Mullo Saint Research

The dominant "stacking" approach to longevity fails due to cellular energy bottlenecks. This paper establishes a three-phase "Energy-First" protocol: NAD+ restoration, followed by autophagy induction, followed by senolytic clearance.

Rapamycin presents a paradox: it inhibits mTOR, which suppresses muscle protein synthesis and immune function—yet low-dose rapamycin improves both in aging populations. The resolution lies in dose timing and cellular preparation. When rapamycin is administered after restoring cellular energy reserves with NAD+ precursors, the 5 mg weekly dose activates autophagy without sustained immunosuppression.

Senolytics kill senescent cells. Killing is the easy part. The cellular debris must be cleared through efferocytosis—a process that requires energy, functional macrophages, and time. This article examines why senolytic therapy produces variable results across clinical trials and individual patients, and how sequential preparation transforms outcomes.

A comprehensive review of NAD+ precursor strategies, enzymatic competition, and clinical evidence for energy-first longevity interventions. Covers biosynthesis pathways, age-related decline mechanisms, sirtuin-PARP-CD38 competition, precursor comparative analysis (NMN, NR, niacin), key human trials, and the rationale for NAD+ restoration as the foundational intervention preceding autophagy induction and senolytic clearance.