19 Week, 2025: dolphin fatty acid benefits and ai digital twins accelerate anti aging therapies

The discovery of C15:0, a fatty acid abundant in dolphin diets, reveals a powerful new longevity nutrient that supports liver function, mitochondrial repair, and cardiovascular health. This challenges outdated views on saturated fats and offers practical supplement and food fortification options for busy professionals seeking metabolic optimization.

Dolphin Study Sparks Breakthrough Longevity Supplement

Researchers at the US Navy Marine Mammal Program and founder Dr Stephanie Venn-Watson identify C15:0, an odd-chain saturated fatty acid abundant in dolphin diets, as an essential longevity nutrient. Through controlled dolphin serum analyses and dietary trials, they demonstrate C15:0’s benefits for liver function, cholesterol reduction, and mitochondrial repair. These findings underpin Fatty15, a peer-reviewed supplement engineered to deliver bioavailable C15:0 for human metabolic health optimization.

Key points:

• Identification of pentadecanoic acid (C15:0) as an essential longevity nutrient through dolphin serum metabolomics.
• Correlation of dietary C15:0 intake with improved metabolic markers and reduced liver disease in bottlenose dolphins.
• Dolphin dietary trials demonstrate C15:0’s effects on lowering cholesterol, reducing inflammation, and repairing mitochondria.
• Development of vegan C15:0 supplement Fatty15, validated by over 100 peer-reviewed studies for bioavailability and safety.
• Proposal to integrate C15:0 into fortified foods, beverages, and infant formulas for broader metabolic health applications.

Why it matters: This discovery challenges prevailing notions that saturated fats are uniformly detrimental by highlighting the therapeutic potential of C15:0, a previously overlooked odd-chain fatty acid. Demonstrating efficacy in a long-lived mammalian model bridges the gap between rodent studies and human application, paving the way for targeted metabolic interventions and evidence-based longevity supplements.

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SGLT-2 Inhibitors Mimic Fasting to Boost Longevity Pathways

Researchers at Healthspan Medical unveiled how SGLT-2 inhibitors, originally developed to lower blood sugar, emulate the metabolic effects of caloric restriction by promoting urinary glucose excretion. This mild energy deficit activates longevity pathways—AMPK, SIRT1—while suppressing mTOR and insulin/IGF-1 signaling, thereby enhancing autophagy, mitochondrial function, and metabolic flexibility. The pharmacological approach offers a practical alternative to strict dietary interventions for promoting healthier cellular aging.

Key points:

• SGLT-2 inhibitors induce mild glucosuria (~60–80 g/day), mimicking a continuous fasting state
• Activated AMPK and SIRT1 pathways enhance fatty acid oxidation, mitochondrial biogenesis, and cellular repair
• Inhibited mTOR and reduced insulin/IGF-1 signaling promote autophagy and reduce pro-growth signaling
• Empagliflozin demonstrated reduced hepatic steatosis, lowered pro-inflammatory M1 macrophages, and increased UCP1 expression in HFD-fed mice
• Early human data show weight loss, improved insulin sensitivity, and cardiometabolic risk-factor reduction

Why it matters: By replicating the cellular effects of caloric restriction without severe dietary changes, SGLT-2 inhibitors may shift the aging paradigm toward pharmacological metabolic reprogramming. This approach could provide a scalable therapy to enhance healthspan, mitigate age-related diseases, and overcome adherence barriers associated with traditional fasting or caloric restriction regimens.

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AI Digital Twins Speed Anti-Aging Therapies

Researchers at Longevity Global integrate machine learning with biomarker analysis to build "aging clocks" and digital twin models that simulate treatment responses. Using virtual clinical trials, they accelerate identification of effective anti-aging interventions, shortening timelines from years to weeks and fostering venture and pharmaceutical investment in precision longevity therapies.

Key points:

• AI-driven digital twins simulate individual aging and treatment responses in silico.
• Epigenetic aging clocks derived from multi-omics biomarkers predict biological age.
• In silico virtual clinical trials shorten evaluation timelines from years to weeks.
• Machine learning identifies candidate senolytics and personalized therapies efficiently.
• Integration of AI models attracts venture capital and pharmaceutical investment.

Why it matters: By harnessing AI to simulate patient-specific aging trajectories and accelerate biomarker identification, this approach promises to transform longevity research, shifting from time-consuming clinical trials to rapid in silico validation. The enhanced efficiency and precision could redefine therapeutic development for aging-related conditions and democratize access to personalized anti-aging therapies.

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Stem Cell EV miRNAs Reverse Cellular Senescence

An aging research team applies miRNA enrichment analysis and an age-related genetic database to isolate a four-strand microRNA cocktail (E5) within stem-cell–derived extracellular vesicles. Delivered to senescent fibroblasts, E5 downregulates p16, p21 and inflammatory interleukins, outperforming native vesicles. In naturally aged mice, systemic E5 injections reduce senescence and DNA damage markers in liver tissue, highlighting a non-senolytic approach to cellular rejuvenation.

