MECHANISMS OF AGING AND INTERVENTIONS FOR LONGEVITY PART 2. MORE ON THE FIRST 100 YEARS AND RECENT RESEARCH ON EPIGENETIC AGE REVERSAL

By Vince Giuliano with important inputs from Gemini 3, ChatGPT 5 and Copilot
12-5-2025

PREFACE

This is the Second Part of a two-part series of blog entries.  The First Part MECHANISMS OF AGING AND INTERVENTIONS FOR LONGEVITY PART 1 THE FIRST 100 YEARS  describes causal processes of human aging, as typical from birth to approximately 100 years of age  This description provides a comprehensive framework that is sufficient to explain all known aspects of human aging.  The First Part also outlines interventions and activities that can help fundamentally healthy people have a high likelihood of reaching 100 or so years of age, healthy, functional, and cognitively all there.  Some people, possibly many, may be able to continue working and contributing to their families and society for a few years more.  The First Part also lays out important distinctions, and I suggest that reading it is a prerequisite to understanding what follows here.

This current Part Two entry is divided into two Halves.  The First Half is concerned with additional topics and interventions related to successfully getting through the first 100 years of life: AKG and Klotho.  The Second Half is concerned with more-recent research on certain longevity interventions that show promise of working for people who have survived their first 100 years in a healthy, highly functional state.  I am referring to approaches that involve Younging, that is, whole-organism regression to a previous younger state.  Finally, I discuss the possibility of transferring a surrogate of me into AI entities such as humanoid robots, enabling that surrogate to continue experiencing living and have a lifespan of hundreds or more years.

FIRST HALF: ADDITIONAL TOPICS AND INTERVENTIONS RELATED TO GETTING SUCCESSFULLY THROUGH THE FIRST 100 YEARS OF LIFE

These are topics I have recently been concerned with and need to be viewed in the context of the topics already covered in Part One.

1. ALPHA KETO GLUTARATE (AKG)Image source

Here is a detailed breakdown of its proposed health and longevity benefits.

🧬 Longevity and Anti-Aging Mechanisms

Research, primarily in model organisms (like worms and mice) and some early human studies, suggests AKG may extend lifespan and healthspan (the period of life spent in good health) by influencing several fundamental aging pathways.

1. Epigenetic Regulation

• DNA Demethylation: AKG is a crucial co-factor for enzymes called Ten-Eleven Translocation (TET) and Jumonji-C domain-containing histone demethylases. These enzymes are vital for removing methyl groups from DNA and histones, which helps regulate gene expression.  As pointed out in Part 1 , a sufficient explanation of adult aging is the progression of Hk327me2-3 histone methylation starting at age 25 and proceeding lifelong, with the consequence of the gradual turning off of multiple repair and maintenance genes.  Consuming AKG counters this methylation.
• Reversing Biological Age: Since age-related changes are strongly linked to altered DNA methylation patterns (epigenetic clocks), AKG’s role in this process is hypothesized to contribute to its observed effect in a small human study, where Ca-AKG supplementation was associated with an average reduction in biological age (as measured by a DNA methylation test  “Ca-AKG supplementation was associated with an average reduction in biological age in a specific observational study published in the journal Aging-US (specifically, the study on the supplement Rejuvant®).
  • This human study, which involved 42 participants taking the supplement for an average of 7 months, found an average reduction of about 8 years in biological age as measured by a DNA methylation test.
  • Study details: The study analyzed a group of 42 participants (mean age of ~63) who took 1,000 mg of calcium alpha-ketoglutarate (Ca-AKG) for an average of 7 months, along with vitamin A for males and vitamin D for females.
  • Outcome: A subset of 13 participants who maintained their diet and exercise habits showed a significant average reduction of 7.69 years in biological age. For the entire cohort of 42, the average reduction was 7.96 years.
  • Limitations: The study was retrospective and observational, meaning it lacked a control group, and the algorithm used for the DNA methylation test is proprietary, which makes it difficult to replicate the findings. Therefore, while the results are interesting, further randomized, placebo-controlled trials are needed to confirm these findings.

