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. 2025 Sep 11;11(1):2557763. doi: 10.1080/20565623.2025.2557763

Childhood trauma and adolescent substance use: an integrative perspective

John P Hoffmann a,✉, Curtis S Hoffmann b
PMCID: PMC12427455  PMID: 40932196

Abstract

This article addresses the complex relationship between childhood trauma and adolescent substance use. Drawing on evidence from neurodevelopmental, psychological/emotional, behavioral, and social research, we determined that childhood trauma, which includes early life stress, adverse childhood experiences (ACEs), and toxic stress, can upset brain development, emotion regulation, and stress-response systems, thereby creating lasting vulnerabilities. These neurological changes both generate and interact with behavioral traits such as impulsivity, poor coping, and emotional dysregulation, thus increasing the risk of substance use as a dysfunctional coping strategy. Social and environmental factors, such as caregiver substance use, peer influences, and community-level disadvantage, further compound these effects. However, individual traits, including effortful control and supportive relationships can attenuate these risks. Moreover, evidence-based interventions that address integrated, trauma-informed, and developmentally appropriate approaches have demonstrated promise in reducing the risks of adolescent substance use among trauma-exposed youth. The article concludes by calling for more conceptual integration across disciplines, longitudinal studies, and culturally responsive prevention, intervention, and treatment approaches.

Keywords: Childhood trauma, adolescent substance use, early life stress, neurodevelopment, ACEs, substance use disorder, developmental psychopathology, intervention

ARTICLE HIGHLIGHTS

Childhood Trauma

  • Childhood trauma includes ACEs, toxic stress, and early life stress, which often co-occur.

  • Traumatic exposures disrupt emotional and physiological functioning and are linked to later substance use.

Neurodevelopmental and Psychological Consequences

  • Childhood trauma affects HPA axis, prefrontal cortex, hippocampus, and amygdala functioning.

  • Trauma-related changes include impaired emotional regulation, heightened stress reactivity, and increased impulsivity.

Pathways to Substance Use

  • Trauma-exposed youth may use substances to self-medicate and manage emotional pain.

  • Neurobiological vulnerabilities, social modeling, and avoidant coping interact to raise risk.

Moderating and Protective Factors

  • Individual traits, including effortful control, secure interpersonal attachments, and structural supports, buffer the risk of substance use or substance use disorders (SUDs).

  • Intersectional and community-level risks highlight the need for tailored interventions.

Implications and Future Research

  • Integrated, trauma-informed, and developmentally sensitive interventions show promise in ameliorating substance use problems.

  • Future research should emphasize longitudinal designs, culturally responsive care, and evaluations of whether trauma-informed programs are implemented appropriately.

1. Introduction

Childhood trauma is an important public health concern that affects several developmental pathways that may lead to adolescent substance use. To better understand the connections between early adversity and substance use, we adopt a developmental psychopathology framework, which highlights the interaction between individual vulnerabilities and environmental settings over time. This approach emphasizes how early disruptions in brain development and emotional regulation, and poor social environments, can interact and lead to behavioral challenges, including substance use or problems related to use.

Unlike previous reviews that address either neurobiological correlates or social predictors of adolescent substance use, this review synthesizes research across levels of analysis: neurodevelopmental, emotional/psychological, and structural. It also incorporates recent findings on epigenetic programming and metabolomic markers that may link trauma to the risk of substance use, especially during adolescence. Our goal is to provide a more integrative and comprehensive view of the development of substance use and the effects of resiliency factors.

We have organized the review into the following sections: (1) definitions and prevalence of childhood trauma and adolescent substance use; (2) neurodevelopmental, epigenetic, and emotional/psychological consequences of trauma; (3) how these factors link trauma to adolescent substance use; (4) moderating and protective factors that affect these links; and (5) evidence-based interventions and implications for future research and practice.

