# NAD+ turnover

> NAD+ consumption | Shop Vital Peptides — Follow NAD+ consumption at Shop Vital Peptides: electron transfer, DNA repair, competing enzymes and a mouse experiment involving CD38.

**The consumption account**

The incoming supply is only half of the account. The different uses of NAD+ are where the story acquires texture.

## Electron transfer

The plus sign is useful. [NAD+ and NADH form a pair involved in cellular oxidation and reduction](https://pubmed.ncbi.nlm.nih.gov/18020963/): the chemistry of passing electrons between reactions. In this role, the molecule cycles between forms. Calling all of that activity ‘consumption’ would muddle the account before it began.

I picture working material circulating through a system, and that less glamorous account suits the chemistry. The [review of NAD+ production, cycling and cellular compartments](https://pubmed.ncbi.nlm.nih.gov/20007326/) makes that system more complicated than a single tank with a level marked on its side. A concentration is a useful measurement; an entire metabolic life has more moving parts.

## PARP1 consumption

PARP1 brings a different sort of demand. The [review of PARP1, DNA repair and cell death](https://pubmed.ncbi.nlm.nih.gov/25283336/) describes NAD+ as a shared substrate for PARP1 and sirtuins. PARP1 activity couples the repair of damaged DNA to the availability of cellular resources; excessive activation can deplete energy and contribute to cell death. This is a review of mammalian cell biology.

Repair has an appealing reputation, and rightly so. Unlimited enthusiasm for a resource seems premature when it follows only from a useful cellular job. The review describes a system with competing demands and consequences when activity becomes excessive. It gives the expenditure a context.

That context becomes very concrete in the [mouse immune cells on the inflammation page](/inflammation), where DNA damage and PARP activity helped create a dependence on NAD+ recycling.

## Age-related CD38 consumption

In [a mouse study of CD38](https://pubmed.ncbi.nlm.nih.gov/27304511/), this NAD+-consuming enzyme became more active with age. Mice lacking CD38 were protected against the age-related fall in NAD+, with preserved SIRT3 activity and improved mitochondrial function. The experiment changes an enzyme genetically in mice. It gives a mechanistic reason to examine the rate of consumption.

The strongest objection, for me, concerns the moving quantities: an incoming supply and an outgoing demand can both change. The ingenuity deserves my admiration; treating a genetically altered mouse as a preview of a human outcome would ask too much of it. The [human-evidence review](https://pubmed.ncbi.nlm.nih.gov/41083806/) describes sparse tissue-specific data and limited clinical efficacy. That leaves plenty of accounting still to do.

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At Shop Vital Peptides, published research sets the terms of my inquiry into cellular demand; this editorial site conducts no business and offers no medical advice.