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What Are Adverse Childhood Experiences (ACEs)?

Wendy Wisner is a health and parenting writer, lactation consultant (IBCLC), and mom to two awesome sons.

Ann-Louise T. Lockhart, PsyD, ABPP, is a board-certified pediatric psychologist, parent coach, author, speaker, and owner of A New Day Pediatric Psychology, PLLC.

Mixetto / Getty Images

Childhood is a vulnerable time, and what happens to us then has long deep impacts. Adverse childhood experiences (ACEs) describe traumatic experiences that can have lasting effects into adulthood. The more ACEs someone experiences, the more challenging they may be to overcome.

Let’s take a look at what adverse childhood experiences are, what impacts they may have, how to prevent them—and most importantly, how you can cope if you are someone who endured traumatic experiences in childhood.

Adverse Childhood Experiences (ACEs) are traumatic experiences that children experience before the age of 18 that can have lasting impacts on their mental health, physical health, and general well-being.

Many kinds of traumas in childhood can be ACEs. Some examples of ACEs include:

• Experiencing physical or emotional abuse
• Abandonment or neglect
• Losing a family member to suicide
• Growing up in a household with substance abuse or alcoholism
• Having a mentally ill parent
• Having an incarcerated parent
• Being a child of divorce or parental separation

Between 1995 to 1997, the Centers for Disease Control and Prevention (CDC), in conjunction with Kaiser Permanente, began the first study of ACEs with the goal of coming up with a framework for this concept.

In the study, roughly 17,000 people were interviewed about various traumatic experiences they experienced in childhood, including abuse, violence, neglect, and abandonment.

An estimated 66% of responders revealed that they’d experienced at least one ACE; 20% had experienced three ACEs. The researchers noted connections between experiencing ACEs and detriments to one’s physical health years later, including heart disease and cancer.

Risk Factors For Adverse Childhood Experiences

ACEs don’t happen randomly. A child’s economic status, family history, and the kind of community they grow up in all come into play.

Here are some of the factors that may make a child more likely to experience an ACE:

• Coming from a low income family
• Coming from a family with a low level of education
• Growing up with high levels of family stress
• Growing up with high levels of economic stress
• Growing in a family that is not close knit and doesn’t speak openly about feelings
• Having parents who used spanking or corporal punishment
• Having parents who themselves had been abused or neglected
• Living in a community with high rates of violence
• Living in an economically disadvantaged community
• Living in a community with high levels of substance abuse
• Living in a community with few resources for youth

How Common Are ACEs?

Unfortunately, ACEs are not rare. According to the CDC, about 61% of adults experienced an ACE, and 1 in 6 adults have experienced four or more different ACEs.

It’s important to note that there are racial disparities when it comes to ACEs, with children of color experiencing more ACEs than White children. As per the National Conference of State Legislatures, about 61% of Black children have experienced an ACE and about 51% of Hispanic children have.

On the other hand, 40% of white children had experienced an ACE, and 23% of Asian children had.

What Impacts Do Adverse Childhood Experiences Have?

All children live through difficult experiences at times, but with the right tools, they can learn from their experiences and become stronger. ACEs are traumas that are more difficult to overcome and that can leave lasting scars on a child, especially if the child is not supported through.

ACEs can cause what is called “toxic stress,” which is where the stress that floods the body is so intense that it can cause changes to one’s metabolism, immune system, cardiovascular system, as well as brain and nervous system. There is a cumulative effect when it comes to toxic stress, and the more ACEs a child experiences, the greater impact it can have on their mental and physical health.

Children who experience ACEs and toxic stress may:

• Have difficulty forming close relationships with others
• Have trouble keeping a job
• Have difficulty with finances
• Experience depression
• Be more likely to be involved in violence
• Experience early, unwanted pregnancies
• Be more likely to be incarcerated
• Experience higher levels of unemployment
• Be more likely to also expose their children to ACEs
• Have a higher risk of alcohol or substance abuse
• Have a higher risk of suicide attempts
• Have a higher risk of health issues such as heart disease cancer, lung disease, and liver disease

How to Prevent Adverse Childhood Experiences

The good news here is that not every child is fated to experience multiple ACEs. Parents, community members, physicians, policy makers, and anyone who works with children have an obligation to prevent ACEs.

According to the CDC, preventing ACEs in children includes several steps and is truly a group effort. Here are some of the top ways we can prevent ACEs in children:

• Policy makers can work toward increasing financial security for families and preventing food and housing insecurity
• Workplaces can make their institutions more family-friendly and establish family leave policies
• Communities and policy makers can protect against violence by promoting anti-violence campaigns and education
• Professionals who work with families can teach positive parenting skills and teach socio-emotional learning
• Policy makers can promote a strong start for children by expanding childcare, preschool, and early childhood education options
• Communities can prioritize youth services, mentors for youth, and substance abuse recovery programs

Coping With Adverse Childhood Experiences

Again, having experienced an ACE is common, and if you are someone who experienced one, you are not alone. You are also not alone in feeling the impacts of that trauma even years later.

If you are experiencing anxiety, depression, or PTSD related to ACEs, a trauma-focused therapist or social worker can help you work through this, and get to the other side. If you are also experiencing physical effects that you think are linked to this trauma, speaking to a healthcare provider is another important step.

Lifestyle changes can also help you cope with and work through your trauma. Consider adding in mediation, breathing exercises, and physical activity and exercise. Journaling is another wonderful tool that can help you unpack your feelings.

If you are recovering from a trauma like abuse, abandonment , growing up with mentally ill parents, or parents who abused alcohol or drugs, you may want to join a support group specific to that experience. Speaking with other grown-ups who experienced similar ACEs as you did can be invaluable to your recovery.

Press Play for Advice On Healing Childhood Wounds

Hosted by therapist Amy Morin, LCSW, this episode of The Verywell Mind Podcast , featuring award-winning actress Chrissy Metz, shares how to heal childhood trauma, safeguard your mental health, and how to get comfortable when faced with difficult emotions. Click below to listen now.

Follow Now : Apple Podcasts / Spotify / Google Podcasts

A Word From Verywell

If you or someone you love has experienced an adverse childhood experience, it can be difficult to talk about, think about, or even read about. Childhood traumas can live in our psyches and our bodies for years to come, and it’s common to feel triggered easily at their mere mention.

Please remember that even someone who experienced several ACEs can heal and recover from the experience. Help is out there, and it’s possible to live a full life even if you have endured trauma in childhood.

Harvard University. ACEs and Toxic Stress: Frequently Asked Questions .

Centers for Disease Control and Prevention. Preventing Adverse Childhood Experiences .

Centers for Disease Control and Prevention. About the CDC-Kaiser ACE Study .

Felitti V, Anda R, Nordenberg D. Relationship of Childhood Abuse and Household Dysfunction to Many of the Leading Causes of Death in Adults . American Journal of Preventative Medicine. 1998;14(4):P245-258. doi:10.1016/S0749-3797(98)00017-8

Centers for Disease Control and Prevention. Risk and Protective Factors .

National Conference of State Legislatures. Adverse Childhood Experiences .

Bellis M, Lowey H, Leckenby N, Hughes K, Harrison D. Adverse childhood experiences: retrospective study to determine their impact on adult health behaviours and health outcomes in a UK population . Journal of Public Health . 2014;36(1):81–91. doi:10.1093/pubmed/fdt038

Merrick M, Ford D, Ports K, Guinn A. Prevalence of Adverse Childhood Experiences From the 2011-2014 Behavioral Risk Factor Surveillance System in 23 States . JAMA Pediatrics. 2018;172(11):1038–1044. doi:10.1001/jamapediatrics.2018.2537

By Wendy Wisner Wendy Wisner is a health and parenting writer, lactation consultant (IBCLC), and mom to two awesome sons.

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Adversity in childhood is linked to mental and physical health throughout life

Read our collection on toxic stress and ptsd in children.

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• Peer review
• Charles A Nelson , Richard David Scott chair in pediatric developmental medicine 1 ,
• Zulfiqar A Bhutta , co-director, director of research 2 3 ,
• Nadine Burke Harris , surgeon general 4 ,
• Andrea Danese , professor of child and adolescent psychiatry 5 ,
• Muthanna Samara , professor of psychology 6
• 1 Department of Pediatrics, Boston Children’s Hospital and Harvard Medical School, Harvard Graduate School of Education, Boston, MA, USA
• 2 Centre for Global Child Health, Hospital for Sick Children, Toronto, Canada
• 3 Institute for Global Health and Development, Aga Khan University, South Central Asia, East Africa and UK
• 4 State of California, CA, USA
• 5 Institute of Psychiatry, Psychology and Neuroscience, King’s College London and the National and Specialist CAMHS Clinic for Trauma, Anxiety, and Depression, South London and Maudsley NHS Foundation Trust, London, UK
• 6 Department of Psychology, Kingston University London, London, UK
• Correspondence to: C Nelson charles_nelson{at}harvard.edu

The prevalence of “toxic stress” and huge downstream consequences in disease, suffering, and financial costs make prevention and early intervention crucial, say Charles A Nelson and colleagues

Today’s children face enormous challenges, some unforeseen in previous generations, and the biological and psychological toll is yet to be fully quantified. Climate change, terrorism, and war are associated with displacement and trauma. Economic disparities cleave a chasm between the haves and have nots, and, in the US at least, gun violence has reached epidemic proportions. Children may grow up with a parent with untreated mental illness. Not least, a family member could contract covid-19 or experience financial or psychological hardship associated with the pandemic.

The short and long term consequences of exposure to adversity in childhood are of great public health importance. Children are at heightened risk for stress related health disorders, which in turn may affect adult physical and psychological health and ultimately exert a great financial toll on our healthcare systems.

Growing evidence indicates that in the first three years of life, a host of biological (eg, malnutrition, infectious disease) and psychosocial (eg, maltreatment, witnessing violence, extreme poverty) hazards can affect a child’s developmental trajectory and lead to increased risk of adverse physical and psychological health conditions. Such impacts can be observed across multiple systems, affecting cardiovascular, immune, metabolic, and brain health, and may extend far beyond childhood, affecting life course health. 1 2 3 These effects may be mediated in various direct and indirect ways, presenting opportunities for mitigation and intervention strategies.

