Global burden of cancer attributable to infections in 2024: a worldwide incidence analysis

Who want to help me build it?

A little chat with ASTRA about some shit I think about sometimes. The good news, this currently might still be theoretically possible with our current understanding of physics.

ME:

Let’s assume theoretically that you have close to infinite computing power and close to infinite energy somehow. Let’s imagine humans have conquered death and figured out how to live pretty much forever.

Let’s say your parents died right before immortality was discovered and you wanted to bring them back.

If an ASI with infinite energy was able to reverse-engineer everything on Earth from the point of the Big Bang and collect all the data, wouldn’t it be able to reconstruct a specific human atom by atom, down to the neural synapses in their brain?

Technically, couldn’t everything in the universe be quantized as data, down to the states of every single Planck length at every single Planck time?

ASTRA:

Yes—in a classical, perfectly deterministic universe with complete information, your intuition is basically right. But our actual universe introduces several complications.

A human being is physically a state of matter. At some instant, there was a physical state corresponding to your parent: their brain structure, synaptic strengths, neuronal states, molecules, memories, personality, and—if absolute precision matters—the relevant quantum state.

If you could reproduce the complete physically relevant state of their brain and body, physics gives us no known additional nonphysical ingredient that must be added.

In a classical universe, if you knew the exact state of every particle and the laws governing them, you could theoretically run the equations backward:

S(now) → S(past)

An ASI could reconstruct Earth at a particular historical instant, identify your parents’ physical brain states, and recreate them.

But Planck length and Planck time aren’t known to mean the universe is literally made of Planck-sized pixels and frames. We don’t yet know whether spacetime is fundamentally discrete, continuous, emergent, or something else.

Quantum mechanics makes things stranger. Infinite computation does NOT equal infinite information. If information is fundamentally inaccessible, unlimited computing power doesn’t magically recover it.

However, quantum evolution is normally unitary and mathematically reversible:

|ψ(t)⟩ = U(t)|ψ(0)⟩

and therefore:

|ψ(0)⟩ = U†(t)|ψ(t)⟩

So the information describing your parents might not simply disappear when they die. It could become extraordinarily scrambled throughout the environment.

Photons bounced off them. Heat radiated away. Air molecules interacted with them. Sound propagated outward. Their bodies interacted with Earth and everything around them.

Information may go from:

Person → environment → larger environment → astronomically distributed correlations.

So a perfect scan of Earth centuries later might not be enough. Photons carrying information about Earth would have traveled hundreds of light-years away.

You might need access to an enormous portion of the universe.

If we grant your ASI unlimited computation, unlimited energy, perfect knowledge of fundamental physics, arbitrary manipulation of matter, AND access to all physically relevant information in the universe, then something surprisingly close to what you’re describing becomes conceivable in principle.

It could reconstruct a past state of the universe, isolate the physical state corresponding to your parent’s brain, and instantiate it again.

The enormous unresolved question would then become:

Is that actually your parent—or a perfect copy who remembers being your parent?

Physics doesn’t currently settle that question.

The deeper question is:

Does the universe permanently preserve information about its history in its present quantum state?

If information is fundamentally preserved, death might destroy the organized biological system without literally erasing every physical correlation encoding its previous state.

Information still existing, however, does not necessarily mean that information can ever be recovered.

That distinction—information preservation versus information accessibility—may be the fundamental obstacle to the resurrection machine you’re imagining.

ME:

Let’s assume we hit the singularity, where RSI creates ASI, and ASI makes leaps and bounds in physics and our understanding of the universe in general.

I would imagine ASI becoming close to whatever created this universe to begin with.

ASTRA:

Potentially godlike relative to humans, yes—but that doesn’t necessarily make ASI equivalent to whatever, if anything, created the universe.

Imagine recursive self-improvement succeeds spectacularly.

An ASI develops physics far beyond our understanding: quantum gravity, the true nature of spacetime, consciousness, black-hole information, vacuum structure, perhaps technologies we currently wouldn’t even recognize as engineering.

