Slate Star Codex
Article
Slate Star Codex is a recurring publication in the Astral Codex Ten archive, appearing 23 times across 23 issues between August 30, 2020 and October 13, 2025. The archive places it in contexts such as “Some of you are probably veterans of my old blog, Slate Star Codex”; “my wage stagnation post on Slate Star Codex (February 2019)”; “The journalist involved hasn’t known about Slate Star Codex for three years”. It most often appears alongside Scott, Trump, United States.
Metadata
- Category: Publications
- Mention count: 23
- Issue count: 23
- First seen: August 30, 2020
- Last seen: October 13, 2025
Appears In
- You’re Probably Wondering Why I’ve Called You Here Today
- Open Thread 158
- Statement on New York Times Article
- Your Book Review: Are We Smart Enough To Know How Smart Animals Are?
- Open Thread 176
- Why Do People Prefer My Old Blog’s Layout To Substack’s?
- Birth Order Effects: Nature vs. Nurture
- I Won My Three Year AI Progress Bet In Three Months
- Open Thread 250
- Prediction Market FAQ
- SSC Survey Results On Schooling Types
- Links For July 2023
- Impact Market Mini-Grants Results
- Highlights From The Comments On Kidney Donation
- Open Thread 308
- Your Book Review: The Family That Couldn’t Sleep
- Triple Tragedy And Thankful Theory
- Book Review Contest 2024 Winners
- ACX Endorses Harris, Oliver, Or Stein
- ACX Survey Results 2025
- Your Review: The Astral Codex Ten Commentariat (“Why Do We Suck?”)
- Meetups Everywhere 2025: Times and Places
- ACX Grants Results 2025
Related Pages
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- Scott (10 shared issues)
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- Trump (5 shared issues)
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- United States (5 shared issues)
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- ACX (4 shared issues)
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- Astral Codex Ten (4 shared issues)
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- Astralcodexten Com (4 shared issues)
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- Australia (4 shared issues)
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- Boston (4 shared issues)
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- Harvard (4 shared issues)
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- Manifold (4 shared issues)
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- ACX (3 shared issues)
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- ACX Grants (3 shared issues)
External Links
Source Context
Recovered passages from the original issue text. When the raw archive preserved outbound links inside the source passage, they are listed directly under the quote.
Welcome to Astral Codex Ten! Some of you are probably veterans of my old blog, Slate Star Codex. Others may be newbies wondering what this is all about.
But for now - welcome to Astral Codex Ten! I am genuinely glad you're here!
3. And better late than never - I recently learned that one of the economists I cited on my wage stagnation post on Slate Star Codex (February 2019) chimed in with a great comment on explaining her work - you can read it here.
Inline links: read it here
In early 2020, I learned the New York Times wanted to write an article about me. They had discovered my real name and wanted to reveal it to the world. Their original pitch – and I don’t know if it was true or not – was that they were interested in how I warned about the coronavirus pandemic very early and urged people to wear face masks before this was standard advice.
Inline links: very early, wear face masks
When I discussed this with the New York Times, they said they were going to reveal my real name anyway. As a protest and an attempt to prevent this from happening, I deleted my blog and replaced it with a post condemning the New York Times’ actions. The post “went viral”, 513,000 people read it, hundreds (thousands?) of people cancelled their New York Times subscriptions in protest, and it was a major scandal. There were some news stories about it at the time – you can read some of them eg here or here. I was proud to receive support from voices like Harvard professor Steven Pinker, Wikipedia founder Larry Sanger, social psychologist Jonathan Haidt, science broadcaster Liv Boeree, and Atlantic editor Yascha Mounk.
In one post, he aligned himself with Charles Murray, who proposed a link between race and IQ in “The Bell Curve.” In another, he pointed out that Murray believes Black people “are genetically less intelligent than white people.”
Inline links: aligned himself with Charles Murray
Okay, so the book doesn't actually talk about predictive processing as such, but since it was about cognition, I couldn't help but think about it. Full disclosure, almosteverything I know about Predictive Processing I learned on Slate Star Codex, so take this with a grain of salt. Given that predictive processing purports to describe what is happening at a really low level, if correct, it almost certainly is how other vertebrate cognition works. This might open up new avenues for experiment and observation that aren't open with humans (no, this isn't a call for vivisection or anything, just building on what has been described above about animals having widely varying cognition that can be tested in different ways). Perhaps even more interesting would be to try to figure out if predictive processing explains the cognition of non-vertebrates like octopodes. I don't really have much further insight on this, but this sounds like yet another place where the fields of (human) psychology/neuroscience and animal cognition could usefully inform each other.
1: I've heard from five people who, despite sending me entries (and in some cases having me get back to them saying I'd gotten them), somehow didn't get entered into the Book Review Contest. The people I know about are the ones who wrote reviews of The Beginning Of Infinity, Gulag+Kapital+Totalitarianism, Plagues And Peoples, Essay On Man, and Origin Of The Human Mind. If you entered but didn't end up either as a finalist or in the Runners-Up Packet, you're also in that category and should send me an email at scott@slatestarcodex.com ASAP so I can fix it. Send it from a different address than you used originally, in case the problem was that your emails end up in my spam filter. My plan is to speed-judge all of them, then pick one extra finalist which I'll present to you next Thursday, then start voting next Friday.
2: I asked you all to vote on entries from the Runners-Up Packet to promote to finalists. There were three clear winners - the two reviews I posted last week, and a review contrasting Peter Zeihan's Disunited Nations with Bruno Macaes' Dawn of Eurasia. I've already posted a Zeihan review, and I worry readers are getting tired of these reviews and don't have the patience for a semi-duplicate, so I'm awarding the new Zeihan review...some prize to be determined later, like "People's Choice" or something, that doesn't involve me making it a finalist. Don't worry, there will be money involved. If you want to read it, you can find it here as "Disunited Nations (2020) vs. Dawn of Eurasia (2017)"
Inline links: here
5: My father, a professor of medicine working at a VA hospital, is trying to do a study and looking for a biostatistician. He can't pay you unless he gets a grant, which he probably won't, but you could get your name on a potentially pretty interesting paper. Interested candidates should know how to mine data from Vinci/Dart, and preferably have some existing relationship with the VA that can save them a painful and potentially impossible onboarding process. If interested, email me at scott@slatestarcodex.com and I'll give him your name.
I think that all of this together is pretty strong evidence that most people prefer the old Slate Star Codex layout to the new Substack-mandated ACX.
This is weird, because the old Slate Star Codex layout was - mostly something I threw together in a day or two. I am widely recognized as not having taste, and the only website I ever developed before this was a Geocities site that was even worse. A few of my web designer friends helpfully smoothed over some rough edges (in one case literally, Apple-style), but the basic design remained my amateurish rush job.
Slate Star Codex: Original version Slate Star Codex: After some web designer friends spruced it up Meanwhile, Substack is run by tech industry veterans who probably hired a team of really experienced designers and thought really hard about every aspect of their product. It doesn’t make any sense at all for me to do a better job than them. So what’s going on?
