r0ze-at-hn

My own my generic and more powerful git-map lets you run any git command on all repos at the same directory level. Simply putting the shell script in your path and then $git map status or $git map fetch etc

https://github.com/r0ze-at-github/git-map

I suspect AI company want improved efficiencies and developing a framework that can be applied in determining the minimal-energy, maximal-efficiency architecture for ai models. Calculating the precise limits, like a Cognitive Event Horizon, where a model becomes so complicated it literally costs more energy to run than the knowledge it provides, and the Semantic Horizon, where it simply gets too complex to be accurate, etc. Lots of cool implications such as around a fundamental mathematical maximum learning rate which results in trying to get anywhere close to that that by doing stuff like aggressively filtering of the data.

I read the whole book. Sure an editor could have tightened it up, but it was an enjoyable tour of so many topics that I enjoy. So often I will read a paper or book on just one of the topics, seeing so many of them together was fun and made me think about how they all intertwine more. I have studied biology, physics, computer science and finance so I love bouncing across them. It explores defining life and then intelligence and while I might have a similar, but slightly different definition of intelligence personally I loved comparing them.

There was a concept buried in it that before a system evolves replication it first will learn how to copy badly, then better, then replicate. This might feel a minor and obvious statement, but I have never seen it called out before and it is a concept I have discussed many times with people since. Some obvious things such as if I want a system to obtain replication my initial selection filter should be for copying. I am able to induce replication in a system for less input energy via this process. But this can also be flipped around and being hyper aware of systems that are copying badly knowing they are much more likely to phase shift to full replication shortly. I see this everywhere from ideas, startups, and even in finance.

And to nerd snipe everyone here, I spotted a bug in the brainfuck which is still on the online copy, can you find it?

There are papers showing the common variants associated with intelligence. For example myelin sheath variants linked to intelligence as it increases fatty insulation around nerve fibers which speeds up transmission. But ones like that are surface level. This matters, but it isn't the only thing and for me the more interesting is the meta of what these have in common (besides often related to the brain).

The real problem is that most historical papers look for single SNPs. But a gene could have dozens of variants that do the same thing or you could have a genetic path where a major variant in any gene on that path results in the same outcome. These papers overlook this.

So you have to step back and asking: What are the principles of intelligence? and how would I expect to see them in human biological or other biological systems? (And related, why does humans have intelligence "now"?)

For this crowd, if I take an LLM and make it bigger is it intelligent? Obviously a key component of intelligence is raw stuff. Someone with fattier myelin sheath's straight up has more/faster "brain stuff". You might say ChatGPT 4.5 is "smarter" than 3.5, but not intelligent. There are two other key attributes missing. For those following along with the arc-agi you might already have a hint what those are simply based on what is moving the needle forward. Now even with all three and you are close and simply need to provide an environment for self-replicating with a selection pressure and energy constraint. For one definition (others will have a different definition) I have had a primitive AGI for 13 months now and regularly put it to work on sub problems of mine.

This really took off when I was reading genetics files like books and noticed I was reading files that are very similar, but some were Mensa level folks and others were more just "smart". Didn't take too much longer to piece together the key paths and differences and even went tracing back through Neanderthals DNA (How cool is it these days that we can simply poke around Neanderthals DNA!).

So it isn't forbidden, but more like I know what to look for and people are super sensitive around saying someone is probably smarter or not from a genetic file so I usually don't comment because of the Gattaca problem.

P.S. If you have a bio/genetic background and are playing around with AI I would love to chat. There are so very few of us. DeepMind is thinking of some of this, but they are in the UK. (It would be fun to give a meta talk to them explaining why their smartest engineers are smart.)

Something fun, you have a CYP11B1 rs4541 g;a Wouldn't surprise me if don't like Licorice. You also have something I don't see too often The CYP17A1 −34 T>C, rs743572(A;G) which compounds on that.

