mechanisms that can be used in new prevention strategies designed to target molecular mechanisms and bolster resilience to the effects of adverse environmental exposures.

In addition to uncovering causal mechanisms, an improved understanding of the genetic determinants of MEB disorders can provide a powerful tool for the study of environmental influences on the development of disorders. Accounting experimentally or statistically for genetic determinants allows for a much more powerful and experimentally controllable assessment of environmental determinants. Thus, genetic approaches should ultimately help to clarify which are the most potent environmental influences in the development of disorders and to prioritize possible biological targets for prevention interventions.

Epigenetics research not only provides support for preventive intervention approaches, as described in this chapter, but also can lead to novel ways of thinking about the design of new and more effective prevention strategies. For example, although the epigenetic causes of disorders are difficult to disentangle from the more traditional effects of learned behavior, growing knowledge of the epigenetically based, transgenerational transmission of maternal care and other behavioral adaptations to the environment raises the possibility that future prevention approaches targeting epigenetic mechanisms may be able to help break cross-generational cycles of such behaviors as violence and substance abuse.

In designing these new interventions, however, it is important to remember that epigenetically transmitted behavioral and emotional dispositions, including stress responsivity, are adaptive for different environmental circumstances (Fish, Shahrokh, et al., 2004). One must therefore take care to ensure that the interventions do not unwittingly produce a mismatch between the newly modified environment and the epigenetically transmitted behavior that was optimized for enhanced survival in the previous, unmodified environment. Such a mismatch could conceivably serve as a risk for pathology, adding a level of complexity to the optimal design of preventive interventions despite the best of intentions in the design and implementation of an intervention.

While theories from developmental neuroscience can inform prevention approaches, findings from prevention trials that suggest causal mechanisms should generate hypotheses that can be tested and further elaborated by basic and clinical neuroscientists using animal models and other neuroscience-based approaches. Therapeutic interventions for already-established human disorders generally offer little insight into the causes of disorders. The fact that penicillin treats pneumonia, for example, does not indicate that the pneumonia is caused by a deficiency of penicillin. As discussed in Chapters 4 and 10, prevention trials permit rigorous testing of causal mechanisms, as well as mediating and moderating effects. If designed in



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