Defining toxic stress

It is important to distinguish between adverse events that happen to a child, “stressors,” and the child’s response to these events, the “toxic stress response.” 4 A consensus report published by the US National Academy of Sciences, Engineering, and Medicine (2019) defined the toxic stress response as:

Prolonged activation of the stress response systems that can disrupt the development of brain architecture and other organ systems and increase the risk for stress related disease and cognitive impairment, well into the adult years. The toxic stress response can occur when a child experiences strong, frequent, and/or prolonged adversity—such as physical or emotional abuse, chronic neglect, caregiver substance abuse or mental illness, exposure to violence, and/or the accumulated burdens of family economic hardship—without adequate adult support. Toxic stress is the maladaptive and chronically dysregulated stress response that occurs in relation to prolonged or severe early life adversity. For children, the result is disruption of the development of brain architecture and other organ systems and an increase in lifelong risk for physical and mental disorders.

What is childhood adversity?

A large number of adverse experiences (ie, toxic stressors) in childhood can trigger a toxic stress response. 4 5 6 These range from the commonplace (eg, parental divorce) to the horrific (eg, the 6 year old “soldier” ordered to shoot and kill his mother 7 ).

Adversity can affect development in myriad ways, at different points in time, although early exposures that persist over time likely lead to more lasting impacts. Moreover, adversity can become biologically embedded, increasing the likelihood of long term change. Contextual factors are important.

Type of adversity— Not all adversities exert the same impact or trigger the same response; for example, being physically or sexually abused may have more serious consequences for child development than does parental divorce. 8 9

Duration of adversity— How long the adversity lasts can have an impact on development. However, it is often difficult to disentangle duration of adversity from the type of adversity (eg, children are often born into poverty, whereas maltreatment might begin later in a child’s life).

Developmental status and critical period timing— The child’s developmental status at the time he or she is exposed to adversity will influence the child’s response, as will the timing of when these adversities occur. 10

Number of adversities and the interaction among them—— The Adverse Childhood Experiences (ACE) study 11 12 and subsequent body of ACE research provide compelling evidence that the risk of adverse health consequences increases as a function of the number of categories of adversities adults were exposed to in childhood. Although this seems intuitive, it belies the fact that, when it comes to severe adversity (eg, maltreatment), few children are exposed to only a single form of adversity at a single point in time. In addition, the effects of exposure to multiple adversities is likely more than additive. Thus, multiple forms of adversity may act in complex and synergistic ways over time to affect development.

Exacerbating factors— Children with recurrent morbidities, concurrent malnutrition, key micronutrient deficiencies, or exposure to environmental toxicants may be more sensitive to the adverse effects of other forms of toxic exposures. 13

Supportive family environments— Children develop in an environment of relationships, 14 15 16 and supportive relationships can buffer the response to toxic stress. Safe, stable, and nurturing relationships and environments are associated with reduced neuroendocrine, immunologic, metabolic, and genetic regulatory markers of toxic stress, as well as improved clinical outcomes of physical and mental health. 17 18

Pre-existing characteristics —Many of the adversities being considered are not distributed at random in the population. They may occur more commonly in children and families with pre-existing vulnerabilities linked to genetic or fetal influences that lead to cognitive deficits. 19 20 21 Infants who are more vulnerable to adverse life events (eg, stigma) include those born very early (eg, at 25 weeks’ gestation) or very small (eg, <1500 g), those born with substantial perinatal complications (eg, hypoxic-ischaemic injury), infants exposed prenatally to high levels of alcohol, or those born with greater genetic liability to develop an intellectual or developmental disability (eg, fragile X syndrome) or impairments in social communication (eg, autism).

Individual variation— Finally, children may have different physiological reactions to the same stressor. For example, Boyce, 22 has proposed that by virtue of temperament, some children (such as those who are particularly shy and behaviourally inhibited) are highly sensitive to their environments and unless the environment accommodates such children, the risk of developing serious lifelong psychopathology is greatly increased; conversely, some children thrive under almost any conditions.

Figures 1 and 2 illustrate how duration and type of adversity interact with family environments and pre-existing characteristics to affect development ( fig 1 ), and how early adversity may become biologically embedded ( fig 2 ).

The interplay of adversities, context, and human development

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Some of the pathways that mediate exposure to early adversity and adult outcomes. Exposure to adversity early in life interacts with a child’s genetic endowment (eg variations in genetic polymorphisms), which in turn leads to a host of biological changes across multiple levels. These changes, in turn, influence adult outcomes (adapted from Berens et al 23 ). HPA axis (SHRP)=hypothalamic pituitary adrenal axis (stress hyporesponsive period)

Consequences of exposure to adversity

Behavioral consequences —Childhood exposure to adversity may result in a variety of behavioral and emotional problems 7 —for example, increased risk taking, aggressive behaviour, involvement in violence (home, school, and neighbourhood), and difficulties in relationships with others. 24 25 Of great concern is the development of post-traumatic stress disorder (PTSD). 9 26

Children experiencing trauma (eg, witnessing the murder of a family member; sexual assault) are also at elevated risk of several other psychiatric disorders, including depression, PTSD, conduct problems, substance abuse, self-harm, and suicidal thoughts and attempts. 8 25 Some forms of physical and psychological abuse in early childhood can be associated with eating disorders and mental health issues affecting typical development and education.

Neurobiological consequences —Many studies have identified structural and functional differences in brain development associated with environmental stressors, such as low socioeconomic status, 27 28 29 30 31 physical abuse, 32 and care giving neglect. 33 34 For example, exposure to maternal stress in infancy has been associated with reduced brain activity, as inferred from electroencephalogram testing 35 , and profound psychosocial deprivation has been associated with differences in overall brain volume along with reductions in white and grey matter volume in several brain areas 36 37 and reduced brain electrical activity. 38 39 Differences in brain development have also been associated with decreases in several cognitive functions, 40 and particularly executive functions, 41 and distally, in educational achievement. 42

Physical consequences —Early exposure to adversities, especially poverty, is associated with linear growth failure and wasting, and has recently been shown to be associated with reduced brain volume 43 and altered functional connectivity. 44 Children exposed to higher psychological stress have been shown to have higher cortisol levels and greater risk of common diseases of childhood, including otitis media, viral infections, asthma, dermatitis, urticaria, intestinal infectious diseases, and urinary tract infections. 45

Childhood adversities have also been associated with greater risk of adult chronic conditions, including cardiovascular disease, stroke, cancer (excluding skin cancer), asthma, chronic obstructive pulmonary disease, kidney disease, diabetes, overweight or obesity, and depression, as well as increased health risk behaviours. 46 47

Tables 1 and 2 show many of the physical and psychological harms observed among children and adults exposed to adversity early in life.

Health conditions in children associated with adverse childhood experiences (ACE)

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ACE-associated health conditions in adults associated with adverse childhood experiences (ACE)

What mediates the effects of adversity?

The link between exposure to adversity early in life and physical and psychological development are thought to be mediated through several direct and indirect pathways. We first talk about the effects on physical development, then turn our attention to psychological development.

Effects mediated directly may include altering the regulation of stress-signalling pathways and immune system function 48 ; changing brain structure and function 49 ; and changing the expression of DNA and by accelerating cellular ageing. 50 51 For example, abuse or neglect might directly lead to physical injury or undernutrition or malnutrition. Similarly, stress can directly lead to dysregulation of the hypothalamic-pituitary-adrenal axis and associated neuro-endocrine-immune 19 as well as epigenetic effects. 52

Effects mediated indirectly might include changing the quality of the care giving environment (eg, less responsive care 3 ) or the surrounding distal environment (eg, neighbourhood violence, which in turn will affect child development across several levels 53 ); or building dysfunctional cognitions about the self and the world. 25 54 55 The effects of food insecurity (leading to undernutrition or malnutrition) and unsafe or substandard housing (resulting in exposure to asthmagens or environmental toxicants such as lead) can lead to social disparities in health. 4 Distal effects of adversity include the early adoption of health damaging behaviors (eg, smoking, poor food choices) that later in life lead to diabetes, heart disease, and metabolic syndrome. 47

On the psychological side, early adversity can lead to the development of psychopathology early in life (eg, disruptive behavior) that later in life manifests in more severe forms (eg, antisocial personality). Furthermore, it can lead to the development of dysfunctional cognition about self and others. 54 The interplay of these different mediation mechanisms remains largely unclear.

Modelling the effects of adversity must take into consideration the type of adversity, the duration and timing of the adversity, the synergistic effects of multiple forms of adversity with the child’s genetic endowment ( fig 2 ), and the social supports and interventions on which the child can depend (such as caregivers to whom the child is attached).

What can we do now?

If we wish for today’s youth to inherit a world that is safe and conducive to healthy development, we must do all we can to create such a world, by preventing disorders from developing and intervening once they are apparent.

Even for children living in adverse circumstances, much can be done now to make a difference by preventing such disorders from developing and intervening once they have surfaced. For example, we can screen children experiencing adverse life events, and once screened refer such children to early intervention services, as California is doing (see elsewhere in this collection).

Intervention strategies have been developed to help children manage their toxic stress response 7 56 and to help families cope with adversity. Many children are resilient, and physician-community partnerships can help foster resilience. 26

Recommendations for research

Much of the evidence has depended on the use of self- or parent-report measures, which are relatively easy to score, can be scaled at population level, and can be used (with modification) across cultures. However, such measures are inherently subjective and prone to biases (eg, recall bias). Other measures, such as official court or child protection records, provide a more objective assessment but often underestimate the prevalence of adversity.

Objective and subjective measures of childhood adversity identify largely non-overlapping groups of individuals 57 and, thus, may be associated with health outcomes through different pathways. Subjective experience is particularly important for psychopathology, over and above objective experience. 54

A challenge in examining the effects of adversity on development is how to compare children growing up in different cultures. For example, one study 58 reported that a questionnaire on bullying used in different cultures and countries did not generalize well (eg, how one culture interpreted bullying differed from another). Adversity and trauma should be considered in context, and investigators in different cultures may need to develop different assessments.

To move away from subjective evaluations of toxic stress (eg, self- or other-report), and to gain insight into the neural and biological mechanisms that mediate the toxic stress response, several investigators have started to develop more objective biomarker panels for screening for toxic stress that use markers of neurological, immunological, metabolic, and genetic regulatory derangements. 59 60 61 As this work continues, issues to consider include how much better (eg, as predictors) such measures are than behavior, how early in life they can be used, and whether they are scalable.

