This seems to have the toughest aspect of gaining consensus.
Need antibody tests now, and ones that work reliably.
first covid death (feb 6) is nearly a month earlier than previously official first US covid death (feb 26), and also from community spread. suggesting it was in the bay area at least half a month earlier than that.
So how do we move this from a collection of anecdotes and immediate dismissal to prioritizing some antibody tests to the bay area. Possibly reopening it faster and keeping it open.
Just acknowledging the possibility can influence public policy, and the research that some other people want to see before they can acknowledge it.
We have no reliable antibody tests, and then won't give the unreliable ones people because they are so rare. So where does the confidence come from that we can rule out this possibility?
What if this is already the "second wave". Something with lower symptoms wouldn't have warranted checking for a new strain, complications and deaths would fit into the normal distribution of last fall's flu season with no outlier spikes. We would then be deep into the second wave and can't even test most for people currently exposed to it, much less having already been exposed. This is enough not to dismiss the hypothesis.
It's not. What is preposterous is advancing the hypothesis without any meaningful evidence, to the detrement of more useful topics, or even useful discussion of the same topic.
It's one thing to be an epidemiologist saying "hey, let's see how we can double check the exact origins of this", which is a potentially useful line of inquery. It's another to take some hypochondriac's third hand retelling of someone else's flu symptoms back in December and jump to the same untested unproven unscientific fear-driven conclusions they did on little more than their wild speculation. Even if they do somehow end up being right, they'll be right in the "broken clock is right twice a day" sense rather than a bringing anything useful to the table sense.
So far, alternative suggestions as to the virus's origins have looked more similar to the latter - with perhaps some undertones of (completely understandable and expected) attempted political diversion (I sure wouldn't want fault for this mess hanging on my neck!) If you have some epidemiologist's proposed study that you're trying to drive funding towards - something that even remotely looks like the former - it'd be a welcome breath of fresh air on the topic, and I'd suggest sharing that as a far more useful and constructive way of advancing the hypothesis.
People like you can help fill gaps of savants saying "this isn't a constructive methodology but it isn't inherently without merit" versus "I don't want to believe that because thats not consensus right now" versus "hm thats interesting maybe worth a look sometime before the 2022 congressional committee to fund the epidemiologists?"
As for hiding within the flu statistics, we test for influenza so these deaths would not have been classified as flu related.
It's possible to have flu and covid-19 but early on it would have been rare. It's probably still somewhat rare.
I am sure flu surveillance samples will be retroactively tested for the virus that causes covid-19. Stanford did this and they have mid to late Feb.
> What if this is already the "second wave". Something with lower symptoms wouldn't have warranted checking for a new strain, complications and deaths would fit into the normal distribution of last fall's flu season with no outlier spikes.
I think you are misunderstanding what wave means here. It means an earlier not as deadly strain/conditions had already occurred, just like in the Spanish Flu in the spring versus the fall deadly resurgance, but at lower orders of magnitude. The strain itself doesn't have to be different if the co-morbidities were different - such as different opportunistic viruses or bacterias being present.
The virus could be the same, the opportunistic additional virus/bacteria could be different.
just like HIV causes no symptoms, until your immune system is down and a different infection (caused by bacteria or virus) kills you. Maybe even a normal "gut" bacteria, or something in your body usually present, is what kills you.
There is research pointing to Sars-Cov-2 attacking T cells directly. Instant AIDS.
In the fall and early winter, there could have been different variables that made it less debilitating and deadly than the spring variables. And in that case the fall and early winter deaths and pneumonia would have blended in to normal distribution.
They do so all the time. They'll advance hypothesis even without ancedotes on the vaguest of hunches, and bias towards Type I pattern recognition errors (https://www.youtube.com/watch?v=1AjLmU0Sfu4). This is in fact half the problem - why anecdotes alone aren't terribly useful, and must be treated with so much caution and skepticism. Needless to say that primary caregivers and epidemiologists are already drowning in such ancedotes as well, they're not exactly aided in us adding more noise to the discussion where they're not even looking.
There is such a thing as "enough anecdotes" - when they're numerous enough to rise to the quantity of being actual statistically measurable data. But you yourself practically admit such ancedotes fail to meet that bar by suggesting some secret first wave that's indistinguishable from the regular flu season in the data. Either the ancedotes form useful data or they don't - you can't have it both ways.
"Enough ancedotes" led us to our current conclusions, not this hypothetical secret first wave stuff you suggest. "Enough ancedotes" say "don't bother looking over there, we've figured it out", on account of failing to rise to the standard of useful statistical data to contradict our current conclusions. We've been checking, and are going to continue to check, for contradictory evidence anyways - despite the lack of usefully contradictory ancedotes - just for thoroughness, given the size, scope, and impact of the epidemic.
> People like you can help
...by spending my time embracing social distancing, masks, calming the histronics of hypochondriacs, and by guiding doubt towards those who deserve it the most and where it's going to be the most useful, actionable, and effective. We have a number of botched pandemic responses - exacerbated by censorship, political manuvering, misinformation, and so much more - with direct lesson to teach us about how to properly react next time, and parts of our government and geopolitics we need to fix. There are ongoing problems like the lack of randomized testing to give us an idea of where we're at now. Things we have hard data for. Things we can change by voting or lobbying our congresscritters or influencing debate or through direct individual action to support those in need, or helping the helpers.
