Page 1
ORIGINAL PAPER
The 2-Repeat Allele of the MAOA Gene Confers
an Increased Risk for Shooting and Stabbing Behaviors
Kevin M. Beaver•J. C. Barnes•Brian B. Boutwell
Published online: 11 December 2013
? Springer Science+Business Media New York 2013
Abstract
morphism in the promoter region of the MAOA gene and antisocial phenotypes. The
results of these studies have consistently revealed that low activity MAOA alleles are
related to antisocial behaviors for males who were maltreated as children. Recently,
though, some evidence has emerged indicating that a rare allele of the MAOA gene—that
is, the 2-repeat allele—may have effects on violence that are independent of the envi-
ronment. The current study builds on this research and examines the association between
the 2-repeat allele and shooting and stabbing behaviors in a sample of males drawn from
the National Longitudinal Study of Adolescent Health. Analyses revealed that African-
American males who carry the 2-repeat allele are significantly more likely than all other
genotypes to engage in shooting and stabbing behaviors and to report having multiple
shooting and stabbing victims. The limitations of the study are discussed and suggestions
for future research are offered.
There has been a great deal of research examining the link between a poly-
Keywords
Add Health ? MAOA ? Shooting ? Stabbing
K. M. Beaver (&)
College of Criminology and Criminal Justice, Florida State University, 634 W. Call Street,
Tallahassee, FL 32306-1127, USA
e-mail: kbeaver@fsu.edu
K. M. Beaver
Center for Social and Humanities Research, King Abdulaziz University, Jeddah, Saudi Arabia
J. C. Barnes
School of Economic, Political, and Policy Sciences, University of Texas at Dallas, Richardson,
TX 75080, USA
B. B. Boutwell
College of Criminal Justice, Sam Houston State University, Huntsville, TX 77341-2296, USA
123
Psychiatr Q (2014) 85:257–265
DOI 10.1007/s11126-013-9287-x
Page 2
Introduction
Serious violent crime represents a pressing public health and safety concern to citizens in
the United States and around the world. To illustrate, there are approximately 5 million
violent victimization events that occur annually in the United States and a large percentage
of these crimes involve the use of lethal weapons, such as guns and knives [29]. Although
statistically rare, murder remains one of the leading causes of death for adolescents and
young adults [13] and the commission of a violent act that does not culminate in a murder
can still leave the victim physically as well as emotionally damaged [17]. The resulting
financial burden that is produced by serious violent behavior, moreover, is astounding, with
some upper-limit estimates indicating that each murder costs taxpayers more than $17
million [6].
Although the consequences associated with personal violence are relatively well-
known, the causes of these extreme violent acts remain poorly understood. There has been
increasing evidence, however, indicating that serious physical violence is the result of a
complex arrangement of neurobiological, genetic, and environmental factors acting indi-
vidually and synergistically [20]. Findings from recent neuroimaging research, for
example, have identified structural and functional differences in regions of the prefrontal
cortex and areas of the limbic system in offenders compared to non-offenders [21–23]. In
addition to neurobiological correlates to extreme violence, including murder, there is now a
wealth of evidence underscoring the role that genetic factors play in the etiology of serious
violent behaviors. The results of a string of meta-analyses have revealed, for instance, that
genes account for approximately 50 % of the variance in antisocial behaviors and serious
violence [7, 16, 19, 26].
Despite the sizeable body of research indicating that violence is highly heritable, the
precise genetic polymorphisms that are related to extreme acts of violence have remained
somewhat elusive. The most promising candidate gene in relation to extreme acts of
violence is the MAOA gene. The MAOA gene has been mapped to the X chromosome at
location Xp11.23-11.4 [15] and has a 30 base pair (bp) variable number of tandem repeats
(VNTR) polymorphism in the promoter region of the gene. The MAOA gene is responsible
for coding for the production of the MAOA enzyme that degrades certain neurotrans-
mitters, such as dopamine and serotonin [28]. This is a functional polymorphism, wherein
different alleles are related to different activity levels for the MAOA enzyme [27]. The
most common way of dividing these alleles is by creating two groups: a group consisting of
alleles that correspond to low MAOA activity and a group consisting of alleles that
correspond to high MAOA activity. Usually, the 2-repeat allele and the 3-repeat allele are
grouped together to create the low MAOA activity genotype while the 3.5-repeat allele,
4-repeat allele, and 5-repeat allele are grouped together to create the high MAOA activity
genotype [5].
