Sure, you can live the rest of your life in a perfectly sterile environment, but then other costs are at play in sustaining that.
It’s an interplay between severity of disease at age, chronic effects, and cost of avoidance.
eniteris
Karma: 172
I agree invoking Chesterton’s Fence may not be exactly fit for purpose.
But since we know it’s purpose (increased workforce participation), you can choose to remove it if it makes sense for your circumstances (able to leave the workforce to take care of your child). Any positive/negative -ternalities of children in daycare (illness, immunity) are not strongly supported, but we do have about a hundred years of history saying that it’s probably not (measurably) harmful.
But also, as with most things, too many changes are happening at once. Is daycare closer to pre-industrial childrearing with larger families and village-raising, compared to modern single-family single-child care? Daycare probably mixes more germs just through larger geographic distance (smaller daycares with more continuous groups of children might work better, but also probably more expensive).
also, do we want preindustrial childcare? child mortality wasn’t great back then, and it is unclear how much of that can be linked to childrearing practices.
no clear answers, only more questions
If the immunity is short-lived, we would not expect the decay to persist (which is does to age 13 independent of age of entry into daycare, Figure 1 and 2). It takes about 3 years for the number of infections to decay back to baseline (no more infections than children who do not go to daycare); if immunity was short-lived, we could expect a spike as one is exposed to new pathogens, then settling to a low baseline level of infection as immunity wanes and reinfection occurs, but we don’t see a higher baseline (or if the baseline is higher, it is hard to see).
One could argue that the decrease in infections is due to age-dependent immune system development instead of an adaptive response, but then the different age-of-enrollment decay curves should overlap, which they do not. Later enrollment does lower the magnitude of the initial spike, which suggests that there might be an effect, but the non-overlapping decay curves implies that adaptive immunity is playing a role.
I do not have children, but I do have a biology PhD, so that’s definitely equivalent. Re: Søegaard et al. 2023
Antimicrobials redeemed were antibacterials (90.5%), anthelmintics (7.8%), and antifungals, antimycobacterials, antivirals and antiprotozoals (combined 1.7%).
[...]
we used prescriptions for antimicrobials as a proxy for infections, but our study does not inform about the potential impact of childcare enrolment on milder infections not requiring treatment or on more severe infections leading to hospitalization. Also, the majority of infections in early childhood are viral rather than bacterial.
they then claim
However, we presume that variations in viral infection rates associated with age at childcare enrolment would resemble those observed for primarily bacterial infection rates in our study. This is supported by the observation that seasonality of viral respiratory infections correlates closely with that of antibiotics use in Danish children.
but skimming through the references “closely correlates” doesn’t seem well supported, other than that both occur more in the winter. Also, the references only track hospitalized viral pneumonia (probably because they don’t have the data for mild infections).
We observed slight increases in the infection rates and cumulative number of infections at ages 14–19 years among children enrolled in childcare during the first 3 years of life compared with peers in homecare, which were most pronounced among girls. [...] Thus, although we adjusted for [a lot of factors], we cannot rule out that the observed increasing rates and cumulative number of infections in adolescence associated with childcare attendance were due to residual socioeconomic confounding.
I’m not sure I’d call the increase “slight”; but there definitely seems to be some issue with the control group.
When enrolling in daycare, there’s a spike of infections, then a decay afterwards, which you would expect if you started developing resistance to infections. So they are acquiring immunity, that is clear; the question is whether this acquired immunity is (on net) beneficial.
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Re: claims
(Quite confident) The most common illnesses (colds and flu) don’t build immunity in general (in kids or adults) because they mutate every year
I’d walk back the confidence on this; just because they mutate every year doesn’t mean it’s not building immunity. Infection generates many different antibodies, and if any of those antibodies bind (even if not perfectly), then it provides immunity. It may not be perfect immunity, but may weaken severity.
And you don’t notice how many times your has fought off an attempted infection, you only notice when it fails.
(Quite confident) The same illness has a greater risk of complications in babies vs. older children and adults
(Moderately confident) The same illness has a greater duration in babies vs. older children and adults
(Moderately confident) Illness during early development is probably more harmful than illness during adulthood
Yes, I’d say that’s generally true. Though there might be a developmental window for immunity (see: allergies) and sometimes the immune response in adults is more dangerous (see: chickenpox).
