Forum Replies Created
The FDA AER system is a completely unscientific shitshow.
Literally anybody – even you right this minute – can access it and enter anything you want.
“I died from HCQ!” would be duly recorded and probably not filtered out.
What are the chances that Pharma goons aren’t busy populating it with complete junk? I dunno – pretty much zero.
You’d think an AER system would be reserved for medically trained people and use tight controls, but that’s not its purpose. It’s meant to gather a lot of noise in case some signal emerges. I get that. If there’s some strange drug interaction that snuck past testing (in know, unpossible, right?) then the AER might pick it up.
But I don’t get anybody reporting straight from it as if it’s meaningful in any way. It’s not. It needs heavy scrubbing and signal amplification first.
Can wearing a mask hurt? No.
Could it help me? Yes.
Could it help others? Yes.
I simply don’t understand how some people can arrange all that into any sort of a controversy.
I’m not aware of any work that demonstrates that SARS2 is expelled as a solitary virus particle of 125 nm diamter. In fact, I rather doubt it would survive long as a stripped down, solitary protein and lipid ball.
Instead droplets of varying sizes are expelled as people breathe, talk, sing or shout. Many of those are truly massive. They fall to the ground within a meter, possibly containing hundreds of millions or billions of virus particles each (becoming ‘fomites’ that people can touch and transfer).
Many more particles are in the 0.5 to 5 micron range that drift about for varying lengths of time and distances depending on too many factors to delve into (such as air currents, humidity, etc).
All of which is a long way of saying that saying the 300nm pore size of an N95 mask is not sufficient to stop a 125nm virus particle is an incorrect characterization. Instead the right question is to ask if the mask stops the spread of the larger particles involved and the answer is “of course.”
Your arguments seem to actually be mainly supporting my hypothesis. Let’s take them one at a time.
The hypothesis is that – we reach herd immunity around 18% -20% sero prevalence. This is not true, when you look at closed systems like cruise ships, prisons or slums where spreading is easy – if you let it, covid will get to 100% of population.
Yes, the above is the hypothesis. However, your next statement doesn’t follow in support of your argument, but rather both of ours. I said in my X + Y + Z equation that people are getting Covid. At least 85% based on some sloppy guessing.
However, I haven’t seen any population yet where there’s been 100% Covid infection. Not on the DP cruise ship, not in prisons…nowhere.
A recent study of slum areas near mumbai has found seroprevalence of 57% . HB-19 does not seem to stop anywhere close to 20%.
That’s certainly interesting and it supports your argument. I haven’t seen seroprevalence numbers that high anywhere else, so would love to see this repeated.
78% of all inmates in Ohio prison, had covid-19.
Well, this is 78% testing positive with a PCR test. This is what I’d predict too. The people with T-Cell immunity would still test positive.
Tellingly, is the next line:
Though prison population is not a representative of general population – it is interesting to see that 95% of those who tested positive are asymptomatic .
The article you linked even goes on to state that very few inmates have died (12, as of the Apr 22nd byline, so that has gone higher since, we presume) and that the vast majority of positives were asymptomatic – which conforms with the XYZ theory.
What we don’t know, which would be great to know, is how many prisoners ended up seropositive. That would help to cement or refute the hypothesis.
Diamond princes cruise ship which is again a different distribution of population had only about 18% asymptomatic cases . It has also shown that strict containment and lockdown measures such as cabin quarantine has reduced the cases R0 drastically inside cruise ship.
Yes, there’s no argument that strict containment reduces the R0. That’s been said by everyone all along. China showed that first. Then Taiwan, New Zealand, South Korea and many others.
However, the article you cite for an “18% asymptomatic cases” figure baffles me. They do some statistical magic on the data and then use language that is less than clear so I cannot follow what they did or if it’s valid. But their own data section includes this:
Summary: Their data table shows that (a) the last date of patient data shows 50.5% asymptomatic and (b) they have no additional information on patient progression after that point. I presume they then tried to fish out the disease progression from the 7 days of data to extrapolate how many of those asymptomatic patients eventually became symptomatic? If so, not actually data, but a model. The best data we have now is that 40% – 45% of all people who contract SARS2 are asymptomatic.
