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. Participants were drawn from the Seattle Social Development Project (SSDP), a nonrandomized controlled trial of the RHC intervention prospectively following youths from 18 elementary schools in Seattle, Washington from 1985 to 2014. Participants who became parents were enrolled in an intergenerational study, along with their oldest biological child and an additional caregiver who shared responsibility for raising the child. Ten waves of data were collected between 2002 and 2018. The present analysis includes 298 SSDP parents, 258 caregivers who identified as a parent or partner of SSDP parent ("co-parent"), and 231 offspring. The SSDP parent sample was composed of 41.6% male, 21.1% Asian or Pacific Islander, 24.2% Black or African American, 6.4% Native American, and 48.3% white individuals. No significant intervention effects were found on adult romantic relationship quality; offspring bonding to co-parent; or co-parent past-month use of cannabis, cigarettes, or binge drinking. Findings highlight the continued need to understand how the benefits of theory-guided universal preventive interventions are sustained across the life course and how they may or may not shape family functioning for those who go on to have families and children of their own.ClinicalTrials.gov Identifier: NCT04075019.

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. Participants were followed through 2014 (age 39 years). Those who became parents were enrolled in an intergenerational study along with their oldest offspring (10 assessments between 2002 and 2018). This study includes young adult offspring (ages 18-25 years; n = 169; 52% female; 4% Asian, 25% Black, 40% multiracial, 4% Native American, 2% Native Hawaiian/Pacific Islander, 25% White, and 14% Hispanic/Latinx) of participants in the original RHC trial. Offspring outcome measures included high school noncompletion, financial functioning, alcohol misuse, cannabis misuse, cigarette use, criminal behavior, internalizing behavior, social skills, and social bonding. A global test across all young adult outcome measures showed that offspring of parents who received the full RHC intervention reported better overall functioning compared to offspring of control group parents. Analyses of individual outcomes showed that offspring of full intervention group parents reported better financial functioning than offspring of control group parents. Findings show the potential of universal preventive interventions to provide long-term benefits that reach into the next generation. ClinicalTrials.gov Identifier: NCT04075019; retrospectively registered in 2019.

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.e., children of nonimmigrants,(CONI)) and to CONI White youth who grew up in small and rural towns. METHODS: Data were from youth who lived in control communities that participated in a community-randomized trial of the Communities That Care prevention system. We compared Latinx CONI (n = 154) with Latinx COI (n = 316) and with non-Latinx White CONI (n = 918). We examined tobacco use in adolescence (any adolescent use, early onset, and chronic use) and young adulthood (any past-year tobacco use, any daily smoking, any nicotine dependence symptoms) with mixed-effects logistic regressions. RESULTS: In adolescence, Latinx CONI had a higher prevalence of any and chronic tobacco use relative to Latinx COI, and of any and early onset tobacco use relative to non-Latinx White CONI. In young adulthood, Latinx CONI were more likely to report tobacco use in the past year, any symptoms of nicotine dependence, and daily smoking relative to Latinx COI; and more likely to report daily smoking relative to non-Latinx White CONI. Generation differences in young adult tobacco use were explained by chronic tobacco use in adolescence. DISCUSSION: The study suggests targeting chronic tobacco use in adolescence to prevent disparities in tobacco outcomes among Latinx young adults from rural communities.

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. RESULTS: Opioid misuse and opioid-specific risk factors shared significant variance with latent substance use and latent substance use risk, respectively, which were strongly associated. A statistically significant residual correlation between opioid-specific risk and opioid misuse remained. CONCLUSION: Young adult opioid misuse reflects a general tendency toward substance use and is strongly predicted by risk for substance use. Opioid-specific risk factors play only a small independent role. Existing evidence-based substance use interventions may be effective in preventing opioid misuse among young adults.

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 current study examined adolescents' polygenic risk scores for aggression in evocative rGEs underlying aggression and family cohesion during adolescence, their contributions to alcohol use in early adulthood (n = 479), and differences between Mexican American and European American subsamples. Results suggest an evocative rGE between polygenic risk scores, aggression, and low family cohesion, with aggression contributing to low family cohesion over time. Greater family cohesion was associated with lower levels of alcohol use in early adulthood and this association was stronger for Mexican American adolescents compared to European American adolescents. Results are discussed with respect to integration of culture and racial/ethnic minority samples into genetic research and implications for alcohol use.

