In part one (click here for part 1) I explained how aging may occur due to information in the epigenome being lost. This means that genes that are meant to be packed tightly away (silenced) become exposed. Once exposed, genes that are not meant to be turned on can be turned on, causing a cell to lose part of its identity. For example, a brain cell will become only 95% brain cell and 5% skin cell because skin genes are being activated. This happens because the gene silencing proteins are constantly leaving ‘home’ to go and fix DNA damage. Sometimes they never find their way home.
What can we do about it? We can slow the loss of epigenetic information by activating our ‘longevity genes’. Our longevity genes are known for having having the ability to keep our cells healthy. We can turn them on by stressing the body in small amounts, a phenomenon known as hormesis (e.g exercise or fasting). Hormesis ‘rocks’ the epigenome but does not cause it to lose information. Keeping our cells healthy is a way to make them more resistant to damage, thereby limiting the distraction of our gene silencing proteins. Of course, we can also limit the amount of DNA damage we get in the first place, by for example, quitting smoking (smoking causes massive DNA damage).
Another thing we can do is boost our NAD levels. NAD is an essential molecule for many critical processes – one being sirtuin activation. Sirtuins are some of the very proteins that silence genes but also repair DNA damage. In yeast, boosting NAD levels has resulted in sirtuins being able to cope with BOTH gene silencing and DNA repair, without losing epigenetic information (the sirtuins always find their way home). What’s more, boosting NAD could even restore the epigenome a little. This restoration could be called age reversal….now it’s getting REALLY interesting.
I’ve already said that information in DNA is not lost. Therefore, we always have the blueprint of our youthful epigenome. The problem is, we lose the ability to read it because epigenetic changes confuse our DNA ‘reading machinery’. In part 3, I’ll explain how one day we may be able to read it again, restore our epigenome, and turn back the aging clock