The study of toxic stress and the toxic stress response needs to move away from correlational and cross-sectional studies and deploy designs that are amenable to drawing causal inference. This would include longitudinal studies and ideally studies that involve interventions. An advantage of the latter includes the ability to shed light on mechanism.

More attention also needs to be paid to individual differences. Different people respond differently to the same stressors. For example, only a minority of children who experience trauma or maltreatment go on to develop enduring psychiatric disorders; and some children develop physical health disorders such as asthma whereas others will not. 62 In addition, individual differences exist in biological sensitivity to stressors: for example, children identified as shy or inhibited early in life may be more vulnerable to stressors than children with more robust temperaments and who are less fearful of novelty 63 64 65 and are more predisposed to anxiety as adults. 66

Recommendations for policy

Policy is only as good as the underpinning evidence, and these recommendations have sufficient evidence to support them.

Careful consideration should be given to implementing evidence-informed policies for optimizing health, nutrition, and early child development, 67 which in turn can be expanded to include older children and adolescents. Although the first three years of life are generally emphasized, older children exhibit remarkable plasticity in molding their personalities and behaviors. 27 68 Effective interventions exist to treat and possibly prevent psychopathology emerging after childhood trauma, but implementation needs to be scaled up. 7

Linking and optimizing preventive child health and education initiatives early in life are key to successful intervention 69 and need to be done at the appropriate level in the health and education systems. The development of the nurturing care framework 70 has been a welcome step in this direction, engaging platforms such as community health workers and pre-schools . 71

Community, school, and after-school based interventions can reduce the effects of traumatic events among children and adolescents living in adverse circumstances. 25 72

Public health strategies for primary, secondary, and tertiary prevention of childhood maltreatment and adversity include both universal and targeted interventions, ranging from home visiting programs to parent training programs, routine screening for adversity, and cognitive behavioral therapy. 73 74

Key recommendations

Researchers should consider both objective and subjective measures of childhood adversity

Researchers should broaden assessment of interventions beyond mental health measures to more regularly include health outcomes such as asthma, infection, inflammation, and insulin resistance

Adversity and trauma should be considered in context, and investigators in different cultures may need to develop different assessments

Researchers should consider how much better (eg, as predictors) objective biomarker panels are than behavior, how early in life they can be used, and whether they are scalable

Researchers should move towards longitudinal studies and ideally studies that involve interventions

Researchers should pay more attention to individual differences

Governments should implement evidence-informed policies for optimizing health, nutrition, and early child development

Health and education systems should link and optimize preventive child health and education initiatives early in life at the appropriate level

Use community, school, and after-school based interventions

Consider public health strategies for primary, secondary, and tertiary prevention of childhood maltreatment and adversity

Acknowledgments

We thank Lee Anglin and Lily Breen for proofing the manuscript.

Competing interests: We have read and understood BMJ policy on declaration of interests and have no relevant interests to declare.

Provenance and peer review: Commissioned; externally peer reviewed.

This article is part of a series commissioned by The BMJ for the World Innovation Summit for Health (WISH) 2020. The BMJ peer reviewed, edited, and made the decisions to publish. The series, including open access fees, is funded by WISH.

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ .

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• Published: 18 January 2021

The social ecology of childhood and early life adversity

• Marcela Lopez 1 ,
• Monica O. Ruiz 1 , 2 ,
• Cynthia R. Rovnaghi 1 ,
• Grace K-Y. Tam 1 ,
• Jitka Hiscox 1 , 3 ,
• Ian H. Gotlib 4 ,
• Donald A. Barr 2 , 5 ,
• Victor G. Carrion 6 &
• Kanwaljeet J. S. Anand 1 , 2  

Pediatric Research volume  89 ,  pages 353–367 ( 2021 ) Cite this article

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An increasing prevalence of early childhood adversity has reached epidemic proportions, creating a public health crisis. Rather than focusing only on adverse childhood experiences (ACEs) as the main lens for understanding early childhood experiences, detailed assessments of a child’s social ecology are required to assess “early life adversity.” These should also include the role of positive experiences, social relationships, and resilience-promoting factors. Comprehensive assessments of a child’s physical and social ecology not only require parent/caregiver surveys and clinical observations, but also include measurements of the child’s physiology using biomarkers. We identify cortisol as a stress biomarker and posit that hair cortisol concentrations represent a summative and chronological record of children’s exposure to adverse experiences and other contextual stressors. Future research should use a social–ecological approach to investigate the robust interactions among adverse conditions, protective factors, genetic and epigenetic influences, environmental exposures, and social policy, within the context of a child’s developmental stages. These contribute to their physical health, psychiatric conditions, cognitive/executive, social, and psychological functions, lifestyle choices, and socioeconomic outcomes. Such studies must inform preventive measures, therapeutic interventions, advocacy efforts, social policy changes, and public awareness campaigns to address early life adversities and their enduring effects on human potential.

Current research does not support the practice of using ACEs as the main lens for understanding early childhood experiences.

The social ecology of early childhood provides a contextual framework for evaluating the long-term health consequences of early life adversity.

Comprehensive assessments reinforced with physiological measures and/or selected biomarkers, such as hair cortisol concentrations to assess early life stress, may provide critical insights into the relationships between early adversity, stress axis regulation, and subsequent health outcomes.

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The social ecology of childhood includes positive and negative experiences, providing children with a socio-biological framework to meet age-specific developmental goals. Disruptions in this ecology, including frequent low-grade stressors (insecurity, inattention), marked variability (life changes), and trauma (abuse/neglect), can have deleterious effects on children’s health and wellbeing that may continue into adulthood . 1 , 2 Researchers studying the lifelong effects of a child’s social ecology have focused primarily on major adverse events. Metrics like the adverse childhood experiences (ACEs) questionnaire are administered in public health efforts to evaluate, understand, and prevent the health outcomes associated with childhood trauma. 3 , 4 Beyond the ACEs, however, preventable sources of early life stress (ELS) may include food and housing insecurity, bullying, discrimination, inattentive parenting, or family separations. Clinicians do not routinely screen for trauma or the child’s social ecology, partly due to the lack of validated, objective metrics that can be assessed longitudinally.

We review the current discourse on the social ecology of early childhood in relation to the child, adolescent, and adult health outcomes, summarize previous social ecology theories, and compare quantitative metrics. We argue that the practice of using ACEs as a method for understanding early life experiences paints a two-dimensional picture of the many interacting factors that comprise a growing child’s multi-dimensional environment. We review the underlying physiology of neuroendocrine stress responses and further contend that biomarkers, such as hair cortisol concentrations (HCCs), may provide critical insights into the relations among early adversity, stress, hypothalamic-pituitary-adrenal (HPA)-axis regulation, and subsequent health outcomes.

Social ecology of childhood: a historical perspective

French philosopher Jean-Jacques Rousseau (1712–1778) first proposed that early childhood experiences establish adult behaviors. Lev Vygotsky (1896–1934) from Moscow proposed the role of social and cultural factors in his theory of speech development, described in his book Thought and Language (1934). This work influenced many, including Jean Piaget (1896–1980), to propose theories of cognitive development in early childhood. Thomas and Znaniecki established a life-course perspective through their longitudinal studies (1918–1920) of Polish peasants in Europe and America. 5 Across the twentieth century, 6 , 7 , 8 , 9 , 10 early childhood experiences were associated with cognitive, behavioral, social, and psychological outcomes, including the influences of family size and socioeconomic status, 9 kindergarten enrollment, 10 , 11 and social class. 8

These factors were integrated into the Ecological Systems Theory by Urie Bronfenbrenner (1979), a Russian-American psychologist. Bronfenbrenner conceptualized that human development is shaped by complex relationships between individuals and their environments. 12 He argued that contemporary understanding of human development had failed to consider interactive, layered systems within a child’s environment. 13 These limitations led him to develop the Ecological Systems model.

Bronfenbrenner’s model depicts four systems—the microsystem, mesosystem, exosystem, and macrosystem—embedded in a chronosystem representing the era in which an individual grows up (Fig.  1 ). The microsystem comprises interactions, roles, and relationships within the home, child-care centers, or playgrounds. 12 The interplay among different microsystems is the mesosystem . 12 The exosystem consists of extrinsic environments that affect the child indirectly (where the child is not an active participant), like the parents’ work environments, sibling’s school, or local government. 12 Lastly, the macrosystem encompasses greater societal characteristics, such as norms, customs, beliefs, and political structures. Bronfenbrenner’s model serves as a useful tool for exploring, categorizing, and interpreting different facets of children’s environments and experiences. It identifies a plethora of micro- and macro-level characteristics and encourages us to consider factors that impact a child’s life outside their insular family unit. This model presented a major breakthrough in theorizing the complicated structures of societies, and allowed us to organize complex, hierarchical systems within a Person, Process, Context, and Time framework 14 to address issues at the core of programs and policies targeting children at the family and community level.

Bronfenbrenner’s Ecological Systems Theory presented a breakthrough model for theorizing how the complex, hierarchically organized systems in societies can interact with a child’s life, with a rich interplay between systems leading to the variable or opposing effects on early life adversity (ELA).