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. The present study tested whether parental AUDs developmentally limited to emerging adulthood (DLAUD) transmit less risk for alcohol problems and alcohol consumption in offspring compared to offspring of parents with AUDs spanning across multiple developmental periods (persistent AUD), as mediated by positive parenting strategies. METHOD: Pathways were examined using longitudinal mediation models (N = 361) comparing offspring with parental DLAUD, persistent AUD, and no AUD. RESULTS: Parents with DLAUD do not transmit the same risk for alcohol problems to offspring as parents with persistent AUD (B = 0.173, SE = 0.067, p < .05); more offspring alcohol problems were associated with persistent AUD than with DLAUD. Positive parenting mediated the transmission of risk from parental AUD to offspring alcohol problems (B = 0.040, SE = 0.019, p < .05) and consumption (B = 0.019, SE = 0.011, p < .05) only when comparing persistent AUD vs. no parental AUD. CONCLUSION: Findings suggest that the developmental period in which parents' recovery occurs is a useful way to categorize "recovered" AUDs versus current AUDs.

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). Genetic predisposition for behavioral undercontrol was captured using a polygenic risk score, and a portion of passive rGE was controlled by including parents' polygenic risk scores. Children's polygenic risk predicted poorer parental monitoring via greater children's impulsivity, indicating evocative rGE, controlling for a portion of passive rGE. Poorer parental monitoring predicted greater children's affiliation with substance-using peers a year and a half later. Results are discussed with respect to gene-environment correlations within developmental cascades.

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. The results support a developmental cascade model in which children's polygenic risk scores predicted greater impulsivity in middle childhood. Impulsivity in middle childhood predicted greater family conflict in late childhood, which in turn predicted greater impulsivity in late adolescence. Adolescent impulsivity subsequently predicted greater substance use in emerging adulthood. Results are discussed with respect to evocative genotype-environment correlations within developmental cascades and applications to prevention efforts.

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. Thus, the current study examined the role of family disorganization, in interaction with genetic risk, in predicting adolescents' delay discounting and subsequent alcohol use. METHODS: Adolescents participated in 4 waves of data collection. Adolescents self-reported their family disorganization at T1, completed a delay discounting questionnaire at T3, and self-reported their alcohol use both at T2 (covariate) and T4 (outcome). Using results from an independent sample, we created a polygenic risk score consisting of dopaminergic genes to index genetic risk for delay discounting. RESULTS: Greater family disorganization predicted adolescents' greater delay discounting, but only for adolescents with low levels of genetic risk for delay discounting. Adolescents with high and mean levels of genetic risk for delay discounting showed elevated delay discounting regardless of their family's disorganization. Greater delay discounting prospectively predicted adolescents' greater alcohol use. Finally, the effects of family disorganization on adolescents' alcohol use were mediated through delay discounting, but only for adolescents with low levels of genetic risk. CONCLUSIONS: Results suggest multiple pathways to delay discounting. Although there are genetically influenced pathways to delay discounting, family disorganization might represent an environmental pathway to delay discounting (and subsequent alcohol use) for a subset of adolescents at low genetic risk. These findings reinforce the utility of family interventions for reducing adolescents' delay discounting and alcohol use, at least for a subgroup of adolescents. Because higher family organization did not buffer against delay discounting among adolescents with high genetic risk, future research should explore other early environmental influences that could protect these high-risk adolescents from developing these risky behaviors.

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. RESULTS: Participants who had an ALDH2*2 allele were more likely to report experiencing all 6 low-dose symptoms and having heightened initial response to alcohol. An interaction was found between ALDH2*2 and ADH1B*2, with ADH1B*2 being associated with heightened self-reported sensitivity to alcohol only in individuals who also possessed 1 ALDH2*2 allele. CONCLUSIONS: These findings suggest the effects of ADH1B*2 may be felt more strongly in Asians who already have some heightened sensitivity to alcohol from possessing 1 ALDH2*2 allele, but who are not too sensitized to alcohol from possessing 2 ALDH2*2 alleles. These results offer additional insight into the discrepant findings that have been reported in the literature for the role of ADH1B*2 in response to alcohol and the development of alcohol-related problems.