What is behind Longevity & Anti-Aging
The cell's master energy sensor — when fuel runs low it ignites fat-burning, glucose uptake and mitochondrial renewal while standing down growth. Evidence A — Human trial evidence.
A sirtuin enzyme that tunes metabolism, DNA repair and mitochondrial health toward the state linked with longer healthspan. Evidence A — Human trial evidence.
NAD⁺ — the coenzyme that powers energy metabolism and fuels the sirtuin longevity enzymes; it declines steadily with age. Evidence A — Human trial evidence.
The cell's self-cleaning and recycling program — it digests worn proteins and organelles and renews the interior. Evidence A — Human trial evidence.
The transcription factor that commands the body's own antioxidant and detoxification arsenal. Evidence A — Human trial evidence.
The master inflammatory switch — indispensable to defend against threat, corrosive when it never stands down. Evidence B — Preclinical.
Senescence and its inflammatory sasp — cells that stop dividing yet linger, spilling signals that age the surrounding tissue. Evidence A — Human trial evidence.
PGC-1α — the master regulator of mitochondrial biogenesis, building new cellular powerplants and oxidative endurance. Evidence A — Human trial evidence.
Insulin sensitivity — how readily cells respond to insulin, the linchpin of metabolic health. Evidence B — Preclinical.
An enzyme that sits on immune cells and eats NAD+. Its expression climbs steadily with age, and it is now the leading explanation for why NAD+ falls at all — not because the body makes less, but because something is consuming more. Evidence B — Preclinical.
Biological cellular aging — the accumulated senescence and epigenetic drift that mark true physiological age. Evidence B — Preclinical.
The rate-limiting enzyme of the salvage pathway. It converts nicotinamide back into NMN so it can become NAD+ again — which is how most tissues keep their supply, since nicotinamide is what every NAD-consuming enzyme leaves behind. Evidence B — Preclinical.
An enzyme that detects broken DNA and builds chains of poly-ADP-ribose to mark the damage for repair. Every chain is built from NAD+, so repair is paid for out of the same pool that runs the sirtuins. Evidence B — Preclinical.
The forkhead transcription factor held in check by insulin and growth signaling — released when nutrients fall to switch on stress-defense and autophagy genes. Evidence A — Human trial evidence.
Evidence on these pathways
AMPK → Insulin Sensitivity. “In model systems, sustained decreases in AMPK activity accompany IR, whereas AMPK activation increases insulin sensitivity.” — AMPK, insulin resistance, and the metabolic syndrome. The Journal of Clinical Investigation, 2013, volume 123, issue 7, pages 2764-2772. doi:10.1172/JCI67227
Autophagy → Proteostasis. “We show that HPK-1 fortifies proteostasis and extends longevity by an additional independent mechanism: induction of autophagy.” — The homeodomain-interacting protein kinase HPK-1 preserves protein homeostasis and longevity through master regulatory control of the HSF-1 chaperone network and TORC1-restricted autophagy in Caenorhabditis elegans. PLoS Genetics; 2017; volume 13; page/elocation not printed on either retrieved record. doi:10.1371/journal.pgen.1007038
CD38 NADase → NAD⁺. “Here we demonstrate that expression and activity of the NADase CD38 increase with aging and that CD38 is required for the age-related NAD decline and mitochondrial dysfunction via a pathway mediated at least in part by regulation of SIRT3 activity.” — CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism. Cell Metabolism, 2016, 23(6), 1127-1139. doi:10.1016/j.cmet.2016.05.006 | PMID 27304511 | PMC4911708 (PMID/PMC from the Atlas receipt list; the DOI was read off the record)
Cellular Aging → Infection Resistance. “This phenomenon, characterized by alterations in both innate and adaptive immunity, increases susceptibility to infections, reduces vaccine efficacy, and contributes to the development of age-related diseases.” — Molecular and Cellular Mechanisms of Immunosenescence: Modulation Through Interventions and Lifestyle Changes. Biology, 2024, 14(1), 17. doi:10.3390/biology14010017
Formulas that act on these pathways
Acts on 10 of these pathways: AMPK, SIRT1, NAD⁺, Autophagy, Nrf2, NF-κB, Senescence / SASP, PGC-1α Biogenesis, Insulin Sensitivity, FOXO.
Acts on 8 of these pathways: AMPK, SIRT1, Autophagy, Nrf2, NF-κB, Senescence / SASP, PGC-1α Biogenesis, Insulin Sensitivity.
Acts on 7 of these pathways: AMPK, SIRT1, Autophagy, Nrf2, NF-κB, Senescence / SASP, Insulin Sensitivity.
Acts on 7 of these pathways: AMPK, SIRT1, Autophagy, Nrf2, NF-κB, Senescence / SASP, Cellular Aging.
Acts on 7 of these pathways: AMPK, SIRT1, Autophagy, Nrf2, NF-κB, PGC-1α Biogenesis, Insulin Sensitivity.
Acts on 7 of these pathways: AMPK, SIRT1, Autophagy, Nrf2, NF-κB, PGC-1α Biogenesis, Insulin Sensitivity.
What this page does not claim
This page names the pathways involved and the published evidence on each. It does not claim that any formula treats, cures or prevents Longevity & Anti-Aging. A pathway opens here only on graded, published evidence, under a standard fixed before the evidence was gathered, and every figure above carries its grade.
These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease.