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16 December 2025

Early Life Adversity and Disordered Eating: Cognitive and Neural Mechanisms

,
and
1
Key Laboratory of Cognition and Personality, Ministry of Education, Southwest University, Chongqing 400715, China
2
School of Psychology, Southwest University, Chongqing 400715, China
*
Author to whom correspondence should be addressed.
Behav. Sci.2025, 15(12), 1739;https://doi.org/10.3390/bs15121739
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Abstract

The mosaic brain evolution perspective states that the relative sizes and functions of brain regions adapt to living environments and behavioural motivation. Early life adversity brings changes to brain structure, function, and patterns of cognitive processing of food cues. Specific brain development patterns are associated with subsequent disordered eating, which, on the one hand, increases the risk of obesity and metabolic syndrome, and, on the other hand, leads to mental health problems, such as depression and anxiety. This review intends to synthesise aberrant brain development indices, describe aberrant brain developmental trajectories, summarise aberrant neural markers of cognitive processing of food cues, conclude how early life adversity affects disordered eating through aberrant brain development patterns, and provide neural implications for future disordered eating research and intervention.

1. Introduction

On 27 April 2022, the General Office of the State Council of China issued the 14th Five-Year Plan for National Health, emphasising the importance of comprehensive interventions targeting health issues and their determinants. Among these, physical fitness has emerged as a national priority. Disordered eating refers to a broad range of maladaptive, psychologically driven eating behaviours that significantly impair physical health and psychosocial functioning (H. Chen & Jackson, 2008). These behaviours elevate the risk of developing eating disorders, obesity, and metabolic diseases. For instance, even short-term binge eating can trigger inflammatory signalling at the cellular level, increase neutrophil counts, and accelerate the development of atherosclerotic plaques (Lavillegrand et al., 2024). In addition, our team found that chronic disordered eating is associated with increased symptoms of binge-eating disorder, bulimia nervosa, and higher obesity risk (H. Chen & Jackson, 2008; Jackson & Chen, 2014; Y. Luo et al., 2023b). Disordered eating has also been linked to psychological problems such as depression, anxiety, self-denial, and even self-injurious behaviours (Yu et al., 2025b). Therefore, investigating the risk factors for disordered eating and its underlying cognitive-neural mechanisms is crucial for the development of effective prevention and intervention strategies for related conditions, such as depression, anxiety, eating disorders, and obesity. Such research holds direct practical relevance for efforts to improve public health and also contributes to the global understanding of eating disorders.
Since 2008, our research team has systematically investigated the psychological and behavioural factors contributing to disordered eating. We have identified sociocultural pressure, negative body image, attentional and memory biases toward food-related cues, and impaired conflict monitoring as significant risk factors for maladaptive eating behaviours (Y. Liu et al., 2019; Y. Luo et al., 2019, 2020a). More recently, large-scale longitudinal studies, behavioural experiments, and neuroimaging techniques, have collected initial evidence suggesting that early life adversity (ELA) may increase the risk of disordered eating in children and adolescents through changes in life history strategies and functional connectivity of the amygdala (Y. Luo et al., 2023a, 2024, 2023b, 2020b).
ELA refers to adverse experiences occurring between birth and age 16, either within the family or broader social environment. These experiences include physical, emotional, and sexual abuse as well as neglect, economic hardship, parental separation or divorce, and exposure to domestic violence (Malave et al., 2022). Despite increased societal awareness of ELA, scholars emphasise its prevalence as a public health challenge and a robust predictor of poor mental and physical health outcomes (Twist, 2024). Similarly, a national policy issued by the General Office of the State Council of China in December 2024 called for improved early development services, highlighting the urgent need to prevent and mitigate the long-term health consequences of ELA. Yet current interventions are primarily behavioural or pharmacological, with limited targeting of the underlying neural mechanisms. This study aimed to review the cognitive-neural pathways linking ELA and disordered eating to provide more effective, mechanism-based prevention and intervention strategies.

Neural Development Patterns of ELA

Mosaic brain evolution perspective suggests that different brain regions may experience adaptive changes in their relative sizes in response to environmental pressures and behavioural demands. Such region-specific neural developmental patterns are thought to reflect the selective evolution of distinct sensory and cognitive capacities (DeCasien & Higham, 2019). Hence, this evolutionary framework provides a compelling lens through which to interpret the neural consequences of ELA. From an adaptive perspective, ELA may signal an unstable or threatening environment in which long-term investments yield limited survival benefits. As a result, individuals experiencing ELA may adopt an accelerated life history strategy that prioritises immediate rewards. Structural and functional changes in brain regions responsible for reward sensitivity and inhibitory control may be a maladaptive consequence of this adaptive calibration (Ellis & Del Giudice, 2019).
Consistent with this view, a growing body of research has documented region-specific alterations in brain development following ELA. For example, emotion- and reward-related areas (e.g., the amygdala, and nucleus accumbens) tend to show accelerated maturation, whereas prefrontal regions implicated in inhibitory control often exhibit delayed development (Chan et al., 2024; Holz et al., 2023; Petrican et al., 2025; Yu et al., 2025a). These findings suggest that ELA may trigger a mosaic pattern of brain development with differential maturation timing across functional systems, reflecting an adaptive response to adversity. However, this adaptive response may compromise long-term emotional regulation, impulse control, and reward processing.

2. Method

Paper Identification and Review

The literature search followed PRISMA guidelines. The full screening workflow is presented in Figure 1. To identify papers to include in the systematic review, we searched PubMed database and Nature Affiliated journals for studies conducted in humans on childhood adversity and disordered eating between 1 January 2015 and 1 May 2025. Childhood adversity was indexed using the following search phrases: “early life stress”, “childhood adversity”, “childhood trauma”, “adverse childhood experiences”, “childhood maltreatment”, “emotional abuse”, “emotional neglect”, “physical abuse”, “sexual abuse”, “physical neglect”, “poverty”, and “environmental unpredictability”. Cognitive and neural mechanism was indexed using “cognitive”, “neural”. Disordered eating was indexed using “overeating”, “emotional eating”, “disordered eating”, “uncontrolled eating”, “binge eating”.
Figure 1. PRISMA flow diagram detailing the literature search and selection process for inclusion in the systematic review.
We included studies that: (1) examined early life adversity (ELA), or subclinical disordered eating symptoms/disordered eating; (2) used neuroimaging methods (structural MRI, resting-state fMRI, or task-based fMRI). We excluded studies that: (1) did not involve neuroimaging, such as genetic research or behavioural research; or (2) focused on clinically diagnosed populations, including eating disorders or other psychiatric or medical conditions.
The initial search yielded 4978 records (PubMed: 3514; Nature and affiliated journals: 1464). After title and abstract screening, 3924 records were removed for being clearly unrelated to the topic. An additional 571 news items, commentaries, or narrative reviews were excluded. We then removed 3353 records that did not involve human neuroimaging. A total of 1054 articles underwent full-text assessment, during which 966 were excluded because they involved clinical populations or did not meet other inclusion criteria. After removing 41 duplicates, 47 studies met all criteria and were included in the final analysis.
Among the 47 studies included, the age composition of samples differed substantially. Based on the mean age reported in each study, 7 examined early childhood groups (0–6 years), 20 involved school-age or adolescent samples, and 20 focused on adult participants. Notably, because early-life adversity is generally defined as exposure occurring before age 16.

3. Results

3.1. Structural Changes, Functional Changes, and Cognitive Processing Patterns Related to ELA

In neuroimaging studies reviewed in latest 5 years (Table 1), structural changes related to ELA showed a certain pattern. For example, Holz et al. (2023) conducted a large-scale cohort study employing machine learning techniques and voxel-based normative modelling to quantify the impact of ELA on brain morphology at the structural level. Their findings revealed widespread structural alterations associated with ELA, including increased volume of the amygdala, hippocampus, and orbitofrontal cortex (OFC), as well as reduced volume of the ventromedial prefrontal cortex (vmPFC) and anterior cingulate cortex (ACC). Importantly, volumetric alterations of the OFC persisted into adulthood, remaining stable at both 25 and 33 years. These results indicate that ELA may accelerate the maturation of emotion- and reward-related regions while delaying the development of brain areas involved in inhibitory control. Such a region-specific developmental trajectory lends empirical support to the ‘accelerated–delayed’ brain development hypothesis in response to early environmental stressors.
Table 1. Summary for Neuroimaging Studies on Early Life/Childhood Experiences and disordered eating.
Functional changes associated with ELA focused on emotional regulation relevant region and network. ELA may lead to premature maturation of emotion perception systems, while concurrently disrupting the development of emotion regulation capacities. This is evidenced by increased negative functional connectivity between the prefrontal cortex and the amygdala (Herzberg & Gunnar, 2020). In addition, the intrinsic variability in brain networks—such as time series variability and functional coupling variability—has been proposed as a marker of the brain’s adaptive capacity to environmental demands. Time series variability reflects a region’s sensitivity to external changes, whereas coupling variability captures the stability of functional integration across networks. In a sample of adolescent girls, increased functional coupling variability was associated with accelerated neurodevelopment, particularly in the visual network, attentional network, and default mode network (DMN). These findings suggest that, in addition to sensory-related systems, variability in networks subserving higher-order cognitive, affective, and social processing (i.e., the DMN) may be a signature of accelerated maturation (Petrican et al., 2025). Moreover, structure–function coupling (SC–FC) is considered to be a key indicator of brain maturation and neural plasticity. Between the ages of 8 and 22 years, SC–FC changes occur in a functional-network-specific manner, with decreases in highly conserved motor regions and increases in transmodal cortices (Baum et al., 2020). A recent birth cohort study tracking 549 children between ages 4.5 and 7.5 years revealed a linear decline in whole-brain structure–function coupling, suggesting a normative age-related reduction in coupling strength. Notably, this decline was steeper in children exposed to high levels of ELA, and this is indicative of accelerated brain development. This acceleration was most evident in transmodal integrative networks, such as the frontoparietal network; however, it was not observed in unimodal sensory networks (Chan et al., 2024). These findings suggest that ELA may expedite the maturation of higher-order brain systems as an adaptive response to environmental challenges. Furthermore, this maturation is potentially at the cost of reduced neural plasticity required for later functional refinement.
Heightened sensitivity in reward-related circuits and the delayed development of executive functions are considered to be key neural markers of atypical brain development associated with ELA. Herzberg and Gunnar (2020) reported that children exposed to early adversity exhibit increased activation in the nucleus accumbens and medial prefrontal cortex during reward tasks, suggesting heightened reward responsivity. Similarly, in gambling paradigms, individuals with histories of ELA display faster and more impulsive decision-making. They opt for high-risk, high-reward choices despite repeated losses, and fail to adjust their strategies to minimise negative outcomes. These behaviours are accompanied by aberrant activation in reward-related regions including the putamen, insula, and precuneus (Birn et al., 2017). Furthermore, children who have experienced high adversity levels demonstrate poorer executive function than their low-adversity peers by age eight years on measures of attention, short-term visual memory, and spatial working memory. Moreover, the developmental trajectories of these functions slow over time, contributing to a widening gap in cognitive performance by adolescence (Wade et al., 2019).
In summary, individuals exposed to ELA may exhibit accelerated development in neural circuits involved in reward and emotion processing. This is thought to be an adaptive response to a threatening environment. However, this adaptation may come at the cost of delayed maturation in brain regions supporting inhibitory control, potentially compromising regulatory capacity in later stages of development. These neurodevelopmental changes may contribute to maladaptive eating behaviours, particularly those characterised by heightened reward sensitivity and diminished impulse control (Yu et al., 2025b).

3.2. Association Between ELA and Disordered Eating

Disordered eating behaviours involve the interplay of three key neural systems: the emotional processing system, the reward circuitry, and the inhibitory control network. Emerging evidence indicates that ELA may accelerate the development of emotion- and reward-related brain regions, while simultaneously delaying the maturation of areas responsible for inhibitory control (Birn et al., 2017; Wade et al., 2019; X. Chen et al., 2023). This imbalance may compromise individuals’ capacity to regulate responses to food-related rewards, thereby increasing the likelihood of maladaptive eating behaviours. Prior research on the neurocognitive mechanisms of disordered eating has primarily focused on the interaction between reward sensitivity and inhibitory control; however, it is essential to consider the regulatory role of the emotional processing system in the ELA context. Structural and functional alterations in emotion-related circuits may modulate both reward responsivity and impulsivity, thereby indirectly contributing to the onset and maintenance of disordered eating.

3.2.1. Structural MRI Evidence

ELA may influence disordered eating behaviours through structural alterations in the brain, particularly in regions involved in emotion regulation and cognitive control (Fujisawa et al., 2015; Gold et al., 2016). Neuroimaging studies have consistently associated early adversity with reduced prefrontal cortical volume and impaired executive functions, including goal-directed behaviour, working memory, and emotional regulation (W. Liu et al., 2020). In contrast, emotion-related circuits such as the amygdala show heightened reactivity and enhanced emotional memory, reflecting a developmental imbalance between affective and regulatory systems.
The inferior frontal gyrus (IFG), a key region within the prefrontal cortex, appears to be particularly affected. Adolescents who engage in emotional or uncontrolled eating often display delayed maturation of the prefrontal cortex, including the IFG and cerebellum (Yu et al., 2025a; Brumback et al., 2016). Longitudinal studies have linked ELA to reductions in overall brain volume, including an 8.6% decrease in total brain volume and significant reductions in the surface area and volume of the right IFG.
White matter abnormalities further support this pattern. Children exposed to ELA exhibit decreased mean diffusivity and increased fractional anisotropy in key tracts connecting the prefrontal cortex and limbic system. These tracts include the cingulum bundle, uncinate fasciculus, and fornix. Reductions in cortical thickness of the IFG have also been observed in maltreated adolescents (Gold et al., 2016). Additionally, IFG abnormalities are consistently reported in populations with ADHD, bipolar disorder, and eating disorders (Fujisawa et al., 2015).
In summary, ELA may alter structural development of the IFG, compromising inhibitory control and increasing susceptibility to reward-driven disordered eating.

3.2.2. Resting States and Task-Based fMRI Evidence

ELA may increase the risk of disordered eating by altering the neural architectures of emotion regulation, reward processing, and inhibitory control. Resting-state fMRI studies have associated self-reported childhood adversity with spontaneous activity in the basolateral and centromedial subregions of the amygdala. In particular, adversity scores can predict both functional connectivity between the bilateral basolateral amygdala and the left IFG and disordered eating behaviour one year later (Y. Luo et al., 2023a). In another retrospective study, adversity scores were positively correlated with attentional bias toward food cues and negatively associated with functional connectivity between the right IFG and the left inferior parietal lobule. This connectivity, in turn, predicted disordered eating severity (Y. Luo et al., 2024). These findings suggest that early adversity may impair prefrontal-parietal circuits underlying inhibitory control, thereby contributing to increased food-related impulsivity.
Task-based fMRI studies further provide evidence for these associations. Compared to women with low levels of ELA, those who had experienced high adversity displayed heightened activation in the amygdala, dorsal striatum (caudate and putamen), medial OFC, and ACC during food-related tasks. Moreover, increased amygdala–putamen connectivity and decreased amygdala–ACC/PFC connectivity were observed in the high-adversity group (Tryon et al., 2013). This suggests a shift toward stronger emotion-to-reward coupling and weaker emotion-to-control integration among individuals with high levels of ELA. Findings from animal models align with these human data. In rats exposed to ELA and later treated with opioid agents, there was reduced activation in the nucleus accumbens core, whereas the central amygdala and prefrontal cortex showed increased activation (Levis et al., 2022). This suggests that early adversity may reshape neural activity within emotion, reward, and inhibitory control circuits, thereby altering sensitivity to food-related stimuli.

3.2.3. Cognitive Processing Patterns

ELA may increase the risk of disordered eating by altering how individuals process food-related reward cues. These alterations are observed across three stages of reward processing—anticipation, consumption, and decision-making. They involve brain regions implicated in emotion, reward, and cognitive control.
During the anticipation of food rewards, individuals with high levels of ELA exhibit heightened activation in brain regions related to gustatory processing (e.g., insular cortex), somatosensory integration, and reward valuation (e.g., the amygdala, and vmPFC) (Hilbert et al., 2018). This increased activation may reflect stronger motivation to seek food to alleviate persistent negative affect stemming from early-life stress.
In contrast, when receiving food rewards, these individuals show attenuated activation in key reward-related regions, such as the dorsal striatum (e.g., caudate nucleus) (Stice & Burger, 2019). This discrepancy between high anticipatory and low consummatory responses can be explained using two theoretical frameworks. The first is incentive sensitization theory, which posits an increased sensitivity to reward cues but a diminished response to the reward itself. The second is the reward deficiency hypothesis, which suggests that food rewards fail to fully compensate for the emotional deficits caused by ELA, resulting in a chronic reward prediction error.
During the decision-making phase, ELA appears to compromise self-regulation. Higher levels of adversity are associated with stronger activation in the vmPFC, amygdala, and striatal regions when evaluating palatable food options. These areas are known to encode hedonic value, and their heightened activity predicts the selection of high-calorie over low-calorie foods (Maier et al., 2015). Furthermore, ELA disrupts effective connectivity among the prefrontal cortex, limbic system, and striatum, weakening the neural mechanisms underlying inhibitory control. Individuals with high ELA may exhibit a maladaptive reward processing profile characterised by heightened anticipation, blunted reward experience, and impulsive food choices. These abnormalities involve both classic reward-related areas (e.g., the amygdala, striatum, OFC, ACC) and regions responsible for higher-order control (e.g., dorsolateral prefrontal cortex). This is a neural basis for increased susceptibility to disordered eating.
Considering the wide-ranging and long-lasting effects of disordered eating, a deeper understanding of how ELA associated brain changes contribute to disordered eating may identify novel brain circuit targets for advanced treatments and preventive strategies.

