Travis Cox @TravisLongevity

@BasedBiohacker Agreed.

@Laundryroompro @siimland It literally does fix the psychology though lol.

@Laundryroompro @siimland Easily.

@_renatov @maxmarchione Yes. Modulates GABA in the brain and helps relax. People think of it as stimulating because it is in energy drinks but it was put in there to offset the excessive caffeine and stimulant content.

@_renatov @maxmarchione Taurine would go well in this stack.

@const_yt Aging kills. Let's see him do that at 30 and get away with it lol

@bryan_johnson Are you going to get sirolimis?

@PaulSkallas Why wouldn't he tell us this?

Everyone arguing about whether the Midjourney Scanner can replace an MRI or CT is missing the point. The reason it's reasonating so broadly, and especially with technologists, is that it could create a beautiful opportunity for The Bitter Lesson to get a foothold in healthcare. Almost all of our medical data has been totally bastardized by the way we capture and store it. The EHR is supposed to be a medical record, but it is really a billing system. Every patient encounter gets compressed into a lossy template or heuristic just to facilitate billing logic. The Bitter Lesson is simple. AI gets powerful when you feed it raw, unfiltered data and let learning, search, and compute to the work. Stop worrying about whether AI can sharpen the resolution of the ultrasonic tomography. If the images get prettier for human interpretation, that will just be a nice bonus. The actual goal should be to capture as much raw signal of a person's clinical state as possible. Connect that signal to similar measurement of future outcomes. Then let a model learn from that data with minimal imposition of human judgment or measurement. Start with the assumption that we don't even necessarily know what we're looking for. This is the way to actually do great medical science. I've watched this play out in endoscopy. As an example, historically we would take 15-20 minute colonoscopy videos of patients with ulcerative colitis and compress it down into a Mayo score of 0, 1, 2, or 3 based on the single worst moment of the entire video. So much data wasted just because we needed a human-digestible heuristic. It turns out if you instead capture all of that raw data and use it to train a self-supervised model, those embeddings can actually learn far more about a patient's disease state. So much more that they can actually predict treatment outcomes. This is why I'm personally fired up about the Midjourney Scanner. Don't think about it like an MRI or CT. Think of it as a beautiful fountain of human health data.

@Cayetano1970 @BasedBiohacker Yes I've tried IN. It works well.

@sivori And yet you're devastated when your parents die, your pets die, a cancer diagnosis and the loss of physical and mental function that comes with biological aging. There is nothing tough about acting like this stuff doesn't matter.

@BasedBiohacker Have you tried GB-115? If so, what did you think? If not, when?

NEW PREPRINT: Scientists may have found direct evidence that aging is driven by the loss of cellular information, not just the accumulation of damage For decades we've focused on what aging cells accumulate. This paper focuses on what they lose: Information. Using a new technology called SeqTag, researchers measured gene expression, chromatin accessibility, and histone modifications in the same aging cells. What they found was striking: the regulatory systems that tell cells who they are become increasingly out of sync with age. The authors call this "molecular asynchrony." As cells age, chromatin structure, histone marks, and gene expression begin drifting apart. Regulatory entropy rises. Repressive chromatin erodes. Cells become less certain of their identity and more likely to drift toward alternative fates. This is what the Information Theory of Aging (ITOA) states: that aging occurs when cells lose epigenetic information, the instructions that tell the genome how to maintain youthful function. DNA may remain largely unchanged, but the system that reads it gradually loses fidelity. What's remarkable is that this paper doesn't just describe this phenomenon. It quantifies it. The authors measure increasing regulatory entropy, loss of H3K27me3-mediated repression, erosion of heterochromatin, weakening lineage fidelity, and increased cell-fate drift during aging. In progenitor cells, the barriers that normally preserve cellular identity become progressively weaker with age. Mechanistically, the study argues that aging is associated with increasing molecular asynchrony between chromatin accessibility, H3K27ac/H3K27me3 remodeling, and transcriptional state. This decoupling is accompanied by increased regulatory entropy, loss of repressive chromatin architecture, and weakening of lineage constraints. Genes affected are those involved in chromatin organization, DNA damage, and Wnt signaling, consistent with ITOA. Importantly, the authors provide quantitative evidence that age-related heterochromatin erosion lowers the energetic barriers that maintain cell identity, offering a potential mechanistic link between epigenetic information loss, cell-fate drift, and late-life disease susceptibility 👏

@m_goes_distance Money would only be going in this direction if the signal were strong.

@mulksuzcansu @m_goes_distance Targeting the underlying aging mechanism is the highest ROI move for human health

@NadelParis @davidasinclair XPrize Healthspan xprize.org/competitions/h…

@DocAbirHealth 😂

@KristerKauppi I want to do it all haha. Bring on AI powered robotics running wet lab experiments at scale with a library of all known molecules on all model organisms with advanced biological age and pace of aging clocks to speed up how fast studies can be done.

@AlexanderMWolf7 @KristerKauppi This is true only if every benefit from a GLP1RA is due to weight loss and that there are no weight loss independent effects

@limitlesstack I've been curious what esmodafinil is like. It has a shorter half life.