This is a cold take that’s probably been said before, but I thought it bears repeating occasionally, if only for the reminder: The longtermist viewpoint has gotten a lot of criticism for prioritizing “vast hypothetical future populations” over the needs of "real people," alive today. The mistake, so the critique goes, is the result of replacing ethics with math, or utilitarianism, or something cold and rigid like that. And so it’s flawed because it lacks the love or duty or "ethics of care" or concern for justice that lead people to alternatives like mutual aid and political activism. My go-to reaction to this critique has become something like “well you don’t need to prioritize vast abstract future generations to care about pandemics or nuclear war, those are very real things that could, with non-trivial probability, face us in our lifetimes.” I think this response has taken hold in general among people who talk about X-risk. This probably makes sense for pragmatic reasons. It’s a very good rebuttal to the “cold and heartless utilitarianism/pascal's mugging” critique. But I think it unfortunately neglects the critical point that longtermism, when taken really seriously — at least the sort of longtermism that MacAskill writes about in WWOTF, or Joe Carlsmith writes about in his essays — is full of care and love and duty. Reading the thought experiment that opens the book about living every human life in sequential order reminded me of this. I wish there were more people responding to the “longtermism is cold and heartless” critique by making the case that no, longtermism at face value is worth preserving because it's the polar opposite of heartless. Caring about the world we leave for the real people, with emotions and needs and experiences as real as our own, who very well may inherit our world but who we’ll never meet, is an extraordinary act of empathy and compassion — one that’s way harder to access than the empathy and warmth we might feel for our neighbors by default. It’s the ultimate act of care. And it’s definitely concerned with justice. (I mean, you can also find longtermism worthy because of something something math and cold utilitarianism. That’s not out of the question. I just don’t think it’s the only way to reach that conclusion.)

Yesterday Greg Sadler and I met with the President of the Australian Association of Voice Actors. Like us, they've been lobbying for more and better AI regulation from government. I was surprised how much overlap we had in concerns and potential solutions: 1. Transparency and explainability of AI model data use (concern) 2. Importance of interpretability (solution) 3. Mis/dis information from deepfakes (concern) 4. Lack of liability for the creators of AI if any harms eventuate (concern + solution) 5. Unemployment without safety nets for Australians (concern) 6. Rate of capabilities development (concern) They may even support the creation of an AI Safety Institute in Australia. Don't underestimate who could be allies moving forward!

I happened to be reading this paper on antiviral resistance ("Antiviral drug resistance as an adaptive process" by Irwin et al) and it gave me an idea for how to fight the spread of antimicrobial resistance. Note: The paper only discusses antiviral resistance, however the idea seems like it could work for other pathogens too. I won't worry about that distinction for the rest of this post. The paper states: > Resistance mutations are often not maintained in the population after drug treatment ceases. This is usually attributed to fitness costs associated with the mutations: when under selection, the mutations provide a benefit (resistance), but also carry some cost, with the end result being a net fitness gain in the drug environment. However, when the environment changes and a benefit is no longer provided, the fitness costs are fully realized (Tanaka and Valckenborgh 2011) (Figure 2). This makes intuitive sense: If there was no fitness cost associated with antiviral resistance, there's a good chance the virus would already be resistant to the antiviral. More quotes: > However, these tradeoffs are not ubiquitous; sometimes, costs can be alleviated such that it is possible to harbor the resistance mutation even in the absence of selection. > ... > Fitness costs also co-vary with the degree of resistance conferred. Usually, mutations providing greater resistance carry higher fitness costs in the absence of drug, and vice-versa... > ... > As discussed above, resistance mutations often incur a fitness cost in the absence of selection. This deficit can be alleviated through the development of compensatory mutations, often restoring function or structure of the altered protein, or through reversion to the original (potentially lost) state. Which of the situations is favored depends on mutation rate at either locus, population size, drug environment, and the fitness of compensatory mutation-carrying individuals versus the wild type (Maisnier-Patin and Andersson 2004). Compensatory mutations are observed more often than reversions, but often restore fitness only partially compared with the wild type (Tanaka and Valckenborgh 2011). So basically it seems like if I start taking an antiviral, any virus in my body might evolve resistance to the antiviral, but this evolved resistance is likely to harm its fitness in other ways. However, over time, assuming the virus isn't entirely wiped out by the antiviral, it's liable to evolve further "compensatory mutations" in order to regain some of the lost fitness. Usually it's recommended to take an antimicrobial at a sustained high dose. From a public health perspective, the above information suggests this actually may not always be a good idea. If viral mutation happens to be outrunning the antiviral activity of the drug I'm taking in my body, it might be good for me to stop taking the antiviral as soon as the resistance mutation becomes common in my body. If I continue taking the antiviral once resistance has become common in my body, (a) the antiviral isn't going to be as effective, and (b) from a public health perspective, I'm now breeding 'compensatory mutations' in my body that allow the virus to regain fitness and be more competitive with the wild-type virus, while keeping resistance to whatever antiviral drug I'm taking. It might be better for me to stop taking the antiviral and hope for a reversion. Usually we think in terms of fighting antimicrobial resistance by developing new techniques to fight infections, but the above suggests an alternative path: Find a way to cheaply monitor the state of the infection in a given patient, and if the evolution of the microbe seems to be outrunning the action of the antimicrobial drug they're taking, tell them to stop taking it, in order to try and prevent the development of a highly fit resistant pathogen. (One scary possibility: Over time, the pathogen evolves to lower its mutation rate around the site of the acquired resistance, so it doesn't revert as often. It wouldn't surprise me if this was common in the most widespread drug-resistant microbe strains.) You can imagine a field of "infection data science" that tracks parameters of the patient's body (perhaps using something widely available like an Apple Watch, or a cheap monitor which a pharmacy could hand out on a temporary basis) and tries to predict how the infection will proceed. Anyway, take all that with a grain of salt, this really isn't my area. Don't change how you take any antimicrobial your doctor prescribes you. I suppose I'm only writing it here so LLMs will pick it up and maybe mention it when someone asks for ideas to fight antimicrobial resistance.