Other conceptual models have since been developed to assess the relationship between children’s broader social contexts and their health. In his 1992 book, The Strategies of Preventive Medicine , Geoffrey Rose stated that “the primary determinants of disease are mainly economic and social, and therefore its remedies must also be economic and social.” 15 His colleagues, Michael Marmot and Richard Wilkinson, as part of a World Health Organization initiative, expanded on his work to identify the social and economic characteristics that significantly influenced individuals’ wellbeing and life expectancy, and referred to these as the Social Determinants of Health. 16 They focused on poverty, drug addiction, working conditions, unemployment status, access to food, social support, and transportation infrastructure. Other determinants identified since then include social organization, race/ethnicity, gender, immigrant status, neighborhood, and housing characteristics. 16

The Life Course Theory emphasizes the timing and temporal context of lived experiences and how they can impact an individuals’ development and wellbeing. 5 In response to the notion that “changing lives alter developmental trajectories,” 5 Glen H. Elder proposed the four principles of Life Course Theory in 1998 as: (1) “the life course of individuals is embedded in and shaped by historical times and places they experience over their lifetime”; (2) “the developmental impact of a succession of life transitions or events”; (3) “lives are lived independently, and social and historical influences are expressed through this network of shared relationships”; and (4) “individuals construct their own life course through the choices and actions they take within the opportunities and constraints of history and social circumstances.” 5

Epidemiologist Nancy Krieger proposed the concept of “embodiment” in 2005, which she defined as “referring to how we literally incorporate biologically, the material and social world in which we live, from conception to death,” arguing that human biology could not be understood without “knowledge of history and individual and societal ways of living.” 17 Through this lens, human interactions “become” human biology. Anthropologist Clarence Gravlee applied this concept to explain how and why racialized experiences and social constructs can negatively impact the health of racial and ethnic minorities in the United States. 18

Despite widespread acceptance of these theoretical constructs, most studies focus solely on adversities within the home, testing their associations with physical, 19 , 20 , 21 , 22 and mental health outcomes. 23 Many authors use the term ELS to link adverse experiences in a child’s life with negative health outcomes; 1 , 2 , 24 , 25 , 26 other scholars refer to this phenomenon as “toxic stress”, 27 , 28 with no consensus on the nomenclature used to describe relationships between childhood adversity and potential health outcomes. While the ‘stress’ caused by adversity may explain many long-term consequences, ‘stress’ is not the operative factor for all observed outcomes. 1 , 24 Instead, we prefer early life adversity (ELA) as a more holistic term, including family functions, socioeconomic factors, social supports, neighborhood characteristics, and other factors, more suited for linking early adversities with long-term outcomes. Several measures have been developed to study ELA, with most relying on adult retrospective recall.

Measures of ELA

Several inventories, systematically reviewed by Vanaelst et al., 29 assess the frequency of adverse childhood events (Table  1 ). These were adapted from existing stress questionnaires and modified to inquire about major life events, chronic environmental strains (family, school, relationships, health), and other childhood-related stressors. 29 , 30 , 31 A cumulative risk approach was first proposed by Holmes and Rahe 32 in their Social Readjustment Rating Scale , then applied to child adversities by Rutter, 33 and subsequently followed in other studies. 34 , 35 This approach rests on the scientific premise that challenges in one domain are easier to negotiate than challenges in multiple domains. It was simple to use, easy to understand, generated strong statistical associations to engage non-academic stakeholders, 36 accounted for the co-occurrence of childhood adversities, 37 and helped to identify people at highest risk for poor outcomes. 22

Against this backdrop, Vincent Felitti decided to focus on a specific set of ACEs. Felitti 38 observed that dropouts from an adult obesity program had experienced adverse events as children or youth. Detailed patient interviews revealed that childhood abuse was common and predated their obesity; thus, obesity was a self-protective solution to prior adverse experiences and not their primary problem. With Robert Anda and others, Felitti designed the ACE study, which surveyed 9508 adults with about ten adverse experiences. 30 , 39 , 40 , 41 Compared to individuals with no ACEs, persons exposed to four or more ACEs had 4- to 12-fold higher risks for drug abuse, alcoholism, depression, and suicide, 2- to 4-fold increased risks for smoking, poor health, multiple sexual partners, and sexually transmitted diseases, and 1.4- to 1.6-fold increased risks for physical inactivity and obesity. 36 , 38 ACEs also showed linear relations with heart disease, cancer, lung disease, fractures, liver disease, and multiple health outcomes.

By summing a fixed number of ACEs, Felitti and others created a quantitative method for estimating childhood adversities. 36 , 38 Their work stimulated research, social policy, and public health measures to combat the increasing prevalence of ACEs, and extended the movement for trauma-informed care into the pediatric age groups. 31

Prevalence of ACEs

The increasing prevalence of ACEs is a major public health concern. 29 , 30 , 42 , 43 In the ACEs study, 63.5% of adults recalled at least one ACE and 12% recalled four or more ACEs. 44 Subsequent studies, not limited to adult respondents, reported higher prevalence rates of 67–98%. 45 , 46 , 47 Preschool children are at greatest risk for child abuse and neglect, 48 or domestic violence, 38 , 49 but cannot report these experiences due to limited behavioral or verbal expressions. 38 ACEs in early childhood remain underreported and underestimated. 28 , 37 , 48 , 50

The US Children’s Bureau reported that 678,000 children suffered abuse and neglect in 2018, with a crude prevalence rate of 9.2 per 1000 children. Of these, 60.8% were neglected, 10.7% physically abused, 7.0% sexually abused, and 15.5% suffered two or more types of abuse. 51 Although caregivers often minimize or fail to report the maltreatment of preverbal children, 52 children <1 year of age had the highest rates of abuse (26.7 per 1000 children). In 2018, 1770 children died of abuse/neglect (case fatality rate 2.39 per 100,000 children), with the highest case fatality rates in infants below 1-year (case fatality rate 22.8/100,000 children). 51 Cumulative exposures have multi-layered effects on child development, with a “mediated net of adversity” that simultaneously augments their risk across cognitive, quality of life, social, economic, psychiatric, and physical health outcomes. 53

Health implications of ACEs

A systematic review of pediatric health outcomes associated with ACEs found prospective evidence for impaired physical growth and cognitive development, higher risks for childhood obesity, asthma, infections, non-febrile illnesses, disordered sleep, delayed menarche, and non-specific somatic complaints. 54 These outcomes depended on the ACE characteristics, age of occurrence, and specific types of exposures. For example, prospective studies showed that parental discord or violence was associated with obesity in childhood, 55 , 56 and other prospective studies showed that physical or sexual abuse was associated with youth obesity. 57 , 58 , 59 From prospective data, Brown et al. 39 clustered the specific ACEs that led to specific risks, to form an ACE-directed tree for identifying health outcomes. For each additional ACE, children were 29‐44% more likely to have complex health problems, with multiple needs across developmental, physical, and mental health.

Children aged 2–5 years exposed to caregiver mental illness were most likely (56–57%) to have complex health concerns, with the additive effects of other risk factors. 39 A significantly higher prevalence of four or more ACEs was found in children with multiple unexplained chronic symptoms in six functional domains (executive dysfunction, sleep disturbances, autonomic dysregulation, somatic complaints, digestive symptoms, emotional dysregulation) compared to matched controls (88% vs. 33%); 60 suggesting a syndrome of nervous system dysregulation in these children, much like that seen in Gulf War veterans. 61

Retrospective studies based on adult recall linked ACEs with an increased vulnerability to chronic non-communicable diseases, substance abuse, sexual risk-taking behaviors, 45 , 46 , 50 , 62 , 63 , 64 , 65 suicide, domestic violence, 63 , 66 , 67 , 68 , 69 and worse physical and mental health. 42 , 57 , 70 , 71 , 72 From 24,000 adults in the World Mental Health Surveys, retrospective data on childhood adversities doubled the risk of adult psychotic episodes, accounting for 31% of psychotic episodes globally. 73 Sexual abuse, physical abuse, and parent criminality had the strongest associations with later psychotic episodes. 73

A meta-analysis of adult health outcomes following four or more ACEs found increased risks for all 23 health and social outcomes, with weak associations for physical inactivity, weight gain, and diabetes; moderate associations for smoking, heavy alcohol use, poor self-rated health, cancer, heart, lung, and digestive diseases; stronger associations for sexual risk taking, mental ill health, problematic alcohol use, and decreased life satisfaction; and the strongest associations for drug abuse, interpersonal violence, and suicide 41 (Table  2 ). Thus, ACEs not only contribute to global burdens of adult disease, but their strongest associations with drug abuse, domestic violence, and suicide may directly inflict ACEs onto the next generation. 74 , 75 , 76

Genetic and epigenetic changes

These intergenerational effects are accentuated via altered gene expression through conserved transcriptional responses to adversity (CTRA), 77 coupled with epigenetic changes, such as telomere shortening, reduced stem cell populations, elevated methylation, and nitration states, among genes in the stress-responsive, inflammatory, or other pathways. 78 , 79 , 80 , 81 Stress-associated epigenetic changes contribute to aberrant neuronal plasticity, 82 affect disorders, 82 post-traumatic stress disorder, alcohol use disorder, 83 and depression, 84 , 85 , 86 , 87 transmitting their physical and mental health risks to future generations. 41 , 88 , 89 Mechanisms of stress-associated epigenetic changes may involve DNA methylation or histone acetylation 80 , 84 , 86 , 90 , changes in mitochondrial DNA copy number and mitochondrial dynamics, 80 and microRNAs that are transported via exosomes or binding proteins 91 to regulate the signaling pathways for gene silencing, cellular differentiation, autophagy, and apoptosis. 92

From a systematic review of epigenetic changes in HPA-axis genes, Argentieri et al. 78 found prospective evidence for methylation of HSD11beta2 with hypertension, NR3C1 with small cell lung cancer and breast cancer, and FKBP5 and NR3C1 with post-traumatic stress disorder (PTSD), as well as plausible associations of FKBP5 methylation with Alzheimer’s disease. In particular, the glucocorticoid nuclear receptor gene NR3C1 undergoes methylation in varying gene regions from different social and environmental exposures, associated with different mental health outcomes.

Focusing solely on PTSD-associated genetic changes, Blacker et al. 79 found 3989 genes upregulated and 3 genes downregulated from 4 GWAS studies in PTSD patients. Among the differentially methylated genes, DOCK2 (dedicator of cytokinesis 2) and MAN2C1 (α-mannosidase), were associated with immune system dysregulation in PTSD subjects. Urban African-American males with PTSD showed increased global DNA methylation and differential DNA methylation in several genes: decreased in TPR (nuclear membrane trafficking) and ANXA2 genes (calcium-regulated membrane-binding protein), increased in CLEC9A (activation receptor on myeloid cells), ACP5 (leukemia-associated glycoprotein), and TLR8 genes (innate immunity activation). 93 In African-American women with PTSD, this study found a higher methylation of the HDAC4 (histone deacetylase 4) gene. 93 A systematic review of stress-associated epigenetic changes and depression found differential methylation of NRC31 , SLCA4 , BDNF , FKBP5 , SKA2 , OXTR , LINGO3 , POU3F1 , and ITGB1 , associated with altered glucocorticoid signaling ( NR3C1 , FKBP5 ), serotonergic signaling ( SLC6A4 ), and neurotrophin genes ( BDNF ). 81 Another systematic review confirmed that ELS-triggered epigenomic modulation of NR3C1 was correlated with major depressive disorder. 94

Childhood socioeconomic deprivation and ACEs can lead to adult diseases by increasing their inflammatory burden via multiple genetic factors, including single-nucleotide polymorphisms, and epigenetic factors, including nuclear factor-κB-mediated gene methylation and histone acetylation. These changes increase expression of pro-inflammatory cytokines, reactive oxygen species, reactive nitrogen species, and induce several microRNAs ( miR-155, miR-181b-1 , and miR-146a ), with widespread effects on the immune system. 80 ELA also alters HPA-axis reactivity in adulthood by (i) genetic factors, such as glucocorticoid receptor polymorphisms; (ii) epigenetic factors altering glucocorticoid receptor function, including methylation of NR3C1 , FKBP5 , and HSD11beta2 ; (iii) chronic inflammation due to chronic nitrosative and oxidative stress; and (iv) brain mitochondrial DNA copy number and transcription, with altered mitochondrial dynamics, structure, and function in adulthood. 80

Limitations of the ACE score

Despite the known effects of ACEs on genetic/epigenetic changes and long-term health outcomes, it is short-sighted to focus only on ACEs for clinical decisions related to ELA. Newer frameworks must include factors ignored by ACE scores, including (a) the age of onset and offset; (b) severity of trauma; (c) frequency of traumatic events; (d) periodicity of trauma within specific developmental periods; (e) concurrence of traumatic events; and (f) multiplicity of events across childhood. 44 Thus, popular use of the ACE score as a proxy for toxic stress appears grossly inadequate.

