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Rahm just tested positive for Covid

iirc... I've posted the study in a response to you in the past (I guess you weren't paying attention lol), here it is again.


That is just a model. It's not real data (or a study of real data). The inputs of the model can be adjusted to make the output say whatever you want. Real data exists that shows that model to be completely wrong and meaningless at this point.
 
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That is just a model. It's not real data (or a study of real data). The inputs of the model can be adjusted to make the output say whatever you want. Real data exists that shows that model to be completely wrong and meaningless at this point.
It is a study/model based on a number of studies.
 
That is just a model. It's not real data (or a study of real data). The inputs of the model can be adjusted to make the output say whatever you want. Real data exists that shows that model to be completely wrong and meaningless at this point.

Of course, that's not the only one....


 
It is a study/model based on a number of studies.

No it's not.

The only thing that was based on "a number of other studies" was the median values they used for incubation period and the distribution of days until symptom onset.

It's just a model. At best, if the model itself is somehow perfect (impossible), the quality of the output can only be as good as the quality of the input.

Honestly, SLUPSU, I'm not going any further explaining to you why this model is irrelevant at this point, because I know how smart you are -- And I know that you too understand it's irrelevance and you're just trying to use it to push me because you don't like my tone when I discuss all the sh*t related to this pandemic.
 
No it's not.

The only thing that was based on "a number of other studies" was the median values they used for incubation period and the distribution of days until symptom onset.

It's just a model. At best, if the model itself is somehow perfect (impossible), the quality of the output can only be as good as the quality of the input.

Honestly, SLUPSU, I'm not going any further explaining to you why this model is irrelevant at this point, because I know how smart you are -- And I know that you too understand it's irrelevance and you're just trying to use it to push me because you don't like my tone when I discuss all the sh*t related to this pandemic.

That's your take, you want to dismiss the statistics (would Kane think?), that's fine. I've just posted other ones and there are more.

What's your go-to study to show that pre and/or asymptomatic spread is low and backs up your stance? Is it the one using nearly the entire population of Wuhan as a data set? No sidestepping allowed, which studies??
 
That's your take, you want to dismiss the statistics (would Kane think?), that's fine. I've just posted other ones and there are more.

What's your go-to study to show that pre and/or asymptomatic spread is low and backs up your stance? Is it the one using nearly the entire population of Wuhan as a data set? No sidestepping allowed, which studies??
Kane thinks the German study is probably close.

Virtually no asymptomatic spread, more than 50% of the cases from that point on are pre-symptomatic.

Makes good sense to me - once people start feeling sick, they probably isolated themselves....

Once I'm convinced something is reasonable, I trust it until I see a reason it is cast into doubt. For now, I'm going with those results.
 
Because:
1) The poster to which I responded referred to asymptomatic spread. Take it up with him. The fact is, early on in this pandemic, public health and the media were leading everyone to believe that people could become infected, walk around living life for days spreading the virus, and never realize they were infected and and spreading it. We now know that's not true.

Regarding presymptomatic, yes, everyone knows there could be a short sliver of time right before your symptoms are realized when you could be contagious. That's common knowledge because we all know that's how the flu, and common colds work too.

The fact that the poster to which I responded expressed the concern as "being asymptomatic and spreading it to others" clearly indicates he's referring to the asymptomatic spread idea that blew up (and has since fizzled and died) early on in the pandemic.

2) Obviously presymptomitic would be a bigger contributer than asymptomatic (since presymptomatic is at least a real thing), but what is your source indicating it to be a significant driver of community spread?
I'm still waiting for your credible sources and numbers illustrating 0% asymptomatic spread.
 
That is just a model. It's not real data (or a study of real data). The inputs of the model can be adjusted to make the output say whatever you want. Real data exists that shows that model to be completely wrong and meaningless at this point.
Please provide your "real" data.
 
Of course, that's not the only one....


That is also just a model.


This one is at least a study of real data/events.

Annnnd.... It finds asymptomatic spread to be 0. :)

This is a very small study, but at least it's an actual study of actual data.
 
That is also just a model.



This one is at least a study of real data/events.

Annnnd.... It finds asymptomatic spread to be 0. :)

This is a very small study, but at least it's an actual study of actual data.

I'm not arguing that asymp spread is not very low, I'm arguing that presym infection is a driver of the pandemic at about 50% of cases, you haven't presented any sources or even commented on what your opinion is with regard to presym spread. You're arguing strongly about something, you have to have an informed opinion about the percentages, right?
 
