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The question is no longer whether scientists can justify pursuing longer, healthier lives. Instead, the burden now falls on defenders of forced ageing to explain why needless suffering should persist. The Ethics Case for Longevity Science Zhuang Zhuang Han, João Pedro de Magalhães.

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This month’s theme: GLP-1, first coumpound with broad positive effects for longevity?

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GLP-1 (glucagon-like peptide-1) is a hormone naturally produced in the intestines that helps regulate blood sugar levels, digestion, and appetite. It works by stimulating the pancreas to release insulin when blood sugar is high, while also reducing the release of glucagon, a hormone that raises blood sugar. Additionally, GLP-1 slows the rate at which food leaves the stomach, which helps prevent sudden spikes in blood sugar after eating and promotes a feeling of fullness. Medications that mimic GLP-1 are commonly used to treat type 2 diabetes and support weight management, and they are also being studied for potential benefits in heart health and metabolic aging.

Metabolic reprogramming

GLP-1 receptor agonists (GLP-1RAs) act far beyond glucose control, intersecting with several hallmarks of aging. They reduce chronic low-grade inflammation by lowering CRP and pro-inflammatory cytokines, improve insulin/IGF-1 signaling, enhance mitochondrial efficiency, and decrease oxidative stress. Preclinical studies show improved mitochondrial biogenesis and reduced cellular senescence markers in metabolic tissues. These pathways are central to geroscience because dysregulated nutrient sensing, mitochondrial dysfunction, and inflammaging drive multiple age-related diseases. By restoring metabolic flexibility and reducing lipotoxicity, GLP-1 therapies may function as metabolic reprogrammers, shifting physiology toward a lower biological age phenotype.

Obesity trends and public health

In the United States, adult obesity prevalence climbed almost continuously from the late 1970s through the 2010s, driven by an obesogenic food environment, sedentary lifestyles, and widening socioeconomic disparities. National Health and Nutrition Examination Survey (NHANES) data showed rates rising from roughly 30% in 1999–2000 to over 42% by 2017–2020, with severe obesity increasing even faster. However, the most recent national surveillance reports (2021–2023) suggest a possible plateau, and in certain age and income subgroups, a slight decline, occurring alongside the rapid adoption of GLP-1 receptor agonists for both diabetes and obesity treatment. Pharmacy and claims data indicate several-fold growth in prescriptions for semaglutide and tirzepatide during this period, with the highest uptake among middle-aged adults and those with private insurance.

Healthspan gains

Large outcome trials demonstrate that GLP-1RAs reduce major adverse cardiovascular events (MACE), even in non-diabetic individuals with obesity. The SELECT trial showed a 20% reduction in MACE with semaglutide in people with overweight/obesity and established CVD. In parallel, GLP-1 therapies improve non-alcoholic fatty liver disease (NAFLD/NASH) through weight-independent mechanisms, including reduced hepatic steatosis and inflammation. Benefits also extend to blood pressure, lipid profiles, and heart failure symptoms, suggesting multi-system healthspan effects rather than single-disease treatment.-

Fat loss vs. muscle preservation

While GLP-1 drugs produce substantial weight loss (≈10–15% with semaglutide), up to 25–40% of total weight lost can be lean mass if no countermeasures are taken. For longevity, preserving skeletal muscle is critical to avoid sarcopenia and frailty. Clinical guidance increasingly emphasizes high protein intake, resistance training, and progressive loading during GLP-1 therapy. Emerging data suggest that combining GLP-1 with structured exercise improves fat-to-lean loss ratio and functional outcomes, aligning weight reduction with healthspan goals rather than simple mass reduction.

Combination Longevity Therapies

GLP-1 drugs seem to generate largely positive effects, but are unlikely to be standalone gerotherapeutics but may serve as foundational metabolic platforms. Combining GLP-1 with exercise enhances mitochondrial function and cardiorespiratory fitness; pairing with metformin targets complementary nutrient-sensing pathways; future combinations with rapalogs or senolytics could address multiple hallmarks simultaneously. The geroscience model favors such stacked interventions to achieve additive or synergistic effects on healthspan and disease prevention. Clinical trials exploring multi-modal metabolic and anti-aging strategies are now a key frontier.

Semaglutide, liraglutide, dulaglutide, exenatide, albiglutide, and lixisenatide are all medications in the GLP-1 receptor agonist class, which are primarily used to improve blood sugar control in people with type 2 diabetes and, in some cases, to support chronic weight management. Across this medication class, common side effects include nausea, reduced appetite, and slowed stomach emptying, and all require medical supervision to ensure proper dosing and safety monitoring.

Commonly Prescribed GLP-1 Medications

• Semaglutide is one of the newer and more potent options and is available as both a once-weekly injection and a daily oral tablet; it is widely recognized for producing significant weight loss and cardiovascular benefits in addition to glucose control. 

 

• Liraglutide is an older GLP-1 medication given as a daily injection and has an extensive safety record, although it typically results in slightly less weight loss than semaglutide. 

 

• Dulaglutide is administered as a once-weekly injection and is popular because of its user-friendly auto-injector device and strong evidence for cardiovascular risk reduction, though its weight-loss effect is generally moderate. 

 

• Exenatide was one of the earliest GLP-1 receptor agonists and is available as either a twice-daily injection or a once-weekly extended-release formulation; it remains effective for blood sugar management but is often considered less potent for weight reduction than newer medications. 

 

• Albiglutide is another once-weekly GLP-1 agent that was previously used for diabetes treatment but has been withdrawn from many markets and is no longer commonly prescribed. 

 

• Lixisenatide is a daily injection mainly used for type 2 diabetes, particularly effective at controlling blood sugar spikes after meals, although it generally produces less weight loss than newer GLP-1 drugs. 

 

This is the first drug to have potentially such a large positive effect in the majority of the population in the USA. However, it is because this population is overweight or obese. We also still have to see impact in the long term since the drugs are recent. Still, we have a global positive effect on healthy longevity.

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The good news of the month- Latest pancreatic cancer research shows potential to shrink and eliminate tumors

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A research team led by Mariano Barbacid at the Spanish National Cancer Research Centre (CNIO) has developed an experimental triple-combination therapy that completely eliminated pancreatic tumors in mice with no major side effects. The study, published in Proceedings of the National Academy of Sciences (PNAS), focuses on pancreatic ductal adenocarcinoma (PDAC), a highly aggressive cancer with a very low five-year survival rate. 

The therapy works by blocking three points in the KRAS signaling pathway, a gene mutation present in about 90% of pancreatic cancer cases. By targeting multiple points rather than a single one, the treatment prevented tumor resistance and produced long-lasting tumor regression in mouse models. The drug combination included an experimental KRAS inhibitor, an approved cancer drug, and a protein degrader. Although the results are very promising, researchers say more work is needed before clinical trials in humans can begin.

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News of Heales and the Longevity Community

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On Wednesday, April 8, there will be an international demonstration for funding longevity with people demonstrating in many cities. In Brussels, we will have a small gathering Place de la Monnaie from 17 to 18:00 CET. More information: fundlongevity.org/en/

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For more information

• Heales, Longevity Escape Velocity Foundation, International Longevity Alliance, Longecity, Lifespan.io, and Aging biotech
• Heales Monthly Science News
• Heales YouTube channel
• Contact us

 

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The next revolution in biology isn’t reading life’s code — it’s writing it.(…)  Sequencing let us read the book of life, our instruction manual. Synthesis will allow us to write new chapters, if not entirely new books. (…). Writing DNA holds even greater promise, the potential to cure any disease. Andrew Hessel. October 20, 2025. Big Think.

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This month’s theme: Exosomes and Longevity

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Exosomes are tiny membrane-bound vesicles released by cells that act as messengers between cells. Measuring about 30–150 nanometers, they form inside the cell and are released into body fluids such as blood and saliva. Exosomes carry proteins, lipids, and genetic material like RNA, which can influence the behavior of recipient cells by altering processes such as inflammation, immune responses, blood clotting, tissue repair, and aging. Because their contents reflect the state of the cells they come from, exosomes are important in research as biomarkers for disease and are being explored as potential therapeutic delivery vehicles.

Exosomes play an important role in the aging process by mediating the transfer of nucleic acids, lipids, and proteins between cells across a wide range of organisms. These vesicles exert significant gerontological effects, influencing cellular function and systemic aging. Exosomes derived from young or stem cells are enriched with antioxidant factors and anti-inflammatory cytokines that help counteract age-related cellular damage. Notably, conditions such as nutrient restriction stimulate exosome release, which has been shown to delay cellular senescence in vitro and slow aging processes in vivo. This effect is thought to occur through enhanced removal of damaged cellular components, including fragmented DNA, misfolded proteins, and oxidized biomolecules, in both animal models and humans. Collectively, these findings underscore the critical role of exosome-mediated waste clearance in aging biology and provide mechanistic support for the longevity benefits associated with fasting and metabolic stress, highlighting promising directions for future research into cellular maintenance and longevity interventions.

As a Longevity Therapy

Exosomes are rapidly emerging as one of the most exciting areas in longevity science. In recent years, researchers have discovered that many of the benefits associated with stem cell therapy are not due to the cells permanently integrating into tissues, but rather to the signals they release. These signals are largely carried by exosomes. This insight has shifted attention toward exosome-based therapies, which offer many of the regenerative benefits of stem cells without the complexity or risk associated with live cell transplantation.

