Introduction
Exposure to potentially traumatic events in early life, or adverse childhood experiences (ACEs), such as interpersonal violence, neglect, accidents, or injuries, is highly prevalent worldwide. A recent meta-analysis by S. Madigan et al. (2023) examined studies including adults from 22 countries and found that 22,4% of participants reported one ACE, 13,0% two ACEs, 8,7% three ACEs, and 16,1% four or more. Further, individuals of racial and ethnic minorities and unhoused individuals report higher rates of ACEs (Madigan et al., 2023). These rates are particularly troubling given evidence that ACEs are associated with a host of negative outcomes among both youth and adults, such as increased risk of poor health, including, but not limited to, obesity, chronic pain, and cardiovascular disease (Birnie, Baram, 2025; Bussières et al., 2023). Moreover, children exposed to ACEs are at greater risk for psychological difficulties, including substance use disorders, impaired interpersonal functioning, and a range of psychiatric disorders (Abou Chabake et al., 2025). These associated impacts result in a substantial economic burden. One meta-analysis estimated annual ACE-attributed costs to be $581 billion (USD) in Europe and $748 billion in North America (Bellis et al., 2019), and economic loss due to reduced healthy life-years has been estimated as high as $13,9 trillion in the United States (Peterson et al., 2023). The troubling rates of ACEs, along with their varied lifelong health and mental health consequences and striking economic burden, reflect the considerable impact of such early life experiences. Thus, it is imperative to continue exploring the pathways through which ACEs may have detrimental long-term effects on well-being.
Given the critical and rapid cognitive development occurring throughout childhood, exposure to ACEs can impair the normative development of cognitive function. Executive function (EF), in particular, is an important cognitive construct involved in the implementation of health-promoting behaviors and self-regulation (Chen et al., 2025). EF can be defined as a collection of higher-order cognitive processes that assist in monitoring and directing thoughts and actions. Individual components of EF include cognitive processes such as working memory, inhibitory control, and cognitive flexibility, and are involved in planning, emotional regulation, and decision making (González-Acosta, Rojas-Cerón, Buriticá, 2021; Hays-Grudo et al., 2021; Lund et al., 2020; Tinajero et al., 2020). Several studies have explored the effects of ACEs on cognition and found impacts on overall intellectual functioning as well as more specific impairments in domains of memory, emotional processing, attention, and EF (González-Acosta, Rojas-Cerón, Buriticá, 2021; Hays-Grudo et al., 2021). Investigations exploring the impact of ACEs on specific domains of EF show negative associations between ACEs and working memory (g = −0,28; [−0,42, −0,14]), cognitive flexibility (g = −0,28; [−0,38, −0,19]), and inhibitory control (g = −0,32; [−0,42, −0,22]; Rahapsari, Levita, 2024). Impairment in EF has been observed following exposure to various individual types of ACEs, including abuse, neglect, and exposure to family member mental illness, as well as cumulative adversity. One meta-analysis revealed that the associations between ACEs and EF processes were consistent across age, sex, and ACE subtypes (i.e., abuse, neglect; Rahapsari, Levita, 2024). Yet, studies examining the role of neglect versus abuse have demonstrated differential effects depending on the type of adversity in both children and adults, and the combination of neglect and abuse experiences may contribute to conflicting findings in the literature (Lund et al., 2022; Lund et al., 2020). For example, a longitudinal examination of adolescents exposed to threat-related (e.g., physical abuse) and deprivation-related (e.g., neglect) ACEs revealed that a history of deprivation-related, but not threat-related ACEs was associated with impaired working memory (β = 0,14; CI95 = [–0,26, −0,01]; Hawkins et al., 2021).