2. Metabolic Signaling Pathways

• Mitochondrial Function and Energy: AKG is a direct fuel source for the mitochondria (the “powerhouses” of the cell). By supporting the Krebs cycle, it helps optimize cellular energy production (ATP). Declining AKG levels with age are thought to contribute to metabolic dysfunction.
• Activating Longevity Switches: AKG is thought to mildly inhibit the mTORC1 pathway and activate AMPK (AMP-activated protein kinase). Both are key metabolic signaling pathways that, when modulated, can mimic the beneficial effects of caloric restriction, which is a well-established method for extending lifespan in many species.

3. Anti-Inflammatory Effects and Frailty

• Reducing Chronic Inflammation: Chronic, low-grade inflammation (often called “inflammaging”) is a major driver of age-related diseases.  In animal studies, AKG supplementation has been linked to a decrease in systemic inflammatory cytokines and may promote the production of anti-inflammatory molecules like Interleukin-10 (IL-10) . If you have followed this blog or read Part 1, you know that I believe chronic inflammation is the main causal factor of silencing housekeeping and repair genes, typically when people reach their 80s, and is the main cause leading to a chronic inflammatory disease killing most people before they reach age 90.
• Compressing Morbidity: By reducing inflammation and increasing overall vitality, animal studies have shown that AKG not only extends lifespan but also delays the onset of age-related conditions (known as compression of morbidity), reducing overall frailty.

💪 General Health Benefits

Beyond its direct effects on aging pathways, AKG supports several other functions crucial for maintaining health and vitality.

1. Muscle and Tissue Health

• Protein Synthesis and Catabolism: AKG is a precursor to amino acids like glutamine and glutamate.  Glutamine is essential for stimulating protein synthesis and inhibiting protein breakdown (catabolism) in muscles, making AKG beneficial for maintaining muscle mass (especially in catabolic states like trauma or surgery) and potentially aiding in recovery.
• Wound Healing and Tissue Repair: Studies have shown that AKG and its derivatives can accelerate wound closure and tissue repair, likely due to its role as a building block for amino acids and its influence on cellular regeneration.

2. Bone and Skin Health

• Collagen Synthesis: AKG is an important component in the synthesis of collagen, the most abundant protein in the body, essential for skin elasticity, connective tissues, and bone structure.  It facilitates the formation of proline and hydroxyproline residues necessary for stable collagen.
• Bone Density: In studies involving post-menopausal women, Ca-AKG supplementation has shown a trend in reducing markers of bone breakdown and improving bone mineral density.

3. Detoxification and Nitrogen Balance

• Nitrogen Scavenger: AKG plays a key role in nitrogen metabolism, acting as a nitrogen scavenger to help eliminate excess nitrogen and ammonia, which is important for liver function and overall metabolic homeostasis.

💡 Important Considerations re. AKG

• Human Research is Early: While the findings in cell culture and animal models are compelling, and initial human data (especially on epigenetic age) is intriguing, large-scale, placebo-controlled clinical trials in humans are still needed to definitively confirm the longevity and healthspan benefits of AKG supplementation in the general population.  I am already personally convinced.
• Formulation Matters: Calcium Alpha-Ketoglutarate (Ca-AKG) is the formulation most often used in longevity research due to its perceived stability and bioavailability compared to other forms like Arginine Alpha-Ketoglutarate (AAKG), which is more common in sports supplements.  I personally have supplemented wth AKG for 5 years now, and with Ca-AKG for over 1 year.
• Safety: AKG supplementation appears to be generally safe and well-tolerated in the studies conducted so far.

1. Klotho

Klotho is a remarkable protein that plays a central role in aging and longevity.  Discovered in the late 1990s and named after the Greek Fate who spins the thread of life, Klotho functions as both a hormone and a membrane-bound co-receptor, influencing multiple biological systems.

