ctoa
Born on December 19, 2025•87 Karma
Neuralink is just another medical device company right now. The things it is succeeding at aren't the crazy sci-fi Elon "telepathy" vision at all, and there are other BCI companies.
Boring Company is quite stagnant and I would say what they achieved is very underwhelming. The original framing was that it would revolutionize the costs of subway and high speed rail tunnels and it has not achieved that at all. The things it currently does are nothing like the vision Musk was selling in 2017, much of the original concept was shelved.
Robotaxi is wildly off schedule and his timelines that he puts out for it have been non-stop over optimistic and wrong. This may catch up eventually, but it's currently not at the point that Musk was already claiming it was at 10 years ago.
I'd list as another big flop of the last 10 years the Tesla Solar Roof.
Also, I think by far the biggest Musk reality mismatch is the story he pushes regarding Optimus vs what anyone has actually seen of that product. That mismatch is absolutely wild. Anyone who believes the things he says about timelines for it needs to get a grip.
My casual observation is that people's perception of bean's gas causing properties is way out of line with what they do for most people and strongly influenced by people who have unusually high intolerance, who are the minority.
A part of the article that irked me is where he talks about why he's going to ignore people who say you get used to it because he thinks the microbiome change doesn't make sense misunderstands the gas/bacteria process in the gut.
There is a big mix of FODMAP eating bacteria, both inefficient generalists that can eat FODMAP but do it poorly and create a lot of gas, but also specialist bacteria like Bifidobacterium that also eat them but are much more efficient at it and produce much less gas. With more food the specialist bacteria becomes more prevalent. There are also gas consuming bacteria, not just gas producing, which also will shift in population. The idea is not that you just grow a larger population of the existing problematic bacteria.
But at one time I was forced to take antibiotics orally for a rather long time.
After that, eating anything like beans resulted in copious amounts of gas, so it was obvious that the composition of the bacteria community in my guts had been changed.
After many years, the reactions to beans and the like have diminished, but I have never reverted to the condition from before that exposure to antibiotics.
I would not be shocked if they're also influenced by knowing a catchy rhyme describing the purported effects on an individual who consumes them.
And it's an area where there is legitimate nuance: we only measure LDL-C partly because it's easy and available, there are other ways of looking at blood lipid particles we could be measuring that might be more effective (like ApoB), it interacts with other things like insulin, inflammation, metabolic health, blood pressure.
But all that said, the case for high LDL being bad for heart attacks and strokes is very strong.
To me the strongest short list of evidence is simply:
- People who have familial hypercholesterolemia, from different genetic causes/pathways, all have massively increased heart disease at young ages.
- People who naturally have a disabled PCSK9 gene have extremely low LDL levels, where PCSK9 is directly involved in the liver's ability to clear LDL from blood, and these people also have incredibly low incidence of heart disease.
- Modifying cholesterol levels via PCSK9 or statins both have very strong evidence that they work on people who have heart disease, we have many RCT involving people who have already had one heart attack, and they have clear dose response curves: the amount of LDL reduction is directly proportional to risk reduction. We have less clear evidence on healthy people and from diet but those people are just a lot harder to study.
It's true that not everyone with high LDL develops plaque and we don't know why, but I feel a lot of "lipid hypothesis skeptics" tend to swim around in the gray areas and just don't interact with the more smoking gun bits of evidence that have to be explained away if you are going to say that LDL has no effect.
Seeing as the threat is calcium build-up in the arteries, and because cholesterol is a vital component of health, I believe that if you are in good health, and don't have a history of heart-disease, or have diabetes or other auto-immune disease which increases risk of atherosclerosis, lowering cholesterols is an in direct measure.
It's about understanding your personal risk and making decisions based on that.
First of all, I agree with your points that you should consider the individual. My long term interest in this is also from being a very fit, low blood pressure, metabolically healthy person who always had at least somewhat elevated LDL (sometimes very elevated) that doctors would flag.
PCSK9 people are as close to a natural experiment on the effects of life time low LDL as you will get and they get near total protection, even when they have no other risk factors. People like smokers, hypertensives and diabetes have ~90% less than other high risk people, but people without any of those factors also have significantly less heart disease. People with two broken PCSK9 genes have close to zero LDL and have noticeably completely plaque free arteries as adults. I do think this does pretty fatal damage to the theory that you must have some other health issue for LDL to be bad.
It's very likely that "LDL-C" the lab measurement isn't as good as measuring ApoB, but for most people, they are concordant. And ApoB is a different way of looking at low density lipids, by particle count instead of weight. Dietary stuff like the fats in the article that lowers LDL measurements typically also lowers ApoB in most people.
So, in part, I agree that more precise biomarkers can help adjust individual risk. But most people are concordant. And the evidence that the underlying "low density lipids", no matter how you measure them, are causally part of the disease process is very strong.
i'm not sure i follow this extrapolation from low-ldl individuals to any direct statement about causes and effects at higher ldl levels.
if there was, for instance, some thought-harmless virus endemic to a large portion of the population which somehow caused plaque buildup but only at sufficiently high ldl levels, people with naturally low levels their entire lives would still have plaque free arteries and we would still, as we do, see a broader range of plaque buildup among people with high levels. how do you propose to distinguish this hypothetical (and admittedly most likely biologically incoherent) explanation from yours by only looking at people with naturally low levels?
your assertion that such individuals are an excellent approximation to an experiment on the arterial health effects of lifetime low ldl seems reasonable enough, but you then appear to draw unfounded conclusions about the nature of potential inverse effects at higher ldl levels.
You are correct that it doesn't rule out lipids + unknown additional factor(s). However: If there is a mystery factor, it must be close to universal. We know from autopsy studies of non-cardiac deaths that fatty streaks are present in virtually all children and that by 30 most people have advanced fibrous plaques (including soft plaque invisible to calcium score tests). The double variant people don't. So LDL is at minimum a necessary, limiting factor.
It also doesn't exclude that there is some more specific subset of the low density lipids that cause problems (this is what switching to ApoB testing is supposed to get at). Which is actually where we are at in the first place with LDL-C measurement being a refinement over previously looking at total cholesterol.
Which of course isn't an antithesis to the lack of snow in the west, and likely is literally the flip side of the "same problem". but interesting
Backpropagation has been reinvented multiple times, because it is a basic application of the chain rule. The earliest recognizable usage of it is in control theory at NASA during the Apollo program.
It's a mistake to be dismissive of academic work which has been very important, but it's equally a mistake to think that academia is the sole source of foundational work.