2. Definitional issues

2.1. Childhood trauma

Childhood trauma is typically defined as exposure by children to events that threaten death, serious injury, or sexual violence; which can be experienced directly, witnessed, or learned about through another source (e.g., parent, sibling, peer) [1,2]. Trauma is not determined only by the event’s objective characteristics, however, but also by the child’s subjective perceptions, including feelings of fear, helplessness, or panic [2,3]. Danese [4], for instance, argued that trauma definitions are not only those that meet the APA’s Diagnostic and Statistical Manual (5th edition) (DSM-V) criteria [1], but also adverse childhood experiences (ACEs) that include neglect, bullying, parental absence, discrimination, and social deprivation. In addition, some researchers use the term early life stress (ELS) or toxic stress to refer to childhood adversities such as maltreatment, exposure to violence, and other adverse experiences listed in ACEs inventories [5].

Observers have noted that while there is clear overlap between ACEs/ELS and traumatic events, the latter are more likely to concentrate on events and experiences that provoke strong emotional and physiological responses that can persist long after they occur [6]. Since childhood traumatic events, ACEs, toxic stress, and ELS have all been the focus of studies of adolescent substance use, however, we do not distinguish these three types of experiences. Rather, we reviewed studies of each to develop our perspective of some complex developmental pathways that can result in substance use.

2.2. Adolescent substance use

Substance use among adolescents involves the consumption of psychoactive substances, including alcohol, tobacco, cannabis, inhalants, cocaine, methamphetamines, heroin, and prescription drugs used improperly. Most youth initiate substance use with alcohol, tobacco, marijuana, or inhalants, yet relatively few move on to other substances like cocaine or opioids. The modal age of first use in the US is 14, with variation across nations [7]. In 2023, about 15% of adolescents in the US used an illegal drug, 14% used a tobacco or nicotine product, and 22% used alcohol in the previous year [8].

Yet, some adolescents begin to use more frequently and thus are at risk of problematic forms of use. The term “substance use disorder” (SUD) is commonly used by the medical community to identify a clinically diagnosed condition denoted by a pattern of continued substance use despite significant cognitive, behavioral, and physiological impairments. According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) [1], an SUD is diagnosed when a person meets at least two of eleven criteria that encompass diminished control, social impairment, risky use, and pharmacological indicators such as tolerance or withdrawal [1]. The disorder is further categorized by severity: mild (2–3 symptoms), moderate (4–5), or severe (6 or more).

Of course, not all adolescents who use illicit substances meet the criteria for an SUD. Many may engage in experimental or episodic use without experiencing a diagnosable condition. Early and frequent use increases the risk of progression to an SUD, however, especially among those exposed to trauma or related experiences. In this article, we use terms such as “substance use,” “substance use problems,” or “SUD” to reflect clinically relevant, non-stigmatizing language. We avoid outdated or stigmatizing terms such as “addict,” “abuser,” or “substance abuse” [9].

In the US, an estimated 2.2 million adolescents had an SUD in 2023 [8]. Yet, this fails to reveal the extent of harm associated with SUDs. A measure that better characterizes the effects of adolescent substance use is the disability-adjusted life year (DALY). The DALY is a composite measure that combines years of life lost due to premature mortality with years lived with disability. Tracking DALYs helps policymakers determine how to allocate resources more effectively by specifying the costs of different diseases and conditions.

Recent estimates have demonstrated a substantial increase in SUD-related DALYs among adolescents in high-income countries—including the U.S.—between 1990 and the early 2020s [10]. This trend suggests an escalating prevalence of long-term health and social consequences related to substance use. The increases in DALYs also intimate that adolescent use is not simply a behavioral issue, but also a key contributor to the global burden of disease. Thus, there is an urgent need across many nations for prevention and intervention strategies that target early use and discourage use from transitioning into an SUD [7].

3. Neurodevelopmental, epigenetic, and psychological/emotional consequences of childhood trauma

3.1. Neurodevelopmental effects

Childhood trauma disrupts brain development and emotional regulation by altering neurological systems, neurotransmitter pathways, and social cognition processes. Some researchers use the term developmental trauma disorder to describe this cluster of impairments, which encompasses PTSD but more generally reflects how early life adversity hinders healthy psychological and behavioral development [11]. These impairments contribute to a large range of emotional and interpersonal challenges across the lifespan [12,13].