A wide range of studies have examined the potential association between MAOA
genotype and antisocial behaviors [14] and theoretical models tying the MAOA genotype
to brain functioning have been supported [3, 18]; but see [8]. The results of these studies
have been relatively consistent in that they tend to indicate that the low MAOA activity
alleles confer an increased risk to antisocial behaviors, but only among males who were
exposed to environmental liabilities, such as childhood maltreatment, abuse, and neglect
[5]. Although the link between antisocial behavior and MAOA has been the most repli-
cated finding in the study of the genetic underpinnings to antisocial phenotypes, there has
been limited evidence bearing directly on whether MAOA is linked to specific acts of
violent behavior. Most studies examining the effects of MAOA tend to examine non-
258 Psychiatr Q (2014) 85:257–265
123
Page 3
specific antisocial behavioral scales or scales that include a wide range of antisocial traits
(e.g., [30]). While such an approach is useful to establish a link between MAOA and
antisocial behavior in general, it is not an appropriate strategy for determining whether
MAOA has behavioral-specific effects. Using an additive scale of antisocial behaviors may
mask important heterogeneity that exists between the individual behaviors and MAOA
genotype such that MAOA may be related to certain types of antisocial behaviors, but not
others. As a result, to further unpack the nexus between MAOA genotype and serious
violence, the current study examines only extreme violence as measured by shooting and
stabbing behaviors.
Another potential shortcoming of the available MAOA research is the way in which the
alleles are broadly grouped into two categories (i.e., a high MAOA activity group and a
low MAOA activity group). Beaver et al. [1] grouped the MAOA genotype into the high/
low dichotomy and reported that the low activity genotype correlated with violent behavior
among gang members. This measurement strategy could mask important variation that
exists for each of the individual alleles and recent research by Guo et al. [9] provides some
support for this possibility. Guo et al. examined the association between MAOA and
delinquent behavior in a longitudinal sample of adolescents and young adults. Unlike prior
research examining MAOA, these researchers estimated the effects of the 2-repeat allele
against all other alleles in data drawn from the National Longitudinal Study of Adolescent
Health (Add Health). Their statistical models revealed that the 2-repeat allele conferred an
increased risk of serious and violent behaviors in both adolescence and early adulthood.
Importantly, Guo et al. also performed a functional analysis and reported that the 2-repeat
allele had a lower level of promoter activity when compared against the 3-repeat and
4-repeat alleles.
In another study, also analyzing the Add Health data, Beaver et al. [2] reported a link
between the 2-repeat allele and the odds of being arrested, the odds of being incarcerated,
and a lifetime measure of antisocial behavior. Unfortunately, neither the Beaver et al. study
nor the Guo et al. [9] study specifically examined the most serious and violent types of
criminal behaviors, but rather grouped together a wide range of antisocial behaviors, some
of which are violent and some of which are non-violent. Given that research has revealed
that violent and non-violent criminal behaviors might have different etiologies [4], the next
important step in the 2-repeat research is to examine this allele’s association with some of
the most violent types of behaviors. Against this backdrop, the current study examines the
effect of the 2-repeat allele on two highly violent behaviors: shooting and stabbing
someone. The findings will help to reveal whether the 2-repeat allele has effects on violent
criminal behaviors rather than antisocial behavior broadly defined.
Materials and Method
Participants
Data for this study were drawn from the DNA subsample of the National Longitudinal
Study of Adolescent Health (Add Health; [10]). Detailed information about the Add
Health, including its sampling design, has been published previously [11, 12, 24]. Briefly,
the Add Health is a longitudinal four-wave study of a nationally representative sample of
American adolescents who were attending 132 middle or high schools during the
1994–1995 academic school year. The first (N = 20,745) wave of data was collected when
respondents were at home along with their primary caregivers. The second wave of data
Psychiatr Q (2014) 85:257–265259
123
Page 4
was collected approximately one-and-a-half years later (N = 14,738). The third round of
interviews were completed in 2001–2002 when the respondents were in early adulthood
(N = 15,197). The fourth wave of data commenced in 2007–2008 when the respondents
were between the ages of 24–32 years old (N = 15,701).
A subsample of subjects was genotyped for a number of genes related to neurotrans-
mission at wave 3. Eligibility was based on whether the respondents were part of a sibling
pair included in the data; respondents who also had a sibling participating in the study were
asked to submit buccal cells for genotyping. Overall, 2,574 subjects agreed to participate.