Bottom line: We are in agreement that cases fall after a first peak. We are in disagreement over the reasons for that. Many seem to think that NPIs alone account for that. Maybe, but the data simply isn’t there for that theory either. I cannot account for why such different country-level approaches all produce the same sorts of graphs. One would think that the weaker NPI countries/regions/states would climb, begin to level out, have a plateau, and then fall slowly. Not what I’m seeing. The data says quick explosion, and an equally quick decline.
I also find it a weak argument to suggest this is entirely due to countries fudging data or suffering from weak testing. Some countries are doing a pretty good job at testing. Germany for instance.
Also, the idea of “waves” or peaks is misleading if simply looking at bumps on a chart. The XYZ hypothesis says there’s one big push that SARS2 will make through a population. If that’s denied via effective NPI’s then that remains as potential energy, as it were, ready to be unleashed if/when fatigue sets in. So a quick pump pushed down by NPIs isn’t that ‘first wave’ I speak of. A long slow burn (aka South Korea) is simply releasing the energy of that first wave slowly over time.
To confirm or refute this theory I’d need to see a second wave in a place that has already had a legit first wave. So in Madrid, but not “Spain” where there are regions that didn’t have a full-blown first wave. So in NYC, but not “the US” where there are states now having their first wave. Again, all the NPIs would do, under this theory, is give you mini bumps along the way as that first wave works through.
The reason I’m pushing the XYZ angle is to see if there isn’t something else happening here that we haven’t uncovered so far. That’s how I operate. It’s my job to constantly ask “is this right?” and “are we missing anything?”
Some, unfortunately, are all tangled up in the idea that the XYZ angle might support Trump. I literally don’t ever consider whether my views might be accidentally supporting or refuting anything that Trump says. Not a factor for me. I also don’t consult what Fauci is thinking, or Merkel or anybody in power.
Just trying to work some theories on a novel virus that fit with the observations…as unemotionally as possible.
/long series of golf claps/
Here’s a chart of the unemployment rates of 7 different states; 3 run by Team Blue, and 4 run by Team Red. All have had (or are having) “a challenging time” with cases, yet the outcomes in some of the states (in terms of unemployment rate) is strikingly different. And in New York and New Jersey, there basically are no cases – herd immunity has been reached, most likely – and yet the “managers” of those states are just not interested in reopening.
Are the team in charge of the Blue States just stupid? Or is it something more? Rules for Rulers might give us a clue. Ruling is all about collecting the treasure, and handing it out to your key supporters.
It turns out, a pandemic lockdown actually allows certain Rulers to do exactly that. Assume the Key Supporters are Silicon Valley mega corporations [AMZN, AAPL, FB, GOOG, NFLX, TWTR]. Assume “the treasure” is real estate or customers controlled by local small business. If you shut down the local economy for long enough, small business will die en masse, and all that wealth will get transferred to the Key Supporters, as if by magic. And you as the Ruler can pretend it is all about “keeping your people safe from COVID-19.”
“Shelter in place! Again!!” [shut small biz]
“Close the schools!” [nobody can work – no childcare]
“Defund the police!” [maximize chaos]
What’s more, a lockdown has the helpful side effect of making everyone miserable. This typically disadvantages the incumbent during an election. “Are you better now, than you were 4 years ago?” Clearly not. I’m not working, I’m having to shelter in place, my kids can’t go to school, the thugs are ruling the streets. I’m blaming Bad Orange Man! I’ll take Basement Biden any day!
Of course this campaign of deliberate economic destruction causes a big hit to tax revenues for all those Blue State Rulers – clearly visible in the unemployment rate in the above chart. Enter Pelosi, and her demand for a $trillion for “the states” – to paper over all that self-inflicted damage. If she holds those $1200 stimulus checks hostage, just maybe she can get Team Red to write a even larger check (funded by us, naturally) to cover the cost of this destructive campaign! How cool would that be?