Given the strong evidence of associations between ACEs and impaired EF, and the importance of these cognitive processes in health-promoting behaviors, it is important to understand the pathways by which this association arises in order to inform intervention and future research. These pathways include biological correlates, as well as psychological and environmental factors that may modify an individual’s susceptibility to the cognitive impacts of ACEs. This review aims to present recent literature on factors relevant to the effects of ACEs on EF, providing an overview of current understanding on this topic, and highlighting important considerations for research and clinical practice.
Biological Mechanisms of ACEs and Executive Function
Stressful experiences activate biological systems that allow an individual to maintain homeostasis and promote survival in the short term. However, intense or chronic stress can result in hyperactivation of these systems and physiological dysregulation. The physiological cost associated with stress-related dysregulation is known as allostatic load and can lead to poor health outcomes over time (Birnie, Baram, 2025). One well-recognized mechanism involved in this process is the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis is a neuroendocrine system that releases glucocorticoid hormones, such as cortisol, in response to stress, resulting in the suppression of the immune system, increased availability of energy, and enhancement of the sympathetic nervous system. However, dysregulation of this system is strongly implicated in a number of physical and mental health disorders (González-Acosta, Rojas-Cerón, Buriticá, 2021; Spencer, Deak, 2017). Overactivation of the HPA axis due to ACEs may affect both structural and functional activity of brain regions associated with cognition, and result in epigenetic changes that affect the expression of glucocorticoid receptors in these areas (Jensen, Berens, Nelson, 2017). Other epigenetic changes relevant to neurodevelopment, and even shortening of telomere length, have also been noted in individuals exposed to ACEs, suggesting that some of these biological changes may be passed down and transmitted to later generations (Barrero-Castillero et al., 2022; Birnie, Baram, 2025; Hays-Grudo et al., 2021). Another contributing factor to allostatic load is inflammation. Higher levels of inflammatory biomarkers are observed in individuals who have experienced ACEs, and chronic low-grade inflammation has been linked to disease, as well as disrupted brain circuitry in these individuals (Nusslock, Miller, 2016).
EF may be particularly vulnerable to biologically mediated disruptions by ACEs due to the protracted development and relative immaturity of associated brain regions, namely the prefrontal cortex (PFC). Past work has found that exposure to early life stress, such as abuse, neglect, or household dysfunction, is associated with alterations of the PFC and related networks (Duffy, McLaughlin, Green, 2018; González-Acosta, Rojas-Cerón, Buriticá, 2021; Sheridan et al., 2022) Individuals with a history of exposure to ACEs exhibit reduced cortical thickness, surface area, and white matter integrity in areas of the PFC known to be involved in EF, including regions associated with working memory, emotional regulation, and decision making (Hays-Grudo et al., 2021; Sheridan et al., 2022). Structural and functional networks important to EF, connecting the PFC, limbic, parietal, and temporal areas of the brain, are also negatively impacted by ACEs (Duffy, McLaughlin, Green, 2018; Park et al., 2021; Sheridan et al., 2022). One study found that experiences of neglect were associated with changes in regions related to cognition and executive function, while abuse was associated with regions involved in emotional processing (Cai et al., 2023). In addition to these macroscopic changes, microscopic alterations associated with plasticity and neurogenesis have been noted in the PFC (González-Acosta, Rojas-Cerón, Buriticá, 2021). These changes may be driven, at least in part, by elevated levels of inflammatory biomarkers, epigenetic changes, and altered glial functioning (Hays-Grudo et al., 2021; Nusslock, Miller, 2016; Núñez-Ríos et al., 2025). However, EF is not impaired universally in those exposed to ACEs. Like the physical and mental health diagnoses associated with these experiences, individual differences exist in how ACEs impact these cognitive skills. Understanding the factors that may put a child at risk or become protective is imperative to our understanding of these experiences and managing the resulting symptoms.
