The relation between dopamine and antisocial behavior : a meta-analysis

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The relation between dopamine and

antisocial behavior: A meta-Analysis

2016

Yvonne de Haan (10837221) and Fardau Verdonk (10834419) Master Forensische orthopedagogiek

Geert Jan Stams and Theo van Leeuwen Amsterdam, 19 april 2016

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Running Head: RELATION BETWEEN DOPAMINE AND ANTISOCIAL BEHAVIOR

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Abstract

A multilevel meta-analysis of 26 published studies, with 26 independent samples containing 133 effect sizes and N = 17.450 respondents was conducted to examine the relation between dopamine and antisocial behavior and possible moderating factors of this association. The results revealed a small overall significant association (r = .084, p < .001) between dopamine and antisocial behavior, indicating that abnormalities in the dopamine system were associated with antisocial behavior, showing the strongest association with anger (r = .416, p = .005). Implications for theory and practice concerning the relevance of the dopamine system for the etiology of antisocial behavior are discussed.

Key words: dopamine, antisocial behavior, problem behavior, meta-analysis, moderator

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Introduction

Criminological research on the etiology of antisocial behavior has shown that both environmental and neurobiological risk factors play a role in the development of externalizing problem behavior (Vaughn, Beaver, & DeLisi, 2009; Zai et al., 2012). Some studies have shown that dopamine and different dopaminergic polymorphisms can cause more or less of an increase in the development of externalizing problem behavior (DeYoung et al., 2006). Moreover, dopamine seems to have an effect on the ability to learn and the sensitivity for reward and punishment, which can influence the susceptibility for behavioral treatment (Blair, 2013). Notably, as the dopamine system seems to influence the development of antisocial behavior, many studies were designed to investigate the strength of this relation. However, as a result of different outcomes of these studies, the following study provides a meta-analysis, investigating the extent to which dopamine and dopaminergic polymorphisms are associated with antisocial behavior.

Antisocial behavior is a frequent precursor of more serious psychopathology (Young et al., 2002). This behavior can be manifested as aggressive, destructive, oppositional, delinquent or conduct problems (Grigorenko et al., 2010), and can cause violation of societal norms and impairment in social, academic, or occupational functioning (Schulz-Heik et al., 2007). To prevent and treat antisocial behavior, it seems important to examine its etiology (Prichard, Jorm, Mackinnon, & Easeal, 2007). Antisocial behavior is multidimensional, which is why its understanding necessarily will involve a host of disciplines (Rhee & Waldman, 2002; Vaughn, Beaver, & DeLisi, 2009). Often, considerable research has focused on environmental influences on the development of behavior (Rhee & Waldman, 2002). The reflection of genetic influences is often not considered. This is unfortunate because disentangling the influences of nature and

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nurture is the first step towards the goal of explaining the etiology of antisocial behavior (Rhee & Waldman, 2002). Also, estimating the relative magnitude of genetic and environmental influences on antisocial behavior is an important step toward the search for specific candidate genes and environmental risk factors underlying this behavior (Rhee & Waldman, 2002). A meta-analysis conducted by Waldman and Rhee (2006) provides evidence indicating that genetic factors, specifically dopamine genes as DRD4, are influential in explaining variance in measures of externalizing problem behavior in the antisocial domain across studies.

In addition to these genetic factors, neurotransmission systems play an important role in the development of antisocial behavior (Raine, 2002a, 2002b). Most studies that pay attention to antisocial behavior and neurological (dis)functions, engage in neurotransmitters norepinepfrine, serotonine and dopamine. Dopamine is known for its contribution to impulsive behavior, attention-deficit/hyperactivity disorder (ADHD) and novelty seeking (Noble et al., 1998; Eisenberg et al. 2007; Carrasco et al., 2006). Impulsivity and ADHD are highly comorbid with aggression and violence (Barkley, 1997), and therefore it is possible that dopamine may also be implicated in the development of antisocial behavior. It has been assumed that the unbalanced presence of dopamine in various areas of the brain can result in a broad spectrum of outcomes, including cognitive, personality, and psychiatric deficiencies (Arnsten & Robbins, 2002; Depue & Collins,1999). Multiple studies have shown that different dopaminergic polymorphisms have influence on the development of antisocial behavior (Boardman et al., 2014). Especially, five dopamine receptor genes (DRD1-5) and the dopamine transporter gene (DAT1) are associated with antisocial behavior (Guo, Roettger, & Shih, 2006; Li, Sham, Owen, & He, 2006; Yang et al., 2007). DRD4 and DAT1 were investigated in a study (Tong Wu, 2013; Vaughn, Delisi, Beaver, & Wright, 2009) that focused on personality traits. There was a significant interaction between minor variants of the DRD2 and DRD4 gene on psychopathic personality traits which are part of

