Epigenetic Resilience to Early-Life Maternal Loss in African Savanna Elephants

Early-life trauma in humans, including maternal loss, is strongly associated with increased risk of chronic diseases, reduced life expectancy, and accelerated biological aging, as measured through epigenetic modifications, such as DNA methylation. Whether similar patterns occur in other long-lived, socially complex non-primate species, however, remains unknown. Elephants share key life-history traits with humans, including longevity, strong social bonds, and advanced cognitive abilities. Yet wild elephant populations face significant anthropogenic and environmental pressures, including poaching, habitat loss, and human-wildlife conflict that can result in maternal mortality and subsequent calf orphaning. We examined whether orphaning of elephant calves was associated with accelerated DNA methylation age and distinct epigenetic signatures. Contrary to our hypothesis and patterns observed in other species, orphaned African savanna elephants exhibited a younger DNA methylation age than non-orphans, no accelerated aging, and only limited differential methylation at CpG sites. At the genome-wide level, chronological age was not associated with differential CpG methylation after correcting for multiple testing. One interpretation of these findings is that elephants may have evolved mechanisms that buffer against epigenetic instability following stressful events. Investigating these protective mechanisms in elephants could inform strategies to mitigate the long-term health impacts of early-life trauma in humans.

In most mammals, early-life adversity, including maternal loss is associated with shorter lifespans and widespread epigenetic alterations. In contrast, we found that orphaned African savanna elephants exhibited a younger epigenetic age compared to non-orphans and showed only a weak distinct epigenetic signature. This unexpected pattern may reflect environmental influences, such as living under human care, or evolutionary adaptations that buffer against epigenetic instability. If the latter is confirmed, such mechanisms could confer resilience to the epigenetic consequences of early-life adversity.