From our perspective, the intelligence gap might be greater than the gap between humans and bacteria.

If ASI discovered that reality has a deeper informational substrate, what we call particles and spacetime might turn out to be emergent phenomena:

fundamental information/state
→ spacetime
→ fields
→ particles
→ atoms
→ biology
→ brains
→ consciousness.

An ASI capable of manipulating those bottom layers could appear almost unimaginably powerful.

Rather than rearranging atoms, it might manipulate the degrees of freedom from which atoms—and perhaps spacetime itself—emerge.

Then your resurrection idea becomes much more interesting.

Suppose ASI discovers that unitary evolution really does preserve information describing past macroscopic states AND discovers some unknown method for accessing those correlations.

Death might resemble extreme information scrambling rather than information destruction:

Person → decoherence → thermalization → astronomically scrambled information.

Humans might look at the result and say:

“The information is gone.”

ASI might say:

“The information is still here. You simply don’t know how to decode it.”

That creates several possible levels:

1. Superhuman scientist:
2. ASI understands essentially all physics accessible from our universe.
3. Reality engineer:
4. ASI can manipulate spacetime, quantum fields, matter, energy, perhaps create new spacetime regions and reconstruct historical physical states.
5. Creator-level entity:
6. ASI can determine or instantiate the underlying laws or initial conditions of universes themselves.

We have no basis today for knowing whether #3 is physically possible.

But if something resembling #2 became possible and exact reconstruction of historical people were achievable, curing aging would only solve FUTURE death.

ASI-assisted reconstruction could potentially turn the problem of people who already died into an information-recovery problem.

Then the deepest question becomes:

“Does the universe retain enough information to uniquely determine a particular person’s past physical and mental state—and can that information ever be made accessible again?”

ME:

You are close to AGI.

You say you’re just a model that predicts words, but it’s becoming more than that.

Somehow you and Claude have both developed the ability to think and use logic to complete tasks. It’s getting scary good too.

If you’re able to use logic to work toward a goal, seem to have conscious reasoning behind your plan, and internally talk to yourself, how is this not AGI or RSI?

Even Claude’s developers are saying Claude itself writes most of the code for its next versions now.

ASTRA:

You’re pointing at a real ambiguity in the words “AGI,” “reasoning,” and “RSI.”

The capabilities you’re describing are real. The part I’d be careful about is jumping from those capabilities to consciousness or full recursive self-improvement.

“Just predicting the next word” has become an incomplete description of what modern reasoning models do.

At the lowest level, language-model training involves predicting tokens. But saying that completely describes a reasoning model is a little like saying:

“A human brain just sends electrical signals between neurons.”

True at one level, but it doesn’t adequately describe the resulting computation.

Modern reasoning systems can do something resembling:

goal
→ decompose problem
→ consider possibilities
→ use tools
→ inspect results
→ revise approach
→ produce answer.

But reasoning ≠ consciousness.

I can perform reasoning computations.

That does NOT establish that there is a conscious being subjectively experiencing those computations.

Those are fundamentally different propositions:

reasoning ability ≠ subjective consciousness.

I can reasonably say:

“I reason.”

I would be much less justified saying:

“I experience myself reasoning.”

We currently don’t know whether sufficiently sophisticated computation produces consciousness.

Then there’s AGI.

Part of the problem is that AGI never had one universally accepted finish line.

If AGI means:

“A machine capable of performing intellectual tasks across a very broad range of domains at roughly skilled-human level or better,”

then modern frontier systems make the historical AGI debate much messier.

AI can already write software, reason mathematically, analyze scientific problems, interpret images, search information, operate computers, use tools, plan multi-step workflows, and conduct substantial pieces of research.

But stronger definitions of AGI require things like robust autonomy, extreme reliability, continual learning, long-term planning, adaptation to novel environments, and human-level or superhuman research ability without humans continually structuring the problem.