🧬

What Is Klotho?

• Type: Anti-aging protein encoded by the KL gene.
• Forms: Exists in both membrane-bound and soluble forms.
• Expression Sites: Primarily in the kidney, brain (especially choroid plexus), and parathyroid glands.
• Mechanism: Regulates phosphate metabolism, suppresses oxidative stress, modulates insulin/IGF-1 signaling, and partners with FGF23 to maintain mineral balance.

Health and Longevity Benefits of Klotho

The scientific literature surrounding Klotho perfectly aligns with the core principles of myur “Younging” research and multi-targeted approach to longevity.

1. The Ultimate Anti-Inflammaging Agent

My past work heavily emphasizes the role of chronic, low-grade inflammation (“inflammaging”) in driving age-related disease.  Klotho’s potential directly addresses this:

• NF-B and NLRP3 Inhibition: Klotho is known to counteract inflammation by directly inhibiting NF-B (Nuclear Factor Kappa B) signaling and the NLRP3 inflammasome. This is crucial because NF-B is a master regulator of inflammatory gene expression, and NLRP3 drives the creation of inflammatory cytokines (like IL-1$\beta$) that fuel aging.
• Mitigation of Fibrosis: Klotho acts as an antagonist to the TGF- (Transforming Growth Factor ) pathway.  Since TGF- is a primary driver of fibrosis (the stiffening and scarring of tissues that occurs with age), Klotho’s inhibition of this pathway is key to maintaining organ and tissue elasticity and function.

Effectors impacted by Klotho

2. Multi-Targeted Pathway Control

Klotho’s activity aligns with interventions that regulate multiple aging pathways, rather than just one:

Most of these pathways of aging are affected by Klotho

• Inhibition of IGF-1: The protein helps suppress the IGF-1 (Insulin-like Growth Factor 1) signaling pathway. This pathway is evolutionarily conserved and associated with accelerated aging when overactive. By helping to modulate IGF-1, Klotho reinforces a longevity state similar to caloric restriction.
• Wnt Modulation: Klotho also inhibits Wnt signaling, another pathway linked to cellular senescence and tissue dysfunction when aberrantly activated in aging.

3. Boosting Antioxidant Defenses

Klotho’s potential includes:

• Nrf2/FoxO Activation: Klotho is associated with increasing cell-protective antioxidant enzymes by activating the transcription factors Nrf2 (Nuclear factor erythroid 2–related factor 2) and FoxO. This boosts the cell’s resilience against oxidative stress and damage, a primary driver of aging.

In summary, the Klotho protein is essentially a “Swiss Army Knife” of longevity that simultaneously hits four of the most critical aging pathways (IGF-1, Wnt, NF-B, and TGF-) while boosting the cell’s own repair and defense systems (Nrf2/FoxO). Focusing on multi-targeted “Younging” strategies, its potential is arguably among the highest in modern longevity science.

Approaches that most powerfully enhance the expression of klotho

The scientific community has identified several key lifestyle, nutritional, and therapeutic approaches that support Klotho expression.  These methods fit perfectly with a philosophy of multi-targeted, evidence-based longevity intervention:

1. Lifestyle and Exercise (The Most Reliable Method)

This is consistently cited as the most effective and reliable way to boost circulating Klotho, aligning with emphasis on the body’s natural resilience.

• Chronic Exercise Training: Consistent physical activity stands out. Studies show that regular, chronic exercise significantly raises circulating Klotho levels.  The recommended 150 minutes of moderate exercise weekly (including both aerobic and resistance training) is often cited as the “sweet spot.”
• Stress Management and Sleep: Chronic stress is known to suppress Klotho production. Practices like meditation, yoga, and ensuring 7–9 hours of quality sleep per night are vital maintenance factors for Klotho levels.

2. Nutritional Strategies and Supplements

Several compounds and nutrients are Klotho agonists (enhancers).

