Melatonin Increased Autophagy dependent on SIRT1, a Longevity Marker

Melatonin declines with age.

Seborrheic keratosis increase with age.

Autophagy declines with age.

Melatonin activates melatonin flux, increasing autophagy.

Blocking Sirt1 blocked melatonin increased autophagy.

Blocking autophagy directly reduced the protection of melatonin.

Increasing autophagy should block or reverse Seborrheic keratosis formation.

Melatonin and Ursolic acid (which increases Sirt1) might ameliorate age related Seborrheic keratosis.

BHB related to exercise and fasting increases autophagy.

I further conjecture that vitamin d levels affects Seborrheic keratosis as keratinocytes have large numbers of vitamin d receptors.

Fasting.

Exercise.

Melatonin.

Ursolic acid. 

Vitamin D.

The above should be negatively associated with Seborrheic keratosis specifically and aging generally!

http://europepmc.org/abstract/med/26918354

Melatonin protects skin keratinocyte from hydrogen peroxide-mediated cell death via the SIRT1 pathway.

Melatonin (N-acetyl-5-methoxytryptamine), which is primarily synthesized in and secreted from the pineal gland, plays a pivotal role in cell proliferation as well as in the regulation of cell metastasis and cell survival in a diverse range of cells. The aim of this study is to investigate protection effect of melatonin on H2O2-induced cell damage and the mechanisms of melatonin in human keratinocytes. Hydrogen peroxide dose-dependently induced cell damages in human keratinocytes and co-treatment of melatonin protected the keratinocytes against H2O2-induced cell damage. Melatonin treatment activated the autophagy flux signals, which were identified by the decreased levels of p62 protein. Inhibition of autophagy flux via an autophagy inhibitor and ATG5 siRNA technique blocked the protective effects of melatonin against H2O2-induced cell death in human keratinocytes. And we found the inhibition of sirt1 using sirtinol and sirt1 siRNA reversed the protective effects of melatonin and induces the autophagy process in H2O2-treated cells. This is the first report demonstrating that autophagy flux activated by melatonin protects human keratinocytes through sirt1 pathway against hydrogen peroxide-induced damages. And this study also suggest that melatonin could potentially be utilized as a therapeutic agent in skin disease.

Joseph Thomas (Tony) Liverman, Jr.