ABSTRACT. Objective: During adolescence, neurobiological maturation occurs concurrently with social and interpersonal changes, including the initiation of alcohol and other substance use. The National Consortium on Alcohol and NeuroDevelopment in Adolescence (NCANDA) is designed to disentangle the complex relationships between onset, escalation, and desistance of alcohol use and changes in neurocognitive functioning and neuromaturation. Method: A sample of 831 youth, ages 12-21 years, was recruited at five sites across the United States, oversampling those at risk for alcohol use problems. Most (83%) had limited or no history of alcohol or other drug use, and a smaller portion (17%) exceeded drinking thresholds. A comprehensive assessment of biological development, family background, psychiatric symptomatology, and neuropsychological functioning-in addition to anatomical, diffusion, and functional brain magnetic resonance imaging-was completed at baseline. Results: The NCANDA sample of youth is nationally representative of sex and racial/ethnic groups. More than 50% have at least one risk characteristic for subsequent heavy drinking (e.g., family history, internalizing or externalizing symptoms). As expected, those who exceeded drinking thresholds (n = 139) differ from those who did not (n = 692) on identified factors associated with early alcohol use and problems. Conclusions: NCANDA successfully recruited a large sample of adolescents and comprehensively assessed psychosocial functioning across multiple domains. Based on the sample's risk profile, NCANDA is well positioned to capture the transition into drinking and alcohol problems in a large portion of the cohort, as well as to help disentangle the associations between alcohol use, neurobiological maturation, and neurocognitive development and functioning. (J. Stud. Alcohol Drugs, 76, 895-908, 2015)

Brain structural development continues throughout adolescence, when experimentation with alcohol is often initiated. To parse contributions from biological and environmental factors on neurodevelopment, this study used baseline National Consortium on Alcohol and NeuroDevelopment in Adolescence (NCANDA) magnetic resonance imaging (MRI) data, acquired in 674 adolescents meeting no/low alcohol or drug use criteria and 134 adolescents exceeding criteria. Spatial integrity of images across the 5 recruitment sites was assured by morphological scaling using Alzheimer's disease neuroimaging initiative phantom-derived volume scalar metrics. Clinical MRI readings identified structural anomalies in 11.4%. Cortical volume and thickness were smaller and white matter volumes were larger in older than in younger adolescents. Effects of sex (male > female) and ethnicity (majority > minority) were significant for volume and surface but minimal for cortical thickness. Adjusting volume and area for supratentorial volume attenuated or removed sex and ethnicity effects. That cortical thickness showed age-related decline and was unrelated to supratentorial volume is consistent with the radial unit hypothesis, suggesting a universal neural development characteristic robust to sex and ethnicity. Comparison of NCANDA with PING data revealed similar but flatter, age-related declines in cortical volumes and thickness. Smaller, thinner frontal, and temporal cortices in the exceeds-criteria than no/low-drinking group suggested untoward effects of excessive alcohol consumption on brain structural development.

Initiation of drinking during adolescence, with or without marijuana co-use, disordered normal brain growth trajectories. Factors possibly contributing to abnormal cortical volume trajectories include peak consumption in the past year and family history of alcoholism.

Background Underage drinking is widely recognized as a leading public health and social problem for adolescents in the United States. Being able to identify at-risk children before they initiate heavy alcohol use could have immense clinical and public health implications; however, few investigations have explored individual-level precursors of adolescent substance use. This prospective investigation used machine learning with demographic, neurocognitive, and neuroimaging data in substance-naïve adolescents to predict alcohol use initiation by age 18. Materials and Methods Participants (N=137) were healthy substance-naïve adolescents (ages 12–14) who underwent neuropsychological testing and structural and functional magnetic resonance imaging (sMRI and fMRI), then were followed annually. By age 18, 70 youth (51%) initiated moderate-to-heavy alcohol use and 67 remained non-users. Random forests classification generated individual alcohol use outcome predictions based on demographic, neuropsychological, sMRI, and fMRI data. Results The final random forests model was 74% accurate, with good sensitivity (74%) and specificity (73%) and included 34 predictors contributing to alcohol use by age 18, including several demographic and behavioral factors (being male, higher socioeconomic status, early dating, more externalizing behaviors, positive alcohol expectancies), worse executive functioning, and thinner cortices and less brain activation in diffusely distributed regions of the brain. Inclusion of neuropsychological, sMRI, and fMRI data significantly increased the prediction accuracy of the model. Discussion Identification of at-risk youth is not validated for clinical use. Its value is for research to address brain mechanisms that predispose to early drinking.

Alcohol intoxication often results in negative consequences; however, specific behavioral and subjective effects vary as a function of individual differences. The present study utilized an alcohol challenge paradigm to examine whether heavy binge social drinkers (HD; n=77), compared to light social drinkers (LD; n=55), exhibit: (1) greater tolerance in psychomotor task performance under the influence of alcohol, and (2) differential perceptions of the impairing effects of alcohol. The study included three test sessions in which participants consumed either a low (0.4 g/kg) or a high (0.8 g/kg) dose of ethanol or a placebo beverage administered in random order and counterbalanced within group. Participants completed the Digit-Symbol Substitution Task (DSST) and the Grooved Pegboard at pre-drink baseline and at multiple time points after beverage consumption. They also completed a scale of perceived impairment at several intervals after beverage consumption. Ethanol impaired performance at the high dose, but not at the low dose (ps<.001). The groups exhibited similar alcohol-induced impairment. However, HD reported lower self-perceived impairment compared to LD, particularly during the early portion of the blood alcohol curve when actual impairment was most pronounced (p<.001). Thus, this study extends prior research in that habitual binge social drinking does not appear to be associated with tolerance to alcohol's impairing effects on select psychomotor skills. Further, results may have implications for alcohol-related harm as binge social drinkers regularly consume intoxicating doses of alcohol but may not be aware of the physical and cognitive impairments produced by alcohol.