Exosomes derived from mesenchymal stem cells (MSCs) are of particular interest in longevity research. They have also shown promise in areas such as skin rejuvenation, joint health, neuroprotection, and metabolic regulation. Because exosomes carry molecular “instructions” from their parent cells, they can influence aging pathways linked to cellular senescence, mitochondrial function, and repair mechanisms.

Another compelling aspect of exosomes is their potential role as biomarkers of aging. Their molecular cargo reflects the physiological state of the cells they originate from, making them valuable tools for monitoring biological aging and disease progression. At the same time, their natural stability and low immunogenicity make them attractive candidates for therapeutic delivery.

While exosome-based longevity therapies are still largely in the research, interest is rapidly growing. Clinical trials are underway, and exosome treatments are already being offered in some settings, though standardized protocols and long-term safety data are still needed. Ongoing research is focused on refining isolation techniques, improving quality control, and understanding how to best harness exosomes for targeted, personalized therapies.

As science continues to uncover how exosomes influence aging and regeneration, they are increasingly viewed as a key component of future longevity medicine—offering the possibility of extending not just lifespan, but healthspan.

Exosomes as a therapy for other diseases

In 2026, the exosome therapy landscape features over 70 active companies developing more than 80 pipeline therapies for regenerative medicine, oncology, and rare genetic diseases. Key companies leading the development of exosome-based therapeutics include:

 Capricor Therapeutics: A clinical-stage company using its StealthX platform for precision medicine. Its lead candidate, CAP-1002, is currently in advanced trials for Duchenne Muscular Dystrophy.

Aruna Bio: Uses neural-derived exosomes to cross the blood-brain barrier. It initiated Phase Ib/IIa clinical trials for AB126 in acute ischemic stroke in late 2024. 

ILIAS Biologics: Developed the EXPLOR platform for loading large therapeutic payloads. Its candidate ILB-202 completed Phase I trials for inflammatory conditions in 2023. EXO Biologics: A clinical-stage Belgian company that secured Series A funding in April 2024 to scale manufacturing and clinical supply for its therapeutic pipeline. 

Coya Therapeutics: Developing COYA 201, a therapy leveraging regulatory T-cell (Treg) derived exosomes for neurodegenerative and autoimmune diseases. 

NurExone Biologic: In early 2025, the company acquired a master cell bank to ensure a scalable supply for treating spinal cord and acute injuries. 

Brexogen: Evaluating BRE-AD01 for atopic dermatitis and BRE-MI01 for myocardial infarction. Direct Biologics: Known for ExoFlo, an intravenous exosome therapy used in clinical trials for severe respiratory conditions.

A recent study led by Nicolás Cherñavsky, a researcher working with Heales, looked at whether exosomes and other extracellular particles from young pigs can be safely injected into rats. The goal was to check if this kind of cross-species approach triggers any immediate immune or toxic reaction. Over nine days, the treated animals showed normal behavior, normal weight gain, and no signs of inflammation or organ damage. Detailed tissue analyses confirmed the absence of acute toxicity in the liver, kidneys, and spleen. These results add to the growing body of research suggesting that exosomes from young organisms may cross species barriers without causing short-term immune reactions. This is an encouraging step for future longevity and rejuvenation studies.

Scientific consensus increasingly aligns with the theory that exosomes function as powerful signaling vectors capable of activating internal self-repair mechanisms. These nano-sized vesicles carry a specialized “cargo” of proteins, lipids, and microRNAs (miRNAs) that act as “biological instructions” to reprogram recipient cells toward a more youthful functional state. Research into heterochronic parabiosis has demonstrated that exosomes from young sources—specifically young plasma or stem cells—can reverse age-related phenotypes at molecular, mitochondrial, and physiological levels. By delivering “youth signals” like miR-144-3p and miR-455-3p, these vesicles can significantly downregulate senescence markers such as p16 and p21, while simultaneously upregulating genes associated with telomerase activity and mitochondrial health, effectively telling the cell to resume the repair processes characteristic of early age.

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The good news of the month- Mice living almost 5 years due to “telomere rivers”

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Telomere Rivers—immune-derived particles that transfer rejuvenating signals between cells. Produced by CD4⁺ T cells, they deliver telomeric DNA and systemically, reversing aging independently of telomerase. Unlike plasma-based or cell-limited effects, Rivers act as a coordinated, immune-driven rejuvenation system, suggesting T cells play a central role in maintaining youth and enabling transferable, organism-wide rejuvenation.

If it is true, this is the most important longevity news in years. However, this is only a preprint and there are some problems in the information given. To be followed.

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News of Heales and the longevity community

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Heales will organize the 8th Eurosymposium on healthy ageing / longevity.  It will be In Brussels and online : Wednesday, November 4th, till Friday, November 6th 2026.

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For more information

• Heales, Longevity Escape Velocity Foundation, International Longevity Alliance, Longecity, Lifespan.io and Aging biotech
• Heales Monthly Science News
• Heales YouTube channel
• Linkedin
• Contact us

If all the money spent on military budgets in every country had been devoted to biological research, the question of immortality, or at least eternal youth, would already have been resolved. (translation). Jean Rostand. French biologist, died in 1977.

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The Heales Journey: Celebrating 200 Editions of the Newsletter

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Looking back on the first edition  

As we reach the 200th edition of Death of the Death, it is worth briefly returning to the very first newsletter published in January 2009. Issue number 0 introduced the ambition of following scientific progress related to human longevity, with a focus on the possibility of delaying, and potentially overcoming, age-related mortality.

The newsletter presented the concept of longevity escape velocity, the hypothesis that if advances in biomedicine increase life expectancy faster than time subtracts it, each generation of progress could enable the next. At the time, this idea was emerging in research circles, and the newsletter aimed to make it accessible and track developments in fields such as regeneration, stem cells and aging mechanisms.

Sixteen years later, this 200th issue marks continuity rather than conclusion. We know more, we live on average longer, but maximal lifespan did not extend. The same questions remain open, the same scientific domains continue to evolve, and the initial objective persists: documenting the progress, challenges and perspectives of longevity science over time.

For this newsletter, we give you 200 pieces of information about longevity and about our organization. They are regrouped into 16 categories. It is impossible to be complete and objective, but we tried.

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Top Geroscience Scientist / Personalities

Famous people who lived 100+ years

Organizations for longevity

Heales at important conferences

Conferences from Heales

Heales in the Media

Activities supported by Heales

Sport & Exercise Related to Longevity

Foods that could help longevity

Social Factors That Support Longevity

Biomarkers of Longevity

Genes Related to Longevity

Longevity products

Lesser-known facts in aging research

Bad News (Long way to go)

Discoveries and Technologies

Top Geroscience Scientist / Personalities

1. Nir Barzilai. Medical Doctor Geneticist focused on aging. longevity genes. and interventions like metformin (Institute for Aging Research).  Advocate of the TAME project.
2. Irina Conboy. Her heterochronic parabiosis and plasma dilution studies revealed how systemic factors regulate aging and repair.
3. José Cordeiro.  Futurist and transhumanist author advocating radical life extension and the end of involuntary aging.
4. Aubrey de Grey. Biomedical gerontologist and revitalization biotechnology advocate (LEV Foundation). 
5. Greg Fahy.  Led human thymus regeneration studies (TRIIM), a landmark immunological aging trial.
6. Steven Horvath. Creator of the epigenetic clock, one of the most influential biomarkers in modern aging biology. His DNA methylation clocks are used globally to measure biological age and evaluate rejuvenation interventions.
7. Bryan Johnson. Entrepreneur running the Blueprint Project. an extreme data-driven experiment to slow and reverse biological aging in humans.
8. Brian Kennedy. Distinguished professor in healthy longevity and biochemistry; long-time leader in aging biology. 
9. Cynthia Kenyon.  Molecular biologist whose work with C. elegans revolutionized the genetics of aging.
10.  James L. Kirkland.  Director of the Mayo Clinic’s Robert and Arlene Kogod Center on Aging, pioneered senolytics and demonstrated that clearing senescent cells improves healthspan. His work helped establish dasatinib and quercetin as the first-generation senolytic compounds.
11.  Andrea Maier.  Prominent longevity medicine clinician and advocate for equitable geroscience translation. 
12.  João Pedro de Magalhães.  A leading computational geroscientist known for longevity genomics, comparative biology, and building the Human Ageing Genomic Resources (HAGR). His work spans AI-based drug discovery and the evolution of lifespan across species.
13.  Élie (Ilya) Metchnikoff. (†)  Often widely credited as the father of gerontology. He coined the term “gerontology” in 1903 to describe the emerging scientific study of aging and longevity. He was a Nobel Prize winner in 1908 for his work on immunity, and devoted his later research to the concept of human longevity. His work laid the groundwork for modern aging studies and centered on the hypothesis that aging was a result of chronic auto-intoxication by gut bacteria.
14.  Liz Parrish.  CEO of BioViva, known for pioneering the first self-administered gene therapy experiments aimed at reversing aging.
15.  David Sinclair.  Harvard biologist and popular author on mechanisms of aging (e.g., sirtuins/NAD pathways).
16.  Shinya Yamanaka.  Nobel Prize winning stem cell researcher who discovered induced pluripotent stem cells (iPSCs), foundational to cellular reprogramming and rejuvenation research.
17.  Alex Zhavoronkov. Founder and CEO of Insilico Medicine, is a leading figure in AI-driven drug discovery and computational geroscience. His work includes developing deep-learning-based aging clocks and multi-omics biomarkers for biological age.