Source here; thanks to Emile for the graph That is, of people with exactly one sibling who read this blog, about 72% of those are the older of the two children in their family, compared to only 29% who are the younger of the two (where by chance we would expect 50-50). This was surprising, because at the time lots of studies had shown there weren’t really birth order effects (that is, firstborn siblings had no major personality differences compared to laterborns). I theorized that maybe for some reason it was easier to find by looking in a heavily-selected group of people and asking members about their birth order, compared to getting a random sample and trying to correlate birth order with things. Sure enough, later amateur research revealed strong birth order effects in physics Nobelists and great mathematicians (and potentially Harvard philosophy students). Given that readers of this blog are highly-educated (about 37% have masters or PhDs) and mostly in STEM (41% programmers of some sort), plausibly birth order affects something about intelligence, education, or STEM orientation (somebody should check literature and peace Nobelists!) Followup research by Less Wrong user “Bucky” determined that the effect fell off with age gaps; the closer in age you are to your sibling, the stronger an effect birth order has: I continue to be confused by this extremely strong effect which most of what we know about psychology says shouldn’t exist. So in 2020, I asked my readership some even more complicated questions about their family situations, in the hopes of teasing out why this is happening. I’ll be honest - I think I over-reached here. I’m not very good at statistics, and this is a weird statistical problem: the dependent variable is whether the case ended up in the sample at all! I wasn’t able to figure out a good way to use most of the data you gave me. And the stuff I did use, I mostly made work by slicing and dicing so much that the sample size got pretty low, even when I started from 8,000 survey respondents. I’m publishing this in the hopes that it will inspire someone else will more domain knowledge to do a sophisticated re-analysis. But for now, here’s what I’ve got. Confirming Old Results With The 2020 Dataset The 2020 dataset also shows a strong birth order effect in people who read this blog. In 2018, among people with exactly one sibling, respondents were 2.51x more likely to be the older sibling than the younger (72%). In 2020, the number was 2.39x (71%). Change with age gap is shown below: Note truncated y-axis This seems to be broadly similar to the 2018 results. There was an anomaly in 2018 where some categories seemed to drop off surprisingly quickly between 7 and 8 years, which I thought might be meaningful. But Bucky’s analysis showed this was probably a coincidence, and indeed it doesn’t show up in the new data. Does Sex Matter For Birth Order Effects? I wondered if there might be a smaller birth order effect for people with opposite-sex siblings. One possible explanation for the birth order effect is children trying to get out of the “shadow” of their older sibling and differentiate themselves in some way. But children are already pretty different from an opposite-sex sibling and might feel less pressure in that situation. But this doesn’t seem to be true. The percent firstborns in sibships of two on the survey was 70% among people with a same-sex sibling, and 71% among people with an opposite-sex sibling; no real difference. Do Biological Or Social Factors Produce Birth Order Effects? All previous results are for biological siblings. But it might be worth asking the question separately for biological vs. social siblings. One could imagine either biological or social causes of the birth order effect. For example, some biologists speculate that pregnancy depletes choline, that it takes a long time for choline stores to recover, and that a second child born within that window will have less choline available to build their nervous system, which could be bad. But also: maybe if you have an older sibling, your parents can’t pay as much attention to you when you’re a kid, and you learn less. This was very hard to test for. Again, I wasn’t able to use traditional statistical tests because I’m trying to determine whether someone was in the sample at all, rather than whether two variables are related. It was easy to check normal birth order because I could compare people with exactly one older sibling to people with exactly one younger. It was harder to do with things like adoption in the mix, because that could introduce a bias: are parents more likely to adopt out their first child (because that’s when they’re most unprepared for parenting)? Are adoptive parents more likely to adopt when they already have children of their own (because they’re comfortable with child-rearing) or less likely (because they really want kids and can’t have them biologically)? I had no way of getting controls for these questions and so I couldn’t do a lot of the analyses I wanted. But I did two relatively weak analyses instead: First, I took the entire set of people in weird situations - people who said their number of social siblings was not the same as their number of biological siblings. In this group of 174 people, biological firstborns made up only 61% of respondents with one sibling, notably less than the 71% in the entire sample. That suggests that the unusual social situations are having an effect. You shouldn’t update on the fact that it’s still higher than 50%, because some of the people’s weird social situations don’t affect their status as social firstborns. Second, I tried to compare people who were firstborn under a biological definition but not a social definition, to people in the opposite situation. There were 40 people in the sample who were biological but not social firstborns, and 60 people who were social but not biological firstborns. Again, this suggests that social firstborn-ness is more important as an explanation than biological firstbornness, although it doesn’t rule out the latter having some effect. I additionally tried to compare two different types of social firstbornness - one where no older siblings lived in the house when you were growing up, and one where your parents had never parented another child. There weren’t many people discordant on these two measures (29 vs. 20 respectively), but for what it’s worth, the ratio was in favor of the first type. Since I wasn’t very confident in my analytical abilities here, I asked Bucky, who knows more and who did good work analyzing the last dataset, to look into this (we worked independently and didn’t tell each other our results until we were done). He writes: It seems to me that the effect is entirely caused by social siblings. I filtered for only people with 1+ biological but 0 social siblings. There were 24 oldest biological children in this group vs 21 2nd children (or 25 youngest children with a large overlap between 2nd oldest and youngest groups). This significantly differed from the ~0.7 fraction of older children in the general surveys (p<0.05 or p<0.01 depending on whether I use the 2nd oldest or youngest as the comparison) and is close to a 1:1 ratio. I then filtered for only people with 0 biological but 1+ social siblings. There were 51 oldest social children and 23 2nd children (or 26 youngest children again with large overlap). This differs significantly from a 1:1 ratio (p<0.001 or p<0.01) and matches pretty well with the 70% of the Birth order effect. I tried doing some filtering by age gap (2-7 years) and the results were compatible with the same result, although the sample sizes got too small to really conclude anything. For dealing with answers left blank I treated them as 0 unless it looked like the whole section had been missed out. If I ignored any respondents who left something blank I got similar results (smaller sample size but ratios are even further in favour of the social hypothesis). I checked for categorisation errors by looking at respondents’ descriptions of their families and they mainly matched pretty well with the numbers given so I think the data should be considered reliable. I did chuck a couple of results out which seemed unreliable and there was one row which was a repeat so your numbers might not match up exactly (plus you have the non-public data). There are a couple of confounders in the analysis such as whether e.g. oldest children are more likely to be adopted or how much you know about your birth family depending on how old one was when the family unit changed etc. I don’t see a realistic way to account for these but I also can’t see any of them being big enough to explain the difference in the results. Hopefully this matches up with what you found! I think this suggests birth order effects are social rather than biological. So What Causes Birth Order Effects? Based on this analysis, it seems unlikely they are biological. Based on my very weak sub-analysis, and on their tendency to decay with larger age gaps, it seems they have more to do with the social presence of a sibling in the house than with any changes in parenting style (ie your parents learn to parent differently). Two explanations that satisfy both those criteria: Parents are able to devote their full attention to parenting their first child, but only half of their attention to parenting their second. Firstborns get more quality time with their parents during the first few years of childhood.
Inline links: here, physics Nobelists, great mathematicians, Harvard philosophy students, Followup research, https://substackcdn.com/image/fetch/$s_!jKaz!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fbucketeer-e05bbc84-baa3-437e-9518-adb32be77984.s3.amazonaws.com%2Fpublic%2Fimages%2F4995a838-7372-40dc-8e51-1b35c811bd43_523x388.png, some even more complicated questions about their family situations, https://substackcdn.com/image/fetch/$s_!CMuv!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fbucketeer-e05bbc84-baa3-437e-9518-adb32be77984.s3.amazonaws.com%2Fpublic%2Fimages%2F8042c21d-a6b7-48f9-bbcc-daf8c136953c_497x339.png
Finally, other people might be able to extract more signal out of this than I was. If you’re interested, you can find the raw data, the original question list, and a description of how to use them here. Note that a few people refused permission for me to republish their data, so you will probably get slightly different numbers than I did.
Inline links: here
In 2018, thanks to the 8,000 of you who filled out the Slate Star Codex Reader Survey, I discovered that higher birth order siblings were much more likely to read this blog than later-borns:
At the time, I wrote: I’m not going to make the mistake of saying these problems are inherent to AI art. My guess is a slightly better language model would solve most of them…for all I know, some of the larger image models have already fixed these issues. These are the sorts of problems I expect to go away with a few months of future research. This proved controversial. Gary Marcus in particular has emphasized how challenging compositionality is for modern language and image models: @sama @gdb @Plinz @ylecun, \n\nEach of you ridiculed my recent title, but this is what the article was actually about: compositionality.\n\nYes, there are many kinds of progress in other directions. \n\nBut compositionality is at the core of intelligence. \n\nNo AGI without it. ","username":"GaryMarcus","name":"Gary Marcus","profile_image_url":"","date":"Sat Apr 09 04:34:37 +0000 2022","photos":[],"quoted_tweet":{"full_text":"Compositionality *is* the wall. \n\nEven “red cube” and “blue cube” on their own are represented unreliably; not one of ten images correctly captures the full phrasal description.\n\nThe images are beautiful, but no match for the precision of language. https://t.co/uvoXUtETwi","username":"GaryMarcus","name":"Gary Marcus"},"reply_count":0,"retweet_count":7,"like_count":54,"impression_count":0,"expanded_url":{},"video_url":null,"belowTheFold":true}" data-component-name="Twitter2ToDOM"> And one of my commenters, Vitor, asked: Why are you so confident in this? The inability of systems like DALL-E to understand semantics in ways requiring an actual internal world model strikes me as the very heart of the issue. We can also see this exact failure mode in the language models themselves. They only produce good results when the human asks for something vague with lots of room for interpretation, like poetry or fanciful stories without much internal logic or continuity. Not to toot my own horn, but two years ago you were naively saying we'd have GPT-like models scaled up several orders of magnitude (100T parameters) right about now (https://slatestarcodex.com/2020/06/10/the-obligatory-gpt-3-post/#comment-912798). I'm registering my prediction that you're being equally naive now. Truly solving this issue seems AI-complete to me. I'm willing to bet on this (ideas on operationalization welcome). I responded to Marcus here, and I responded to Vitor by making a bet on whether AI image models could draw some compositionality-heavy pictures by 2025. The specific terms we agreed on: My proposed operationalization of this is that on June 1, 2025, if either if us can get access to the best image generating model at that time (I get to decide which), or convince someone else who has access to help us, we'll give it the following prompts: 1. A stained glass picture of a woman in a library with a raven on her shoulder with a key in its mouth 2. An oil painting of a man in a factory looking at a cat wearing a top hat 3. A digital art picture of a child riding a llama with a bell on its tail through a desert 4. A 3D render of an astronaut in space holding a fox wearing lipstick 5. Pixel art of a farmer in a cathedral holding a red basketball We generate 10 images for each prompt, just like DALL-E2 does. If at least one of the ten images has the scene correct in every particular on 3/5 prompts, I win, otherwise you do. DALL-E can’t do any of these: If I were being kind, I would give it the farmer in the cathedral. But I am being unkind, so the farmer in front of the cathedral doesn’t count. II. There are now at least four more AI image models available: Google Imagen announced May 2022.
