NAD+ Decline & Aging

Nicotinamide adenine dinucleotide (NAD+) is arguably the most critical molecule in the aging equation. It serves as an electron carrier in mitochondrial energy production, a substrate for sirtuins (the longevity enzymes), a substrate for PARPs (DNA repair), and a signal molecule for CD38 (immune regulation). By age 60, NAD+ levels have declined approximately 50% from their peak.

Why NAD+ Declines

The decline is driven by increasing CD38 activity (an NAD+-consuming enzyme upregulated by chronic inflammation), decreased NAMPT expression (the rate-limiting enzyme in NAD+ biosynthesis), and accumulated DNA damage requiring PARP activity.

The Midas Approach

The Midas Protocol includes NAD+ 500mg for direct restoration, alongside BPC-157 and TB-500 to reduce chronic inflammation (which drives CD38 upregulation), and FOXO4-DRI to clear senescent cells (a major source of inflammatory SASP factors). This multi-pathway approach addresses both NAD+ supply and the upstream causes of its decline.