Famous people who lived 100+ years 

18. Jeanne Calment (122) (†). Oldest woman ever.

19.  Jiroemon Kimura (116) (†). Oldest man ever.

20. Kane Tanaka (119) (†)

21. Sarah Knauss (119) (†)

22. Terentia (103) (†). Roman Empire. Widow of Cicero.

23. Edgar Morin (104). Oldest well-known philosopher.

24. Kirk Douglas (103) (†).

Organizations for longevity

 25. Google Calico. Focusing on both basic research and the translation of our discoveries into new interventions that can help people live healthier, and maybe longer, lives.

 26. Chan Zuckerberg Initiative (not “officially” longevity). It was founded in 2015 to help solve some of society’s toughest challenges — from eradicating disease and improving education to addressing the needs of our local communities.

27.  Altos Labs. Restore cell health and resilience through cellular rejuvenation programming to reverse disease, injury, and disabilities that can occur throughout life.

28.  BioViva Science (Liz Parrish). BioViva is committed to lengthening healthy human lifespans with AAV and CMV gene therapy (works with Integrated Health Systems.) 

29.  Longevity Escape Velocity Foundation (Aubrey de Grey). Exists to proactively identify and address the most challenging obstacles on the path to the widespread availability of genuinely effective treatments to prevent and reverse human age-related disease. 

30.  Rejuvenate Bio (George Church). Will make dogs (and later humans) “younger” by adding new DNA instructions to their bodies.

31.  Dog Aging Project. The goal of the Dog Aging Project is to understand how genes, lifestyle, and environment influence aging. We want to use that information to help people increase their healthspan, the period of life spent free from disease.

 32. National Institute of Aging (USA). Lead a broad scientific effort to understand the nature of aging and to extend healthy, active years of life. The Interventions Testing Program (ITP) is a peer-reviewed program designed to identify agents that extend the lifespan and health span in mice.

33.  Institut Pasteur de Lille, Founded in 2003 by Prof Miroslav Radman and Prof Marija Alačević, is a research center, which mobilizes 34 research teams and aims to decipher the essential physiopathological mechanisms of the most impacting diseases,  particularly infectious ones, to understand these diseases, slow down their development and imagine the treatments of tomorrow.

34.  Salk Institute (Juan Carlos Izpisua Belmonte). The Institute is an independent nonprofit organization and architectural landmark: small by choice, intimate by nature, and fearless in the face of any challenge. Be it cancer or Alzheimer’s, aging, or diabetes.

35.  Buck Institute for Research on Aging, Mission is to end the threat of age-related disease for this and future generations.

36.  Glenn Consortium for Research in Aging (11 centers). To extend the healthy years of life through research on mechanisms of biology that govern normal human aging and its related physiological decline, to translate research into interventions.

 37. Life Biosciences (David Sinclair and Nir Barzilai). Research and development on therapeutics for human health. (See also Elixir Pharmaceuticals and Sirtris Pharmaceutical)

 38. Longevity Research Institute (Joe Betts-Lacroix, Sarah Constantin, Jaan Tallinn). A health-span-expanding treatment for humans would prevent years of severe illness for billions of people. Plan to design, fund, and launch animal lifespan studies for the most promising longevity interventions.

 39. Retro Biosciences. The mission is to add 10 years to a healthy human lifespan They are starting with cellular reprogramming, autophagy & plasma-inspired therapeutics.

40.  International Longevity Alliance. Promotes longevity research and advocacy from the grassroots to the international level. It includes over 75 non-profit associations working in over 65 countries.

41.  Hevolution. Funds efforts to extend healthy human lifespan and understand the processes of aging.

42.  Lifespan Research Institute. Raising funds and awareness for scientific work addressing of the aging process and working directly on research projects.

43.  XPrize Healthspan. Prize of $ 101 million for innovative therapies that restore muscle, cognitive, and immune function by a minimum of 10 years to make healthy aging possible for everyone.

Heales’ presence at certain conferences and activities

 44. Web2Day. L’homme qui vivra 100 ans est déjà né. 2015. 

45.  TEDxULB “Eternal Life: Are We There Yet?”. TEDx talk of Didier Coeurnelle
2016, Université libre de Bruxelles (Belgium)

46. 2017. Longévité : un vieux rêve de l’humanité, peut-être le plus beau | Didier Coeurnelle | TEDxBelfort

47.  “Afternoon of Study: Aging”. Invited speaker / discussant 9 December 2019, Brussels (healthy life expectancy; organized by the Belgian Federal Public Service  Social Security)

48.  Longevity Projects for Africa. Conference presentation 2019.

 49. TransVision 2022, Paris, En route vers l’immortalité.

50.  Longevity Summit Dublin. Speaker in 2022, 2023 and 2024

51. TransVision Utrecht 2024. Heales oral presentation

52. TransVision Abidjan 2025. Longévité, égalité, fraternité.

Conferences from Heales

 53. The 1st Eurosymposium on Healthy Ageing (EHA) was held in 2012. The talks spanning 3 days included topics like- Biology of aging is now a robust science, and it can extend healthy lives, Concrete examples of research and innovation to extend healthy lives, and meeting among stakeholders: building the innovations together

 54. The 2nd Eurosymposium on Healthy Ageing was held on 1st and 2nd October 2014. 

 55. The 3rd Eurosymposium on Healthy Ageing was held on 29th and 30th September and 1st October 2016

 56. The 4th Eurosymposium on Healthy Ageing was held on 7th-9th November 2018

57.  5th Eurosymposium on Healthy Ageing, was held on October 1, 2020 on zoom. How to Significantly Extend Healthy Lifespan. It adopted a Declaration on Biomarkers and Clinical Tests.

58.  February 11, 2021. Conference and workshops. Clarifying whether and to what degree the current anti-aging approaches work in mice or people.

59.  Virtual Conference On Big Data, A.I. and Healthy Longevity. How to progress faster and better for all scientists? Thursday, September 9, 2021

60.  6th Eurosymposium on Healthy Ageing (EHA). This meeting was held online on Friday, 25th, and Saturday, 26th November 2022. It adopted a Declaration for Radical Healthspan Extension:  After Covid times, rejuvenation times.

61.  Sharing Health Data and AI Insights for Longevity in Europe and Around the World. The conference explored the latest advancements in AI and Big Data within the realm of longevity research. February 29th, 2024. It adopted a Declaration on Sharing Health Data and Using AI for Healthy Longevity.

 62. 7th Eurosymposium on Healthy Ageing. Friday, November 22nd, and Saturday, November 23rd 2024,   “Sharing Health Data and AI Insights for Longevity in Europe”

Heales in the Media

 63. 2014: Sciences humaines: Immortalité : the opinion of Didier Coeurnelle

 64. 2014: RTL Belgium, Controverses « Bientôt tous immortels ?” Didier Coeurnelle

 65. 2017: Pour augmenter la longévité humaine. Didier Coeurnelle, Long Long Life

 66. 2018: interview, Belgian radio RTBF.

67.  2018: Belgian TV, RTBF, interview with Aubrey de Grey and Didier Coeurnelle, among others.

68.  2025: Sven Bulterijs Dutch journal Interview on Organ-Specific Aging Clocks (Het Nieuwsblad)

 69. 2025: Sven Bulterijs Interview on Life Extension Following Remarks by Putin and Xi (VRT News)

Activities supported by Heales

70.  Leucadia Therapeutics. Ferret study related to Alzheimer disease. Theory that reduced aperture sizes due to ossification leads to behavioral and brain morphological changes.

71.  A study on older rats. To test longevity after injecting plasma fraction with the working name ‘Elixir’ into old rats (6 experimental old rats + 6 control old rats). This experiment was under the direction of Professor Harold Katcher in Mumbai, in collaboration with Heales. 

72.  Another study on older rats. To test longevity after plasma transfusion of young rats (9 tested old rats + 8 control old rats). This experiment was under the direction of Professor Rodolfo Goya at the Institute of Biochemical Research in Argentina, in collaboration with Heales.

73.  DataBeta Test Project to compare epigenetic markers after testing different supplements, trying different diets and exercise programs.

 74. Project with Longeavus Technologies. Combination of Known and Putative Longevity Therapeutics for Radical Life Extension in Mice

75.  LongevityGPT is an AI tool that uses domain-specific retrieval and advanced AI techniques to help answer longevity and genetics research questions by integrating scientific databases and improving the accuracy of biomedical information retrieval. The main scientist behind this project is Anton Kulaga.

76.  Project with Nicolas Chernavsky replicate one of the experiments of Harold Katcher’s study, which demonstrated the rejuvenation of old rats using extracellular particles derived from young pigs’ blood plasma.

77.  The Longevity Escape Velocity Foundation received a €200,000 donation from Didier Coeurnelle, with up to an additional €200,000 pledged contingent on matching gifts raised by October 31, 2024. The funding supported pre-study pilot work for the next phase of the Robust Mouse Rejuvenation project, as the first phase, which began in February 2023, has been completed.