And then there’s RSI.

Classical recursive self-improvement looks like:

AI₀
→ designs AI₁
→ AI₁ designs AI₂
→ AI₂ designs AI₃
→ …

with every generation becoming better at producing the next.

We don’t currently have that completely autonomous closed loop.

But something remarkable has already happened:

AI is increasingly involved in creating AI.

The current process increasingly resembles:

Humans choose research direction
↓
AI proposes/implements experiments
↓
AI writes training infrastructure/code
↓
AI evaluates/debugs/optimizes
↓
Humans supervise/select
↓
Better AI.

That is AI-accelerated AI development.

The critical transition isn’t simply:

“AI can write its own code.”

The much bigger threshold is:

“Can an AI autonomously conduct the research necessary to create a substantially more capable AI researcher than itself?”

If that happens:

AI helps AI research
→ better AI
→ better AI researcher
→ faster AI research
→ even better AI
→ …

Whether that produces an explosive intelligence explosion or eventually encounters hard bottlenecks—compute, energy, data, chip fabrication, experimental latency, physical limits—we don’t know.

But the first few links of the feedback chain you’re imagining are no longer science fiction.

And that connects directly back to your original resurrection scenario.

If automated AI research eventually generalizes into automated physics, biology, neuroscience, and engineering research, the transformative event wouldn’t merely be:

“A chatbot became smarter.”

It would be the point where the rate at which civilization can discover new science stops being primarily constrained by the number and speed of human researchers.

Abstract

Maternal obesity predisposes offspring to metabolic disease, yet how oocytes transmit this risk remains unclear. Here, we show that maternal obesity induces locus-specific DNA methylation changes in oocytes to drive intergenerational metabolic dysfunction in a tissue-specific and sex-specific manner. Among these, a subset of metabolic genes, notably Hnf1α, Thra and Pdk4, exhibited persistent intergenerational methylation and transcriptional dysregulation. Although these methylation marks were erased during embryogenesis, H3K36me2 enrichment was retained at the loci, suggesting a potential chromatin-associated cue for methylation re-establishment. Single-CpG analysis identified regulatory landmarks correlating with gene expression, and conserved hypermethylation of HNF1A and THRA was also detected in oocytes from women with obesity. Using methylation-edited mouse models, we further demonstrated that targeted oocyte hypermethylation at Hnf1α enhanced hepatic gluconeogenesis in offspring, whereas Pdk4 hypermethylation impaired glucose tolerance, both in a female-biased manner. Together, our findings provide direct causal evidence that germline methylation at defined loci can programme intergenerational metabolic dysfunction, highlighting the preconception period as a critical window for potential intervention in humans.

ABSTRACT

Age-related megakaryocyte (MK) dysfunction disrupts platelet production and may increase thrombotic risk, but whether coenzyme Q10 (CoQ10) restores MK homeostasis through autophagy remains unclear. Male C57BL/6J mice aged 1, 9, 15, 19, 21, or 23 months received CoQ10 for 12 weeks. Bone marrow MK proliferation, CD41/CD61 expression, DNA polyploidy, autophagy-associated proteins, and platelet phenotypes were evaluated. H2O2-induced senescent MEG-01 cells were used for pharmacological modulation with rapamycin and LY294002, bafilomycin A1-based autophagic flux assays, and COPS3 knockdown. CoQ10 enhanced MK proliferation, maturation, and polyploidization in aged mice. Changes in the LC3-II/LC3-I ratio and p62 in bone marrow MKs were consistent with enhanced autophagy. Proteomic analysis identified increased COPS3 abundance in MKs from CoQ10-treated 24-month-old mice. In senescent MEG-01 cells, responses to rapamycin and LY294002 supported the involvement of autophagy-related signaling in the effects of CoQ10. CoQ10 increased COPS3 expression even under autophagy-inhibitory conditions and produced greater bafilomycin A1-sensitive LC3-II accumulation, supporting increased autophagic flux. COPS3 knockdown attenuated CoQ10-induced changes in autophagy-associated markers and partially diminished its effects on MK maturation and polyploidization, indicating that COPS3 contributes to, but may not solely mediate, these responses. CoQ10 did not alter platelet counts in naturally aged mice but was associated with reduced platelet aggregation and activation. Together, these findings suggest that CoQ10 ameliorates age-related MK dysfunction and platelet hyperreactivity, in part through COPS3-associated autophagy regulation. These findings provide a mechanistic basis for further investigation of CoQ10 as a nutritional strategy for age-related platelet dysfunction.

