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ACEs: Best Practices

Future Research

Adverse Childhood Experiences: Future Research Directions

Roy Wade, MD, PhD, MPH; Cari Jo Clark, ScD; and Megan H. Bair Merritt, MD, MSCE

Advances in a diverse set of disciplines have led to an increased understanding of the mechanisms by which ACEs predispose individuals to poor health outcomes. ACEs have been linked to health damaging behaviors, poor psychosocial health, and physiologic disruptions in the developing brain and regulatory systems, thereby increasing risk for disease. With this new knowledge, there has been growing interest in the role that health care providers and community-based organizations can play in identifying ACEs and fostering resilience in patients and clients. For this to occur most effectively, however, researchers must develop a more nuanced understanding of the following: (1) how biological embedding contributes to health outcomes along the life course, including ways in which to measure physiological changes in the clinical setting; (2) how ACEs differentially affect diverse populations; and (3) how to effectively prevent ACEs and mitigate their impact.

Syntheses of the literature have begun to comprehensively characterize how ACEs “get under the skin.”1,2 Research has elucidated, in part, the process by which increased production of stress hormones leads to alterations in underlying molecular pathways and inflammatory mediators, eventually causing multisystem impairments.3,4,5,6 However, the field lacks standard, feasible “biomarkers” that can be used clinically to predict patient outcomes.  Specifically, more research is needed to understand the cascade of biological changes that occur as part of alterations in stress physiology, the clinical relevance of changes in specific physiologic markers, and the responsivity of these changes to intervention.  Development of such biomarkers may help clinicians treat and counsel patients and may set the stage for intervention development.

Although ACE-related studies to date have demonstrated a strong association between ACE score and adverse adult health, it is unclear how ACEs differentially affect specific populations or how ACEs contribute to the persistence of health disparities. 

  • Does the constellation of salient ACEs differ by race/ethnicity, socio-economic status, urban/suburban/rural location, socio-cultural group, immigration/refugee status, and sexual orientation? If the constellation of relevant ACEs differs by population, screening questions may need to be tailored to specific populations. 
  • Does poverty interact with ACEs to potentiate their impact?  To date, there have not been published studies examining the breakdown of ACEs by socio-demographics and analyzing these associations to determine how they may differently contribute to health outcomes among at risk populations.
  • Disparities have been noted in exposure to ACEs (e.g., by socio-economic status7 and by sexual orientation8). However, it is not clear whether differences in experiences with ACEs help account for some health disparities. If ACEs do account for part of this variance, then developing effective preventive strategies will be critical in ameliorating disparities.

Understanding the potential differential impact of ACEs by socio-demographic group may open up new strategies to bend the health-care cost curve and improve longstanding outcomes for vulnerable populations.

While the association between adult health outcomes and ACEs has been clearly documented,9,10,11,12,13 this association has not been firmly established for pediatric health outcomes. The strongest associations between ACEs and pediatric health outcomes has been documented with developmental, mental, and behavioral health.14,15 Studies that have looked for associations between ACEs and pediatric physical health outcomes have demonstrated links between ACEs and poor overall physical health but failed to investigate associations with common pediatric chronic illnesses.16,17  Further, as with much of the ACEs literature, the majority of the research investigating child and adolescent health impact suffers from limitations and biases associated with self-report of both the exposures and the outcomes, limiting the strength of the findings. With increasing trends in obesity, insulin resistance, and asthma among other chronic pediatric medical conditions, the association between ACEs and these chronic health conditions must be further explored, ideally using objectively defined measures of health impact.  Studying ACEs in pediatric populations allows researchers to follow participant cohorts prospectively rather than retrospectively, as has been done in most ACE-related studies. In addition, investigating ACEs in pediatric populations will offer researchers the opportunity to disentangle the timing related to exposure to ACEs, physiologic changes in stress reactivity, development of risky coping strategies, and acquisition of health conditions.

