Early-life adversity leads to both mental and physical illness in adulthood. One type of adversity is injury at the hands of a care-giver—non-accidental trauma. A recent report in this journal examined young children presenting with traumatic injury and compared DNA methylation between those with and those without indicators of non-accidental trauma. They found that 27 CpG sites within FKBP5 gene were differentially methylated. This finding makes sense, as FKBP5 plays significant roles both in responses of the central nervous system to stress and in regulation of the immune system, thought to be deregulated by adverse childhood experiences (ACEs). Non-accidental injury to a child frequently occurs within a context of low scores for social determinants of health, such as food and housing security. These factors may drive vulnerability to, or directly cause, epigenetic changes. While there are many limitations to our current technology for analysis of DNA methylation levels, and this study had a relatively small sample size, the findings still offer a strong potential target for early molecular diagnosis, a biomarker to follow interventions, and a starting point for further research. The life-long impact of ACEs was reported 25 years ago, yet biological mechanisms leading to persistence across the lifespan remain mysterious.
