Question 1

What is nanoNAD+ and how does it differ from standard NAD+ supplements?

Accepted Answer

Conventional NAD+ in liquid solution forms large molecular clumps and aggregates exceeding 50 to 500 nanometers, preventing transdermal pore absorption and causing injection site burning. nanoNAD+™ is a patent-pending breakthrough that declumps NAD+ into uniform single molecules measuring 1.92 nm (verified via Particle Technology Labs Dynamic Light Scattering analysis). It is produced via Saccharomyces cerevisiae yeast fermentation, yielding 100% pure biologically active Beta-NAD+.

Question 2

What is Dr. Fenton LeBon's 5-Step Mitochondrial ReGenesis Cycle?

Accepted Answer

The 5-Step Mitochondrial ReGenesis Cycle is Dr. LeBon's clinical protocol for restoring cellular energy to maximum capacity: 1) Substrate Fueling with nanoNAD+™ to feed Complex I; 2) Sealing Inner Membrane Holes using SS-31 (Elamipretide) to stabilize cardiolipin; 3) Surveillance Tagging with PINK1/Parkin to flag depolarized organelles; 4) Quality Control Clearance with MOTS-c peptide to trigger autophagic cleaning; and 5) Active Biogenesis with Urolithin A and PQQ to stimulate PGC-1α replication of fresh mitochondria.

Question 3

Why does Dr. LeBon compare NAD+ and mitochondria to an oil refinery?

Accepted Answer

Dr. LeBon uses the Industrial Energy Analogy: NAD+ is the crude oil, mitochondria are the refinery, and ATP is the refined high-octane gasoline. Supplying crude oil without repairing holes in the refinery cristae will not yield ATP output. Conversely, having a pristine refinery without adequate crude oil leaves the cell dormant. Both fuel and membrane infrastructure must be optimized together.

Question 4

How does nanoNAD+ cross the blood-brain barrier to support neural recovery?

Accepted Answer

Due to its single-molecule 1.92 nm hydrodynamic diameter, intranasal nanoNAD+ rapidly traverses the cribriform plate directly into the central nervous system. In neural tissue, extracellular NAD+ is metabolized into adenosine, which binds inhibitory adenosine A1 receptors in the amygdala and hippocampus. This engages a neurological brake on presynaptic glutamate release, dampening traumatic fear generalization and hyperarousal while replenishing neuronal ATP.