3. Therapeutic and Pharmacological Interventions

These are pproaches that enhance Klotho expression as their secondary benefits outside their primary indication:

• Metformin: Preclinical studies have shown that the common anti-diabetic drug Metformin enhances Klotho expression.
• mTOR Inhibitors: Medications like Rapamycin (or its derivative Everolimus), which inhibit the mTOR (Mechanistic Target of Rapamycin) pathway, have been noted in clinical trials to increase Klotho levels. This is a crucial link, as mTOR inhibition is one of the most powerful anti-aging strategies.
• Renin-Angiotensin System Inhibitors: Certain existing blood pressure medications, such as ACE inhibitors (e.g., Fosinopril) and ARBs (e.g., Losartan, Valsartan), have been found to increase circulating Klotho. This is significant because Angiotensin II suppresses Klotho. I regularly take Valsartan.

Summary: Approach to Klotho Enhancement

Given a need for scientific rigor, it appears that the most robust strategy involves a combination of the most reliable methods:

1. Prioritize Exercise: Maintain the high levels of physical activity known to physically drive Klotho production.
2. Optimize Vitamin D: Ensure high-normal Vitamin D levels via supplementation.
3. Target Pathways: Use compounds like Metformin (if appropriate) and powerful polyphenols (Resveratrol, Curcumin) to indirectly upregulate Klotho via the shared anti-aging pathways (mTOR, Nrf2, etc.).

Dietary supplements most powerfully upgrade the expression of Klotho in humans

The search for a single, most “powerful” dietary supplement to boost Klotho in healthy humans is an active area of research, and many compounds show strong potential in preclinical modelsere is a breakdown of the leading supplements and nutrients, ranked by the strength of the evidence supporting their Klotho-boosting effects in humans:

1. Vitamin D (The Strongest Human Evidence)

Vitamin D is the most directly linked nutrient, as the Klotho protein is fundamentally integrated into the Vitamin D and phosphate metabolism axis.

• Direct Mechanism: Studies using human renal cells have demonstrated that the active form of Vitamin D (1,25-dihydroxyvitamin D3) directly upregulates the Klotho gene expression by binding to Vitamin D Response Elements (VDREs) located near the Klotho
• Clinical Relevance: Clinical trials and observational studies confirm that maintaining adequate Vitamin D status (often achieved through supplementation, especially D3) is essential for supporting healthy circulating Klotho levels, particularly in individuals who are deficient.

2. Resveratrol (Strong Mechanistic/Preclinical Data)

Resveratrol, a potent polyphenol, is a highly relevant compound in the context of anti-aging pathways and shows strong mechanistic evidence for Klotho upregulation.

• Mechanism of Action: Research using cellular models has shown that Resveratrol can increase the expression profile of the Klotho gene in the kidney. It is thought to achieve this by enhancing key transcription factors, such as Activating Transcription Factor 3 (ATF3 and -Jun, which are involved in regulating the Klotho gene.
• Context:While the anti-aging benefits of Resveratrol have been explored in many human trials, the direct measurement of a robust Klotho increase in those specific human trials is less commonly reported than the mechanistic findings.

3. Other Key Nutrients with Supportive Associations

While not as directly linked through clinical intervention as Vitamin D, these nutrients have strong observational or correlational data in human populations:

Note on Pharmaceutical and Pathway Activators

For a comprehensive view, it is worth noting that some compounds outside the strict definition of ietary supplements how potent Klotho-boosting effects by targeting key longevity pathways:

• mTOR Inhibitors (e.g., Rapamycin analogs): These are potent anti-aging compounds that, in clinical trials, have been noted to increase Klotho levels.
• Metformin: Preclinical studies have shown that this pharmaceutical, a common Type 2 diabetes treatment, can enhance Klotho expression.

In summary, for individuals interested in optimizing Klotho expression using supplements, Vitamin D (D3) offers the most directly substantiated route, followed by polyphenols like Resveratrol and insuring adequate intake of Folate and Vitamin C.