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antisocial behavior (Tong Wu, 2013). However, although research has been done on dopaminergic polymorphisms, it is still unclear which polymorphism is accountable for which behavior (Beaver, Wright, DeLisi, Walsh, Vaughn, & Boisvert, 2007). A study from Beaver et al. (2007) shows that neither DRD2 nor DRD4 show significant effects on antisocial behavior, but DRD2 interacted with DRD4 to predict variation in adolescent externalizing problem behavior and in adult antisocial behavior. This raises the question in which way specific dopamine genes have influence on the development of antisocial behavior.

To date, there are a few reasons why recent programs for preventing and treating antisocial behavior seem to have small effects. First of all, most programs lack in giving attention to and treating neurobiological (dis)functions (Moffit, 2005; Vaughn, Beaver, & DeLisi, 2009;). Moreover, Blair (2013) suggested that small effects of interventions are caused by symptoms of antisocial behavior. Explaining this, people with antisocial behavior show impairment in aspects of decision making, specifically in reinforcement learning and the representation of reinforcement expectancies (Blair, 2013). This impairment may relate to antisocial behavior and may result into the possibility that they are less sensitive for punishment and reward. This may be caused by the lack of activation in the amygdala and the corresponding release of dopamine by distress cues (Blair, 2013; Reuter, Weber, Fiebach, Elger, & Montag, 2009). Consequently, people with antisocial behavior do not show an increased attention to distress cues and any emotional responses on these cues (Blair, 2013). Taking the role of dopamine into account, this may be an important contribution to the effectiveness of treatment. Due to levels of dopamine, one can be assigned to a treatment that fits the neurobiological state of a person (Vaughn et al., 2009). This may improve the possibility to develop more effective treatment of youth with antisocial behavior.

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Due to previous research, it is evident that there are connections between dopamine and antisocial behavior. However, despite all the research that has been done, studies investigating the etiology of antisocial behavior and the relation with dopamine have different outcomes (Zai et al., 2012). Therefore, we conducted a meta-analysis to investigate the strength of the relation between dopamine and the development of antisocial behavior. Moreover, a meta-analysis will allow us to investigate if moderators influence this relation. According to this, all articles, published in the last 15 years and pertaining to this research were collected. We expect to find a relation between dopamine and antisocial behavior, and that the interaction between DRD2 and DRD4 may predict the development of antisocial behavior.

Method Inclusion Criteria

For the current meta-analysis, multiple inclusion criteria were formulated. First, antisocial behavior has been operationalized as externalizing problem behavior, which includes psychopathic traits, conduct disorder, criminal behavior, delinquency, violent behavior, aggressive behavior and anger. We excluded other types of antisocial behavior (for example, substance use and ADHD) and co-morbidity from the current meta-analysis to increase the comparability of the outcome measures in the studies (Hofer & Piccinin 2009). Second, only studies that examined the relation between dopamine and antisocial behavior were included to create the possibility to calculate effect sizes. Third, articles which were older than 15 years were excluded due to new insights of research focused on dopamine and to keep the information up to date.

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All studies addressing the relation between dopamine and antisocial behavior and which were published before May 2015 were included in the current meta-analysis. For collecting articles which contained information about the relation between dopamine and antisocial behavior the electronic databases PiCarta, Web of Science, Science Direct, PubMed, Google Scholar, CogNet were used. The search string included two combined variables: an antisocial behavior element and a dopamine element. For the antisocial behavior element, the following keywords were used: ‘psychopathic traits’, ‘conduct disorder’, ‘criminal behavior’, ‘delinquency’, ‘anger’, ‘externalizing behavior’. For the dopamine element, the following keywords were used: ‘genes’, ‘genetic influence’, ‘dopamine’, ‘DRD1’, ‘DRD2’, ‘DRD3’, ‘DRD4’’, and ‘DAT1’. Furthermore, references sections of review articles and important articles about the relation between antisocial behavior and dopamine were inspected for qualifying studies.