That's your take, you want to dismiss the statistics (would Kane think?), that's fine. I've just posted other ones and there are more.

What's your go-to study to show that pre and/or asymptomatic spread is low and backs up your stance? Is it the one using nearly the entire population of Wuhan as a data set? No sidestepping allowed, which studies??

NIH meta analysis of 54 relevant studies RE household transmission with 77,758 participants. You've seen this before, and commented on it. And there are many more where this came from.


BTW, I first found this one when I was reading a CDC study regarding children in schools. That CDC study indicated how they observed no (or very little) transmission from asymptomatic contacts, then commented how that is consistent with with the findings of other studies - And cited this as an "other" study. So, it's good enough for the CDC to cite in the context of downplaying the real world existence of asymptomatic spread.
 
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I'm not arguing that asymp spread is not very low, I'm arguing that presym infection is a driver of the pandemic at about 50% of cases, you haven't presented any sources or even commented on what your opinion is with regard to presym spread. You're arguing strongly about something, you have to have an informed opinion about the percentages, right?

If I haven't commented on what is my opinion with regard to presymptomatic spread (and that is true), then how are you reading that I'm "arguing strongly about it?"

The conversation on this thread was about asymptomatic spread (on which I do have good data and thus pretty strong position). You showed up and started preaching about presymptomatic spread - Which is different. If you go back and look at the receipts, I never argued against you with regard to presymptomatic spread. I only asked you where your (%) number came from, because, frankly, I haven't seen much hard/reliable data on presymptomatic. And then when you cited a few models, I pointed out that they are just models and meaningless. I've never -- and I'm certainly not in this thread -- "argued strongly" one way or another about presymptomatic spread.

I have not seen any data one way or another that gives me any confidence to have strong thoughts on how significant of a contributor presymptomatic spread is to community spread.

Edit: My intuition would tell me that presymptomatic is likely pretty significant in the home, but I don't even have a guess as to how significant it would be in the community, for a few different reasons.
 
Kane thinks the German study is probably close.

Virtually no asymptomatic spread, more than 50% of the cases from that point on are pre-symptomatic.

Makes good sense to me - once people start feeling sick, they probably isolated themselves....

Once I'm convinced something is reasonable, I trust it until I see a reason it is cast into doubt. For now, I'm going with those results.

Makes good sense to me - once people start feeling sick, they probably isolated themselves....

And there is the unknown factor. There are people who don't care if they're sick and go out in public anyway. There are people who may have very mild symptoms and don't realize they are sick. Others may have those mild symptoms and realize they'll sick but not enough to avoid going out in public.

You may very well be correct on the percentage of pre-symptomatic spread, but there seems to be no way to quantify it.
 
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If I haven't commented on what is my opinion with regard to presymptomatic spread (and that is true), then how are you reading that I'm "arguing strongly about it?"

The conversation on this thread was about asymptomatic spread (on which I do have good data and thus pretty strong position). You showed up and started preaching about presymptomatic spread - Which is different. If you go back and look at the receipts, I never argued against you with regard to presymptomatic spread. I only asked you where your (%) number came from, because, frankly, I haven't seen much hard/reliable data on presymptomatic. And then when you cited a few models, I pointed out that they are just models and meaningless. I've never -- and I'm certainly not in this thread -- "argued strongly" one way or another about presymptomatic spread.

I have not seen any data one way or another that gives me any confidence to have strong thoughts on how significant of a contributor presymptomatic spread is to community spread.

Edit: My intuition would tell me that presymptomatic is likely pretty significant in the home, but I don't even have a guess as to how significant it would be in the community, for a few different reasons.
I do have to say, you're right on that. I have no idea why the "pre-symptomatic" spread thing came from.

Perhaps because from a pandemic standpoint, you cannot tell if it is asymptomatic OR pre-symptomatic before lots of people have been infected and the initial spreader becomes symptomatic.
 
If I haven't commented on what is my opinion with regard to presymptomatic spread (and that is true), then how are you reading that I'm "arguing strongly about it?"

The conversation on this thread was about asymptomatic spread (on which I do have good data and thus pretty strong position). You showed up and started preaching about presymptomatic spread - Which is different. If you go back and look at the receipts, I never argued against you with regard to presymptomatic spread. I only asked you where your (%) number came from, because, frankly, I haven't seen much hard/reliable data on presymptomatic. And then when you cited a few models, I pointed out that they are just models and meaningless. I've never -- and I'm certainly not in this thread -- "argued strongly" one way or another about presymptomatic spread.

I have not seen any data one way or another that gives me any confidence to have strong thoughts on how significant of a contributor presymptomatic spread is to community spread.