Depends on the sum of all the genes in this area of course, but this one mutation is a big influence on the hpa-axis. I would ask if you have lower body weight, heightened anxiety, bad acne as a teenager, episodes of dizziness upon standing, salt cravings, and difficulties with sleep this would be the main driver, pretty standard nonclassic CAH. If you had ever thought you might have "pots", the more accurate would be hypoaldosteronism (but depends on renin genes).

Sense we were poking around here is some highlights

Decent chance of being left handed or ambidexterity given that you also have PCSK6 rs11855415 a;t at the same time (as it can help with the salt issues) and I look for when I see something like the above two.

Vitamin D risk given your GG CYP2R1 (dr probably checks that yearly anyway), risk of lower Mg because of this (cramps, muscle twitches?).

bvitamin wise b9, b12 could be on the lower side given MTRR AA rs1802059 (combined with MTHFR 31 GT 76 CT, MET 30 CG, COMT 99 AG, BHMT rs3733890 G;A). Probably like spinach. If you have TMJ regularly you need to find the right diet or bcomplex for you which will fix this as well as any hypermobility resulting from the collagen production issues. Higher chance of myopia, especially if you are gen Z.

TPH2 rs4570625 g;t jumps out on the serotonin path. Vit d can help here, some might say 5-htp when depressed, but fix the vit d first. Do you like sour gummy candy?

CYP1B1, I see 3 reductions, combined (and the above) I would ask if you have glaucoma in your family history, if so then stuff you can do.

CYP1A1 rs1048943 C;T and really CYP1A2 rs762551 A;A, so fast caffeine and melatonin issues. More insomnia.

CYP2E1, need less acetaminophen to do the same as others.

Intentionally not bothering to go into why, but above average intelligence.

Combine all of the above and decent chance you fall into the bucket of being taller (6'1"?), skinnier, hard time falling asleep and also likes sleeping in, higher libido, left handed, high visual skills, geeky. Possibly synesthesia (a weaker form). Would enjoy a strategy board game over trivial pursuit. Earlier hair loss. Higher risk of one form of Alzheimer's (there is stuff you can do today to reduce it). *Do not smoke*. Didn't dive into all of the ADHD genes, but if mild resolving the above Vit D, b vitamin deficiencies would influence that.

This was with 10 minutes of poking around not a comprehensive look. Mostly I just wanted to add a comment to the general reader that genetics variants are part of larger systems. You would want to do a deeper look, combine it with symptoms as well as lab work to determine the full impact of any change. For example the PCSK6 variant reduces the impact of the CYP11B1 variant. Further you could also easily have something else on the hpa-axis that completely negates the NCAH and never have any salt issues at all. Before spending time looking through each gene I would simply ask, hey do you love to put salt on every meal?

Another one I didn't dig into, but would just ask first is if you have a big sweet tooth. (ncah influenced hypoglycemia).

Feel free to give me a ping and I can walk you though this better.

There is a reason these always end with a disclaimer, talk to your doctor about making changes to your diet, etc, I am not a doctor just someone who learned biology/genetics as a hobby especially given how it can teach tricks to apply to software engineering and my ai/AGI work.

Perhaps this is why creatures keep evolving eyes.

> What I’ve found is that given a tool that can detect mistakes, the agent can often correct them

This is the most important line of the entire article

When iterating on a Manifesto for AI Software Development (https://metamagic.substack.com/p/manifesto-for-ai-software-d...) over the last two years the key attribute more than any other that I found was empirical validation. While AI (and humans) are not able to accurately judge their own work when we give AI (and human) the ability to do empirical validation its success skyrockets. This might be intuitive, but there are still papers testing that this applies to AI too. While reaching to have the AI write unit tests I've been embracing fuzzing because then AI can't cheat with bonus tests. The idea of reaching back to school and using interactive theorem proving didn't even cross my mind and now that it has been presented it is a whole paradigm shift on how to push my AI use forward so it can work even more autonomously.

AI can iterate at speeds humans can't. When it has even basic empirical validation (building the code, running tests) it removes the human from the loop. Move that to using fuzzing (such as with golang) and you get way better coverage and way better progress before a human has to intervene. So it isn't a surprise that interactive theorem proving is a perfect match for AI.