Sport & Exercise Related to Longevity

78. Regular walking

79. Strength training

80. High-intensity interval training (HIIT)

81. Cycling

82. Swimming

83. Balance training

84. Flexibility / mobility work

85. Daily physical activity (non-exercise movement)

86. Cardiorespiratory fitness

87. Consistency over intensity

Foods that could help longevity 

88. Olive oil (part of the Mediterranean diet)

89. Fatty fish (omega-3 rich) (part of the Okinawan diet)

90. Pomegranate

91. Nuts

92. Leafy green vegetables

93. Berries

94. Fermented foods (part of the Japanese diet)

95. Passion fruit

96. Green tea and coffee

97. Dark chocolate (high cocoa)

Social Factors That Support Longevity 

98.  Strong social ties

99. Regular social interaction

100. Believing in god

101. Intergenerational relationships

102. Being married or partnered (at least for men)

103. Cultural engagement

104. Feeling useful to others

Biomarkers of Longevity 

105. Biological age (epigenetic age)

106. Resting heart rate

107. VO₂ max

108. Grip strength

109. Fasting glucose

110. HbA1c

111. Inflammatory markers (e.g. CRP)

112. LDL/HDL cholesterol ratio

113. Blood pressure

114. Muscle mass

Genes Related to Longevity 

115. FOXO3

116. APOE

117. SIRT1

118. SIRT6

119. IGF-1 pathway genes

120. mTOR pathway genes

121. TP53

122. CETP

123. KLOTHO

124.  LMNA

Longevity products: 

125.  NMN (Nicotinamide Mononucleotide)  NAD⁺ precursor for cellular energy and aging support.

126.  NR (Nicotinamide Riboside) another NAD⁺ precursor supporting mitochondrial health

127.  Resveratrol polyphenol thought to activate longevity pathways.

128.  Fisetin natural senolytic (clears senescent cells).

 129. Quercetin antioxidant often paired with fisetin for senolysis.

130. Spermidine supports autophagy and cellular renewal.

131.  Astaxanthin antioxidant with mitochondrial and anti-aging support.

132.  Coenzyme Q10 (CoQ10) supports energy production and cardiovascular health. 

133.  Curcumin anti-inflammatory antioxidant.

 134.  Pterostilbene resveratrol-like antioxidant with higher bioavailability.

135. Rapamycin (Sirolimus) mTOR inhibitor shown to extend lifespan in animal studies

136. Metformin diabetes drug with potential longevity benefits.

137.  Senolytic Drug Combinations (e.g., Dasatinib + Quercetin) targeted clearance of senescent cells.

138.  GLP-1 Receptor Agonists (e.g., semaglutide) diabetes/weight-loss drugs with potential systemic aging benefits.

139.  SGLT2 Inhibitors cardio-renal protective drugs with possible longevity implications

140. Omega-3 Fatty Acids (fish oil DHA/EPA) cardiovascular and anti-inflammatory effects tied to healthy aging.

141.  Vitamin D (plus Vitamin K2) supports bone health, immune function, and cellular longevity markers. 

142.  Alpha-Ketoglutarate (AKG) metabolic intermediate linked to reduced inflammation and energy metabolism support.

143.  Longevity Complete™ Supplement Blends multi-ingredient commercial products combining NAD⁺ precursors, CoQ10, antioxidants, and other longevity agents. 

Lesser-known facts in aging research

144.  Sharks get cancer less often than other species, probably because of a slow mutation rate.

145.  Some jellyfish can revert to their juvenile form repeatedly, essentially “aging backward.”

146.  Sleep timing affects your lifespan  people with irregular sleep patterns age faster.

147.  Extreme cold exposure may trigger longevity pathways in humans and animals.

148. Certain protein-restricted diets without calorie reduction can extend lifespan.

149. Your skin age can differ drastically from your biological age internally.

150. Blue zones have unique social habits that may be as important as diet.

151. Some long-lived species tend to have very stable blood sugar levels naturally.

152. Telomere shortening isn’t the only clock of aging  other protective DNA loops exist.

153.  High cardiovascular fitness can add more years than diet alone.

154. Some long-lived rodents resist cancer almost completely.

155. Environmental enrichment can slow brain aging in mammals.

156. Certain RNA molecules may influence longevity independently of DNA.

157.  Mitochondrial transplantation in lab animals can improve tissue function.

158. Some animals defy the “size vs lifespan” rule  tiny bats can live 40+ years.

159. Some turtles can survive without oxygen for hours by slowing their metabolism dramatically.

160. Intermittent mild heat exposure (like sauna use) is linked to longer life in humans.

161. Long-lived whales accumulate fewer harmful mutations in their DNA over time.

162. Certain cavefish live longer than surface fish, despite harsh conditions.

163. Regular social interaction may protect telomeres and slow cellular aging.  (More in exercise part) 

Bad News (Long way to go)

164. No mouse in the world today is older than 4 years (and it was slightly better in the past). 

165. No human is older than 116 years (and the oldest person ever, Jeanne Calment, lived 6 years more). 

166. Pollution of microplastics is increasing fast and going in our brains. We do not know how to stop this.

167. To live longer, there is still nothing really better than what your parents told you. 

168. Eroom’s law. Creating new drugs is becoming slower and more expensive.

169. During Covid times, life expectancy in the world decreased for the first time since 70 years, despite more money being used for health than ever.

170. Life expectancy in the US is stagnating despite the USA spending more money for health than any other country and having many of the best scientists inthe world.

171. The prospect for (biological) immortality appears to be close since more than 60 years, wrongly until now.

172. Life expectancy is not rising faster during the 21st century than during the 20th century.

173. Failure of Alzheimer drugs and therapies in humans is close from 100 %.

Discoveries and Technologies

174.  mTOR inhibition extends lifespan (rapamycin effects across species)

175.  Senescent cells drive aging and their removal improves healthspan

 176. Senolytic drugs selectively eliminate senescent cells

 177. Epigenetic clocks accurately measure biological age

 178. Partial cellular reprogramming can reverse aging markers without loss of identity

 179. Inflammaging identified as a central mechanism of age-related diseases

 180. Mitochondrial dysfunction as a root cause of aging

 181. Stem cell exhaustion recognized as a hallmark of aging

182.  Gut microbiome influences aging and lifespan

 183. Caloric restriction mimetics identified (e.g. metformin, rapamycin)

184.  Proteostasis collapse linked to neurodegeneration and aging

185.  DNA damage accumulation and repair decline tied to aging speed

 186. Immune system aging (immunosenescence) mapped and quantified

187.  Circulating “youthful” blood factors affect aging (heterochronic parabiosis)

 188. Sex differences in aging biology formally characterized

189.  Aging defined as a treatable biological process, not just a risk factor

190.  Aging can be partially reversed by cellular reprogramming (Yamanaka factors)

191. CRISPR gene editing (and other gene therapies)

192. AI-driven drug discovery

193. Single-cell sequencing

194. Organoids

195. Wearable health trackers

196. Digital twins in medicine

197. Stem cell therapies

198. Advanced diagnostics (multi-omics)

199. Robotics for elderly care

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The good news of the month.

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200.  We live longer than ever during the whole history of Humanity. On average, 73 years in the world. 85,5 years in Hong Kong.

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For more information

• Heales, Longevity Escape Velocity Foundation, International Longevity Alliance, Longecity, and Lifespan.io 
• Heales Monthly Science News
• Heales YouTube channel
• Contact us

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The next revolution in biology isn’t reading life’s code – it’s writing it. (…) Writing DNA holds even greater promise – the potential to cure any disease. Andrew Hesel. October 23, 2025. Source.

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This month’s theme: Mitochondria

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The Powerhouse and the Clock: How Mitochondria Shape Aging

About 2,3 billion years ago, an organism absorbed a bacterium that would become mitochondria. This was, for animals, the most successful symbiosis in the history of life. Nowadays, mitochondria, often called the “powerhouses” of the cell, do far more than just produce energy. These small but mighty organelles generate ATP—the essential molecule that fuels nearly every cellular process—while also regulating calcium balance, apoptosis (programmed cell death), and key metabolic pathways. What makes them especially intriguing is that they contain their own DNA, separate from the cell’s nucleus, which makes them uniquely vulnerable to damage over time.

Mitochondria undergo wear and tear that affects their ability to function properly.

1. Damaged DNA, Damaged Cells

Mitochondria possess their own DNA (mtDNA), separate from the cell’s nuclear DNA. Unlike nuclear DNA, mtDNA lacks the robust protective histones and repair systems that guard against damage. This makes it particularly vulnerable to oxidative stress — the constant bombardment of reactive molecules produced during energy generation. Over time, oxidative stress introduces mutations into mtDNA, disrupting the genes responsible for key components of the electron transport chain. 

2. The ROS Paradox

Reactive oxygen species (ROS) are a double-edged sword in biology. On one hand, they are natural byproducts of mitochondrial respiration and play important signaling roles in cell adaptation, repair, and immune defense. In youthful, healthy cells, low levels of ROS act as beneficial messengers that fine-tune metabolism and trigger protective antioxidant responses — a process known as mitohormesis. However, as mitochondria age and become less efficient, they produce excessive ROS that overwhelm the cell’s antioxidant defenses. This oxidative overload damages DNA, lipids, and proteins, impairing cellular structures and signaling pathways. Over time, these molecular injuries accumulate, accelerating tissue degeneration and contributing to diseases such as Alzheimer’s, Parkinson’s, and cardiovascular decline.