My favorite quote of 2020 applies: “everything that happens in an election year, regardless of how disconnected it might seem, is about the election.”
The total disfunction embedded in all of this: what we can expect during the Fourth Turning.
My favorite quote; “Never let a good crisis go to waste.”
I think of everything in terms of “ANDs” not “ORs” I think SARS2 is an awful virus that is very real AND I think the usual bevy of terrible actors used it to cement their power, wealth and control.
It’s a both AND, not an either OR.
Great observations on the state level unemployment Dave. Makes sense.
As always, appreciate the opportunity to dig through the data for interpretations.
Here’s what I’m pretty certain about.
- At least 45% of people catch SARS2 and don’t progress to Covid, in fact they have no symptoms at all. These people are only known about because of contact trace testing and special situations like the Disaster Princess or countries that actually test pretty much everybody.
- Therefore in places with weak testing, like the US, vastly more people are exposed than we know about.
- The PCR test returns a hefty chunk of both false positives and false negatives.
- With different countries and even different states/provinces/regions administering different tests at different rates, our data is mediocre at best.
- For whatever reason(s), pre-pubescent children are virtually pre-immune to SARS2/Covid.
As fuzzy as the case testing may be, it’s still directionally correct. Not perfect, but still useful.
With that said, it makes sense to also back up and view the macro data.
- Are your hospitals overflowing?
- Are bed counts up or down?
- Is your excess mortality higher, rising, or declining?
Based on the fact that I cannot find evidence of either overflowing hospitals or excess deaths remaining elevated *after* the first wave, I have to conclude that for whatever reason, Covid is not as big of an issue after the first wave (which is usually a pretty awful thing).
It’s an issue, for sure, and I don’t want to catch it if I can avoid it, and it’s a terrible assault on some people’s bodies, and all of that – but it also follows a similar pattern in country after country.
Okay, so it’s hypothesis time. Why would it do that?
Certainly we could posit that in country after country the people become alert to the disease, take precautions, and governments apply reasonable containment programs. Boom! The R0 falls.
But this strikes me as unlikely because of the vastly different cultures and government responses involved. Why should the graph of Mauritania look so similar to NY? Why does the daily death chart of Sweden resemble that of a dozen other countries?
In terms of formulating an hypothesis this is where I allow myself to consider all sorts of possibilities. It’s something I’m well wired for. I am willing to let go of my prior beliefs, ideas and opinions to try and see things with new eyes.
So the other possibility that explains all these similar charts in dissimilar countries is that we’re actually tracking a beast of a virus whose dominating characteristics define the shapes of the charts.
Anything short of a draconian lockdown, and exceptionally rigorous follow-on actions (such as China’s) the Honey Badger virus runs rampant through every half-assed approach as if they didn’t even exist at all.
This would explain the similarities. Weak containment, shoddy tracing, and don’t-test-don’t-tell policies all lead to the same outcome.
Declining case counts coupled to the declining hospitalizations + declining excess mortality all point to one conclusion; SARS2 is running out of new hosts to infect.
I can’t think of any other reasonable interpretation. We can either attribute that to the exceptional efforts of wise governments and clued-in populations or we have to posit something else.
Which brings us to the herd-immunity hypothesis. Early modeling based on the high R0 suggested that you’d need 80%+ exposed people with circulating antibodies to achieve that. We’re nowhere near that.
So then how do we account for the case declines even though seroprevalences are weak (by accepted herd immunity standards) in every tested area?
We do that by hearkening back to the T-cell immunity evidence. For immunity we’ve got B-cell (humoral, or antibody based) and we’ve got cell-mediated.
We have to account for the fact that a significant portion of those exposed don’t display any symptoms at all. Or extremely mild symptoms. That means only one thing; they’ve got either complete or significant immunity. Right from the get-go.
