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The HUM2N clinic’s founder, Dr. Mohammed Enayat, credits a regimen of vitamin B complex, magnesium, and omega-3 fatty acids with reversing his biological age. These supplements work by enhancing energy metabolism, regulating enzymatic processes, and combating inflammation, which collectively promote cellular vitality and resilience.

Key points

  • Vitamin B complex enhances energy metabolism, DNA repair, and nervous system function.
  • Magnesium regulates over 300 enzymatic reactions, improves sleep, and mitigates inflammation.
  • Omega-3 fatty acids (EPA/DHA) reduce systemic inflammation and support cardiovascular and brain health.

Why it matters: This approach suggests affordable, non-invasive strategies can modulate cellular aging markers and inflammation, potentially transforming preventive healthcare and broadening therapeutic options in longevity research.

Q&A

  • What is biological age?
  • How do GlycanAge and TruAge tests work?
  • Why are B vitamins important for aging?
  • Can lifestyle changes replace supplements?
  • What role do senolytics have in longevity?
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A multidisciplinary team investigates biohacking strategies—nutrigenomics, advanced supplementation, stem cell therapies, gene editing, and AI-driven personalised medicine—to modulate aging pathways, aiming to extend healthspan and mitigate age-associated diseases through integrated technological interventions.

Key points

  • Nutrigenomics-driven dietary strategies target gene–nutrient interactions to regulate aging-related pathways.
  • Senolytic compounds and NAD+ precursors clear senescent cells and restore cellular energy for improved function.
  • CRISPR gene therapy combined with AI analytics enables personalised editing and prediction of longevity outcomes.

Why it matters: Integrating genomics, AI, and regenerative techniques could shift aging interventions from trial-and-error supplementation to precision-based longevity therapies with broader disease prevention impact.

Q&A

  • What is nutrigenomics?
  • How do senolytic compounds work?
  • What are NAD+ boosters?
  • How does AI personalise longevity therapies?
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A team of Chinese scientists investigates metformin’s potential as an anti-aging intervention by examining its effects on cellular energy regulation and organ protection in both human cohorts and primate models. They report a 30% reduction in mortality before age 90 among postmenopausal women, and demonstrate metformin activates AMPK pathways to mitigate inflammation, protect vital tissues, and enhance metabolic resilience against age-related diseases.

Key points

  • 30% reduction in mortality risk before age 90 among postmenopausal women in epidemiological analysis.
  • Metformin activates AMPK to reduce inflammation and improve insulin sensitivity.
  • Primate studies show organ protection and slowed brain aging via AMPK-driven gene activation.

Why it matters: By targeting aging processes rather than individual diseases, metformin offers a scalable strategy to prevent multiple age-related disorders and extend healthspan.

Q&A

  • How does AMPK activation by metformin promote longevity?
  • What evidence supports metformin’s organ-protective effects in primate models?
  • Can healthy individuals use metformin for anti-aging benefits?
  • What are the limitations of current research on metformin’s geroprotective role?
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The Vatican Longevity Summit in Rome brought experts including Nobel laureates to examine ethical and technical advances for healthy aging. Discussions emphasized intergenerational dialogue and technology-driven healthcare reforms, providing practical policy examples to enhance equity and wellness.

Q&A

  • What is the Vatican Longevity Summit?
  • How does technology affect healthy aging?
  • Why is intergenerational communication emphasized?
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