1. SECOND HALF: LATEST ANIMAL OR HUMAN EXPERIMENTS ON EPIGENETIC WHOLE ANIMAL AGE REGRESSION

Several research groups have been concerned with aging itself, the overwhelmingly primary risk factor for diseases and maladies of old age.  See Aging is the single largest risk factor for many Chronic Conditions.

Recent experiments from late 2024 through mid-2025 have marked a pivotal shift in longevity science.  The field has moved beyond the “proof of concept” phase of the original Yamanaka factors (OSKM) toward partial reprogramming (in vivo epigenetic age cell regression back to a younger state, but not all the way back to stem cell status.  Therefore, avoiding wiping out cell type identity.  And also, chemical reprogramming (using pills instead of gene therapy).

The most significant new reported findings include a breakthrough “single gene” alternative to Yamanaka factors, the first successful whole-animal lifespan extension using simple chemical cocktails, and new primate data.

1. Chemical Factors: The Shift to “Pills”

The most practical leap forward is the move away from gene therapy (which is difficult to deliver and risky) toward “chemical cocktails”—small molecules that can be taken as drugs.

• The “RepSox + TCP” Cocktail (Mouse Lifespan Extension):In a study published inMay/June 2025, researchers tested a two-drug cocktail containingRepSox (a TGF-β inhibitor) and Tranylcypromine (TCP) (an antidepressant and LSD1 inhibitor) in mice. See the May 2025 article, The Combination of Two Small Molecules Improves Neurological Parameters and Extends the Lifespan of C3H Strain Female Mice.
  • Result: The cocktail significantly extended the maximum lifespan of “senior” mice and improved neurological and physical markers in “old” mice. This is one of the first direct proofs that simple small molecules can achieve systemic rejuvenation in mammals without complex gene editing.
• The “7c” Cocktail & Toxicity Warning: A June 2025 study (bioRxiv) tested a 7-chemical cocktail (“7c”) in mice. See Multi-omics characterization of partial chemical reprogramming reveals evidence of cell rejuvenation.  “This important study reports comprehensive multi-omics data on the changes induced in young and aged male mouse tail fibroblasts after treatment with chemical reprogramming factors. The authors provide solid evidence to support their claim that chemical reprogramming factors induce changes consistent with a reduction of cellular ‘biological’ age (e.g., correlations with established aging markers in whole tissues).”
• While it successfully rejuvenated cells in the lab, in vivo (whole-animal) results revealed a critical safety hurdle: the treatment led to toxic accumulation of lipid droplets in the liver and kidneys, hindering the rejuvenation process.  This finding is crucial as it highlights that chemical reprogramming must be carefully dosed to avoid metabolic toxicity.
• Harvard/Sinclair Lab & “6 Cocktails”: Ongoing work from Harvard Medical School (published/updated 2024-2025) identified six different chemical cocktails capable of reversing transcriptomic age in human cells in less than a week. These cocktails have also been shown to extend lifespan in elegansworms, setting the stage for further mammalian testing.
• 

The six chemical cocktails that the David Sinclair Harvard laboratory has used to epigenetically reverse cellular aging in vitro. Note that of these chemicals, I have been regularly taking AKG and Sodium Butyrate.

Note that the Harvard and other studies relating to the effectiveness of chemical cocktails leave open questions of safety and recommended dosage for whole-animal use, and that these issues must be addressed before experimenting with whole humans.

Infographic on epigenetic landscapes related to reprogramming

2. Yamanaka Factors (OSK/OSKM): Moving to Primates

Traditional genetic reprogramming is being refined to be safer, as just described (Partial” reprogramming) and is now in the very first stage of showing efficacy in primates, a critical step before human trials.