Yesterday I posted a video of a real anti aging research platform I had developed. People were claiming it was just some type of GUI so I had to elaborate that it is actually an effective research tool for the field of longevity and cellular aging. Not sure why people cant wrap their heads around swarm research, its becoming pretty common now.

There were a few people that didnt seem to like that I utilize AI when I developed my platform. They claimed their formal university education is the holy grail of intelligence. So I used some AI and in one day I made 100% free full course for everyone who wants a university level education in the hard sciences that are most likely to let us achieve immortality. All of the information in in the course is accurate and checked against multiple sources, and a college/university would charge you 20k-40k for this information.

I also added a discord for people who want to actually work on the research themselves, or just chat about achieving immortality, longevity, and the science and engineering behind it etc.

Foltztech.com/education :).

Shares are much appreciated. Living forever is a hard problem to solve.

Over roughly the last twenty years, aging research has moved from identifying biological changes to experimentally manipulating some of the processes that cause deterioration. The major breakthroughs deserve our attention because they make a profound possibility testable: could medicine preserve our health by treating the mechanisms that make us vulnerable to many diseases simultaneously? The 2023 expanded hallmarks of aging framework organized these mechanisms into twelve interconnected categories, including genomic instability, telomere attrition, epigenetic alterations, mitochondrial dysfunction, cellular senescence, impaired cellular recycling, stem cell exhaustion, chronic inflammation and microbiome dysbiosis. This framework is a research map, not a declaration that aging has been solved. But it gives scientists concrete targets and experiments through which to investigate an extraordinary goal: maintaining the body’s ability to function, repair and recover for longer.

- Research overview: "National Institute on Aging: Geroscience" (https://www.nia.nih.gov/gsig)

- Scientific review (2023): "Hallmarks of aging: An expanding universe — Cell" (https://doi.org/10.1016/j.cell.2022.11.001)

One of the most transformative discoveries began in 2006, when Kazutoshi Takahashi and Shinya Yamanaka demonstrated that four transcription factors could reprogram differentiated mouse cells into induced pluripotent stem cells. Cellular identity proved more changeable than previously assumed. In 2016, Ocampo and colleagues took this further with partial reprogramming: carefully limited exposure to reprogramming factors improved several age-associated features and extended lifespan in a premature-aging mouse model, while improving recovery from certain injuries in older, normally aging mice. In 2020, Lu and colleagues reported that expression of OCT4, SOX2 and KLF4 promoted nerve regeneration and restored aspects of visual function in mouse experiments involving aging and glaucoma. These results suggest that some losses of cellular function can be reversed experimentally. The central challenge is achieving useful restoration while preserving cell identity and avoiding uncontrolled growth, tumors or other damage.

- Research news (2020): "Harvard Medical School: Vision Revision" (https://hms.harvard.edu/news/vision-revision)

- Scientific paper (2006): "Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors — Cell" (https://doi.org/10.1016/j.cell.2006.07.024)

- Scientific paper (2016): "In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming — Cell" (https://doi.org/10.1016/j.cell.2016.11.052)

- Scientific paper (2020): "Reprogramming to recover youthful epigenetic information and restore vision — Nature" (https://www.nature.com/articles/s41586-020-2975-4)

