Advertisement
Not a member of Pastebin yet?
Sign Up,
it unlocks many cool features!
- 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 There has been a great deal of research examining the link between a polymorphism 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 environment. 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 AfricanAmerican 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.
- 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
- 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 wellknown, 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 individually 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 neurotransmitters, 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 replicated 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 non258 Psychiatr Q (2014) 85:257–265
- 123
- 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) 85:257–265 259
- 123
- 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 neurotransmission 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 MAOAuVNTR polymorphism [27]. Primer sequences were as follows: forward, 50
- ACAGCCT
- 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 dichotomous 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
- 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 selfreports 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 Genotype 2R 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) 85:257–265 261
- 123
- 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 polymorphism 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 Genotype 2R 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
- 262 Psychiatr Q (2014) 85:257–265
- 123
- 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, the analyses for the current study were confined to African-American males because
- of the low base rate of Caucasian males carrying the 2-repeat allele which precluded the
- ability to calculate any multivariate statistical models. Future studies should expand on these
- 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
- Caucasians carry this rare allele [25, 30], the sample sizes will need to be sufficiently large to
- increase the statistical power needed to detect small-to-moderate effects of the 2-repeat allele.
- 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 This research uses data from Add Health, a program project designed by J. Richard
- 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.
- 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) 85:257–265 263
- 123
- 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 metaanalysis. 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 documentation]. 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, maltreatment, 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 monoamine 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 Personality 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 prefrontal 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 Bandeeen-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
- 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 Neuroscience 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) 85:257–265 265
- 123
Advertisement
Add Comment
Please, Sign In to add comment
Advertisement