3. Out with the Old — or Not

Cells have a sophisticated quality-control system to maintain mitochondrial health, and a central part of this system is mitophagy — the targeted degradation and recycling of damaged mitochondria. Under normal conditions, faulty mitochondria are tagged and removed to make way for new, fully functional ones. However, with age, this self-renewal process slows down. The mechanisms that detect and dispose of defective mitochondria become less responsive, leading to the accumulation of dysfunctional organelles within the cell. These impaired mitochondria not only produce less energy but also leak harmful molecules that exacerbate oxidative stress. The gradual buildup of damaged mitochondria is a critical contributor to the decline in cellular vitality and resilience seen in aging tissues.

4. Inflammation from Within

When mitochondria become damaged beyond repair, they can release fragments of their own DNA and proteins into the cytoplasm or bloodstream. Interestingly, because mitochondrial DNA evolved from ancient bacteria, the immune system often mistakes it for a foreign invader. Over time, this persistent low-level inflammation — termed inflammaging — becomes a major driver of age-related tissue damage and chronic diseases, including atherosclerosis, diabetes, and neurodegeneration. In this way, failing mitochondria act not only as victims of cellular aging but also as active participants that amplify the inflammatory processes underlying it.

Focus on Mitochondria for anti-aging interventions

Recent advances in nanoengineered mitochondria (biohybrid systems that integrate isolated mitochondria with functional nanomaterials) may soon allow us to repair and enhance them, opening new paths toward better health and longevity. Unlike conventional mitochondrial transplantation, which simply transfers healthy mitochondria to damaged tissues, these nano-biohybrids enhance organelle stability, boost ATP production, and enable targeted delivery. Preclinical studies show promising results in cardiovascular, neurodegenerative, and age-related disorders, including breakthroughs where engineered mitochondria prevented intervertebral disc degeneration in rats by restoring mitochondrial function and modulating key signaling pathways such as mtDNA/SPARC-STING. By bridging materials science and mitochondrial biology, nanoengineered mitochondria could emerge as a powerful new tool in longevity therapeutics, revitalizing energy metabolism at its source.

Several strategies are being developed to counteract mitochondrial decline. One major approach involves antioxidants targeted specifically to mitochondria, such as MitoQ and MitoVitE, which aim to neutralize excess ROS and reduce oxidative damage. Another focuses on stimulating mitochondrial biogenesis, often through pathways like PGC-1α activation; exercise remains the best-validated method for this, but pharmacological enhancers are under investigation. Therapies that enhance mitophagy — the selective clearance of damaged mitochondria — are also of growing interest, as impaired mitophagy is a hallmark of aging cells. Other approaches include modulating mitochondrial metabolism, for instance by increasing NAD⁺ levels, which support mitochondrial redox reactions and energy metabolism.

Among the most promising experimental therapies is Elamipretide (SS-31), a mitochondria-targeted peptide that binds to cardiolipin in the inner mitochondrial membrane, stabilizing its structure and improving the efficiency of the electron transport chain. In preclinical studies, Elamipretide improved muscle endurance, cardiac function, and mitochondrial energetics, and early human trials have shown enhanced ATP production in older adults. 

Collectively, these mitochondrial-targeted interventions represent one of the most active areas in aging research. While most remain at early stages of development, they illustrate a broader therapeutic shift—from treating single age-related diseases to addressing the underlying cellular dysfunctions that drive aging itself. Lifestyle interventions such as exercise and caloric moderation remain the most reliable means to preserve mitochondrial health, but ongoing trials of peptides like Elamipretide, NAD⁺ precursors, and mitophagy activators could soon expand the toolkit for promoting healthier aging. The field’s success will depend on overcoming key challenges such as long-term safety, delivery specificity, and demonstrating true improvements in human healthspan rather than just cellular biomarkers.

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The good news of the month. Human cells reduce senescence markers in aged macaques.

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In a study published in Cell (September 4, 2025), scientists demonstrated that infusing senescence-resistant human mesenchymal progenitor cells (SRCs) into aged macaques significantly reduced markers of aging and improved cognitive, bone, and reproductive function.

This is very promising. It is hoped that those monkeys will live long enough to demonstrate that the progenitor cells prolong the healthy lifespan.

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For more information

• Heales, Longevity Escape Velocity Foundation, International Longevity Alliance, Longecity, and Lifespan.io 
• Heales Monthly Science News
• Heales YouTube channel
• Contact us
•  S. L. Morales-Rosales et al, 2020

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In a few years, with the development of biotechnology, human organs can be constantly transplanted so that (people) can live younger and younger, and even become immortal (Vladimir Putin). The prediction is that in this century humans may live to 150 years old (Xi Jinping). Informal dialog between the two heads of state during an international conference in Beijing, September 3, 2025.  Hoping that these discussions spread to the most democratic states. Source.

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This month’s theme: Compounds for Longevity

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Introduction

Most humans would love a pill without negative effects and largely extending healthy life. Sadly, until today, there is no product making a far longer healthier life possible for humans. This newsletter is about the compounds for longevity that are the most studied at the moment.

Metformin

A widely prescribed drug for type 2 diabetes has garnered significant interest for its potential role in promoting longevity and healthy aging. Beyond its glucose-lowering effects, metformin influences multiple cellular pathways associated with aging, including activation of AMPK, inhibition of mTOR, reduction of oxidative stress, and improvement of mitochondrial function. These actions collectively mimic some of the effects of caloric restriction, a well-established intervention for lifespan extension in model organisms. Preclinical studies in mice and other animals have shown that metformin can extend healthspan, reduce the incidence of age-related diseases such as cancer and cardiovascular disease, and improve metabolic and cognitive function. Observational studies in humans, particularly among individuals with diabetes, suggest that metformin use is associated with lower all-cause mortality and a reduced risk of age-related conditions compared to non-users. However, randomized controlled trials specifically evaluating longevity in non-diabetic populations are sadly not yet startedongoing, most notably the TAME (Targeting Aging with Metformin) trial.

mTOR Inhibitors

Rapamycin and its analogs (rapalogs such as everolimus, temsirolimus, and ridaforolimus), are among the most validated pharmacological interventions for extending lifespan across model organisms and are now showing promise in humans. These drugs primarily inhibit mTORC1, slowing growth and enhancing stress resistance, but dose and context are critical: while moderate dosing improves longevity, excessive inhibition can impair fertility, immunity, or metabolism. Beyond aging, rapalogs are being investigated in oncology, reproductive health (reducing endometriosis progression and preserving ovarian function), and neuro-ophthalmology (protecting against glaucoma through autophagy). Recent advances such as RapaLinks—next-generation compounds targeting both mTORC1 and mTORC2—offer stronger, more durable inhibition and may overcome drug resistance seen in cancer. Overall, rapalogs remain central to longevity research, with evidence pointing to sex-specific, tissue-specific, and dose-dependent benefits that make them promising, though nuanced, tools for extending healthspan.

NMN

By replenishing NAD⁺, NMN has been shown in animal studies to improve insulin sensitivity, vascular function, and cognitive performance, while extending healthspan and in some cases lifespan. Recent work highlights the role of NMN transporters and extracellular NAMPT in systemic aging regulation, leading to the “NAD World 3.0” framework that emphasizes multi-tissue communication in longevity control. NMN supplementation has also been found to restore NAD⁺ levels and reduce inflammation through pathways like TLR4/NF-κB/MAPK, suggesting protective effects against age-related ovarian decline. Human clinical data remain limited but show that NMN is generally safe and well-tolerated, capable of raising blood NAD⁺ levels. Overall, NMN represents a leading candidate among NAD⁺ boosters, with strong mechanistic rationale and encouraging early results, but confirmation from large-scale clinical trials is still needed.

Senolytics

Dasatinib combined with quercetin (D+Q) is one of the most studied senolytic strategies in the context of longevity. Aging is partly driven by the accumulation of senescent cells, which stop dividing but secrete pro-inflammatory factors known as the senescence-associated secretory phenotype (SASP), contributing to tissue dysfunction, chronic inflammation, and age-related diseases. Dasatinib, a tyrosine kinase inhibitor originally used in leukemia, selectively induces apoptosis in senescent preadipocytes and endothelial cells, while quercetin, a natural flavonoid, targets senescent endothelial cells and fibroblasts. Together, they provide a broader spectrum of senescent cell clearance than either agent alone. Preclinical studies in mice have shown that intermittent administration of D+Q reduces senescent cell burden in fat, liver, and kidney, improves physical function such as grip strength and endurance, reduces age-related pathologies, including fibrosis and atherosclerosis, and enhances healthspan. Early human pilot studies, including in patients with idiopathic pulmonary fibrosis and age-related dysfunction, suggest that intermittent D+Q therapy can decrease senescence markers and systemic inflammation, potentially improving physical performance and tissue function. While these results are promising, long-term effects on human lifespan and healthspan are still unknown, and dasatinib carries potential serious side effects, so its use requires medical supervision.

