't trust the paper based on what they wrote in just the abstract and citations. If you read something and immediately find the first paragraph to be wrong do you trust the person's expertise going forward?

He also does touch on other issues if you read the thread.

He is irreverent but friendly and interacts with those he critiques sometimes. It seems like pretty normal science discussion to me.

[Corraleno]

2 minutes ago, EmseB said:

And again, I don't know about plenty of evidence vs. a baseline of normal or even normal in the course of other viruses. That was my original post today, that these exact issues were seen after and during the common cold.

Well clearly "these exact issues" that the UCSF researchers saw were not seen after the common cold, unless you know of studies where autopsies of people who died of the common cold found very distinctive patterns of damaged heart muscle fibers.

[EmseB]

I feel like this is the exact opposite of the HCQ discussion in terms of who is now more accepting of retrospective observational and in vitro studies and if or what action should ensue. Except I am not @Pen. 🤣

[Corraleno]

6 minutes ago, square_25 said:

I don't care much about what people stick in their introduction, no. That's just fluff people put in that's totally separate from their actual research. The only time DH talks about people's intros is when he complains that they don't mention his work when they should 🤣. But otherwise, no, it has absolutely nothing to do with how good their research is. And the fact that someone's dismissing a paper based on it seems very strange to me. 

 

No, this scans as very sloppy to me. He doesn't engage with the science at all. He just dismisses it because he dismissed the German paper already, and this one cited the German paper (because of course it did... it's one of the few other papers on the same topic!) 

His whole schtick seems to be snarky, dismissive comments about other people's research, and he clearly didn't even read ANY of the actual research or data. He read the first line of the abstract (which of course doesn't include references, abstracts never include references), then he finds the references in the paper that relate to the first line of the abstract, dismisses them as "irrelevant" and says the paper is not worth reading. How could he possibly know if they're irrelevant to the actual research if he didn't bother to read the research? One of the references he dismissed as irrelevant is about stem-cell derived heart tissue, which is what they used in the in vitro part of the study. So clearly relevant to the actual research, but he wouldn't know that from only reading the first line of the abstract. 

I looked at his list of publications and none of them have anything to do with virology, he appears to focus on heart attacks and coronary artery disease. So, with zero background in this area, he is dismissing the work of multiple academic researchers who specialize in this exact area, without even reading the paper, because he gets attention on social media for being snarky and dismissive. Not impressed.

[EmseB]

14 minutes ago, square_25 said:

Because they are different people? I don't understand the question. I'd obviously not pay attention to anything published by the Surgisphere people.

Sorry, I was speaking generally not about surgisphere or these people in particular.

I mean, who can ever say about causation? But yes, there's been an athlete heart attack death after a COVID infection. 

So what does that mean vis a vis all sports? I mean, we still have NBA, NFL, MLB going, AFAIK.

Right, which is why the in vitro study and the autopsies are INTERESTING -- they suggest that our vague feeling that something's weird is going on may be justified. I don't remember people having reports of crazy heart dysfunction after colds... it's possible they had cardiac inflammation they didn't know about, of course, but I don't remember reports of striking heart rate symptoms, for example. 

 

 

[EmseB]

1 minute ago, Corraleno said:

His whole schtick seems to be snarky, dismissive comments about other people's research, and he clearly didn't even read ANY of the actual research or data. He read the first line of the abstract (which of course doesn't include references, abstracts never include references), then he finds the references in the paper that relate to the first line of the abstract, dismisses them as "irrelevant" and says the paper is not worth reading. How could he possibly know if they're irrelevant to the actual research if he didn't bother to read the research? One of the references he dismissed as irrelevant is about stem-cell derived heart tissue, which is what they used in the in vitro part of the study. So clearly relevant to the actual research, but he wouldn't know that from only reading the first line of the abstract. 

I looked at his list of publications and none of them have anything to do with virology, he appears to focus on heart attacks and coronary artery disease. So, with zero background in this area, he is dismissing the work of multiple academic researchers who specialize in this exact area, without even reading the paper, because he gets attention on social media for being snarky and dismissive. Not impressed.

Wait, isn't this all rather dismissive? Are you an expert in the field??

[Corraleno]

4 minutes ago, EmseB said:

I feel like this is the exact opposite of the HCQ discussion in terms of who is now more accepting of retrospective observational and in vitro studies and if or what action should ensue. Except I am not @Pen. 🤣

A study in which the cause of the damage was unequivocally demonstrated in vitro (thus eliminating the possibility that the damage was caused by some other agent or by pre-exiting conditions), and then confirmed by autopsy in 100% of the patients whose tissues they had access to. 