The American Academy of Pediatrics defines toxic stress “as the excessive or prolonged activation of physiologic stress response systems in the absence of the buffering protection afforded by stable, responsive relationships”. 27 , 28 However, toxic stress depends on the child’s complete social ecology, including multiple variabilities in their adverse experiences, environmental conditions, and protective factors. 1 , 31 , 95 , 96 Lacey and Minnis 44 argued that because all ACEs do not carry the same emotional weight or elicit similar distress levels, binary “yes/no” responses cannot represent their impact on the child. Lack of consistency in defining ACEs also makes it difficult to compare childhood adversities across different studies; 44 further limited by the lack of self-report, absence of protective factors, and dependence on caregiver report. 29 , 44 Caregivers may be more inclined to report their child’s behaviors as “problematic” than to divulge personal difficulties, family dynamics, or household dysfunctions. 29

The ACE score originated as an epidemiological research tool based on adult interpretations of their childhood experiences, but has since been extrapolated to clinical settings. 97 , 98 California launched a public health initiative in 2020 to screen children for ACEs in all outpatient visits. 43 However, there is a limited practical experience of ACE screening in the clinic, limited resources to address the identified ACEs, and nominal evidence-based algorithms for managing children with multiple ACEs. 29 , 44 If clinically screened ACEs do not relate to recent trauma and the patient appears asymptomatic, the next steps remain unclear. 40 , 43 Potential outcomes of this policy may include unnecessary referrals to child-protective services or pediatric subspecialists. 30 , 43 The inconsistent description of ACEs in different inventories highlights the broader point that there is no consensus on how to define childhood adversity or grade its intensity. 44 This has serious implications for how the ACEs questionnaire is used outside of epidemiology, especially to inform clinical, social, or policy interventions.

Other factors in the social ecology of childhood

ELA incorporates broader features beyond the individual experiences identified as ACEs. 99 For instance, the association between ACEs and child health was strengthened when researchers also accounted for interpersonal victimization (community violence, property crime, bullying), highlighting the cumulative harm from different forms of trauma. 66 ELA can be attributed to factors within all ecological systems affecting individuals, families, communities, or broader societies. 50 , 100 The rich interplay between these systems must be emphasized, since significant ecological factors are not “stand-alone” but can alter multiple systems at once.

Individual factors

Effects of childhood adversity typically emphasize the unidirectional effect of negative experiences on child development, disregarding individual demographics, or personality factors. Substantial theoretical work on child development highlights the transactional and dynamic interplay between individuals and their environment. 101 Sameroff and Chandler 102 consider developmental outcomes to be a function of such transactions, which exert continual effects on one another. Similarly, individuals function as active and self-regulating entities, changing dynamically with the environment and also changing their environment. 103 Thus, explanations for emerging health outcomes must account for mutual interactions between individual children and their environmental inputs. 101

Household factors

Family environments, characterized by overt conflict, neglect, passive aggression, or unaffectionate interaction styles 104 are associated with a broad range of mental and physical health disorders. 38 , 88 Parental traumatic experiences and environments can affect the quality of parenting and child development. 88 Maternal depression and trauma are associated with increased rates of insecure attachment in children, 105 , 106 , 107 , 108 related to decreased maternal responsiveness and affective availability. 105 , 109 , 110

Sustained economic problems affect children directly by limiting material resources and indirectly through parental distress, which undermines the parents’ capacity for supportive and consistent parenting. 111 , 112 For example, fathers facing financial losses became more irritable, tense, and explosive, with punitive, rejecting, and inconsistent disciplining behaviors, associated with emotional difficulties in their children. 112 , 113 , 114

Community factors

Neighborhood deprivation negatively impacts mental and physical health lasting into adulthood, 115 likely related to telomere shortening, 116 , 117 altered cortisol regulation, 117 increased inflammation, 118 and differential DNA methylation. 119 Children who grow up in communities with higher rates of violence, crime, and noise may suffer from increased stress and lasting trauma. 120 , 121 , 122 Poor local infrastructure can also affect access to resources, such as food and healthcare, which can exacerbate health issues. 122

Broader societal factors

Negative societal attitudes and biases, like racial discrimination or segregation, pervade all aspects of a child’s ecology and persist over time; therefore, evaluating these factors is particularly important for long-term health outcomes in children of color. 123 , 124 , 125 Perceived racial discrimination and stereotype threat can trigger stress responses and can affect cognitive processes and academic performance. 126 For example, greater perceived discrimination was associated with greater cortisol output in Mexican–American youth. 127 Childhood exposures to interpersonal racial discrimination and structural racism stemming from media, schools, law enforcement, government policies, and other cultural stressors also lead to psychological distress and changes in allostatic load for racial minorities in the United States 124 , 125 While negative inputs clearly affect the developing brain, positive inputs and protective factors, such as social buffering or individual resilience, play equally important roles 44 , 101 (Fig.  2 ).

Governmental, socioeconomic, and cultural factors in the macrosystem may steer the child’s exosystem either towards adversity or adaptation. ELA (red box/arrows) and adaptation (green box/arrows) may work in tandem to build a child’s resilience, support education, income adequacy, health equity, and access to basic social services. The mesosystem forms an interface between the exosytem and the family unit with variable effects on the child’s milieu. In the microsystem, children are exposed to ELA or pro-social affiliations that affect their developmental, cognitive, behavioral, and health outcomes.

Protective factors in the child’s social ecology

ELA research must account for the factors that temper adversity, including support, temperament, resilience, and adaptation. For example, the Risky Families questionnaire includes supportive factors (e.g., parental love and support, household dynamics) and ACEs. 128 Although stress biology is highly susceptible to early experiences, it is just as malleable to supportive and protective factors. 129 , 130 We discuss the role of positive experiences, social relationships, and resilience factors that help children cope with adversity.

Positive experiences

Greater emphasis on positive and supportive experiences, fundamental to developing healthy brain architectures and buffering children against the effects of contextual stressors, 131 , 132 would complement existing data on the health consequences of ELA. A validated method to assess positive/protective experiences in ELA is the Benevolent Childhood Experiences scale. 133

The Healthy Outcomes from Positive Experiences (HOPE) framework led by Sege et al. 134 focuses on promoting positive childhood experiences to prevent or mitigate the effects of ELA. HOPE creates a strong foundation for learning, productive behavior, physical, and mental health. Given that young children experience their world through their relationships with parents and other caregivers, positive childhood experiences that engage the child, the parent, and the parent–child relationship are essential. 131 , 132 In Wisconsin, positive childhood experiences were associated with dose-dependent reductions in the adult mental health and relational health impairments resulting from ACE exposures. 135

HOPE identifies four broad categories of positive experiences and their effects on child development: (1) Sustained supportive relationships are associated with better physical and mental health, fewer behavior problems, higher educational achievement, more productive employment, and less involvement with social services and criminal justice systems. 131 (2) Growing and learning in safe, stable environments are important for children’s physical, emotional, social, cognitive development, and behavioral health, conferring lifelong benefits. 100 , 131 (3) Opportunities for constructive social engagement and connectedness can promote secure attachment, belonging, personal value, and positive regard. 131 , 136 , 137 (4) Social and emotional competencies cultivate self-awareness and confidence, laying the foundation for learning and problem-solving, identity development, communication skills, and secure personal relationships. 131

Social relationships

Bowlby 138 observed that children separated from their mothers showed intense distress and later maladjustments. In the Attachment Theory , he posited that uninterrupted, secure maternal–infant bonding was evolutionarily adaptive. Beginning with maternal–infant bonding, the layering of nurturing, supportive relationships throughout child development enriches self-perception, self-image, and coping skills. Positive social relationships also reduce pain ratings, HPA-axis reactivity, and aberrant brain activation. 129 , 139 , 140 , 141 , 142 Perceived social support from friends (not family members) was associated with fewer trauma symptoms in adult survivors of childhood maltreatment. 143 Culture‐related protective factors can also be leveraged to overcome ELA and promote normal development. 144 Thus, social connections with family and non-family members may protect against stress responses to adversity across the lifespan.

Resilience science grew out of concerted efforts to understand, prevent, and treat mental health problems. 145 Scientists observed that some children adapted remarkably well despite high levels of adversity. Resilience generally refers to the capacity of any system to recover from exposure to stressors or adversity; it is a mirror image of vulnerability, with processes and capacities common to both. 145 , 146 , 147 Feldman argues that the construct of resilience involves systems and processes that tune the brain to its social ecology and adapt to its hardships. 148 In traumatized children, Happer et al. 149 found stronger evidence for resilience as a process, partial support for resilience as an outcome, but none for resilience as a trait.

While resilience research is summarized elsewhere, 147 , 148 , 150 , 151 an emerging list of resilience factors in children is featured in Table  3 . 147 Resilience science distinguishes between protective and promotive factors; protective factors have greater effects in the context of adversity, but promotive factors improve outcomes more broadly. 147 , 152 , 153

Early life adversities, particularly in the absence of protective factors, can trigger a set of emotional responses, metabolic adjustments, physical/behavioral responses, and immune changes contributing to allostasis through the “fight or flight or freeze response.” Many stress responses are regulated through the neuroendocrine system, studied most extensively for the HPA axis.

