The Effect of MAOA and Stress Sensitivity on Crime and Delinquency: A Replication Study

Published date01 August 2018
Date01 August 2018
Subject MatterArticles
Journal of Contemporary Criminal Justice
2018, Vol. 34(3) 336 –353
© The Author(s) 2018
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DOI: 10.1177/1043986218770001
The Effect of MAOA
and Stress Sensitivity on
Crime and Delinquency:
A Replication Study
Christa C. Christ1,2, Joseph A. Schwartz3,
Scott F. Stoltenberg2, Jonathan R. Brauer4,
and Jukka Savolainen5
Across several meta-analyses, MAOA-uVNTR genotype has been associated with
an increased risk for antisocial behavior among males who experienced early
life adversity. Subsequently, early life stress and genetic susceptibility may have
long-term effects on stress sensitivity later in life. In support of this assumption,
a recent study found evidence, in two independent samples, for a three-way
interaction effect (cG × E × E) such that proximate stress was found to moderate
the interactive effect of MAOA-uVNTR and distal stress on crime and delinquency
among males. In light of recent developments in cG × E research, we attempted to
replicate these findings in an independent sample of university students. Our results
failed to support any cG × E or cG × E × E effects reported in the original study.
Implications of a failed replication and general concerns for future cG × E research
are discussed.
monoamine oxidase A gene, antisocial, distal stress, proximate stress, childhood
1Hamilton College, Clinton, NY, USA
2University of Nebraska–Lincoln, NE, USA
3University of Nebraska, Omaha, NE, USA
4Indiana University, Bloomington, IN, USA
5University of Michigan, Ann Arbor, MI, USA
Corresponding Author:
Christa C. Christ, Department of Psychology, Hamilton College, Clinton, NY 13323, USA.
770001CCJXXX10.1177/1043986218770001Journal of Contemporary Criminal JusticeChrist et al.
Christ et al. 337
Candidate gene-by-environment (cG × E) research has grown exponentially in recent
years, with applications to a variety of social science topics. Concern for the integrity
of this agenda has also increased due to low overall replicability of scientific literature
more broadly (Baker, 2016), and cG × E findings specifically (Duncan & Keller, 2011;
Risch et al., 2009). A recent article provided recommendations to address the chal-
lenges of cG × E research in response to the issues brought forth by the National
Institute on Alcohol Abuse and Alcoholism (Dick et al., 2015). We find these recom-
mendations, subsequently discussed, to be a compelling means toward efficient prog-
ress in understanding the underlying genetic architecture of complex behavioral
phenotypes, and we rely on them here to evaluate current cG × E research.
The purpose of cG × E research is to examine the potential contribution of specific
genetic variants to an observable outcome (i.e., “phenotype”) in the context of varying
environmental factors. However, because the effect of any one genetic variant is likely
to be extremely small (Chabris, Lee, Cesarini, Benjamin, & Laibson, 2015; Kendler,
2013), large samples (e.g., N > 1,000) are needed to secure sufficient power for detect-
ing a main effect of a candidate gene and, therefore, even larger sample sizes would be
needed to reliably detect cG × E effects (Heo & Leon, 2010). With this in mind, inde-
pendent replications of cG × E findings prior to publication are recommended, but also
do not sufficiently address all the issues raised by Dick et al. (2015).
In addition to a lack of sufficient statistical power, two additional methodological
concerns with cG × E research are noteworthy. First, genetic variants are often selected
and modeled without a clear theoretical link to the phenotype of interest. In particular,
studies targeting candidate genes of the “usual suspect” variety, such as MAOA, are
inconsistent with the polygenic contribution to most complex traits (Dick et al., 2015).
Second, there is considerable heterogeneity in the operationalization and measurement
of environmental factors (Dick et al., 2015). The review of “stress” measurements in
particular has been shown to be widely variable in terms of validity, severity, type, and
time period, suggesting that replication of studies involving stress as an environmental
moderator are essential (Monroe & Reid, 2008; Uher & McGuffin, 2010). Despite
these limitations, the existing literature appears to provide strong a priori reasons to
consider the MAOA-uVNTR genotype as a potential moderator of the association
between exposure to stressful experiences and criminal behavior. The results of mul-
tiple meta-analyses support the finding that MAOA-uVNTR genotype moderates the
association between environmental adversity and risk for antisocial behavior (Byrd &
Manuck, 2014; Ficks & Waldman, 2014). Moreover, the MAOA-uVNTR has a known
effect on the rate of transcription of the MAOA gene (Sabol, Hu, & Hamer, 1998).
Based on these findings, and in light of the methodological issues surrounding
cG × E research, the present study aims to replicate the results from a recent article by
Wells et al. (2017) focusing on the interactive effect of MAOA-uVNTR genotype and
stress on delinquent behavior. The findings from Wells et al. (2017) found proximal
life stress to be associated with increased risk for criminal behavior in males. Critically
important for the present study, they found this association to be stronger among males

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