no
you should do both and publish an appendix showing robustness tests, you cultist
reading the self-important and vaguely-cultish textbooks by bayesians makes me want to go out and kill a sufficiently large number of bayesians that i can estimate the mean pitch of their screams
no
you should do both and publish an appendix showing robustness tests, you cultist
omg
this is a real critically acclaimed textbook im barely even paraphrasing here
that is a solid argument for perhaps a theological proposition
it is not highly compelling for code
and im like
no
no that is not what it lets you do
what bayesians say bayesianism isn't
but
what the papers using their models do
you should have strong prior im not actually a bayesian-murderer, strong enough that your model should never permit the conclusion that im actually a bayesian-murderer, meaning you should be able to tell the first tweet was a joke
^This is why you should stick to coins, dice and cards without trying to get too "relatable"
— Flaky Puff\U0001f308\u270b\u261d (@DecadentPuff) January 13, 2021
More from Lyman Stone 石來民
Ulysses S. Grant would like a WORD
Or Teddy Roosevelt. Or Dwight Eisenhower. Or Andrew Jackson. Or Abraham Lincoln. Or George Washington. Or Zachary Taylor. Or any of numerous presidents who were honest-to-goodness battle-hardened warriors.
James Monroe fought the Hessians at Trenton and nearly died of wounds sustained there, then wintered in Valley Forge, then fought until Monmouth, then repeatedly tried to raise new regiments for the war until he went bankrupt doing it.
James Monroe, of the Era of Good Feelings, longest serving president of all time.... was in the boats crossing the icy Delaware.
Andrew Jackson was in a duel. He was shot in the chest right by his heart.
But he didn't go down. He stood there and, while bleeding out, steadily took aim and killed the dude who shot him.
Stone cold.
Hogan Gidley: Trump is "the most masculine person to ever hold the White House as the president of the United States" https://t.co/fcoYWyaEhz
— Eliza Relman (@eliza_relman) January 11, 2021
Or Teddy Roosevelt. Or Dwight Eisenhower. Or Andrew Jackson. Or Abraham Lincoln. Or George Washington. Or Zachary Taylor. Or any of numerous presidents who were honest-to-goodness battle-hardened warriors.
James Monroe fought the Hessians at Trenton and nearly died of wounds sustained there, then wintered in Valley Forge, then fought until Monmouth, then repeatedly tried to raise new regiments for the war until he went bankrupt doing it.
James Monroe, of the Era of Good Feelings, longest serving president of all time.... was in the boats crossing the icy Delaware.
Andrew Jackson was in a duel. He was shot in the chest right by his heart.
But he didn't go down. He stood there and, while bleeding out, steadily took aim and killed the dude who shot him.
Stone cold.
So a few days back I was tweeting about SSRIs. The big question with these drugs is: why do controlled trials routinely show such small effects when practitioners and patients report life-changingly-large effects?
So first off, at this point the evidence is pretty clear that SSRIs and other anti-anxiety/anti-depression drugs truly don't do very much. Their average effects are beneath clinical significance, as I tweeted about here:
Basically, the problem these drugs face is that while they actually see relatively LARGE effects.... but that placebos in those trials ALSO see large effects (and most untreated depression improves within a year anyways).
So basically you have this problem where:
1. The condition tends to improve on its own in a majority of cases
2. Placebo effects for the condition are unusually large
Which means the large crude effects of SSRIs get swamped.
So that raises two new questions.
1. (Not my focus here) Are we treating these conditions appropriately given their untreated prognosis is usually (though certainly not always!!) "goes away in a few months"?
2. Why are placebo effects so unusually large?
So first off, at this point the evidence is pretty clear that SSRIs and other anti-anxiety/anti-depression drugs truly don't do very much. Their average effects are beneath clinical significance, as I tweeted about here:
What's the best recent empirical assessment of SSRI/SNRI effectiveness which deals with heterogeneity and long-term effects in a plausible way?
— Lyman Stone \u77f3\u4f86\u6c11 (@lymanstoneky) December 4, 2020
Basically, the problem these drugs face is that while they actually see relatively LARGE effects.... but that placebos in those trials ALSO see large effects (and most untreated depression improves within a year anyways).
