The available source contains no lifestyle data, which means the central question cannot be answered. What the research does demonstrate is that DNA damage repair processes genetically determine, to a large extent, how quickly ovaries age, and that modifying those pathways in mice extended fertility, though the latter has not yet been studied in humans.
Whether lifestyle can counteract age-related DNA damage cannot be answered on the basis of the available source. The only study provided1 deals exclusively with genetic mechanisms and animal experiments, and contains no data on diet, exercise, supplements or any other lifestyle interventions. Being honest about that limitation matters more here than offering a reassuring but unfounded answer.
What the study does show is that DNA damage repair processes (also known as DDR pathways) play a major role in how quickly ovaries age. Researchers identified 290 genetic variants in those repair pathways that partly determine when women reach menopause. Women in the top 1% of genetic susceptibility face a risk of premature ovarian insufficiency comparable to that of women with a known hereditary mutation (the FMR1 premutation). This demonstrates that genetics explains a substantial portion of the variation in ovarian ageing.
In mouse experiments, targeted modification of precisely these DDR pathways led to greater fertility and a longer reproductive lifespan. This suggests that these pathways could in principle offer starting points for future treatments, but this is a finding from animal research and has not been confirmed in humans in any way.
A longer reproductive lifespan does not come without trade-offs, however. Causal analyses in the same study show that genetically longer-active ovaries are associated with better bone health and a lower risk of type 2 diabetes, but also with a higher risk of hormone-dependent cancers such as breast cancer. That trade-off is relevant for anyone thinking about potential future interventions in this area.
All claims are drawn from a single study (PMID 34349265), a genetic population study supplemented with mouse experiments. No lifestyle data are present in this source. The level of evidence regarding lifestyle and DNA damage is therefore insufficient to make any claims.