NAD supresses Akt activation via SIRT7-FKBP51-PHLPP

I was surprised that Niacin (vitamin B3) significantly increases the type of OCD that one can describe as “being stuck, like the signal “I did that already” doesn’t come through”.

Since this happened clearly after Niacin, I decided to research if Akt/GSK3b has anything to do with NAD (a very important molecule that reflects energy production).

It turns out, there is a Sirtuin 7 protein that deactivates AKT (!):

• SIRT7 regulates the acetylation of FKBP51, which then regulates Akt activation
• Acetylated FKBP51 enhances Akt activity by blocking its interaction with PHLPP-Akt
• SIRT7 deacetylates FKBP51 at two major lysine residues
• SIRT7 suppresses Akt activation and modulates cell sensitivity to genotoxic agents

Damn, so trying to boost energy by using NAD will actually lower Akt signalling, which means GSK3b will shut other important proteins, Nrf2 including.

In simple English: boosting NAD have a good change to increase oxidative stress due to increased activation of GSK3b.

This makes so much sense now.

If you have OCD that makes you stuck in compulsion, chances are, your NAD level is okay (but not necessary), but GSK3b is overactive because of inhibited Akt.

Quick and dirty fix

Eating carbs to increase insulin level - insulin stimulates Akt and by that inhibits GSK3b. But this will work for only one hour, then insulin level drops and overactive GSK3b comes back.

Fix 2

Chromium supplement (just a small dose). Chromium amplifies Akt signalling.