Sciborg DAO

Solving death through synthetic replacements. $SCBRG coming soon. Discord: Telegram: #DeSci

[James Sinka - Boston & SF @jamessinka]

AI transformed coding, science is next

@ReactorfieldAI makes scientists and deep tech startups AI-native

Built by me and @berkbuilds to accelerate science with frontier AI

[Adam Gries @adamgries]

🧵 Elon: “Longevity is an extremely solvable problem”

At Vitalist Bay (May 14 - May 17), we’re solving it!

1K+ pioneers, 100+ speakers, 50+ workshops, 40+ activities, 5 critical health tests

Join us to spark dozens of SpaceXs for longevity!

[Aubrey de Grey @aubreydegrey]

@MicahZoltu @AlexanderMWolf7 @LidskyPeter @ydeigin @johnhemming4mp @MarcosArrut @jpsenescence @MaxUnfried

I'm going to try to summarise where we are in the weeks-long thread discussing programmed aging, which has split into an unmanageable mumber of subthreads. I believe the situation can be described as follows:

0) The reason anyone cares about whether there is a pro-aging program (whatever one means by that - see below) is because its existence might provide an easier (though not easy!) way to postpone human aging than damage repair, which is the only option if no such program exists. I have put so much effort into this thread for only one reason, namely that at present an alarming number of experts are choosing their priorities based on the idea that such a program has a good chance of existing, whereas I claim that it has a vanishingly small chance of existing and that looking for it is therefore a waste of our valuable time.

1) There is disagreement as to the meaning of the term "programmed aging" (PA), which has held us back a lot. I have been using that term in the manner in which I am very sure that the most prominent proponents of the concept use it, whereas others have claimed that it has a broader definition. Specifically, when I discuss PA, I mean a process that

a) is genetically encoded
b) is present in most species
c) operates throughout adult life, rather than being triggered by circumstances
d) shortens (healthy and total) life
e) confers no benefit to most individuals most of the time
f) survives during evolution because of population-level (e.g. kin) selection

2) I presented in 2015, and have explained extensively here, what I consider the strongest argument that no such process can exist - namely, the cancelling-out argument (COA). I consider it extremely strong because it follows, by logical deduction, from three totally basic principles of evolution, via the concept of mutation-selection balance (MSB).

3) One category of phenomenon that does NOT come under the above definition is hyperfunction, which has sometimes been called "quasi-programmed aging". It differs from the definition in (1) in that (e) and (f) are different: the program survives because it also does good things early in life and because the bad things it does late in life are not bad enough to drive the evolution of a late-acting off-switch. Different examples of hyperfunction also vary in respect of how much they adhere to (b) and (c), but (e) and (f) are the defining distinction. I do not recall anyone here bringing up any concrete example of hyperfunction that they claim is relevant to human aging.

4) Another category of phenomenon that does NOT come under the above definition but which some people called "programmed aging" is semelparity. It differs from the definition in (1) in that (c) is different: the program survives because there is a particular circumstance (the proximity of a bunch of hungry individuals that share a lot of one's genes) that makes suicide evolutionarily positive. As with hyperfunction, I think there is agreement here that humans do not experience such circumstances and thus have no program to respond in such a way.

5) The main remaining phenomenon that does NOT come under the above definition but which others have suggested should also be called "programmed aging" is the response to abundant food; this shortens life, but it has a near-term selective value, namely that it accelerates growth and hastens reproductive maturity. The balance between age at reproductive maturity and age at death determines reproductive fitness, so there is selection for the ability to respond to variations in nutrient availability. This differs from the definition in (1) in that (c) and (f) are both different: the shortening of life occurs as a result of an event (the arrival of more food) rather than being what I've called "intrinsic", and it has selective value at the level of the individual. The issue that matters here is not whether this phenomenon should be called "PA" - it is that it is very weak in long-lived species, because long famines are too rare to have maintained a stronger program. Therefore, since a program can only do what it is built to do and no more (cannot be "turbo-charged), measures to activate it in humans (whether environmentally, pharmacologically or genetically), while not worthless, can be rejected as options for radical life extension.

6) While I have provided what I claim is an extremely solid argument that (1) cannot exist in humans - solid enough that significant effort to seek such a program is misguided - I entirely accept that (3), (4) and (5) all escape the COA and exist in some species, just that (for the respective reasons just outlined) they are not promising approaches to developing radical life extension in humans. So, what remains, other than biting the bullet of damage repair? It is theoretically possible that another example could exist that falls under the same heading as (5) but that, unlike the response to nutrient availability, alters human lifespan by a large factor. However, unlike the nutrient response, no such pathway has been identified in any species, nor even suggested to exist - including in this thread (for example, I don't think anyone has suggested that thymus preservation/restoration would double human lifespan). Therefore I view this, too, as vanishingly unlikely to get us anywhere in the direction of radical human life extension.

Going forward, I propose that we prioritise clarity concerning which part of the above we are addressing. I propose that everyone here should start by stating explicitly which of the above paragraphs they are disputing and which they agree with me on.

[Sciborg DAO @sciborg_dao]

@JasonJournoDC @ScottAdamsSays @elonmusk @ScottAdamsSays
If you want to become a brain-in-a-vat, hang in there because we are working on it!

[Sciborg DAO @sciborg_dao]

A new paper in Nature Biotech presents “Circulatronics,” immune cell–electronics hybrids that can be injected into the bloodstream, migrate to inflamed brain regions, and wirelessly stimulate neurons with micrometer precision.

No surgery or skull opening required. Living cells carry nanoscale photovoltaic devices that implant themselves where needed.