The initial search resulted in 65 articles. This was narrowed down to 50 articles by inspection of the abstract and the method section, including studies examining all kinds of genetic influence on different kind of behaviors. After excluding the studies with other types of antisocial behavior, genetic factors and co-morbidity, a total of 26 studies (with 133 effect sizes, and 17.450 respondents) met the inclusion criteria. Not all studies contained independent data sets. Many studies had overlapping samples and used the same waves of the Add Health-trial. Table 1 shows the study characteristics of the included studies.

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Running Head: RELATION BETWEETN DOPAMINE AND ANTISOCIAL BEHAVIOR Table 1 Characteristics of included studies

Study Study characteristics Sample characteristics

Year N # r (M) PR IF Design DV SR Continent Instrument Dopamine Gender Age Type sample

Beaver 2007 872 12

(0.044)

Yes 2.0 LONG CD/AB No America DSM IV, GT DRD2,

DRD4 Males <18 Comm. Guo 2006 116 3 16 (0.0972)

Yes 4.522 LONG SD/VD Yes America SR, GT DAT1,

DRD2 Mixed 12-23 Comm. Vaughn 2009 257 4 1 (0.0661)

Yes 1.622 LONG CB Yes America SR, GT DAT1 Mixed <18 Comm.

Dmitrieva 2010 119 6 (0.0773)

Yes 5,884 CROSS CB Yes Russia SR, ZKQ, GT DRD4 Mixed <18 CS

Chen 2007 41 3

(0.4418)

Yes .429 CROSS AB Yes America SR,

Interview,GT DAT1, DRD2, DRD4 Males 12-19 CS Wu 2013 257 4 3 (0.0386)

Yes 2.378 LONG PPT Yes America SR. FFM, GT DAT1,

DRD2, DRD4

Mixed <18 Comm.

Delisi 2009 232 8

(0.1229)

Yes 1.662 CROSS CB Yes America SR,

questionnaire DRD2 Women Comm. Prichard 2007 209 6 6 (0.0097)

Yes 2.774 LONG AB Yes Australia SR, GT DBH, DRD2 Mixed >18 Comm.

DeYoung 2006 177 2 (-0.1027)

Yes 13.75 0

CROSS AB Yes America GT, WISC,

questionnaire, SR

DRD4 Males <18 CS

Zai 2012 288 22

(0.0709)

Yes 4.230 CROSS AB Yes Canada Questionnaire, GT, SR DRD2, DRD4 Mixed <18 CS Mota 2013 559 2 (0.1194)

Yes 2.048 CROSS CD No America DSM IV, GT DRD4 Mixed <18 CS

Hohmann 2009 298 6 (0.1012)

Yes 2.871 CROSS EB Yes Europe Questionnaire, GT, SR DRD4 Mixed <18 CS Buckholtz 2009 30 2 (0.2566) Yes 14.97 6

CROSS PPT No America Brainscans, PPT, fMRI, and PPI Overall/Dop amine Unkno wn >18 CS

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N = number of participants; # r (M) = number of effect sizes (mean); PR = peer review; IF = impact factor of journal; SR= self report; design = cross-sectional or longitudinal; CROSS = cross-sectional design; LONG = longitudinal design; CD = conduct disorder; AB = antisocial behavior; SD = serious delinquency; VD = violent delinquency; CB = criminal behavior; AB = aggressive behavior; PPT = psychopathic personality traits; EB = externalizing problem behavior; GT = genotyping; BS = blood sample; Exp. = experiment; CS = clinical subsample; Comm. = community sample.

6 0.0774) GT, SR DAT1

Chen 2005 132 3

(0,2705)

Yes 1.152 CROSS PPT/AB Yes America GT, screening, SR DRD2, DAT1 unkno wn unkno wn CS Boardman 2014 724 1 (0.1880)

Yes 1.662 LONG SD/VD Yes America Interview, SR, GT DAT1, DRD2 Mixed <18 Comm. Grigorenko 2010 421 1 (0.0300)

Yes 2.269 CROSS AB/CD No Russia GT,

K-SADS-PL

DRD4 Male <18 CS

Nikitopoulos 2014 296 1 (0.0600)

Yes 3.957 CROSS EB Yes Europe Video-calls, questionnaires, GT, SR

DRD4 Mixed <18 Exp.

Schulz-Heik 2008 372 1 (0.0030)

Yes 2.274 CROSS CD No America DIS, BS DAT1 mixed >18 Exp.

