Assignment: Genetic and Biological Aspects of Criminal Behavior

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Forensic Science International 237 (2014) 40–45

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Forensic Science International

j o u r n a l h o m e p a g e : w w w . e l s e v i e r . c o m / l o c a t e / f o r s c i i n t

Review Article

Behavioral genetics and criminal responsibility at the courtroom

Roberto Tatarelli a,*, Antonio Del Casale a,b, Caterina Tatarelli c, Daniele Serata a,d, Chiara Rapinesi a,d, Gabriele Sani a, Georgios D. Kotzalidis a, Paolo Girardi a,d

a Department of Neurosciences, Mental Health, and Sensory Organs (NESMOS), School of Medicine and Psychology, Sapienza University, Sant’Andrea Hospital,

Rome, Italy b Department of Psychiatric Rehabilitation, Fondazione ‘‘P. Alberto Mileno Onlus’’, Vasto, CH, Italy c Unit of Hematology, School of Medicine and Psychology, Sapienza University, Sant’Andrea Hospital, Rome, Italy d Department of Neuropsychiatry, Villa Rosa, Suore Ospedaliere of the Sacred Heart of Jesus, Viterbo, Italy

A R T I C L E I N F O

Article history:

Received 24 October 2013

Received in revised form 21 December 2013

Accepted 22 January 2014

Available online 31 January 2014

Keywords:

Genetics

Criminal responsibility

Liability

Violent crimes

Sentence

A B S T R A C T

Several questions arise from the recent use of behavioral genetic research data in the courtroom. Ethical

issues concerning the influence of biological factors on human free will, must be considered when

specific gene patterns are advocated to constrain court’s judgment, especially regarding violent crimes.

Aggression genetics studies are both difficult to interpret and inconsistent, hence, in the absence of a

psychiatric diagnosis, genetic data are currently difficult to prioritize in the courtroom. The judge’s

probabilistic considerations in formulating a sentence must take into account causality, and the latter

cannot be currently ensured by genetic data.

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

2. Genetic determinants of aggression and impulsivity in humans. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

3. Genetic constitution, violent impulsive behavior, and criminal responsibility: the problem of the causal link . . . . . . . . . . . . . . . . . . . . . . . . 41

3.1. Scientific methodological elements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

3.2. Neurobiological factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

3.3. Epistemological elements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

4. Conclusions and future directions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

1. Introduction

Worldwide sentence guidelines for judges permit punishment mitigations for defendants with demonstrated reduced mental capacity due to a psychiatric illness, whose intentionality and free

* Corresponding author at: Department of Neurosciences, Mental Health, and

Sensory Organs (NESMOS), Sapienza University, School of Medicine and Psychology,

Sant’Andrea Hospital, Via di Grottarossa 1035-1039, 00189 Rome, Italy.

Tel.: +39 0633775951; fax: +39 0633775342.

E-mail address: [email protected] (R. Tatarelli).

will were reduced at the time of the criminal act. As a consequence the court may establish compulsory internment and treatment in a psychiatric institution, sentence reduction, or both.

Recent cases show that molecular behavioral genetics are currently becoming influential on courts. While lawyers during the 1990s advanced guilt limitation due to putative brain serotonergic deficiency of their clients, the courts mostly rejected their claims and the sentences were little affected by expert testimony of genetically-determined reduced ability to control one’s own impulses [1]. However, in 2009, a judge of an Italian appeals court reduced by one year the prison sentence of an adult immigrant with schizophrenia who had killed another immigrant

R. Tatarelli et al. / Forensic Science International 237 (2014) 40–45 41

by mistake, believing that the victim was the one who was mocking him. The Court of Assizes of Appeal of Trieste supported that in accordance with the results of tests matching ‘‘numerous international studies’’, certain elements in the murderer’s genetic code ‘‘significantly increased the risk that he would develop impulsive aggressive behavior’’. [2]. Since the murderer was found to be a carrier of a few genetic variants that existing literature data associated with a predisposition to aggressiveness, the court reduced the final sentence from nine years and two months to eight years [2–6].

