An intricate yet crucial area for comprehending long-term psychological and neurological implications is the interplay of Early Life Stress (ELS), anxiety, and cognitive development. This interplay becomes particularly significant when considering how stress responses, especially during early developmental periods, can shape both emotional regulation and cognitive functioning across the lifespan. Stress is our response to events that disrupt, or threaten to disrupt, our physical or psychological functioning (Lazarus & Folkman, 1984; Taylor, 1991) [1]. Unfortunately, stress has been a common part of life since the 1990s—something few of us can avoid altogether. It is a complex phenomenon that arises in response to outside circumstances or events known as stressors. People's varied physical and psychological responses to the same experience are an interesting aspect of stress.[1].

Adverse childhood experiences (ACEs), or childhood adversities, refer to a wide range of potentially stressful experiences that occur in childhood. The most widely used ACE scales, ie, the conventional ACEs, include 10 items covering abuse, neglect, and household challenges from the Centers for Disease Control and Prevention (CDC)–Kaiser Permanente ACE Study [2]. An additional set of expanded ACEs have been included to measure community-level stressors such as neighborhood or school bullying and unsafe communities. In addition, several new ACE indicators (eg, somatic illness or death of family members) have also been reported to be prevalent and should be considered in ACE-related studies [2]. The term Early Life Stress (ELS) broadly refers to stress occurring in childhood (prior to the age of 18). It is a term that covers a wide range of adverse experiences a child might encounter, including, but not limited to, exposure to toxins, nutritional restriction, abuse, neglect, and limited family resources [3]. According to Nakamu et al., childhood stress called Early Life Stress (ELS) includes neglect, physical and psychological abuse, sexual abuse, and events such as loss of caregiver, relationship constructing, bullying, accidents and illnesses, natural disasters, and wars (Agid et al., 2000; Heim et al., 2004; Heim et al., 2003) [4]. Looking at the definitions and explanations, we can say that Adverse Childhood Experiences (ACE) causes Early Childhood Stress (ELS). And thus, in this paper, Adverse Childhood Experiences (ACE) and Early Childhood Stress (ELS) are used almost interchangeably.

Clinical observations and studies by authoritative psychiatrists and pediatricians, such as John Bowlby and Donald Winnicott, emphasized the crucial role of early life experiences in shaping individuals’ psychological health [5]. They have the potential to seriously impair the brain's normal growth and development, which could have long term psychological and physiological repercussions [6]. Stress in early life is linked to a high prevalence of mental illnesses that are significant public health issues, including schizophrenia, attention-deficit/hyperactivity disorder, post-traumatic stress disorders, and anxiety or depressive behavior [7].

The childhood period is a critical period, as the nervous system is highly plastic. According to Alberini and Travaglia (2017), the majority of stressful occurrences take place throughout adolescence and right after birth. The nervous system loses its plasticity due to stimuli input, changes in excitatory and inhibitory synapses, and synaptic pruning. According to earlier research, stress causes changes in the structure, connection, and function of the developing brain on a number of levels [8]. Such impairments in the brain increase vulnerability to psychiatric disorders. Thus, stress during childhood has impacts on the neurological system’s development and persists throughout adulthood [4, 9].

Cognitive development, encompassing the maturation of mental processes like memory, attention, and executive functions, plays a pivotal role in how individuals perceive and manage future anxiety and stress [10]. These mental processes develop with the development of an individual’s brain. Anxiety, as defined by the American Psychological Association is an emotion characterized by feelings of tension, worried thoughts, and physical changes like increased blood pressure, while the DSM characterizes it as excessive worry and apprehensive expectations [11]. It is suggested that cognitive abilities of threat perception, future thinking, and generalization may underlie anxiety [12]. Anxiety phenomena are highly prevalent during the development of children [10].

The study of the interconnectivity of these three concepts is something that is very important for future interventions and programmes to help individuals deal with long term effects. This paper aims to understand the effects of ELS on anxiety and cognitive brain development. 

Understanding Early Life Stress (ELS)

Stress refers to an organism’s insufficient physiological response to any mental, emotional, or physical pressure, whether real or imagined. Various forms of stress imposed at different life stages can affect individuals, such as early-life stress (ELS) and adult stress. Reputable psychiatrists and pediatricians like John Bowlby and Donald Winnicott highlighted in their clinical observations and research the critical role that early experiences—particularly the bond between an infant and its mother or caregiver—have in determining an individual's psychological well-being [5].