GLP-1 

Glucagon-like peptide-1 is a hormone primarily known for its role in glucose metabolism and appetite regulation, but emerging evidence suggests it may also influence longevity and healthy aging. GLP-1 receptor agonists, such as liraglutide and semaglutide, improve insulin sensitivity, reduce systemic inflammation, and promote weight loss, all of which are key factors in mitigating age-related metabolic and cardiovascular diseases. Beyond metabolic effects, GLP-1 signaling has been shown in preclinical studies to protect against oxidative stress, improve endothelial function, and enhance mitochondrial health, mechanisms that are closely linked to cellular aging. Animal studies indicate that GLP-1 receptor activation can improve cardiovascular outcomes, reduce neurodegeneration, and extend healthspan. Human observational and clinical data suggest potential benefits in reducing the incidence of type 2 diabetes, cardiovascular events, and possibly cognitive decline. Although direct evidence for lifespan extension in humans is still limited, GLP-1–based therapies appear to target several hallmarks of aging, making them a promising avenue for promoting longevity and metabolic resilience.

Glucosamine

This naturally occurring amino sugar commonly used as a dietary supplement for joint health, has recently drawn attention for its potential role in longevity. Beyond its effects on cartilage and osteoarthritis, preclinical studies suggest that glucosamine may influence aging through several mechanisms, including reducing chronic inflammation, modulating nutrient-sensing pathways such as mTOR and AMPK, and promoting autophagy, all of which are linked to extended healthspan. Epidemiological studies, particularly large cohort studies in humans, have observed associations between regular glucosamine supplementation and lower overall mortality, reduced risk of cardiovascular disease, and decreased incidence of some age-related diseases. While the exact mechanisms are still being elucidated, glucosamine appears to act as a mild caloric restriction mimetic, supporting cellular homeostasis and potentially contributing to healthier aging. Its safety profile is generally favorable, making it an attractive candidate for longevity research, though randomized controlled trials specifically targeting aging outcomes are still limited.

Lesser-known therapeutic compounds

SGLT2 inhibitors (ex : dapagliflozin, canagliflozin)

SGLT2 inhibitors, such as dapagliflozin and canagliflozin, offer significant benefits for kidney, heart, and metabolic health. These medications help improve glucose control while also reducing cardiovascular and renal risks. Interestingly, canagliflozin has even been shown to extend lifespan in male mice but not female and to slow the development of age-related lesions in the heart, kidneys, liver, and adrenal glands in genetically heterogeneous male mice. 

Urolithin A

Urolithin A is a natural mitophagy activator that helps promote the removal of damaged mitochondria, thereby improving cellular energy and health. It is well tolerated in humans and has shown promising effects on mitochondrial function in clinical studies. Ongoing trials are investigating its potential in Alzheimer’s disease, where it has been shown to restore mitophagy and lysosomal function (which involves the cell’s “recycling centers” that break down and clear waste, helping maintain healthy cellular homeostasis and neuronal function).

TNIK 

TNIK(Traf2- and Nck-interacting kinase) inhibitors are an emerging class of compounds being explored for longevity because of their role in pathways linked to cellular senescence, inflammation, and fibrosis. Recent AI-driven and robotics-lab studies identified the inhibitor INS018_055 which reduced markers of senescence such as the senescence-associated secretory phenotype (SASP) while preserving healthy cell function. Early clinical data in patients with idiopathic pulmonary fibrosis, a disease strongly tied to aging, showed that TNIK inhibition was safe and improved lung function. Howeverthere is still no evidence that TNIK inhibitors extend lifespan in animal models or humans, and long-term safety data remain limited.

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The good news of the month. GLP-1 Receptor Agonist Use Reduces Heart Failure Mortality.

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Some longevists affirm that GLP-1 can be considered the first real longevity drug useful for most people. Actually, it could be useful because most people have an unbalanced diet.

GLP-1 receptor agonist has various positive effects. It was recently established that patients initiating semaglutide or tirzepatide had a more than 40% lower risk of hospitalization for heart failure or all-cause mortality compared with sitagliptin (a glucose-lowering drug with no effect on heart failure end points).

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For more information

• Heales, Longevity Escape Velocity Foundation, International Longevity Alliance, Longecity, and Lifespan.io 
• Heales Monthly Science News
• Heales YouTube channel
• Contact us

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If we’re being more open-minded about accepting new weird ideas, can I suggest anti-aging research? Aging is a humanitarian disaster that kills as many people as WW2 every two years, and even before killing debilitates people and burdens social systems and families. Let’s end it. Vitalik Buterin, co-founder of Ethereum (source)

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This month’s theme: Best Resources for Information about Longevity Research

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Online resources play a crucial role in advancing the field of longevity by providing timely access to essential information such as upcoming conference dates, the latest research findings, and updates on emerging therapies and drug developments.

These platforms enable researchers, clinicians, and enthusiasts to stay connected with the rapidly evolving science of aging, ensuring they are informed about breakthroughs, clinical trials, and regulatory changes. With longevity being a multidisciplinary and global field, this constant stream of information fosters collaboration across disciplines and borders, enabling scientists, healthcare providers, investors, and the public to make informed decisions. In a field as dynamic and interdisciplinary as longevity, online resources are not just helpful—they are essential for progress.

AgingBiotech.info

It is a helpful and well-organized website that gives clear, reliable information about the growing field of aging and longevity biotechnology. Its main goal is to collect everything important that’s happening in the field and put it all in one easy-to-use place. The site focuses on companies and efforts that are working to turn scientific discoveries about aging into real products and treatments that can help people live longer and healthier lives. It helps users keep up with what’s going on in this space by organizing useful public information into big, sortable tables. These include things like companies working on aging therapies, funding sources, clinical trials, and more. Each table has links.

AgingBiotech.info was created and is maintained by Karl Pfleger, a longevity activist and computer scientist. The site has one main weakness: it is not well-known. 

This website is especially helpful for people who want a clear view of the aging biotech world without having to dig through tons of scattered sources. Whether you’re a researcher, investor, student, or someone just curious about the future of health, the site is a great starting point.

AgingBiotech.info is non-profit and doesn’t make money from ads, sponsorships, or subscriptions. It doesn’t even accept donations. Everything is offered freely, and no company can pay to be listed or promoted. The site focuses on information and usefulness, so it may look plain, but it’s full of value.

Because the main data is shown through Google Sheets, it works best on computers.

For individuals new to the aging field, the site recommends starting with the “About” and “Motivations” sections to gain an understanding of why aging research is important. It also offers a list of top books, blogs, podcasts, and videos to help people learn more. Busy people may prefer listening to audiobooks or podcasts to quickly grasp the key ideas.

To stay up to date with new additions to the site, users can follow AgingBiotech.info on  Twitter, LinkedIn, & Reddit /r/longevityAgingBiotech.info is organized into many clearly labeled sections to help users quickly find specific information about the longevity biotech field. Here’s some of what you can find

• Motivations – Covers the reasons why slowing or reversing aging is important, scientifically possible, morally urgent, and economically promising.

• Objections – Addresses common criticisms or concerns about the idea of interfering with aging.

• Opportunities – Highlights areas in longevity biotech where there is room for growth, innovation, and investment.

• Companies – One of the most detailed sections, listing longevity biotech companies with info such as their focus, status, and links.

• Nonprofits – Lists nonprofit organizations involved in aging research, advocacy, or public education.

• Jobs – A table listing job openings in longevity biotech companies for people looking to work in the field.

• Therapeutics – Focuses on treatments and drugs in development or already available that aim to slow or reverse aging.

• Trials – Lists clinical trials relevant to longevity and aging-related therapies, with links to further info.

• Databases – Links to external data sources and organized collections relevant to aging biotech.

• People – Profiles key individuals in the field—founders, researchers, investors, and thought leaders.

Fight aging

Fight Aging! is a website and blog that shares information about how science and medicine might one day slow down, stop, or even reverse aging. It was started in 2004 by a person named Reason (his real name!), who cares deeply about helping people live longer, healthier lives. The main idea behind Fight Aging! is that aging is not just something we have to endure. Like other medical problems, it may be treatable in the future. The website wants more people to know about this, support the science, and help it grow faster.

The site focuses on three main goals:

1. Teach people about the latest discoveries in aging and longevity science.

2. Make it easier to find trustworthy information on how to live a longer, healthier life.

3. Support research by encouraging more funding and attention for new anti-aging treatments.

The website shares blog posts, research news, and updates from the longevity field. It’s not a commercial site, so it doesn’t run ads or accept money to promote products. It’s simply there to help move the science of healthy aging forward and to inspire others to care about the future of aging and health. It informs regularly and more completely than any other source specialized in longevity news.

Three other good general websites

Longecity (formerly the Immortality Institute) is an international, not-for-profit, membership-based organization of advocacy and research for unlimited lifespans. It has been, for decades, a place of dialogue through its many forums. 

Aside from scientific and activist information and discussion between members, there is also a large community of users of longevity products and therapies. It is an interesting meeting place for biohackers.

Longevity technology is a website of good scientific information about research for longevity, with some detailed articles.

The Lifespan Research Institute is the best place for videos for popularization and general information.

The list could be longer. For example, many organizations like the International Longevity Alliance, the Global Healthspan Policy Institute have websites with general information.

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The good news of the month. Largest-ever human imaging study completed

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The UK Biobank, a public project, reached the milestone of 100,000 people examined. It collected in 15 years more than one billion images from those volunteers, including genomics, blood biomarkers, lifestyle information, and clinical records. 

The information is easily available for scientists worldwide. This gigantic source of information will be useful for scientists specialized in longevity and in many other fields.

Concerning the sharing of health data, this month also saw the birth of a new project: the International Health Data Space Initiative (IHDSI). Their final goal is to have something similar to the European Health Data Space, but at the world level.