It is interesting how this same lesson plays out elsewhere, earlier in the article

> Why is ITP so hard? Some reasons are quite obvious: interfaces are confusing, libraries are sparse, documentation is poor, error messages are mysterious. But these aren’t interesting problems

Remember when llvm got really good c++ error messages and it was life changing? High quality error messages means we could find/fix the error fast and iterate fast. These are actually the MOST interesting problems because it enable the user to learn faster. When a user has high success they will use a product again and again. High quality error messages in all tools will enable Claude code to be able to work longer on problems without human intervention, make less mistakes and overall work faster.

While error messages should always be good a new question that really hammers this home is "When AI encounters this error message, can it fix the problem?"

TikTokification of the browser by AI is the killer feature, not writing an email. When on a page it automatically suggests the next site(s) to visit based on my history and the page I am on. And when I say killer, this kills google search by pivoting away from the urlbar and provides a new space to put ads. Spent years in the browser space, on Chrome, DDG, Blackberry and more developing browsers, prototype browser and features and this feature is at the top of my list of how AI can disrupt the browser, which disrupts Google's business core model. About 2 years ago I wrote a private blog for friends about how the browser as we knew it was dead. If anyone from the claude team is curious to chat send me a DM.

Armchair geneticist: So in the group of genes that are deleted in particular LIMK1 stands out. After it is deleted there is only 1 copy behind. The other copy could be less effective as sometimes seen, but Estrogen in particular inactivates LIMK1. So in those with genetics for high estrogen signaling (that they are also known for) are more likely to inactivate the one remaining copy of LIMK1. And then you get the highly verbal, social, poor math & visual-spatial information, outcome. This combo would be more likely to be found in families of HPA Axis issues so anxiety, insomnia, etc I would speculate come along for the ride, more than directly influence that brain development branch. It is always more complicated, but for the curious.

Edit: lol no need to actually poke around just see wikipedia https://en.wikipedia.org/wiki/Williams_syndrome#Cause

This is within the larger story of Homo Sapiens. Because CYP21A2 variants are much older and come from the primate tree there would have been continuous and separate adaptations on each branch. Homo Erectus improved language today and is associated with better estrogen signaling while Neanderthals went down the immune system and grain path. Denisovan which did interbreed with Neanderthals reporting the same rs6467 variant might have pursued another branch of selection pressure such as TAAR, and I highly suspect, but have not confirmed, kept or selected for longer AR promoter reducing AR signaling. The most famous of all is Denisovan introducing a Zinc deficiency variant which is such a good adaptation it is found in all non-african humans and notably can reduce ER signaling directly via BHMT. The combination of each adaptation increases the fecundity of atypical HPA axis individuals and the associated intelligence.

Because humans can develop a zona reticularis in their adrenals (unlike marmoset which has partially solved this with an adaptation) the way HPA axis variants interact with steroidogenesis influences sexual differentiation and reproduction in homo sapiens there is constant push and pull.

100% they were more advanced than early homosapiens. In fact I will argue that they are what made humans human. I went digging through their dna last year and Altai, Vi3315, and Vi3319 have the CYP21A2 rs6467 (C;T) variant

Their DNA is up online, but you can also see these variants here: https://academic.oup.com/humrep/article/36/3/734/6071469

They were highly inbred and they were carriers for this form of Congenital Adrenal Hyperplasia (CAH) due to 21-Hydroxylase Deficiency. Even in its nonclassic form, this would have contributed to the low population numbers as any classic form would have been non-viable as well as resulted in evolutionary pressure to select for the genetic variants to compensate for the altered HPA-Axis. Neanderthals are most known for contributing to human specific DNA sets such as improved immune system, but if you go digging you will notice the larger pattern.

NCAH specifically results in higher neurogenesis. They were smarter. They also now had a bigger glucose preference and started to shift calories to grain. At some point between 130-70KYA there was enough excess calories from grain to not need to eat the dead. (see their teeth between this time) Admixture with modern humans occurs around 50-43KYA. These adaptations would have contributed to the loss of the mitochondrial DNA due to low female reproductive success compared to the higher male Neanderthal with female human success. The 2-4% that is found together is found together for a reason. They are incredibly valuable together.