4. Discussion

As a systematic review, this study synthesises evidence across multiple domains to examine the cognitive and neural mechanisms linking Early Life Adversity (ELA) to subsequent disordered eating, highlighting specific patterns of brain development that may underlie this association. Results indicate that ELA exerts pervasive effects on the development and function of neural circuits. Specifically, it appears to accelerate the maturation of emotion- and reward-related brain regions while delaying the development of areas responsible for inhibitory control.
Therefore, efforts to promote children’s physical and mental development should prioritise reducing adverse factors embedded in the family, school, and community environments. Additionally, future research should investigate how the two distinct dimensions of ELA—specifically, abuse and neglect—differentially shape this neural development trajectory.
Despite the identified imbalance (accelerated emotion/reward versus delayed inhibitory control), few studies have directly related this pattern to subsequent disordered eating symptoms. Moving forward, integrating findings from clinical and preclinical research will be essential for identifying the precise neurobiological mechanisms that causally mediate the effects of ELA on maladaptive eating. This neuro-developmental imbalance may fundamentally impair an individual’s capacity to regulate responses to food-related rewards, thereby heightening the likelihood of maladaptive eating behaviours.
Understanding these neural mechanisms not only helps to eliminate the stigma associated with abused or neglected children—as their behaviours are manifestations of a brain injury, not them being “innately bad”—but also provides precise targets for scientific intervention.
The most crucial implication of these findings is the recognition that these ELA-related brain changes are often adaptive responses rather than permanent damage, underscoring the remarkable neuroplasticity available during childhood and adolescence. Interventions which provide a stable, safe, responsive, and supportive environment—such as high-quality alternative care, trauma-focused psychotherapy, and school-based support—can actively help these children’s brain development trend toward repair and recovery.

5. Limitations

However, several limitations of this review should be clarified. First, we did not examine potential moderators of the neurodevelopmental pathways linked to disordered eating. Our focus was on how ELA-related patterns—accelerated maturation of emotion–reward systems and delayed development of inhibitory control—may converge to shape vulnerability. As a result, other influences such as gender, age, socioeconomic status, or comorbid conditions were not considered. These factors remain important, and future work should test how they modify the link between early adversity and eating-related outcomes at different developmental stages.
Second, the imbalance model outlined here is conceptual and derived from indirect evidence. Its assumptions have not been tested through direct statistical modelling, and any causal interpretation should be viewed as provisional. Longitudinal neuroimaging studies will be essential for validating or revising this framework.
Finally, most studies included in this review focused on early childhood, adolescence, and young adulthood. This concentration in younger samples should be noted, as it limits the generalisability of the findings to later developmental periods.

6. Conclusions

Early life adversity (ELA) exerts pervasive effects on the development and function of neural circuits, thereby increasing the risk of disordered eating and obesity across the lifespan. Specifically, it can accelerate the maturation of emotion- and reward-related brain regions while delaying inhibitory control related regions. This neurodevelopmental imbalance may impair an individual’s capacity to regulate responses to food-related rewards, thereby heightening the likelihood of maladaptive eating behaviours and increasing the risk of obesity. Addressing how ELA disrupts the intricate interplay among the emotion, reward, and inhibitory control systems remains a major challenge for contemporary neuroscience and psychiatry, requiring consideration of both the molecular regulation of these systems and the developmental trajectories of individual brain regions.

Author Contributions

Conceptualization, Y.L.; methodology, Y.L.; software, Y.L.; validation, Y.L. and J.Z.; formal analysis, Y.L.; investigation, Y.L.; resources, Y.L.; data curation, Y.L.; writing—original draft preparation, Y.L. and J.Z.; writing—review and editing, Y.L., J.Z. and H.C.; visualisation, Y.L. and J.Z.; supervision, H.C.; project administration, H.C.; funding acquisition, H.C. All authors have read and agreed to the published version of the manuscript.

Funding

This research was funded by National Natural Science Foundation of China (No. 32271087); National Social Science Foundation of China (No. 22&ZD184); the Innovation Team of Philosophy and Social Science in Universities of Chongqing (7110200530).

Institutional Review Board Statement

Not applicable.

Data Availability Statement

No new data were created or analysed in this study.

Conflicts of Interest

The authors declare no conflicts of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Abbreviations

The following abbreviations are used in this manuscript:
ELAearly life adversity
OFCorbitofrontal cortex
vmPFCventromedial prefrontal cortex
ACCanterior cingulate cortex
DMNdefault mode network
IFGinferior frontal gyrus

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