Inline links: https://slatestarcodex.com/2020/06/10/the-obligatory-gpt-3-post/#comment-912798, here, bet, https://substackcdn.com/image/fetch/$s_!_gqe!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fbucketeer-e05bbc84-baa3-437e-9518-adb32be77984.s3.amazonaws.com%2Fpublic%2Fimages%2F6138ab0d-3a82-4eb9-a328-bf38ea0f6b10_632x784.png, announced
2: The past year has been a terrible time to be a charitable funder, since FTX ate every opportunity so quickly that everyone else had trouble finding good not-yet-funded projects. But right now is a great time to be a charitable funder: there are lots of really great charities on the verge of collapse who just need a little bit of funding to get them through. I’m trying to coordinate with some of the people involved. I haven’t really succeeded yet, I think because they’re all hiding under their beds gibbering - but probably they’ll have to come out eventually, if only for food and water. If you’re a potential charitable funder interested in helping, and not already connected to this project, please email me at scott@slatestarcodex.com. I don’t want any affected charities to get their hopes up, because I don’t expect this to fill more than a few percent of the hole, but maybe we can make the triage process slightly less of a disaster.
And I tried to make the same point in Axiology, Morality, Law (2017), where I said:
Inline links: Axiology, Morality, Law
I later discussed whether there could be exceptions to this (like “what if by giving one person a paper cut you could end all disease forever?”) but I hope that it’s still clear that in most normal situations following the rules is the way to go. This isn’t super-advanced esoteric stuff. This is just rule utilitarianism, which has been part of every discussion of utilitarianism since John Stuart Mill in the 1800s. See also The Dark Rule Utilitarian Argument For Science Piracy.
Inline links: The Dark Rule Utilitarian Argument For Science Piracy
If you have an idea for a prediction-market-related company, feel free to run it by me. You can reach me at scott@slatestarcodex.com.
Taken from the 2020 Slate Star Codex Survey. SSC/ACX readers are a heavily-selected population and nothing about them necessarily generalizes to anyone who isn’t an SSC/ACX reader. But you are an SSC/ACX reader, so maybe they generalize to you. Most of these questions are heavily confounded by different types of people going to different schools. In a few cases, I’ve made feeble efforts to get past this, in other cases I haven’t tried. All of this is rough and weak, you don’t need to comment to tell me this.
Inline links: 2020 Slate Star Codex Survey
As always, you can try to replicate my work using the publicly available SSC Survey Results. If you get slightly different answers than I did, it’s because I’m using the full dataset which includes a few people who didn’t want their answers publicly released. If you get very different answers than I did, it’s because I made a mistake, and you should tell me.
Inline links: SSC Survey Results
12: Big thanks to Adam Piovarchy, who included me as a coauthor in his recent article in Philosophical Studies, Epistemic Health, Epistemic Immunity, and Epistemic Inoculation. He said he was inspired by old Slate Star Codex posts including Cowpox of Doubt and wanted to give me shared credit. This is a typical example of the process of turning SSC/ACX posts into journal articles, in that 1) you’re completely welcome to do it and 2) I probably won’t contribute anything to the process beyond my permission, sorry.
13: Sort of distantly related: Roman “bayesyatina” Achisov and a group of Russian ACX fans (don’t you guys have other things to worry about over there?!) have turned my short story Ars Longa, Vita Brevis into a shockingly-professional-feeling short film! Currently only in Russian, sorry, but you can make YouTube awkwardly translate the subtitles by clicking on the gear icon on bottom → Subtitles (CC) → Translate → Auto-Translate → English. If the Translate option doesn’t appear, select Russian subtitles and then try the process again. They say they might have official English subtitles up soon, in which case I’ll link this again, but I’m excited and want to link it now too:
Inline links: Ars Longa, Vita Brevis
My only regret with this grant is that Max undervalued himself, so all his money is going to his investor. Max, please get in touch with me at scott@slatestarcodex.com about having me retroactively recoup some of your other expenses if you want.
Thanks again to everyone who participated, whether as project leader, investor, or judge. And thanks especially to Austin Chen, Rachel Weinberg, and the rest of the Manifund and Manifold teams for the technology and organization that made this possible. If we owe you money, expect an email from Manifund sometime in the next two weeks. If you don’t get it, email me at scott@slatestarcodex.com.
If he holds a rule “preserve bodily integrity” because he notices that helps him avoid bad things - and if he makes exceptions whenever there are cases where preserving bodily integrity imposes costs, or prevents a benefit - then I propose he’s using it as a heuristic for what he really wants, which is something like trying to stay healthy and safe while balancing that out with satisfying his other values. People tend to crystallize heuristics at different levels, and maybe he’s chosen to crystallize this one here. But I bet we could come up with lots of cases he hasn’t considered before, and find that the heuristic really isn’t that crystallized - if someone invents something new which is approximately as body-integrity-violating but also approximately as beneficial as vaccines, Stephen will support it.
Inline links: crystallize heuristics at different levels
…really you don’t even have to do that. I find the morality/axiology distinction helpful here. You can have a concept of morality such that it’s pretty weak and you’re more or less following it correctly, while maintaining a concept of axiology where you’re not a perfect saint doing the maximally beneficial thing at all times (and that’s fine).
Inline links: the morality/axiology distinction
…or maybe I’m being unfair to Stephen. Here Lone Ranger demonstrates a different reason to stick with coarse-grained heuristics even when there’s evidence that they fail in your specific case: you don’t believe the evidence, you don’t trust the people presenting the evidence, and you suspect the whole thing is an op. This is epistemic learned helplessness, and it’s adaptive in a lot of situations.
Inline links: epistemic learned helplessness
2: Related: I’m trying to figure out how to share applications with judges, and it’s more complicated than it sounds. To make it easier, please don’t send any extremely secret (can’t even be shown to non-me judges) applications via the form. If you have these (which I don’t recommend), send them to my email (scott@slatestarcodex.com) directly, using the form as a guide. I’ll update the form to reflect this. Don’t worry, I’ve manually taken out the nonpublic applications I’ve already gotten.