This sentence took into account biological data to further back the clinical diagnosis of schizophrenia. The scientific basis for backing the judgment was wide, as it was derived from studies focusing on specific populations of patients, who all had a diagnosis of schizophrenia (for example, [7–16]), not from population studies. In the same year, a Tennessee court, accepting a Monoamine Oxidase A (MAOA) gene variant per environment interaction (MAOA-L � childhood abuse), reduced the charge of a defendant from first degree murder to voluntary manslaughter [17]. In fact, the jury felt not like giving a death penalty after a forensic psychiatrist produced evidence that the defendant had a ‘‘warrior gene’’ conferring him vulnerability in some conditions, and condemned the defendant to a 32-year imprisonment [18]. The defendant appealed twice to further reduce his penalty, but the judge rejected most of his arguments [19,20], sticking to the facts and not taking into account further genetic considerations.

Currently, several defendants attempt to blame their own genetic constitution for their crimes and to ask for penalty mitigation during court sentencing. This raises issues of both ethical and moral nature mainly concerning the influence of biological factors on human free will, the risk of incurring in a deterministic eugenic science, the distinction between scientific knowledge sensu strictu (epistemological) and knowledge in a broader sense (gnoseological), the problem of the interpretation of scientific research data, and the problem of the sentence and its reduction.

The Italian psychiatrist Lombroso was first to propose in 1876 an empirical biological theory of criminal behavior [21]. According to this theory, some people are born rather than become criminals, and manifest different characteristic ‘‘atavistic’’ physical traits, such as their cranial structure, nose size, jaw jutting, jug ears, skin wrinkles, tattoos, that result from a regression to a more primitive state of evolution, which may facilitate their identification. For Lombroso, only one third of the criminal population belongs to this group of people, while other ‘‘criminaloids’’, with just some of the atavistic traits of criminality, may be influenced by an adverse environment [21].

The debate focused lately on genetic and aggressive behaviors, with two different standpoints emerging. On one hand, some consider the baby as entering the world as a ‘‘blank slate’’ and that environment, not heredity, determines all behavior [22,23]. On the other hand, others go back to Lombroso, supporting that harboring a gene alteration is basic and that the environment just facilitates the expression of aggressive–impulsive behavior. The more deterministic theories, according to which the antisocial, violent, and aggressive behaviors of some criminals are completely genetically-triggered, are now almost completely been put aside, but the current revision of the Lombrosian concepts is not much of a theoretical advance, as they only take into account the recently emerged epigenetics, but this is only pushing the issue forward.

In this paper we will discuss a number of questions that arise from the use of behavioral genetic research data in the courtroom. A major problem concerns the relationships between specific genomic structures of defendants and their intentionality at the time of the criminal act (criminal responsibility).

2. Genetic determinants of aggression and impulsivity in humans

Several geneticists estimated that the risk of aggressive behavior, both reactive and proactive, is influenced by genetic factors by about 40–50%; different twin studies showed them to play a greater role in adulthood and in men, compared to women [24–27].

The risk of inducing antisocial behavior may grow exponen- tially when harmful genetic and environmental factors synergisti- cally interact in the same (pathological) direction [28]. The enzyme monoamine oxidase A (MAOA), which degrades amine neuro- transmitters, such as norepinephrine, epinephrine, serotonin, and dopamine, has been shown to play a key role in the regulation of aggressive behavior. In fact, its gene has been called ‘‘warrior gene’’; inactivating mutations in its coding region significantly correlated with aggressive and impulsive behaviors [29]. Evidence of gene/environment interaction has been provided that carriers of the low-activity MAOA variant who were exposed to physical or psychological abuse in childhood have a significantly higher risk of impulsive, aggressive, and violent behaviors in late adolescence and early adulthood [30].

The polymorphism that was found to be mostly involved in aggression and violence is the variable number of tandem repeats (VNTR), which is located 1.2 kb upstream of the coding region in the MAOA promoter, and has an average of four alleles, with 3, 3.5, 4, and 5 30-bp tandem repeats.

Alleles with two repeats (low enzyme expression) showed correlations with increased levels of delinquency and violent behaviors, as compared to the other MAOA-VNTR variants, while the allele with 4-repeat (high enzyme activity) was correlated with lower levels of impulsive aggression in boys [31,32].

