Astral Codex Ten

University of Florida

15 min read

University of Florida

Article

University of Florida is a recurring organization in the Astral Codex Ten archive, appearing 2 times across 2 issues between June 29, 2023 and December 07, 2023. The archive places it in contexts such as “Jennifer Miller, an endocrinologist at the University of Florida”; “Professor Jeffrey Hillman of the University of Florida”. It most often appears alongside Aaron, Aaron Silverbook, Aella.

Metadata

  • Category: Organizations
  • Mention count: 2
  • Issue count: 2
  • First seen: June 29, 2023
  • Last seen: December 07, 2023

Appears In

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.

Sure, Whatever, Let's Try Another Contra Caplan On Mental Illness
June 29, 2023 · Original source
Liking Pepsi more than Coke. You could think of this as a preference for drinking Pepsi over drinking Coke - or as an internal state marked by a strong repulsion to Coke plus a strong attraction to Pepsi. In the first two situations, it’s much more natural to use internal-state language, and in the sixth, it’s much more natural to use preference language. The middle three aren’t obvious, which is why we’re having this debate. The Buddhists say desire is suffering, and sometimes this is literally true. An itch is the clearest example; it’s in an almost perfect superposition between raw suffering and pure desire (to scratch yourself). Is it a preference or a constraint? It’s both - a preference to scratch one’s self, and a constraint to be forced to feel suffering if you don’t scratch yourself. While the person may choose whether or not to scratch themselves, they cannot choose whether or not to feel the suffering. Put a gun to their head and say “stop feeling suffering when you don’t scratch yourself” and they will have no choice but to die. It’s possible, although bizarre, to think of normal preferences like the preference for Pepsi over Coke this way. You could say “this person has the constraint that they will feel suffering when they are forced to drink Coke instead of Pepsi”. It’s not very useful. But it’s possible. Whether it’s more useful to think of any given situation as a preference or a constraint depends on things like whether you can easily satisfy the preference, whether the preference is ego-syntonic or ego-dystonic, and whether it seems normal by social standards. Consider Prader-Willi syndrome, caused by damage to a region of chromosome 15. Symptoms tend to include short limbs, mental retardation, and extreme hunger. Here’s how the NYT describes this last problem (content warning for body horror): One result is a heightened, permanent sensation of hunger. “They describe it as physical pain,” Jennifer Miller, an endocrinologist at the University of Florida who treats children with Prader-­Willi, told me. “They feel like they’re going to die if they don’t get food. They’re starving.” Parents must lock their pantries, refrigerators and trash cans, and their children frequently lie and steal to get something to eat. They have been known to memorize credit-card numbers and secretly phone for delivery, use a drill to remove the door from a locked refrigerator and break into a neighbor’s garage and eat, uncooked, an entire frozen pizza. And here’s how it describes one particular patient’s last moments: In 2004, Peter and Gayle Girard held their annual Christmas Eve party for family members at their home in Orlando, Fla. Before dinner, they set out chips, vegetables and dip, shrimp, a bowl of punch and sodas. Their 17-year-old son, Jeremy, had Prader-­Willi, and they often hosted events at their home so he could join in while they kept an eye on him — as they believed they were doing that night. But the next morning, Jeremy’s belly was distended, and he complained of pain. At the emergency room, doctors pumped his stomach, but his condition worsened. A day passed before surgeons discovered that his stomach, which had been distended long enough to lose blood flow and become septic, had ruptured. Jeremy died that night. Only afterward did the Girards learn that other family members saw him eating more than he should have but didn’t alert them. I insist on calling Prader-Willi syndrome a disease, and a serious one, even though the extreme hunger of Prader-Willi is continuous with/shades into the normal hunger where I would like a slice of pizza. My preference for pizza is so easily satisfied that it rarely bothers me. It’s ego syntonic - I am fine with being the sort of person who likes pizza. It’s socially normal - everyone likes pizza. It doesn’t cause much trouble - it wouldn’t improve my life much if I stopped wanting pizza. So I think of it as a preference. If it were otherwise - the extreme hunger of someone with Prader-Willi - it would be more natural to talk about it as a compulsion, a sense of extreme pain inflicted on me when I wasn’t eating enough, something ontologically similar to a stomach flu that also produces extreme pain in the abdominal region. IV. None of this really addresses Caplan’s most recent post, which is, I think, a much worse point. His current post says that either you have to believe that mental illness doesn’t exist and is just voluntary preferences which are stigmatized by society, or you have to believe that homosexuality is objectively a mental illness. Not only are each of these incoherent ideas, they’re not even the same incoherent idea! You could easily accept one of the incoherent ideas and reject the other! Consider the following three positions: Down’s Syndrome is a terrible disease that inflicts vast suffering on its victims. Also it inflicts suffering on society by making people unproductive. We should be very angry about this, and do everything we can do make people with Down’s Syndrome normal.