(Weak guess) Daycare environments are more conducive to disease spread than schools for older kids and the number of possible illnesses is very high; there isn’t just a limited number of things you catch once
Daycare environments are more conducive to disease spread probably due to a lot more touching and less sanitation. I think the number of possible illnesses is very high, but it’s a mix of things you can catch once and things that mutate that build (partial) immunity (see point one).
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Immunologically speaking I don’t think we understand development enough to give strong recommendations. Exposure is definitely helpful in building an adaptive immune response, but what age is best is an open question. Vaccines definitely have less side effects than an infection, but (some) vaccines might produce antibodies biased towards one protein instead of the whole virus, which may not provide as broad immunity.
In my opinion Chesterton’s Fence remains in place (especially if it’s cost-effective for other reasons), but more research is required.
And the worst: making sense of art. I sometimes ask Claude for interpretation of something, and it’s rather weird to see how typically my own takes are just plain worse. I don’t know how to feel about this, except that perhaps one could get better with practice.
Art is, to wit, how it makes you feel, and recursively why the art is making you feel. Everything else is gravy (served with dead author).
Though yes context is often important, especially when trying to discern Authorial Intent, and learning about context can definitely allow you to reinterpret the art. But that’s not necessary.
The Sentinelese has been reproductively isolated for probably less than twenty generations, which can be sufficient for speciation (given strong selection pressures), but relatively unlikely. So I don’t think it’s necessary to assume that speciation has occurred.
(aside, estimates of Sentinelese isolation are full of wild speculation and misinformation. We have no genetic samples from North Sentinel Island, which means we have no evidence. All estimates are speculation, with an upper bound at a few thousand years due to shared ethnographic artifacts. Missing artifacts (metalworking, etc.) may or may not help establish a lower bound, but is confounded by natural resources available on the island. Also, going back more than tens of generations would imply a high amount of inbreeding given the limited carrying capacity of the island, which could theoretically be sustained with strong selection.)
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Imagine a forest with one species of frog. Then a road is built through the forest, separating the forest in two. The day after the road is built, I discover that there are now two reproductively isolated groups of frogs! Are these now different species?
(under most species frameworks) No! That’s preposterous. The two populations have been isolated for less than a day. Sure, they may at some point in the future diverge (and now natural selection is acting on the two groups differently), but at this point the two species are genetically identical.
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But now imagine you stumble across on species of frog in one forest, and a similar-looking frog in a different forest. The two population are reproductively isolated. Are they the same or different species?
Well, you might ask how long they’ve been reproductively isolated for, since if the forests were connected yesterday then we converge on the same scenario as above. A week, a month, a year, a decade, a century, a millennium, a million years. At some time of separation we cannot reject [no speciation] out of hand, or, rather, number of generations, since that’s what matters in (genetic) speciation. And in nature, we can generally assume that the groups have been isolated from each other for thousands of generations (unless the barriers are human-made, or with recorded history, and because our genetic divergence estimation tools don’t work well for times less than that).
Can they produce fertile offspring? Well, no, not in nature, since that’s what reproductive isolation means. Maybe you can put two of them in a box and test it out manually, but you don’t have the funding to do that. And genetics don’t help too much in determining hybridization potential.
(an aside, what counts as producing fertile offspring? If they can produce fertile offspring via IVF, but never crossbreed if you cage them together because they don’t have the same mating calls or compatible mating apparatus or look funny to each other or sleep at different times of the day, does that count as producing fertile offspring? this is why “natural populations that are reproductively isolated” is added to the definition)
So you have two groups of frogs, isolated from each other for thousands of generations. Evolution is acting upon them as two different groups. But they look suspiciously similar. Do you call them different species?
I could go either way, and lean towards labelling them as different species until we have evidence to the contrary. Otherwise one of the forests might be bulldozed before we can gather the evidence.
If the humans become sufficiently anti-interbreeding for
six hundred thousand generations (which is how long ago the crows have been split, and twice the number of generations that humans have separated from chimps) then yes I think you may consider it as a speciation line.EDIT: I used the wrong numbers, that’s probably the upper bound. The lower bound is 400 generations. Am looking for more precise divergence timelines than “Pleistocene glaciation”
EDIT2: So the mutations in coloration seem to have arisen around 400-500kya. So that’s about 14-16 thousand generations.