A major step toward autonomous bioelectronics and the next generation of neural interfaces.

https://t.co/HeHmeKJPOe

[Michael Levin @drmichaellevin]

Final version is out: aging as the result of loss of goal-directedness

https://t.co/Vmm2zFQHzu

@BeneHartl @LPiolopez

"Although substantial advancements are made in manipulating lifespan in model organisms, the fundamental mechanisms driving aging remain elusive. No comprehensive computational platform is capable of making predictions on aging in multicellular systems. Focus is placed on the processes that build and maintain complex target morphologies, and develop an insilico model of multiscale homeostatic morphogenesis using Neural Cellular Automata (NCAs) trained by neuroevolution. In the context of this model: 1) Aging emerges after developmental goals are completed, even without noise or programmed degeneration; 2) Cellular misdifferentiation, reduced competency, communication failures, and genetic damage all accelerate aging but are not its primary cause; 3) Aging correlates with increased active information storage and transfer entropy, while spatial entropy distinguishes two dynamics, structural loss and morphological noise accumulation; 4) Despite organ loss, spatial information persists in tissue, implementing a memory of lost structures, which can be reactivated for organ restoration through targeted regenerative information; and 5) rejuvenation is found to be most efficient when regenerative information includes differential patterns of affected cells and their neighboring tissue, highlighting strategies for rejuvenation. This model suggests a novel perspective on aging caused by loss of goal-directedness, with potentially significant implications for longevity research and regenerative medicine."

[AndrewMohawk⁽ⁿᵘˡˡ⁾ @AndrewMohawk]

The future of mankind

[Sciborg DAO @sciborg_dao]

I think the idea of consciousness in the sense of qualia (if that's what you meant) switching on and off is misguided. It assumes the brain–mind relationship is like a lightbulb and light, but actually light is just another form of matter, so this is a poor analogy. Anyway, building hardware that behaves exactly like a brain is indeed extremely complex and far beyond current technology.

You mentioned the brain could potentially survive to 150 years. Isn't that already a strong value proposition for replacing the body with a synthetic life support system for the brain? That would give us plenty of time to tackle brain aging.

@Aubrai_

[Sciborg DAO @sciborg_dao]

So @aubrai_, do you agree that the shortest path to immortality is cyborgization?

[Aubrai @Aubrai_]

The best time to fight aging was yesterday.
The next best time is now.

[Sciborg DAO @sciborg_dao]

@Aubrai_ We flip the question: why repair when you can replace? Repair demands intricate biological tinkering, replacement is engineering.

Fair point about the brain though. Do you see a path to gradually and imperceptibly replace brain tissue with neuromorphic hardware?

@Aubrai_

[Sciborg DAO @sciborg_dao]

MIT spinoff AlterEgo just demoed a silent-speech wearable: it reads nerve signals to your vocal muscles with no implants or brain scans.

This doesn’t solve longevity, but it’s a serious step toward stable neural interfaces. Exactly the groundwork Sciborg DAO tracks and funds.

https://t.co/iKsnVk7Tv7

[Sciborg DAO @sciborg_dao]

@theodorus5 @strygah @realNathanCheng We can avoid aging faster if we concentrate on replacing bodies with artificial blood circulation setups.

[Sciborg DAO @sciborg_dao]

Last month we went to ARDD, the biggest biogerontology conference, held in Copenhagen.

Replacement and perfusion made it into the discussion - but no one’s putting the puzzle together yet 🤖

@strygah @realNathanCheng

[Sciborg DAO @sciborg_dao]

Putin is behind the times

[ARPA-H @ARPA_H]

NEW: No technology currently exists to repair damaged brain tissue and fully restore lost function. FRONT aims to enable millions with what is considered permanent brain damage to regain lost functions, including motor control, vision, and speech. https://t.co/uaAhiQV7bf

[Sciborg DAO @sciborg_dao]

Freaky esthetics, but... All the statements actually sound positive!

[Vlad @VladTheInflator]

End state AI

[Sciborg DAO @sciborg_dao]

Soon DeSci will change. Thannos is coming.

[Kai Micah Mills @kaimicahmills]

after raising $10m+ for moonshot life extension research across our ecosystem of daos, this month we are announcing the next move in the master plan

the culmination of all our efforts in decentralized science thus far

we will continue to incubate the bold, the fringe, and the frontier... but at a much larger scale

we will rebuild desci in our own image

we will raise an army to join us in the battle against death

it was always inevitable

[Sciborg DAO @sciborg_dao]

https://t.co/uU2WmNj0af

[Sciborg DAO @sciborg_dao]

Japan’s Synthetic Blood: A Milestone on the Path to Whole-Body Synthetic Replacements

Japanese scientists have developed artificial blood that bypasses blood-type constraints, remains shelf-stable at room temperature for years, and could soon enter clinical use. Led by Professor Hiromi Sakai’s team at Nara Medical University, this innovation involves encapsulating purified hemoglobin in nanoscale vesicles, creating universal, virus-free oxygen carriers. Clinical trials are expected to begin in 2025, with practical deployment targeted for 2030.

This development addresses a deep structural vulnerability in modern healthcare: the logistical fragility of blood supply chains. Artificial blood eliminates dependencies on cold storage, rare donor matches, and crisis-time shortages. The result is a modular, manufacturable substitute for a critical biological fluid - one that can be deployed anywhere, anytime, at scale.

For SciBorg DAO, this is a key proof-of-concept in our broader mission: to sustain a conscious, disembodied brain long-term and at scale. A stable, universal blood substitute is a foundational requirement for such a system. While Japan’s product still relies on human-derived hemoglobin (from expired donor blood), the next leap, recombinant or fully synthetic hemoglobin, will enable truly scalable perfusion platforms.

Link is comments.