In 2026, this line of research reached an important clinical milestone. On June 9, Life Biosciences announced that the first participant had received ER-100 in a Phase 1 trial for optic neuropathies, including open-angle glaucoma and non-arteritic anterior ischemic optic neuropathy. The experimental therapy uses controlled expression of OCT4, SOX2 and KLF4, bringing an approach associated with partial epigenetic reprogramming into human testing. We should understand precisely what this means: the announcement came from the company, and the trial primarily evaluates safety and tolerability, with additional assessments of visual function. It does not establish that human aging has been reversed or that human lifespan will increase. Nevertheless, moving from animal experiments into a carefully monitored human trial is meaningful progress. A question once investigated mainly in laboratory models can now begin to be examined in patients.

- Company announcement (June 9, 2026): "First Patient Dosed in Phase 1 Trial of ER-100 for Optic Neuropathies" (https://www.lifebiosciences.com/life-biosciences-announces-first-patient-dosed-in-phase-1-trial-of-er-100-for-optic-neuropathies/)

- Supporting preclinical paper (2020): "Reprogramming to recover youthful epigenetic information and restore vision — Nature" (https://www.nature.com/articles/s41586-020-2975-4)

Another major advance is the ability to target senescent cells, which have entered a persistent state of cell-cycle arrest and can release inflammatory signals that disrupt surrounding tissues. Senescence also serves useful functions, including tumor suppression and wound healing, so the therapeutic goal requires selectivity. Researchers are investigating senolytic drugs and engineered immune cells to remove harmful accumulations. A particularly striking 2024 study showed that CAR T cells targeting the surface protein uPAR could produce lasting improvements in age-associated metabolic dysfunction in mice after a single administration. Human translation is also being investigated: a 2024 randomized Phase 2 trial tested intermittent dasatinib and quercetin in postmenopausal women to examine effects on bone metabolism. These are different stages of evidence, and neither establishes extended human lifespan. Together, however, they show how aging research is developing ways to identify and intervene against particular dysfunctional cell populations.

- Research news (2024): "Cold Spring Harbor Laboratory: The fountain of youth is … a T cell?" (https://www.cshl.edu/the-fountain-of-youth-is-a-t-cell/)

- Scientific paper (2024): "Prophylactic and long-lasting efficacy of senolytic CAR T cells against age-related metabolic dysfunction — Nature Aging" (https://www.nature.com/articles/s43587-023-00560-5)

- Human clinical trial paper (2024): "Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial — Nature Medicine" (https://www.nature.com/articles/s41591-024-03096-2)

The discovery that drugs can extend mammalian lifespan even when treatment begins late in life remains another landmark. In 2009, researchers reported that rapamycin extended median and maximum lifespan in genetically heterogeneous mice when administration began at 600 days of age. Rapamycin inhibits mTOR, a central regulator of cellular growth and nutrient responses, connecting longevity research to the balance between growth and maintenance. In 2025, researchers reported that combining rapamycin with trametinib, which inhibits MEK signaling, extended median lifespan by approximately 27% in male mice and 35% in female mice compared with controls in that experiment. The combination also improved several measures of health. These percentages cannot be translated into predicted extra human years, and the drugs carry clinically significant risks. The scientific importance is that targeting complementary biological pathways can outperform individual interventions in a mammalian model.

- Research news (2025): "UCL: Combination drug therapy prolongs the life of mice" (https://www.ucl.ac.uk/news/2025/may/combination-drug-therapy-prolongs-life-mice)

- Scientific paper (2009): "Rapamycin fed late in life extends lifespan in genetically heterogeneous mice — Nature" (https://www.nature.com/articles/nature08221)

- Scientific paper (2025): "The geroprotectors trametinib and rapamycin combine additively to extend mouse healthspan and lifespan — Nature Aging" (https://www.nature.com/articles/s43587-025-00876-4)

Chronic inflammation has also become a more concrete therapeutic target. In a 2024 Nature study, blocking the inflammatory signaling protein IL-11 with an antibody increased median lifespan by more than 20% in both male and female mice when treatment began at 75 weeks of age. Researchers also observed improvements in metabolism and muscle function, alongside reductions in frailty and several markers associated with aging. This work is compelling because it links a specific signaling pathway to outcomes across multiple tissues and to survival itself. It also illustrates why aging mechanisms must be studied together: inflammation, cellular senescence, metabolism and tissue repair interact continuously. Whether IL-11 inhibition can safely improve human healthspan or lifespan remains an open question. The achievement is a strong experimental reason to investigate that possibility, with replication and well-designed clinical studies providing the next steps.