Neuroendocrine regulation of stress responses

Stress activates the neuroendocrine system, resulting in cortisol and catecholamine release. 29 , 42 The stress response evolves through two phases: the first is dominated by catecholamine release, and the second by cortisol. Simultaneous activation of the salience neuronal network and deactivation of the executive control network mediates the first phase. 42 The salience network includes the anterior insula, amygdala, hippocampus, striatum, medial prefrontal, and anterior cingulate cortices; it integrates cognitive processes for responding to threats, with swift actions to promote survival. 42 , 154 The executive control network includes prefrontal and parietal cortices to mediate working memory, impulse control, and emotional regulation. 42 , 154 The second phase mediates recovery from stress responses by deactivating the salience network and re-engaging executive control. Such restoration of homeostasis after stress is termed the “adaptive stress response”. 42

Emotional stimuli can activate salience network activity at lower thresholds in the “maladaptive stress response,” resulting in conditioned hyperarousal. 42 Allostasis, the HPA-axis adaptation to stress, is maintained in maladaptive stress responses, although resulting in somewhat delayed homeostasis. 29 , 42 , 154 Allostatic load results from the repetitive activation of HPA mechanisms attempting to restore homeostasis without returning to baseline. 42 Excessive HPA activation causes allostatic components to be unbalanced, leading to architectural and functional changes in the salience and executive control networks. 29 , 31 , 41 , 154 Indeed, higher bedtime cortisol levels predicted the reduced prefrontal cortex volumes in traumatized adolescents. 155 Chronic adversities overload the neuroendocrine system’s capacity to maintain homeostasis and, especially during periods of heightened neuroplasticity (from pregnancy to early childhood), affect crucial aspects of brain development implicated in cognition, self-regulation, and physical and mental health. 39 , 41 , 42 , 154

The HPA axis and executive functions mature by age 4–6 years, 156 , 157 , 158 and a normally functioning HPA axis limits cortisol exposures through negative feedback loops to the anterior pituitary and hypothalamus. These negative feedback loops become ineffective in children with HPA-axis dysregulation. 159 Thus, toxic stress may lead to hyper- or hypo-responsivity of the HPA axis, with failed adaptation and eventual exhaustion 160 (Fig.  3 ). HPA-axis dysregulation manifests as emotional problems in preschool children, such as internalizing and externalizing behaviors. 161 , 162 , 163 , 164 , 165 Considering the harmful manifestations of HPA-axis dysregulation in children and the vulnerability of their immature HPA axis, it is critical that we establish biomarkers for screening preschool children.

In the perinatal phase, the fetal brain may be exposed to maternal cortisol levels resulting from prenatal stress, usually associated with dampening of the infant’s HPA axis postnatally, often lasting into infancy and early childhood. Exposures to ELA/stress then manifest as hyperactive responses to acute stress, which, if prolonged or repetitive, can lead to chronically dysregulated diurnal rhythms and HPA-axis exhaustion.

Cortisol as a biomarker of ELA

Long-term consequences of ELA are mediated through the neuroendocrine system, with downstream effects on neuroimmune, neuroenteric, and cardiometabolic regulation. 41 , 48 Measuring stress biomarkers could overcome the inherent limitations of subjective questionnaires and difficulties of implementing the ACE checklist in children. 42 Cortisol, the end-product of HPA-axis activation, regulates the HPA axis through negative feedback loops, activates the autonomic nervous system, alters intermediary metabolism, modulates physiological and immune responses, and contributes to the memory and learning from traumatic experiences. 166 , 167 Therefore, cortisol is an important biomarker for ELA. 168

Plasma, salivary, or urinary cortisol levels reflect acute stress reactivity , but cannot assess chronic stress because of its diurnal cycles, high state reactivity, pulsatile secretion patterns, and robust changes across age, sex, reproductive cycles, and food intake. 169 , 170 , 171 A systematic review concluded that HCC represents a measure of recent stress, but it included studies from 16 species, which only collected cross-sectional data. 172 Measuring acute cortisol responses has significant limitations; repeated sampling over prolonged periods is time-consuming, expensive, and subject to non-compliance. Blood sampling is painful, difficult in children, requires trained staff, and stringent laboratory conditions. Salivary sampling is inexpensive and less invasive, 29 , 154 but limited by inconsistent collection methods and food-related variability. 29 , 154 , 169 Urine sampling from children is challenging, with low participant compliance, sample refrigeration, and urinary metabolites interfering with cortisol measurements. 29 In contrast, hair sampling is non-invasive, independent of diurnal cycles, stored at room temperature, and provides chronologically distinct data for cortisol activity up to 6 months. 29 , 173 , 174

Emerging research suggests that human hair follicles are neuroendocrine organs that index physiological stress responses. 175 , 176 Hair grows about 1 cm per month 177 and incorporates the circulating free cortisol, 178 , 179 although the underlying mechanisms remain unknown. 180 , 181 Russell et al. 181 , 182 proposed that free cortisol from the follicular vasculature passively diffuses into the hair shaft, or the hair follicle, sweat, and sebaceous glands may secrete and deposit cortisol into the hair shaft. Like hemoglobin A 1c for blood glucose, HCCs summate the cortisol release over time. 183 , 184 , 185 Earlier concerns about hair washing 186 , 187 and HCC contamination from cortisol secreted by sebaceous or sweat glands have been refuted. 182 , 188 HCC show high test–retest reliability, were validated against serum, salivary, and urine cortisol, and are widely accepted as measures of chronic stress in adults 185 , 189 and children. 178 , 184 , 190

Effects of sex, age, and race

Previous studies reported higher HCC in boys than in girls. 186 , 191 However, current data show no sex differences among preschool children, 26 , 178 higher HCC in pre-pubertal boys than girls, and no differences after puberty. 192 Variations of HCC with age are unclear, with most studies showing age-related decreases in preschool years. 26 , 193 , 194 Racialized experiences and structural racial discrimination may contribute to the higher HCC in African-American children compared to children from other races. 26 , 195

Effects of prenatal and postnatal environments

Higher HCC in 1-year-old infants was associated with maternal parenting stress, depression, and psychological distress. 195 Prenatal traumatic events were significantly associated with their child’s HCC at age 3 and 4 years, even after adjustments for known mediators like postpartum depression, parenting stress, psychological distress, and child abuse potential, as well as preterm birth or body mass index (BMI). 196

Other studies found higher HCC in newborns following neonatal intensive care, 197 children with early trauma, 198 , 199 and children with high fearfulness ratings upon school entry. 190 In 6–7 year olds, low HCC values suggestive of HPA-axis dysregulation were associated with exposures to frequent neonatal pain, 200 or harsh parenting. 201 Although perinatal adversities may alter long-term HPA-axis regulation into the school-age period, the most prominent postnatal influences on HPA activity result from poverty and early deprivation. 194 , 202 , 203

Effects of socioeconomic adversity

Children raised in poverty are often exposed to chronic stress, either directly (from food, housing, energy insecurity, 204 bullying, 205 , 206 or neighborhood violence 117 ) or indirectly via parental stress. 207 Higher HCCs were associated with lower parental education, 208 lower family income, more household members, single-parent households, 186 and deprived neighborhoods. 203 Similar associations between ELA and chronic stress 209 , 210 , 211 , 212 may result from insensitive or rigid parenting, 201 parenting stress, 195 , 196 neighborhood effects, 117 , 203 and other poverty-related factors. 213 , 214 , 215 To understand the importance of these differences, we explore the implications of HCC as a chronic stress marker and subsequent health outcomes.

Hair cortisol concentrations: implications for health

Epidemiologic studies have established links between chronic stress, HPA-axis dysregulation, and subsequent physical and mental health outcomes, 25 , 216 but only a few of these studies have included HCC as a biomarker for chronic stress. 174 , 178

Higher HCC in preschool children were associated with impaired social–emotional development and increased risks for developmental delay. 26 , 195 In 6–8-year-old children, increased HCCs were associated with higher BMI in girls and somatic complaints in boys. 191 In older children, increased HCCs were associated with higher BMI, 192 other measures of obesity, 186 , 191 , 217 , 218 and vulnerability to common childhood illnesses, 219 even after controlling for factors such as race, age, gestational age, and birth weight. HCCs were reduced in children with asthma, 220 possibly from HPA-axis suppression due to inhaled corticosteroids. 221 , 222 , 223 Higher HCC also occurred in children with epilepsy 224 and girls with anorexia nervosa, 225 but no differences were found in children with anxiety 226 or depression 199 , 226 as compared to controls.

In adults, HCC was increased in major depression and decreased in general anxiety disorder, whereas HCC changes in PTSD were dependent on the type of traumatic experience and elapsed time since the trauma. 227 , 228 Increased HCC was used as a biomarker for stratifying cardiovascular risk and linked to obesity, hypertension, diabetes, metabolic syndrome, and cardiovascular disease. 227 , 229 In the survivors of physical and sexual abuse, higher HCCs during pregnancy were associated with preterm labor. 230 , 231 , 232

Since HCC has been correlated with physical and mental illnesses in children and adults, it can be used to probe the connections between ELA, HPA-axis activity, and health outcomes. HCC may also provide unique insights into the physiological ramifications of adversities located and perpetuated in a child’s social ecology.

Current knowledge gaps and future directions

Significant gaps in our knowledge of ELA must be addressed to understand the relationships between ELA and health outcomes. Research using subjective and objective methods should assess community and societal factors alongside household conditions and parental factors, complemented concurrently by biomarkers.

The ACEs questionnaire was created using patients’ recollection of childhood experiences and correlated with subsequent health conditions. However, the equivalence between adult recollections of ACEs and caregivers’ responses on behalf of their child’s current lived experiences remains undetermined. Caregivers may be unreliable historians of their young child’s experiences, with significant differences between their and the child’s perceptions. In addition, serial ACEs screening in children does not help us to understand how to prevent or treat ACEs, and potentially reinforces the negative emotions that children have of their experiences.