Bentley 2010 328 2 (0.2094)

Yes 6.459 CROSS AB No America Blood samples, and assessments

DRD2 Mixed <18 Exp.

Jorm 2001 660 4

(0.0333)

Yes 2.159 CROSS EB Yes Australia Questionnaires, BS, SR

Dopamine Mixed <18 Exp. Propper 2007 169 2

(0.0885)

Yes 3.307 CROSS EB No America Observations, CBCL, BS

DRD4 Mixed <18 Exp.

Young 2002 790 3

(0.0347)

Yes 6.335 CROSS EB Yes America CBCL, DNA

screening, SR

DAT1 Mixed <18 Exp.

Lee 2007 183 16

(0.0240)

Yes 3.416 CROSS AB No America BS, diagnostic research

DAT1 Mixed <18 Exp.

Barnes 2013 107

8 1 (0.0700)

Yes 1.210 CROSS EB Yes America SR, BS Dopamine males >18 Exp.

Butovskaya 2013 138 6 (0.1781)

Yes 5.578 CROSS AB Yes Africa Questionaire (AQ), SR, DNA research

DRD2, DAT1

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Running Head: RELATION BETWEETN DOPAMINE AND ANTISOCIAL BEHAVIOR

Variables and Study Characteristics

Included studies have been coded according to the guidelines of Lipsey and Wilson (2001). Antisocial behavior was the dependent variable. Dopamine was the independent variable. Dopamine was coded as a moderator variable: DRD2, DRD4, DAT1, DBH, DRD2xDRD4, DAT1xDRD4. No studies assessed DRD1 and DRD3. Antisocial behavior was divided in nine categories that could possibly moderate the relation between the independent and dependent variable: antisocial behavior not otherwise specified, externalizing problem behavior, conduct disorder, aggressive behavior, anger, criminal behavior, psychopathic traits, delinquency and violent behavior. The various factors with a potential moderating effect on the relation between dopamine and antisocial behavior were coded. These moderators were study and sample characteristics. Study characteristics added in the moderator analysis were publication year, whether the study was peer reviewed or not, impact factor of the journal in which the study was published, the design of the study (cross-sectional versus longitudinal) and the continent of the study. Sample characteristics were gender (all male/female or mixed sample) and the age of respondents which were gathered in groups (adolescents, toddlers, children, adults, all ages, children/adolescents).

Calculation and Analysis of Effect Sizes

Effect sizes were transformed into the correlation coefficient r. The effect size, correlation coefficients were calculated using formulas from Lipsey and Wilson (2001). A positive correlation indicates the relation between the development of antisocial behavior and abnormalities in the dopamine system. An effect size was coded as zero in case the study only reported that the relation was not significant (Lipsey & Wilson, 2001). The continuous moderator’s publication year and impact factor were centered around the means. For categorical variables, dichotomous dummy variables were created. Outliers in effect sizes (> 3.29 SD from the mean; Tabachnik & Fidell, 2007) were winsorized. Correlation coefficients r were recoded into Fisher z-values (Lipsey and Wilson 2001). After the analyses, the Fisher z-values were transformed into correlation coefficients again for interpretation and reporting. Standard errors and sampling variance of the effect sizes were estimated using formulas by Lipsey and Wilson (2001).

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Twenty-six studies reported about the relation between dopamine and antisocial behavior, resulting in a different number of effect sizes per study. It is possible that two effect sizes from the same study are more alike than effect sizes from other studies. The assumption of independent effect sizes underlying traditional meta-analytic methods was therefore violated (Hox, 2002; Lipsey & Wilson, 2001). We applied a multilevel approach to the current meta-analysis in order to deal with the interdependency of effect sizes (Rhee & Waldman, 2002). A three-level model random effects model was used to account for three levels of variance, including the sampling variance for each effect size (level-one), the variance between effect sizes within studies (level-two), and the variance between studies (level-three) (Wibbelink & Assink, 2015). We used likelihood-ratio-tests to compare the deviance scores of the full model and the models without variance parameters on level two or three to determine if the level-two and -three variance was significant, indicating heterogeneous effect sizes. In case the effect sizes are considered to be heterogeneous, we proceeded to moderator analysis, since the differences between the effect sizes may be explained by outcome, study and sample characteristics. The current meta-analysis was conducted in R, using the metafor-package, restricted maximum likelihood estimation and the Knapp and Hartung-method (Wibbelink & Assink, 2015).