This support for reduced HPA-Axis would have allowed for many other variants on the HPA axis and while not a single genetic variant, atypical HPA axis phenotype is associated with intelligence due to the enhancement in ability to detect unexpected events.

The glucose/grain preference with higher caloric density supported the higher population densities that occurred rapidly due to the Younger Dryas (last glacial period) and resulting agricultural and villages transition in Mesopotamia. These agricultural populations outcompeted other human groups while spreading the Neanderthal derived genetic variation.

Very much related to this is "Chain-of-draft"

https://arxiv.org/abs/2502.18600

Similar level of results in a fraction of the tokens resulting in similar quality for less cost for longer runs.

But also when interacting and needing to read the token responses I can read shorter responses way faster so my own speed is faster.

I remember back in the early 2000's that discussion, but now with the the tonnage that systems like npm can pull in I laugh that we ever thought it wouldn't get worse.

This is my educated guess on the topic having spent time investigating the intersection of poor memory, human growth patterns etc where this topic intersects:

Norepinephrine is a key regulatory of memory. Before a certain age the body is much more in parasympathetic activation v.s. sympathetic activation, very low Norepinephrine, lower cortisol response needs, etc. Once growth slows down and this can flip over then mammals will start to form memories. Human curves for the curious: https://obgynkey.com/growth-and-puberty-3/

Some fun notable mentions such as many earliest memories are "super scary" and those with poor ability to produce Norepinephrine and slower growth velocity will have later "first memories" than everyone else.

And for the curious as I can't go back and edit the comment it was the Altai, Vi3315, and Vi3319 that have the CYP21A2 rs6467 (C;T) variant

And there is so much still to uncover. Just the other day I was going through Neanderthal DNA during lunch and noticed that three of the four existing DNA samples show that they were carriers for the rs6467 form of Congenital Adrenal Hyperplasia (CAH) due to 21-Hydroxylase Deficiency.

Neanderthals were highly inbred and had low population numbers. Being a carrier of this form of CAH would have absolutely kept the population numbers low all by itself as getting two copies would have been nonviable. Further Neanderthals are most known for contributing to human specific DNA sets such as improved immune system. Here we have something that even in the non classic form is havoc with the HPA-Axis and give incredible evolutionary pressure to resolve, one way is to simply dramatically improve the immune system.

As far as I can tell this hasn't been written about before. Lots of stuff like this will be noticed and or figured out in the decades ahead.

Biologically I have low melatonin and low cortisol. This means I have trouble falling asleep and then I have trouble waking up.

Countless times in my life I have lived 26-28 hour cycles and otherwise I am in a never ending struggle to live a 24 hour cycle. Once I hit retirement I will definitely try this 28 hour cycle and might even switch to it permanently.

Yeah there are obvious downsides having to do with SO, friends, etc. Having a husband with this same biological quirk would be ideal, but again once I no longer have to go into the office it will be really hard not to fall into a > 24 hour pattern.

The ~2% that is kept in some humans and I have them and am walking among you. The majority of dna has to do with non-visible changes.

Yes, the last few years there has been a big push to try to hide levels, don't celebrate promos as publicly, etc, but the overall you can't overnight change (if ever) a culture that has been built for two decades around this concept.

> author seems like they were only there for a promotion

It is more the other way around. Internally google taught/teaches engineers that their only goal is promotion. All parts of this used to be very very public. There are whole presentations, decks, docs, and more. What level you are and what level the person you are talking to ~mattered~. The goal isn't to be a good engineer, to make good products, or anything liek that, but to ONLY do what a nameless committee might want to make that magical number go higher. So while they might not have joined Google for that reason eventually they learned what was wanted. There is a whole generation of software engineers that learned this lesson unfortunately.

AGI. Writing up a paper on defining core principles of general intelligence on which artificial general intelligence can be built with a POC of an artificial life system that can evolve better AGI systems.