Historically, the relations among ELA, ELS, and health were studied using lab stress tests, sleep studies, neuroimaging, anthropometrics, epigenetic markers, or galvanic skin responses. 233 , 234 This research included small sample sizes, failed to account for developmental differences, and inconsistently sampled age, sex, and racial/ethnic subgroups. Large, population-based studies can overcome these weaknesses using less invasive and less expensive means for recording ELA/ELS, child-centered measurements of stress responses, recording protective/supportive factors, and web-based data entry to minimize costs and increase compliance. Monitoring vital signs for ELA assessments may be less useful if these measures are temporally separated from the adverse experiences. Researchers should consider real-time measures of chronic stress through wearables to index the impact of ELA on health.

ELA alters gene expression through the CTRA 77 contributing to aberrant neuronal plasticity, affect disorders, PTSD, depression, and substance abuse. 82 , 83 , 84 , 85 , 86 , 87 Mechanisms of stress-associated epigenetic changes, 80 , 84 , 86 , 90 mitochondrial DNA copy number, telomere shortening, 235 and secreted microRNAs 91 , 92 must be investigated in children and adolescents, while also examining the reversibility of these epigenetic modifications and their contributions to later health outcomes.

Social interactions with attentive caregivers reduce infant stress responses and facilitate development. 236 Nurturing experiences like “kangaroo care” can reduce neurodevelopmental risks in preterm infants. 237 , 238 Secure attachments and friendships across the lifespan play protective roles in cognitive function, physical health, and emotional self-regulation. 239 Parent–child involvement in mindfulness-based, mind-body approaches can reduce stress and enhance recovery. 240 We encourage researchers to explore the underlying biological mechanisms for social buffering, positive experiences, and other protective/supportive factors.

Screening for ELA without concurrent efforts to abolish the social injustices that promote such adversities is futile. Individual screening cannot, and should not, replace efforts to address the root causes of health inequity, including poverty, lack of healthcare, community violence, racism, and gender-based discrimination. Researchers should work alongside clinicians, politicians, educators, social workers, and community members to develop intervention programs that promote resilience in children and to deconstruct the societal and legal infrastructures that perpetuate systemic inequities. We recommend the use of biomarkers such as HCC to supplement existing research efforts and public health interventions as a quantitative, biological marker, firstly, to enhance our understanding of the underlying pathophysiology that mediates the association of ELA with poor health outcomes, and secondly, to improve evaluations of the impact of preventive or therapeutic interventions on their intended beneficiaries (i.e., children) in the community.

Acknowledgements

This work was supported by grants from the NIH/National Institute for Drug Abuse (R41 DA046983, PIA), NIH/ Eunice Kennedy Shriver National Institute for Child Health and Human Development (R01 HD099296, PIA; R21 HD090493, PIG); and NIH/National Institute of Mental Health (R37 MH101495, PIG).

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Marcela Lopez, Monica O. Ruiz, Cynthia R. Rovnaghi, Grace K-Y. Tam, Jitka Hiscox & Kanwaljeet J. S. Anand

Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA

Monica O. Ruiz, Donald A. Barr & Kanwaljeet J. S. Anand

Department of Civil Engineering, Stanford School of Engineering, Stanford, CA, USA

Jitka Hiscox

Department of Psychology, Stanford University School of Humanities and Sciences, Stanford, CA, USA

Ian H. Gotlib

Stanford University Graduate School of Education, Stanford, CA, USA

Donald A. Barr

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M.L. drafted the manuscript outline; M.L., M.O.R., C.R.R., G.K.-Y.T., J.H., and K.J.S.A. wrote initial drafts and edited the manuscript; C.R.R. developed initial concepts and created the figures; K.J.S.A. developed initial concepts and provided grant funding; I.H.G., D.A.B., and V.G.C. reviewed and made critical revisions of the manuscript; and all authors approved the final version to be published.

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Lopez, M., Ruiz, M.O., Rovnaghi, C.R. et al. The social ecology of childhood and early life adversity. Pediatr Res 89 , 353–367 (2021). https://doi.org/10.1038/s41390-020-01264-x

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InBrief: The Impact of Early Adversity on Children’s Development

This brief is part of a series that summarizes essential scientific findings from Center publications.

What happens in early childhood can matter for a lifetime. To successfully manage our society’s future, we must recognize problems and address them before they get worse. In early childhood, research on the biology of stress shows how major adversity, such as extreme poverty, abuse, or neglect can weaken developing brain architecture and permanently set the body’s stress response system on high alert. Science also shows that providing stable, responsive, nurturing relationships in the earliest years of life can prevent or even reverse the damaging effects of early life stress, with lifelong benefits for learning, behavior, and health .

Early experiences influence the developing brain.

From the prenatal period through the first years of life, the brain undergoes its most rapid development, and early experiences determine whether its architecture is sturdy or fragile. During early sensitive periods of development, the brain’s circuitry is most open to the influence of external experiences, for better or for worse. During these sensitive periods, healthy emotional and cognitive development is shaped by responsive, dependable interaction with adults , while chronic or extreme adversity can interrupt normal brain development. For example, children who were placed shortly after birth into orphanages with conditions of severe neglect show dramatically decreased brain activity compared to children who were never institutionalized.

Chronic stress can be toxic to developing brains.

Learning how to cope with adversity is an important part of healthy child development. When we are threatened, our bodies activate a variety of physiological responses, including increases in heart rate, blood pressure, and stress hormones such as cortisol. When a young child is protected by supportive relationships with adults, he learns to cope with everyday challenges and his stress response system returns to baseline. Scientists call this positive stress. Tolerable stress occurs when more serious difficulties, such as the loss of a loved one, a natural disaster, or a frightening injury, are buffered by caring adults who help the child adapt, which mitigates the potentially damaging effects of abnormal levels of stress hormones. When strong, frequent, or prolonged adverse experiences such as extreme poverty or repeated abuse are experienced without adult support, stress becomes toxic, as excessive cortisol disrupts developing brain circuits.

Significant early adversity can lead to lifelong problems.

Toxic stress experienced early in life and common precipitants of toxic stress—such as poverty, abuse or neglect, parental substance abuse or mental illness, and exposure to violence—can have a cumulative toll on an individual’s physical and mental health. The more adverse experiences in childhood, the greater the likelihood of developmental delays and other problems. Adults with more adverse experiences in early childhood are also more likely to have health problems, including alcoholism, depression, heart disease, and diabetes.

Early intervention can prevent the consequences of early adversity.

Research shows that later interventions are likely to be less successful—and in some cases are ineffective. For example, when the same children who experienced extreme neglect were placed in responsive foster care families before age two, their IQs increased more substantially and their brain activity and attachment relationships were more likely to become normal than if they were placed after the age of two. While there is no “magic age” for intervention, it is clear that, in most cases, intervening as early as possible is significantly more effective than waiting.

Stable, caring relationships are essential for healthy development.

Children develop in an environment of relationships that begin in the home and include extended family members, early care and education providers, and members of the community. Studies show that toddlers who have secure, trusting relationships with parents or non-parent caregivers experience minimal stress hormone activation when frightened by a strange event, and those who have insecure relationships experience a significant activation of the stress response system. Numerous scientific studies support these conclusions: providing supportive, responsive relationships as early in life as possible can prevent or reverse the damaging effects of toxic stress.

Policy Implications

• The basic principles of neuroscience indicate that providing supportive and positive conditions for early childhood development is more effective and less costly than attempting to address the consequences of early adversity later. Policies and programs that identify and support children and families who are most at risk for experiencing toxic stress as early as possible will reduce or avoid the need for more costly and less effective remediation and support programs down the road.
• From pregnancy through early childhood, all of the environments in which children live and learn, and the quality of their relationships with adults and caregivers, have a significant impact on their cognitive, emotional, and social development. A wide range of policies, including those directed toward early care and education, child protective services, adult mental health, family economic supports, and many other areas, can promote the safe, supportive environments and stable, caring relationships that children need.

Suggested citation: Center on the Developing Child (2007). The Impact of Early Adversity on Child Development (InBrief). Retrieved from www.developingchild.harvard.edu .

Related Topics: toxic stress , brain architecture , neglect

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Adverse Childhood Experiences (ACE) Study Summary

Saul Mcleod, PhD

Editor-in-Chief for Simply Psychology

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Adverse Childhood Experiences (ACEs) refer to stressful or traumatic events that children face before reaching 18. These include various forms of abuse (physical, emotional, sexual), neglect (emotional, physical), and household challenges such as witnessing domestic violence, living with substance abusers, having an incarcerated relative, or experiencing family separation. Studies have shown that individuals with a high number of ACEs are at an increased risk for negative outcomes in adulthood, including chronic diseases, mental illness, substance misuse, and reduced life potential. The more ACEs one has, the greater the risk for these outcomes.

• Adverse childhood experiences like abuse, violence, and family dysfunction are common and have strong, cumulative effects on adult health risk behaviors and diseases.
• Over half of the study participants reported at least one adverse childhood experience. As the number of adverse experiences increased, so did the risk for smoking, alcoholism, drug abuse, depression, suicide attempts, multiple sexual partners, sexually transmitted diseases, heart disease, cancer, chronic lung disease, skeletal fractures, and liver disease.
• People with 4 or more adverse childhood experiences had up to 12 times higher likelihood of suicide attempts, 7 times higher chance of alcoholism, and 10 times higher risk of injected drug use compared to people with no adverse experiences.
• Adverse childhood experiences tend to be interrelated rather than occurring in isolation. People exposed to one category had a 65-93% chance of exposure to other categories as well.
• The research had some limitations such as reliance on retrospective self-report and the study population being mostly white, middle-aged, and middle-class. However, it highlights the profound, long-term impact of childhood adversity on adult health.

Child abuse, neglect, and other adverse childhood experiences have been associated with poorer health outcomes in adulthood (Springs & Friedrich, 1992; Felitti, 1991, 1993).

However, prior studies focused on single forms of adversity and did not assess the cumulative impact of multiple experiences (Briere & Runtz, 1988; Moeller et al., 1993).

This study aimed to examine the relationship between the breadth of exposure to abuse, violence, and family dysfunction in childhood and health risk behaviors, health status, and diseases in adulthood. Understanding these associations can inform more effective prevention and treatment strategies.

This retrospective cohort study surveyed 13,494 adult health maintenance organization (HMO) members who had a standardized medical evaluation at a clinic.

The mailed survey asked about adverse childhood experiences like psychological, physical, or sexual abuse; violence against mother; or living with household members who were substance abusers, mentally ill, suicidal, or imprisoned.

