Memorial Day weekend is a good reason not to worry about reporting cases or deaths. FDA declines to respond with making it easier to get treatments we have in ample supply, or to update the vaccines. Congress refuses to fund anything at all, really.
Thanks again for writing these up. Between you and Naked Emperor one can save an absolute fuck-ton of crap to sift through, and I really appreciate it.
Honest question: Do we have any reason to read "COVID deaths" as "Deaths caused by COVID" instead of "Deaths with COVID?" if it is not explicitly written out in the report in question? I ask because I haven't seen any reason to do so from the beginning of the pandemic, and things like the "Total COVID-19 patients in acute care or intensive care" graph immediately jump out at me as saying "This isn't necessarily because they have COVID, but they just happen to have COVID and be there for whatever reason, including having COVID." Maybe I have just been an academic too long and cynically assume that if they could say "They are there because of COVID" without lying they absolutely would, but instead word it so you could be mislead to make it seem like a more important result than it is. (That's about 90% of conference paper presentations, right there.) Is there some reason to believe it is not just misleading with statistics and language?
Kristen Fortney (the CEO quoted in that article about aging) is Good People and the absurd journalistic framing is not her fault. It's just good sense to use COVID-19 as a timely application for the geroprotective drugs you've been developing anyway since before they were cool.
The COVID-19 drug they're working on is a prostaglandin receptor antagonist. https://en.wikipedia.org/wiki/Prostaglandin_DP1_receptor
Very roughly, this blocks the "bad kind of inflammation" (more allergic-like, Th2-ish, mast cells, eosinophils) that becomes more common with age and chronic disease and makes old sick people less able to fight off infection. It's totally plausible that targeting PTGTR1 would be good for COVID-19, other infectious diseases, and maybe even as a preventative for the healthy elderly.
My guess is that it's not very root-cause-y, and thus might not do much for other chronic diseases of aging or overall lifespan, but infectious disease is a leading cause of death in the elderly so it's pretty high impact even if all it does is keep old people from dying of pneumonia.
Preprint on an Israeli study of Paxlovid treatment seems it may not prevent hospitalizations for under 65 cohort.
I can't help but wonder what that "Covid-19 Death Rates for People 65+" graph would look like with another line for "previously infected".
Anyway, on the anti-aging front, the most relevant effort I can think of would be Dr. Fahy's thymus regeneration work, since it directly targets regenerating the immune system.
Results to date have been pretty impressive.
I'll be traveling - but I'm going to anticipate that you'll forget about Juneteenth, which will be an interesting case. It's officially a federal holiday, likely to be haphazardly observed publicly/privately. Big impact on reporting? Or not so much?
Re aging: Do you know of the idea that aging, (more specifically the Hayflick limit, https://en.wikipedia.org/wiki/Hayflick_limit ) is an organisms response to not dying of cancer.
So in brief, with ~a billion cells how do you stop one from going cancerous and killing the organism. Well you give it a maximum cell divide counter. (The Hayflick limit.) Once a cell reaches the limit, it stops dividing and perhaps you have a little tumor but the cell doesn't take over the entire body. The long term effect of having a limit is aging. So cancer and aging are two sides of the same coin. (The 'coin' being how do a billion cells form an organism.) I think I heard this idea first on a podcast by Eric Weinstein with his brother Bret. "All our mice are broken" https://www.youtube.com/watch?v=JLb5hZLw44s It's a bit of a torturous conversation... And as far as I know all our mice are still broken. (broken in that they were accidently breed to have very long telomeres.) Edit, The idea is called the 'reserve-capacity hypothesis', and Gwern has a copy of the original paper. https://www.gwern.net/docs/longevity/2002-weinstein.pdf