Early Life Stress (ELS) encompasses a wide range of adverse experiences occurring during critical developmental periods, including the prenatal stage, infancy, childhood, and adolescence. As mentioned in the introduction, these stressors include, but are not limited to, abuse, neglect, loss of parental care, hunger, extreme poverty, and exposure to violence in familial, community, or educational settings. Prenatal adversities, such as elevated maternal anxiety, malnutrition, and other stressful living conditions, are also considered part of ELS due to their impact on fetal neurodevelopment [13]. Consistent with previous research, the National Comorbidity Survey Replication (NCS-R) evaluated twelve binary ACEs that occurred prior to the age of 18 and were divided into three categories: direct maltreatment (e.g., physical abuse, sexual abuse, and neglect), parental maladjustment (e.g., mental illness, substance abuse, criminality, and domestic violence), and interpersonal loss (e.g., parental death, divorce, or other types of separation) [14]. They also included other challenges including severe family financial difficulty and childhood illnesses that could be fatal. The substantial and enduring impact of ELS on developmental outcomes is highlighted by the substantial body of evidence indicating that these early adversity considerably raise the likelihood of long-term cognitive, emotional, and psychological challenges.

While stress can positively impact behavior and brain health, chronic stress can also have substantial and persistent negative effects. Early life stress (ELS), particularly childhood physical, sexual, and emotional abuse has been linked to poor general health outcomes in adulthood [15]. In a study of 44,066 people, those who had more than three ELS events had a four to twelvefold increase in addictive substance abuse, depression, and suicide [16]. Stress in early life has also been linked to personality disorders and the development of schizophrenia. Given the plasticity of the central nervous system during childhood, it has been proposed that traumatic experiences during sensitive periods of brain development are likely to have adverse long-term effects on brain function and adaptation  [17]. Understanding the centrality of stress to depression, many candidate biomarkers of depression, including smaller hippocampal volume, disruptions in HPA-axis functioning and elevated peripheral inflammation, are also linked with exposure to early adversity. However, there is a paucity of data on the possible physiological changes associated with adverse childhood experiences [18]. The ACE study described adverse experiences as “common, stressful and traumatic exposures affecting the (neuro) development of children”.

The ACE hypothesis posits that adverse or stressful childhood experiences such as abuse and neglect, or growing up in a dysfunctional household, create common vulnerability to social, emotional and cognitive impairments that lead to increased risk of poor health behavior, social adjustment and physical and mental illness [19]. The first wave of the study conducted in 1995/1996 included seven adverse events in the definition of ACEs, namely sexual, physical and emotional abuse, and household dysfunction. The second wave in 1997 updated the list to ten with the addition of emotional and physical neglect and parental divorce or separation [19]. The latter study also became the basis for expert recommendations to expand the definition of ACEs to include exposures experienced in high income as well as low to middle income countries (LMICs), including the domains of socio-economic status, peer to peer and community violence [19].

According to research, 15.5% of children and adolescents suffer from psychological distress associated with adverse childhood experiences (ACEs), such as abuse, neglect, and dysfunctional households [20]

Complex brain systems are involved in the mechanisms that underlie children's stress response. The hypothalamic-pituitary-adrenal (HPA) axis, which controls how the body reacts to stress, is essential to this. Prolonged stress can cause the HPA axis to become dysregulated, which raises cortisol levels and has a negative impact on brain growth and function. In particular, long-term exposure to stress hormones can harm the development of brain areas like the hippocampus and prefrontal cortex that are essential for controlling emotions and processing information. Early interventions are crucial to reducing the long-term effects of ELS since these neurobiological changes raise the risk for a number of mental health conditions, such as anxiety, depression, and cognitive deficits [8].

Impact of ELS on the brain

The impact of ACEs also depends on the timing of the ACE in relation to sensitive periods of brain development [21]. As mentioned above, the childhood period is a critical period, as the nervous system is highly plastic. According to Alberini and Travaglia (2017), the majority of stressful occurrences take place throughout adolescence and right after birth. Now, looking at the brain and its various parts, we see varied changes caused by ACE or ELS. Neuroimaging studies examining the impact of early life stress (ELS) have consistently focused on structural and functional changes in key brain regions implicated in emotional regulation, memory, and stress response.