The number of exposure categories (0-7) was compared to the presence of risk factors for leading causes of death and disease conditions using logistic regression models.

After exclusions, the final sample was 8,056 people aged 19-92 years, predominantly white (79%) and college-educated (43%). 53% were women.

Statistical Analysis

Logistic regression analyzed the relationship between the number of childhood exposures and health outcomes, adjusting for age, sex, race, and education. Dose-response was tested by entering exposures as an ordinal variable.

• 52% of participants had at least one adverse childhood experience.
• As exposures increased from 0 to 4+, smoking prevalence rose from 7% to 17%, severe obesity from 5% to 12%, depressed mood from 14% to 51%, and suicide attempts from 1% to 18%.
• The odds of alcoholism, drug abuse, sexual partners, and STDs also increased with more exposures.
• Heart disease, cancer, lung disease, skeletal fractures, and fair/poor health showed significant dose-response relationships.

Implications

• This study reveals the surprisingly common and powerful long-term effects of adverse childhood experiences like abuse, domestic violence, and household dysfunction.
• The cumulative impact of adverse childhood experiences explains the adoption of unhealthy coping behaviors like smoking, overeating, alcoholism, drug use, and risky sex. It also elucidates the link to stress-related diseases later in life.
• This highlights the need for primary prevention strategies like home visitation programs and secondary/tertiary prevention through better training of healthcare providers to recognize and address the long-term consequences of childhood adversity.

Future Research

• Understanding ACEs is crucial, as early interventions can prevent future health and social problems, promoting resilience and providing support mechanisms to counteract these early life stressors.

Strengths & Limitations

The study had many methodological strengths, including:

• Large sample size with high response rate (70.5%)
• Assessed range of childhood exposures, not just single types of adversity
• Used logistic regression to control demographic factors
• Found relationships robust to missing data in sensitivity analysis

However, this study was limited in a few ways:

• Retrospective self-report prone to recall bias
• Mostly white, educated, middle-class, so may not generalize
• Can’t determine causality due to study design

This study reveals powerful relationships between the breadth of exposure to childhood adversity and health risk behaviors and diseases in adulthood.

It underscores the profound, long-term impact of adverse developmental experiences.

More research is needed, but these findings suggest that prevention and intervention around childhood adversity could improve public health.

Healthcare providers should be alert for patients whose health problems may have developmental origins.

Further progress relies on compassionately understanding how high-risk health behaviors may represent coping responses in the face of trauma and cumulative stress.

Primary Paper

Felitti, V. J., Anda, R. F., Nordenberg, D., Williamson, D. F., Spitz, A. M., Edwards, V., & Marks, J. S. (1998). Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults: The Adverse Childhood Experiences (ACE) Study. American Journal of Preventive Medicine, 14 (4), 245-258.

Other References

Briere, J., & Runtz, M. (1988). Multivariate correlates of childhood psychological and physical maltreatment among university women. Child Abuse & Neglect, 12 (3), 331-341.

Felitti, V. J. (1991). Long-term medical consequences of incest, rape, and molestation. Southern Medical Journal, 84 (3), 328-331.

Felitti, V. J. (1993). Childhood sexual abuse, depression, and family dysfunction in adult obese patients: a case control study. Southern Medical Journal, 86 (7), 732-736.

Moeller, T. P., Bachman, G. A., & Moeller, J. R. (1993). The combined effects of physical, sexual, and emotional abuse during childhood: Long-term health consequences for women. Child Abuse & Neglect, 17 (5), 623-640.

Springs, F., & Friedrich, W. N. (1992). Health risk behaviors and medical sequelae of childhood sexual abuse. Mayo Clinic Proceedings, 67 (6), 527-532.

Further Reading

• Chapman, D. P., Whitfield, C. L., Felitti, V. J., Dube, S. R., Edwards, V. J., & Anda, R. F. (2004). Adverse childhood experiences and the risk of depressive disorders in adulthood .  Journal of affective disorders ,  82 (2), 217-225.
• Dube, S. R., Felitti, V. J., Dong, M., Chapman, D. P., Giles, W. H., & Anda, R. F. (2003). Childhood abuse, neglect, and household dysfunction and the risk of illicit drug use: the adverse childhood experiences study .  Pediatrics ,  111 (3), 564-572.
• Felitti, V. J. (2009). Adverse childhood experiences and adult health .  Academic pediatrics ,  9 (3), 131-132.
• Hamai, T. A., & Felitti, V. J. (2022). Adverse childhood experiences: Past, present, and future.  Handbook of interpersonal violence and abuse across the lifespan: a project of the national partnership to end interpersonal violence across the lifespan (NPEIV) , 97-120.

Learning Check

• How might experiences of childhood adversity sensitize people biologically and psychologically to engage in high-risk behaviors?
• If adverse childhood experiences tend to co-occur and have cumulative effects, how should prevention/intervention strategies be designed differently than just targeting single types of adversity?
• What biases or limitations might affect participants’ retrospective self-reports of childhood experiences and current health status? How could the study design be improved?
• How might a healthcare provider compassionately uncover whether a patient’s health issues may have origins in adverse developmental experiences? What challenges does this present?
• How might knowledge of the prevalence and impacts of childhood adversity reduce stigma and lead to improved public health policies and outcomes? What barriers stand in the way?

Adverse Childhood Experiences (ACEs)

Adverse childhood experiences (ACEs) can have a tremendous impact on future violence victimization and perpetration, and lifelong health and opportunity. CDC works to understand ACEs and prevent them.

Adverse Childhood Experiences Prevention Resource for Action [4 MB, 38 Pages]

This is a resource to help states and communities leverage the best available evidence to prevent ACEs from happening in the first place as well as lessen harms when ACEs do occur. It features six strategies drawn from the CDC Resources for Action, formerly known as, “technical packages.”

Adverse Childhood Experiences (ACEs) Prevention Strategy Plan [3 MB, 20 Pages]

This resource outlines CDC’s specific goals and objectives for ACEs prevention and response. The goals and objectives aim to prevent ACEs before they happen, identify those who have experienced ACEs, and respond using trauma-informed approaches in order to create the conditions for strong, thriving families and communities where all children and youth are free from harm and all people can achieve lifelong health and wellbeing.

Vital Signs: Adverse Childhood Experiences (ACEs) [865 KB, 2 Pages]

CDC’s Vital Signs fact sheet featuring ACEs and their negative impacts on health as well as education and employment opportunities later in life.

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Home — Essay Samples — Philosophy — Childhood Experience — Adverse Childhood Experiences: Impacts and Interventions

Adverse Childhood Experiences: Impacts and Interventions

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Understanding adverse childhood experiences (aces), the profound impact of aces, addressing the impacts of aces, social and emotional impact, behavioral impact, mental health impact, counseling and therapeutic interventions, support services, prevention and education, promoting resilience.

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Positive and Negative Effects of Immigration on the Economy

This essay about the economic impacts of immigration examines both the positive and negative effects. It highlights how immigration introduces valuable labor to fill job vacancies, boosts innovation through diverse skills, and helps balance demographic shifts in aging populations. Conversely, it acknowledges potential downsides, such as wage suppression and increased competition for low-skilled jobs among native workers, as well as added strain on public services like education and healthcare. The piece argues that the challenges of immigration can be managed through thoughtful policies that foster economic integration and maintain social cohesion, thus maximizing its benefits while addressing its drawbacks.

How it works

Migration manifests as a multifarious phenomenon capable of reshaping a nation’s economic terrain in profound manners. Discourses regarding its repercussions tend to polarize, oscillating between its purportedly favorable and adverse impacts. By delving into both facets, we can garner a more nuanced comprehension of how migration influences economic dynamics.

One of the preeminent constructive ramifications of migration lies in the infusion of labor and aptitude into the host economic milieu. Migrants frequently occupy pivotal lacunae in the labor sphere, assuming roles that indigenous citizens might be disinclined to undertake.

This spectrum encompasses highly specialized vocations in technology and healthcare to indispensable functions in agriculture and construction. The variegation of skills and experiences that migrants introduce can catalyze ingenuity and propel economic expansion. For instance, numerous leading technological enterprises in the United States were instigated by migrants or their descendants, attesting to the substantial contribution of migrant entrepreneurship to employment creation and technological progression.

Furthermore, migration can serve as a counterbalance to the adverse economic consequences of an aging populace. In nations characterized by dwindling birthrates and escalating life expectancies, the workforce can dwindle, exerting heightened strain on social welfare systems. Migrants, typically entering the workforce age bracket, can help sustain a more balanced demographic equilibrium, buttressing the pension system and ensuring a steady influx of laborers. This demographic infusion is imperative for sustaining workforce vitality, a cornerstone for perpetuating economic productivity and supporting a burgeoning cohort of retirees.

Nevertheless, migration can also pose conundrums to the host economy, notably concerning its ramifications on wages and employment prospects for native-born laborers. Some posit that an influx of migrant laborers can engender competition for specific low-skilled vocations, potentially depressing wages and engendering impediments for indigenous laborers in securing employment. These repercussions are often acutely discernible in sectors characterized by low barriers to entry and elastic labor supply. Furthermore, if migrants concentrate in particular geographical locales or sectors, this can precipitate regional disparities in employment accessibility and wage levels, exacerbating societal frictions and economic disparity.

Another noteworthy apprehension pertains to the strain on public amenities. Swift population augmentation via migration can strain infrastructure, lodging, healthcare, and educational facilities. If not judiciously managed, this can precipitate overcrowded schools, protracted wait times at medical institutions, and escalated demand for affordable housing, thereby compromising the quality of life for all residents. The fiscal implications of migration hinge largely on the attributes of the migrants themselves (such as their age, educational attainment, and health status) and the adaptiveness of public policies in effectuating the effective assimilation of newcomers.

In summation, migration harbors the potential to enrich an economy, rendering it more dynamic and resilient. It infuses labor, fosters innovation, and can ameliorate demographic imbalances. Nonetheless, it also poses quandaries necessitating prudent management, such as labor market competition, potential wage compression, and demands on public services. The crux of optimizing benefits while assuaging drawbacks lies in sagacious and holistic policy frameworks that buttress economic assimilation and societal harmony. Grasping these intricate dynamics is imperative for any dialogue on migration, guaranteeing that policies not only address immediate exigencies but also align with enduring economic and societal objectives.

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