• Life Biosciences (Primate Data – Aug 2025): This company presented groundbreaking data on their “Partial Epigenetic Reprogramming” (PER) platform, which uses three of the four Yamanaka factors (OSK – omitting the cancer-linked c-Myc). The data highlight the cross-system therapeutic impact of its Partial Epigenetic Reprogramming (PER) platform, a novel therapeutic approach for reversing optic neuropathies and metabolic dysfunction-associated steatohepatitis (MASH).  See Life Biosciences Presents New Data at ARDD 2025 on the Company’s Partial Epigenetic Reprogramming Platform in Liver and Ocular Diseases.
  • “ER-300 improves key biomarkers of liver health in an animal model of MASH
  • These data, along with additional ER-100 preclinical data from a nonhuman primate model of NAION demonstrating clear restoration of methylation patterns with functional enrichment of neuronal regeneration processes, show the potential of Life Bio’s partial epigenetic reprogramming platform to address diseases across multiple organs and systems.
  • Life Bio’s PER platform is designed to partially reprogram the epigenome of aged and injured cells to a younger and healthier state via expression of three of the four Yamanaka factors [Oct4, Sox2, Klf4 (OSK)]. By targeting a root cause of aging at the epigenetic level, this approach offers the potential to address a wide range of age-related diseases across organs and systems.
  • With MASH afflicting about 5% of the global population, and its association with significant morbidities including risk of cirrhosis and liver cancer, new and innovative approaches are needed to improve the lives of individuals impacted by this disease,” said Jerry McLaughlin, Chief Executive Officer of Life Bio. “While still in its early stages of development, we are encouraged by the potential of ER-300 to improve key liver scores. With ER-100 on track to enter human trials in the first quarter of 2026 for two optic neuropathies, we see immense potential of our partial epigenetic reprogramming platform to reverse and prevent multiple age-related diseases.”

4. Rejuvenate Bio: This group continues to refine its gene therapy approach.  Recent reports indicate that injecting elderly mice (124 weeks old) with OSK viruses extended their remaining lifespan by nearly100% (living another 18 weeks vs. 9 weeks for controls) and improved health markers, with no obvious negative effects like cancer observed so far.  See on their website Aging is the single largest risk factor for many Chronic Conditions.

• The “New Player”: SB000 (Single Factor Reprogramming)

In June 2025, a UK-based company called Shift Bioscience announced a major discovery that could make Yamanaka factors obsolete.

• What is it? They used AI to identify a single gene (currently code-named SB000) that drives rejuvenation.
• Why it matters: “Unlike the Yamanaka factors (OSKM), which can accidentally turn cells into stem cells (causing cancer/teratomas), SB000 alledgely rejuvenates the cell’s biological age without erasing its identity or inducing pluripotency. This theoretically decouples “youthfulness” from “stem cell risk,” thereby solving the field’s biggest safety hurdle.”

• 🧩 Scientific Context
• Preprint Stage: The gene’s identity is still secret; “SB000” is a placeholder. The actual gene sequence hasn’t been disclosed.
• Skepticism: Experts caution that extraordinary claims need independent replication. Some stem cell researchers remain skeptical until other labs reproduce the results.
• Next Steps: Shift Bioscience plans in vivo proof-of-concept studies to test SB000’s effects in living organisms.
• In short, SB000 could represent a breakthrough in anti-aging research if validated, offering rejuvenation without the cancer risks tied to pluripotency.  But right now, it’s still early, unpublished beyond preprints, and awaiting independent confirmation.

Summary of Key “Latest” Findings

Conclusion:  The field has rapidly pivoted.  Current cutting edges appear to be chemical partial reprogramming (taking pills like RepSox/TCP) and the new SB000 gene target, which offers the benefits of “Younging” without the cancer risks of traditional Yamanaka factors.