The brain experiences significant developmental changes during childhood and adolescence, such as the cortex becoming thinner, the cortical surface area increasing and then decreasing, and the volume of white matter connections continuing to grow [22]. These changes have been linked to cognitive functioning. To gain a deeper understanding of the mechanisms behind latent vulnerability and resilience, it is imperative to investigate the ways in which ACEs impact brain development [13]. Reduced grey matter quantities in the orbitofrontal cortex and hippocampus, among other brain regions, have been associated with abuse during childhood [19].

Neuroimaging studies on childhood adversity started with a strong focus on the effects of severe early caregiver adversity, for example in institutionalized children or children exposed to childhood maltreatment. Many psychiatric disorders emerge during adolescence [23].  Due to the well-established significance of fronto-limbic areas in the hypothalamic-pituitary-adrenal (HPA) axis functioning in response to stress, the majority of studies concentrated on the fronto-limbic network, which includes the frontal cortex, hippocampus, and amygdala. Some of the strongest links between childhood adversity and the hippocampus, a structure essential for memory consolidation and HPA-axis feedback inhibition, have been found. When combining meta-analyses and reviews, the most consistent results are seen in the corpus callosum, fronto-limbic regions, fronto-striatal regions, and fronto-subcortical association fibers [13]. The hypothalamic–pituitary–adrenal (HPA) axis is closely linked to the primary mechanism behind the negative effects of early stress. The preservation of the organism's homeostasis is connected to the HPA axis. When confronted with stressful events, this axis permits the immunological response to be suppressed, energy to be mobilized, and the sympathetic division of the autonomic nervous system to be activated in general. Early-life stress exposure and the resulting hyperactivity of the HPA axis, however, have long-term consequences for behavior, cognition, and the brain regions supporting the latter [23]. In humans, the hyperactivity of the HPA axis can first change the baseline levels of glucocorticoids, specifically cortisol. Following extended exposure, it may impact the anatomical and functional arrangement of limbic regions, including the cingulate gyrus, the amygdala, the hippocampus, the hypothalamus, the orbital PFC and mPFC, and others [24]. Given the importance of stress in depression, exposure to early adversity is also associated with a number of potential biomarkers of depression, such as reduced hippocampal volume, abnormalities in HPA-axis functioning, and increased peripheral inflammation [18].

Subregions of the hippocampus and amygdala have been shown to alter in volumetric analyses of people who were repeatedly exposed to various stimuli as children, including physical and sexual abuse [24]. These structural alterations, which may be caused by abnormal neurogenesis and plasticity, are correlated with poor cognitive abilities, including learning and short-term memory. Changes in the corpus callosum and cingulate gyrus also point to impaired hemisphere-to-hemisphere communication and emotional control deficiencies.

Neuroimaging methods have also allowed the identification of correlations between neuroanatomic and functional alterations and early exposure to different types of traumatic events. In this regard, changes at the level of both cortical and subcortical structures have been documented [25]. 

Cognitive Development in the context of ELS

The effects of early stress have also been explored on a cognitive level. A strong association has been established between abuse and failures in different memory modalities, as well as poor development of school skills, and low scores on attentional tests and abstract reasoning [24]. Verbal memory assessment in people who experienced various forms of abuse as children has been the subject of numerous investigations; all but one of these studies revealed that the participants performed poorly on the tasks designed for this purpose. In particular, one study examined individuals who had been exposed to abuse and/or domestic violence at a young age; another examined those who had experienced physical and/or sexual abuse and discovered short-term verbal memory impairment; two studies only looked at women who had experienced sexual abuse; one examined verbal declarative memory changes, while the other found no changes in explicit verbal and visual memories. Lastly, another study discovered that neglected individuals have issues with verbal memory and certain executive skills [26].  Furthermore, in a study that also assessed other cognitive functions, it was discovered that victims of various forms of maltreatment had altered visuospatial memory, women who had experienced sexual abuse performed poorly on short-term memory tests, and victims of physical abuse as children also had altered associative and instrumental learning [24].

In the first place, as was previously noted, the hyperactivity of the HPA axis can change the baseline levels of glucocorticoids, and in the case of humans, cortisol. The cingulate gyrus, the amygdala, the hippocampus, the hypothalamus, the orbital PFC and mPFC, and other limbic structures may be affected in terms of their structural and functional organization during extended exposure. There is a correlation between these structural modifications and significant functional changes. For instance, it has been demonstrated that hypercortisolemia has a significant impact on the structure and function of the hippocampus, as demonstrated by certain pathologies that show up as a reduction in mental functions like short-term memory retention [24].

