Yeah I mean, if you and I were to play the word-guessing game where you needed to guess what next word I'm thinking of, there's always uncertainty in your guess because it's a game of partial information - you can't fully observe my inner state. But that doesn't mean you couldn't evolve a strategy that spends a really long time thinking and analyzing to get asymptotically close to the best guess. There's no limit on that intelligence.
I kinda agree with you and I understand your point but I also think there is a social-ethical reality that if a doctor finds something they must treat it. The two options are 1. doing nothing, or 2. reducing cancer risk and you get unnecessary biopsies.
You're thinking of this as there being an objective positive utility for not dying of cancer and a objective negative utility for biopsies, and there being an objective optimal "rational" tradeoff that the best radiologist can optimize for to get their "nearly certain" detection threshold.
But frankly - the tradeoff for the value of a human life is perhaps the most uncertain thing one could choose. It lies in the eyes of the patient if the worry and time associated with a false detection is worth their reduced chance of death. The ethical uncertainty expressed in the OP - are these unnecessary biopsies worth it - is warranted.
> This is why the paper presented does not support the claim that LDL is the sole source of heart disease
Is that what we were arguing about? I guess it was. At some point in thinking about this my frame must have shifted into agreement with you. Of course there are other causes of heart disease besides LDL, like blood pressure, duh. The smooth dose response is about the particular gene not being linked to heart disease through something other than LDL, roughly.
What do you think of Dr. Schooling's response that the Mendellian effects might be inflated? I think they had a good defense but was not entirely convinced they hadn't sidestepped the issue that Schooling was getting at, wasn't sure either way.
I think maybe you are saying that there may be some way that the genes affect heart disease not through LDL, and therefore MR does not apply because the "exclusion restriction" [1] fails here? Or are you talking about a different assumption?
The cited study addresses this, which is why I pointed to figure 3. They argue that if genes were causing heart disease not through LDL in any meaningful way, you wouldn't expect such a clean dose-response consistency across different genetic variants - it would be more jagged.
Across different genetic variants, lower lifetime LDL -> lower risk of death. Check out figure 3.
The causality of LDL -> plaque buildup -> 55-60% [1] of heart disease related deaths is also well understood, so it seems clear to me that preventing plaque buildup in the first place prevents over half of heart disease related deaths.
Would like to know if you disagree, "Minimize LDL at all costs" goes current mainstream medical guidance, so I'd like to disconfirm my beliefs if possible.
Here is the chief editor of JAMA internal medicine arguing there is not enough evidence to prescribe statins for primary prevention in those 40+: https://www.natap.org/2016/HIV/ied160021.pdf
Yes. You can define a regex matching what you want, and every regex can be compiled into a state machine (https://en.wikipedia.org/wiki/Nondeterministic_finite_automa...). Then at each character you make a step in your state machine. You pause the output while the regex is not matching.