Serotonin transporter (5-HTT) is a transmembrane protein that allows the reverse transport of serotonin from the synaptic cleft to the presynaptic neuron. In the promoter region of the serotonin transporter SLC6A4 encoding gene, which is located on chromo- some 17q11.2 [33], a functional insertion–deletion polymor- phism 5-HTTLPR has been found. Differently from the small (S) allele of 5-HTTLPR, the long (L) allele contains a 44-bp insertion. The S variant correlates in mice with low expression of the transporter and a consequent reduction of the transport of serotonin [34].

Pavlov and colleagues (2012) [35] reported that the presence of the genotype SS can explain 5% of the inter-individual variance in aggressive behavior in humans. The S allele was significantly associated with increased aggression and impulsivity in children [36,37], adopted children [38], adolescents [39], girls and young women [40], cocaine-dependent individuals [41], and patients with personality disorders [42,43].

Other genes, including genes for the estrogen, androgen, and serotonin receptors, for tryptophan hydroxylase, for the dopamine transporter, beta-hydroxylase, and receptors, and catechol-O- methyl transferase have also been involved in the genetics of impulsive and aggressive behaviors (for a review, see [35]).

Taken together, these data suggest that human aggression levels may correlate with multiple genetic factors.

3. Genetic constitution, violent impulsive behavior, and criminal responsibility: the problem of the causal link

So far we have discussed the role of different specific genes and alleles involved in impulsive/aggressive behaviors. We will now expose the factors that do not permit to clearly establish a causal link between genetic constitution, impulsive/aggressive behaviors, and criminal responsibility in determining intentionality at the time of the criminal act. For example, for genuinely genetic

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diseases, like phenylketonuria [44] and trisomy 21 [45], the mere presence of a given gene may be associated with the lack of responsibility of affected individuals, but the current state of knowledge does not allow to consider specific gene patterns per se as infirmities from a medico-legal viewpoint, so in most other cases, where psychiatric disorders are invoked to reduce responsi- bility, the relationship between genes and criminal act is not so straightforward.

3.1. Scientific methodological elements

Most studies focusing on genetic and impulsiveness/aggression mainly included individuals with psychiatric, personality, or neurological disorders/disturbances. Furthermore, those providing evidence suggesting a significant role of genetic factors in impulsivity and aggression are often characterized by relatively small population samples. This limitation frequently leads to inconsistent results and increases the probability of type 1 and type 2 errors, as stated in a recent review that stressed the need for new studies with increased samples, to increase the statistical power [35]. In fact, studies focusing on the link between aggressiveness/impulsiveness and serotonin transporter gene (5- HTTLPR) S allele were underpowered. These studies also included heterogeneous samples, some showing correlations between S allele expression and impulsive aggression and some not. For example, Han et al. [46] reported a correlation in patients with psychotic disorders, while Nolan et al. [15] did not find such correlations, Courtet et al. [47] found and Zalsman et al. [48], Baca- Garcia et al. [49], and Zalsman et al. [50] did not find correlations in suicide attempters, Sukonick et al. [51] and Sweet et al. [52] found, while Assal et al. [53], Ha et al. [54], and Prichard et al. [55] did not find correlations in patients with Alzheimer’s disease, Beitchman et al. [37] found and Davidge et al. [36] did not find a correlation in children with history of aggressive behavior, and finally Zalsman et al. [48] did not find any correlation in adolescents with violent suicidal behavior. This correlation between S allele and aggression/ impulsivity has been reported in cocaine dependents [41], adolescents with drug use [39], adolescents with aggressive and/or delinquent behavior [56], offenders, people with conduct disorders or violent behaviors [42,56,57], and male adoptees [38], always in small samples, but these results should await confirmation in larger samples.

Genetic studies of MAO genes and aggression/impulsivity also have similar limitations. They often included dissimilar cohorts, such as women diagnosed with panic attack [58], men only [59], maltreated children [31,32], adolescents and young adults [60], the results of which cannot be extended to the general population. Moreover, MAOA gene expression effects may differ among different ethnic groups [61,62]. More large scale-studies of the general population are needed.