This is the weekly visible open thread. Post about anything you want, ask random questions, whatever. ACX has an unofficial subreddit, Discord, and bulletin board, and in-person meetups around the world. 95% of content is free, but for the remaining 5% you can subscribe here. Also:
(This report was, as it happens, published in the exact same month as The Family That Couldn’t Sleep.) DTM came to know the family well. He befriended them by way of two members of their younger generation, Lisi – a woman terrified by the shadow of the disease, and Ignazio – the doctor she had married, who was more terrified by the shadow of the disease. Ignazio put together the pieces of the family puzzle, consolidating all the disparate diagnoses into a single disorder and filling out a lot of blank spots on family trees. When DTM came along, he was able to help Ignazio make the case that the family would benefit from the spotlight – that greater awareness of FFI could lead to a cure both for them and for a slew of other prion diseases. As it so happens, he is one of those nonfiction authors who serve as a character in their own story. DTM has some form of progressive muscular palsy. He is, or at least was in 2006, not entirely sure what it is. The relatively unimpressive state of genetics at the time had not identified his causative mutation, though it looked a lot like one of the rarer forms of Charcot-Marie-Tooth disease2. DTM is pragmatic about this, the way everyone chronically ill is either pragmatic or doomed. Whatever he has, it is a defect in protein structure; his peripheral nerves decay not because of a problem with the nerves themselves but an inability of their scaffolding to hold them together, as he puts it. The last chapter of the book dwells on this, on the web of connections popping up between a thousand disorders. DTM’s disease is something vaguely similar, if you squint, to an exceptionally slow-progressing motor neurone disease; if you jump another level out, you see amyloid plaque diseases like Huntington’s and Alzheimer’s, and if you jump yet another level out, you see something like prions. His interest in the Venetian family was driven by this. Some of its members thought this a beautiful act of sympathy; others thought him a grotesque parody of themselves, an onlooker, a gawker, peddling their tragedy to salve his relatively insignificant problems. They are, he thinks, both right. That’s the beginning, and that’s the end. What happens in the middle? --------------------------------------------------------- The Venetian family lends the book its title, but they’re really more of a framing device. The Family That Couldn’t Sleep is separated into four parts, of which the first and fourth – the shortest by far – deal with the family. Part 2 is kuru, the king of fucked up diseases you read about in clickbait Weird Medicine listicles. Let’s talk about kuru! Kuru, is, famously, the prion disease you get if you eat another person’s brain. Well, not quite. It’s a prion disease that became endemic amongst women in the Fore society, who ritually ate brains, one of which had an inherited or spontaneous prion disease. This is an important note – there’s a tendency (which the book’s later chapters engage in) to assume cannibalism just has a Prion Disease Generator attached. If you eat people who don’t have prion diseases, you won’t suddenly get one. Uh, don’t eat people. Anyway, part 2 is DTM’s historiography of Fore-Westerner first contact. It’s hilarious. Papua New Guinea is a frankly ridiculous place; one of the all-time best Lyttle Lytton winners (worst first sentence from a hypothetical or, in this case, real work) was “Papua New Guinea is so violent that more than 820 languages are spoken there”. The native residents were so hostile to outsiders that all the colonial empires had cut their losses – and when you think about the places they colonized, that says something. After the First World War, PNG was ripped from its nominal German ‘owners’, but no one else wanted the place. So, of course, they gave it to the Australians. It was thirty years and another war before we actually made contact. 1940s Australia was as ‘settled’ as it’d ever be; the cities were bustling and the interior was mapped. The kind of explorer who two centuries before would be heading to new continents had to console himself with Pacific islands. Console he did. The native peoples of the PNG coasts were hostile enough to the wannabe-colonialists that the Australians, flying planes overhead, were the first people to discover that the island’s inland was populated too. No one had broken through on land. In all this deep and angry rainforest, the Fore were the furthest out. They lived far into the island’s mountainous interior; DTM describes their territory as “nearly vertical”. Calling people primitives is a bit passe these days for understandable reasons, but no other term comes to mind. The Fore had no name for themselves; we call them by an exonym, “the people to the south”. They weren’t, to be clear, hunter-gatherers – they were slash-and-burn agriculturalists, but very well-fed ones. Despite the tendency in grain-focused cultures for poor agriculturalists to be stunted/malnourished, the Fore were a remarkably healthy people. Well, except for the famous bit. The first remarkable thing about the Fore was just how quickly they wanted to assimilate. Most PNG tribes weren’t particularly enthused by Western offers of injections/tractors/radios/Christianity. Yet as soon as the Australians arrived, the Fore made ceasefires in their wars with other tribes, volunteered to help large-scale Australian projects on the coast, started planting and trading coffee, and enthusiastically participated in censuses. It’s the only first-contact narrative I’ve seen where the colonizers were concerned about how badly the other guys wanted to be colonized. The next was the one that got their names in the history books. Australian officials started to notice a remarkable lack of women in Fore camps. Some tribes sequestered their women, particularly when Westerners were around, so at first they thought nothing of it. The high rate of unpartnered young men, though, was way out of PNG norms. DTM tells this part fantastically. The Fore chapters drip with the dread of dramatic irony. When the first breakthrough comes, you have to catch your breath: “Tiny” Carey noted something in the middle of August 1950 that deepened this mystery. He noticed that near the village of Henganofi there had been an unusual number of deaths. “It appears,” he wrote his superiors, “natives suffer from stomach trouble, get violent shivering, as with the ague, and die fairly rapidly.” [...] McArthur investigated a little more [...] One day in August 1953 he ran into more of the shivering people Tiny Carey had seen several years before: “Nearing one of the dwellings, I observed a small girl sitting down beside a fire. She was shivering violently and her head was jerking spasmodically from side to side.” It would be quite some time before anyone figured out what caused it – but the problem, as DTM notes, was that its cause wasn’t possible. Everyone priored that the weird undescribed disease in the Fore lands was some nocebo sorcery-sickness. Vincent Zigas, the first actual doctor sent to work with the Fore, tried to placebo-effect them and failed miserably: On the way, Apekono stopped at a hut and showed Zigas his first kuru victim. “On the ground in the far corner sat a woman of about thirty,” the doctor wrote. “She looked odd, not ill, rather emaciated, looking up with blank eyes with a mask-like expression. There was an occasional fine tremor of her head and trunk, as if she were shivering from cold, though the day was very warm.” It was almost exactly the tableau McArthur had witnessed in 1953. Zigas, though, was a doctor. He could do more than look—or so he thought: “I decided I might as well try my own variety of magic,” he remembered. He rubbed Sloan’s Liniment, a balm for sore muscles, on her and declared to her family and his guide: “The sorcerer has put a bad spirit inside the woman. I am going to burn this spirit so that it comes out of her and leaves her. You will not see the fire, but she will feel it. The bad spirit will leave her and she will not die.” The lotion penetrated the woman’s skin and she writhed in pain. “Get up! Walk!” Zigas commanded theatrically. “The woman struggled feebly as if to rise, then, exhausted, started to tremble more violently, making a sound of foolish laughter, akin to a titter.” That evening Apekono asked Zigas not to try to cure any more kuru victims; “Don’t use your magic medicine anymore. It will not win our strong sorcery.” This was a disaster. The Fore were so cooperative precisely because they hoped “Western magic” could conquer theirs. As it became clear it couldn’t, they turned hostile. The Australians had hoped to “modernize a Stone Age people”; now all their subjects were dropping dead before their eyes, from what they could only assume was a “hysterical reaction” to colonization itself. So, to solve this, they needed a batshit insane American. Carleton Gajdusek is one of the characters who dominates The Family That Couldn’t Sleep. He couldn’t not. You could put him in a car commercial and he’d dominate it. Gajdusek was a physician with a rare, intense combination of science and practice. He was a romanticist, a field worker, and a lover of everything strange. He’d been an army doctor, a government conspiracy-cover-upper, and a postdoc under Linus Pauling who described his intent as “to straighten out Pauling’s ideas about proteins”. He hated civilization, in a slightly-to-Ted’s-centre sense, and was passionate about “primitives and isolates”. He jumped at the chance to work in Papua New Guinea; he planned to conduct a multi-site study on child development in such cultures, and relished the opportunity to live in a “primitive” environment himself. He did all this so he could rape kids. Oh, he did it for the scientific curiosity and love of medicine, but he also did it so he could rape kids. Gajdusek was a pedophile in the actual-lifelong-exclusive-paraphilia sense, as opposed to the “metonym for child molester” sense. Some people who roll snake-eyes on the Sexuality Dice repress it, but some are perfectly happy to act on it; Gajdusek was #2 in its fullest form, the kind of guy who believes that a well-lived life includes raping some kids. DTM doesn’t shy from this, not for a moment. It’s the first thing he tells you about Gajdusek. It couldn’t not be; you couldn’t talk about why he went to PNG otherwise. When Gajdusek landed in PNG, he first found the place too civilized. He’d been promised a land of “cannibal savages” – where were they? After some traipsing, he found them, right where he was promised. The Fore were perfect for Gajdusek. They had some kind of medical mystery that’d been lost on everyone else. They ate each other, in exactly the way he loved detailing in his diaries (“”Women and children, particularly, partake of the human flesh,” he noted with pleasure”). As kuru cases popped up, he aggressively recorded them. He wrote lovingly detailed notes that