Link to the University of Pittsburgh Homepage
Link to the University Library System Homepage Link to the Contact Us Form

THE DEVELOPMENT OF ANTISOCIAL BEHAVIOR: GENES, BRAIN AND ENVIRONMENT AS DIRECT AND INTERACTIVE PREDICTORS OF ANTISOCIAL BEHAVIOR FROM EARLY CHILDHOOD TO YOUNG ADULTHOOD

Hyde, Luke Williamson (2012) THE DEVELOPMENT OF ANTISOCIAL BEHAVIOR: GENES, BRAIN AND ENVIRONMENT AS DIRECT AND INTERACTIVE PREDICTORS OF ANTISOCIAL BEHAVIOR FROM EARLY CHILDHOOD TO YOUNG ADULTHOOD. Doctoral Dissertation, University of Pittsburgh. (Unpublished)

[img]
Preview
PDF
Primary Text

Download (1MB) | Preview

Abstract

Antisocial behavior (AB), including physical and sexual aggression, destruction of property, theft, and violation of serious rules, has been of particular interest to researchers and the general public because of its large cost to society and negative impact on perpetrators and victims, its chronic nature and trajectory, and the difficulty in preventing and treating AB. Although recent views of AB have emphasized the complex interplay between biology and the environment (Jaffee et al., 2005; Reiss, 2005; Rutter, 1997), little empirical work has connected genetic variability, neural reactivity and environmental risk in understanding the development of AB in early adulthood. Thus, the current study sought to advance our understanding of AB in an ethnically diverse sample of 310 young men followed prospectively from age 1.5 to age 20 through measurement of amygdala reactivity to threat, variability in genes affecting serotonin signaling, cumulative environmental risk during early childhood and early adolescence, and measures of AB during adolescence and at age 20. Contrary to our hypotheses, we found that AB across adolescence and at age 20 was related to lower amygdala reactivity to threat, regardless of the level of callous traits also present. Also contrary to our hypotheses, we found that variants in serotonin genes previously linked to lower amygdala reactivity were related to callous traits as well as AB in the presence of high callousness. Imaging genetics models that linked variability in specific serotonin genes, amygdala reactivity, and AB were not supported. Similarly, little support was found for Imaging Gene by Environment interactions in which the interactions between genetic variability and environmental risk were linked to AB via their association with neural reactivity. Results highlight the difficulty in testing complex models of the likely interactions between genes, brain and environment in understanding AB and suggest a specific role of amygdala reactivity in AB.


Share

Citation/Export:
Social Networking:
Share |

Details

Item Type: University of Pittsburgh ETD
Status: Unpublished
Creators/Authors:
CreatorsEmailPitt UsernameORCID
Hyde, Luke Williamsonlwh2@pitt.eduLWH2
ETD Committee:
TitleMemberEmail AddressPitt UsernameORCID
Committee ChairShaw, Danielcasey@pitt.eduCASEY
Committee Membercampbell, Susansbcamp@pitt.eduSBCAMP
Committee Membermanuck, Stephenmanuck@pitt.eduMANUCK
Committee Memberforbes, Erikaforbese@upmc.eduERIKA
Committee MemberHariri, Ahmadahmad@haririlab.com
Date: 26 September 2012
Date Type: Publication
Defense Date: 12 July 2012
Approval Date: 26 September 2012
Submission Date: 31 July 2012
Access Restriction: 5 year -- Restrict access to University of Pittsburgh for a period of 5 years.
Number of Pages: 148
Institution: University of Pittsburgh
Schools and Programs: Dietrich School of Arts and Sciences > Psychology
Degree: PhD - Doctor of Philosophy
Thesis Type: Doctoral Dissertation
Refereed: Yes
Uncontrolled Keywords: Antisocial behavior; conduct disorder; fMRI; neuroimaging; molecular genetics; callous-unemotional; violence;
Date Deposited: 27 Sep 2012 02:20
Last Modified: 26 Sep 2017 05:15
URI: http://d-scholarship.pitt.edu/id/eprint/13247

Metrics

Monthly Views for the past 3 years

Plum Analytics


Actions (login required)

View Item View Item