Finally, although the “ACEs Next Steps” document has discussed strategies for intervention and for building resilience, few are evidence-based.  Increasingly, “on the ground” organizations that are implementing intervention strategies must partner with researchers so that epidemiologically rigorous tests of ongoing programs occur.  In research trials, home-visiting and parenting programs designed to strengthen families have shown some limited efficacy among certain populations and in low-income urban communities.18,19,20 Numerous cognitive behavioral therapy programs also have shown efficacy in improving outcomes for children with significant adversity, though most of these therapy programs are only available in a limited number of communities. Cost-effectiveness studies may help promote broader dissemination. Future research must continue to identify cost-effective, evidence-based strategies that strengthen at-risk families and provide meaningful support for all patients/clients who have been affected by ACE exposure.

References and Resources

1. Miller GE, Chen E, and Parker KJ. Psychological stress in childhood and susceptibility to the chronic diseases of aging: moving toward a model of behavioral and biological mechanisms. Psychol Bull. 2011;137:959–997.

2. Shonkoff JP and Garner AS. The lifelong effects of early childhood adversity and toxic stress. Pediatrics. 2012;129;E232–E246.

3. Szyf M, McGowan P, and Meaney MJ. The social environment and the epigenome. Environ. Mol. Mutagen. 2008;49;46–60.

4. Gunnar M and Quevedo K. The neurobiology of stress and environment. Annual Review of Psychology 2007;58:145–73.

5. McEwen BS. Stress, Adaptation, and Disease: Allostasis and Allostatic Load. In Neuroimmunomodulation: Molecular Aspects, Integrative Systems, and Clinical Advances, Ann NY Acad Sci. 1998;840:33-44.

6. McEwen BS and Gianaros PJ. Stress and allostasis-induced brain plasticity. Annual Review of Medicine 2011; 62:431–45.

7. Adverse Childhood Experiences Reported by Adults—Five States, 2009. MMWR. 2010;59(49);1609-13.

8. Andersen JP and Blosnich J. Disparities in Adverse Childhood Experiences among Sexual Minority and Heterosexual Adults: Results from a Multi-State Probability-Based Sample. PLoS ONE 2013;8(1):e54691.

9. Felitti, VJ, Anda RF, Nordenberg D, et al. Relationship of Childhood Abuse and Household Dysfunction to Many of the Leading Causes of Death in Adults. American Journal of Preventive Medicine. 1998;14:245-58.

10. Edwards VJ, Holden GW, Felitti VJ, Anda RF. Relationship between multiple forms of childhood maltreatment and adult mental health in community respondents: results from the adverse childhood experiences study. American Journal of Psychiatry 2003;160:1453–60.

11. Hillis SD, Anda RF, Dube SR, et al. The association between adverse childhood experiences and adolescent pregnancy, long-term psychosocial consequences, and fetal death. Pediatrics. 2004;113:320-7.

12. Dong M, Giles WH, Felitti VJ, et al. Insights into causal pathways for ischemic heart disease: adverse childhood experiences study. Circulation 2004;110:1761–6.

13. Brown DW, Anda RF, Tiemeier H, et al. Adverse childhood experiences and the risk of premature mortality. American Journal of Preventive Medicine.2009;37:389–96.

14. Finkelhor D. Improving the adverse childhood experiences study scale. JAMA Pediatrics 2013;167:70.

15. Schilling EA, Aseltine RH, and Gore S. Adverse childhood experiences and mental health in young adults: a longitudinal survey. BMC Public Health.2007;7:30.

16. Flaherty EG, Thompson R, Litrownik AJ, et al. Adverse childhood exposures and reported child health at age 12. Academic Pediatrics. 2009;9:150–6.

17. Flaherty EG, Thompson R, Litrownik AJ, et al. Effect of early childhood adversity on child health. Arch Pediatr Adolesc Med 160, 1232–1238 (2006).

18. Coyne JC and Kwakkenbos L. Triple P-Positive Parenting programs: the folly of basing social policy on underpowered flawed studies. BMC Medicine 2013;11:11.

19. Wilson P, Rush R, Hussey S, et al. How evidence-based is an ‘evidence-based parenting program’? A PRISMA systematic review and meta-analysis of Triple P. BMC Medicine 2012;10:130.

20. Bodenmann G, Cina A, Ledermann T, and Sanders MR. The efficacy of the Triple P-Positive Parenting Program in improving parenting and child behavior: a comparison with two other treatment conditions. Behav Res Ther 2008;46:411–27.

© 2015 by Academy on Violence and Abuse

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