Adolescence is a particularly vulnerable neurodevelopmental period marked by high rates of engagement with risky alcohol use. This review summarizes the cognitive and neural consequences following alcohol use during adolescence from longitudinal design studies in humans and animals. Findings from human adolescent studies suggest that binge drinking and heavy alcohol use is associated with poorer cognitive functioning on a broad range of neuropsychological assessments, including learning, psychomotor speed, attention, executive functioning, and impulsivity. adolescence is memory, visuospatial functioning, Alcohol use during associated with accelerated decreases in gray matter and attenuated increases in white matter volume, and aberrant neural activity during executive functioning, attentional control, and reward sensitivity tasks, when compared to non-drinking adolescents. Animal studies in rodents and nonhuman primates have replicated human findings, and suggest cognitive and neural consequences of adolescent alcohol use may persist into adulthood. Novel rodent studies demonstrate that adolescent alcohol use may increase reward responsiveness of the dopamine system to alcohol later in life, as well as disrupt adolescent neurogenesis, potentially through neuroinflammation, with long-lasting neural and behavioral effects into adulthood. Larger longitudinal human cognitive and neuroimaging studies with more diverse samples are currently underway which will improve understanding of the impact of polysubstance use, as well as the interactive effects of substance use, physical and mental health, and demographic factors on cognition and neurodevelopment.

Objective: Data on the neurodevelopmental and associated behavioral effects of light to moderate in utero alcohol exposure are limited. This retrospective investigation tested for associations between reported maternal prenatal alcohol use and psychological, behavioral, and neurodevelopmental outcomes in substance-naive youths.Methods: Participants were 9,719 youths (ages 9.0 to 10.9 years) from the Adolescent Brain Cognitive Development Study. Based on parental reports, 2,518 (25.9%) had been exposed to alcohol in utero. Generalized additive mixed models and multilevel cross-sectional and longitudinal mediation models were used to test whether prenatal alcohol exposure was associated with psychological, behavioral, and cognitive outcomes, and whether differences in brain structure and resting-state functional connectivity partially explained these associations at baseline and 1year follow-up, after controlling for possible confounding factors.Results: Prenatal alcohol exposure of any severity was associated with greater psychopathology, attention deficits, and impulsiveness, with some effects showing a dose-dependent response. Children with prenatal alcohol exposure, compared with those without, displayed greater cerebral and regional volume and greater regional surface area. Resting-state functional connectivity was largely unaltered in children with in utero exposure. Some of the psychological and behavioral Send correspondence to Ms. Lees

This review provides the first systematic and quantitative synthesis of the literature examining the relationship between binge drinking, cognition, brain structure and function in youth aged 10 to 24 years. PubMed, EMBASE, Medline, PsychINFO and ProQuest were searched for neuroimaging, neurophysiological, and neuropsychological studies. A total of 58 studies (21 neuroimaging, 16 neurophysiological, 21 neuropsychological) met the eligibility criteria and were included in the review. Overall, abnormal or delayed development of key frontal executive-control regions may predispose youth to binge drink. These abnormalities appear to be further exacerbated by the uptake of binge drinking, in addition to alcohol-related neural aberrations in reward-seeking and incentive salience regions, indexed by cognitive deficits and maladaptive alcohol associations. A meta-analysis of neuropsychological correlates identified that binge drinking in youth was associated with a small overall neurocognitive deficit (g = −0.26) and specific deficits in decisionmaking (g = −1.70), and inhibition (g = −0.39). Using the Grades of Recommendation, Assessment, Development, and Evaluation (GRADE) Evidence Profile, the certainty in outcomes ranged from very low to low. Future prospective longitudinal studies should address concomitant factors, exposure thresholds, and age-related vulnerabilities of binge drinking, as well as the degree of recovery following discontinuation of use.