Results

Table 2 presents the results of the multilevel meta-analysis. The overall association between dopamine and antisocial behavior can be found in this table, as well as the results of the moderator analyses. Only moderator variables with a significant contribution to the relation between dopamine and antisocial behavior are presented.

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Overall Relation Dopamine and Antisocial Behavior

A significant association was found between dopamine and antisocial behavior (r = .084 (SE = .019), t (132) = 4.460; p < .001), suggesting that there is a significant overall relation between dopamine and antisocial behavior.

The likelihood ratio test comparing models with and without between-study variance (level 3) showed that significant variance was present at the between-study level (X2 = 5.795, p =

.016). The variance between the effect sizes within studies (level 2) was significant as well (X2 =

43.522, p < .0001), indicating a heterogeneous effect size distribution. About 19 % of the total effect size variance was accounted for the sampling variance (level 1), 6 % for the variance between effect sizes within studies (level 2), and 75 % for the variance between studies (level 3). In case of heterogeneous effect size distributions, moderator analyses are advised to investigate whether the variance between the effect sizes can be explained by specific factors, regardless of the significance of the overall effect size. Therefore, we conducted moderator analyses on sample and study characteristics, problem behavior, and dopamine. Table 2 shows the results of the moderator analyses.

Sample Characteristics

Gender did not moderate the relation between dopamine and antisocial behavior: F(2, 130) = .469; p = .627. Man nor women were significantly related with the association between dopamine and antisocial behavior. Neither did the age of the respondents moderate the relations between dopamine and antisocial behavior: F(5, 127) = 1.346, p = .249.

Study Characteristics

None of the study characteristics had a moderating effect on the relation between dopamine and antisocial behavior. The continents in which the articles were written and where research were done, did not moderate the relation between dopamine and antisocial behavior:

F(2, 128) = .524; p = .718.

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The moderator problem behavior had a significant effect on the relation between dopamine and antisocial behavior: F (8, 124) = 2.169, p = .034. Antisocial behavior not otherwise specified (reference category) did not show a significant mean association (r = .038, p = .431). In this moderator analysis, dopamine only had a significant effect on anger (r = .416, p = .005). None of the other antisocial behavior categories had a significant effect (externalizing problem behavior, conduct disorder, aggressive behavior, criminal behavior, psychopathic traits, delinquency and violent behavior).

Dopamine

In relation to antisocial behavior different types of dopamine did not moderate the relation between dopamine and antisocial behavior: F(6, 126) = 1.720, p = .122.

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Table 2 The overall results and moderator effects relation between sports participation and juvenile delinquency

Study ES b0 (r) t0 b1 p F(df1,df2)

Overall association between dopamine and antisocial behavior

26 133 .084 Moderator variables Antisocial behavior (RC) Externalizing problem behavior Conduct disorder Aggressive behavior Anger Criminal behavior Psychopathic traits Delinquency Violent behavior 26 133 .038 -.038 .046 .152 .416 .096 .133 .190 .036 .791 -.005 .129 1.860 2.847 .971 1.087 1.477 -.028 -.000 .008 .114 .377 .058 .094 .152 -.002 .431 .996 .897 .065 .005 ** .333 .279 .142 .997 F(8, 124) = 2.169

# studies = number of independent studies; # ES = number of effect sizes; t0 = difference in mean r with zero; t1 = difference in mean r with reference category; mean r = mean effect size (r); F(df1,d f2) = omnibus test; RC = reference category * p\.05; ** p\.01

Discussion

Antisocial behavior is multidimensional, which is why its understanding necessarily will involve a host of disciplines (Rhee & Waldman, 2002; Vaughn, Beaver, & DeLisi, 2009). Criminological research on the etiology of antisocial behavior has shown that both environmental and neurobiological risk factors play a role in the development of externalizing problem behavior. Contemporary research indicates that a number of genes implicated in the neurotransmission process, specifically dopamine, are correlated with antisocial behavior (Wu & Barnes, 2013). Building on this evidence, the current study collected information to examine the relation between dopamine and antisocial behavior.