A consistent result found in neuroimaging studies is that trauma-related stress alters the structure and function of the prefrontal cortex (PFC), amygdala, and hippocampus, which are brain regions that operate together to regulate emotions, detect threats, and support memory and decision-making [5,14]. Chronic early life stress (ELS) may also result in increased amygdala reactivity, diminished hippocampal volume, and enervated connectivity between the PFC and amygdala [15–17]. These changes may lead to heightened vigilance, emotional reactivity, and difficulty interpreting ambiguous social cues. Although these responses are adaptive in risky environments, they can become maladaptive in everyday settings [18].

Early trauma also affects the hypothalamic–pituitary–adrenal (HPA) axis, which regulates the body’s stress response. Heightened HPA activation that results from trauma exposure leads to elevated cortisol levels, but over time, chronic activation results in dysregulated cortisol patterns. This is associated with compromised cognitive functioning, poor decision-making, and neurotoxic effects on hippocampal development [19,20]. In addition, trauma-related effects on dopaminergic pathways have been associated with altered reward sensitivity, anhedonia, and increased vulnerability to mood disorders [21,22].

3.2. Epigenetic effects

Another physiological mechanism by which which childhood trauma exerts long-term effects is epigenetic modification, especially through changes in DNA methylation, histone modifications, and non-coding RNAs. These changes do not alter the DNA sequence itself but regulate when and how genes are expressed, often in response to environmental stressors [23,24]. Traumatic experiences during sensitive developmental periods have been linked to altered methylation of genes that regulate the stress response and neuroplasticity, including NR3C1 (glucocorticoid receptor) and compromised BDNF (brain-derived neurotrophic factor). These are vital for HPA axis regulation, synaptic plasticity, neurogenesis, learning, memory, and cognitive function [25–28]. Like some of the mechanisms discussed earlier, stress-induced epigenetic alterations can lead to prolonged HPA axis dysregulation, increased vulnerability to disorders such as PTSD and depression, and disruptions in normal psychological and cognitive development, which may contribute to later health-risk behaviors [29,30]. In general, epigenetics research supports the view that childhood trauma leaves lasting physiological marks that may shape long-term behavioral outcomes.

3.3. Psychological and emotional effects

Meta-analyses have shown that trauma-related symptoms are linked to emotional dysregulation and maladaptive personality factors in children and adolescents, including impulsive aggression, affective liability, difficulty returning to emotional baseline, uncooperativeness, self-centeredness, heightened novelty and risk seeking, impulsivity, and lack of future planning [31,32]. These impairments are not simply comorbid features of trauma but appear to mediate the severity and persistence of future behavioral and mental health risks [32].

Several mechanisms likely underlie these impairments. The heightened attention to threat cues, hypervigilance, and problems reacting to negative or neutral stimuli mentioned earlier can become embedded over time and thus contribute to interpersonal difficulties, mood disorders, and aggressive behaviors [33,34]. The adoption and functionality of effective coping strategies are also diminished in many trauma-exposed young people [35].

To compound these challenges, meta-analyses have discovered that ELS is associated with deficits in executive function and social cognition, which can disrupt a child’s ability to interpret and respond to social cues in a normative manner [36]. These impairments often persist into adolescence and adulthood, especially when caregivers fail to provide sufficient emotional support and guidance or therapeutic interventions are not available.

4. The association between childhood trauma and adolescent substance use

A substantial body of research has established a significant connection between childhood trauma and adolescent substance use [37,38]. This section reviews current understanding of this connection by examining the multifaceted mechanisms through which early life adversity increases vulnerability to substance use and substance use disorders (SUDs). By considering neurological, emotional/psychological, and structural factors – including their potential intersectional effects – we have aimed to present a comprehensive integrated framework for understanding this deleterious association.

4.1. Neurodevelopmental pathways

Trauma in early life exerts enduring effects on brain systems that regulate stress, emotion, and behavioral control. These changes can help explain increased vulnerability to substance use during adolescence. Rather than fading once the threat is removed, the trauma response often continues through hyperarousal, emotional dysregulation, and increased sensitivity to perceived risks. As discussed earlier, these outcomes are connected to structural and functional changes across three interconnected brain systems: the limbic system (which includes the amygdala and hippocampus), the prefrontal cortex (PFC), and the HPA axis [39].

