STRESS, GENES, AND GENERALIZABILITY ACROSS GENDER: EFFECTS OF MAOA AND STRESS SENSITIVITY ON CRIME AND DELINQUENCY*

• Published date: 01 August 2017
• DOI: http://doi.org/10.1111/1745-9125.12147
• Date: 01 August 2017

STRESS, GENES, AND GENERALIZABILITY ACROSS

GENDER: EFFECTS OF MAOA AND STRESS

SENSITIVITY ON CRIME AND DELINQUENCY∗

JESSICA WELLS,1TODD ARMSTRONG,2

DANIELLE BOISVERT,1RICHARD LEWIS,1

DAVID GANGITANO,3and SHEREE HUGHES-STAMM3

1Department of Criminal Justice and Criminology, Sam Houston State

University

2School of Criminology and Criminal Justice, University of Nebraska—Omaha

3Department of Forensic Science, Sam Houston State University

KEYWORDS: stress, antisocial behavior, biosocial, monoamine oxidase A (MAOA)

gene

In the current study, we extend the gene-by-environment interaction (cGxE) litera-

ture by examining how a widely studied polymorphism, the MAOA upstream variable

number tandem repeat (MAOA-uVNTR) interacts with distal and proximal stressors

to explain variation in crime and delinquency. Prior research findings have revealed

that MAOA-uVNTR interacts with single indicators of environmental adversity to

explain criminal behavior in general-population and incarcerated samples. Neverthe-

less, the genetically moderated stress sensitivity hypothesis suggests that increased risk

for criminal behavior associated with variation in the MAOA-uVNTR can be best

understood in the context of both distal stress during childhood and proximal stress

in adulthood. Therefore, we employed Tobit regression analyses to examine a gene–

distal–proximal environment (CGxExE) interaction across gender in a sample of

university students (n=267) and with data from the National Longitudinal Study

of Adolescent to Adult Health (Add Health; n=1,294). The results across both sets

of analyses demonstrate that variation in the MAOA-uVNTR interacts with distal

and proximal stress to lead to increased risk for criminal behavior in males. Although

proximal life stress is associated with an increase in crime and delinquency, this effect is

more pronounced among MAOA-L allele carriers that have experienced distal stress.

∗Additional supporting information can be found in the listing for this article in the Wiley Online

Library at http://onlinelibrary.wiley.com/doi/10.1111/crim.2017.55.issue-3/issuetoc.

Direct correspondence to Jessica Wells, Department of Criminal Justice and Criminology, Col-

lege of Criminal Justice, Box 2296, Sam Houston State University, Huntsville, TX 77341 (e-mail:

jmw057@shsu.edu).

This study was supported by an Enhancement Grant for Professional Development from the Of-

fice of Research and Sponsored Programs at Sam Houston State University. Sponsors were not

involved in the development of study methodology or in any aspect of study implementation, data

analysis, or report writing. Data were taken from Add Health, a program project directed by

Kathleen Mullan Harris and designed by J. Richard Udry, Peter S. Bearman, and Kathleen

Mullan Harris at the University of North Carolina at Chapel Hill and funded by Grant P01-

HD31921 from the Eunice Kennedy Shriver National Institute of Child Health and Human

C2017 American Society of Criminology doi: 10.1111/1745-9125.12147

CRIMINOLOGY Volume 55 Number 3 548–574 2017 548

MAOA, STRESS SENSITIVITY, CRIME, AND DELINQUENCY 549

In heritability studies, researchers have found that approximately 50 percent of the

variance in antisocial behavior is attributable to genetic factors (Rhee and Waldman,

2002). Nevertheless, much work is still needed to uncover the precise developmental

pathways through which genetic variation contributes to risk for antisocial behav-

ior, including criminal behavior. One method to capture developmental influences

is through the study of candidate gene-by-environment (cGxE) interactions. Such

interactions are consistent with the multilevels perspective within developmental

psychopathology. This perspective suggests that development of diverse forms of psy-

chopathology, including patterns of pronounced antisocial behavior, is influenced by

complex interactions between systems operating at multiple levels, including biological

and environmental processes (Cicchetti and Dawson, 2002; Cicchetti and Toth, 2009;

Masten, 2007). Consistent with this perspective, most contemporary research into

molecular genetic influences on antisocial behavior is aimed at testing these influences

in the context of the cGxE model. Within the cGxE model, genetic influences on

antisocial behavior result in increased risk for antisocial behavior in interaction with

environmental variation. Among research testing the cGxE model is a large group of

study results showing that a polymorphism in the monoamine oxidase A (MAOA)

gene moderates the association between environmental adversity and increased risk

for antisocial behavior, including crime (Byrd and Manuck, 2014; Ficks and Waldman,

2014).

Although the application of the cGxE model has shown that genetic risk for antiso-

cial behavior is often entirely contingent on the co-occurrence of environmental risk,

cGxE models may be limited as they mostly rely on a single, unitary measure of the

environment. The treatment of environment as a unitary phenomenon is challenged by

research results showing the independent contributions of stress at different stages of

development (Hammen, Henry, and Daley, 2000) and study findings demonstrating that

the neurodevelopmental consequences of early life (distal) stress may lead to increased

sensitivity to later (proximal) stressors (Frodl and O’Keane, 2013). Generalized to the

study of molecular genetic influences on psychopathology, the results of this research

reveal a developmental pathway for psychopathology where genetic variation influences

sensitivity to proximal stress through an interaction with distal stress. Essentially, this

genetically moderated stress sensitivity hypothesis proposes a gene-by-distal environ-

mental stress by proximal environment stress interaction, cGxExE (Homberg and van

den Hove, 2012). cGxExE interactions have recently been found by two studies in which

researchers examined the development of depression (Grabe et al., 2012; Starr et al.,

2014). Here, we test the generalizability of the genetically moderated stress sensitization

hypothesis to the explanation of crime and delinquency by focusing on MAOA-

uVNTR1and both distal and proximal stressors in a sample of university students

and in a sample from the National Longitudinal Study of Adolescent to Adult Health

(Add Health).

Development, with cooperative funding from 23 other federal agencies and foundations. Special

acknowledgment is due to Ronald R. Rindfuss and Barbara Entwisle for assistance in the original

design. Information on how to obtain the Add Health data files is available on the Add Health web-

site (http://www.cpc.unc.edu/addhealth). No direct support was received from Grant P01-HD31921

for this analysis.

1. MAOA-uVNTR =monoamine oxidase A upstream variable number tandem repeat.