Risk and Protective Factors
One established and well-researched correlate of ACE exposure and impairments in EF is the development and maintenance of internalizing symptoms (Russell et al., 2025; Sætren, Augusti, Hafstad, 2021). Internalizing symptoms, characterized by distressing internal states such as anxiety and depression, are the most common psychiatric disorders across adolescent and young adult populations (Conley, Hilt, Gonzales, 2023; Silva et al., 2020). The association between ACEs and internalizing symptoms has been supported in investigations of youth and adults (Hawes, Allen, 2023; Nelson et al., 2017). One meta-analysis of studies examining trajectories of depression in adults who reported ACEs demonstrated that adults with a history of ACEs were 2,66 to 3,73 times more likely to develop depression and had earlier onset of depression (Nelson et al., 2017). Notably, one cross-sectional investigation in a sample of youth explored the role of executive dysfunction in the association between ACEs and internalizing symptoms and found that EF mediated this link (R2 = 0,077). Specifically, greater executive dysfunction was associated with both greater cumulative ACEs and greater internalizing symptom severity (Asselman et al., 2025). Given the integral role of these cognitive processes in emotion regulation, deficits in these domains can lead to significant difficulties in managing and understanding intense emotions, which in turn confer greater risk for internalizing symptoms (Russell et al., 2025; Sætren, Augusti, Hafstad, 2021). This is consistent with work indicating that emotion regulation may mediate the association between ACEs and inhibitory control (β = 0,03, CI95 = [0,002, 0,08]) (Tinajero et al., 2020). However, it is difficult to infer the directionality of these associations, and evidence is mixed (Brieant, King-Casas, Kim-Spoon, 2022; Freichel et al., 2024).
Notably, past work suggests that a history of ACEs is associated with poorer treatment outcomes among adults receiving interventions for internalizing symptoms, particularly if multiple ACEs are endorsed (Giampetruzzi et al., 2023). There is also evidence that targeting EF in treatment may serve to improve internalizing symptoms. Among adolescents, cognitive training interventions have also demonstrated promise in improving emotional (η²p = 0,11) and cognitive control (η²p = 0,10 to 0,46) and reducing internalizing symptoms (η²p = 0,22) (Carballo-Marquez et al., 2025). Further, a meta-analysis of studies examining the effects of working memory training on reducing internalizing symptoms found it to be effective in improving emotion regulation (g = 0,24) and reducing symptoms of anxiety (g = 0,16) (Cui et al., 2024).
Beyond internalizing symptoms, executive dysfunction is associated with a wide range of psychiatric disorders that are frequently observed among individuals with histories of childhood adversity (Lund et al., 2022; Lund et al., 2020). The development of post-traumatic stress disorder (PTSD) and dissociative symptoms following childhood trauma is also linked to executive dysfunction. Childhood sexual abuse accompanied by greater symptoms of PTSD has also been negatively correlated with working memory and attention (r = –0,387 to –0,684) (Rivera-Vélez et al., 2014). Even when including individuals without clinical diagnoses, dissociative symptoms have been connected to poorer verbal memory and disruptions in EF (r = –0,373 to –0,556) (Rivera-Vélez et al., 2014). Additionally, recent work suggests that difficulties in EF observed among individuals diagnosed with PTSD after exposure to ACEs persist into adulthood (Lund et al., 2022). These patterns suggest that trauma-related cognitive deficits may exist along a continuum, with clinically significant symptoms emerging at higher levels of adversity.