So if we posit that herd immunity is achieved when XX% (insert arguments here) of the population has immunity then our efforts need to be focused on the inputs for immunity.
- X% are simply “pre-immune.” This includes the very young. We don’t know the mechanisms yet or how effective they are at transmission even if they aren’t seriously affected. TBD.
- Y% develop cellular immunity and don’t go down the antibody pathway. We don’t yet know how many people this is or how long this lasts.
- Z% develop traditional antibodies. So far we see this at 10% to 15% wherever tested. We don’t know how long this lasts, or if ADE is a downstream risk.
X + Y + Z = (min threshold) and then you’ve got herd immunity.
Guessing wildly, I might place those at X = 45%, Y = 25% and Z = 10% – 15% which adds up to 80% to 85%.
So the theory is, as presented, that SARS2 is actually vastly better at sweeping through a population than we have appreciated, it devastates far too many lives but doesn’t really impact the vast majority (through the first 6 months at least…the rest is TBD), and it burns out rather quickly from an epidemic standpoint.
However, it is now endemic and anything other than a proper lockdown with strict adherence to mask wearing and full on contact tracing and quarantine, will lead to an eventual escape of HB-19 back into your population.
New Zealand, most of Australia, South Korea, Taiwan, China, etc., are all in full containment mode.
Most other countries lack the resources and/or political will for such a program, and that explains all those similar charts all over the world.
As always, if/when the data changes, I’ll shift again!
By the way, for the critics in the Youtube comments noting that “Spain is experiencing a second wave, so your theory is wrong” should really look at this chart comparing the initial seroprevalence and the new case clusters.
Seems to me that the new outbreak in formerly low seroprevalence regions supports the hypothesis laid out rather than refutes it.
Just wondering…do those swing high candles correlate with HHS taking over case counts from CDC?
Something funny going on there…
It is interesting to know that “No bat in world history has ever been confirmed to directly infect (dock with hACE2) humans” – but does this lack of evidence is really an evidence of absence?
No, not all on its own, of course.
But consider that SARS2 didn’t just allegedly jump from a bat/+? able to bind human ACE2 with vastly higher affinity than any other tested specie, but also to bind to CD147, Neuropilin, and 3 or 4 other receptors/matrix proteins.
Weird, right? Any one of those other possible binding sites would be sufficient for some level of infection and replication. How odd that so many were stacked up ready for ONE BIG JUMP – all at once. Not just to humans, but the mink farms in the Netherlands have been wiped out (by humans terminating infected animals, not due to direct killing of ferret family members by SARS2), and cats and tigers and even dogs get it too. One would think such a capable virus would have been detected out in the wild by now.
So in the scheme of ‘preponderance’ the table is heavily tilted towards ‘not natural’ rather than a legit, rare but possible zoonotic jump.
Far more likely, in the preponderance game, is the idea of directed tinkering to insert the PRRA site, and then do a whole bunch of serial passages in cells and then some live animal passages…followed by some sort of release, accidental or otherwise.
Again – I know, I know – I’m talking again about the Comex default that never happens and is never gonna happen!
But then again…
August is a tame month for gold and nothing ever happens. Ever. September and December are *&always* the hot months for contracts.
Except in 2020.
Check this out:
A record amount of first notices stood for delivery. In A.U.G.U.S.T.
My friends, that is very notable! As in, this time may be different.
We shall see…
Funny thing about virus evolution…it can happen a LOT faster in the lab.
The evolutionary clock is assuming a rate of mutations, both synonymous and non-synonymous. Count those up and multiply by the average time per mutation and – voila! – you get the age of the divergence.
Thing is, those are the sorts of things that are routinely sped up in the lab, either by performing very aggressive serial passages which speed up the clock or by actively introducing mutagens, which is also a thing.
Any time I see an ‘article’ like this one that pre-supposes that any changes must have happened naturally and therefore the assessed evolutionary 50-70 year span proof that this happened outside of a lab … well, I know I am being misled.
That’s not how deductive logic actually works.