Epithalon & NAD+:
Longevity Peptide Science
Founded on 40 years of Russian longevity science · St. Petersburg Institute of Bioregulation & Gerontology
Epithalon is the only peptide with published telomerase activation data in human somatic cells — backed by four decades of peer-reviewed research from Prof. Vladimir Khavinson. Combined with NAD+ restoration for sirtuin pathway reactivation, these compounds address the two most fundamental hallmarks of cellular aging: telomere attrition and mitochondrial collapse.
Two Pillars of Cellular Aging
Telomere Shortening
Every somatic cell division trims the telomeric TTAGGG repeat sequences capping chromosomes. After ~50 divisions (the Hayflick limit), critically short telomeres trigger permanent replicative senescence or apoptosis — the cellular clock of aging.
Telomerase activation via Epithalon (Ala-Glu-Asp-Gly tetrapeptide) resets this clock. Prof. Khavinson's published trials demonstrate measurable telomerase induction in human somatic cells — the first peptide with this validated mechanism.
In animal longevity models, Epithalon-treated subjects showed 33–68% lifespan extension correlated with preserved telomere length across generations of cell division.
NAD+ Depletion
NAD+ (nicotinamide adenine dinucleotide) is the central metabolic coenzyme fueling over 500 enzymatic reactions. From age 20 to 50, intracellular NAD+ levels drop approximately 50% — a decline now recognized as a primary driver of the aging phenotype.
The sirtuin pathway (SIRT1–SIRT7) requires NAD+ as an obligate substrate. When NAD+ falls, sirtuin activity collapses — halting epigenetic reprogramming, mitochondrial biogenesis via PGC-1α, and DNA repair. NAD+ restoration directly reactivates these longevity pathways.
NMN and NR are the two clinically studied NAD+ precursors that efficiently cross the cell membrane and boost intracellular NAD+ in human trials, with NMN showing superior bioavailability in recent head-to-head data.
Hallmarks Addressed by This Protocol
When to Start a Longevity Protocol
NAD+ decline and telomere shortening begin in your 20s. The optimal intervention window varies by decade.
Telomeres are still relatively intact. This decade is about establishing the sirtuin pathway and protecting against the first wave of NAD+ decline.
NAD+ has declined significantly. Telomere shortening accelerates. Mitochondrial dysfunction becomes measurable. This is the most critical intervention window.
Multiple hallmarks are active simultaneously. Comprehensive multi-compound stacking addresses telomere attrition, NAD+ depletion, and epigenetic alterations in parallel.