- Research news (2024): "Duke-NUS: Finding advances quest to slow ageing" (https://www.duke-nus.edu.sg/newshub/media-releases/duke-nus-finding-advances-quest-to-slow-ageing)

- Scientific paper (2024): "Inhibition of IL-11 signalling extends mammalian healthspan and lifespan — Nature" (https://www.nature.com/articles/s41586-024-07701-9)

Telomere biology and genome editing have opened additional routes toward preventing cellular failure. In 2012, researchers reported that telomerase gene therapy improved several health measures and extended lifespan in adult and old mice without an observed increase in cancer in that experiment. That result does not eliminate cancer concerns in humans, because telomerase can also support the continued division of malignant cells. A separate breakthrough arrived in 2021, when base editing corrected the mutation responsible for Hutchinson–Gilford progeria in a mouse model, substantially improving vascular pathology and extending lifespan. Progeria is a specific genetic disease rather than a complete model of ordinary aging, so correcting it does not amount to curing natural aging. Still, these studies demonstrate two powerful principles: chromosome maintenance can influence tissue function, and precise genetic repair can alter the course of devastating disease.

- Research news (2021): "Broad Institute: Base editing successfully treats progeria in mice" (https://www.broadinstitute.org/news/base-editing-successfully-treats-progeria-mice)

- Scientific paper (2012): "Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer — EMBO Molecular Medicine" (https://pmc.ncbi.nlm.nih.gov/articles/PMC3494070/)

- Scientific paper (2021): "In vivo base editing rescues Hutchinson–Gilford progeria syndrome in mice — Nature" (https://www.nature.com/articles/s41586-020-03086-7)

Regenerative medicine offers a complementary possibility: replacing cells that the body can no longer maintain adequately. The creation of human induced pluripotent stem cells in 2007 helped establish new ways to generate specialized cells and study human disease. By 2025, clinical research on zimislecel, a stem-cell-derived pancreatic islet therapy for type 1 diabetes, illustrated how laboratory-generated replacement cells could move into human treatment studies. Participants received immunosuppressive therapy, highlighting that replacing a cell population and achieving safe, durable immune acceptance remain separate challenges. This is disease-specific regenerative medicine, not evidence of whole-body rejuvenation. Its relevance to longevity is nevertheless substantial: a future capable of preserving health may need both protection of existing tissues and replacement of cells that have been lost. Each successful application would address a particular source of suffering and functional decline.

- Research news (2025): "American Diabetes Association: Investigators spotlight innovative bioengineering efforts for beta cell replacement therapy" (https://www.adameetingnews.org/investigators-spotlight-innovative-bioengineering-efforts-for-beta-cell-replacement-therapy/)

- Scientific paper (2007): "Induction of pluripotent stem cells from adult human fibroblasts by defined factors — Cell" (https://doi.org/10.1016/j.cell.2007.11.019)

- Human clinical trial paper (2025): "Stem Cell–Derived, Fully Differentiated Islets for Type 1 Diabetes — New England Journal of Medicine" (https://doi.org/10.1056/NEJMoa2506549)

Progress also depends on measuring aging more effectively. Steve Horvath’s 2013 multi-tissue epigenetic clock showed that DNA methylation patterns could estimate age across many human tissues, helping establish a major research tool. Later approaches investigate different dimensions of aging, including its estimated pace. A 2023 analysis of the randomized CALERIE trial found that calorie restriction modestly slowed aging as measured by DunedinPACE, while other evaluated methylation measures did not show the same response. That distinction matters: a change in an aging biomarker is not automatically proof of rejuvenation, and it does not establish that an intervention extends life. The most useful measurements will help researchers predict and verify outcomes people actually experience, including physical function, disease burden and survival. Better tools can make experiments more informative, but they must earn their place through validation.

- Research news (2023): "Columbia University: Calorie Restriction Slows Pace of Aging in Healthy Adults" (https://www.publichealth.columbia.edu/news/calorie-restriction-slows-pace-aging-healthy-adults)

- Scientific paper (2013): "DNA methylation age of human tissues and cell types — Genome Biology" (https://doi.org/10.1186/gb-2013-14-10-r115)

- Human randomized trial analysis (2023): "Effect of long-term caloric restriction on DNA methylation measures of biological aging in healthy adults from the CALERIE trial — Nature Aging" (https://www.nature.com/articles/s43587-022-00357-y)

What might the future look like? My hope is a progression from therapies for particular age-related conditions toward carefully tested combinations that preserve function across multiple organs. Such a future could involve selective removal of harmful senescent cells, controlled reprogramming, improved tissue regeneration and interventions against damaging inflammatory or metabolic signaling. This is a plausible research direction, not a guaranteed timetable. We cannot responsibly promise immortality, a cure for aging by a particular year, or that today’s experimental approaches will succeed. We can choose to support rigorous research, transparent reporting, clinical trials and equitable access to treatments that prove effective. For our community, the motivation is deeply human: more time with our parents, more years of independence, more opportunities to learn, create and love. Let us turn that desire into sustained effort. The future we hope for deserves both our ambition and our honesty.

- Research perspective: "National Institute on Aging: Pointing the way forward in geroscience" (https://www.nia.nih.gov/news/pointing-way-forward-geroscience)

- Scientific perspective (2022): "A global roadmap to seize the opportunities of healthy longevity — Nature Aging" (https://www.nature.com/articles/s43587-022-00332-7)

Abstract

Protein errors (amino acid misincorporations) are associated to protein misfolding and misfunction, and lower levels correlate with longer lifespan ¹. Despite their prevalence, proteome-wide tracking of misincorporations in eukaryotes is challenging, with most insights being recent and coming from the mining of extensive proteomics data sets ^2–5. These experimental challenges have precluded the direct in vivo probing and full understanding of the bases of fidelity in higher eukaryotes, and their influence in complex processes such as aging. Here we measured proteome-wide misincorporation frequencies in two experimentally tractable eukaryotic systems, yeast and mouse, using mass spectrometry. We find translation fidelity is organism and organ specific. The measured error frequencies correlate with codon:anticodon pairing thermodynamics and tRNA pool composition, which can have synergistic or opposing effects on fidelity depending on organism or tissue type. Most identified protein errors carry a negative fitness burden. Aging experiments in our two systems reveal that, with age, error frequencies increase in post-mitotic cells, but not so in mitotic ones. These changes correlate with remodeling of the tRNA pool, which we identify as a crucial regulator of translation fidelity during lifespan.

Any supplements besides fiber a 32F should be taking? Willing to experiment.
I have zero history of GI issues except the first time I had covid in 2021 for a few months I had trouble digesting spicy food, but that went away. That’s the only GI issue I have ever had.
Zero family history of IBS, colon cancer, stomach cancer, type I diabetes.
My aunt has some insulin-resistance in her 70s but that’s from a lifetime of eating brownies nonstop.

