Adverse Childhood Experiences: Addressing Health Disparities through Prevention, Early Detection, and Intervention

Last Updated: July 14, 2020

Disclosure: None
Pub Date: Monday, Dec 18, 2017
Author: Krista M. Perreira, PhD and Linda C. Gallo, PhD
Affiliation: University of North Carolina School of Medicine, Department of Social Medicine (Dr. Perreira) and San Diego State University, Department of Psychology (Dr. Gallo)

Adverse childhood experiences (ACEs) are associated with a variety of poor health behaviors and deleterious health outcomes including cardiometabolic disorders and cancer. The AHA Scientific Statement on Childhood and Adolescent Adversity and Cardiometabolic Outcomes adroitly describes the health consequences of ACEs, the bio-behavioral mechanisms underlying these effects, and the socio-demographic factors that can modify the impact of ACEs on health.1 In this commentary, we discuss the challenges of defining and measuring ACEs, identifying their prevalence, understanding their determinants and taking steps to prevent, detect, and intervene in ACEs before they compromise health. We approach this discussion through a psychosocial stress model of disease and with an emphasis on the structural determinants of health.2-4 In doing so, we bring the discussion of ACE into the context of research on health disparities.

Defining and Measuring ACEs

Suglia and colleagues1 define ACEs as “subjectively perceived threats to the safety or security of the child’s bodily integrity, family, or social structures.” From the perspectives of the psychosocial stress model3,5 and the ecobiodevelopmental framework,6 the combination of severe, prolonged, and repeated adversity with a lack of necessary coping resources (especially buffering support from a protective adult relationship) creates “toxic” stress. These experiences can accumulate over the life course, get “under the skin” through neurobiological, behavioral, psychological, and epigenetic mechanisms, and ultimately contribute to poor health.7-9

Common measures of ACEs include items assessing household dysfunction (e.g., parental mental illness, substance use, incarceration, and divorce), exposure to violence, and child maltreatment. Asked retrospectively of adults, ACE measures are similar to measures of stressful and traumatic life events in adults,10 and are subject to many of the same criticisms, including recall error, response biases, and differences in event interpretation. ACE scales also aggregate across experiences that may differentially affect health. Scores typically sum and equally weight all events, thus presupposing that only the quantity of experiences (and not their timing, severity, or form) matters. However, this is unlikely to be accurate. For example, multiple experiences of physical or sexual abuse across several years may have a far different influence on health than living with a parent or sibling with a mental illness. Moreover, there may be sensitive developmental periods during which the biological embedding of adverse experiences is intensified.7 ACE scales also focus attention on some sources of adversity while neglecting others. In research with children of immigrants and refugees, extreme economic hardship, food scarcity, discrimination, and fears of deportation are important considerations. Similarly, ACEs may need to include victimization or rejection from peers and siblings, or exposure to violence in the community.11 In short, as research on ACE progresses, deeper reflection on its conceptualization and measurement is needed.

Prevalence of ACEs

Exposure to adverse child experiences is common, with 59% of US adults reporting at least one ACE in 2009, and 8.7% reporting 5 or more ACEs.12 Prevalence varies by indicators of socioeconomic status (SES) such as education and poverty. In a 2011-2012 survey of children 0-17 years, less than 10% with family incomes at least 400% of poverty had experienced two ACEs compared to 35% of children with family incomes less than 100% of poverty.13 Similarly, 30% of children in households where neither parent had graduated from college reported two or more ACEs versus 13% of those with at least one college educated parent. Prevalence also varies across race/ethnicity groups, with non-Hispanic American Indian/Alaskan Native children (40.3%), non-Hispanic black children (31.1%), and Hispanic children of multiple races (32.75%) most likely to report two or more lifetime ACEs, followed by non-Hispanic white, Hispanic, Native Hawaiian/Pacific Islanders (about 20% for all groups), and non-Hispanic Asian children (5.3%).13 Prevalence is also high globally. A recent review of data from 93 countries estimated that 44% of children from developed countries and 59% from developing countries - more than 1 billion children overall - had experienced or witnessed physical, emotional, or sexual violence within the past year.14 Because they focus on a limited range of experiences, these prevalence figures likely underestimate ACEs. Additional research is needed to understand the full scope and impact of these occurrences

Determinants of ACEs

While most research on ACEs has focused on adult health consequences rather than determinants of ACEs, evidence suggests that exposure to adversity stems from the social, economic and institutional structures that shape an individual’s access to resources and the patterns in their daily lives.4,15 ACEs are not randomly distributed in the population, but are an endogenous, downstream determinant of health. To reduce the public health burden of ACEs, we must identify and intervene in the upstream social, economic, and institutional determinants of adversity.

