Full length articleContextual risks linking parents’ adolescent marijuana use to offspring onset
Introduction
Marijuana use is relatively common among adults in the U.S. (30.2% among 19–28 year olds; Johnston et al., 2013a) and, as with use of other substances, becomes increasingly prevalent across adolescence. In 2012, lifetime prevalence of marijuana use among 8th, 10th, and 12th graders in the Monitoring the Future (MTF) Study was 15.2%, 33.8%, and 45.2%, respectively (Johnston et al., 2013b). Recent legalization of recreational marijuana use in several U.S. states may reflect increasingly liberal use norms and may lead to increased availability and modeling of marijuana in the homes and communities of adolescents. At the same time, however, there is increasing evidence that marijuana use may have serious effects on the developing brains of adolescents, including increased risk for disorders such as schizophrenia (Arseneault et al., 2004, Bossong and Niesink, 2010, Moore et al., 2007). Earlier onset also is associated with heavier and more persistent use, marijuana use disorder, and negative socioeconomic consequences during early adulthood (Broman, 2009, DeWit et al., 2000). Consequently, there is good reason to delay onset among youth. The identification of modifiable risk and protective factors will inform prevention efforts to do so.
Many risk and protective factors relevant to marijuana use may be of similar relevance to other commonly used substances (Hansen et al., 1987). Social influences such as those related to parenting, peer group, and neighborhood on use of any specific substance in adolescence often overlap with those for use of other substances and for the general category of problem behaviors (Dishion and Patterson, 2006, Hicks et al., 2004). Additionally, polysubstance use is common in adolescence (Leatherdale et al., 2009), and onset of one kind of substance use hastens onset of others (Kosterman et al., 2000). Thus, models of risk for marijuana use onset should accommodate the likelihood that some risks tend to be generalized rather than substance specific. Identifying pathways of association that are of special importance in relation to marijuana use would aid the refinement of prevention programs.
Parent substance use is an important risk factor for child use, and some research has focused on marijuana specifically (Duncan et al., 1995, Washburn and Capaldi, 2014a, Washburn and Capaldi, 2014b). Most studies measure parent substance use in adulthood (e.g., Bailey et al., 2009). However, across early adulthood, marijuana use becomes less probable and quantity of use decreases even among chronic users (Washburn and Capaldi, 2014a). Thus, parental use in middle adulthood may represent atypical and problematic behavior, and variability in parents’ prior use, which may have long-term influences, is ignored. We focus here on marijuana use during parents’ adolescence, and examine the extent to which it is associated with family and peer contexts that lead to their children's marijuana use onset.
Genetic studies generally support a heritable component to substance dependence, but environmental influences are stronger in adolescence and for earlier stages of use (e.g., onset; (Dick, 2011, Kendler et al., 2008, Lynskey et al., 2010). Thus, parents transmit risk for marijuana use, in part, through the social contexts in which offspring are raised. Social contextual models of marijuana use in adolescence are derived from those proposed for alcohol use (e.g., Conger and Rueter, 1996, Kerr et al., 2012) and emphasize parents’ influence on both home and peer environments that model use, communicate deviant norms, and offer (or fail to limit) access to marijuana. Consistent with these notions, the age trends in marijuana use prevalence identified in MTF were paralleled by clear trends toward older youth more often having friends who use marijuana, personally approving of trying it, less often believing that occasional use is harmful, and being able to easily get it (Johnston et al., 2013b).
In the present study, fathers who have been studied since childhood participated with their offspring and their offspring's mothers in an ongoing prospective study of risk for alcohol and drug abuse. Factors from children's family and peer contexts potentially linking parents’ adolescent marijuana use with risk for child onset were examined, including those known to confer generalized risk for adolescent problem behaviors (parental monitoring and deviant peers; e.g., Dishion and Patterson, 2006). Then – as in our prior work on alcohol-specific risk (Kerr et al., 2012) and drawing on prior studies of marijuana (e.g., Ellickson et al., 2004) – outcome-specific risk factors were examined; specifically, having friends who use marijuana, exposure to marijuana use, and perceived parent disapproval of child marijuana use. Models also controlled for whether children had shown onset of alcohol use. This approach highlighted predictive paths to marijuana use onset that were not better explained by generalized risk processes shared with use of this more commonly encountered substance.
The study offers several other advances over prior work. Given the design of the study, adolescent marijuana use histories were known for all fathers, who tend to be less represented in developmental research. Additionally, most risk factors were measured using multiple informants, and substance use by fathers and their children were measured prospectively. Finally, the discrete-time survival analysis approach is especially relevant given the sensitivity needed to model onset and examine how risk may accumulate with development.
Study hypotheses were as follows: (a) parents’ marijuana use during their own adolescence will be associated with an earlier onset of marijuana use among their children; (b) the intergenerational transmission of such risk will be largely indirect through general contextual risks in the family and peer contexts, including peer deviance and less parental monitoring; (c) parent marijuana use will be associated with several outcome-specific risks for child marijuana use: namely, having friends who use marijuana, exposure to marijuana use, and low perceived parent disapproval of child use; (d) these general and specific factors will hasten the onset of marijuana use, beyond what would be predicted from child alcohol use. We also control for child gender, given the earlier substance use onset observed in boys in this and other samples (Capaldi et al., under review, Kosterman et al., 2000).
Section snippets
Participants
The present study was based on 93 fathers (recruited as children to the Oregon Youth Study [OYS]; Capaldi and Patterson (1989) and assessed regularly to the present day); their biological children (n = 146; 83 girls), 85 of the children's mothers, and 90 of the fathers also participated in the Three Generational Study (3GS). Children had to have participated in at least one of the four waves between ages 11 and 19 years as of March, 2014 to be included in the present analyses. A minority (38.4%, n
Descriptives and correlations
Descriptive statistics for all study variables are given in Table 1. Child marijuana use onset increased across adolescence, from 2% or less by age 13 years, to approximately 50% at ages 17–19 years; 36.3% showed onset. Boys’ rates of marijuana use onset exceeded girls at the first three assessments but were essentially equal by ages 17–19 years. Relative to girls, boys were monitored less by their parents (t[144] = 3.10, p = 0.002), were 4.46 times more likely to have consumed at least one whole
Discussion
Findings of this prospective intergenerational study indicate that adolescents who more often used marijuana were more likely to raise children in family and peer contexts that encouraged or failed to inhibit children's early onset of marijuana use. In such families, parents less closely monitored their children's whereabouts and associates, children had more contact with deviant peer groups, more often had seen someone use marijuana, and believed their parents would disapprove less if they
Role of funding source
This research was supported by the National Institutes of Health (NIH), U.S. PHS Award Number R01 DA015485 from the National Institute of Drug Abuse (NIDA), R01 AA018669 from the National Institute on Alcohol Abuse and Alcoholism (NIAAA), and R01 HD46364 from the National Institute of Child Health and Human Development (NICHD) awarded to Dr. Capaldi. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH, NIAAA, NICHD, or NIDA.
Contributors
All authors have approved the final article. Dr. Kerr was a co-investigator on the larger project, supervised the data analyses, and conceptualized and wrote the introduction and discussion of the article. Dr. Tiberio conducted the data analyses, wrote the method and results, and critically reviewed the final article. Dr. Capaldi was the Principal Investigator on the larger project, contributed to article conceptualization and analytic interpretation, and critically reviewed the final article.
Conflict of interest statement
No conflict declared.
Acknowledgements
We thank Shivan Tucci and the Oregon Youth Study-Three Generational Study team for high-quality data collection, Sally Schwader for editorial assistance, and Lee Owen and Karen Yoerger for data management.
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