[Corraleno]

3 minutes ago, EmseB said:

Wait, isn't this all rather dismissive? Are you an expert in the field??

I'm dismissing the opinion of one random cardiologist who (1) has no expertise in the area of the UCSF research and (2) admits he didn't even bother to read the paper.

I'm not sure why anyone would take seriously someone's dismissal of a paper they never read? I can't imagine the reaction if I'd turned in a paper in grad school saying I hadn't bothered to read the paper I was critiquing, but I did read the first line of the abstract and I looked up 3 of the references, and I thought the references were irrelevant to the paper (that I didn't read), therefore I have debunked the research. 

[Pen]

19 minutes ago, EmseB said:

I feel like this is the exact opposite of the HCQ discussion in terms of who is now more accepting of retrospective observational and in vitro studies and if or what action should ensue. Except I am not @Pen. 🤣

 

What?

 

[ktgrok]

4 hours ago, EmseB said:

And many other cardiologists have debunked that paper over and over, or at least called it out for significant errors and it has been revised. And it was a preprint.

I honestly don't understand the sentiment that we want fully vetted RCTs for something like HCQ but a preprint with a lot of errors should be taken on, "Well, the authors said..."

No..no they haven't. There are not a lot of errors in it, and no one is basing treatment off of it anyway. It is something showing possible issues, and a need for further study. 

They don't have controls or whatever because it wasn't that kind of a study. Like, you can have a study that compares stuff, and you can have just basic research, looking at what happens to cells when exposed to something. That is what they were doing. And they found results they were not expecting, and shared those results. Period. 

 

 

[Corraleno]

12 minutes ago, square_25 said:

I think she's talking about the German study, which hasn't been debunked, per se, but was absolutely sloppy and deserves the pushback, from what I've seen. (I haven't followed it very closely, but that's my impression.) 

Well I think the problem is that *we* were talking about the UCSF study, and she was responding to those posts as if we were talking about the German study, which is totally different in every way. And then when I specifically linked the UCSF study, she repeated the claim that it had been criticized, changes had been demanded, etc. So that seems to have led to a lot of confusion since AFAIK, there has not been any substantive criticism of the UCSF research so far.

Edited September 13, 2020 by Corraleno

[Corraleno]

1 minute ago, square_25 said:

Right. Criticizing this research substantively would require doing real work, anyway... you'd have to try the same experiment and get different results, or inspect heart tissue from more autopsies, or find a similar pattern of damage in control subjects... it's not just a matter of looking through their numbers and seeing issues. 

I think there could also be methodological critiques — like someone with a background in this type of research might claim that a certain step or procedure had introduced other factors they hadn't accounted for, or that there may be other mechanisms than the one they posit (protease cleaving or whatever). Or someone who did a lot of autopsies might say that they had seen that type of damage as a result of some other cause (which wouldn't disprove that what they saw was caused by Covid, only that it might be caused by other things as well).

Other issues that have been (incorrectly IMO) raised as "critiques" of the research are really more suggestions for further research. Could this damage be caused by other types of viruses? That's an obvious area for further research, both in vitro and port-mortem. Are there ways of testing whether this type of damage exists in a living person? That would be incredibly useful if researchers can develop a way of measuring that. But none of those things are in any way a critique of the actual research.

[EmseB]

I had to run errands so haven't caught up on posts, but here is another discussion I found helpful:

 

[EmseB]

I also found this discussion of the discredited/revised jama paper helpful as to why rushing to print or preprint can have long lasting problems in the covid era.

 

[Pen]

“An observational study in the Netherlands found a possible link to low levels of vitamin K and severe cases of COVID. Scientists suggest that poor Vitamin K status may be linked to the breakdown of lung tissues, which is often seen in patients with severe cases of COVID (1). Remember that observational studies do not show cause and effect, and more research is needed to explore the possible link.”

 

Dofferhoff, A.S.; Piscaer, I.; Schurgers, L.J.; Walk, J.; van den Ouweland, J.M.; Hackeng, T.M.; de Jong, P.A.; Gosens, R.; Lux, P.; van Daal, H.; Maassen, C.; Maassen, E.G.; Kistemaker, L.E.; Vermeer, C.; Wouters, E.F.; Janssen, R. Reduced Vitamin K Status as A Potentially Modifiable Prognostic Risk Factor in COVID19. Preprints 2020, 2020040457 (doi: 10.20944/preprints202004.0457.v2)

 

ETA: I wonder if it might also relate to breakdown of heart tissues. 