Edit: My intuition would tell me that presymptomatic is likely pretty significant in the home, but I don't even have a guess as to how significant it would be in the community, for a few different reasons.
Well, you seem argumentative in responses to me.

Yes, the conversation started as one about asymptomatic spread and I was clearly changing that to make a point, which was talking about asymptomatic spread alone is misguided. Whatever point you're trying to make regarding really low asymptomatic spread is made meaningless by the existence and prevalence of presymptomatic spread.
It's funny to me that you commented that presymptomatic spread might be significant in an in-home (and unmasked) situation... it's almost like your afraid to buy into a high level of presymptomatic spread because of that.
 
Well, you seem argumentative in responses to me.

Yes, the conversation started as one about asymptomatic spread and I was clearly changing that to make a point, which was talking about asymptomatic spread alone is misguided. Whatever point you're trying to make regarding really low asymptomatic spread is made meaningless by the existence and prevalence of presymptomatic spread.
It's funny to me that you commented that presymptomatic spread might be significant in an in-home (and unmasked) situation... it's almost like your afraid to buy into a high level of presymptomatic spread because of that.

N.L.,
This is the map I always try to follow for where I go:
1. With no knowledge and/or understanding myself, and no data: No opinion. Or, if a hypothesis seems to make a lot of sense and has overwhelming support, then that.
2. With a basic/fundamental understanding, but no data: Whatever hypothesis that seems to make the most sense between those I hear/learn from others, and the one Occam's razor tells me.
3. With a solid understanding, but no data: Whatever hypothesis that seems to make the most sense between those I hear/learn from others, and the one Occam's razor tells me. (same as above)
4. When data is introduced, I follow that data. The quality and quantity of the data determines how far I follow it, but the data drives my opinion/position.

For me, simply, the effect of presymptomatic community spread falls into #1. It's easy to understand how presymptomatic spread would/could be significant in the home. In the community, there are a lot more factors at play that make it harder to have a strong opinion. If perfect data emerged tomorrow making it clear that presymptomatic spread in the community was anywhere between insignificant and significant, I would not be surprised.

And I'm not "afraid" to buy into anything. Like everyone else, I usually don't enjoy finding out that I'm wrong about something... But unlike (seemingly) so many others, I would rather experience the short term pain to the ego that comes with learning/admitting I was wrong than experience the long term pain of continually trying to support and defend an opinion/position where which the evidence shows it to most likely not be correct.

Two examples of this:
- Asymptomatic spread. I'm kinda embarrassed to say that I didn't do any of my own research and fully bought into that conspiracy theory - hook, line and sinker - like many others. I repeated it in conversation and online, and contributed to the misinformation. But as time went by without much in the way of scientific proof or evidence, I started to wonder about it. Then, when studies/data like the one I linked above started coming out, I realized I was most likely wrong and changed my position.
- Airborne transmission (as we have sparred on in the past). As you know, I was in the camp that believed infectable virus was shed on the droplets of coughs/sneeze/spittle and could only travel a little further than those droplets... But as more relevant data came out, I began to question my accepted understanding on that, and now it seems most likely that I was in fact wrong and not only can infectable virus travel considerably further than the droplets (especially in the case of a sneeze), but some virus might even shed from normal breathing exhales (most likely in the exhales following a sneeze, but still). There's some nuance involved, but generally that is where the data shows us to most likely be with regards to that, so I was wrong before, and this is where my opinion is today.
 
N.L.,
This is the map I always try to follow for where I go:
1. With no knowledge and/or understanding myself, and no data: No opinion. Or, if a hypothesis seems to make a lot of sense and has overwhelming support, then that.
2. With a basic/fundamental understanding, but no data: Whatever hypothesis that seems to make the most sense between those I hear/learn from others, and the one Occam's razor tells me.
3. With a solid understanding, but no data: Whatever hypothesis that seems to make the most sense between those I hear/learn from others, and the one Occam's razor tells me. (same as above)
4. When data is introduced, I follow that data. The quality and quantity of the data determines how far I follow it, but the data drives my opinion/position.

For me, simply, the effect of presymptomatic community spread falls into #1. It's easy to understand how presymptomatic spread would/could be significant in the home. In the community, there are a lot more factors at play that make it harder to have a strong opinion. If perfect data emerged tomorrow making it clear that presymptomatic spread in the community was anywhere between insignificant and significant, I would not be surprised.