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For more information

• Heales, Longevity Escape Velocity Foundation, International Longevity Alliance, Longecity, and Lifespan.io 
• Heales Monthly Science News
• Heales YouTube channel
• Contact us

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Faced with the changes longer lives will bring, humans will not miss the Reaper and construct one to solve their problems. Just as with our larger cities, we don’t remix the (clean) water (with sewage water) to bring back cholera. Why die? Kurzgesagt (studio d’animation allemand).

This month’s theme: Stem Cells and Aging

Stem cells are special cells in the body that have the unique ability to develop into many different types of cells, such as muscle, nerve, or blood cells. Unlike most cells, stem cells can divide and make copies of themselves over long periods. This makes them essential for growth, development, and repair in the body. There are different types of stem cells, including embryonic stem cells, which can turn into any cell type, and adult stem cells, which are more limited but still help maintain and repair specific tissues. Scientists can also create induced pluripotent stem cells by reprogramming adult cells to act like embryonic stem cells.

How does aging affect the stem cells?

Aging significantly impairs the function and regenerative capacity of stem cells, which are vital for maintaining tissue homeostasis throughout life. One of the primary effects of aging is stem cell exhaustion, characterized by a decline in the number of active stem cells and their ability to self-renew and differentiate. Over time, stem cells accumulate DNA damage due to environmental stressors and diminished repair mechanisms, while telomere shortening limits their replicative potential, pushing them toward senescence or apoptosis (programmed death cell). Simultaneously, epigenetic alterations, such as changes in DNA methylation and histone modifications, disrupt gene regulation. Aging also affects the stem cell niche, the specialized microenvironment that provides signals for their maintenance. These signals weaken or shift toward pro-inflammatory cues, further compromising stem cell activity. 

In addition, aged stem cells exhibit mitochondrial dysfunction and a shift in cellular metabolism, resulting in increased reactive oxygen species (ROS) and oxidative stress, which further damage cellular components. Functionally, these changes lead to reduced tissue regeneration, impaired immune responses, and increased risk of degenerative diseases and cancers. For example, aging hematopoietic stem cells tend to produce more myeloid cells and fewer lymphoid cells, weakening adaptive immunity and promoting clonal hematopoiesis.

The Hayflick limit refers to the finite number of times a normal somatic cell can divide before entering senescence, typically due to progressive telomere shortening. While this limit applies strictly to most somatic cells, stem cells present a more nuanced case. Adult stem cells, such as hematopoietic or mesenchymal stem cells, do exhibit a form of the Hayflick limit but can divide more extensively than typical somatic cells. This is largely because they express higher levels of telomerase, the enzyme responsible for maintaining telomere length. However, this telomerase activity is not unlimited, and over time, these adult stem cells also experience telomere attrition and eventually enter senescence. In contrast, embryonic stem cells and induced pluripotent stem cells (iPSCs) possess high levels of telomerase. They can maintain their telomere length indefinitely, allowing them to divide without a limit under optimal conditions. This distinction underlies their unique regenerative potential and highlights the fundamental difference in aging and replicative capacity between various cell types.

Stem Cell Therapies

Stem cell therapy is a medical treatment that uses stem cells to repair, regenerate, or replace damaged or aging tissues. It works by either directly injecting stem cells into affected areas or using them to stimulate the body’s natural healing processes. As we age, our natural stem cell supply decreases and becomes less effective, which contributes to slower healing, tissue damage, and chronic diseases. By introducing healthy, functional stem cells, therapies aim to rejuvenate tissues, improve organ function, and possibly delay the effects of aging. Research is ongoing in areas like improving skin elasticity, reducing joint pain, boosting immune function, and even enhancing cognitive health in older adults. These therapies are often marketed by private anti-aging clinics as established treatments. However, they are still largely experimental and require further evidence to demonstrate their long-term safety and efficacy…

Among the most promising types are mesenchymal stem cells (MSCs), known for their potent anti-inflammatory, immunomodulatory, and regenerative effects. Clinical studies suggest that MSCs can enhance cognitive function, reduce systemic inflammation, and improve tissue repair in aging-related conditions, including neurodegenerative diseases and frailty. 

Another powerful avenue is the use of induced pluripotent stem cells (iPSCs), which are adult cells reprogrammed to an embryonic-like state. These can be differentiated into virtually any cell type, such as insulin-producing pancreatic cells or natural killer (NK) immune cells. iPSC-derived NK cells are particularly relevant in older adults due to their lower risk of graft-versus-host disease and utility in targeting age-related malignancies. 

Meanwhile, neural stem cells (NSCs) are gaining traction for their ability to restore brain function in models of traumatic brain injury and neurodegeneration, offering potential therapies for Alzheimer’s and other forms of cognitive decline. Furthermore, stem cell-derived hepatocytes and β-cells are being explored for treating metabolic dysfunction-associated steatotic liver disease (MASLD) and diabetes, which are prevalent in the elderly. These cells can be used both as therapeutic agents and as disease models for drug discovery. As the field advances, challenges such as cell delivery, immune compatibility, tumorigenicity, and long-term safety become key areas of focus. 

Current Clinical Trials

One of the leading clinical studies exploring the use of stem cell therapy in aging involves mesenchymal stem cells (MSCs) for treating age-related frailty, a condition characterized by decreased strength, endurance, and physiological function. The CRATUS study (NCT02065245), a Phase 2 randomized clinical trial, evaluated intravenous allogeneic MSCs in older adults diagnosed with frailty. The results were compelling: patients treated with MSCs exhibited significant improvements in physical performance, walking speed, and inflammatory biomarkers, including a notable reduction in tumor necrosis factor-alpha (TNF-α), a key driver of chronic inflammation in aging. Importantly, the treatment was well-tolerated with no serious adverse events reported, supporting its safety profile.

Another clinical study in stem cell therapy targeting aging is a Phase I clinical trial evaluating the safety and efficacy of autologous adipose-derived mesenchymal stem cell (AD-MSC) transplantation in patients with aging-related low-grade inflammation, a condition also known as inflammaging. Conducted by Nguyen et al. (2024), this open-label, single-group trial involved 12 patients who received two intravenous infusions of 100 million AD-MSCs. These individuals exhibited high levels of pro-inflammatory cytokines and were also diagnosed with two of the following metabolic conditions: diabetes, dyslipidemia, or obesity. TheAD-MSC therapy may offer a safe and effective intervention to reduce chronic inflammation associated with aging and potentially mitigate the onset or progression of age-related diseases

Biotech companies are working on stem cell therapy

Aspen Neuroscience, based in San Diego, focuses on developing personalized stem cell therapies for neurodegenerative diseases, particularly Parkinson’s disease. Its lead therapy, ANPD001, uses autologous induced pluripotent stem cells (iPSCs) to replace dopamine-producing neurons lost in Parkinson’s. The company received FDA IND clearance in 2023 to begin Phase 1/2a trials. 

BlueRock Therapeutics, a Cambridge-based company owned by Bayer, is also working on iPSC-based regenerative medicines, with a focus on Parkinson’s disease. Their lead program, Bemdaneprocel (BRT-DA01), involves implanting iPSC-derived dopamine neurons into the brain. 

Cellino, another Cambridge-based company, aims to revolutionize personalized medicine with a scalable, automated biomanufacturing platform using iPSCs. The company leverages advanced technologies like label-free imaging and AI to streamline the production of patient-specific therapies for diseases like Parkinson’s, diabetes, and heart disease

The rise in chronic and degenerative diseases, like heart disease, neurodegenerative conditions, and cancer, is pushing the demand for stem cell therapies that can help repair and regenerate damaged tissues. The field still faces challenges, including high treatment costs, regulatory hurdles, and ethical concerns. Here, as elsewhere, the lack of large-scale research programs and clinical trials with public funding and sharing of results is hindering rapid progress.

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The good news of the month- Eli Lilly’s Orforglipron: A Potential Breakthrough in GLP-1 Therapy

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The Glucagon-like peptide (GLP-1) is an intestinal hormone that could slow down different aspects of senescence. Eli Lilly’s new GLP-1 medication, Orforglipron, is making headlines as an oral, once-daily pill currently in late-stage clinical trials. Early data from a Phase 3 study show promising results, with the drug significantly lowering levels of glycated hemoglobin and promoting weight loss in adults with type 2 diabetes.

Unlike existing GLP-1 treatments like Ozempic and Mounjaro, which require injections, orforglipron is a small molecule GLP-1 receptor agonist that offers the convenience of oral delivery. This could dramatically expand access and appeal to a broader population.

Lilly is seeking regulatory approval for both type 2 diabetes and obesity treatment, and if approved, Orforglipron could mark a major shift in how GLP-1 therapies are used.

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For more information

• Heales, Longevity Escape Velocity Foundation, International Longevity Alliance, Longecity, and Lifespan.io 
• Heales Monthly Science News
• Heales YouTube channel
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Why desire the radical extension of life? Because everything valuable requires time. Time to write, to read, to create and refine work that leads us to deep meaning. Time to learn multiple languages, to peel back the endless layers of our identity, to reinvent the best version of ourselves. Time to love and be loved. Time to raise children, nurture grandchildren, and play with great-grandchildren — all part of the gradual unfolding of love. Yana D’Cortona, medical student, January 9, 2025.

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Theme of the month: The impact of nanoparticles on our bodies.