Edited September 13, 2020 by Pen

[Pen]

https://youtu.be/8nqgZn9Izv8

Autopsies

 

[Corraleno]

58 minutes ago, EmseB said:

I had to run errands so haven't caught up on posts, but here is another discussion I found helpful:

OK, I read through as much of that thread as I could and the only actual "critiques" I saw were:

(1) A post from someone who did not appear to have read the study who said that since the heart tissue was derived from stem cells, the findings only applied to neonates.But they found exactly the same things in adults.

(2) Various people attacking the guy who posted it, saying he was creating fear and panic and the study was probably "bollocks," with no actual critique.

(3) Many people who also apparently didn't read the actual article saying that everyone knows viruses cause myocarditis, so why is this news.

(4) Several people linking to this one guy, Francois Balloux, whose incisive critique was as follows: "3 people who died had heart damage, likely before #COVID19 infection already. They also showed that the virus can kill cells in test tubes, but as someone mentioned, bathing the cells in orange juice would likely have had the same effect than 'virus juice'." Which again demonstrates a total lack of understanding of what the results actually show and an unwillingness to even read the paper. 

If anyone can find an actual scientific critique of the methods, materials, results, or conclusions of the UCSF research, please link it. Because so far this is all just people who can't even be bothered to read the damn study tweeting totally uninformed comments. 🙄

[EmseB]

35 minutes ago, Corraleno said:

OK, I read through as much of that thread as I could and the only actual "critiques" I saw were:

(1) A post from someone who did not appear to have read the study who said that since the heart tissue was derived from stem cells, the findings only applied to neonates.But they found exactly the same things in adults.

(2) Various people attacking the guy who posted it, saying he was creating fear and panic and the study was probably "bollocks," with no actual critique.

(3) Many people who also apparently didn't read the actual article saying that everyone knows viruses cause myocarditis, so why is this news.

(4) Several people linking to this one guy, Francois Balloux, whose incisive critique was as follows: "3 people who died had heart damage, likely before #COVID19 infection already. They also showed that the virus can kill cells in test tubes, but as someone mentioned, bathing the cells in orange juice would likely have had the same effect than 'virus juice'." Which again demonstrates a total lack of understanding of what the results actually show and an unwillingness to even read the paper. 

If anyone can find an actual scientific critique of the methods, materials, results, or conclusions of the UCSF research, please link it. Because so far this is all just people who can't even be bothered to read the damn study tweeting totally uninformed comments. 🙄

That isn't what I linked so having trouble finding where it's directing you. For number 1 in your post, for example, he addresses that exact thing in the thread that you are taking issue with. He is a scientist offering scientific critique while also praising the paper on its merits.

For number four, Francious Balloux is the director of University College London genetics institute who has done extensive research on covid, not just some rando.

Most of the docs commenting are researchers/cardiologists/fellows/scientrandom. None of them are covid or science deniers. They tend to make fun of people who are or who promote "cures" like hcq or vitamins without rcts. Those are the people I'm reading, not random commenters in the threads, sorry if the links are not working properly. I have actually found really well reasoned discussion between researchers and docs and scientists on Twitter that has actually tempered a lot of the fear mongering I find in headlines. I see that you've already decided to dismiss it out of hand, or I've given bad links so the discussion isn't fully fleshed out, but it isn't all the nonsense you're making it out to be.

Edited September 13, 2020 by EmseB

[Corraleno]

42 minutes ago, EmseB said:

That isn't what I linked so having trouble finding where it's directing you. For number 1 in your post, for example, he addresses that exact thing in the thread that you are taking issue with. He is a scientist offering scientific critique while also praising the paper on its merits.

For number four, Francious Balloux is the director of University College London genetics institute who has done extensive research on covid, not just some rando.

Most of the docs commenting are researchers/cardiologists/fellows/scientrandom. None of them are covid or science deniers. They tend to make fun of people who are or who promote "cures" like hcq or vitamins without rcts. Those are the people I'm reading, not random commenters in the threads, sorry if the links are not working properly. I have actually found really well reasoned discussion between researchers and docs and scientists on Twitter that has actually tempered a lot of the fear mongering I find in headlines. I see that you've already decided to dismiss it out of hand, or I've given bad links so the discussion isn't fully fleshed out, but it isn't all the nonsense you're making it out to be.