Studies have shown that early trauma and adversity lead to cortisol dysregulation and increased allostatic load, impairing the body’s ability to return to homeostasis after stress [40]. These neuroendocrine changes contribute to chronic activation of the amygdala (heightening threat detection), diminished activity in the PFC (reducing executive control), and vulnerability to risk-taking behaviors. The combined effects increase the risk of impulsivity, sensation seeking, and poor emotional regulation, which have each been consistently associated with substance use initiation and progression [41,42].

In addition to these processes, epigenetic changes that result from trauma and affect stress regulation might increase the risk of substance use over time [43]. Research has also revealed that metabolomic signatures found disproportionately among trauma-exposed individuals are associated with an escalated risk of SUDs [44]. In general, these research findings demonstrate that trauma-related neurodevelopmental pathways operate across multiple levels, from hormone systems and cellular markers to emotional functioning, and thus reinforce the view that trauma is intricately related to adolescent substance use and SUDs.

Though not comprehensive, one way to envision the pathway from childhood trauma to substance use and SUDs is with a “fire” analogy. As illustrated in Figure 1, trauma is the “match” that serves to “ignite” neurological and emotional/psychological vulnerabilities. These then affect behavioral outcomes and contribute to adolescent substance use. As noted in the previous section, trauma disrupts stress-response regulation (via the HPA axis), impairs emotion regulation (via the prefrontal cortex and amygdala), weakens memory/contextual control (via the hippocampus), and reduces intrinsic reward sensitivity (via dopaminergic systems). These alterations during early neurobiological development interact with epigenetic processes and environmental exposures (such as local models of substance use) – analogous to a house fire growing and becoming more difficult to control – to promote traits such as impulsivity, risk-seeking, and emotional dysregulation. Together, these factors increase the likelihood of substance use as a maladaptive coping mechanism during adolescence.

Figure 1.

Figure 1.

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Analogy of the effects of childhood trauma to a house fire.

4.2. Psychological and behavioral pathways

Cognitive and behavioral mechanisms also play a key role in linking childhood trauma to substance use. Studies have shown that ACEs, for example, are associated with poor decision-making among adolescents, which mediates the relationship between childhood trauma and substance use initiation [45]. Moreover, the self-medication hypothesis suggests that substance use is reinforced through its temporary relief of negative affect or trauma-related symptoms, perhaps by dampening certain neurological functions that contribute to overactive threat responses and emotional dysregulation [46,47].

This latter point is supported by research suggesting that the avoidance-based coping strategies used by many adolescents with trauma histories places them at risk of employing substance use to achieve emotional relief [48]. Further, the threat-based schemas, mistrust, and heightened vigilance found among trauma exposed youth contribute to risk-taking behaviors and associations with deviant peers [49], both established risk factors for substance use.

4.3. Interpersonal pathways

The social environment can significantly compound trauma-related risks, as well as be a source of trauma and stress. Adolescents exposed to ACEs and ELS frequently grow up in households and neighborhoods where substance use is modeled or normalized, and where adult supervision is limited by the demands on parents of living in disadvantaged households [37,50]. Trauma often occurs in settings of instability, neglect, or caregiver substance use, all of which can increase adolescents’ access to substances while reducing protective supervision [51].

In addition, exposure to parental substance use, particularly when co-occurring with neglect or abuse, not only increases access to substances and provides social models of use but also weakens protective attachment bonds [52]. Moreover, childhood trauma increases the probability of associating with deviant peers, thus indirectly elevating substance use risk through these associations [49].

4.4. Cumulative and intersectional effects

The relationship between trauma and substance use exhibits a clear dose-response pattern. Multiple studies, including Zhu et al.’s [38] meta-analysis, have reported graded increases in the odds of substance use and SUDs with each additional ACE or life stressor. This effect persists across substance types – including alcohol, cannabis, tobacco, and illicit drugs – from adolescence into adulthood [53,54]. For example, youth experiencing four or more ACEs have a two- to fourfold higher odds of early initiation of substance use, polysubstance use, and progression to SUDs [38,55].