But entertaining the conspiracy theorist fueling armchair "hypothesizing" about alternative virus origin stories? Does our political and epidemic policy really change if, say, technically this started several months earlier than we realized in Russia? This "maybe hypothetically a second wave!" still kicked off in China, regardless. I don't see the hypothetical policy changes. I don't see the upside. I don't see how this hypothesizing "helps". I think, in fact, that it hurts - by further stressing people out when they're already stressed out (which has real health impacts), and driving them towards unreasonable levels of distrust in the scientific method and community (which has been very upfront about the many things that are actually properly unknown about this epididemic). I think it's the same nonsense that leads to the antivax mindset. It reminds me of gaslighting.
And so, on this topic, I think helping means poking all the obvious holes I can in said "hypothesizing" - as a perhaps useful example to follow - as to how one might differentiate this armchair debate from actual reasonable doubt. On the off chance that I'm wrong, it invites a proper useful rebuttal or counter-argument. On that note, I again emphasize:
>> If you have some epidemiologist's proposed study that you're trying to drive funding towards [...] it'd be a welcome breath of fresh air on the topic, and I'd suggest sharing that as a far more useful and constructive way of advancing the hypothesis.
But since you seem to be hypothesizing about 2022 congressional committees instead of any of the stuff actively being looked into while half the bloody economy has been put on hold, I won't hold my breath.
Thanks for the invitation. Lets see where the goal post is here
> Either the ancedotes form useful data or they don't - you can't have it both ways.
In this case they do if you test for antibodies. We can't test for antibodies. It has been gaslighting from you to willingly ignore what the limitations of data are and how to solve them, if this is a term that bothers you make sure to look at it from my perspective as well, are you recycling this argument for everything epidemiologists aren't currently doing and everything that doesn't currently have consensus? Or is it just for me, either way I don't think you have factored in the exact argument here and I'll get to that:
> Does our political and epidemic policy really change if, say, technically this started several months earlier than we realized in Russia?
Yes it does, because it means the bay area is safe and can change its own policy. I don't see how you missed this in your effort to convert the word hypothetical into a pejorative.
> But since you seem to be hypothesizing about 2022 congressional committees
This was hyperbole but also likely what is going to happen. After the dust has cleared, Congress makes committees to see what exacerbated dysfunction - and they may then notice this discrepancy in the bay area as well. Meaning that it has nothing to do with a national policy decision because my hypothesis is relevant on a local level for the Bay Area as this whole thread made abundantly clear. For everywhere else it is merely interesting.
The difference is that one major economic center of the US can resume with a level of certainty and forward guidance.
My primary point of this exercise is that you are rejecting this possibility out of principle, recycled from rejecting a wide universe of possibilities, without factoring in what this one actually could change. So I hope thats clear now.
> In this case they do if you test for antibodies
I'm not sure if this is a disagreement in framing or what. I encourage retroactive testing for antibodies, however, I do so in spite of ancedotal data failing to form useful data that suggests such tests will contradict the currently understood origins of the virus. Finding antibodies for samples taken in December, for example, sounds like it would be interesting and potentially useful science - for the very reason that it contradicts the data formed by said ancedotes.
>> Does our political and epidemic policy really change if, say, technically this started several months earlier than we realized in Russia?
> Yes it does, because it means the bay area is safe [...]
Wait what? How the heck would that conclusion follow? If there was some safer first wave originating from outside of China, and we're now in the middle of a dangerous second wave, then we're still dealing with a second dangerous wave! Are you... assuming some confounding variable is what's causing this to be dangerous, and assuming said confounding variable isn't present in the bay area? On what basis? For how long? There are confounding variables - the age of the victims, societal mask use, possibly weather conditions, and more to boot I'm sure... but I'm completely unaware of any that would suggest the bay area is somehow "safe", regardless of the origin of this thing. If anything, it might suggest that the confounding variables are changing to make this thing more dangerous.
The worldwide spread is giving us a huge sample size under varying conditions, the better to understand said confounding variables. It seems like a bit of a stretch to assume that any additional hypothetical early sample points are going to give us terribly much more insight as to what said confounding variables are, when we've turned half the planet into an involuntary testbed already - if there are indeed such confounding variables that would make parts of the world "safe" - and a stretch beyond the breaking point of common sense to assume that those insights will automatically make the bay area specifically safe when this thing is killing people just up the coast.
> [...] and can change its own policy. I don't see how you missed this in your effort to convert the word hypothetical into a pejorative.
Hypothesizing is great, and a fundamental part of the scientific process - which is why I don't wish to sully the term by conflating it with biased wishful thinking and conclusion jumping. I also haven't missed e.g. the bay area and California at large joining the Western States Pact, and their ability to make/change their own policy.
What I have completely missed is even the hypothetical logic train to "the bay area is safe". I have attempted to guess at it above, but it has so many holes that I fear I must be (unintentionally, I promise!) strawmanning you - and that you clearly must have some other train of logic leading to that conclusion that I'm simply failing to synthesize on your behalf. Perhaps you stated it elsewhere and can simply point me to the right part of that thread?
"Safe" meant "maybe we don't need a lockdown as long either" or that "a larger portion of the population than you might think doesn't need to be in lockdown" and that it loses utility to keep them in lockdown. At the very least, it would allow for the Mayors offices in bay area counties, and the Governors offices to take a holistic view at the blanket order - or FUTURE blanket orders when this flares up again throughout the year. But only after antibody tests occurred.