Inline links: Here’s how the NYT describes
Defying Cavity: Lantern Bioworks FAQ
December 07, 2023 · Original source
It lacks a peptide that its species usually uses to arrange gene transfers with other bacteria. The antibiotic helps it win the Darwinian competition in your mouth to become King Of The Oral Bacteria. The alcohol metabolism means it won’t produce lactic acid (and so won’t cause tooth decay). The peptide knockout prevents it from transferring genes back and forth with other bacteria that might either inactivate it or leak its advantage. 1.1: Where did this come from? Who invented it? Professor Jeffrey Hillman of the University of Florida. In 1985, he was surveying the microorganisms on his graduate students’ teeth (as you do). One grad student had an unusual strain of S. mutans with a natural version of mutations 1 and 2 (it produced mutacin-1140, and was resistant to it). Hillman realized the potential, and spent the next few decades adding mutations 3 and 4 and testing the results. 1.2: So how did it end up with a tiny startup in 2023? Professor Hillman started a company “Oragenics” and applied for FDA approval. The FDA demanded a study of 100 subjects, all of whom had to be “age 18-30, with removable dentures, living alone and far from school zones”. Hillman wasn’t sure there even were 100 young people with dentures, but the FDA wouldn’t budge from requiring this impossible trial. Hillman gave up and switched to other projects (including an intranasal COVID vaccine!) Aaron heard this story and figured that brash, move-fast-and-break-things Silicon Valley biotech might be able to find an alternative route to commercialization. The strain was off-patent, so he first tried to synthesize it himself from the clues in Hillman’s published papers. When that didn’t work, he made a deal with Oragenics for 10% of profits in exchange for samples and the full recipe. 2: How do you use it? To apply, you brush your teeth with a special pumice-based product that removes your existing tooth bacteria, then swab it on with a q-tip. One dose is sufficient; once you use it, it’s in your mouth approximately forever. 2.1: As users kiss their loved ones, who kiss others in turn, will this spread exponentially and take over the world? There was originally some concern about this, but no. Remember, the original bacterium was found in the wild, in a random grad student’s mouth forty years ago. There must be thousands of people walking around with various naturally-occurring BCS3-L1-like things. So probably this isn’t a risk for some kind of weird pandemic. Existing mouth bacteria have fortified their position and have a strong home field advantage. This is why you need to brush your teeth with the special product to apply Lumina. Lantern’s safety documents note that couples who kiss constantly do end up with similar oral microbiomes. So maybe enough kissing - especially kissing just after a dental cleaning when your existing bacteria are at their weakest - could spread the strain accidentally, very slowly. This rate of spread would be comparable to the rate of spread of every other mouth bacterium. 2.2: When a user kisses their newborn baby, will it spread to the baby? Okay, this one is true. Babies have no existing mouth bacteria, and get theirs from their parents’ kisses. Not necessarily their first kiss as a newborn (newborns have no teeth, and BCS3-L1 needs teeth to live), but their first kiss after teeth grow in. If you get this, you’re probably getting it for your whole future family line. 2.3: If you wanted to get rid of it, could you? Some kind of extreme course of oral antibiotics that nukes everything growing in your mouth would probably eradicate BCS3-L1, but this hasn’t been tested and would have side effects. 3: Is it dangerous to have bacteria secreting an antibiotic in your mouth? Does this mean you’re on a weak antibiotic all the time? There are already bacteria secreting antibiotics in your mouth. Microbes are in constant war with other microbes, and antibiotics are one of their favorite weapons - remember, penicillin comes from a fungus. Because bacteria secrete just enough antibiotic to clear their local area, these are tiny quantities, much less than you’d get from taking a medical-grade antibiotic pill. Lantern says the levels of mutacin-1140 dilute to irrelevance “tens of microns” away from the secreting bacteria. In any case, it’s a weak antibiotic that doesn’t survive the digestive tract (Hillman originally hoped to market the antibiotic too, but found it didn’t get absorbed and broke down too quickly). Neither the grad student with the original strain nor any of Hillman’s test subjects had any noticeable health issues. See also Lantern’s Safety Review FAQ. 3.1: Is it bad to disrupt your normal mouth microbiome? When talking about BCS3-L1 “taking over” the mouth, this just means it takes over the streptococcus mutans niche. There are still other bacteria and fungi in the mouth. The mutacin antibiotic might still disrupt these other bacteria (probably not fungi). But strains like BCS3-L1 already exist in the wild (eg the original grad student), and lots of bacteria and fungi secrete antibiotics, so it doesn’t seem like having mutacin-secreting organisms in your mouth makes you some extreme oral microbiome outlier. If you eat a normal Western diet, your mouth microbiome is already pretty far from the design specs, and it’s unclear if using Lumina makes things worse. 