Currently, most prevention efforts are famed as universal interventions. However, despite the demonstrated efficacy of many prevention programs, variability in response is the rule with some participants responding very little and others accounting for the bulk of the positive impact of the program. Better understanding the processes associated with better and worse response to prevention is a critical first step in refining and adapting existing programs, or alternatively designing new prevention programs with enhanced outcomes. Because vulnerabilities to substance use, emotional problems, risky sexual behavior and other behavioral problems are influenced by a combination of environmental, genetic, and epigenetic factors, mediated in part through psychological processes (Kreek et al., 2005; Rutter et al., 2006), the study of genetic and epigenetic vulnerability and susceptibility factors provides an important starting point for efforts to address this critical need.
A growing body of research on differential genetic susceptibility indicates that efforts to enhance prevention impact may benefit from consideration of the contribution of individual genetic differences to treatment response (Brody et al., 2013). In addition, the recent expansion of genetic research to include a focus on epigenetic change provides considerable promise for the development of indicated prevention and individually tailored prevention efforts. However, before this promise can be realized, a number of theoretical and practical challenges remain. Thus, through this special section, we propose to provide a foundation for a new era of prevention research in which the principles of prevention science are combined with genomic science.
In the current special section we will bring together authors to deal with genetic and epigenetically driven processes relevant to depression, substance abuse, and sexual risk taking. Together they will comment on, and provide data relevant to, assessment, research and statistical methods, development of biomarkers, and implementation strategies with disadvantaged and high-risk populations. The papers will help to inform the development of a new generation of prevention programs that go beyond universal programs and sensitively target key processes while providing greater precision regarding prediction of population-level impact.
Brody, G. H., Beach, S. R. H., Hill, K. G., Howe, G. W., Prado, G., Fullerton, S. M. (2013). Using genetically informed, randomized prevention trials to test etiological hypotheses about child and adolescent drug use and psychopathology. American Journal of Public Health, 103 Suppl 1:S19-24. doi: 10.2105/AJPH.2012.301080.
Kreek M. J., Nielsen D. A., Butelman E. R., LaForge K. S. (2005). Genetic influences on impulsivity, risk taking, stress responsivity and vulnerability to drug abuse and addiction. Nature Neuroscience, 8, 1450-1457.
Rutter M., Moffitt T. E., Caspi A. (2006). Gene-environment interplay and psychopathology: Multiple varieties but real effects. Journal of Child Psychology and Psychiatry, 47, 226-261.
Currently, most prevention efforts are famed as universal interventions. However, despite the demonstrated efficacy of many prevention programs, variability in response is the rule with some participants responding very little and others accounting for the bulk of the positive impact of the program. Better understanding the processes associated with better and worse response to prevention is a critical first step in refining and adapting existing programs, or alternatively designing new prevention programs with enhanced outcomes. Because vulnerabilities to substance use, emotional problems, risky sexual behavior and other behavioral problems are influenced by a combination of environmental, genetic, and epigenetic factors, mediated in part through psychological processes (Kreek et al., 2005; Rutter et al., 2006), the study of genetic and epigenetic vulnerability and susceptibility factors provides an important starting point for efforts to address this critical need.
A growing body of research on differential genetic susceptibility indicates that efforts to enhance prevention impact may benefit from consideration of the contribution of individual genetic differences to treatment response (Brody et al., 2013). In addition, the recent expansion of genetic research to include a focus on epigenetic change provides considerable promise for the development of indicated prevention and individually tailored prevention efforts. However, before this promise can be realized, a number of theoretical and practical challenges remain. Thus, through this special section, we propose to provide a foundation for a new era of prevention research in which the principles of prevention science are combined with genomic science.
In the current special section we will bring together authors to deal with genetic and epigenetically driven processes relevant to depression, substance abuse, and sexual risk taking. Together they will comment on, and provide data relevant to, assessment, research and statistical methods, development of biomarkers, and implementation strategies with disadvantaged and high-risk populations. The papers will help to inform the development of a new generation of prevention programs that go beyond universal programs and sensitively target key processes while providing greater precision regarding prediction of population-level impact.
Brody, G. H., Beach, S. R. H., Hill, K. G., Howe, G. W., Prado, G., Fullerton, S. M. (2013). Using genetically informed, randomized prevention trials to test etiological hypotheses about child and adolescent drug use and psychopathology. American Journal of Public Health, 103 Suppl 1:S19-24. doi: 10.2105/AJPH.2012.301080.
Kreek M. J., Nielsen D. A., Butelman E. R., LaForge K. S. (2005). Genetic influences on impulsivity, risk taking, stress responsivity and vulnerability to drug abuse and addiction. Nature Neuroscience, 8, 1450-1457.
Rutter M., Moffitt T. E., Caspi A. (2006). Gene-environment interplay and psychopathology: Multiple varieties but real effects. Journal of Child Psychology and Psychiatry, 47, 226-261.