he sent back to his Australian advisor. He wrote with intensity, with exclamation marks, with the joie de vivre of a man just where he wanted to be. Gajdusek smothered the Fore with ‘cures’ that never worked, but they didn’t get angry at him. As DTM dryly puts it: “Their children trusted him, and that was enough for them.” At some point, someone suggested sending an anthropologist...or an epidemiologist...or literally anyone with more credentials than Gajdusek and Zigas3. Gajdusek threw a shitfit, convinced this one-and-a-half-man team was enough to Solve The Problem Forever. But he got bored eventually – running off with another tribe with, as his diary notes at length, an apparent custom of youths ritually fellating older men – and Zigas, I dunno, the book neglects him a bit here. So they managed to sneak in some anthropologists. The husband-and-wife team of Robert Glasse and Shirley Lindenbaum4 were the first involved parties to give a shit about the Fore as people, rather than as colonial subjects/medical mysteries/walking sex toys. What they uncovered was fascinating. The Fore were cannibals, yes, but they were recent cannibals. They didn’t have an ancient tradition of eating their dead, like the other visitors assumed. They happened to be in contact with some cannibal groups, and after a Fore man died of “sorcery”, they thought: well, what would happen if we ate him? “People tasting it expressed their approval. ‘”This is sweet,” they said, “What is the matter with us, are we mad? Here is good food and we have neglected to eat it.”” If not for the wild coincidence that the first Fore cannibalism victim had a prion disease, kuru would never have existed. Glasse and Lindenbaum started to put together the pieces. They’d been sent down to rule out a genetic explanation – to track the kinship ties of the Fore and see how the disease ran through families. It didn’t run through families in any coherent sense, but it sure did run through cannibalism. The clincher was the age distribution. The Fore, ever enthused by colonialism, quit eating each other as soon as the Australians arrived. Children stopped dying of kuru shortly after; they simply weren’t exposed to the infectious agent. The couple sent the news to Gajdusek, who was off raping kids somewhere else. In the next part of the book, DTM runs through Gajdusek’s many conjectures of kuru’s cause – more like sketches or abstract paintings than like true hypotheses. Gajdusek was annoyed that someone else was doing something he “totally could’ve done”, and even more annoyed that another lab was running similar experiments – an attempt at a vaccine for a particular sheep disease had accidentally created a prion generator. But he was happy to swoop in and claim the credit for what he was starting to think of as “slow viruses”, an infection that somehow lays dormant for years. DTM portrays Gajdusek perfectly, in that “real life has no need for verisimilitude” way. Gajdusek was at once a brilliant man, an all-consuming narcissist, an entertaining character, and a monster beyond redemption. A lesser book might pick one or two. The Family That Couldn’t Sleep portrays him as all four, and on a personality level (as opposed to a scientific one), the Gajdusek-focused parts are some of the most gripping. --------------------------------------------------------- Outside of the jumps between the Venetian family and everything else, The Family That Couldn’t Sleep is not siloed. The narratives of all prion diseases are deeply intertwined. This is what makes it a great book. It’s 300 pages of dramatic irony. You read the whole thing, waiting for the eureka moment – the point everyone realizes they’re looking at the same cause. It does, however, make it a tad difficult to review or synopsize. The book’s story is so weird – and, often, so at odds with conventional wisdom that trickles down about the Fore et al – that you have to recap quite a bit, and the book steadfastly resists recapping. The next couple chapters after we depart from Gajdusek’s credit-claiming are mostly about experiments with various prion diseases. They’re scientifically fascinating. Unlike some medical-books-for-general-audiences (cough, How Not to Study a Disease), DTM never talks down to the reader. He assumes someone reading a 300-page book about prions is smart and wants to learn about prions. He also has – you can feel it in his words – the agonizing experience of spending his life on the other side of the doctor’s desk, trying to beat into whoever he’s talking to that no, seriously, you don’t need to lie to him or try explain a complex disease at a fourth-grade level. The first prion disease studied was scrapie. Scrapie was a big deal – it starved and killed large shares of British sheep flocks, making it a serious economic problem. Veterinary researchers had tried to prevent or cure it for centuries. It was a veritable graveyard of ambitions: Quintessential was D. R. Wilson at the Moredun Institute in Scotland, who worked in the middle of the last century for more than a decade trying, with mounting frustration, to kill the scrapie agent. He found that it survived desiccation; dosing with chloroform, phenol, and formalin; ultraviolet light; and cooking at 100 degrees centigrade for thirty minutes. The scrapie researcher Alan Dickinson told me he remembered Wilson at the end of his career as “very, very, very quiet. Of course, that was after his breakdown.” “Now it is our turn to study prions. Perhaps we should approach the subject cautiously.” The problem, as DTM explains, is that prion diseases were impossible. They violated 20th-century understandings of biology. Proteins “were no more alive, and no more infectious, than bone”. Prion diseases seemed to have too many causes – genetic, infectious, and sporadic. They looked infection-like in some ways, but patients didn’t produce virus antibodies. Sheep exposed to scrapie, or chimps infected with kuru, took years to develop symptoms. Their facts did not fit together. In the 1960s, people started wondering. The unifying trait of prion agents was that they had to be denatured to be destroyed. Was this a particularly small virus defined by its protein coating? Or – even more outre – was it pure protein, no DNA at all? No one could figure out quite how the latter worked, but it was tempting. Gajdusek, by now a major figure in this field, kept a foot in both worlds. He didn’t want to stake his reputation on a no-DNA hypothesis, but he certainly sympathized. Enter Prusiner. Stanley Prusiner was Gajdusek’s counterpart. Where Gajdusek seemed permanently manic, Prusiner was deliberate and exacting. He entered Gajdusek’s “slow viruses” field in the early 1970s after a chance encounter with a CJD patient. He relished the laboratory in a way Gajdusek didn’t at all, and set out to optimize the hell out of his projects. Prusiner set out to isolate the smallest infectious particle in the scrapie agent. He injected tons of hamsters (hamsters got sick faster than mice) with increasingly tiny scrapie proteins, hoping to determine whether the Minimum Viable Scrapie was DNA. By the mid-1980s, he’d produced something so small it couldn’t possibly be a virus. Denaturing it destroyed it; exposing it to nucleic acid dissolvers actually made it stronger. Emboldened by this discovery, Prusiner set out to anoint himself the King of Prions. Here emerges something of a Voldemort-Umbridge distinction – the difference between cartoonish villainy and banal evil. Gajdusek is a bad guy because he rapes kids. Prusiner is a bad guy because he is the most grotesque stereotype of the Advisor/Peer Reviewer from Hell made flesh. Everything Prusiner did was to build his reputation atop a pile of skulls. When recruited as a peer reviewer for other prion papers, he wrote negative reviews to undermine their authors. He worked his grad students to the bone and intentionally destroyed their careers, telling them he’d “ruin them” if they entered prion research as competitors. He lied about the origin of the protein-only hypothesis, claiming he originated it a decade after it was actually conjectured. But hey, he was good at getting grants. I was surprised reading a lot of this, because for all the time I’ve been aware of it, the cause of prion disease has seemed settled. “Oh yeah, it’s a protein that gets all fucked up.” But DTM goes through just how unsettled it was right up through to The Family That Couldn’t Sleep’s publication. Serious confirmation only arrived a couple years later. Many people were deeply critical of the prion hypothesis – often, it seemed, because they loathed Prusiner too much to go along. Throughout the book, he cuts an uncharismatic figure. Gajdusek and Prusiner both won the Nobel for discovering prions, decades apart. This tells you something – the “discovery” of prions can be construed quite a few ways. Gajdusek formulated the hypothesis; Prusiner proved it. Gajdusek was grievously offended by Prusiner’s Nobel, perceiving his rival – not inaccurately – as a follower who never originated any ideas of his own. But Gajdusek was offended from a federal prison cell, so how’d that work out for him? Fascinating as all this is, no one published a book about prions in the mid-2000s because it was about kuru or FFI. They published books about prions because teenagers were dying, and people wanted to know why. DTM lays the seeds for part 3 – the mad cow section – in part 1. This is a discussion of scrapie, the longstanding prion disease of sheep. Scrapie was a medical mystery for centuries (remember poor D. R. Wilson), precisely because of the intuitive implausibility of prions. The scrapie chapter is a great history-of-science piece, covering the agricultural productivity revolutions of the 18th century, the surfeit of bizarre origins veterinarians concocted, and the treatments that never worked. Scrapie is not transmissible to humans – well, we hope. It’s concerningly transmissible to primates. But it’s been around for a long, long time, and it doesn’t epidemiologically look like humans get it...we hope. Anyway, you ever tried to generalize from one example? The British government did! In the mid-1980s, strange reports started coming out of the UK’s farms. Farmers were describing a new disease where dairy cows – incredibly docile creatures, under normal circumstances – turned hostile, kicking them as they went into the milking stalls. The symptoms looked to all the world like scrapie. Epidemiologists tracing the outbreaks found a unifying link with “cake” – animal protein feed sweetened with molasses. The scrapie-like symptoms must have traced to an infected sheep. But scrapie doesn’t transmit to humans, so it must be okay to keep slaughtering them, right? We all know how this ended. The best term for the British response to the mad cow outbreak is “cacklingly evil conspiracy”. The agricultural industry really, really didn’t need a huge zoonotic outbreak – so it decided it didn’t have one. They first suppressed all mentions that the disease looked like scrapie, then – when this became impossible – hyped up that scrapie doesn’t transmit to humans, so there’s nothing to worry about. The formal name