The IQ of those who experienced maltreatment as children has not been extensively studied. While other studies examined the impact of the link between childhood abuse and the later development of post-traumatic stress disorder (PTSD) on intelligence, some of these used the IQ variable to control the results of more complex and specific functions, such as executive functions [24]. Stress throughout childhood has also been found to affect other higher mental functions, such as language in those who experienced any form of abuse or domestic violence and visual-motor integration in those who experienced neglect combined with physical abuse. Thirteen studies included people who had been physically abused, evaluating changes in IQ, school abilities, and cognitive and executive functions; six studies included people who had been sexually abused, mostly women, and evaluated executive functions almost exclusively; and the same number of studies and functions evaluated people who had been neglected as children. Three research assessed the executive functions of adults who had early institutional deprivation, and six more studies assessed those who had experienced domestic violence, family trauma, or dysfunction in the home as children. There were more studies evaluating changes in cognitive/executive skills linked to early stress exposure than evaluating changes in general intelligence or academic performance [24].

The most researched higher mental functions are executive functions, which also show the greatest changes in reaction to stress in early life. Planning, problem-solving, abstraction, reasoning, working memory, inhibitory control, decision-making, and cognitive flexibility are some of these executive functions. Early institutional deprivation has been shown in numerous studies to have a substantial impact on cognitive flexibility, working memory, inhibitory control, targeted attention, and decision-making. People who had early physical and/or emotional abuse or neglect, family trauma, or dysfunction in the home have also been shown to have altered working memory. Furthermore, it has been seen that individuals who have experienced physical abuse do poorly on cognitive flexibility tasks, while those who have experienced sexual abuse, neglect, or familial trauma perform poorly on inhibitory control tasks [24].

Another executive function that is assessed in those who experienced early stress is attention, which includes sustained, visual, and auditory modalities. All study participants, regardless of whether they had experienced family trauma, physical abuse combined with neglect, or abuse or neglect alone, exhibited attention problems. According to a study, children who had an acute stressful experimental event showed changes in their sustained attention, and when they experienced parental stress, their attentional vulnerability increased [24].

People who experienced early neglect have also been reported to have difficulties with planning and problem-solving. Ironically, one study discovered that participants who experienced both physical abuse and neglect fared worse on executive functions like reasoning, abstraction, and problem-solving, but they outperformed those who had only experienced neglect [24].

Early life adversity can produce biological memories that weaken multiple developing body systems such as the stress response, cardiovascular and immune systems, and metabolic regulatory controls [19].

Development of Anxiety and anxiety disorders

Anxiety, as defined by the American Psychological Association is an emotion characterized by feelings of tension, worried thoughts, and physical changes like increased blood pressure, while the DSM characterizes it as excessive worry and apprehensive expectations [11]. Anxiety disorders are diagnosed when an individual’s experience of fear and/or anxiety becomes excessive and impairs functioning.Anxiety disorders are the most prevalent psychiatric disorders. There is a high comorbidity between anxiety (especially generalized anxiety disorders or panic disorders) and depressive disorders or between anxiety disorders, which renders treatment more complex. Anxiety disorders are the most prevalent psychiatric disorders (with a current worldwide prevalence of 7.3% [4.8%-10.9%]—Stein et al, in this issue p 127). Generally speaking, women are more prone to develop emotional disorders with an onset at adolescence; they are 1.5 to 2 times more likely than men to have an anxiety disorder [27]. Among children with typical development , the point prevalence estimates for some of the most common anxiety disorders are 0.5-3.0% for Separation Anxiety Disorder (SAD), 0.3-2.5% for Social Phobia (SoP), and 0.4-2.5% for Generalized Anxiety Disorder (GAD). However, each anxiety disorder develops differently throughout childhood and adolescence. Anxiety diagnoses tend to be more prevalent in females than males, but these sex differences generally do not emerge until adolescence. In studies of young children, no sex differences in prevalence are typically found for any anxiety disorder [28].

Globally, over 300 million people were living with an anxiety disorder in 2019, accounting for nearly 29 million disability adjusted life years. Anxiety disorders are among the most common mental health burdens globally, and are 40 % more common among women compared to men. Generalized anxiety disorder, marked by excessive worry, cognitive avoidance, and intolerance of uncertainty, is highly comorbid with depression, suicidality, and subtypes of anxiety [29].