I just read Balloux's entire twitter feed back to August 25th, when the UCSF study was first released, and the ONLY references I can find to the UCSF study are (1) a link to Darrell Francis's comment on the paper that he didn't read, and the comment I quoted above. There is no critique of the paper. He seems to have a beef with the person whose twitter feed he posted on (Eric Topol), as he made some personal comments about him, but Eric Topol had nothing to do with the UCSF research. He also seems to believe that Covid is strictly a respiratory disease that does not cause any cardiac damage other than what might occur with any other virus, and therefore any study that claims to show cardiac damage is by definition bogus. He frequently retweets comments (not research, but comments) by other cardiologists saying that they're not seeing any unusual cardiac damage and therefore covid is strictly a respiratory disease.  He may not be "just some rando" but his personal opinion does not outweigh the opinions of many other cardiologists and researchers who feel otherwise based on their own practices and research. 

Can you quote some of the critiques you can see in the twitter thread which specifically address the UCSF research? Because I cannot find one single critique of it. All I can find are claims like the ones below,  which refer to generic "adverse cardiac effects" and do not address the specific findings of the UCSF team. They're just saying "yeah, yeah, viruses can affect the heart, so what?" No one is citing evidence that that the very specific damage to heart muscle fibers the UCSF team found is not a potentially serious issue, or that the same thing is caused by many other diseases, or that their methodology was flawed. 

 

[Pen]

9 hours ago, square_25 said:

You’re doing a lot of argument by authority in this thread. I agree that you’re linking real people who have the right to an opinion, but there are also real people who disagree.

Why can’t we agree that we don’t know yet and there’s cause for concern?? That seems like an extremely minimal statement. 

 

Out of curiosity, why does agreeing matter? 

 

 

[Ausmumof3]

7 hours ago, kdsuomi said:

CA has the lowest number of patients with COVID in the ICU and also in the hospital since early April, and the positivity rate is under 4%, so that's all good news. 

Glad you guys have some good news.

[EmseB]

16 hours ago, square_25 said:

You’re doing a lot of argument by authority in this thread. I agree that you’re linking real people who have the right to an opinion, but there are also real people who disagree.

Why can’t we agree that we don’t know yet and there’s cause for concern?? That seems like an extremely minimal statement. 

I was responding to the critique that they were just random Twitter folks by giving their credentials. I responded to her points specifically. How can I respond that specific point without listing credentials?? I left this convo last night because I feel that you're now just picking apart things to disagree with for some reason I can't figure out. If I can't respond to a specific point about the people I'm linking (links that were asked for!) by explaining who they are, then I'm at a loss. Of course there are people who disagree! I was asked to provide links to the disagreements in this thread.

I don't know a lot of things. I do know that making billion dollar policy decisions affecting many lives based on headlines based on studies like these heart studies is something I disagree with. I also think that said headlines are putting fear into the hearts of many and after reading quite a bit, I think unnecessarily. I read many scientists and researchers who have informed that opinion and seen enough junk science pre-published and published in the last six months that I am not tending to lean the other way, but rather seen more sense in being wary of anything coming out about covid sequelae right now. I think this is a bad virus that is much worse for some people. I think anecdotes of said cases are unhelpful for informing public health policy which by it's very nature cannot continue on a covid-only approach. I think caution, masking, and distancing is prudent. 

I hope you and yours remain healthy, square_25. I don't know how to have this discussion with you though.

[Ausmumof3]

24 minutes ago, EmseB said:

I was responding to the critique that they were just random Twitter folks by giving their credentials. I responded to her points specifically. How can I respond that specific point without listing credentials?? I left this convo last night because I feel that you're now just picking apart things to disagree with for some reason I can't figure out. If I can't respond to a specific point about the people I'm linking (links that were asked for!) by explaining who they are, then I'm at a loss. Of course there are people who disagree! I was asked to provide links to the disagreements in this thread.

I don't know a lot of things. I do know that making billion dollar policy decisions affecting many lives based on headlines based on studies like these heart studies is something I disagree with. I also think that said headlines are putting fear into the hearts of many and after reading quite a bit, I think unnecessarily. I read many scientists and researchers who have informed that opinion and seen enough junk science pre-published and published in the last six months that I am not tending to lean the other way, but rather seen more sense in being wary of anything coming out about covid sequelae right now. I think this is a bad virus that is much worse for some people. I think anecdotes of said cases are unhelpful for informing public health policy which by it's very nature cannot continue on a covid-only approach. I think caution, masking, and distancing is prudent. 

I hope you and yours remain healthy, square_25. I don't know how to have this discussion with you though.

I guess my question would be if there’s a chance that 25pc of people are experiencing heart damage are we better to err on the side of caution or not?