Yet, trauma does not affect all youth equally. Intersectional identities, including race, ethnicity, gender, and sexual orientation, shape both exposure to trauma and access to coping resources and social support. Swedo et al. [56] found, for instance, that LGBTQ+ and racially marginalized youth report higher rates of trauma and associated health risks, some resulting from experiences with discrimination and racism. Studies also show that ACEs and traumatic experiences have stronger effects on substance use in certain subpopulations due to these overlapping sources of adversity and systemic marginalization [38,56].

4.5. Moderating and protective factors

Although the link between childhood trauma and substance use is well-established, not all individuals exposed to ELS or adversity develop substance-related problems. Studies have shown that various protective factors operating at the individual, interpersonal, and macro-levels can buffer the impact of trauma on the risk of adolescent substance use and SUDs.

4.5.1. Individual-level factors

At the individual level, self-regulation capabilities and personality traits such as high effortful control, optimism, and emotional resilience are associated with a lower risk of substance use among trauma-exposed youth [57,58]. For example, youth who exercise effortful control – the ability to regulate one’s impulses, respond flexibly to stressful situations, and modulate their responses – are less likely to use illicit substances than similarly traumatized youth. They also tend to be less impulsive and have more secure self-concepts. This further minimizes their risk of using psychoactive substances as coping mechanisms. Although the neurological factors that may serve as protective mechanisms, such as enhanced neuroplasticity, are not fully understood, some youth may have neurological structures or processes that improve resilience over time.

4.5.2. Interpersonal and structural factors

Youth’s interpersonal relations play a central role in protection against trauma effects. Secure attachments to non-abusive caregivers, positive peer relationships, and engagement with supportive adults in school or community settings have potent buffering effects [58,59]. Adolescents who experience parental warmth and responsiveness, even with a background of trauma, demonstrate greater resilience and are less likely to engage in substance use [57]. Those who spend time with supportive non-deviant peers are also at lower risk of substance use, perhaps because their peers provide them with coping resources when the detrimental effects of trauma emerge [60].

Religion and spiritual practices may offer protection against substance use among trauma-exposed adolescents. LeTendre and Reed [61] found, for instance, that while religiosity does not fully moderate the ACEs-SUD link, it does independently reduce the likelihood of developing an SUD, possibly by providing supportive social environments and positive adult role models. On the other hand, some studies have shown that any effect of positive religious coping on mental health or behaviors is independent of the effects of trauma-exposure [e.g., 62].

Finally, structural factors such as socioeconomic stability and neighborhood safety influence substance use and SUDs. Community violence, for example, is a distinct type of adverse experience that amplifies the likelihood of mental health challenges among residents and is associated with higher rates of adolescent substance use [63–65]. As noted by Hoffmann and Jones [37], community violence, as well as discrimination and lack of access to health care, can also reinforce the effects of other traumatic experiences, especially when adolescents lack access to safe environments and support systems.

However, family relations and community resilience can mitigate the effects of structural challenges [66]. For instance, close family relationships and parental support have been shown to buffer the detrimental effects of individual trauma for youth living in unstable or violent communities [67]. Supportive neighborhood organizations, youth programs, accessible mental health services, and strong school–community partnerships also buffer the effects of trauma by increasing interpersonal connections, providing prosocial adult role models, and nurturing a sense of safety and belonging. These protective community-level resources can disrupt patterns of disadvantage and reduce the likelihood that trauma-exposed youth will turn to illicit substances as a coping mechanism.

Figure 2 furnishes a simplified version of the model that emerges from a developmental psychopathology framework and synthesizes recent research findings on the effects of trauma on development. Note that it links childhood trauma to neurodevelopmental factors, which, in turn, affect emotional and psychological outcomes. These can combine with environmental factors to affect the risk of substance use initiation, regular use, and the risk of SUDs and relapse. However, several other potential moderating factors described in this section are absent from the figure, so it is not intended to show all potential influences that link trauma to substance use.

Figure 2.

Figure 2.

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Proposed pathway from childhood trauma to adolescent substance use.

