Effects of age at first substance use and psychiatric comorbidity on the development of substance use disorders
Introduction
In this paper, we first examine what Anthony and Petronis called the “uncertainty whether early-onset drug use exerts an independent effect on risk of later drug problems, even though it might presage and serve as a vulnerability marker for later problems”(Anthony and Petronis, 1995). Using retrospective data, they showed that the risk of adult drug problems was linearly related to age at onset of drug use, being twice as high in adults reporting first use before age 13 as in those with first use after age 17. However, the time from first use to problem use was around 4 years, irrespective of age at first use among problem users. Here we look at the situation in adolescence, but using prospective data. Many previous research findings have established that early onset of drug use is associated with later problem use (Andreasson et al., 1992, Boyle et al., 1992, DeWit et al., 2000, Kandel et al., 1986, Kaplan et al., 1986, Mills and Noyes, 1984, Robins and Murphy, 1967, Robins and Przybeck, 1985, Yamaguchi and Kandel, 1984). We have found no prospective study testing for a linear relationship between age at onset and probability of later problem drug use in adolescents, but retrospective analysis of the Ontario Mental Health Supplement data (DeWit et al., 2000)found a nonlinear relationship, with the highest risk in those reporting first use at 13–14 for alcohol abuse and 11–12 for alcohol dependence.
Second, we explore the effects of early psychiatric disorders, including conduct disorder (CD), on both the likelihood and the timing of the transition from substance use to substance use disorders (SUD). It is well established that early problem behavior is associated with later drug use and abuse (Anderson et al., 1989, Jessor and Jessor, 1977, Kandel et al., 1978, Kaplan, 1980, Monnelly et al., 1983, Smith and Fogg, 1979, Vaillant and Milofsky, 1982, Wingard et al., 1979). However, most of the studies cited start in adolescence. In this paper we examine an earlier developmental period, beginning at age 9 and following children through to age 16. We examine the effects of a range of psychiatric disorders with onset by age 15 on risk for substance use disorders by age 16.
In her analysis of the (retrospective) Epidemiologic Catchment Area (ECA) data, Robins proposed a more specific hypothesis than one of a general association between conduct problems and SUD.
Abuse is extremely rare for those free of (early) conduct problems, no matter how early substance use began. At every other level of conduct problems, however, the earlier that use begins, the greater is the likelihood of substance abuse …. For those first using substances before age 20, the number of conduct problems was an even better predictor of substance abuse than was age of onset (before or after age 15). Among those beginning substance use before age 15 with seven or more conduct problems, more than half developed substance abuse; with only one conduct problem, only 5% did so. When first use occurred between ages 15 and 19, there is still a large effect from number of conduct problems, but the control for age of first use somewhat reduced their impact.”(Robins and McEvoy, 1990) (p. 196).
If it is the case that early CD increases the risk of adult SUD, a logical extension is to expect early CD also to drive the onset of adolescent SUD. Here we test this hypothesis, and also examine the impact of other psychiatric disorders on the transition from use to abuse/dependence.
The present study also adds to the literature in the following ways: (1) It follows a representative population sample of youth prospectively from childhood into adolescence. (2) It uses structured psychiatric interviews with parent and child to generate a range of DSM-IV psychiatric diagnoses. (3) The sample contains both boys and girls, unlike many previous studies. (4) The statistical methodology incorporates the effects of psychiatric comorbidity on transitions from the prior use of substances to SUD. (5) Use of a hierarchical Bayesian modeling approach permits the analysis of a complex, stratified data set that addresses some issues of dynamic age and covariate effects.
Section snippets
Study population
The Great Smoky Mountains Study (GSMS) is a longitudinal study of the development of psychiatric disorder and substance use and abuse in a predominantly rural area of the southeastern United States. Full details of the study design and instruments used can be found elsewhere (Costello et al., 1996). Briefly, a representative sample of 9, 11, and 13-year olds was recruited from 11 counties in western North Carolina using a household equal probability design. A two-phase sampling procedure was
Rates of onset
Table 1 shows the reported rates of age specific incidence for psychiatric disorders, substance use, and substance use disorder at each age. The rate of onset at a given age was computed by dividing the weighted number of reported onsets by the weighted total number of subjects interviewed since the age of onset after removing subjects who had onsets previously. There was no SUD before 12, but onsets increased rapidly thereafter, affecting 9.25% of the sample by age 16. Among the substance use
Conclusions
The goal of these analyses was to test some of the ideas about the development of substance use disorders that scholars have derived mainly from the scrutiny of studies using retrospective recall of ages at onset of both substance use and other psychiatric disorders. We adopted a hierarchical Bayesian dynamic modeling approach to assess the precise developmental impact of risk factors on SUD, showing that the effects evolved over time. For example, if a static regression such as GEE had been
Acknowledgements
This research was supported by grants from the National Institute of Drug Abuse (1R01DA11301-01) and the William T. Grant Foundation, and a National Institutes of Health Independent Scientist Award to the last author.
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2021, NeuropharmacologyCitation Excerpt :Young adolescence appears to be a crucial time for the initiation of problematic alcohol use; many individuals who begin drinking during early adolescence tend to rapidly escalate their use, with more than ten percent accelerating to meet alcohol use disorder (AUD) criteria within the first year of initiation (Faden, 2006; Forman-Hoffman et al., 2017; Masten et al., 2009). This early introduction to alcohol use has been associated with numerous long-lasting alterations to brain function, brain structure, and behavior (Crews et al., 2016; Spear, 2018; Squeglia et al., 2014), including increased rates of anxiety, depression, and AUD later on (Duncan et al., 1997; Grant and Dawson, 1997; Hawkins et al., 1997; Pitkanen et al., 2005; Sung et al., 2004; Wolford-Clevenger and Cropsey, 2019). Our understanding of the effects of adolescent alcohol comes largely from studies that have used exposures yielding BECs of 150–250 mg/dL, far exceeding the definition of binge-level exposure [80 mg/dL (NIAAA, 2004),].