There are three NAD boosting strategies.

Increasing the supply of NAB precursors is just one way.

The other two are having the body make more by activating NAB synthesizing enzymes,

or have the body use less by, for example,

conserving it, by using less.

Besides Sertuins, the major consumers of NAD are PARP-1 and CD-38.

Parp 1 is an enzyme that uses NAD to repair DNA.

The more oxidative DNA damage, the more single and double-stranded DNA breaks.

The more enzymes like PARP-1 need to be activated to come to the rescue.

This uses up a lot of NAD.

As DNA damage accumulates with age,

the rising need for repair enzymes like PARP-1

causes a major drain on NAD levels.

Exposing cells in vitro to DNA-damaging agents such as gamma radiation or genotoxic chemicals

can cause an 80-90 percent drop in NAD levels within a matter of minutes.

This has led to the search for Park 1 blockers to preserve NAD levels within a matter of minutes. This has led to the search for PAR-1 blockers to preserve NAD levels,

but rather than blocking DNA repair, why not work to prevent so much damage in the first place?

For example, the severe oxidative stress of a high-fat diet

can lead to PARP-1 activation and NAD depletion in mice, but NAD levels

can be dramatically restored by feeding them purple sweet potato color, the natural anthocene

and pigments found in purple sweet potatoes. Or, of course, you can just not feed them a high-fat

diet. DNA repair is a good thing.

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