So basically you have this problem where:
1. The condition tends to improve on its own in a majority of cases
2. Placebo effects for the condition are unusually large
Which means the large crude effects of SSRIs get swamped.
So that raises two new questions.
1. (Not my focus here) Are we treating these conditions appropriately given their untreated prognosis is usually (though certainly not always!!) "goes away in a few months"?
2. Why are placebo effects so unusually large?
More from Culture
I just finished Eric Adler's The Battle of the Classics, and wanted to say something about Joel Christiansen's review linked below. I am not sure what motivates the review (I speculate a bit below), but it gives a very misleading impression of the book. 1/x
The meat of the criticism is that the history Adler gives is insufficiently critical. Adler describes a few figures who had a great influence on how the modern US university was formed. It's certainly critical: it focuses on the social Darwinism of these figures. 2/x
Other insinuations and suggestions in the review seem wildly off the mark, distorted, or inappropriate-- for example, that the book is clickbaity (it is scholarly) or conservative (hardly) or connected to the events at the Capitol (give me a break). 3/x
The core question: in what sense is classics inherently racist? Classics is old. On Adler's account, it begins in ancient Rome and is revived in the Renaissance. Slavery (Christiansen's primary concern) is also very old. Let's say classics is an education for slaveowners. 4/x
It's worth remembering that literacy itself is elite throughout most of this history. Literacy is, then, also the education of slaveowners. We can honor oral and musical traditions without denying that literacy is, generally, good. 5/x
As someone\u2019s who\u2019s read the book, this review strikes me as tremendously unfair. It mostly faults Adler for not writing the book the reviewer wishes he had! https://t.co/pqpt5Ziivj
— Teresa M. Bejan (@tmbejan) January 12, 2021
The meat of the criticism is that the history Adler gives is insufficiently critical. Adler describes a few figures who had a great influence on how the modern US university was formed. It's certainly critical: it focuses on the social Darwinism of these figures. 2/x
Other insinuations and suggestions in the review seem wildly off the mark, distorted, or inappropriate-- for example, that the book is clickbaity (it is scholarly) or conservative (hardly) or connected to the events at the Capitol (give me a break). 3/x
The core question: in what sense is classics inherently racist? Classics is old. On Adler's account, it begins in ancient Rome and is revived in the Renaissance. Slavery (Christiansen's primary concern) is also very old. Let's say classics is an education for slaveowners. 4/x
It's worth remembering that literacy itself is elite throughout most of this history. Literacy is, then, also the education of slaveowners. We can honor oral and musical traditions without denying that literacy is, generally, good. 5/x
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https://t.co/6cRR2B3jBE
Viruses and other pathogens are often studied as stand-alone entities, despite that, in nature, they mostly live in multispecies associations called biofilms—both externally and within the host.
https://t.co/FBfXhUrH5d
Microorganisms in biofilms are enclosed by an extracellular matrix that confers protection and improves survival. Previous studies have shown that viruses can secondarily colonize preexisting biofilms, and viral biofilms have also been described.
...we raise the perspective that CoVs can persistently infect bats due to their association with biofilm structures. This phenomenon potentially provides an optimal environment for nonpathogenic & well-adapted viruses to interact with the host, as well as for viral recombination.
Biofilms can also enhance virion viability in extracellular environments, such as on fomites and in aquatic sediments, allowing viral persistence and dissemination.
Viruses and other pathogens are often studied as stand-alone entities, despite that, in nature, they mostly live in multispecies associations called biofilms—both externally and within the host.
https://t.co/FBfXhUrH5d
Microorganisms in biofilms are enclosed by an extracellular matrix that confers protection and improves survival. Previous studies have shown that viruses can secondarily colonize preexisting biofilms, and viral biofilms have also been described.
...we raise the perspective that CoVs can persistently infect bats due to their association with biofilm structures. This phenomenon potentially provides an optimal environment for nonpathogenic & well-adapted viruses to interact with the host, as well as for viral recombination.
Biofilms can also enhance virion viability in extracellular environments, such as on fomites and in aquatic sediments, allowing viral persistence and dissemination.