Genotyping was conducted in a coordinated effort between Add Health and researchers at
the Institute of Behavioral Genetics in Boulder, Colorado [12].
Genotyping Procedures
A variant of a previously developed assay was used to genotype subjects for the MAOA-
uVNTR polymorphism [27]. Primer sequences were as follows: forward, 50ACAGCCT
GACCGTGGAGAAG-30(fluorescently labeled), and reverse, 50-GAACGTGACGCT
CCATTCGGA-30. This assay resulted in PCR products of 291 (2-repeat allele), 321 (3-
repeat allele), 336 (3.5-repeat allele), 351 (4-repeat allele), and 381 (5-repeat allele) bps.
Two independent raters scored the genotypes. MAOA genotypes were divided into two
groups: one group consisted of subjects who possessed the 2-repeat allele and the other
group consisted of subjects who possessed the 3-repeat, 3.5-repeat, 4-repeat, and 5-repeat
alleles. Because MAOA is X-linked and because shooting and stabbing tend to be almost
exclusively carried out by males, the current study excludes females from the analyses.
Measures
Shooting and stabbing were measured with two interrelated items. During each of the four
waves of data collection, respondents were asked to indicate whether they had shot or
stabbed someone during the previous 12 months. Responses were coded dichotomously,
where 0 = did not shoot or stab someone in the past 12 months and 1 = shot or stabbed
someone in the past 12 months. The first shooting and stabbing measure was a dichoto-
mous measure that indicated whether the respondent had ever shot or stabbed someone
across all four waves of data. This item was coded such that 0 = did not shoot or stab
someone and 1 = shot or stabbed someone. Overall, 5.6 % of the sample reported having
shot or stabbed someone at some time during the first four waves of data collection. The
second shooting and stabbing item was designed to measure repeat shooting or stabbing.
This item was created by summing across all four wave-specific shooting and stabbing
items. The resulting value indicated the total number of waves for which the respondent
indicated they had shot or stabbed someone. In total, 4.7 % of the sample reported shooting
or stabbing someone at one wave, 0.8 % of the sample reported shooting or stabbing
someone at two waves, and 0.1 % of the sample reported shooting or stabbing someone at
three waves. There were no subjects who reported shooting or stabbing someone at all four
waves.
To take into account the potentially confounding effects of race, a single-item variable
was included to measure racial status. During wave 1 interviews, interviewers indicated
which race best described each subject. The data for the current study were analyzed using
subjects who were either Caucasian or African-American.
260 Psychiatr Q (2014) 85:257–265
123
Page 5
Findings
Findings from previous research have indicated that the frequency of the 2-repeat allele
varies significantly across races (e.g., [25, 30]). As a result, the analysis begins by
examining the frequency of the 2-repeat allele separately for Caucasians and African
Americans. Overall, the 2-repeat allele was carried by 0.1 % of Caucasian males and by
5.2 % of African-American males. These frequencies were double-checked using self-
reports of race instead of interviewer-reported race and the results were nearly identical.
Importantly, these allelic frequencies parallel those reported in other samples (e.g., [25,
30]). Given the extremely low prevalence of the 2-repeat allele in Caucasian males, all of
the subsequent analyses were conducted within the African-American male subsample.
After cases were excluded for missing data, the final analytical sample size was N = 133
African-American males, including 6.0 % who possessed the 2-repeat allele (three 2-repeat
carriers were dropped because of missing data on the shooting or stabbing variables).
Next, the association between the 2-repeat allele and the dichotomous shooting or
stabbing variable was examined by estimating a binary logistic model. The results of this
analysis are presented in Fig. 1, where the predicted probabilities are contained as bar
graphs and the parameter estimates are included in the caption. As can be seen, the
predicted probability of shooting or stabbing someone for respondents with alleles other
than the 2-repeat allele was 0.07. In contrast, the predicted probability of shooting or
stabbing someone for subjects with the 2-repeat allele was 0.50. The parameter estimates
for this equation revealed that the 2-repeat allele exerted a statistically significant effect on
the odds of shooting or stabbing someone (OR = 12.89, p\0.05).