5. Interventions and treatment for trauma-exposed youth

Preventing and treating the neurodevelopmental, personality, and interpersonal effects of childhood trauma are critical for minimizing the risk of adolescent substance use and SUDs. Although preventing trauma exposure is a worthy goal that requires the attention of policymakers, recent studies have offered several effective interventions and treatment programs that mitigate the effects of trauma, help youth build resilience, and address co-occurring risks. These programs operate at several levels, including in early childhood and adolescent settings.

5.1. Integrated and trauma-informed treatment models

There is increasing support for trauma-informed models that integrate substance use and mental health services for youth with a history of trauma and adversity. Becker et al. [68], for example, noted that trauma-focused cognitive behavioral therapy (TF-CBT) and other exposure-based methods reduce the risk of substance use and posttraumatic stress symptoms when tailored to youth. Some treatment providers are understandably concerned that trauma exposure programs might threaten youth with co-occurring SUDs, yet research suggests this concern is unsubstantiated. In general, exposure-based cognitive behavioral models lead to better outcomes among adolescents than standard SUD treatments alone [69].

Grummitt et al. [70] have similarly emphasized the importance of addressing co-occurring trauma and SUDs using integrated treatment approaches. As noted earlier, youth with trauma histories often have challenges with affect regulation, avoidance behaviors, and mistrust of adults, which can impede the effectiveness of standard SUD treatment. Integrated treatments such as motivational interviewing combined with skills-based CBT and family-based interventions that address trauma symptoms and substance use in tandem are effective alternatives to standard treatments.

5.2. Early childhood interventions

Promising early childhood interventions have emerged in recent years under the sobriquet trauma-informed care (TIC) in early childhood education and care (ECEC) settings [71]. These offer an opportunity to prevent the consequences of childhood trauma for youth before they begin formal schooling. Furthermore, multi-tiered systems of support, which range from universal teacher training and targeted classroom support to intensive individualized interventions, are becoming more common in ECEC centers and have demonstrated promising results for improving behavioral and emotional outcomes among trauma-exposed children [72]. Although the long-term effects of these support systems on adolescent substance use have not been fully evaluated, reducing early behavioral risks may diminish future risks of substance use and SUDs.

5.3. Family- and community-based interventions

Some scholars have argued that trauma-focused interventions require multiple components that target family settings, especially those involving parental substance use, mental health challenges, and intimate partner violence (IPV) [73]. These family-level factors are associated with both childhood trauma exposure and adolescent substance use. Programs that teach parenting skills and include mental health treatment, when augmented by CBT, have been shown to improve parenting practices and reduce maladaptive behaviors among children [74]. Community interventions that include supplemental income or public resources may also reduce stress-related parenting risks and improve functioning among economically disadvantaged families.

5.4. Targeting the mechanisms and mediators of risk

According to Grummitt et al. [70], prevention programs are most effective when they focus on modifiable mediators linking childhood adversity to substance use. These include some of the individual-level factors mentioned earlier, such as externalizing behaviors, emotion dysregulation, post-traumatic stress symptoms, impulsivity, and substance use coping motives. Interpersonal mechanisms include poor parent or caregiver attachment and deviant peer influences. Preventive interventions targeting these factors, including school-based life skills training, social-emotional learning programs, and family therapy, can diminish the likelihood of early substance use among trauma-exposed youth.

5.5. Trauma-informed systems and organizational change

At a systems level, trauma-informed interventions and treatment modalities have been increasingly adopted in pediatric and adolescent health care settings. Goldstein et al. [75], for instance, reviewed 16 recent studies and concluded that implementing SAMHSA’s [76] 10-domain trauma-informed care framework across health care systems improves provider readiness, patient outcomes, and organizational safety. Key elements of this framework include focused staff training, screening and referral for trauma, and policy changes to ensure care that avoids retraumatizing clients. Although the studies assessed by Goldstein et al. [75] focused on health systems generally, adolescent SUD treatment programs that adopt trauma-informed principles may achieve better client engagement, retention, and outcomes, especially for trauma-exposed young people.

