NAD+ references

Mouse experiments

Cheng and colleagues: mitochondrial NAD+ transport in mouse liver. Deleting SLC25A47 increased liver lipid content and promoted tumors. This is the experiment behind the opening question about protection and cellular context.

Camacho-Pereira and colleagues: CD38 and age-related NAD+ decline in mice. Deleting a consuming enzyme preserved NAD+ and improved mitochondrial function. I value the contrast between disturbing supply in one experiment and consumption in the other.

Human precursor trials

Conze and colleagues: NR safety and metabolism in healthy overweight adults. An 8-week randomized trial measuring whole-blood NAD+ and tolerability.

Yi and colleagues: NMN in healthy middle-aged adults. A 60-day randomized trial reporting blood, walking and quality-of-life findings.

Yoshino and colleagues: NMN and muscle insulin sensitivity. A 10-week trial in prediabetic postmenopausal women, with a positive muscle finding and unchanged body composition and HbA1c.

Vinten and colleagues: the 2025 human clinical-evidence review. The useful counterweight to expansive aging claims: limited efficacy and scarce tissue-specific data.

Cellular supply, repair and growth

Covarrubias and colleagues on NAD+ metabolism during aging and Katsyuba and colleagues on homeostasis in health and disease cover the larger biology.

Zapata-Pérez and colleagues on human NAD+ homeostasis examine how supply becomes disturbed. Groth and colleagues on metabolism, stress and infection describe the biosynthetic pathways.

Elhassan and colleagues on metabolic disease, Ying on NAD-dependent cellular functions and Kar and colleagues on the CD38–NAD+ axis expand the account of consumption, signaling and repair.

Aleo and colleagues on extracellular NAD in human skin fibroblasts studied cells in culture. I give it a specific boundary here because a cell-surface experiment has sometimes been stretched into an account of human infusion behavior.