The last analysis that was conducted was designed to examine the association between
the 2-repeat allele and the total number of waves that the subject reported shooting or
stabbing someone. Given that this measure was highly skewed, the association was
examined by estimating a negative binomial regression equation. Figure 2 contains a
graphical depiction of the predicted rate of change along with the parameter estimates in
the caption. As this figure shows, the predicted rate of change is 0.10 for respondents who
0
0.1
0.2
0.3
0.4
0.5
0.6
Other Genotype2R Genotype
Predicted Probability of Shooting or Stabbing Someone
Fig. 1 Predicted probabilities of lifetime prevalence of shooting or stabbing someone (N = 133). Note
Parameter estimates for logit equation: b = 2.56, SE = .79, OR = 12.89, p\0.05; all equations corrected
for the clustering of observations in families by using the ‘‘cluster’’ command in STATA10.0; any cases
missing a family ID number were dropped from the analyses
Psychiatr Q (2014) 85:257–265261
123
Page 6
possess alleles other than the 2-repeat allele, but the predicted rate of change is 0.63 for
respondents who carry the 2-repeat allele. The parameter estimates generated from the
negative binomial analysis indicate that this association between the 2-repeat allele and the
total number of shooting or stabbing incidents is statistically significant (exp(b) = 6.51,
p\0.05).
Discussion
There has been a great deal of interest in examining the specific genetic polymorphisms
that are associated with antisocial behavior in general and specific categories of antisocial
behavior, such as violence or aggression, in particular [5, 14]. Even so, there has been
comparatively less empirical attention paid to the potential link between certain genetic
markers and specific antisocial behaviors. The current study partially addressed this gap in
the literature by examining whether MAOA genotype was related to shooting and stabbing
behaviors during adolescence and adulthood. Analysis of data drawn from the National
Longitudinal Study of Adolescent Health revealed two key findings. First, carriers of the
2-repeat allele of MAOA were significantly more likely than carriers of all other alleles to
report having shot or stabbed someone at least once during their lifetime. Second, the
2-repeat allele was also related to the total number of waves in which the subject reported
shooting or stabbing someone. In short, the 2-repeat allele confers an increased risk of
shooting and stabbing multiple victims over the entire life course.
Although to our knowledge, this is the first study to link a specific genetic polymor-
phism to shooting and stabbing behaviors and to having multiple shooting and stabbing
victims, there are a number of issues that should be addressed in future studies to determine
the robustness of the results. First, almost all of the prior research examining the effects of
MAOA on antisocial behaviors has pooled the 2-repeat allele together with the 3-repeat
allele [14]. As the results of this study indicate, however, this approach may be misguided
as the most powerful effects may be found within the 2-repeat allele and combining the
0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
Other Genotype2R Genotype
Predicted Rate of Change for the Total
Number of Times of Shooting and Stabbing
Fig. 2 Predicted rate of change for the total number of times of shooting or stabbing someone (N = 133).
Note Parameter estimates for negative binomial equation: b = 1.87, SE = .54, exp(b) = 6.51, p\0.05; all
equations corrected for the clustering of observations in families by using the ‘‘cluster’’ command in
STATA10.0; any cases missing a family ID number were dropped from the analyses
262Psychiatr Q (2014) 85:257–265
123
Page 7
2-repeat allele with the 3-repeat allele may attenuate the main effects of MAOA [9].
Supplemental analyses (not reported) revealed that when the 2-repeat allele and the
3-repeat allele were combined, this genotype was unrelated to the odds of shooting or
stabbing someone.
Second, and relatedly, analysis of the Add Health data revealed that the 2-repeat allele
conferred an increased risk of shooting and stabbing behaviors and that these effects were
independent of environmental factors. These findings stand in stark contrast to much of the
extant MAOA research which has revealed that MAOA only has effects on antisocial
behaviors in the presence of environmental liabilities. The differential effects, however,
could be because the 2-repeat allele has independent effects whereas the 3-repeat allele
only has effects when paired with an environmental risk factor. Future research needs to
explore this possibility in much greater detail.
Third, and importantly, all of the existing research examining the effects of the 2-repeat
allele on antisocial behaviors has analyzed data from the Add Health. While the current
study extends previous research by showing that the 2-repeat allele has relatively strong
effects on some of the most violent types of criminal behaviors, the findings should be
viewed cautiously because they do not represent a completely independent analyses from
those conducted by Guo et al. [9] and Beaver et al. [2]. Future research is needed that
examines the effects of the 2-repeat allele in a sample that is distinct from the Add Health.
Moreover, the study focused on a rare event, in a small sample, with a low base rate of the
2R allele. While the findings are statistically significant, they could have been influenced
by small changes in the cell sizes of the 2 9 2 table (between the 2R allele and shooting/
stabbing). Thus, the reader should exercise appropriate caution when interpreting the exact
values presented here.