Another important point regards the fact that the presence of possible culprit polymorphisms has not been investigated in all the population of criminal convicts, hence, there is no evidence whether they should be considered as valid for sentence reduction in these particular cases in which they were advocated. Further- more, if it was proved that these same aggressivity/impulsivity- related polymorphisms are present also in other convicted people as well, whose lawyers failed to ask for sentence reduction, if sentenced, these convicted people may a posteriori claim sentence reduction such as those obtained in the above-mentioned cases. This would multiply the output of legal cases unnecessarily and increase further the social cost of crime. The presence of DSM-IV or -5 psychopathology might be causally related with the perpetrated crime beyond the presence of aggressive impulsiveness-related genes, hence it is on clinical grounds that the possible sentence reduction should be considered, independently from the presence

or absence of culprit genes. The presence of these genes, should the results pointing to their involvement in criminal acts be obtained, might increase the odds for the crime to occur, but their pathophysiological link with the crime should be demonstrated before asking for sentence reduction in cases where the convict’s DNA analysis yields positive results.

Few exceptions to the small sample rule are found. Haberstick et al. [63] reported a significant correlation between aggressive behaviors in middle childhood and the expression of the 5-HTTLPR S allele in a sample of 366 families from the general population. Gonda et al. [64] found a significant correlation between aggressive behavior and the same S allele in 169 psychiatrically healthy Hungarian women. Finally, Sysoeva et al. [40] showed some measures of hostility to have a significant effect on the -HTTLPR polymorphism in 112 girls (Moscow school students) and young women (university students at the Biological Department) and in 67 girls who were qualified synchronized swimmers; however, the distribution of LL and SL variants, though not that of SS variant, was different between the athletes and the controls and the study had other methodological flaws as well.

3.2. Neurobiological factors

Even adopting a biological approach and excluding the interpersonal relational factors, the transition from gene to behavior involves many intermediate steps. Lesh et al. [65] presented a unified model to explain the transition from a genetic substrate to psychological symptoms in patients with schizophre- nia. This model could also be adapted to connect genotype to aggressive/impulsive personality traits, bringing forward the attempt already made by Baum [17]. The first step could regard alterations of those genes which control neurotransmitter synthesis and disposition and concerns the cell nucleus, the cytoplasm, and synaptic events. Among transmitters, those mostly linked with the pathophysiology of aggression are epinephrine, norepinephrine, dopamine, and serotonin. The second step concerns the brain neurocircuitry in which these neurotransmit- ters are involved. Altered function of these circuits may be expected and may be shown to correlate with impulsivity and aggression through functional neuroimaging, which may also evidentiate differences between people who are aggressive/ impulsive and those who are not, or show correlations between a given activity and specific brain activation patterns. This comprises functional connectivity and both activation responses to aggression-related stimuli or tasks and stable patterns of activity, that could be related to personality traits.

One of the genes called in question, in particular the 5-HTTLPR gene, has not been associated only with aggression directed to others or to objects, but also to self-directed aggressiveness, as it was found to be related with suicide risk [66]. The reasons why the same gene may direct aggression toward self or others and which factors may intervene to shift from one to another are currently obscure. However, it should be stressed that the SS allele is not only related to aggression behavior only, but is a depressive behavior marker in various psychiatric conditions [67–74] and encodes also some aspects of obsessive–compulsive behavior in OCD patients [75] and psychotic symptoms in schizophrenia [76].

However, even if some gene forms could be shown to possibly constraint a person to displaying criminal behavior, one must first obtain enough data showing that other people without those gene polymorphisms or mutations are immune from such behavior. Furthermore, one must show that all the possessors of these polymorphisms and/or mutation would be forced to display this behavior, for lack of criminal responsibility to be claimed. Moreover, even if such conditions are met, the potential effects of genes and SNPs related to the ‘‘aggressive/impulsive phenotype’’

R. Tatarelli et al. / Forensic Science International 237 (2014) 40–45 43

might be modulated by epigenetic interactions, such as epistasis, and these may even prove to be protective toward criminal behavior. Prior to collecting such data, it would be preferable to leave things as they are and rely on clinical assessment and on what is already known about psychiatric conditions and criminal responsibility.

Last, it is frequently argued that ‘‘extended prison sentences can exacerbate the perpetual cycle of violence as it is well known that there is a violence problem within prisons, and because environ- ment also plays a role in triggering a genetic disposition for violence, the highly stressful and hostile environment of most prisons could seriously hinder a prisoner’s ability to learn to control his behavior’’ [77]. However, this could also apply to people who do not possess these genetic characteristics, shifting the problem on the environmental conditions in prisons in general.