We found that only one adverse childhood experience predicted higher anxiety a year later - reporting the presence of depression or suicide among household members. It is probable, though beyond the scope of this study to verify, that family genetic inheritance contributes to some of this association. Genetic analysis shows around 30 % of current anxiety symptoms may be attributed to genetic factors. Future research may endeavor to parse out contributions to anxiety that are genetically-linked or products of the social environment among people in rural sub-Saharan Africa. The data add to observations from South Africa that adults in sub-Saharan Africa who report more child maltreatment experience higher levels of anxiety. The finding supports the need to monitor not only specific adverse experiences but also cumulative totals of adversities. Previous research has found generalized anxiety produces substantial societal costs through decreased work productivity, increased demand of health services, and comorbidities with other mental and physical health conditions [29].

Gender and socio-economic factors of ELS

Socioeconomic status, gender, and cultural context are critical dimensions that shape the experience of adverse childhood experiences (ACEs) and their downstream effects on anxiety and cognitive development. Lower SES is consistently linked to greater exposure to ACEs—such as abuse, neglect, and household dysfunction—due to increased stress, deprivation, and reduced access to resources. As mentioned above, childhood poverty specifically correlates with structural brain changes—reductions in gray and white matter—and heightened amygdala activation alongside diminished prefrontal cortex function, which together contribute to elevated anxiety and poorer working memory outcomes. Gender, on the other hand, plays a distinct role, with females more prone to internalizing disorders, including anxiety and depression, while males more often exhibit externalizing behaviors; biological, social, and cultural influences all contribute to this divergence . Empirical studies highlight gender-specific pathways: girls may demonstrate stronger anxiety responses following ACEs, whereas boys often show greater externalizing symptoms, though exceptions exist across contexts. Ignoring these intersecting dimensions oversimplifies ACEs research and may obscure critical pathways through which adversity affects mental health and cognition, ultimately undermining efforts to design effective, context-sensitive prevention and intervention strategies.

Adverse Childhood Experiences (ACEs) are widespread across both high-income and low- and middle-income countries (LMICs), with significant implications for public health and developmental outcomes. In the original ACE study, approximately 60% of participants reported at least one ACE, and over 10% had experienced five or more. This prevalence was mirrored in subsequent U.S. surveys and in Wales, where 60% and 47% of respondents, respectively, reported at least one ACE. In LMICs, the rates are even higher: 85% of adolescents in a Brazilian cohort experienced at least one ACE, with females reporting more adverse events, and 76% of Vietnamese university students reported similar experiences. Although definitions vary, South African studies also reveal high exposure levels—18.3% and 19.5% of rural and urban adolescents reported frequent physical and emotional abuse, respectively. In one national study, emotional abuse affected 54.7% of women and 56.4% of men, while 39.1% of women and 16.7% of men reported sexual abuse before age 18 [19].

Several individual, household, and community-level factors heighten vulnerability to ACEs.

Despite global concern, few studies in LMICs use the cumulative ACEs framework. Research often isolates single exposures, overlooking the complex interplay among various adversities [19]. A systematic review found that prevalence of four or more ACEs ranged from 1% to 32%, with the highest observed in a middle-income country. These patterns underscore the urgency of preventing ACEs in resource-constrained settings facing multiple public health burdens. Notably, markers of poverty correlate with sexual and psychological abuse and later symptoms of depression among South African youth. Inequalities in developmental and health outcomes often begin prenatally and are exacerbated by cumulative ACE exposure, particularly in LMICs where over 250 million children under five are at risk of not reaching their full potential [19].

Girls are more likely to experience sexual abuse and greater cumulative adversity. Globally, child maltreatment—including emotional abuse (36%), physical abuse (22%), neglect (16%), and sexual abuse among girls (18%)—is strongly predictive of adult mental health outcomes. Meta-analyses show a 68% increased risk of adult anxiety for those reporting any maltreatment, with even higher risks linked to specific types such as sexual abuse (90%) and physical abuse (56%). Although research from sub-Saharan Africa is limited, existing data confirm similar trends. One study found that among multiple ACEs, only the presence of household depression or suicide significantly predicted anxiety a year later [29]. This may reflect genetic influences, with heritability accounting for approximately 30% of anxiety symptoms [30].

Thus, while genetic predispositions may play a role, the structural and cumulative nature of ACEs remains a modifiable and urgent target for intervention. Preventing ACEs is not only essential for reducing psychological distress but also a necessary step toward achieving health equity and social justice in LMICs [19].

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