Last,theanalysesforthecurrentstudywereconfinedtoAfrican-Americanmalesbecause
of the low base rate of Caucasian males carrying the 2-repeat allele which precluded the
abilitytocalculateanymultivariate statisticalmodels.Futurestudiesshouldexpandonthese
findings and examine the effects of MAOA for African Americans, Caucasians, and other
racial/ethnic groups. Since approximately 5.5 % of African-Americans and less than 1 % of
Caucasianscarrythisrareallele[25,30],thesamplesizeswill needtobesufficientlylargeto
increasethestatisticalpowerneededtodetectsmall-to-moderateeffectsofthe2-repeatallele.
Until studies are conducted that are able to simultaneously examine both African Americans
and Caucasians, it would be premature to speculate as to the potential ramifications of the
2-repeat allele in explaining any of the well-known crime trends.
Acknowledgments
Udry, Peter S. Bearman, and Kathleen Mullan Harris, and funded by P01-HD31921 from the Eunice
Kennedy Shriver National Institute of Child Health and Human Development, with cooperating funding
from 17 other agencies. Special acknowledgement is due to Ronald R. Rindfuss and Barbara Entwisle for
assistance in the original design. Persons interested in obtaining data files from Add Health should contact
Add Health, Carolina Population Center, 123 W. Franklin Street, Chapel Hill, NC 27516-2524
(addhealth@unc.edu). No direct support was received from grant P01-HD31921 for this analysis.
This research uses data from Add Health, a program project designed by J. Richard
References
1. Beaver KM, DeLisi M, Vaughn MG, Barnes JC: Monoamine oxidase A genotype is associated with
gang membership and weapon use. Comprehensive Psychiatrcy 51:130–134, 2010.
2. Beaver KM, Wright JP, Boutwell BB, Barnes JC, DeLisi M, Vaughn MG: Exploring the association
between the 2-repeat allele of the MAOA gene promoter polymorphism and psychopathic personality
Psychiatr Q (2014) 85:257–265263
123
Page 8
traits, arrests, incarceration, and lifetime antisocial behavior. Personality and Individual Differences
54:164–168, 2013.
3. Buckholtz JW, Meyer-Lindenberg A: MAOA and the neurogenetic architecture of human aggression.
Trends in Neurosciences 31:120–129, 2008.
4. Burt SA: Are there meaningful etiological differences within antisocial behavior? Results of a meta-
analysis. Clinical Psychology Review 29:163–78, 2009.
5. Caspi A, McClay J, Moffitt TE, Mill J, Martin J, Craig IW, Taylor A, Poulton R: Role of genotype in the
cycle of violence in maltreated children. Science 297:851–854, 2002.
6. DeLisi M, Kosloski A, Sween M, Hachmeister E, Moore M, Drury A: Murder by numbers: Monetary
costs imposed by a sample of homicide offenders. The Journal of Forensic Psychiatry and Psychology
21:501–513, 2010.
7. Ferguson CJ: Genetic contributions to antisocial personality and behavior: A meta- analytic review from
an evolutionary perspective. Journal of Social Psychology 150:1–21 2010.
8. Fowler JS, Alia-Klein N, Kriplani A, et al.: Evidence that brain MAO A does not correspond to MAO A
genotype in healthy male subjects. Biological Psychiatry 62, 355–358, 2007.
9. Guo G, Ou X-M, Roettger M, Shih JC: The VNTR 2 repeat in MAOA and delinquent behavior in
adolescence and young adulthood: Association and MAOA promoter activity. European Journal of
Human Genetics 16:626–634, 2008.
10. Harris KM: The National Longitudinal Study of Adolescent Health (Add Health), Waves I & II,
1994–1996; Wave III, 2001–2002; Wave IV, 2007–2009 [machine-readable data file and documenta-
tion]. Chapel Hill, Carolina Population Center, University of North Carolina at Chapel Hill, 2009.
11. Harris KM, Florey F, Tabor J, Bearman PS, Jones J, Udry JR. The National Longitudinal Study of
Adolescent Health: Research Design [www document]. URL: http://www.cpc.unc.edu/projects/
addhealth/design, 2003.
12. Harris KM, Tucker Halpern C, Smolen A, Haberstick BC: The national longitudinal study of adolescent
health (add health) twin data. Twin Research and Human Genetics 9:988–997, 2006.
