LOTS of things affect epigenetics. It currently appears to be a messy, relatively non-deterministic process with lots of different pathways crossing wires with lots of other different pathways.
A snapshot of my mental model of epigenetics (warning: epigenetics/histone modifications are not my particular field of study): "The methylator slides along DNA to methylate histone tails at location 32 of histone 2 while in simultaneous competition the demethylator demethylates methyl groups of histone 1 at locations 4, 12 and 18 under most conditions, or location 32 of histone 2 IFF it is within three histones of an acetylated histone which itself has its acetylation competing with a deacetylator - constantly. And if a certain set of marks occur appropriately in combination, a set of neighboring histones wrap up and hide themselves and their DNA - preventing its hidden DNA from being used in that cell until some other mechanism can unwrap that section. Oh, and (most of) those marks are copied to children/daughter cells right along with the copying of DNA."
Because it's so fickle, non-deterministic, and tangled (unlike it's DNA counterpart) it's actually pretty hard to study and is currently (like this afternoon, down your street) a topic of a significant amount of cutting edge research. As the wikipedia article above shows, the 'Histone Code' is still a work in progress, and it now appears unlikely that there is a 1:1 relationship between this chemical mark and that effect, very much unlike the very nice deterministic relationship we found between DNA->RNA->Protein.
One common change I've read about that bubbles up to normal life is the capability of nicotine to affect histone acetylation. It seems to rapidly alter histone modifications so as to make other habits/actions more addictive [1] (precisely in a way that we now know THC does not - the original 'gateway drug' mis-extrapolation).
A snapshot of my mental model of epigenetics (warning: epigenetics/histone modifications are not my particular field of study): "The methylator slides along DNA to methylate histone tails at location 32 of histone 2 while in simultaneous competition the demethylator demethylates methyl groups of histone 1 at locations 4, 12 and 18 under most conditions, or location 32 of histone 2 IFF it is within three histones of an acetylated histone which itself has its acetylation competing with a deacetylator - constantly. And if a certain set of marks occur appropriately in combination, a set of neighboring histones wrap up and hide themselves and their DNA - preventing its hidden DNA from being used in that cell until some other mechanism can unwrap that section. Oh, and (most of) those marks are copied to children/daughter cells right along with the copying of DNA."
Because it's so fickle, non-deterministic, and tangled (unlike it's DNA counterpart) it's actually pretty hard to study and is currently (like this afternoon, down your street) a topic of a significant amount of cutting edge research. As the wikipedia article above shows, the 'Histone Code' is still a work in progress, and it now appears unlikely that there is a 1:1 relationship between this chemical mark and that effect, very much unlike the very nice deterministic relationship we found between DNA->RNA->Protein.
One common change I've read about that bubbles up to normal life is the capability of nicotine to affect histone acetylation. It seems to rapidly alter histone modifications so as to make other habits/actions more addictive [1] (precisely in a way that we now know THC does not - the original 'gateway drug' mis-extrapolation).
[1] https://www.nih.gov/news-events/nih-research-matters/why-nic...