While individual psychological symptoms play a key role in shaping cognitive outcomes, their impact unfolds within broader social, cultural, and economic contexts. Unfavorable environments, particularly those marked by low socioeconomic status (SES), increase the likelihood of ACE exposure, as well as intensify the negative effects of early adversity (OR = 1,18, CI95 [0,99, 1,40] to 1,51, CI95 [1,09, 2,09]) (Maguire-Jack et al., 2021). Evidence on the direct association between various socioeconomic factors and EF is mixed, with one study finding that parental education positively predicts EF in trauma-exposed preschoolers (β = 0,23), but monthly family income does not (β = 0,09) (Cohodes et al., 2020). Children experiencing severe forms of low SES, such as homelessness, have been found to exhibit lower EF performance, particularly on tasks related to working memory and impulsivity (r = 0,558 and r = 0,511, respectively), highlighting the pervasive influence of these contexts on cognitive development (Fry et al., 2020). Further, paternal arrest and incarceration has been linked to deficits in attention/working memory, cognitive flexibility, and lower academic achievement during middle childhood (Haskins, 2016). Preliminary evidence also suggests that among justice-involved youth, a history of maltreatment may indirectly predict externalizing and internalizing symptoms through global EF deficits (β = 0,28) (Dennis et al., 2024). Research on children adopted after experiencing extreme neglect in both physical and emotional care shows that globally depriving environments led to significantly poorer EF compared to children adopted from institutions that, though psychosocially depriving, met children’s basic physical needs (Merz, McCall, Groza, 2013). In addition, children adopted before 18 months, as opposed to after (d = 0,56 and 0,61), and those who spent more time with their families before institutional placement (r = 0,29), demonstrated better EF outcomes (Hostinar et al., 2012; Merz, McCall, Groza, 2013), pointing to a time-sensitive protective effect of family care, though this effect may depend on the severity of deprivation (Chumakova et al., 2022; Chumakova et al., 2020).
Notably, nurturing environments and the availability of protective resources are essential for buffering the negative impacts of early adversity and fostering successful adaptation. Factors related to caregiving and a child’s environment also appear to be a viable target for intervention. Children placed in foster care after neglectful institutional care showed marked improvements in inhibitory control and neural functioning compared to those who remained in institutional settings (d = 0,57) (McDermott et al., 2012). Children experiencing homelessness display greater EF skills when parents support the autonomy of their children, which has been associated with better academic and housing outcomes (Distefano et al., 2024; Fry et al., 2020). Moreover, warm and cognitively stimulating caregiving not only fosters EF development but also shields children from the cascading effects of other risk factors, such as maternal depression (r = 0,04) (Baker, Kuhn, 2018) or institutional neglect (McDermott et al., 2012). Ultimately, research has shown that the presence of stable family routines and clear rules, coupled with strong, responsive relationships, is instrumental in fostering healing and enabling successful adjustment in high-risk children (Turgeon et al., 2023; Younas, GutmanYounas & Gutman, 2023)
Discussion and Conclusions
ACEs are highly prevalent and associated with impairment in EF. Many factors underlie, compound, or buffer this association, including biological mechanisms, psychological factors, and environments. More specifically, ACEs have been associated with HPA dysregulation, genetic and epigenetic changes, and structural and functional differences in brain regions associated with EF at both the macroscopic and microscopic levels. ACEs and EF are also associated with the onset and maintenance of internalizing symptoms and other clinical presentations, such as PTSD, and EF may represent a valuable treatment target to improve prevention or treatment outcomes in some cases. Finally, Environmental factors such as SES, quality of care, and disruptions to parental support also have a substantial influence on EF and represent possible areas of prevention. However, several areas warrant continued research to elucidate the effects of ACEs on EF. Further investigations into how the combination and interaction of biological changes impact EF, as well as how protective factors may influence biological systems, are warranted to gain a more holistic perspective of mechanisms underpinning the effects of ACEs. Additional research on the directional or reciprocal associations between EF and psychopathology is also necessary to clarify the impacts of ACEs and how EF might be most effectively targeted in treatment. Moreover, greater research regarding the timing and severity of such factors, and the degree to which EF may be recovered after these experiences, may aid in the prevention of these impacts. Due to the narrative nature of this brief review and the numerous factors involved, speculation on potential combinations of factors that might consistently result in EF deficits is beyond the scope of the current study. However, the literature represented here provides a helpful and current overview of the associations between ACEs and EF and highlights the importance of understanding and considering the context and cognitive impacts of these early life experiences in both research and clinical practice.