3.2: Will the other bacteria develop resistance to the antibiotic? Mutation 4 prevents BCS3-L1 from “leaking” its own resistance. Although in theory other bacteria could develop resistance, mutacin-1140 is a hard antibiotic to develop resistance to, and the other bacteria would have to do it in the short period before BCS3-L1 kills them off and establishes its own home field advantage. In practice, Professor Hillman found that BCS3-L1 remained dominant over many years and nothing developed resistance to it. Even if a mutacin-resistant strain does develop in one person’s mouth, it will have a hard time getting to anyone else’s mouth, so widespread immunity is unlikely. 4: Is it dangerous to have bacteria secreting alcohol in your mouth? Will you get drunk? Most people already have some alcohol-secreting bacteria in their bodies. (there’s a condition called auto-brewery syndrome where those bacteria get out of control and produce enough alcohol to make someone drunk. It’s vanishingly rare in real life, but more common in the legal system: “You gotta believe me, Officer, it was just auto-brewery syndrome!”) The average person has enough of these bacteria in their gut to have a natural blood alcohol level - even after zero drinks - of about 0.1 mg/dl. Under pessimistic assumptions, BCS3-L1 will add another 0.2 mg/dl, bringing the total to 0.3. This is still a pretty normal number that some people have naturally (it would bring the average customer from the ~50th to the ~80th percentile of natural blood alcohol). It’s also far from the usual threshold for feeling tipsy (30 mg/dl) or too drunk to drive (80 mg/dl). Under more realistic assumptions, the amount of alcohol produced by BCS3-L1 probably isn’t significant even by the very low standards of natural blood alcohol concentrations. 4.1: Are there some unusual scenarios where this amount of alcohol might matter? I don’t think Lantern has studied Breathalyzers. Since the alcohol is directly in your mouth, it might have disproportionate effect on a Breathalyzer compared to alcohol in your blood. I think it’s probably still too low to matter, but this is a wild guess. There is conjecture that “non-alcoholic steatohepatitis”, a liver disease in which non-alcoholics get the same kind of liver damage that alcoholics usually get, might be associated with endogenous blood alcohol in the high normal range. If I’m understanding this paper right, it’s probably because the gut produces levels of alcohol consistent with auto-brewery syndrome, the liver goes into overdrive and metabolizes it away (prevents auto-brewery syndrome from developing), but the liver is damaged in the process the same as if it had to go into overdrive to metabolize normal binge drinking. Since BCS3-L1 produces much less alcohol than auto-brewery, I think it wouldn’t cause non-alcoholic steatohepatitis, even though it might produce final blood alcohol levels similar to those associated with the condition. I was originally worried that Lumina might activate Antabuse, an anti-alcoholism drug that prevents drinking by causing a very unpleasant (sometimes dangerous) reaction to ethanol. There are some past cases of Antabuse being activated by really trivial quantities, like the alcohol in a chicken marsala dish or a mouth wash. But no, I think BCS3-L1 is less than this too. Chicken marsala can contain several grams of alcohol per serving, but BCS3-L1 probably only produces a few milligrams per day. If you swallow 1/10 of your mouthwash, that’s about 200 mg of alcohol - again, BCS3-L1 is probably only a few milligrams a day. Antabuse usually activates around a BAC of 5 mg/dl; BCS3-L1 only gives you a BAC of about 0.3 mg/dl. Again, this really is a tiny amount of alcohol. There might be other edge cases like these. Lantern offers a $100 bounty to anyone who can come up with one they haven’t thought of yet (and sometimes extra if you’re willing to help them research them). 4.2: Has anyone tested this in real life? As mentioned before, the mutacin-releasing strain (with mutations 1 and 2) exists in the wild and was extensively tested by Professor Hillman. The full strain with all four mutations has undergone some testing by Dr. Hillman, but nobody had officially infected themselves with it until two months ago, when Aaron finally synthesized it and tried it on himself. He says he’s usually “a lightweight” as far as alcohol goes, and hasn’t felt any different over the past two months. When first infected, BCS3-L1 makes up almost 100% of the microbiome (because you deliberately removed all your other bacteria, then infected yourself with it). Over time, other bacteria creep back in; over an even longer period (years?), BCS3-L1 reclaims lost territory and reaches a steady state. But the point is that Aaron probably has already passed his period of highest BCS3-L1 activity, and felt nothing. My wife infected herself about a month ago, and I haven’t noticed her having worse judgment or becoming more impulsive. But at baseline she was the sort of person who would infect herself with an untested genetically-modified bacteria strain, so there might be floor effects. 5: What’s the plan to sell Lumina? The plan is: Phase 1: (January 2024) Sell to biohackers in Prospera for $20,000.
Inline links: an intranasal COVID vaccine, made a deal, recipe, To apply, Safety Review FAQ, auto-brewery syndrome, in the legal system, this paper, can contain, https://substackcdn.com/image/fetch/$s_!My2N!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2F9200a48f-2549-40ba-9b4a-73c3e19fe93a_569x393.png