5 ms·

People don't advance a hypothesis without enough anecdotes to say "look over there" People like you can help fill gaps of savants saying "this isn't a construc

People don't advance a hypothesis without enough anecdotes to say "look over there" 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?"

sjg007 6y ago
We would have seen a higher death rate if the virus was here earlier. 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.
- pm_me_ur_fullz 6y ago
  > We would have seen a higher death rate if the virus was here earlier. > 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.
  - sjg007 6y ago
    We know this is not true because the mutation rate is too low.
    - pm_me_ur_fullz 6y ago
      I specifically wrote "/conditions" to predict that specific rebuttal. 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.
MaulingMonkey 6y ago
> People don't advance a hypothesis without enough anecdotes to say "look over there" 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 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.

sjg007 6y ago

We would have seen a higher death rate if the virus was here earlier. 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.

pm_me_ur_fullz 6y ago
> We would have seen a higher death rate if the virus was here earlier. > 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.
- sjg007 6y ago
  We know this is not true because the mutation rate is too low.
  - pm_me_ur_fullz 6y ago
    I specifically wrote "/conditions" to predict that specific rebuttal. 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.

MaulingMonkey 6y ago

> People don't advance a hypothesis without enough anecdotes to say "look over there" 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 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.