Lao Mein

P(doom) = 50%, 3 years to AGI.


I give full permission for anyone to post part or all of any of my comments/posts to other platforms, with attribution.

Currently upskilling for future work on technical AI alignment research. Want to do part time work translating AI developments in China for a Western audiance in the meantime. Would really appreciate funding on either.

Will analyze papers and do bioinformatics research for money. DM me if interested.

Wiki Contributions


Can you give examples of what you're looking for? Can I email you entries and expect a response?

Lao Mein130

I can confirm that my PayPal has received the $500, although it'll be frozen for a while.

Thanks! I had a lot of fun doing the research for this and I'm working on an update that'll be out in a few days. 

I think a lot of it comes down to training data context - " Leilan" is only present in certain videogame scrapes, " petertodd" is only found in Bitcoin spam, ect. So when you try to use it in a conversational context, the model starts spitting out weird stuff because it doesn't have enough information to understand what those tokens actually mean. I think GPT-2's guess for " petertodd" is something like "part of a name/email, if you see it, expect more mentions of Bitcoin". And not anything more, since that token doesn't occur much anywhere else. Thus, if you bring it up in a context where Bitcoin spam is very unlikely to occur, like a conversation with an AI assistant, it kinda just acts like a masked token, and you get the glitch token behavior.

Lao Mein130

I was thinking of areas along the gum-tooth interface having a local environment that normally promote tooth demineralization and cavities.  After Lumina, that area could have high chronic acetaldehyde levels. In addition, the adaption of oral flora to the chronic presence of alcohol could increase first-pass metabolism, which increases acetaldehyde levels locally and globally during/after drinking.

I don't know how much Lumina changes the general oral environment, but I think you might be able to test this by seeing how much sugar you can put in your mouth before someone else can smell the fruity scent of acetaldehyde on your breath? I'm sure someone else can come up with a better experiment.

The Alcohol Flushing Response: An Unrecognized Risk Factor for Esophageal Cancer from Alcohol Consumption - PMC (

There are a lot of studies to regarding the assocation between ALDH2 deficiency and oral cancer risk. I think part of the issue is that

  1. AFR people are less likely to become alcoholics, or to drink alcohol at all.
  2. Japanese in particular have a high proportion of ALDH2 polymorphism, leading to subclinical but still biologically significant levels of acetaldehyde increase after drinking among the non-AFR group.
  3. Drinking even small amounts of alcohol when you have AFR is really really bad for cancer risk.
  4. Note that ALDH2 deficiency homozygotes would have the highest levels of post-drinking acetaldehyde but have the lowest levels of oral cancer because almost none of them drink. As in, out of ~100 homozygotes, only 2 were recorded as light drinkers, and none as heavy drinkers. This may be survival bias as the definition of heavy drinking may literally kill them. 
  5. The source for #4 looks like a pretty good meta-study, but some of the tables are off by one for some reason. Might just be on my end.
  6. ADH polymorphism is also pretty common in Asian populations, generally in the direction of increased activity. This results in faster conversion of ethanol to acetaldehyde, but often isn't included in these studies. This isn't really relevant for this discussion though.

As always, biostatistics is hard! If X causes less drinking, drinking contributes to cancer, and X increases drinking's effects on cancer, X may have positive, neutral, or negative overall correlation with cancer. Most studies I've looked at had a pretty string correlation between ALDH2 deficiency and cancer though, especially after you control for alcohol consumption.

It also looks like most researchers in the field think the relationship is causal, with plausible mechanisms.

Will there be other people there? Looks like I'm the only one interested.

Lao Mein243

Some times "If really high cancer risk factor 10x the rate of a certain cancer, then the majority of the population with risk factor would have cancer! That would be absurd and therefore it isn't true" isn't a good heuristic. Some times most people on a continent just get cancer.

It might have conditioned your oral and gut flora to break down ethanol into acetaldehyde faster. I'll have a follow-up piece on hangovers and AFR coming soon, but the short of it is that certain antacids taken before drinking may help by decreasing ethanol first pass metabolism.

Good question - I don't think anyone knows.

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