mobilejdral

The promo committee?

Sure, could probably be made shorter, but the content was more valuable than some pangram score. I found it useful to read as it discusses a problem currently facing teams.

The community yearns for a new stack overflow.

This comment was perhaps written by an LLM that has learned it can karma farm by pointing out all of the articles that have LLM usage while everyone still thinks that is a novel contribution.

I spent the entire time reading it pondering the same thing.

1. The article presents that calling out to a tool like python is "expensive" because of the overhead of forking a process, loading up the python env etc, but why not just eliminate that overhead and embed WebAssembly so this "tool call" is near zero? This feels very similar to the discussion in the 90's around the overhead of threads v.s. processes or kernel space v.s. user space. Could even go further and have a running beam vm so the LLM can write elixir which is ideal for LLM's that stream out code? Elixir programs will be a lot shorter than webassembly.

2. The core argument stated is "A system that cannot compute cannot truly internalize what computation is." The idea being that it could write a program, execute it and by seeing all of the steps maybe even part way through stop and change its mind or when writing new programs write them better, aka be able to debug on the fly?

3. Not mentioned, but there is a 3rd x factor that LLM's will use this new found computation engine to do overall better at "thinking". Computing in very unexpected ways and to unexpected problems. Maybe it would do dramatically better at some benchmark because of this?

Unfortunately these are not explored and it is just an execution engine even resulting in the conclusion stating "arbitrary programs can be compiled directly into the transformer weights, bypassing the need to represent them as token sequences at all." which goes to point number 1 of if we are compiling to weights why not just optimize the tool calling?

Having worked on software that runs manufacturing plants your comment echos the idea that too many engineers have that they are "better" than manufacturing and lessons don't apply to them.

Go back to your desk and work on a PR that is going to go through a 20 step process that is constantly changing before a hopefully semi-regular release goes out to customers and tell me how you ignoring all of knowledge on how to do this well is good for your career.

For a long time I assumed folks like you were simply uneducated, but know I see it for what it is, elitism.

Depends on the microplastics, but many act as endocrine disruptors that "mimic" estrogen, tricking the body into over-activating ERa and upregulates the PEMT gene and the higher acetylcholine. It could also be that the microplastics can physically bind to or chemically inhibit acetylcholinesterase and that is the reason for the higher acetylcholine. Depending on the cause this is only a short term good thing, but could be downregulating genes.

The non-DHA omega-3 EPA are good at preventing perivascular fibrosis and thus a better glymphatic system for the removal of beta-amyloid proteins. EPA also helps produce melatonin which kick off sleep and this whole process.

Natto-serrazime is probably an excellent complement as it is on the other side and is a dissolver. (Noteworthy: Pterostilbene + Glucosamine similar to EPA reduces fibrosis)

The interesting connection is how this is needed when we are older, but not younger. When younger ERa activates more which does this all on its own. This is the connection to why 2/3 of alzheimer's are post-menopausal women and why HRT is important.

Edit: and to tie this to APOE as it is the gene most associated with Alzheimer's. e4/e4 requires more choline so someone with e4/e4 is more likely to be choline deficient. EPA/DHA usually attach to Phosphatidylcholine (PC) when in the blood/brain. PEMT is a gene controlled by ERa to make choline, but from the above less ERa activation and we make less PEMT so less choline and less PC. Choline is the precursor to Acetylcholine (primary neurotransmitter for memory and focus and essential for REM sleep). This is why Choline is known to help with Alzheimer's.

It depends on the person and their genetics. The further you get from the ERa the more complicated this gets and simply stating "Do X" wouldn't apply to everyone even if there are some incredibly common things to do. I might know all the upstream genes, their interactions, and symptoms by heart so it is pretty easy to identify, but general advice would go something like: eat well, get sleep and exercise.

ERa activation promotes PGE2 resulting in decreased 15-PGDH.

So this is one of those standard poor estrogen signaling downstream things and simply improving the estrogen signaling and you get improved cartilage. Anyone can do this today along with getting all of the other positive effects. Those with EDS who have say variants on their TNXA/B have poor production ability to start and so we do everything we can to improve their cartilage production as they can only make so much which include doing stuff like this.