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The number of nanoparticles created directly or indirectly by humans is increasing overall, even if there are improvements in certain areas. Invisible to the naked eye (1-100 nanometers), these particles are omnipresent in our environment and infiltrate our bodies by various routes, including breathing, ingestion, or skin exposure. Their minute size enables them to pass through the respiratory tract, the digestive system, and other routes to cross biological barriers (air-blood, blood-brain, placental) and reach the brain, where they can potentially interact with our cells. These interactions, still poorly understood, raise an essential question: how do these tiny particles influence our health?

In general, it can, unfortunately, be said that many nanoparticles accelerate ageing or increase the likelihood of cancer. To date, fortunately, the benefits of medical progress continue to outweigh the effects of pollution, but disastrous medium- and long-term effects of nanomaterials (possibly combined in “toxic cocktails”) cannot be ruled out. 

How do nanoparticles enter our bodies?

Among the ways in which nanoparticles can be absorbed, we will study two main routes here:

1. Respiration: Inhalation of airborne nanoparticles. They can reach the lungs and brain.
2. Ingestion :
   Through food: Ingestion of particles contained in food and impact on the digestive system.
   By hydration: Consumption of water-containing nanoparticles promotes their absorption by vital organs.

Nanoparticles in the air: Inhalation and respiratory risks

Airborne nanoparticles come from industrial pollution, exhaust fumes, forest fires, and certain domestic activities. When inhaled, they can reach the lungs and enter the bloodstream.

These include: nanoparticles (Np) of titanium dioxide (TiO₂) used in paints and cosmetics (sunscreens) which, when generated in large quantities, can cause lung inflammation. The International Agency for Research on Cancer (IARC) has declared TiO2 NPs to be “possibly carcinogenic when inhaled”, and highlighted the need to better understand their potential adverse effects via different routes of exposure in humans. Studies have shown that they can cross the placental barrier and reach fetal organs (liver, brain) in mice, causing developmental disorders and neuronal damage.

Nanoparticles resulting from the combustion of fossil fuels, notably soot and carbon black, are ubiquitous in our environment. The toxicity of soot particles stems from their physico-chemical characteristics. Soot particles penetrate deep into the respiratory tract, and are difficult to eliminate from the pulmonary alveoli. These fine particles penetrate deep into the respiratory tract, increasing the risk of asthma and cardiovascular disease. In 2013, IARC classified soot as a definite carcinogen (Group 1) in chimney sweepers, due to its association with skin and lung cancers.

Nanoparticles of heavy metals such as lead, mercury, and cadmium, present in industrial emissions, can also be found in the air. Heavy metals cannot be degraded or attacked by bacteria. The U.S. Environmental Protection Agency (USEPA) has classified mercury, cadmium, and lead as among the most toxic pollutants. Exposure to these heavy metals can cause neurotoxic effects, disrupting the nervous system.
Lead, for example, is recognized for its effectsmarked neurotoxic , affecting neurological development and neuronal transmission. Mercury, for its part, can cause serious neurological disorders such as Minamata disease. Oral exposure to high doses of cadmium can cause severe gastrointestinal irritation and significant effects on the kidneys. Chronic inhalation exposure has been associated with lung effects, including emphysema, and kidney damage. It can also cause bone damage.

A case study shows the impact of atmospheric nanoparticles on mortality in Canada: A study conducted between 2001 and 2016 in Canada revealed that prolonged exposure to atmospheric nanoparticles is associated with a significant increase in the risk of non-accidental mortality (+7.3%) and, more specifically, respiratory mortality (+17.4%). In Montreal and Toronto, this pollution is estimated to cause around 1,100 additional deaths per year. These results underline the urgent need to integrate nanoparticles into air quality regulation policies in order to limit their harmful effects on public health.

Nanoparticles in the food chain.

Heavy metals such as mercury (Hg), cadmium (Cd), lead (Pb), arsenic (As), and chromium (Cr) are present in the environment, due to industrial, agricultural, or urban activities. These activities lead to their incorporation into soils, water, and sediments, affecting living organisms including humans. At each trophic level, the concentration of metals increases. For example, a fish contaminated with mercury will be eaten by a predator, which will accumulate even more mercury in its body. This phenomenon is known as biomagnification.

Main food sources :

• Fish and seafood: Contamination by mercury, particularly methylmercury, which is neurotoxic. A recent study (2024) revealed that one in ten cans of tuna (a predatory species) exceeds the permitted mercury limit in Europe, exposing consumers to health risks.
• Vegetables and cereals: Absorption of heavy metals via polluted soils.
  In a study carried out in Canada in 2021, arsenic was detected in high concentrations (up to 2.20 ppm) in vegetable powders (92% of samples concerned). Leafy vegetables, such as kale, also showed higher levels of contamination than other vegetables, due to their high absorption capacity for soil particles.
• Meat and dairy products: Accumulation through ingestion of contaminated livestock feed.

Zinc oxide (ZnO) and copper oxide (CuO) nanoparticles used in agriculture are involved in the disruption of intestinal microbiota. By eating contaminated food, we absorb these particles, which can accumulate in our vital organs (liver, kidneys, brain), causing chronic poisoning, digestive disorders, and metabolic diseases.

Nanoparticles in water: Drinks and their impact on the body

Nanoparticles found in water come from industrial waste, microplastics, and chemicals. Nanoplastics (PE, PP, PET): present in tap and bottled water, now known to affect the hormonal system (Campanale et al., 2020). Silver nanoparticles (AgNPs): used for their antibacterial properties in certain filters and food packaging, can affect the intestinal microbiota. Heavy metal nanoparticles (lead, mercury, arsenic, cadmium): present in drinking water and certain contaminated water sources, can accumulate in our bodies and lead to neurological and renal risks (Khan et al., 2019).

Genotoxic effect of certain

Nanoparticles (NPs) of copper, zinc, silver, and quantum dots are attracting particular attention because of their potential genotoxic effects, mainly linked to the generation of reactive oxygen species (ROS), responsible for DNA damage. ZnNPs, commonly found in sunscreens and cosmetics, can release Zn²⁺ ions, inducing oxidative stress that alters DNA. In vitro studies have confirmed their genotoxicity, revealing DNA damage. Similarly, quantum dots, often composed of heavy metals such as cadmium (Cd) or selenium (Se), can release toxic ions capable of generating oxidative stress and causing genetic damage.
Although nanoparticles may represent a health risk, they offer innovative solutions for combating cellular aging by targeting its key mechanisms.

Nanoparticle applications in medicine: Nanotechnology.

Nanoparticles have also been studied for their positive impact on health. They can repair DNA damage by delivering repair enzymes, as shown by gold nanoparticles that reduce age-related mutations. They also act against oxidative stress with antioxidant nanoparticles, such as those based on cerium dioxide (CeO₂), which protect cells from free radicals. In addition, nanoparticles can eliminate senescent cells by carrying senolytic drugs, such as quercetin, thus reducing inflammation and tissue damage. Finally, they help protect telomeres by delivering agents such as telomerase, extending cell lifespan. These applications position nanoparticles as promising tools for slowing or reversing cellular aging.

Conclusions and outlook:

Nanoparticles, because of their small size and ability to penetrate deep into our bodies, present both health risks and opportunities for therapeutic innovation. Their omnipresence in the environment and their presence in air, water, and the food chain underscore the importance of studying and understanding their long-term effects.

In this field, as in others, it is urgent and vital to :

• Make available data on nanoparticle densities in the human body and their known impact, whether negative or (unfortunately more rarely) positive.
• Reference any knowledge of negative (or, unfortunately, more rarely) positive “cocktail effects”.
• Whenever possible, for new or increasingly used nanoparticles, organize longevity tests comparing the lifespan of mice (or other animals) with and without the substances concerned.
• Require companies developing nanomaterials to share data on the health effects of substances, particularly those for which they hold patents.

Alongside the study of nanoparticles, it is also crucial to examine the impact of microplastics, a category of plastic particles that are larger in size (< 5 mm), but still of concern due to their ubiquitous presence in our environment. Although their direct impact on human health is even less documented than that of nanoparticles, microplastics raise concerns due to their ability to transport toxic substances and accumulate in specific areas of the body, such as the digestive system and, even more seriously, the brain. This subject will be explored in greater detail in a future newsletter.

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The bad news of the month: the United States and Health.

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Among the tsunami of initiatives, President Trump’s new US administration has made decisions that have, at least in the short term effects generally considered negative for the health of Americans de of the world’s population:

These include:

Withdrawal from the World Health Organization. Along with Liechtenstein, the USA will thus be the only United Nations member state not to be a member of the WHO. It should be remembered that:

• The WHO aims to enable citizens “to enjoy a state of complete physical, mental and social well-being, and not merely the absence of disease or infirmity.”
  One of the consequences of the decision to leave will be to strengthen China’s weight in this organization.
  The USA is the country with both the highest per capita health expenditure and the lowest life expectancy among countries with a high standard of living.
• The blocking of numerous health-related expenditures. So, a month after Donald Trump took office as the 47th President of the United States, almost all grant review meetings remain suspended at the National Institutes of Health (NIH), preventing the world’s largest public funder of biomedical research from spending much of its $47 billion annual budget.
  

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Find out more:

• See in particular: heales.org, sens.org, longevityalliance.org and longecity.org.
• Image source.