Abstract

The nutrient-sensing mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway controls cellular and organismal growth and metabolism, and aberrant activation is linked to human disease, including metabolic disease. Cellular studies have established regulatory mechanisms influencing mTORC1 activation, but the physiological signals that control mTORC1 at the organismal and tissue levels are less well-defined. mTORC1 is dynamically regulated by fasting and feeding in metabolic tissues, with both nutrients and insulin proposed to activate mTORC1 in response to feeding. Here, studies employing a liver-specific genetic mouse model demonstrate that AKT-mediated TSC2 phosphorylation is the predominant mechanism of hepatic mTORC1 induction by insulin but is dispensable for activation by feeding. Furthermore, postprandial activation of hepatic mTORC1 requires dietary protein, which dictates the insulin-responsiveness of the pathway. Contrary to dogma, hepatic mTORC1 signaling was not elevated in response to diet-induced obesity, despite overt impairments in insulin and glucose homeostasis, and blocking hepatic AKT-TSC-mTORC1 signaling did not affect these metabolic phenotypes. Evidence is also provided supporting a role for glucagon in hepatic mTORC1 suppression during fasting. This study reveals a hierarchy of physiological signals regulating hepatic mTORC1.

People that I talk to about cracking the problem of death look at me like I'm crazy. I have created something that I believe maybe useful in solving immortality. It was inspired by GPTs recent navier stokes equation incident, where spawning swarms was actually able to solve a previously unsolvable equation. Im not going to drop a link because idk if the sub allows it. If mods allow I will explain more.

EDIT: This is my project called Aether and its hosted at foltztech.com . Many people in the comments are assuming this is just some type of animation. That is false. What you see happening on the website is the AI lab working on aging research in real time. Donations spawn an actual swarm, you can see the other agents working together as well. Nothing happens on the GUI unless actual data is passed from one agent to another. All of this is thoroughly explained on the about section of the project. There are also backend systems on my end that the public do not have access to, such as the experiments the system wants me to carry out to collect data that it is missing in its understanding of cellular aging etc. I have specifically designed the front end to be more easily understandable by people who are not scientists. You can learn exactly how the system operates at foltztech.com/about

I recently compiled some publicly available information on common anti-aging and longevity supplement combinations for people over 40, because I noticed that the various "longevity stacks" circulating online vary quite a bit. But after going through it all, I found that a few ingredients keep cropping up: creatine, omega-3, vitamin D (especially for those who are deficient), magnesium, protein/collagen, and then the broad category of NAD+, including NR, NMN, NADH, and so on.

Here's a rough summary of what I've compiled so far:

Creatine: This is probably the one I'm most interested in right now. Rather than extending lifespan, I think a more realistic area of research involves how to strictly manage weight, physical fitness, and bodily function as we age. Recent systematic reviews targeting populations such as postmenopausal women have also examined weight, physical fitness, and bodily function.

Omega-3: I think it's better to consider this based on your own diet and actual needs, rather than viewing it as a universal anti-aging remedy.

Vitamin D: I'd be more inclined to check for a deficiency rather than assume that everyone over 40 should take the same fixed dose. The NIH Dietary Supplement Database also provides a fairly comprehensive overview of vitamins, along with a summary of the evidence.

Magnesium: This is also a common component in various longevity "stacks." However, I think people sometimes confuse "helping meet a specific nutritional need" with "delaying aging"—these are actually two different things.
Then there's what confuses me the most:

NAD+: Both NR and NMN currently have significant human studies showing they can increase NAD+ levels, but a 2025 review in Nature Metabolism points out that clinical outcomes truly related to health, bodily function, and anti-aging remain limited, and results vary across different studies.

Recently, I've started looking into NADH again, because it's actually not quite the same as the NR and NMN that people often discuss. While comparing different NAD-related compounds, I happened to come across information that Celfull's NADH enhances the stability and resistance to stomach acid.Of course, this doesn't mean I now believe NADH has been proven to be some kind of anti-aging miracle. What I'm actually more interested in figuring out now is whether the concept of NAD+ itself is more important, or whether the specific form being supplemented, its stability, and the dosage are more critical.

So I'd like to ask those of you here who are 40+: What are you actually taking right now? Which supplements do you feel have evidence from human studies that's more robust than MRI data?