NAD+ (High Dose)

What it is

NAD+ (nicotinamide adenine dinucleotide) is a coenzyme found in every living cell, not a peptide, though it is sold through the same telehealth category because of overlapping interest in cellular and metabolic health. NAD+ acts as a co-substrate for sirtuins, a family of deacylase enzymes that regulate aspects of metabolism, and maintaining adequate NAD+ levels is one proposed avenue for supporting mitochondrial function (Role of NAD+ and mitochondrial sirtuins in cardiac and renal diseases, Nat Rev Nephrol, DOI 10.1038/nrneph.2017.5). There is no FDA-approved injectable NAD+ product for wellness use; NAD+ offered through this pathway is a compounded preparation, not an FDA-approved drug product.

This high-dose option is intended for patients whose provider, after reviewing history and any prior response to a standard NAD+ regimen, determines a higher dose may be appropriate as a maintenance step up rather than a default starting point. NAD+ is available after a licensed-provider evaluation, and if a prescription is issued it is compounded through a US-licensed compounding pharmacy.

Van Peptides connects patients with an independent network of US-licensed providers who evaluate whether NAD+, and at what dose, fits your goals and history. We do not diagnose, prescribe, or dispense, and we do not employ the providers or the pharmacy.

What the literature has explored

Preclinical work has shown that restoring NAD+ levels, including through precursor supplementation, can activate SIRT1 and correct aspects of mitochondrial dysfunction in animal models, supporting the broader hypothesis that NAD+ availability is a limiting factor in mitochondrial health (NAD(+)-dependent activation of Sirt1 corrects the phenotype in a mouse model of mitochondrial disease, Cell Metab, DOI 10.1016/j.cmet.2014.04.001). Review literature has extended this reasoning to cardiac and renal tissue, proposing NAD+ repletion as a plausible therapeutic avenue across several organ systems, though this work is largely mechanistic and preclinical rather than large-scale human outcome data (Nat Rev Nephrol, DOI 10.1038/nrneph.2017.5).

Dose-ranging data specifically comparing higher-dose to standard-dose NAD+ administration in humans is limited, and most of the mechanistic story comes from animal and cell-based models rather than controlled human trials. Outcomes are individual, and any decision to pursue a higher dose over a standard maintenance dose is a clinical judgment best made between you and a licensed provider, not a default upgrade this page recommends.

We describe the sirtuin and mitochondrial mechanism because it is genuinely the subject of active research, but we do not present a higher dose as a fix for the aging process or a guarantee of a specific cellular outcome in you. The honest framing is that NAD+ biology is compelling and still being worked out in humans.