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This systematic review assessed the current evidence base of substance use prevention programs for Indigenous adolescents in the USA, Canada, Australia and New Zealand. The authors investigated (a) the outcomes, type, setting and context of prevention programs; (b) the common components of beneficial prevention programs; and (c) the methodological quality of evaluations of included prevention programs. The authors searched eight peer-reviewed and 20 grey literature databases for studies published between 1 January 1990 and 31 August 2017. Data extracted included type of program (culturally adapted, culture-based or unadapted), the setting (school, community, family or multi-setting), delivery (computerised or traditional), context (Indigenousspecific or multi-cultural environment) and common components of the programs. Program evaluation methodologies were critically appraised against standardised criteria. This review identified 26 eligible studies. Substance use prevention programs for Indigenous youth led to reductions in substance use frequency and intention to use; improvements in substance-related knowledge, attitudes and resistance strategies; and delay in substance use initiation. Key elements of beneficial programs included substance use education, skills development, cultural knowledge enhancement and community involvement in program development. Five programs were rated as methodologically strong, seven were moderate and fourteen were weak. Prevention programs have the potential to reduce substance use among Indigenous adolescents, especially when they are developed in partnership with Indigenous people. However, more rigorously conducted evaluation trials are required to strengthen the evidence base.

Globally, Indigenous populations experience a disproportionately higher burden of disease related to substance use. Effective prevention of harm related to substance use is a key strategy for improving the health and wellbeing of Aboriginal and Torres Strait Islander peoples in Australia. To inform preventative approaches, this review synthesised the evidence of risk and protective factors of substance use and related harms among Aboriginal and Torres Strait Islander peoples. Eight peer-reviewed and two grey literature databases were systematically searched for quantitative or qualitative studies assessing factors associated with substance use and related harms among Aboriginal and Torres Strait Islander peoples, published between 1 January 1990 and 30 April 2018. Study quality was assessed using validated instruments. Risk or odds ratios were extracted or calculated and factors were summarised in an ecological model into individual, relationship, community, societal or culturally-distinct levels. Thirty-eight relevant studies were identified and reviewed. Individual-level risk factors for substance use were identified including low socio-economic status, high psychological distress, poly drug use and being male. Relationship-level factors were peer pressure and partner/family substance use; protective factors were supportive environments and positive role models. Community-level risk factors included availability of substances. Culturally-distinct factors included cultural connection as a protective factor, but cultural obligations around sharing was a risk factor. Societal risk factors included intergenerational trauma caused by government policies. These findings highlight the importance of tailored preventative approaches for Aboriginal and Torres Strait Islander communities that address identified risk factors and promote protective factors across all ecological levels.

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Background An emerging body of literature has indicated that broad, transdiagnostic dimensions of psychopathology are associated with alterations in brain structure across the life span. The current study aimed to investigate the relationship between brain structure and broad dimensions of psychopathology in the critical preadolescent period when psychopathology is emerging. Methods This study included baseline data from the Adolescent Brain and Cognitive Development (ABCD) Study® (n = 11,875; age range = 9–10 years; male = 52.2%). General psychopathology, externalizing, internalizing, and thought disorder dimensions were based on a higher‐order model of psychopathology and estimated using Bayesian plausible values. Outcome variables included global and regional cortical volume, thickness, and surface area. Results Higher levels of psychopathology across all dimensions were associated with lower volume and surface area globally, as well as widespread and pervasive alterations across the majority of cortical and subcortical regions studied, after adjusting for sex, race/ethnicity, parental education, income, and maternal psychopathology. The relationships between general psychopathology and brain structure were attenuated when adjusting for cognitive functioning. There were no statistically significant relationships between psychopathology and cortical thickness in this sample of preadolescents. Conclusions The current study identified lower cortical volume and surface area as transdiagnostic biomarkers for general psychopathology in preadolescence. Future research may focus on whether the widespread and pervasive relationships between general psychopathology and brain structure reflect cognitive dysfunction that is a feature across a range of mental illnesses.