[EmseB]

2 hours ago, Ausmumof3 said:

I guess my question would be if there’s a chance that 25pc of people are experiencing heart damage are we better to err on the side of caution or not?

I would want to know what you meant by erring on the side of caution, what you meant by "a chance", what is considered heart damage, and can we say definitively that covid is causing said damage or is the damage pre-existing and we see it because we are scanning people who have had covid. I would want to know what is damage relative to what happens to our hearts when we get any other myriad of viruses. Is it recoverable or permanent? So many questions based on what you are asking.

There are studies that find correlations between x and y all the time. In fact, a lot of that type of thinking and application of those studies and wanting to err on the side of caution is the heart of the anti-vax movement. It's profoundly unscientific, IMO, and not good for making public health policy that has to balance a ton of other factors.

Edited September 14, 2020 by EmseB

[frogger]

31 minutes ago, EmseB said:

I would want to know what you meant by erring on the side of caution, what you meant by "a chance", what is considered heart damage, and can we say definitively that covid is causing said damage or is the damage pre-existing and we see it because we are scanning people who have had covid. I would want to know what is damage relative to what happens to our hearts when we get any other myriad of viruses. Is it recoverable or permanent? So many questions based on what you are asking.

There are studies that find correlations between x and y all the time. In fact, a lot of that type of thinking and application of thise studies and wanting to err on the side of caution is the heart of the anti-vax movement. It's profoundly unscientific, IMO, and not good for making public health policy that has to balance a ton of other factors.

 

I was under the impression that current public health policy is based on not overwhelming the hospitals but I suppose some states could be doing things differently but I don't see a lot of them acting that way. Heck, Arizona just tried to work in more ability to expand or "surge" or whatever.

 

I appreciate that my city acted when we could see continually increases and an estimate to less than 6 weeks capacity last month and acted and currently we are on a downward trend but already open more as our Rt is less than 1. Don't know that it will stay that way but considering the US numbers I seriously doubt it's more than that in most states. I don't study every state though.

 

Part of the stories the media is pushing may be to convince the young people to cooperate. Partly, because other media outlets have basically told them if you aren't elderly or have big risk factors, it's no problem, which isn't true because no one knows and we do know many die or have long term damage, we just don't knowthe percentage.

The truth is we don't know. We should be telling people to think about spread, no matter your age, and do the things that get the most bang for your buck. Think and be helpful so the government isn't tempted to force you. 

 

It really appears most don't want to act until they see the hospitals over run already or they see first hand a bunch of deaths. It's like they can't look forward and project or understand exponential growth.  You have to keep growth down. No matter what if growth continues the problem will be harder, not easier to control. 

Edited September 14, 2020 by frogger
I swear my space bar is out to get me.

[Ausmumof3]

4 hours ago, EmseB said:

I would want to know what you meant by erring on the side of caution, what you meant by "a chance", what is considered heart damage, and can we say definitively that covid is causing said damage or is the damage pre-existing and we see it because we are scanning people who have had covid. I would want to know what is damage relative to what happens to our hearts when we get any other myriad of viruses. Is it recoverable or permanent? So many questions based on what you are asking.

There are studies that find correlations between x and y all the time. In fact, a lot of that type of thinking and application of those studies and wanting to err on the side of caution is the heart of the anti-vax movement. It's profoundly unscientific, IMO, and not good for making public health policy that has to balance a ton of other factors.

 

4 hours ago, EmseB said:

I would want to know what you meant by erring on the side of caution, what you meant by "a chance", what is considered heart damage, and can we say definitively that covid is causing said damage or is the damage pre-existing and we see it because we are scanning people who have had covid. I would want to know what is damage relative to what happens to our hearts when we get any other myriad of viruses. Is it recoverable or permanent? So many questions based on what you are asking.

There are studies that find correlations between x and y all the time. In fact, a lot of that type of thinking and application of those studies and wanting to err on the side of caution is the heart of the anti-vax movement. It's profoundly unscientific, IMO, and not good for making public health policy that has to balance a ton of other factors.

Err on the side of caution would mean encouraging athletes or anyone on an intense exercise program to get scanned and checked before returning to play.  At the same time as getting some data together on what the typical rate of myocarditis in athletes is.  If it doesn’t already exist.  It shouldn’t be that hard to get scans on 20-30 healthy volunteers for comparison, to at least get an idea if we’re looking for something.

and on an individual level I’m adding it to my list of reasons why I don’t want covid till we know a lot more about it.  Yes there’s lots of viruses that don’t have long lingering after effects.  There’s also a heck of a lot that do.

 

Edited September 14, 2020 by Ausmumof3