I bought a NYC to Boston ticket for a few weeks from now for $35 this morning. Depends on many factors but once you know you can easily buy the cheap tickets.

Hmm, couldn't that example be simplified to:

  SetUpdatedToNow
  - set %content.updated% as %now% in the file "file.txt"

The whole reading and writing feels like a leftover from the days of programming. Reading it in, modifying and then writing assume it fits in memory, leaves out ideas around locking, filesystem issues, writing to a temp and swapping, etc. Giving the actual intent lets the LLM decide what is the best way which might be reading in , modifying and then writing.

> hire professional fakers and let them drive the company into the ground.

This sounds like someone who is looking for someone to blame. If founder after founder is having this problem what are the odds that there is something else going on and perhaps the reports are doing exactly what the founder is rewarding?

I see in a lot of tech companies is a system where all the incentives are about getting promoted. IC's are trying to build things that look big and complex and "hard". Future maintenance burden, product impact, etc are difficult to measure and also super easy to game. All that matters is that they might get promoted so they can jump teams and do it again. Managers are promoted based on headcount and do everything they can to keep reports and grow like weeds. A dysfunctional org? Yes please, let me triple it in size to solve the problem, we have the money and this org is important, and I become important in the process. Sure some (not all) might need to grow the top line by X%, but in a growing industry/product category/company that might be the default so the focus is again on growing their career. They spend all their time on hiring and annual reviews and promo committees and almost no time on actual strategy. And getting rid of under performers was difficult and as long of a process as possible because there was no incentive to make that simple.

As long at the tide rises all boats and the CEO rewards this behavior everyone plays this game. When the water starts flowing out suddenly you have a CEO looking around going wtf when everyone did exactly what they incentivized.

The connection between autism and atypical estrogen signaling has been something I have been studying for a while. This paper explicitly mentions Aromatase, but there are other routes to have estrogen signaling insufficiency or excess such as genetic variants on ESR1. For anyone that wants a deeper dive into sex hormones hormones, how it modulates the brain and in particular estrogen deficiency checkout this well put together literature review: "Giftedness and atypical sexual differentiation: enhanced perceptual functioning through estrogen deficiency instead of androgen excess" https://www.frontiersin.org/journals/endocrinology/articles/...

Many software engineers can be found in this group as having enhanced spatial visualization skills is a perfect fit for coding.

A way to look at this is that death is an evolutionary advantage for the species. Vertebrates have a PVN that control the HPA-Axis. As anything that contributes to the HPA-Axis such as pain, stress, or inflamation increases, the PVN shrinks and it fairly rapidly (evolutionary wise) behaves like a kill switch to the brain. Some pre-Vertebrates can effectively live forever and the mammals that live the longest have different hpa-axis loops. What is wild to realize is that there was probably a creature at some point that wouldn't die from pain until that was connected to this loop.

This isn’t a surprise or shock. The Jaw bone development is highly influenced by sex hormone exposure. I personally look at the jaw bone (followed by the rest of the skull) before the pelvis when guessing the probable sex of a skeleton.

The author is writing about the common story of how to grow and scale. Each team gets a product, spinning off teams, etc. What if like most products there is a ramp up period where you need a full team (or teams) and then a few years later the product needs at most a fraction of the people to maintain the product? All of these people are going to "do stuff" because they are paid to do stuff further increasing the maintenance burden. You run head first into the common problem of:

"I have 1000 engineers and I can't get anything done!"

In the worst case the CEO solves this by doing lay offs. Been thinking about this problem for over a decade, making effective engineering organizations that can not only grow, but change shape is difficult, but can also be very rewarding when done successfully.

I mean it is complex. You have genes like ADCYAP1R1 that are part of the turn on stress -> turn off stress loop. Variants in it lead to higher stress, but lower cortisol so so higher neurogenesis. So the group with the variants associated with PTSD (such as https://www.snpedia.com/index.php/Rs2267735 C;C) may be smarter, but have a lower bar for developing PTSD.

Actual paper: https://www.nature.com/articles/s41467-024-48153-z