3.3. Epistemological elements

Despite an exclusively biological approach to psychological phenomena proved to be useful in understanding their biological substrates and of heuristic value in finding new treatments, this approach is not to be intended as comprehensive. The psychody- namic approach allows for investigating the mechanisms of instinctual drives involved in the development of the personality of an individual, which underlies his/her behavior. These mechanisms are strongly influenced by his/her current and past experiences. The consideration and explanation of these mechan- isms by purely biological approaches may be only partial and reductionist.

Although epigenetics may come into play when considering culture, the human psyche and culture have a complementary relationship and mutual inherence. It is impossible to have a proper understanding of an individual when dissociating the study of culture from that of the psyche [78,79].

When dealing with attribution of liability in psychiatric forensic cases, even advanced laboratory and instrumental techniques cannot currently back sufficiently clinical observation [80], so it is out of question that instrumental psychiatry could decently substitute clinical psychiatry. Furthermore, phenomena occurring during the encounter between two individuals cannot be discern- ible neutrally and a historically. Such phenomena are not currently reducible to an objective list [81]. Current biological paradigms in psychiatry are piecemeal and patchy, thus their value in forensic consultation must be placed in an adequate frame and cannot supersede psychiatric judgment based on clinical, anthropophe- nomenological, and psychopathological considerations.

Briefly, there is no sufficient scientific support to state that specific gene patterns, which have been claimed to predispose to aggression, would make the carriers incapable of repressing a given behavior, thus rendering them unable to select among a set of socially appropriate, acceptable behaviors. A specific gene or single nucleotide polymorphism or a set of them may increase the odds of occurrence of a given behavior, but we currently lack sufficient knowledge to determine a complete chain of cause-effect events inevitably leading to that behavior. The cause-effect link is what might tell something about responsibility or its lack. Even admitting that some gene pattern may increase the probability that a person may display a given, say, aggressive behavior, there is still no proof that this gene pattern acted to limit the person’s options of behavioral displays at the time the behavior occurred, therefore temporarily limiting her/his freedom of choice and, consequently, responsibility. When a judge is looking for responsibility and when geneticists themselves express the effect of genes in terms of responsibility, some confusion may be expected [6]. In taking a decision, a judge must decide whether there is enough evidence for responsibility, and this is a

probabilistic process; however, she/he judges about the probabili- ty that the purported evidence has been causal in determining the criminal behavior, i.e., that the evidence ensured at the time the crime was committed that the individual had limited freedom of will, hence responsibility for her/his actions. The judge must decide about juridical evidence, and genetic evidence is currently not such, it is only biological evidence.

4. Conclusions and future directions

Based on available genetic data, despite some association found in specific populations or in the general population between specific genes or patterns and aggressive behavior, it is not possible to trace a linear cause–effect relationship between gene presence and displaying of behavior. Until more data are gathered to establish clear relationships between gene patterns and behavior, it is ethically very questionable to employ such genetic data in the court. Until that time, courts will have to rely on clinical judgment in psychiatric cases. Thus, investigations in the direction of establishing the genetic underpinnings of behavior are welcome and needed, but their partial or controversial results should not be used as evidence in the courtroom. This is the only way to avoid that Aristotelian dy�nami& (Realität) supersedes Ene0 rgeia (Wirk- lichkeit). Judges take their decision on the basis of probabilities, but to balance the evidences they have to prioritize them hierarchical- ly. Although genetic data may be given due consideration in the courtroom, they should presently be considered lower in a hierarchy where psychopathological considerations must play a primary role and be considered according to the specific case.

Financial & competing interests disclosure

In the past two years, Paolo Girardi has received research support from Lilly, Janssen, and Springer Healthcare, and has participated in Advisory Boards for Lilly, Otsuka, Pfizer, Schering, and Springer Healthcare and received honoraria from Lilly and Springer Healthcare. All other authors of this paper have no relevant affiliations or financial involvement with any organization or entity with a financial interest in, or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

This work has not been supported by any funding.

Acknowledgments

The authors wish to thank Ms. Mimma Ariano, Ms. Ales Casciaro, Ms. Teresa Prioreschi, and Ms. Susanna Rospo, Librarians of the Sant’Andrea Hospital, School of Medicine and Psychology, Sapienza University, Rome, for rendering precious bibliographical material accessible, as well as their Secretary Lucilla Martinelli for her assistance during the writing of the manuscript.

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