of the disease, “bovine spongiform encephalopathy”, was supposedly chosen to optimize for unfamiliarity – it wouldn’t fit well in a headline. They emphasized, extensively, that there was nothing to worry about. Ever. At some point, people started asking questions. If there was nothing to worry about, why was the agricultural industry panicking so hard? As things became ever more worry-inducing, this turned down ludicrously twisting paths: Meanwhile, the Southwood Working Party and the experts who advised it were learning on the job. They learned, for instance, that the BSE agent entered the animal through the mouth and then followed the digestive tract into the organs that try to filter out infections—the tonsils, the guts, and the spleen—and from there traveled into the peripheral and central nervous system, and finally arrived at the brain. They also learned that pasties, meat pies, and even some baby foods contained tissues from a lot of those organs. So the Southwood Working Party recommended banning these organs, but only from baby food. This started a chain reaction of consumer doubt: if infected cow organs were unsafe for babies, how could they be good for adults? The government then banned offal, as the organs were collectively called, in all human food but gave the industry a grace period to get it out of the feed supply. Then pet food manufacturers began to wonder if what drove cows mad might not also drive dogs, cats, and parrots mad. The feed they sold came from concentrate made of the same sick animals that had previously made up the meat and bone meal farmers used. Their trade group decided to put a similar ban in place—immediately. So for five months it was safer to be a dog than a human in Britain. DTM spends pretty much this whole section of the book making fun of the British government. To be fair, they deserved it. They killed hundreds of kids in agonizing and preventable ways – they could take some ribbing. This is all throughout the mid-1980s to early-mid 1990s. Through this period, it wasn’t yet clear that mad cow could spread to humans. The panic was clear, and deserved, but it didn’t yet have a match for its powder keg. It would alight. The first suspected case of vCJD – human mad cow – was in 1994. Fifteen-year-old Vicky Rimmer developed a sudden, strange disease. Doctors gave her months to live...until she died in 1998. A couple other suspected cases trickled down through the mid-90s, including a young man who made meat pies for a living, whose grieving mother received a letter from the Prime Minister that “humans do NOT get mad cow disease”. (That must’ve been fun.) Soon, they couldn’t deny it any longer. On March 20, 1996, Stephen Dorrell, the health secretary, stood up in Parliament to announce the news that had already appeared as a tentative conclusion in scientific journals and as rumor in newspapers for the previous two years: British beef was killing British teenagers. The first confirmed death was that of Stephen Churchill, a nineteen-year-old student from Wiltshire, who died in May 1995. Back in 1989, at the Southwood Working Party’s suggestion, the government had set up a surveillance unit in Edinburgh to watch for any evidence that BSE had crossed to humans. One worry had been that if BSE passed to humans, how would anyone know it? How would you recognize something you had never seen? It turned out to be easy: Churchill and the nine other teenagers who had gotten sick had spectacular amyloid plaques in their brains, chunks of dead protein almost visible to the naked eye. If sporadic CJD was a whisper, BSE-caused prion disease was a shout. The investigators sat open-mouthed looking at slides whose damage, they feared, portended the most severe epidemic in modern British history. This part of the book is not fun. It lacks the insane personalities and duelling careers of the other entries. It is an honest chronology of the vCJD epidemic – a gruesome failure of the agricultural industry, the one system that everyone is vulnerable to. The government and industry had completely violated their duty of care to citizens and consumers. They were paying the price. No one would buy British beef anymore – not while they watched their children die. Now here’s the thing: this is ethnography, not historiography. The Family That Couldn’t Sleep is a book from the mid-2000s. The epidemic was not at all in the rear view mirror. There were piles of unanswered questions that DTM constantly alludes to. We have eighteen years more hindsight than he did then. What do we know now? --------------------------------------------------------- In 2006, the vCJD epidemic looked like it was going to be a lot better than the worst fears. BSE itself was a huge problem for the cattle industry, but honestly, no one is too sympathetic to the cattle industry. People were not going to die in anywhere near the numbers believed. We had all sorts of reassuring data coming out about this, which DTM chronicles. We were learning that only some genotypes seemed susceptible to vCJD. We didn’t see any older people die of the disease. We were seeing numbers drop, such that vCJD must have a pretty short incubation period. Anyway, all of this is wrong! The Family That Couldn’t Sleep was written in the candidate gene era. Back then, the nascent field of human genetics was sure it was about to Solve Polygenism. Yes, the simple Mendelian monogenic patterns popular a few decades back clearly didn’t apply to common diseases, but how many variants could there be? We were about to discover the five genes influencing 20% of Alzheimer’s risk each, the five genes influencing 20% of heart disease risk each, etc., and once we were done we’d just do gene therapy and cure Alzheimer’s. A paper on autism genetics from 1999 was so outre as to speculate there might be as many as fifteen genes involved. The fact we are now using the term “omnigenic model” should tell you roughly how well this worked out. Do you remember SNPedia? If you were a 2014 Slate Star Codex reader, you might. 2014 was still pretty candidate gene. People were out there publishing papers saying a single variant could increase your life expectancy by 15 years. SNPedia was a site that beautifully categorized all of these, so you could do 23andme or whatever, look up your results on SNPedia, and make horrible life choices.5 It was eventually bought out by one of the consumer DNA companies, so no one ever edited it again, making it a great time capsule of early-mid 2010s behavioural/medical genetics takes. SNPedia will excitedly explain to you that common genetic variants make you immune to vCJD. They cite a 2009 post from the now-archived 23andme blog titled “No Good Evidence That Potential Pool of Mad Cow Disease Victims Is Expanding”, explaining how fears of late-onset vCJD are clearly debunked by new Scientific Knowledge. Everyone who developed vCJD in the 1990s and 2000s had an M/M genotype in a particular part of the PRNP prion gene, so the roughly half the population with M/V or V/V genotypes were immune. The Family That Couldn’t Sleep buys this, too. In fact, it buys it in an even more agonizingly 2000s way. The first sign that transmissible prion diseases weren’t genotype-restricted should’ve been the growth hormone kids. You might have heard this story – from the late 1950s through mid-1980s, human growth hormone produced from brain tissue was used as a treatment for pituitary dwarfism, until it turned out to spread CJD if the originating brain was infected. DTM discusses this, to set the scene for the genetics thing. He mentions what was the state of the art at the time – that a disproportionate share of both the growth hormone kids and sporadic CJD cases were V/V homozygotes. This, uh – so the book was written in the mid-2000s, yeah? Yeah. The conclusion DTM drew – and this was a common conclusion at the time – was that homozygosity somehow made you more vulnerable to CJD, and M/M homozygosity made you vulnerable to BSE-borne CJD in particular. We cannot criticise the author for not predicting the future, but we live in the future, and can say how this worked out. Turns out, nope, M/V heterozygotes totally get vCJD. After a British man in his 30s died of CJD in 2016, he was found to have vCJD and an M/V genotype. He was tested for vCJD only because he was exceptionally young for someone with a sporadic prion disease – meaning people developing it later in life would be missed6. Did you know up to 1 in 2000 people in the UK have latent vCJD? There is one line in The Family That Couldn’t Sleep that stopped me dead in my tracks when I read it: What happens to the Italian family in the end depends less on their own actions than on the world’s interest in prion diseases, which they cannot control. If lots of people are afraid of getting variant CJD, the family benefits. If fear of prion disease goes the way of the fear of swine flu or Ebola, then they will be orphaned again. THIS BOOK IS FROM 2006! Three years before the swine flu pandemic! Eight years before the Ebola pandemic! “If you’re looking for a sign, this is it.” --------------------------------------------------------- The last section of The Family That Couldn’t Sleep addresses BSE fears in America and a nascent internet subculture DTM calls “Creutzfeldt Jakobins” – people who track American CJD cases, trying to spot vCJD patterns. When reading his description of the Creutzfeldt Jakobins, my mind constantly, uncontrollably turned to covid. Here it was – an online community of people deeply skeptical about a disease’s official story, tracking every contradiction, every implausibility, every statistic that failed to apply to the individual. Self-described “redneck hippies” and “soccer mom Republicans” teaming up to find the truth hidden behind an impossible world. You know what they’re doing now. I’ve always combined a deep interest in medicine with a healthy distrust for it. People who are constitutionally inquisitive, anti-authoritarian, and suspicious about official narratives tend to end up skeptical of at least some mainstream claims in the field. This is not to say I think you should take bleach enemas or something, just that I understand the impulse behind concluding the US government was covering up a local vCJD wave. Traditionally, sporadic prion diseases are said to have a prevalence of one in a million. (Hold on to that for a second.) The last section of the book is a chronology of Americans finding bizarrely more than one in a million of their friends dying of sporadic CJD, often at inexplicably young ages, sometimes in geographical clusters. This is understandably suspicious. Then DTM goes on to reassure us by saying none of these cases were confirmed to have an M/M genotype, which OH GOD OH FUCK A number of high-profile people in the prion world, including Gajdusek, are clarified as not believing sporadic prion diseases exist. You get the impression DTM doesn’t, either. Now, how common are prion diseases? Eric Vallabh Minikel has an answer for you! Eric and his wife Sonia are prion researchers from a rather unique background – after Sonia was diagnosed as having a single-gene mutation with ~100% penetrance for prion