Long-term Effects of the Raising Healthy Children Intervention on Family Functioning in Adulthood: A Nonrandomized Controlled Trial.

Some universal prevention programs, such as Raising Healthy Children (RHC), have shown persisting and wide-ranging benefits in adulthood, long after the intervention has ended. Recent studies suggest that benefits may continue into the next generation as well. This study examines whether the RHC intervention, delivered in childhood, may promote healthy family functioning among participants who now have families of their own.

Testing Cross-Generational Effects of the Raising Healthy Children Intervention on Young Adult Offspring of Intervention Participants.

This study tested whether effects of a preventive intervention delivered in elementary school showed benefits for the young adult offspring of intervention recipients over 20 years later. The Raising Healthy Children (RHC) intervention, trialed in 18 public schools in Seattle, Washington, from 1980-1986 (grades 1-6), sought to build strong bonds to family and school to promote school success and avoidance of substance use and illegal behavior. Four intervention groups were constituted: full, late, parent training only, and control.

Tobacco Use Patterns From Adolescence to Young Adulthood Among Latinx Youth From Rural Communities.

Purpose: To examine patterns in adolescent and young adult tobacco use, comparing Latinx foreign-born children and children of foreign-born parents (i.e., children of immigrants(COI)) to Latinx US-born children of US-born parents (i.

Young adult opioid misuse indicates a general tendency toward substance use and is strongly predicted by general substance use risk.

Objective: To examine whether young adult opioid misuse reflects a general tendency toward substance use and is influenced by general substance use risk or whether it is a different phenomenon from other drug use.

Methods: At ages 23 (2016) and 26 (2019), a panel of young adults (n = 3794 to 3833) in the United States self-reported their past-month substance use (opioid misuse, heavy drinking, cigarettes, cannabis) and substance-specific risk factors (perceptions of harm; approval of use; and use of each substance by friends and romantic partners). Structural equation models examined non-opioid and opioid-specific associations between latent risk and substance use factors.

Polygenic risk, family cohesion, and adolescent aggression in Mexican American and European American families: Developmental pathways to alcohol use.

Poor family cohesion and elevated adolescent aggression are associated with greater alcohol use in adolescence and early adulthood. In addition, evocative gene-environment correlations (rGEs) can underlie the interplay between offspring characteristics and negative family functioning, contributing to substance use. Gene-environment interplay has rarely been examined in racial/ethnic minority populations.

The relation of parent alcohol disorder to young adult drinking outcomes mediated by parenting: Effects of developmentally limited versus persistent parent alcohol disorder.

Background: Parent alcohol use disorder (AUD) is a well-established risk factor for the development of offspring AUD and is associated with poor parenting. However, few studies have examined heterogeneity in trajectories of parental AUD and its influence on adolescent offspring drinking, and no studies to date have considered the differential risk to offspring conferred by parental AUDs that are limited to early adulthood. Specifically, AUDs limited to the period of emerging adulthood may confer less risk to a child's environment as recovery following emerging adulthood coincides with the typical ages of entry into the parenting role.

Affiliation with substance-using peers: Examining gene-environment correlations among parent monitoring, polygenic risk, and children's impulsivity.

Parental monitoring can buffer the effect of deviant peers on adolescents' substance use by reducing affiliation with substance-using peers. However, children's genetic predispositions may evoke poorer monitoring, contributing to negative child outcomes. We examined evocative genotype-environment correlations underlying children's genetic predisposition for behavioral undercontrol and parental monitoring in early adolescence via children's impulsivity in middle childhood, and the influence of parental monitoring on affiliation with substance-using peers a year and a half later (n = 359).

Predicting substance use in emerging adulthood: A genetically informed study of developmental transactions between impulsivity and family conflict.

Deviance proneness models propose a multilevel interplay in which transactions among genetic, individual, and family risk factors place children at increased risk for substance use. We examined bidirectional transactions between impulsivity and family conflict from middle childhood to adolescence and their contributions to substance use in adolescence and emerging adulthood (n = 380). Moreover, we examined children's, mothers', and fathers' polygenic risk scores for behavioral undercontrol, and mothers' and fathers' interparental conflict and substance disorder diagnoses as predictors of these transactions.

Testing the Relations Among Family Disorganization, Delay Discounting, and Adolescent Alcohol Use: A Genetically Informed Study.

Background: Delay discounting is a potential etiological factor in adolescents' alcohol use, making it important to understand its antecedents. Family disorganization might contribute to delay discounting, but few studies have tested this relation. Moreover, because delay discounting is heritable, the effects of family disorganization on delay discounting might be moderated by adolescents' genetic risk for delay discounting.

ALDH2 and ADH1B interactions in retrospective reports of low-dose reactions and initial sensitivity to alcohol in Asian American college students.

Background: A mechanistic model has been proposed for how alcohol-metabolizing gene variants protect individuals from the development of alcohol use disorders, with heightened sensitivity to alcohol being an early step (endophenotype) in this model. This study was designed to determine whether possession of 2 alcohol-metabolizing genes variations, the aldehyde dehydrogenase ALDH2*2 allele and the alcohol dehydrogenase ADH1B*2 allele, was associated with self-reported sensitivity to alcohol at low doses and at initial use.

Methods: Asian-American college students (N=784) of Chinese and Korean descent were genotyped at the ALDH2 and ADH1B loci and assessed for lifetime alcohol symptoms following 1 or 2 drinks and level of response to alcohol during the first 5 lifetime drinking episodes.