Nanostructured electrode materials and flexible-substrate engineering for wearable multi-analyte biosensors in diabetes monitoring and personalized care: a comprehensive review.

Adolescent substance use remains a pressing public health concern (Harris and Weitzman ). Early initiation of alcohol, cannabis, nicotine, and other substances can cascade into academic failure (Wills et al. ), mental health problems (Boden et al. ), poorer physical health (Hamidullah et al. ), and substance use disorders in adulthood (Jordan and Andersen ; Volkow et al. ). Adverse childhood experiences (ACEs), including abuse, neglect, and household dysfunction, are a risk factor for substance misuse (Grummitt et al. ), estimated to account for 13%–29% of drug use and 5%–14% of smoking cases in the United States (Grummitt et al. ; Hughes et al. ). Foundational work demonstrated that individuals with four or more ACEs have a 4‐ to 12‐fold increased risk for alcoholism and drug abuse (Felitti et al. ), and subsequent research confirms adolescents with higher ACE scores initiate substance use earlier and progress more quickly to hazardous use (Leza et al. ; Ports et al. ). While the association is well‐established, the specific neurocognitive mechanisms explaining how early adversity translates into substance use remain an area of active investigation, with most studies employing cross‐sectional designs. To clarify these mechanisms prospectively, this study leverages longitudinal Adolescent Brain Cognitive Development (ABCD) Study data to examine executive function (EF) as a pathway linking cumulative and domain‐specific childhood adversities to early adolescent substance use initiation. Vulnerability models suggest neurocognitive liabilities, such as EF deficits resulting from early adversity, act as premorbid risk factors creating a predisposition for addiction (Luciana ). EF is a multifaceted construct of higher‐order cognitive processes, including inhibitory control, working memory, and cognitive flexibility, that support self‐regulation and goal‐directed behavior (Diamond ; Miyake et al. ). A recent meta‐analysis concluded early adversity significantly reduces lifespan cognitive control, emphasizing EF as a mediator of ACEs' effects on later health and behavioral outcomes (Rahapsari and Levita ). Weaker EF skills have been linked to impulsivity, risk‐taking, and greater substance use across adolescence and young adulthood (Casey and Jones ; Luciana ), and longitudinal studies consistently show low preschool behavioral control predicts earlier and more problematic substance use by early adulthood (Dick et al. ; McGue et al. ; Peeters et al. ; Wilson et al. ). Importantly, ACEs are associated with deficits in daily‐life EF (Ifroh and Gai ; Trossman et al. , ), with these deficits being one of the most frequently reported neurocognitive consequences of childhood maltreatment (Kavanaugh et al. ). This vulnerability is particularly pronounced during adolescence, a period characterized by heightened risk‐taking and an imbalance between a rapidly maturing reward system and a still‐developing prefrontal cortex responsible for executive control (Casey and Jones ; Spear ; Sturman and Moghaddam ). Neurobiological models explain chronic stress from adversity disrupts the maturation of these prefrontal and frontoparietal networks, compromising the neural circuits subserving EF (McLaughlin and Sheridan ; Teicher et al. ; Trossman et al. ). A growing body of research provides direct support for a mediational model where executive dysfunction links adversity to substance misuse. For example, Ifroh and Gai () found EF deficits partially mediated the relationship between ACEs and health‐risk behaviors, including smoking and vaping, in Indonesian adolescents. This pathway has also been established neurobiologically, with trauma‐affected brain networks predicting future high‐risk drinking via their impact on executive dysfunction (Silveira et al. ). Furthermore, Trossman et al. () identified a crucial methodological nuance, finding that self‐reported global executive dysfunction, capturing EF difficulties in daily life, mediated the link between adversity and poor mental health, whereas performance on discrete, lab‐based core executive skills did not. However, a competing explanation exists for the relationship between EF and substance use. Neurotoxicity models propose that substance use is the causal agent that leads to subsequent changes in normal brain development, resulting in EF deficits and a loss of control (Castellanos‐Ryan et al. ), which subsequently increases the propensity to seek substances (Scott et al. ; Squeglia et al. ; Wilens et al. ). Much of the existing research examining the ACEs‐EF‐substance use pathway, however, has relied on cross‐sectional designs, making it difficult to establish which mechanism is operating in the EF‐substance use link.