disease, they left their previous jobs to dedicate their lives to curing it. It turns out, when you run the numbers, you get not one in a million but 1 in 5000 people dying of prion diseases. This is best described as “nightmarishly high”. I’m normed on genetic disorders. A genetic disorder that affects one in five thousand people is pretty common! I have known, in person, completely unselected, just from “random people I’ve met in my life in a non-medical context”, someone with a ~1/250k syndrome and someone with a ~1/50k-100k syndrome. I don’t think anyone in my extended family knows someone who died of a prion disease. I feel like it would’ve come up if they did! Prion diseases have distinctive phenotypes. Not distinctive enough, apparently, to avoid a lot of CJD being misdiagnosed as Alzheimer’s – but diagnosis is consistently insane. Something DTM reiterates throughout The Family That Couldn’t Sleep is just what prion dementia looks like. The characteristic dementia in prion diseases spares something – “self” or “recognition” or “reflection” – that is not spared by Alzheimer’s, or by most common dementias. Shouldn’t this be, uh, noticeable?7 They kill rapidly, often over the course of months, and often onset in midlife. ALS shares this pattern and is way, way more common than prion diseases; you hear about ALS far more in the “disorder people actually have” sense. What am I missing here? Anyway: 1 in 2000 prevalence of latent vCJD in the UK + extreme lack of clarity over whether scrapie is human-transmissible + blood donations spread vCJD + sporadic CJD prevalence keeps going up = ??? (Yes, I am annoyed that most countries have lifted their ban on UK blood donors, thank you for asking!) --------------------------------------------------------- But back to the book. The “American chapter” is one-third about the country’s response to vCJD, one-third about the Creutzfeldt Jakobins, and one-third about chronic wasting disease. The last part is the most interesting. Chronic wasting disease is a prion disease of deer. Like scrapie, it “probably, we hope” isn’t human-transmissible (eat venison at your own risk). Under natural circumstances, deer shouldn’t get prion diseases: A prion plague should not be possible among ruminants in the wild. Deer are not cannibals, as the cows that spread BSE were forced to be; and, because deer and elk are not domesticated, they do not have enough contact with one another to spread a prion infection the way sheep are thought to spread scrapie. But deer do not live as they used to live, humans having once again brought their ambitions to bear on the natural course of things. The Family That Couldn’t Sleep is a book of medical anthropology. Anthropology of the Veneto, anthropology of Papua New Guinea, anthropology of 1990s Britain. Here, it is an anthropology of America. Americans, having won the world, still fight to win their own backyard. The North American continent is geographically diverse, cutting through rain-snow-shine, mountains jutting over plains, cities sprawling into wilderness, habitations criss-cross dotted with surprisingly few empty zones. Go somewhere like Denver, the Mile High City, three million people fighting against nature. Few other countries have anything like this; geographically vast polities usually have uninhabitable blocks. Australians are twenty-five million people clustered against the shore. It still surprises me, after all this time, how every US state has a meaningful city8. Midcentury Denver, growing and sprawling out across its mountains, started to run into their natural inhabitants – deer. Starvation is one way nature adjusts the deer population to the available food supply. People did not usually see this process, but in the 1950s and 1960s Colorado became more densely settled, reducing forested areas and forcing deer to look longer and harder for food. At the same time, the state enacted conservation laws, limiting when and where hunters could shoot. Soon emaciated deer began wandering onto the lawns and through suburban streets looking for a meal. People began to feed them, only to find that they died anyway. They would drop dead by haystacks, along highways, and in flower beds. In the late 1960s, a young biologist named Gene Schoonveld tried to figure out why the deer starved even when they were fed.9 He deprived some deer of food for a while, “[h]e cut windows in their stomachs to see what went on inside, and then he began to feed them”. While this was going on, he had a control group of healthy, well-fed deer as backups in case anything went wrong. It did...but not to the experimental group. The pen in which the deer were kept also housed sheep, which, it turned out, were scrapie carriers. The deer somehow acquired scrapie – there’s a huge unanswered question here, which DTM doesn’t address. How did they get scrapie? They didn’t eat the sheep, presumably. Did it somehow transmit from casual contact? This is not supposed to happen. And yet: the deer in the sheep pen started dying of a mysterious scrapie-like disease, one never reported before, that would go on to infect thousands. These deer were released into the wild. Ten years later, the first reports of chronic wasting disease came out. The disease spread across deer and elk in the western half of the country. By the turn of the millennium, cases were exploding – and lost all geographical restriction. DTM can report up to 2005, at which point it was floating around Upstate New York. This kind of spread doesn’t track natural deer migration. That’s irrelevant, because nothing about CWD’s spread is natural. We shift gears into an anthropology of the American hunter. The hunter wants to shoot the most impressive buck, to bag himself one with as many “points” as possible – one whose antlers branch out most. A “ten-point buck” has five branches on each horn: Original by Ric McArthur Nature doesn’t make enough bucks with perfectly symmetrical ten-point horns. To fill the demand, the market had to step in. Thus was born the deer farm industry, which raises captive deer in better genetic and nutritional conditions than Nature permits, then ships them across the country so hunters who couldn’t get legit ten-point bucks get the taxidermy piece for their wall. These are controversial amongst hunters and illegal in numerous states – but the industry is big enough to spread CWD. (The kind of hunter who needs a deer shipped to his house is the kind of hunter who will fumble killing it.) Another problem is supplemental feeding – leaving out protein-enriched food for deer to eat. This produces “trophy class animals at an earlier age”, but again, what’s in that protein? (“It is much like feeding your cows 41 percent protein cottonseed cake during the winter to raise the protein level in the cow’s diet to a level that will maintain acceptable production”, says that article from 1991.)10 The book segues into a vignette. CWD was new in Wisconsin in the early 2000s, and the state’s Department of Natural Resources was optimistic it could eradicate it. In a state with a love of hunting, you could, in theory, recruit people to kill every single deer in a 400-square-mile radius: In many states, the state would have had to call out the National Guard for such an onslaught, but hunting is a passion in Wisconsin. Hunters shoot 450,000 deer every year, more than in any other state. “I’m looking for ardent hunters to help us, unless fear or their wives keep them away,” one DNR official told a Milwaukee magazine. The state extended the normal hunting season and waived the usual limit of one buck per hunter, and the hunters came out in force. The whole affair was gruesome – one official called it “hunting for slob hunters”. If you’re trying to eradicate a prion disease, you can’t very well let people take the carcasses home to eat. Bodies piled up in control stations, decomposition mingling with bleach. The 2002 hunt established a base rate of 2% for chronic wasting disease in Wisconsin deer, with the most affected areas getting up to 10%. Further hunts in 2003, 2004, and 2005 spread to wider and wider areas – and didn’t move the needle one bit. This is to say that CWD is quite a bit more common in the American deer population than BSE ever was in British cattle. Since publication, it’s popped up in Norway and South Korea. Notably, Norway doesn’t allow for the import of cervids, raising numerous questions about how it got there. There are no unambiguous cases of CWD transmission to humans, and in vivo/in vitro primate studies have mixed results. There sure are some unusually young hunters with sporadic CJD, though. But don’t worry, most of them aren’t M/M homozygotes! There is an absolute ton going on in this book. I’ve had to skim over whole sections. Parts that couldn’t be easily slotted into a narrative review include: When Gajdusek was invited to a party at Prusiner’s house, he was horrified to find his rival had purchased hundreds of New Guinean statues – all with the genitals removed.
Inline links: 2, Lyttle Lytton, 3, 4, a couple years later, concerningly transmissible to primates, omnigenic model, you might, 5, SNPedia, a 2009 post, https://substackcdn.com/image/fetch/$s_!N93S!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2Fced2eca3-ec58-40b8-8c13-debdb559ab8f_651x601.png, Yeah., nope, M/V heterozygotes totally get vCJD, 6, up to 1 in 2000 people in the UK have latent vCJD, bleach enemas, has an answer for you, 7, blood donations spread vCJD, going, up, 8, 9, not supposed to happen, https://substackcdn.com/image/fetch/$s_!0J8B!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2F2a64b287-a7c6-4d82-bbe1-da949fc93118_1024x683.png, Ric McArthur, controversial, amongst, hunters, illegal in numerous states, trophy class animals at an earlier age, 10, Norway, South Korea, mixed results, sure are
[An old Slate Star Codex post describes] systems trying to thrive [versus] systems trying to survive. Just as with the political left-right dichotomy that Scott described in these terms, this distinction between these types of systems is most obvious when both are in conflict with each other, such as when Silicon Valley startups complain that the regulations of the systems trying to ensure survival are stopping them from thriving, or when opponents of nuclear power proclaim themselves uninterested in the low price of this energy.
3rd: How The War Was Won, reviewed by Jack Thorlin. Jack previously worked as an attorney at the Central Intelligence Agency, and is now an assistant professor at the University of Arkansas School of Law. First place gets $2,500, second place $1,000, third place gets $500. Email me at scott@slatestarcodex.com to tell me how to send you money; your choices are Paypal, Bitcoin, Ethereum, check in the mail, or donation to your favorite charity. Please contact me by October 21 or you lose your prize. The other Finalists were: Autobiography Of Yukichi Fukuzawa, reviewed by Jason Rhys Parry. Jason is a researcher at Sapienship. He has a new tech and culture-themed Substack called Blueprint Canopy. You can read his debut post "The Sci-fi Career Guide" for a taste of things to come. He also tweets at @JRhysParry.
