The first cluster of studies zeroes in on the close relationship between emotional distress and problematic digital media use. Zhou and Feng demonstrated that loneliness partially mediated the association between social anxiety and smartphone addiction in Chinese college students, hinting that socially anxious young adults may reach for their phones, in part, to cope with interpersonal disconnection. Zhu and colleagues, studying a similar population, found that negative emotions and problematic phone use went hand in hand with poorer life satisfaction and mental health. Tian and colleagues extended the picture with adolescent athletes, showing that resilience was associated with lower mobile phone addiction, an effect explained by reduced anxiety and depressive symptoms. Taken together, these findings converge on a clinically important message: problematic smartphone use is not simply a matter of excessive exposure to technology, but is often embedded in broader difficulties with affective regulation, distress tolerance, and adaptive coping.

A second group of articles emphasizes that addiction-related behaviors take shape within relational and environmental contexts that can either buffer or amplify risk. In a two-wave longitudinal study with children, Wei and Xu found that a more positive school climate predicted lower internet gaming addiction one year later, with deviant peer affiliation acting as a mediator and sensation seeking as a moderator. The results underscore the importance of school environments as potential risk or protective factors during development, a point with obvious implications for prevention programs aimed at children before gaming habits harden into compulsive patterns.

Family dynamics emerged as another powerful contextual force. Xu and colleagues reported that excessive parental psychological control was associated with greater psychological distress in Chinese university students with smartphone addiction. Intriguingly, it was inhibitory emotion regulation, rather than cognitive reappraisal, that helped explain this relationship, suggesting that maladaptive family environments may raise addiction risk not only directly but also by eroding the very self-regulatory capacities that would normally protect against compulsive behavior. Li and colleagues broadened the scope further by examining cosmetic surgery addiction in Chinese adults, finding that adverse childhood experiences, defined as a range of traumatic events before age 18, were linked to greater symptom severity, with insecure attachment and self-alienation serving as mediating factors. Although this form of addiction differs from digital or substance-related addictions, it points to the same long-term role of early adversity, disrupted attachment, and impaired self-related processes in driving compulsive, reward-seeking behavior.

The neurobiological heart of the collection comes from three complementary studies probing how reward circuitry and executive networks miscommunicate. Zhang and colleagues used resting-state functional MRI and dynamic causal modeling to compare brain connectivity in adults with tobacco use disorder against non-smokers. They found altered effective connectivity between the default mode network, an internally oriented circuit active during self-referential thought, and the central executive network, which governs working memory and cognitive control. Specifically, connectivity from the right dorsolateral prefrontal cortex and the medial prefrontal cortex was increased, and this pattern predicted heightened motivation for smoking. If confirmed in larger samples, the authors argue, these findings would support the view that addiction involves altered interactions between internally oriented and executive-control circuits, and they raise the possibility that network-level markers could eventually aid early assessment or risk stratification in clinical settings.

Sensation seeking, a trait long associated with adolescent risk-taking, received its own neural spotlight. Qianlan and colleagues examined sensation seeking, reward sensitivity, and risk adjustment in young adults facing uncertain conditions, measuring behavior alongside electroencephalographic responses. High sensation seekers adjusted more poorly to varying levels of risk and showed weaker neural responses to reward. The findings link reward-related personality traits to reduced flexibility in decision-making under uncertainty, a combination that could help explain why some young people persist in risky choices even as evidence of mounting losses accumulates. The editors note that these promising results deserve expansion with advanced neuroimaging and cognitive modeling techniques that can dissect the precise computational failures involved.

Genetics added a third layer to the mechanistic story. Emond and colleagues genotyped two dopaminergic polymorphisms, ANKK1 rs1800497, better known as Taq1A, and COMT rs4680, along with one nicotinic polymorphism, CHRNA4 rs1044396, in American children aged nine to twelve. All three variants had previously been linked to internet and video gaming addiction. The results showed that the Taq1A polymorphism, which is associated with reduced dopamine sensitivity, was related to higher problematic media use scores in these pre-adolescent children. Although replication in larger samples is needed, the study illustrates how genetic differences in reward sensitivity may quietly shape addiction vulnerability well before the transition to adolescence, potentially setting the stage for later compulsive behaviors.

Together, the mechanistic studies strongly support the core premise of the Research Topic: addiction risk in youth is best understood through the dynamic interplay of genetic predisposition, reward sensitivity, emotion regulation systems, and executive functions. Heightened reward seeking, reduced adaptability to risk, altered large-scale brain connectivity, and possible dopaminergic genetic vulnerability all describe pathways through which impulsive or compulsive behaviors may outpace still-maturing control systems. Crucially, the editors stress that these vulnerabilities are not purely biological. They are shaped by mental health status, family relationships, school context, and adverse early experiences, meaning that any account of youth addiction limited to brain or genes alone would be incomplete.

The translational value of the collection is reinforced by studies on assessment and intervention. Diaz-Guerra and colleagues validated the Executive Functions Scale for University Students, known as UEF-1, in a large sample of Cuban university students. The scale focuses on academic skills and self-regulation in Spanish-speaking populations, and the results supported its seven-factor structure, covering domains such as self-regulation, behavioral monitoring, decision-making, and emotion regulation. This contribution matters psychometrically and conceptually, because culturally appropriate tools are essential for identifying executive-function profiles relevant to addiction risk in diverse populations. Meanwhile, Haenjohn and colleagues piloted the Integrative Cognitive Neuropsychological Program for Inhibitory Control, or ICNIC, in Thai adults with substance use problems. The program combined psychoeducation, behavioral control skills, and computerized tasks aimed at improving inhibition and reducing impulsivity. Participants reported greater self-efficacy in behavioral control, although accuracy rates on visual and auditory Substance Stop Signal Tasks measuring motor inhibition to drug cues did not improve. Even with this mixed pattern, the editors suggest that gains in perceived control may emerge before measurable changes in specific inhibitory processes, meaning multifaceted approaches to cognitive control hold promise for treatment.

Finally, two contributions situate addiction within a broader developmental framework. Using a very large national sample of South Korean adolescents, Jeong and colleagues showed that earlier alcohol use and smoking predicted a later increase in addiction risk, and that smartphone overdependence interacted with substance-related behaviors. Behavioral addictions and substance-related risk behaviors, in other words, may reinforce each other over development rather than unfold in isolation. Complementing this empirical work, Lozano Wun and Luciana reviewed developmental models of addiction and argued for a dual-systems perspective in which an imbalance between reward-related systems and executive control during specific phases of adolescence, interacting with individual differences, heightens vulnerability to reward-seeking behaviors. Both developmental timing and individual differences matter: addiction risk is not static across adolescence, and future prevention efforts may need to be tailored to specific developmental windows. The editors conclude that the collection points toward operational targets for prevention and intervention, including strengthening inhibitory control and emotion regulation, promoting resilience, addressing early adverse experiences, and improving family and school environments, while future longitudinal, multimodal, and cross-cultural research will be essential to clarify causal mechanisms and translate these findings into developmentally sensitive interventions.

Subject of Research: Developmental and neurobiological mechanisms of addiction vulnerability in adolescents and young adults

Article Title: Editorial: Executive functions, reward systems, and addiction in adolescents and young adults

Article References: Editorial: Executive functions, reward systems, and addiction in adolescents and young adults. (n.d.). https://doi.org/10.3389/fradm.2026.1835532

Image Credits: AI Generated

DOI: 10.3389/fradm.2026.1835532

Keywords: addiction, adolescence, executive functions, reward systems, smartphone addiction, tobacco use disorder, sensation seeking, default mode network, dopamine genetics, emotion regulation, developmental psychology, public health