I don't understand why you would need Tailscale, for example -- shouldn't your VPS have a static address to which you can reach out from your home and also connect remotely, making Tailscale superfluous?

Would that meant that building rust is slower, but everything else is the same, and you don't have to maintain a fork of another complex project?

I have personal knowledge ofcases with acknowledged errors and apologies that have also resulted in the hospital eating the full cost of care.

Before I dive back into the literature, as you claim to be stating this in good faith... is the "good" load-bearing here? Relentlessly attacking methodology is an easy way to make this kind of general claim.

Also, are you talking narrowly about a group of people that has had COVID but never had a prior COVID vaccination? (In which case is it still a "booster"?) Or is a proper steelman of your position that anyone that has had COVID, regardless of prior vaccinations exposure, does not benefit from additional vaccination in any meaningful sense?

Alzheimer's disease is a specific subtype of dementia; this article seems to be more focused on vascular dementia (or at least vascular risk factors) -- why I was curious about the relationship between e.g. smoking and fructose.

The association of fructose has been studied directly in the context of AD, and the hazard ratio is modest (and not necessarily dose-dependent) [0]:

> After adjustment for sex, age, MMSE at baseline, education level, SBP, treatment of hypertension, LDL, uric acid, prevalent diabetes mellitus, current smoking, alcohol consumption, dietary fiber intake, total energy intake, sugar in beverage, seafood, red meat, fried foods, animal fat, personal income, marital status, physical activity index, and BMI in the Cox regression model, participants with consumption of fructose more than 7 servings/week showed a higher risk of all-cause dementia and AD dementia (HR: 1.49, 95% CI: 1.14–1.84, P for trend < 0.001 for all-cause dementia; HR: 1.60, 95% CI: 1.22–2.01, P-trend < 0.001 for AD dementia) than subjects with no consumption for fructose. And the results remained comparable for participants with medium consumption of fructose (HR: 1.46, 95% CI: 1.30–1.79, for all-cause dementia; HR: 1.52, 95% CI: 1.14–1.91, for AD dementia) (see Table 2).

I haven't seen anything about the fructose content of brains of AD patients; do you have a (preferably non-video) reference / source?

[0]: https://www.sciencedirect.com/science/article/pii/S227458072...

I agree that people should be cautious, but I think you are significantly misunderstanding [3].

"Toxicity" != death -- toxicity is merely "some evidence of a toxic effect" -- possibly as simple as a transiently abnormal blood test with no symptoms or sequelae, ever.

Single (accidental) doses of up to 200 mg / kg are routinely recommended to be managed at home [0], i.e. "you don't really need to go to the emergency department for this." For me, a fairly average 79kg male, this would be about 16g.

Please consult with your local poison control if you have concerns or questions!

[0]: https://pubmed.ncbi.nlm.nih.gov/16496488/

Definitely no instructor involved, just a dumb 20 year-old living in Puerto Rico. It admittedly was dangerous, but I am living evidence that it was far from a "surefire" way to die. It was one of a hundred ways in which I put my life at risk during my 20s. ¯\_(ツ)_/¯

> As for the specifics that may have prevented you from doing what you wanted: If you breathe too shallow or too slow, you won't clear enough CO2.

I'm confident I was doing it sufficiently well to accomplish a longer period of breath holding than I otherwise would have been able to sustain, as evidenced by having done so (in addition to the usual symptoms of lightheadedness, confusion, loss of vision, near-syncope -- yes I agree quite uncomfortable). I know people on HN love to idolize Wim Hof, but in this context minute ventilation is not that difficult of a concept; I'm usually able to estimate the response in a paralyzed patient's PCO2 fairly well when making changes to their tidal volume and rate.

I didn't search for too long, but here's at least one relevant document, in which otherwise untrained subjects were able to achieve a substantial reduction in CO2 (17.4 vs 29.0) with a mere 15 seconds of hyperventilation, leading to an extra 23 seconds of breath holding prior to involuntary breathing moments. The peripheral O2 sat nadir in the hyperventilation group appears to have been identical to the non-hyperventilation group after the first trial (Fig 8b, looks like ~94%) and was only statistically significantly lower on trials 2-5: <https://pmc.ncbi.nlm.nih.gov/articles/PMC10363065/>

EDIT: your comment is otherwise entirely correct, particularly at sea level.

Neither of us could get it below 98%, and this was at a mile of elevation (UNMH in Albuquerque).

Certainly is not defeating thermodynamics, assuming calorie absorption is not disrupted somehow it's likely the above.

We have wildly heterogeneous data just within the US!

And again, how exactly is this interface going to work? How does the AI determine how hard to press on an abdomen, and where, and how does it press there once it has that information?

PSA and troponin seem trivial to get. Did you look?