Research has confirmed that multiple layers of etiological risk, including individual genetic risk, proximal environmental experiences (e.g., parenting and family relationship characteristics), and neighborhood context (e.g., neighborhood disadvantage, social organization, and exposure to community violence), influence the development of children's conduct problems (CP;aggressive and rule-breaking behaviors comprising diagnosable and sub-threshold Conduct Disorder). To date, however, we little insight into the interplay between genetic and contextual risks for child CP, or the role that proximal risks may play in this relationship. The current application outlines a novel and unique research design intended to do just this. In particular, we will sample 500 middle-to-low income child twin families that reside in one of a range of disadvantaged neighborhood contexts (i.e., from moderately to extremely disadvantaged). This "at-risk" twin sampling strategy constitutes a significant advance over current epidemiological twin studies in regards to studies of contextual risk, as such samples contain relatively few at-risk families. As a result, extant twin studies are typically unable to meaningfully explore the role of contextual risk as an etiological moderator of child outcome. We will then augment our innovative sampling approach with an in-depth assessment battery that includes comprehensive assessments of the twins'and the parents'psychological and behavioral profiles, videotaped parent-child and family interactions, interviews assessing exposure to community violence, questionnaires completed by the twins'teachers, and census tracking of the family's neighborhood. We will also collect an (unrelated) neighborhood informant sample to report on social organization and crime in each family's neighborhood. State-of-the-art behavioral genetic analyses will then examine both how contextual risk factors, both alone and in combination with proximal risk factors, moderate genetic predispositions for child CP. This innovative sampling and design strategy will allow us to meaningfully integrate, for the first time, the genetic, proximal, and contextual risk factors thought to underlie the development of child CP, and accordingly, has the potential to significantly advance our understanding of the origins of child conduct problems.

Public Health Relevance

The proposed study intends to establish how neighborhood contextual risk (both alone and in combination with more proximal risks) moderates genetic risk for child CP. Such findings should ultimately inform individually-tailored interventions aimed at the amelioration of child CP.

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Research Project (R01)
Project #
5R01HD066040-04
Application #
8462648
Study Section
Behavioral Genetics and Epidemiology Study Section (BGES)
Program Officer
Esposito, Layla E
Project Start
2010-07-25
Project End
2015-05-31
Budget Start
2013-06-01
Budget End
2014-05-31
Support Year
4
Fiscal Year
2013
Total Cost
$547,370
Indirect Cost
$156,362
Name
Michigan State University
Department
Psychology
Type
Schools of Arts and Sciences
DUNS #
193247145
City
East Lansing
State
MI
Country
United States
Zip Code
48824
Burt, S Alexandra; Klahr, Ashlea M; Klump, Kelly L (2015) Do non-shared environmental influences persist over time? An examination of days and minutes. Behav Genet 45:24-34
Klahr, Ashlea M; Klump, Kelly L; Burt, S Alexandra (2014) The etiology of the association between child antisocial behavior and maternal negativity varies across aggressive and non-aggressive rule-breaking forms of antisocial behavior. J Abnorm Child Psychol 42:1299-311
Klahr, Ashlea M; Thomas, Katherine M; Hopwood, Christopher J et al. (2013) Evocative gene-environment correlation in the mother-child relationship: a twin study of interpersonal processes. Dev Psychopathol 25:105-18
Burt, S Alexandra; Klump, Kelly L (2013) The Michigan State University Twin Registry (MSUTR): an update. Twin Res Hum Genet 16:344-50