In your case it might simply be that there was not enough of this kind of tasks in the training data.

*head bangs in approval*

I agree in general, but not with this strong phrasing. I've let AI build a good amount of non-trivial code. But my consistent experience is that it works best when guided by an experienced coder who can correct it, and when implementing well-known algorithms rather than coming up with novel solutions.

Example: I let it write up a quadtree implementation in a language for which there was no ready solution online. It took 2-3 correcting prompts to get a good result. I could've done it myself but it would've likely taken a few hours to get it all right instead of the half or so hour it took with AI. The important part for me was that there's nothing unknown in how to implement a quadtree. All the AI needs to do is take the 100s of existing implementations and translate them into a different language.

True but too simplified. The Luddites had an entirely different motivation: The fact that factories now employed women and children at very low rates meant that the men lost their status in the family as bread winners and head of household. That was a major social disruption, which we don't have with AI.

I'd compare it more to teamsters or wagoners when cars became common. Your job is threatened by a different way of doing the same thing, a way to which your skills don't cleanly transition. Some choose to pick up the new tech, some want the old ways to persist.

In the end, coachmen became chauffeurs, because rich people prefer to be driven around oder driving themselves, no matter if it's a horse or an engine doing the pulling. But much fewer teamsters and wagoners became truck drivers.

Oh, forgot to link the dry density for you: here you go. 341kcal/100g. Aka 3,41kcal/g.

Which, like I said, should be obvious, since they're almost entirely carbs (~4kcal/g) and protein (~4kcal/g), and they're, as noted, dry (12-16% moisture). It would be quite the trick indeed to get something that is dry and and is almost entirely comprised of things that are 4kcal/g to be 1,38kcal/g! ;)

Just in case you need help:

Your calculation: 195g (dry weight) × 1.38 kcal/g = 269 calories per pound of cooked beans.
Correction: Because you used 1.38 kcal/g (the cooked density) as if it were the dry density, you essentially diluted the calories twice.
The Actual Math: 195g of dry beans * 3.4 kcal/g (actual dry density) = 663 kcal.

When those 195g of dry beans absorb water to weigh 454g (1 pound), they still contain those same 663 calories (since water has zero calories).

Canned beans are ALREADY COOKED. *facepalm*. You can eat them straight out of the can.

which is waaaay more than I would want to eat at a sitting.

I can't think of a single ingredient - any ingredient - that I would want to eat exclusively as my diet, so this is a really stupid argument.

In general, "damping pleasure" is not most people's experience with GLP-1 agonists. What it does is more like separate pleasurable experiences from having an urgent need to continue doing them.

I'd believe the Iceland numbers. I had a doctor once who wanted to get me on antidepressants, and got mad when I didn't want to, and completely ignored my pleadings of "But I'm not depressed", "I enjoy life", "I'm probably the least depressed person you'll meet", etc. He just really liked his patients to be on it. The Icelandic medical system is very into anything that "medicates symptoms" rather than treating diseases. For example, during COVID, it was essentially impossible to get drugs like paxlovid, but they made parkodín (tylenol with codeine) over-the-counter.

In most modern societies medication is usually a last resort.

I'm going to take a wager that if I were to open your medicine cabinet right now, there would be painkillers in it, which you take as will when you get headaches, body aches, etc.

Yes, different people have different baseline hunger levels. This is well accepted in the scientific community.

Please read: Cooked bean variety.

The "beans in your pantry" data you're looking at are probably per serving. Here, let me grab the beans in *my* pantry. Roland BLACK BEANS Habichuelas Negras Supreme Calidad. Net weight 15.5 OZ / 439g. Serving size: 130g. Calories per serving: 180.

There's 453,6 grams per pound, so that's 0,968 pounds. 439/130 = 3,15 servings, times 180 calories = 567. In 0,968 pounds, that's 586 calories.

Or look online. "172 grams of black beans (cooked, boiled, unsalted) contains 227 Calories." Do the math.

I'm not sure exactly how you expect something that is 70% carbs (of which are 36% fibre) and 26% protein to be low-cal. Do you think it has the moisture content of celery or something?

BOTH of them? :-)

I'm thinking about starting a very low dose when the pills come out in Europe. That gives an extra year for more data.

For me it's purely about health (well, about 90% about healthj). I'm a marginal case weight-wise, but the overall health impact profile looks spectacular. If a pill seems likely to add a number of healthy years to my lifespan, yes please. But the more data the better.

One thing that held me back was, I'm very averse to addiction, to anything that might have withdrawal symptoms. People report being ravenous and needing to eat all the time when they quit. BUT - the data shows that after one year, people still retain about 25% of their weight loss, and at two years they're about baseline (some above baseline, some below - the "above" people may be due to sarcopenic obesity, in that you put fat back on faster than muscle, and so your metabolism is lower until the muscle comes back). This is very different from when you diet to lose weight and then stop dieting - you're not ravenous at all, you finally have satiation.

But given the weight regain stats, and the general way these work, what I think is going on is: when you lose weight, you've been training yourself for months on how to ignore or alleve your hunger pangs, so when you stop, you're well trained to it. Whereas GLP-1 agonists are just the opposite: you don't even need to think about resisting the temptation to eat, it just comes naturally; you can get pleasure from something, such as a tasty dessert, without feeling the need to eat everything on your plate; pleasure and craving get separated. So people who just suddenly cut off from GLP-1 agonists are "mentally unarmed" for the reversal. The weight-regain stats however suggest that it doesn't leave you long-term disabled in this regard; that you're just back to your old self once you readjust, whatever that old self may have been.

I haven't read these particular studies, but a lot of the fascinating impacts of GLP-1 agonists occur whether the person loses weight or not. For example, the cardiac benefits are massive, like 2/3rds of the scale of benefits of being on statins, and it apparently occurs independent of weight loss.

One of the annoying things about our wetware is that systems aren't isolated; a "part" that gets used for one thing might also be used for half a dozen unrelated things.

Please understand that there is a balance. Taking things to "reduce inflammation" or to "boost the immune system" run counter to each other. Inflammation *is* the reaction of the innate immune system. The immune system defends not just against pathogens, but also cancer. If you shut down the immune system too much, you can shut down cancer surveillance, which I don't need to stress, is a bad thing.

The downside to inflammation is that, yes, it is damaging. Needless inflammation is bad. And, as an added twist, from a personal example: my mother has Sjögren's and MALT lymphoma in the salivary glands. Sjögren's is an autoimmune condition that attacks exocrine glands. In doing so, it triggers a nonstop immune reaction in the salivary glands and the development of lymphoid tissue, with lymphocytes constantly proliferating. This nonstop proliferation runs the risk of - as in my mother's case - developing mutations that lead to lymphoma. So too much of a needless immune reaction can also cause cancer.

The immune system is an extremely complex, with hundreds of known cytokines, each causing various activation / suppression effects in others and having various other interactions with the body. So it's extremely hard to say, if you tweak this one thing, what will be the overall impact in the long term?

These GLP-1 agonists inhibit the NF-kB pathway and downregulate pro-inflammatory cytokines like TNF-a, IL-6, and IL-1. We think that this sort of downregulation is probably in general beneficial, in that in most cases it should not weaken cancer surveilance, and actually can help with certain types of cancers (but still can be harmful to some). Everything is situation dependent, and there's a lot we don't know.