And I'm not "afraid" to buy into anything. Like everyone else, I usually don't enjoy finding out that I'm wrong about something... But unlike (seemingly) so many others, I would rather experience the short term pain to the ego that comes with learning/admitting I was wrong than experience the long term pain of continually trying to support and defend an opinion/position where which the evidence shows it to most likely not be correct.

Two examples of this:
- Asymptomatic spread. I'm kinda embarrassed to say that I didn't do any of my own research and fully bought into that conspiracy theory - hook, line and sinker - like many others. I repeated it in conversation and online, and contributed to the misinformation. But as time went by without much in the way of scientific proof or evidence, I started to wonder about it. Then, when studies/data like the one I linked above started coming out, I realized I was most likely wrong and changed my position.
- Airborne transmission (as we have sparred on in the past). As you know, I was in the camp that believed infectable virus was shed on the droplets of coughs/sneeze/spittle and could only travel a little further than those droplets... But as more relevant data came out, I began to question my accepted understanding on that, and now it seems most likely that I was in fact wrong and not only can infectable virus travel considerably further than the droplets (especially in the case of a sneeze), but some virus might even shed from normal breathing exhales (most likely in the exhales following a sneeze, but still). There's some nuance involved, but generally that is where the data shows us to most likely be with regards to that, so I was wrong before, and this is where my opinion is today.
Very well put. You follow the Scientific Method much better than most of our so called scientists that have been working on this mess. As a scientist, over the years I've grown to have great distain for 3 things: bureaucracy, bullshit and bad science.
 
This is a simple question for anyone who can explain it. What is the difference between "asymptomatic" and "pre-symptomatic" as you are using those terms? Aren't all pre-symptomatic persons also asymptomatic?
 
Agree, getting old fast. Anyone that comes down with Covid now only has to look in the mirror to assign blame.

The other part I don't understand is why some are saying it was developed way too fast. My question: so science was suppose to take their time when some of our hospitals were at a breaking point and hundreds of thousands of people were dying ? Well. I do get it.....some are locked into their initial thoughts and won't admit they might be wrong even if hit with all kinds of evidence.

Is the vaccine perfect ? No, probably not. But it is the reason we're coming out of this thing and we'll be able to watch CF this Fall.

Right now the data suggests this is one of the best vaccines ever created.
 
Agree, getting old fast. Anyone that comes down with Covid now only has to look in the mirror to assign blame.

The other part I don't understand is why some are saying it was developed way too fast. My question: so science was suppose to take their time when some of our hospitals were at a breaking point and hundreds of thousands of people were dying ? Well. I do get it.....some are locked into their initial thoughts and won't admit they might be wrong even if hit with all kinds of evidence.

Is the vaccine perfect ? No, probably not. But it is the reason we're coming out of this thing and we'll be able to watch CF this Fall.

I don't know of anyone who thinks it was not the obviously smart thing to do - accelerate the vaccine and take a few shortcuts. As you say, it saved hundreds of thousands of people.

Obviously Fauci wanted to go slow and emphasize all the trials that needed done when he was saying there would NEVER be a vaccine by the end of the year (2020), but as pointed out earlier - Fauci certainly is not a very smart man. Trump, no doubt for his own political reasons, as well as ending the pandemic, wanted to get there as fast as humanly possible.

Of course, it is true that taking these shortcuts leaves SOME VERY SMALL uncertainty, but easily worth the risk...

What might be confusing you is that other people are also noting that for the young and healthy, the odds of getting meaningfully sick from Covid are also VERY SMALL.

And so, we are trying to estimate two very small probabilities....a tough thing to do.
 
But do they affect reproduction? We know that they synthesize proteins that do not occur naturally in the human body. We also know that mRNA trials in animals were halted due to animals dying upon reinfection from antibody dependent enhancement. I guess since they eliminated the lab rats due to high death rates on this stuff, millions of Americans were eager to take their place.

My view, if you are extremely vulnerable to COVID, then get the experimental shots. If you are at low risk (most children and working aged adults), then you are rolling the dice on the risk to benefit.

Not sure where some of you keep saying animal studies were halted. There are plenty of studies with no adverse events. Here’s one on reproduction
 
This is a simple question for anyone who can explain it. What is the difference between "asymptomatic" and "pre-symptomatic" as you are using those terms? Aren't all pre-symptomatic persons also asymptomatic?
pre-symptomatic is a cute buzz word to try to hide the fact that a large percentage of people who test positive for covid never have symptoms.
 