(the crows have been merged into the same species as of 2025; they were the same species but were split in 2002 due to pre-genetic evidence. probably merged again due to genetic evidence)
I would strongly recommend reading Species Concepts in Biology for a history and explanation of the current system(s). In summary, there are multiple joints at which you can carve reality, and which joints you choose to carve depends on why you are carving reality in the first place.
As someone who studies viruses of bacteria, how are you supposed to apply the Biological Species Concept to asexual organisms anyways? Are there no bacterial “species”? But we need a way to categorize and talk about them, even if they’re not a species under the BSC. Even if this will group bacteria together whose genome lengths can vary by an entire order of magnitude.
Fundamentally, the Species Concept is the same problem. We need a way to categorize and talk about animals, so we find ways to categorize them based on how useful the categories are. Birds are feathered reptiles. Reptiles are non-feathered reptiles. We form these categories not because they carve reality at the phylogenetic joints but because these categories are useful. Fish are fish. Trees are trees.
(Viral species are even worse. Linear phylogenetic inheritance is thrown out the window. Everything is modular and recombines with each other.)
I don’t really follow the IUCN or like the focus on “biodiversity” for its own sake (just expose them to mutagens if you want more genetic diversity) (I also have philosophical issues with “conservation”—what, exactly, are you conserving and why is that time more worth conserving than any other time?) I’m probably informed by my study: in my opinion everything is a bag of genes, and genes constantly flow between them; species aren’t real and are just useful lines to draw in a continuum of gene flow, which constantly changes over time.
all human populations are biologically capable of mutual gene flow, so all humans would be the same species.
But can you verify it? Do you have experimental evidence that a human from location A can form fertile offspring with a human from remote location B? That’s why geographical isolation is used to define species; because they (mostly) don’t overlap, we don’t have evidence if they can or cannot interbreed. Only when we have evidence of hybridization can we start discussing whether to collapse them into the same species (ring species notwithstanding).
Also, I don’t know nearly enough about plant hybridization, but I’m pretty sure that plants can hybridize extremely easily and if we applied only an “interbreeding” species concept the categories would collapse into uselessness.
In Search of Lost Time—A Review
Yeah the paper seems more like a material science paper than a biology paper. There was no test/simulations/discussion about biological function; similar to DNA computing/data storage, it’s mostly interested in the properties of the material than how it interfaces with pre-existing biology.
They did optimize for foldability, and did successfully produce the folded protein in (standard bacterial) cells. So it can be produced by biological systems (at least briefly), and more complex proteins had lower yields.
Their application they looked at was hydrogels, and it seems to have improved performance there? But functioning in biological systems introduces more constraints.
It’s not really that they made it have more hydrogen bonds, they made it longer and therefore more hydrogen bonds. It’s like having a piece of velcro, and then using a bigger piece of velcro. Yes, the bigger velcro will be stronger. The AI was mostly used to design the scaffolding of the velcro.
They didn’t test whether it’s biologically functional (though that’s not really important if you only care about biomechanics).
Though the tintin protein is already absurdly huge, and I’m pretty sure that the time it takes to translate it is longer than the division time of a(n average) cell. And these scientists made it even bigger (or rather, one domain of it even bigger and didn’t make the rest of the protein).
Also, he has a noticeable lack of confusion about key NPCs–Oak is consistently Oak, the player character is never “the red-hatted NPC”, and he can pick out gym leader Erika from a lineup.
I’m a little lost on this front. A person who has never encountered Pokemon before would not recognize the Oak or Erika sprite on-sight; why should the AI vision model? Perhaps one could match the Oak sprite to the full size Oak picture at the beginning of the game, but Erika? Erika can really only be identified by sprite uniqueness and placement in the top center of the gym.
I would instead think the newer models are just trained on more Pokemon, and hence can better identify Pokemon images.
Minor correction on genome sizes:
DNA phage genomes have a median size of ~50kb, whereas RNA phage genomes are more around the 4kb mark.
Similarily, mammalian DNA viruses are usually >100kb, but their RNA viruses are usually <20kb.
Oddly enough the smallest known virus, porcine circovirus, is ssDNA, mammalian, and only 1.7kb
But yes, mammalian viruses are generally more difficult to culture, probably downstream of mammalian cells being more difficult to culture. Phages also typically only inject their genetic material into the cells, which bootstraps itself into a replication factory. Mammalian viruses, which generally instead sneak their way in and deliver the payload, often deliver their genetic material alongside proteins required to start the replication.