Link and Phelan’s seminal treatise on the fundamental causes of disease highlights the importance of SES as a potential determinant of ACEs.15 SES is related to exposure to ACEs and many of the health conditions stemming from them.16,17 SES is not simply a confounding variable in the relationship between ACE and health, but an indicator of differential access to knowledge, power, prestige, and resources that children and their families can utilize to both protect themselves from and cope with threats.

Likewise, Dresseler and colleagues’4 structural-constructivist model highlights the racialization of social, economic, and institutional structures in society. Racial/ethnic differences in the prevalence of ACEs reflect the historical and contemporary constraints on opportunity and resources, which affect every aspect of life. From this viewpoint, prevention of ACEs requires intervention at the local, state, and federal levels. For example, laws and law enforcement practices that promote racial/ethnic disparities in prosecution, sentencing, and punishment must be addressed;18 racial/ethnic disparities in access to mental health and substance use services must be improved;19 and community resources for supporting parents must be strengthened.20

Intervening to Reduce the Impact of ACEs

In addition to primary prevention through policy and community level changes, secondary prevention to limit the deleterious impact of ACEs, and tertiary prevention and treatment for individuals experiencing mental or physical health sequela, are critical. Importantly, not all individuals who experience ACEs suffer negative health and social outcomes, a phenomenon often described in terms of “resilience”. Resilience reflects a person’s capacity to effectively cope with toxic stress so that it becomes tolerable and its impact is limited.21,22 Research suggests varied modifiable factors that can promote resilience, including children’s self-regulation, social skills, sense of personal agency, and socio-familial factors, such as proximity to a reliable, trustworthy adult caregiver.23

Education and healthcare settings represent important contexts for surveillance and intervention strategies to promote resilience and reduce the impact of ACEs by strengthening family support systems, teaching positive parenting skills, and fostering child socioemotional and language skills.24,25 Such approaches are effective in short circuiting the association of ACEs with behavioral and mental health problems.26 Moreover, recent evidence suggests that they may protect against deleterious physical health outcomes. A pilot study showed that a supportive parenting intervention for black/African-American children aged 11 and their parents reduced the association between ACEs and prediabetes,27 and between depression and accelerated epigenetic aging (DNA methylation) as measured in the offspring at age 25.28 Although preliminary, these promising findings demonstrate that the physical and mental health consequences ACEs can be addressed.


The AHA statement provides substantial evidence that ACEs play a role in cardiometabolic health outcomes across the lifespan, and identifies important directions for future research. We echo these calls for additional research to address questions around conceptualization and measurement, prospective associations, determinants and consequences, while continuing prevention, surveillance, and intervention efforts. To be maximally effective, at limiting both exposure to and consequences of ACEs, multi-sectoral programs are needed that target structural factors, communities, families, and individuals. With at least one billion children affected by ACEs globally, research addressing ACEs and how to reduce their impact is of critical importance.


Suglia SF, Koenen KC, Boynton-Jarrett R, Chan PS, Clark CJ, Danese A, Faith MS, Goldstein BI, Hayman LL, Isasi CR, Pratt CA, Slopen N, Sumner JA, Turer A, Turer CB, Zachariah JP; on behalf of the American Heart Association Council on Epidemiology and Prevention; Council on Lifelong Congenital Heart Disease and Heart Health in the Young; Council on Genomic and Precision Medicine; Council on Cardiovascular and Stroke Nursing; and Council on Quality of Care and Outcomes Research. Childhood and adolescent adversity and cardiometabolic outcomes: a scientific statement from the American Heart Association [published online ahead of print December 18, 2017]. Circulation. doi: 10.1161/CIR.0000000000000536.


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-- The opinions expressed in this commentary are not necessarily those of the editors or of the American Heart Association --