Key points:

• Four-miRNA cocktail (E5) derived from stem cell EVs modulates senescence.
• Delivery via extracellular vesicles reduces SA-β-gal activity by ~30% in fibroblasts.
• E5 downregulates p21, p16, IL-1β and IL-6 through PCAF and HIPK2 suppression.
• In 24-month-old mice, systemic E5 dosing lowers senescence and DNA damage markers in liver tissue.
• Non-senomorphic approach spares cell viability while targeting aging pathways.

Why it matters: This miRNA-loaded EV approach offers a non-senolytic alternative that reprograms aging cells without inducing cell death, potentially reducing side effects of current therapies. By targeting multiple senescence pathways, it could pave the way for precise, rejuvenative treatments in age-related diseases.

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UNITY's UBX1325 Senolytic Yields Vision Gains in DME Trial

UNITY Biotechnology’s Phase 2b ASPIRE trial evaluates UBX1325, a novel senolytic targeting senescent retinal cells to treat diabetic macular edema. Against aflibercept, UBX1325 demonstrates non-inferior vision gains overall and superior outcomes in a moderately aggressive patient subgroup, guiding future pivotal studies.

Key points:

• UBX1325 is a small-molecule senolytic targeting anti-apoptotic pathways in senescent retinal cells
• Phase 2b ASPIRE trial compared UBX1325 monotherapy against standard aflibercept in DME patients
• Primary endpoint was non-inferiority in BCVA averaged between weeks 20 and 24
• Subgroup with moderately aggressive DME showed superior BCVA improvements with UBX1325
• Future plans include 36-week data release and proteomic analyses of aqueous humor markers

Why it matters: This trial provides the first replicated clinical evidence that senolytic therapy can improve outcomes in age-related retinal disease. It validates senescent cell clearance as a viable mechanism, potentially opening new therapeutic avenues for DME and broader age-associated pathologies beyond existing anti-VEGF treatments.

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DT-109 Peptide Reverses Atherosclerosis in Primates

Researchers in a collaborative study evaluate DT-109, an orally deliverable tripeptide, for its effects on advanced atherosclerosis and vascular calcification in cynomolgus monkeys. Administered daily alongside a high-cholesterol diet, DT-109 significantly reduces lesion formation, inflammatory signaling, and arterial calcification while promoting smooth muscle cell contractile marker expression. These findings suggest a multifaceted therapeutic approach to combat cardiovascular disease by targeting inflammasome pathways and plaque stability.

Key points:

• Orally administered DT-109 (Gly-Gly-Leu) peptide at 150 mg/kg/day in cynomolgus monkeys.
• Five-month treatment with a cholesterol-rich diet showed significant reductions in aortic and coronary lesion size.
• DT-109 downregulates pro-inflammatory genes NLRP3, AIM2, CASP1 and oxidative stress markers NCF2, NCF4.
• Treatment reduces vascular calcification and macrophage content while increasing SMC contractile markers ACTA2, CNN1, TAGLN.
• In vitro assays confirm DT-109 inhibits NLRP3 inflammasome activation and smooth muscle cell calcification.

Why it matters: These results demonstrate a novel peptide-based strategy that combines anti-inflammatory and anti-calcific actions to address advanced atherosclerosis, a leading cause of cardiovascular mortality. By demonstrating efficacy in primate models, DT-109 bridges the gap between rodent research and human application, offering a promising route to more effective, orally available therapies that can regress plaque and restore vascular function.

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Senolytics Reverse Spinal Disc Aging and Relieve Back Pain

Researchers employ o-vanillin and RG-7112 in sparc–/– mice, targeting accumulated senescent cells in intervertebral discs. Oral administration clears these cells, lowers SASP-driven inflammation, improves vertebral bone quality, and reduces pain marker expression in the spinal cord through p53/MDM2 inhibition and senomorphic activity.

Key points:

• Oral o-vanillin and RG-7112 synergistically clear senescent cells in sparc–/– mouse discs.
• Senolytic treatment markedly reduces SASP factor release and local inflammation in IVD tissue.
• Cleared senescence correlates with lower disc degeneration scores and restored ECM integrity.
• Vertebral bone quality improves, and expression of spinal cord pain markers decreases post-treatment.
• RG-7112 blocks p53/MDM2 interaction to induce senescent cell apoptosis; o-vanillin acts as a senomorphic agent.

Why it matters: By demonstrating that targeted senolytic therapy can reverse established disc degeneration and alleviate chronic back pain, this study shifts the paradigm from symptomatic management to disease modification. It highlights a translational pathway for combining natural senomorphics with targeted apoptosis inducers to tackle age-related disorders driven by cellular senescence.

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