6. Conclusion

The relationship between childhood trauma and adolescent substance use represents a complex interplay of neurobiological, psychological, behavioral, social, and environmental factors. Our review has illuminated some key insights with important implications for research, prevention, and treatment.

First, childhood trauma influences developing neural systems, particularly those governing stress response, emotion regulation, reward processing, and executive function. These effects can produce a neurobiological vulnerability to substance use through multiple, and often intersecting, pathways, including heightened stress reactivity, impaired emotional regulation, altered reward sensitivity, and compromised decision-making. The “fire” analogy presented in this article illustrates how trauma can ignite these vulnerabilities, creating conditions that increase the risk for substance use as a maladaptive coping mechanism.

Second, psychological and behavioral pathways mediate this relationship. Trauma-exposed youth often develop threat-based schemas, utilize avoidance-based coping strategies, and have difficulties with emotion regulation and interpersonal relationships. These conditions can increase vulnerability to substance use as a form of self-medication or emotional escape. Social and environmental factors, including exposure to others who use psychoactive substances, diminished parental supervision, and association with deviant peers, can further compound these risks.

Third, the relationship between trauma/ACEs and substance use exhibits a dose-response pattern, with each additional adverse experience incrementally increasing risk. However, this relationship is not ineluctable. Several protective factors, such as self-regulation, certain personality traits, secure attachments, positive peer relationships, and community resources, can mitigate the association between childhood trauma and adolescent substance use or SUDs. A better understanding of these protective factors is important for developing effective interventions.

Finally, recent evidence has demonstrated the effectiveness of integrated, trauma-informed approaches to prevention and treatment. Early childhood interventions, family- and community-based programs, and treatments targeting mediators have shown promise in reducing the effects of trauma on adolescent substance use. Implementing trauma-informed systems across education, healthcare, and community settings is a critical step toward addressing this public health challenge.

7. Future perspectives

To increase our understanding of trauma’s effects on substance use, future research must focus on longitudinal, developmental designs that examine how different types and combinations of childhood trauma affect trajectories of substance use, mental health, and resilience over time. Studies should also incorporate multilevel data, including biological (e.g., epigenetic and metabolomic markers), emotional/psychological, and social domains. This will allow researchers to map out causal pathways more precisely, which is needed for identification and intervention. Moreover, research designs should emphasize diverse and marginalized populations to understand better how systemic inequities influence both risk and resilience. Sampling strategies must ensure adequate representation of racial/ethnic minorities, LGBTQ+ youth, and those in low-resource environments, who often experience disproportionate trauma and have less access to protective services.

From a clinical and policy standpoint, our review also leads us to call for a shift toward comprehensive, developmentally appropriate, and culturally sensitive trauma-informed care models that promote resilience and reduce behavioral risks [76]. Prevention efforts should begin early by identifying trauma-exposed children and providing them with effective early childcare. Parenting interventions should also be emphasized since parents are often behind much of the early life trauma experienced by children [77]. Yet, it’s vital that these efforts extend into adolescence with integrated school- and community-based programs. For youth already affected by trauma and substance use, service systems must provide coordinated treatment that addresses co-occurring disorders rather than treating trauma and substance use separately [78,79]. Effective implementation also requires systemic investment in staff training, trauma screening tools, and organizational support to prevent retraumatization. Finally, future program evaluations must move beyond efficacy trials to include implementation science questions: What works for whom, in which settings, and under what conditions [80]?

Attention to these issues will ensure that trauma-informed care is not just conceptually sound but can also be functionally successful across diverse settings. Moreover, such efforts have the potential to disrupt intergenerational cycles of trauma and substance use, which could eventually improve outcomes for vulnerable children and adolescents across diverse populations.

Author contributions

John P. Hoffmann conceived of the initial idea for the manuscript and its organization. John P. Hoffmann and Curtis S. Hoffmann conducted literature reviews on the topic and developed the key arguments. Both authors discussed the results and wrote sections of the manuscript. Curtis S. Hoffmann created the figures. John P. Hoffmann was responsible for final editing and responding to reviews.

Disclosure statement

No potential conflict of interest was reported by the authors.

References

Papers of special note have been highlighted as either of interest (•) or of considerable interest (••) to readers.

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