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Mind & Brain, the Journal of Psychiatry

a number of samples from around the world (eg, Australia, Sweden, and England).

What is remarkable about this body of work is that it has

yielded consistent findings that cut across the various methods (eg, twin vs twin-sibling design), sampling proce- dures (eg, retrospective recall vs prospective assessment), and country of origin. What’s more, these findings fall logically into a developmental model of substance use risk that not only complements the rationale for intervention presented in the previous section, but in fact helps integrate the various perspectives offered.

The first critically important yield of the work to date is an atypical finding for genetically informative studies*although one that makes developmental and conceptual sense. Across the vast majority of published studies, adolescent use of substances has shown particularly strong evidence for shared environmental effects*simply put, environmental influences that promote similarity amongst family members. Recent reviews and empirical papers have shown this to be the case for tobacco use, alcohol use, and marijuana use.2327 Shared environmental effects are found to be robust for either initiation (eg, classifying subjects into having tried a sub- stance vs not having tried a substance) or level of use in adolescence (eg, quantifying usage such as the number of days out of the past month that a given substance was used). This finding has held up across country of origin as well as study design (so that it is not just found, for example, in the classic twin method). The consistency of the findings across methods and samples may thus speak to a particularly strong current of environmental influence on initial use of sub- stances in adolescence.

There may be, of course, multiple streams of environmental

influence that impact adolescent use and have similar effects on siblings living together. From the intervention perspective, social dynamics between siblings and mutual friendships have stood out as explanatory factors within the genetic epidemiological models, particularly for tobacco use and alcohol use.2832 For example, the amount of time that siblings spend together, and whether or not they have mutual friends, significantly moderates the shared environmental effect on adolescent substance use.53 These findings have been interpreted as a form of social contagion. A corollary to this scenario is that lack of appropriate parental monitoring and limit setting would set up a particularly conducive family environment for social contagion, both in terms of siblings within the family being more likely to be exposed to substance use by peers and friends, and also directly impacting each other’s likelihood of use.

How does this ‘‘contagion’’ model of initiation of substance

use in adolescence connect with risk for progression to higher levels of use including abuse and dependence? In genetically informative studies*particularly prospective longitudinal projects*there have been opportunities to examine the genetic and environmental influences underlying progression. Here a very different story has emerged: the role of shared environmental factors has been negligible in that it

M&B 2011; 2:(1). July 2011 52

does not explain sibling similarity for higher levels of use of tobacco, alcohol, or marijuana. What does explain sibling similarity for progression of substance use is genetic influence.26,33,54 It is important to emphasize that the strong evidence suggesting genetic influence on progression from initiation to varying levels of misuse and abuse cuts across the primary substances studied (tobacco, alcohol, and mari- juana). While the literature supporting the heritability of substance dependence and abuse is vast and has emerged over the last two decades, the point to be emphasized here is that the genetic epidemiological models suggest that herit- ability becomes dominant as an explanatory factor for progression from use in adolescence to abuse/dependence in adulthood. A recent paper by Agrawal and Lynskey34 provides a very nice review of this evidence for multiple substances.

The emergence of a developmental gene-environment model

This ‘‘two-stage’’ developmental genetic epidemiological model*which emphasizes shared environmental influences on initiation and early use and genetic influences on progression*sits well with the arguments made previously in support of intervention aimed at adolescent substance use by bringing into play a unifying developmental model. The two-stage model suggests different classes of influence that may be operative at different points in the trajectory. It supports strongly the idea that psychosocial factors may be particularly important in terms of shaping risk for early use of substances*but these same factors are not so relevant when we consider why some adolescents progress to problematic use while others do not. So we have here a first piece of a developmental gene-environment model*an emphasis on the psychosocial climate of peer and family influences and a number of interconnected risk factors that could serve as rational and empirically supported targets for psychosocial intervention. What is noteworthy here is the idea that genetically informative studies have yielded a consensus that implicates environmental risk processes anchored at a specific developmental stage and thus supports directly the idea that psychosocial intervention may be particularly effective in redu- cing substance use in early adolescence.

The point for intervention scientists is that psychosocial

interventions would likely not directly impact genetically mediated predispositions to escalating use and abuse of substances. Rather, psychosocial interventions may be con- ceptualized as having the potential for indirect effects on the genetic pathways by serving to blockade continual use of substances that are believed to ‘‘turn on’’ these genes that react to the active addictive chemicals in tobacco, alcohol, and marijuana. At this point, we have the basis for a framework for one model of psychosocial intervention: to modify the likelihood of gene expression via environmental intervention. What is especially notable about the prior and ongoing genetically informative work is that essential roles of environmental and genetic risk factors are being articulated, along with the way in which they intersect in developmental time. This is much

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