Parietal P3 and midfrontal theta prospectively predict the development of adolescent alcohol use

Abstract

Background Subclinical adolescent alcohol use is highly prevalent and may have deleterious effects on important psychosocial and brain outcomes. Prior research has focused on identifying endophenotypes of pathological drinking, and the predictors of normative drinking remain understudied. This study investigated the incremental predictive value of two potential psychophysiological endophenotypes, P3 amplitude (an index of decision making) and midfrontal theta power (a correlate of attentional control), for prospectively predicting the expression and initiation of alcohol use emerging in adolescence. Methods A large (N = 594) epidemiological sample was prospectively assessed at ages 11/14/17. Alcohol/substance use was assessed at all ages via a computerized self-report inventory. EEG was recorded at age-14 during a visual oddball task to elicit P3 and theta. Results Reduced target-related P3 and theta at age-14 prospectively predicted drinking at age-17 independent of one another. Among alcohol-naive individuals at age-14, attenuated P3 and theta increased the odds of new-onset alcohol behaviors 3 years later. Importantly, the endophenotypes provided significant incremental predictive power of future non-clinical alcohol use beyond relevant risk factors (prior alcohol use; tobacco/illicit drug initiation; parental alcohol use disorder). Conclusions The current report is the first of our knowledge to demonstrate that deviations in parietal P3 and midfrontal theta prospectively predict the emergence of normative/non-pathological drinking. P3 and theta provide modest yet significant explanatory variance beyond prominent self-report and familial risk measures. Findings offer strong evidence supporting the predictive utility of P3 and theta as candidate endophenotypes for adolescent drinking.

Midfrontal Theta Activity in Psychiatric Illness: An Index of Cognitive Vulnerabilities Across Disorders

“…During oddball and Go/No-Go tasks, reduced FM has been found in participants with active AUD and those with short-and long-term abstinence (103)(104)(105). These effects may present as a risk factor for AUD, rather than a consequence of the disorder, as reduced FM in early adolescence predicts problematic drinking (106).…”

Internal consistency and test–retest reliability of the P3 event‐related potential (ERP) elicited by alcoholic and non‐alcoholic beverage pictures

“…Future prospective studies also could characterize differences between the Alcohol Cue P3 (or ACR-P3) and the P3-AR within an ontogenetic framework (Perkins et al, 2020;Senner et al, 2015). The P3-AR reflects a heritable (Carlson & Iacono, 2006), domaingeneral cognitive deficit that increases risk for externalizing psychopathology, including substance use, as a premorbid liability (Harper et al, 2021;Joyner et al, 2020;Perlman et al, 2013). In contrast, the Alcohol Cue P3 is theorized to be an alcohol-specific indicator reflecting consequences of alcohol userelated reinforcement learning processes (Bartholow et al, 2007(Bartholow et al, , 2010.…”

“…In contrast, the Alcohol Cue P3 is theorized to be an alcohol-specific indicator reflecting consequences of alcohol userelated reinforcement learning processes (Bartholow et al, 2007(Bartholow et al, , 2010. 11 Accordingly, whereas P3-AR is observable prior to and predicts the onset of substance involvement (Harper et al, 2021;Iacono et al, 2003;Perlman et al, 2013), in theory the Alcohol Cue P3 should not differentiate individuals' alcohol use trajectories prior to onset of use. Also, unlike P3-AR, which is largely unaffected by substance use (Joyner et al, 2020;Perlman et al, 2009), increasing alcohol involvement should be expected to exacerbate Alcohol Cue P3/ACR-P3.…”

Using multivariate endophenotypes to identify psychophysiological mechanisms associated with polygenic scores for substance use, schizophrenia, and education attainment

“…Moreover, while our previous report focused on schizophrenia polygenic risk, it is unknown whether endophenotypes index the polygenic liability for other psychological phenotypes, such as substance use ( Liu et al 2019 ; Pasman et al 2018 ) or educational attainment ( Lee et al 2018 ). A ‘multivariate endophenotype’ approach, leveraging the covariation across many endophenotypes using statistical techniques like principal component analysis (PCA), may also improve power to detect polygenic effects ( Gilmore, Malone, & Iacono, 2010 ; Harper, Malone, & Iacono, 2019a ; Iacono, Carlson, & Malone, 2000 ; Jones et al 2006 ; Price et al 2006 ). Multivariate endophenotypes have potentially greater explanatory power than any single endophenotype because they combine the unique and shared (genetic) variance explained across many endophenotypes and help capture the multiple biological and cognitive pathways giving rise to a single phenotype ( Gottesman & Gould, 2003 ).…”