I mostly stand by the reasoning in my 2016 post, Slate Star Codex Endorses Clinton, Johnson, Or Stein. But you can read a better and more recent argument against Trump’s economic policy here, and against his foreign policy here. You can read an argument that Trump is a dangerous authoritarian here.
I think the strongest argument against Trump is the argument from authoritarianism. But what is authoritarianism in this context? As I argued years ago, Trump isn’t Hitler, isn’t going to put people in death camps, and probably his approval rating among minorities won’t even dip below the 30s. So what am I worried about?
Inline links: As I argued years ago
Actually we can do this very easily, because the paint-throwers broke the law, and the fossil fuel executives didn’t. Unless you’re the dumbest sort of naive consequentialist, you punish people who have violated bright-line norms, not people doing stuff you think is subtly damaging, even if the subtle damage may add up to more harm than the bright-line norm violations. You do this because it’s the prerequisite for having civilization at all: everyone disagrees on what’s subtly damaging, but everyone should be able to get behind protecting paintings. If people come together and form institutions to prevent bright-line violations everyone agrees on, and you pervert them or to fight your preferred battle against subtle damage, eventually those institutions lose credibility and you can’t do either.
Inline links: you punish people who have violated bright-line norms
http://slatestarcodex.com/Stuff/ACXPublic2025.xlsx
http://slatestarcodex.com/Stuff/ACXPublic2025.csv
Thanks again to everyone who took the survey! If you want to investigate the answers in more depth, download the public data (.xlsx, .csv)
The SSC-era is highlighted in blue. You can see that it shows something a bit like a classic sigmoidal adoption curve (but wearing a top hat). Post engagement starts low, before rapidly shooting up in 2014-15. It peaks in April 2016 – which is highlighted in red in this and all subsequent graphs so you can track peak engagement - before dropping back to a steady level of around 400-600 comments per post for the next three years. Notably, the run of posts that most people regard as being the ‘Golden Age’ for Scott’s writing happens much earlier than peak engagement with the comments section. People disagree about where this run of exceptionally good posts in quick succession start and ends, but I think you could safely say it has definitely begun by the time of The Control Group is Out of Control (although I would date it a little earlier, personally) and ends with either The Toxoplasmosa of Rage or Untitled – basically 2014 has a high density of ‘important’ posts.
Complexity of thought – Perhaps the most important feature distinguishing the ACX Commentariat from other, lesser, blogs is that some really smart people comment here and give novel and well-nuanced takes on a topic. If this ever disappeared it would not matter about any of the other three features, because the Commentariat would effectively be dead anyway. To me, these broad categories represent the unique and positive features of the SSC/ACX Commentariat, and the extent to which they are present is a reasonable indicator of comment section quality, especially if they are all present at the same timepoint and that timepoint happens to line up with peak engagement in 2016 (this is foreshadowing). To generate data on the ACX Commentariat, I scraped the comments section of every post Scott has made since 2013. The Old Ones whisper of a blog that existed before even Slate Star Codex, but since I’m not 100% certain we’re encouraged to talk about the older blog (and nobody dates the golden era of Scott’s writing to pre-2013 anyway) I kept my scraping to just the two websites we’re definitely allowed to talk about; Slate Star Codex (SSC) and Astral Codex Ten (ACX). The main points of failure with my scraping were Subscriber-only threads (which my algorithm virtuously refused to read as it wasn’t a subscriber) and battling with the Substack UI to get all the comments to load for me simultaneously on larger threads. Nevertheless, between my incompetent code and the jaunty Substack UI I only dropped a few comments on even very long threads, so I figured the data scrape would be adequate for the use-case I had for it. I then used a bunch more janky code (some written by me, some written by ChatGPT) to try and quantify the levels of depth, freedom, politeness and complexity of each comment. I captured 2460 individual posts, and approximately 1.8m comments. Of the 24,486 unique comment authors, around 40% have made only one comment to the blog. The most prolific poster is the irrepressible Deiseach, at 20,685 contributions. Deiseach is also the only commentor to have made a comment on both the first post in my sample and the last, so has been with the blog a very long time! Only one other commentor has made more contributions than Scott (11,249), and this is John Schilling (11,607). The quality of data on individual users is not great for the ACX era (Substack seems to record missing author data in a few different ways, and sometimes swallow data for no reason) but I’m happy to give the rank ordering of anyone else who cares to know their specific level of clout in this niche community - I myself am the 799th most prolific contributor to the comments section (225 comments). I’m also delighted to share my raw data with anyone interested – the summary statistics per post are here. The scraped comments themselves are about 2Gb so I don’t know where I can host them but if anyone has any ideas (and Scott doesn’t mind) I’ll share them too. I know that some of the post titles seem to have turned into hieroglyphics, but as far as I can tell it is cosmetic only and won’t affect any of the actual data – it is a symptom of a cool hidden feature of Microsoft Excel where it open UTF-8 encoded CSVs in a way that garbles special characters for no particular reason. Considering each of these factors in turn: Depth of engagement with a topic
This graph shows that around 9% of comments will contain at least one token indicating the comment is discussing a sensitive topic, with a range of about 6% to 14%, disregarding the very early years where small sample size made the data more variable. There wasn’t any one ‘sensitive’ token in particular which correlated exceptionally well with the rise and fall of this 6% to 14%, which implies to me that we have correctly identified a general factor of ‘willingness to discuss sensitive topics’ (or possibly that the peaks and troughs correspond to peaks and troughs in the external landscape – ie specific touchpoints and lulls in the Culture War – which would also be fine for the purpose we’re putting it to). This is an imperfect measure because it only tracks if someone is using a sensitive phrase and not whether they are using it in a heretical way (cf. ‘fifty Stalins’ here). However, I thought in the context of ACX posts the approach was probably reasonable – sensitive phrases are only likely to appear if they are being discussed a lot, and we know from the previous section that discussion depth is high both now and during the 2016 peak engagement period. It isn’t necessarily true that deep discussion implies spirited debate - some political discussions on reddit can go into the thousands of comments without anyone ever actually expressing a counter-orthodoxy view – but I think in the specific context of ACX it is reasonable, because we don’t generally have norms of expressing substanceless agreement. Hopefully, therefore, the changing ratio of socially or professionally sensitive phrases to phrases not included in my dictionary would tell us something about the willingness of the comment section to engage in potentially emotive discussions at any point in time. The relationship of occurrence of these tokens to engagement with the comment section is hard to draw clear conclusions from – although the peak does indeed look to be about 2016 or 2017 the data are noisy, and strongly affected by the choice of words to include in my dictionary. I picked the dictionary before I saw the data, but perhaps a different set of words would have given a different result, especially if I had a better way of identifying sensitive discussions around COVID (‘ivermectin’ was the only COVID-related word I could think of that became politicised in the same way ‘microaggression’ or ‘misgender’ did). Nevertheless, I would say this gives some weak support to the idea that 2016 was a turning point in SSC Commentariat free speech norms (and strong support to the idea that the start of ACX was a low point for discussion of sensitive topics) I include below a few specific sensitive phrases which I thought were interesting. Do note the different scales on each graph. Of particular interest to me is the ‘SJW’ graph, which has a really clear peak at exactly the high point of Commentariat engagement. I will return to this graph later in the review. Politeness
Many cities have regular Astral Codex Ten meetup groups. Twice a year, I try to advertise their upcoming meetups and make a bigger deal of it than usual so that irregular attendees can attend and new readers can hear about the meetups. This is one of those times.
Meetup Czar Note: If Cassander claims to be running ACX Everywhere, this is false. We have fully split with Cassander, and ask that he no longer use the Astral Codex Ten or Slate Star Codex brand.
Contact: Joey Contact Info: me[a t]joeym[period]org Time: Wednesday, September 10th, 6:00 PM Location: Armistice Coffee Roosevelt, 6717 Roosevelt Way NE Suite 101, Seattle, WA 98115. I'll be in the back covered area, with a sign that says "Astral Codex Ten Meetup". Coordinates: https://plus.codes/84VVMMHJ+4XJ Group Link: https://www.meetup.com/seattle-rationality/events/; https://www.lesswrong.com/groups/PmvZmMxBtxE87PHZf; https://discord.gg/6qk [remove this bit] jG5heDC
Of the 42 grantees, 40 have answered our email asking for confirmation that they still want the grant. I’m still waiting for confirmation emails from Lewis Wall and Nishank B. If you’re reading this and don’t think you got a confirmation email, check your spam folder. If it’s not in your spam folder, email me at scott@slatestarcodex.com. If you can’t reach me or I don’t respond, DM me on Substack or Twitter. I’ll give you until November 1 to get in touch, after which point the grant will be withdrawn. There are also a few projects so deep in stealth I don’t have permission to share their existence; I will mention these as they become public.
If any of you are unhappy with how you have been credited or not-credited, please email me at scott@slatestarcodex.com.
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