Anti-Aging & Longevity

The "Anti-aging and longevity" series isn't built around wellness language - it's built around the concrete hallmarks of aging: mitochondrial dysfunction, telomere attrition, epigenetic drift, and NAD+ decline. These are validated peer-reviewed targets, not fashion concepts, and the catalog is organized around them rather than around market promises.

NAD+ drops by roughly 50% between age 30 and 60 (Yoshino et al., Cell Metabolism 2018) - and because NAD+ is the substrate for the sirtuin family (SIRT1-7), that loss directly constrains DNA repair and mitochondrial biogenesis. Epitalon (Ala-Glu-Asp-Gly), a tetrapeptide modeled on epithalamin from the pineal gland, was characterized by Vladimir Khavinson's group at the St. Petersburg Institute of Bioregulation - in cell lines it raises TERT expression (the catalytic telomerase subunit) and extends the replicative ceiling of human fibroblasts (Khavinson et al., Bull Exp Biol Med 2003).

MOTS-c and Humanin are mitochondrially-derived peptides - encoded not in the nucleus but inside mitochondrial DNA itself. MOTS-c activates AMPK and, in myotube models, raises insulin sensitivity (Lee et al., Cell Metabolism 2015). Humanin binds IGFBP-3 and BAX and, in Alzheimer's models, reduces apoptosis in hippocampal neurons (Hashimoto et al., PNAS 2001). For researchers focused on healthspan, these four - NAD+, Epitalon, MOTS-c, Humanin - cover different axes of aging, not one universal lever.

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