That's very interesting, thanks for sharing! I would be interested to see if this is related to autophagy modulation and oxidative stress given that prolonged periods of feast vs. fast may result in lower cellular turnover, and as a result, higher incidence of mutation, degradation, and greater levels of stored toxins.

Anecdotal evidence suggests intermittant and medium-term fasting promotes not only autophagy in general, but release and processing of toxins from freed lipids with ketosis. With more new cells, less malformed or damaged DNA should be present, so would that affect the DunedinPACE DNAm algorithm? For those with more time and interest, I noticed some relevant sources cited at the bottom of the report. Of particular interest are the ones regarding telomeres, the validity of the different DNAm clocks, and intermittant fasting.