Comorbidity between alcohol dependence and illicit drug dependence in adolescents with antisocial behavior and matched controls

Department of Psychiatry, Virginia Commonwealth University, Ричмонд, Virginia, United States
Drug and Alcohol Dependence (Impact Factor: 3.42). 10/2006; 84(1):85-92. DOI: 10.1016/j.drugalcdep.2005.12.003
Source: PubMed


Knowledge regarding the causes of comorbidity among substance use disorders can have significant impact on future research examining the etiology of these disorders. Unfortunately, the conclusions of past studies examining the comorbidity among substance use disorders are conflicting; some studies emphasize familial influences common to multiple substances, while others emphasize substance-specific influences. Discrepancies in results may reflect different analytical approaches or differences in the samples. Here, we examine the causes of comorbidity between alcohol dependence and illicit drug dependence in adolescents.
We ascertained a clinical sample of adolescents treated for antisocial behavior and substance use disorders and their siblings and a matched control sample. A model fitting approach was used to test 13 alternative hypotheses for the causes of comorbidity.
The best supported hypothesis for the comorbidity between alcohol dependence and illicit drug dependence was a model hypothesizing that comorbid disorders are alternate forms of a single underlying liability. The next best fitting models were two of the correlated liabilities models (correlated risk factors and reciprocal causation).
The results suggest that the best hypotheses explaining the comorbidity between alcohol and illicit drug dependence in adolescents are that alcohol dependence and illicit drug dependence are manifestations of a single general liability to develop substance dependence or that there are separate liabilities that are highly correlated.

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    • "There is substantial evidence that similar genetic factors influence liability to multiple substance use disorders (e.g. Kendler et al. 2003a, 2007; Rhee et al. 2006; Young et al. 2006; Xian et al. 2008; Sartor et al. 2010; Palmer et al. 2013). Most notably, Kendler et al. (2007) identified two genetic factors, corresponding to the covariance across licit (alcohol, nicotine, caffeine) and illicit (cannabis, cocaine) drugs; however, the genetic factors were highly correlated (r = 0.82). "
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    ABSTRACT: Genetic influences contribute significantly to co-morbidity between conduct disorder and substance use disorders. Estimating the extent of overlap can assist in the development of phenotypes for genomic analyses. Multivariate quantitative genetic analyses were conducted using data from 9577 individuals, including 3982 complete twin pairs and 1613 individuals whose co-twin was not interviewed (aged 24-37 years) from two Australian twin samples. Analyses examined the genetic correlation between alcohol dependence, nicotine dependence and cannabis abuse/dependence and the extent to which the correlations were attributable to genetic influences shared with conduct disorder. Additive genetic (a2 = 0.48-0.65) and non-shared environmental factors explained variance in substance use disorders. Familial effects on conduct disorder were due to additive genetic (a2 = 0.39) and shared environmental (c2 = 0.15) factors. All substance use disorders were influenced by shared genetic factors (r g = 0.38-0.56), with all genetic overlap between substances attributable to genetic influences shared with conduct disorder. Genes influencing individual substance use disorders were also significant, explaining 40-73% of the genetic variance per substance. Among substance users in this sample, the well-documented clinical co-morbidity between conduct disorder and substance use disorders is primarily attributable to shared genetic liability. Interventions targeted at generally reducing deviant behaviors may address the risk posed by this shared genetic liability. However, there is also evidence for genetic and environmental influences specific to each substance. The identification of these substance-specific risk factors (as well as potential protective factors) is critical to the future development of targeted treatment protocols.
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    • "A second related consideration is that the mechanisms that induce the observed correlations between tobacco and cannabis use may also vary across development. In the case of alcohol and illicit drug dependence, Rhee et al. (Rhee et al., 2006) found that in adolescents, a model where a single liability underlying both alcohol and illicit drug dependence fit significantly better than the traditional correlated risks model, which has been shown to be a reasonable fit to data on adult twins (Kendler et al., 2003b; Kendler et al., 2007). "
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    ABSTRACT: Using twins assessed during adolescence (Virginia Twin Study of Adolescent Behavioral Development: 8-17 years) and followed up in early adulthood (Young Adult Follow-Up, 18-27 years), we tested 13 genetically informative models of co-occurrence, adapted for the inclusion of covariates. Models were fit, in Mx, to data at both assessments allowing for a comparison of the mechanisms that underlie the lifetime co-occurrence of cannabis and tobacco use in adolescence and early adulthood. Both cannabis and tobacco use were influenced by additive genetic (38-81%) and non-shared environmental factors with the possible role of non-shared environment in the adolescent assessment only. Causation models, where liability to use cannabis exerted a causal influence on the liability to use tobacco fit the adolescent data best, while the reverse causation model (tobacco causes cannabis) fit the early adult data best. Both causation models (cannabis to tobacco and tobacco to cannabis) and the correlated liabilities model fit data from the adolescent and young adult assessments well. Genetic correlations (0.59-0.74) were moderate. Therefore, the relationship between cannabis and tobacco use is fairly similar during adolescence and early adulthood with reciprocal influences across the two psychoactive substances. However, our study could not exclude the possibility that 'gateways' and 'reverse gateways', particularly within a genetic context, exist, such that predisposition to using one substance (cannabis or tobacco) modifies predisposition to using the other. Given the high addictive potential of nicotine and the ubiquitous nature of cannabis use, this is a public health concern worthy of considerable attention.
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    • "While substance-specific factors have been supported, the high rates of comorbidity among nicotine, alcohol, and illicit substances have led many researchers to concentrate on risk factors that may be common across multiple substances. For example, Rhee and colleagues (2003) utilized simulated family data to discriminate between 13 different models of comorbidity defined by Neale and Kendler (1995), and then applied this methodology in a clinically ascertained adolescent sample (Rhee et al., 2006). Results suggested that two models were equally likely to explain the patterns of comorbidity observed. "
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