I have heard nothing about Mending Wall, so here’s my impressions as a first time reader:
Mending Wall React Comment
I can’t quite parse “Something there is that doesn’t love a wall”. It’s repeated twice, so it’s obviously important. I’m projecting my ambiguity to whether we should love the wall or not.
Later: oh, “Something there is” is equivalent to “There exists something”, practically, entropy; poetically, ???elves???
Classic ambiguous Frost on whether hunters actually destroy walls or not.
It’s obviously a commentary on “good fences make good neighbors”, the same way Dulce et Decorum Est is a commentary on the Latin phrase. This neighbor appears to be good (annual mutual wall maintenance, out-door game), but his insistence on the wall where it serves no purpose (his father’s saying, thus giving into tradition) gives the author the thought of his neighbor as an “old-stone savage armed”, upon contemplating whether the wall is to keep things in or out.
But these thoughts are “mischief” by the author, so are possibly a problem for the sake of a problem.
Also, I don’t think he tackles my interpretation of the phrase, which is about clear communication about boundaries. Frost focuses on the literal interpretation. Would apple trees outcompete pines, or vice versa? the neighbor’s insistence on a clear boundary could make sense.
Summary:
Walls are victims to entropy and must be maintained. Perhaps actively destroyed by hunters?
The mere existence of a wall can be sufficient to imagine the Other as a threat.
Please question Appeal to Tradition.
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Good imagery and Frost style, but I still find The Road Not Taken to be more clear and more succinct.
Nothing from Savitsky? My personal favorites are Millenium’s Dawn and The Stuff That Dreams are Made Of, but Hacker’s Heaven gets a shout out too.
A Casino Odyssey in Cyberspace by localroger (author of Metamorphosis of the Prime Intellect) takes place in the same post-scarcity universe. How do you have a casino under post-scarcity?
Spoilers
“The Bugsy [currency] is backed by human misery. The one thing you can buy with a Bugsy that you can’t simply ask Prime Intellect for is the suffering of another bona fide human being. Not a facsimile or a simulation or a recording, but a real live person who feels as you feel.”
It seems they were literally using the nonpathogenic attenuated anthrax strain used for vaccines.
marginal bioterrorist
I’m not sure a marginal bioterrorist can train an AI model to obfuscate a DNA sequence to bypass the sequence scanning, but I concede it’s definitely easier to do than recode an organism. I’m not really sure what the skillset/resources of a marginal bioterrorist are.
But we should watch out for proliferation/commercialization of recoded organisms, since recoded organisms would be easier to recode further (if they introduce a new codon, just modify the synthetase to load a different amnio acid).
A marginal bioterrorist could probably just brew up a vat of anthrax which technically counts. Advanced labs definitely have more capacity for modification, but they still need to source the pathogens.
I’m not a fan of the phage synthesis paper as there was a lot of post-generation filtering and failures going on and the AI-generated phages were basically the same. There’s a couple interesting new mutations, but a lot of them are noncoding/synonymous/in nonessential genes.
Judging by your writing I think you missed a new paper red-teaming DNA synthesis screening software. They’re using AI to create proteins that function the same but with different amino acids (probably conformation-based) which bypasses the DNA screening, because screening (probably) isn’t translating and throwing it into Alphafold and comparing it to known toxins. Though the paper didn’t test whether the AI-generated toxins are actually toxic, but we can assign that a reasonable probability.
That being said...translating DNA to protein with standard codon table is just one encoding scheme. And we can recode organisms to use a different encoding scheme. And no DNA screening would be able to catch it, since they have no knowledge of the nonstandard codon table you’re using.
Also thanks for bringing up the Germy Paradox; I seemed to have missed that sequence.
I don’t think your framing is helpful.
I framed the question as “is it better to get sick earlier or later” and you said “actually, it’s better not to get sick”. Yes, that is technically correct, but is also not engaging with the question, and also not at all practical.
EDIT: perhaps I read your comment incorrectly, but this is how I interpreted it.
I think from context and from the article I’m commenting on that it was obvious I was talking about relatively mild childhood infections with few long-term effects (that we know of). I was not talking about polio, or HIV, or Ebola. I thought it was clear, but perhaps it was not.
There is a separate question on whether what we think are benign childhood infections have long-term negative consequences that we consider normal or normative. That may be possible, but given the wide prevalence of these pathogens the question again becomes whether you are infected earlier or later, or if you can spend your life in a sterile bubble.