Cerebral Blood Flow and Vascular Function Are Impaired in Adults Who Report Adverse Childhood Events

Introduction: Adverse childhood events (ACEs), including abuse, neglect, or severe household dysfunctions, have been associated with the development of premature cardiovascular disease (CVD) during adulthood. Acute and intense emotional stress leads to structural changes in the brain that reduce cerebral blood flow, specifically in the medial prefrontal cortex (mPFC). In response, the body releases stress hormones and mediators that cause peripheral vascular dysfunction, a prognostic marker of CVD. Whether or not ACEs predispose adults to reductions in mPFC blood flow and associated peripheral vascular dysfunction has yet to be investigated. Hypothesis: This study sought to test the hypotheses that ACEs contribute to reductions in mPFC blood flow and associated peripheral vascular dysfunction. Methods: Fifty-three young adults (34 ± 3 yrs), with no evidence of overt CVD, were divided into a high (HiA) and no (NoA) ACE group based on their self-reported ACE questionnaire score: HiA: ACE score ≥ 4 (n=17) or NoA: ACE score = 0 (n=36). Near-infrared spectroscopy was utilized to assess blood flow (tHb), O 2 delivery (O 2 Hb), and O 2 consumption (HHb) in the mPFC. Peripheral vascular function was determined using the flow-mediated dilation (FMD) technique. Results: The HiA group had a significantly ( p =0.009) lower tHb compared to the NoA (56 ± 4 vs. 69 ± 3 μM, respectively). In addition, O 2 Hb and HHb were significantly ( p ≤0.04) reduced in the HiA when compared to the NoA. Likewise, FMD was significantly ( p =0.001) lower in HiA (6.3 ± 0.7%) compared to NoA (9.4 ± 0.5%). Significant associations were also identified between ACEs and tHb ( r = -0.574; p =0.001) and between tHb and FMD ( r =0.477; p =0.021). Conclusion: For the first time, we have documented that blood flow in mPFC is reduced and vascular function is impaired in adults who reported ACEs compared with adults who did not report ACEs. Notably, individuals exposed to a greater number of ACEs present with lower cerebral blood flow and higher CVD risk. Future studies are warranted to evaluate possible mechanisms underlying these dysfunctions as well as potential therapeutic interventions to reduce as well as to prevent the exacerbated CVD risk observed in individuals exposed to ACEs.