13. Heron M: Deaths: Leading causes for 2007. National Vital Statistics Reports 59:1–95, 2011.
14. Kim-Cohen J, Caspi A, Taylor A, Williams B, Newcombe R, Craig IW, Moffitt TE: MAOA, mal-
treatment, and gene-environment interaction predicting children’s mental health: New evidence and a
meta-analysis. Molecular Psychiatry 11:903–913, 2006.
15. Levy ER, Powell JF, Buckle VJ, Hsu YP, Breakefield XO, Craig IW: Localization of human mono-
amine oxidase-A gene to Xp11.23-11.4 by in situ hybridization: Implications for Norrie disease.
Genomics 5:368–370, 1989.
16. Mason DA, Frick PJ: The heritability of antisocial behavior: A meta-analysis of twin and adoption
studies. Journal of Psychopathology and Behavioral Assessment 16:301–323, 1994.
17. Menard S: Short- and long-term consequences of adolescent victimization. Youth Violence Research
Bulletin:1–16, 2002.
18. Meyer Lindenberg A, Buckholtz JW, Kolachana B, et al.: Neural mechanisms of genetic risk for
impulsivity and violence in humans. Proceedings of the National Academy of Sciences 103:6269–74,
2006.
19. Miles DR, Carey G: Genetic and environmental architecture of human aggression. Journal of Person-
ality and Social Psychology 72:207–217, 1997.
20. Raine A: From genes to brain to antisocial behavior. Current Directions in Psychological Science
17:323–328, 2008.
21. Raine A, Buchsbaum MS, Stanley J, Lottenberg S, Abel L, Stoddard J: Selective reductions in pre-
frontal glucose metabolism in murders. Biological Psychiatry 36:365–373, 1994.
22. Raine A, Buchsbaum M, LaCasse L: Brain abnormalities in murderers indicated by positron emission
tomography. Biological Psychiatry 42:495–508, 1997.
23. Raine A, Meloy JR, Bihrle S, Stoddard J, LaCasse L, Buchsbaum MS: Reduced prefrontal and increased
subcortical brain functioning assessed using positron emission tomography in predatory and affective
murderers. Behavioral Sciences and the Law 16:319–332, 1998.
24. Resnick M, Bearman P, Blum R, Bauman K, Harris K, Jones J, Tabor J, Beuhring T, Sieving R, Shew
M, Ireland M, Bearinger L, Udry J: Protecting adolescents from harm: Findings from the National
Longitudinal Study of Adolescent Health. Journal of the American Medical Association 278:823–832,
1997.
25. Reti IM, Jerry Z Xu, Jason Yanofski, Jodi McKibben, Magdalena Uhart, Yu-Jen Cheng, Peter Zandi,
Oscar J Bienvenu, Jack Samuels, Virginia Willour, Laura Kasch-Semenza, Paul Costa, Karen Bande-
een-Roche, William W Eaton, Gerald Nestadt: Monoamine oxidase A regulates antisocial personality in
whites with no history of physical abuse. Comprehensive Psychiatry 52:188–194, 2011.
264 Psychiatr Q (2014) 85:257–265
123
Page 9
26. Rhee S-H, Waldman ID: Genetic and environmental influences on antisocial behavior: A meta-analysis
of twin and adoption studies. Psychological Bulletin 128:490–529, 2002.
27. Sabol S, Hus S, Hamer D: A functional polymorphism in the monoamine oxidase A gene promoter.
Human Genetics 103:273–279, 1998.
28. Shih JC, Chen K, Ridd MJ: Monoamine oxidase: From genes to behavior. Annual Review of Neuro-
science 22:197–217, 1999.
29. Truman JL, Rand MR: Criminal victimization, 2009. Washington, DC: Bureau of Justice Statistics, US
Department of Justice, 2010.
30. Widom CS, Brzustowicz LM: MAOA and the ‘‘cycle of violence:’’ Childhood abuse and neglect,
MAOA genotype, and risk for violent and antisocial behavior. Biological Psychiatry 60:684–689, 2006.
Author Biographies
Kevin M. Beaver, PhD is a professor in the College of Criminology and Criminal Justice at Florida State
University and a visiting distinguished professor at King Abdulaziz University.
J. C. Barnes, PhD is an assistant professor in the School of Economic, Political, and Policy Sciences at the
University of Texas at Dallas.
Brian B. Boutwell, PhD is an assistant professor in the Department of Criminal Justice and Criminology at
Sam Houston State University.
Psychiatr Q (2014) 85:257–265265
123
Download full-text 