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The overall finding from the meta-analysis shows a signiﬁcant association between dopamine and antisocial behavior, indicating that there is a signiﬁcant relation between dopamine and antisocial behavior (r = .084, p < .001). The distribution of effect sizes was heterogeneous, indicating that there was variation between the effect sizes within and across studies, possibly explained by moderators. Therefore, we conducted moderator analyses on sample characteristics, study characteristics, type of problem behavior and dopamine. The moderator analyses showed that sample characteristics, including gender and age of the respondents, study characteristics and type of dopamine did not influence the relation between dopamine and antisocial behavior. As type of dopamine does not seem to be a significant moderator, this rejects our hypothesis that in particular the interaction between DRD2 and DRD4 predicts the development of antisocial behavior.

In this study, type of antisocial behavior was the only significant moderator, with anger showing the largest (and only significant) effect (r = .416, p = .001). Reuter, Weber, Fiebach, Elger, and Montag (2009) consider anger to be a key symptom of antisocial behavior, often co-occurring with aggression, which can be observed by means of concrete described symptoms. As antisocial behavior not otherwise specified involves a broad range of symptoms, the relation with dopamine might be obscured by its large heterogeneity.

There are some limitations of this study. First of all, this study included many articles which used the Add Health Data. Therefore, it might be possible that different articles with different topics show related information based on the same data. Moreover, since the Add Health data are a nationally representative sample of youth, it is possible that very few individuals with antisocial behavior were captured by the sample. For future work it will be necessary to use respondents which are chosen randomly. Third, Plomin, Owen and McGuffin (1994) argue that scientists have suggested that there are many genes influencing human behavior in an epistatic, polygenic, and pleiotropic manner. Finding an association between dopamine and antisocial behavior only reflects a very small portion of the total genetic variance of antisocial behavior.When placed in context, the current findings, though relatively small in effect size, are consistent with this and the understandings (and research) of the genetic influence on the development of antisocial behavior (Viding et al., 2010; Zuk, Hechter, Sunyaev, & Lander, 2012). The fourth limitation is that many articles did not give much attention to the operationalization of different types of problem behaviors (Wu & Barnes, 2013). Therefore, it

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might be possible that different described problem behaviors overlap in the description. It will be important for future research to establish the degree to which the current measures of antisocial behavior overlap with other well-known scales tapping psychopathology. The fifth limitation is that the moderator antisocial behavior did have many categories, which were not filled with the same amount effect sizes. Consequently, findings based on this moderator should be interpreted cautiously.

Despite the limitations, the current meta-analysis has several strengths. First of all, as there is a need of getting more information about the etiology of antisocial behavior, this article has put light on the neurobiological part of it. Second, this study only included peer-reviewed and published articles with strong designs. Third, by using an advanced multilevel approach that allowed inclusion of multiple effect sizes per study, comprehensive moderator analyses were possible, leading to a better understanding of (the lack of) moderating inﬂuences. Third, we increased the comparability of the studies included in the meta-analysis by excluding all the articles which contained co-morbidity of problem behavior.

Finally, we argue that the large within/between study heterogeneity of the association between the dopamine system and antisocial behavior sets limits to the interpretation of this meta-analytically established relation, because there is not much explanation for this heterogeneity. In this sense, we agree with Miller (2010), who stated that the relation between a biological entity and a psychological construct does not reduce a psychological phenomenon to a biological characteristic. We conclude that antisocial behaviors, in their complexity, depend on the interplay between genetic influences, brain functioning and the social environment.

However, there are still major problems in this field with respect to replication and contradictory research findings, which warrant further investigation (Dick et al., 2015; Duncan & Keller, 2011; Jaffee, Price, & Reyes, 2013). For the future, it will be important to analyze the mechanisms of and interactions between genetic/neurobiological factors and environmental factors in the creation of antisocial behavior. Moreover, more research on dopamine is necessary in order to understand how dopamine plays a role in the development of antisocial behavior.

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Conclusion

Despite all the research that has been done, little is known about the etiology of antisocial behavior and its relation with dopamine. This study aimed to provide more information on the association between dopamine and antisocial behavior. The results of this multilevel meta-analysis showed that overall dopamine was related to antisocial behavior. This might indicate that abnormalities in the dopamine system are associated with antisocial behavior. There was only one significant moderator, which was type of antisocial behavior. Other moderators, study characteristics, dopamine, age, and gender, were not related to the relation between dopamine and antisocial behavior. More investigation is necessary to gain knowledge on the relation between the dopamine system and antisocial behavior. The role of dopamine in the development of antisocial behavior may be an important factor to take into account when examining the effectiveness of treatment (Vaughn, Beaver, & DeLisi, 2009).

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