I think that is a fair statement. Truth lags legend in most cases. It was proven that the virus is almost impossible to spread on hard surfaces a year ago. yet, here we are cleaning hard surfaces every few minutes. The CDC stated that 3 feet social distancing is as good as six feet yet, in most cases, six feet was still being enforced.

But in the case of Rahm, them's the rules. As a kid working in a large computer company, I had an argument with my boss because he was bustin me on some data from a report. The report was wrong. He said, "Oblie, the report may be right or the report may be wrong. but it is the report which is used to run the company". The PGA needs to reconsider the rule but under the circumstances, they had no choice. Rahm should have been vaxxed, he had plenty of opportunities. Its like a golfer complaining about getting a bad lie in the ruff. You don't want bad lies, don't hit it into the ruff. To Rahm's credit, he isn't complaining.
Your last sentence is critical. Rahm ISN'T complaining. It is the rest of us saying the rule is idiotic.
 
So back to OP and the PGA and Rahm and the stupidity [not enforceability ] of the rule. What I think I have read is as follows
. If you have been vaccinated you do not need to be tested.
. If you haven't been vaxxed you must get tested and if positive you are tossed. [asymptomatic or not]

.Is it not true that even if you have been tested you can contract the virus and get either mild symptoms or remain. asymptomatic? [at least that is the logic I think for continuing masking etc even after being vaxxed]

.So how is Rahm any different from any other pro out there who has been vaxxed but could [like Rahm] be asymptomatic but carrying the virus? This seems like a clear double standard or at least example 1259 of mixed messages sent by various groups.
 
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So back to OP and the PGA and Rahm and the stupidity [not enforceability ] of the rule. What I think I have read is as follows
. If you have been vaccinated you do not need to be tested.
. If you haven't been vaxxed you must get tested and if positive you are tossed. [asymptomatic or not]

.Is it not true that even if you have been tested you can contract the virus and get eiother mild symptoms or remain. asymptomatic? [at least that is the logic I think for continuing masking etc even after being vaxxed]

.So how is Rahm any different from any other pro out there who has been vaxxed but could [like Rahm] be asymptomatic but carrying the virus? This seems like a clear double standard or at least example 1259 of mixed messages sent by various groups.

At the point that he was tested, then told, there is no difference. You are correct.

If Rahm doesn't have natural immunity from previous infection, he would have a higher likelihood of becoming symptomatic than someone who is vaxed.... But yeah, until that happens, basically the same.

Note, if Rahm becomes symptomatic, there could be a sliver of time where he could be contagious right before he realizes symptoms.
 
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At the point that he was tested, then told, there is no difference. You are correct.

If Rahm doesn't have natural immunity from previous infection, he would have a higher likelihood of becoming symptomatic than someone who is vaxed.... But yeah, until that happens, basically the same.

Note, if Rahm becomes symptomatic, there could be a sliver of time where he could be contagious right before he realizes symptoms.
I agree with what you are saying. So you have "a small sliver of time" that he could be more contagious contrasted to EVERY pro who was vaxxed potentially carrying some virus. So you have 1 man with with a small sliver of time vs 100 pros who have a smaller chance but still a chance to be carrying the virus. Sure sounds like a dumb rule.
 
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NIH meta analysis of 54 relevant studies RE household transmission with 77,758 participants. You've seen this before, and commented on it. And there are many more where this came from.


BTW, I first found this one when I was reading a CDC study regarding children in schools. That CDC study indicated how they observed no (or very little) transmission from asymptomatic contacts, then commented how that is consistent with with the findings of other studies - And cited this as an "other" study. So, it's good enough for the CDC to cite in the context of downplaying the real world existence of asymptomatic spread.

I Didn't have a chance to look at this study when you first posted it. In the context of this discussion, it does nothing to clarify presymptomatic spread.

ps... isn't this "study" a statistical model? you seemed to have a problem with that before.
 
I Didn't have a chance to look at this study when you first posted it. In the context of this discussion, it does nothing to clarify presymptomatic spread.

ps... isn't this "study" a statistical model? you seemed to have a problem with that before.

You are correct that that study is not good at all for determining the role PRE-symptomatic spread plays. I don't think I ever claimed it was, and if I did, that was a misunderstanding. It has a very poor definition for a presymptomatic transmission (IMO), so I only think it's valuable for illustrating the relative difference in likelihood of asymptomatic vs symptomatic.

And no, that study is absolutely not a statistical model. What makes you think that? It's a meta-analysis of other studies that recorded and studied actual transmissions. No data in the study came from a model, or modeling of their own.
 
Rahm tweeted out that he has tested negative twice and is now eligible to complete at the USOpen this weekend
 
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