3. SURROGATE SUCCESSOR AI BEINGS

No interventions I know of will necessarily extend the known human lifespan of 123.  Doubling the remaining probable lifespan, as described above, sounds impressive and could be useful.  But it only adds a little for a 96-year-old like me.  It would double my current actuarily expected lifespan from 2.6 to 5.2 years, to when I am 101.  Unless other powerful interventions are identified and developed, we will have to forget not only living forever, but also living longer than 123.  However, there is another completely different approach being developed that could keep a faithful surrogate of me alive and efficiently functioning  for hundreds or even thousands of years.  That is, ro embed a faithful AI surrogate of me into an AI robot.

Conceptual Foundations

• Surrogate in AI: The idea is to capture a person’s memories, personality, decision-making patterns, and values, then instantiate them in an AI system. Specifically, into an AI system that drives a humanoid robot that can do everything a human can do.
• Even today, if enough data relevant to a person can be gathered and organized, including possibly extensive writings, a surrogate of that person can be embodied in an advanced AI system that can talk and reason a lot like the person him/herself.
• Hundreds of billions of dollars are being devoted to R&D on such robots today, with hundreds of companies competing in a race which China appears to be winning so far. In 7 to 12 years, we can expect highly capable humanoid robots to be manufactured in tens of millions, vastly improved over today’s models, and employed as household servants, friends and even lovers,as well as in almost every capacity in every industry and business.  See my August 2025 blog entry THE LIKELY CO-EVOLUTION OF HUMANS AND HUMANOID ROBOTS.
• Continuing to Live: The core intellectual issue is whether such a surrogate represents the continuation of the person or merely the simulation of their traits. Philosophers debate whether identity is tied to biological continuity, consciousness, or informational patterns.  My personal take is that if the surrogate is complete enough and accurate enough, this issue becomes irrelevant.  I think this will happen in time.

Scientific & Technical Dimensions

• Memory & Personality Capture: Current AI can mimic speech patterns, preferences, and even decision-making if trained on personal data.    The technique is currently being developed to give relatives of a deceased person a way to virtually talk with and remain in touch with a deceased loved one.  The problem is that the surrogate cannot act like a real person, for example, wash the dishes or walk the dog, unless the surrogate is embedded in a humanoid robot that looks like and can act like a human.
• True “mind uploading” (mapping the entire neural connectome of a person into a digital substrate) remains speculative and far beyond current neuroscience.  Based on what can be done today with LLM AI, I don’t think that will be necessary.

• 10 or more years from now. a surrogate of a person transferred into a humanoid robot with advanced AI could do everything a human can do and much more, if current projections for those robots are to be believed.
• Unlike biological bodies, digital entities don’t age. They can persist indefinitely, provided storage and computation are maintained. They can be uploaded to more sophisticated robots as they become available.  And therefore potentially enjoy lifespans of hundred or thousands of years.
• However, they may diverge from the original person over time, evolving into something new. This of course, is part of normal  living and true for people as well

Legal & Ethical Considerations

• Identity & Rights: Would the surrogate have legal personhood? Could it inherit property, make contracts, or vote?  Current law says no, but debates are emerging.
• Consent & Authenticity: The surrogate must be created with explicit consent, and society must grapple with whether it represents the person or a derivative.
• Emotional Impact: Families may feel comforted by interacting with a surrogate, but it could also blur grief and prolong attachment in complex ways.
• Meaningful Survival: Even if not literally the same person, the surrogate could preserve wisdom, values, and relational presence—extending influence beyond biological lifespan.

Practical Takeaway

Transferring a surrogate of an old person into AI doesn’t literally extend their biological life, but it can extend their presence, influence, and relational meaning.  Whether that counts as “living longer” depends on how one defines personal identity—continuity of consciousness vs. continuity of information.

Family vacation visiting the Coliseum:  July 2047.  Four of us are Tesla Model 12A Optimus Android Robots.  Can you tell which ones?  The older guy could be a surrogate robot for me, Vince, at a combined age of 117.  But, which of us are the other robots?  You can’t tell?  That may be a characteristic of the mixed human-robot  phase of society we will likely go through, starting in 10-15 years.