Gene Heritability Associated with Violent Behavior

(1) A man who has committed several violent rapes is on trial and his lawyer argues that the man cannot help himself because his behavior is the result of his genetic make-up. The man's father and brother also have a history of violent crime. In defense of his position, the lawyer cites studies reported in 1993 on a small Dutch family indicating that some people inherit a propensity toward violent behavior. Affected individuals in this family were shown to have a mutation in the monoamine oxidase gene involved in the breakdown of neurotransmitters. Do you think that the sentencing of the man on trial should depend in part on this type of scientific study? Are people with known genetic alterations responsible for their actions? Should all individuals with a criminal record of violence be genetically tested for suspected mutations and, if tests prove positive, should repeat offenders be jailed for life or undergo sterilization in exchange for lighter sentences?

"Am I my brother's keeper?" This question which Cain replies to God contains the most imposing issue facing man's system of justice. How can we truly know whether someone is guilty or not? In this world, those who commit the most terrible crimes, besides the rare exceptions, will never confess their deeds. The fact is that the root of all evil is not embedded in the crimes that men commit. Rather, their ability to deceive. That, along with the fact that men are not omniscient beings is at the route of human violence in crime. However, current scientific research is trying to find the answer to our infantile pursuit of justice. Current scientific research may revolutionize our undiscerning and naive approach to crime and genetics.

Throughout the history of mankind, human violence has permeated every generation. This idiosyncrasy brings humans to ask: where does violence originate from? To begin to understand where violence originates from, violence itself must be understood. Intuitively, there are different types of violent behaviors that are exhibited by human beings. Violent behavior is typically categorized by impulsive violence or premeditated violence. It is important to make this distinction because it is likely that these two subtypes span from two different bases of biological aggression (5). Other issues, such as age that violent acts or tendencies began, are important to consider when determining if gene heredity was involved. Even the method of violence (murder - close encounter or use of weapons, assault and battery, rape, etc.) likely has their own respective causes. Accounting for these violent behaviors can be a daunting task as there are so many factors that could be conditioning people for violence. Factors that could potentially affect violence are biological (activity and/or imbalance in the brain/body, disorder, disease, syndrome, etc.), genetic (inherited disease, disorder, or predisposition to violence), environmental (location, toxins, stressors, etc.), and social characteristics (upbringing/child-rearing, schooling, siblings, family abuse, etc.). According to researchers, "violent and criminal behavior are likely related to complex and social circumstances, but heritable factors have also been implicated(3)".

In the last decade, many studies have been conducted on these factors in combination with evidence linking a polymorphism in the monoamine oxidase A (MAOA) gene and impulsive violent behavior. MAOA has arguably been the clearest link between genetic variations associated with aggression, due to the enzyme that catabolizes monoamines (3). The MAOA allelic variation is an X-linked gene, which has been studied and associated with impulsive aggression in humans and animals (3). Due to the X-linked MAOA gene males tend to be homozygote which is further supported by the majority of females being heterozygous (3). Furthermore, the female homozygotes act more like the male hemizygotes (see Figure 4 in back), in that they usually receive one of the genes (3). The polymorphism is located in the promoter region of the monoamine oxidase A gene and is characterized by a variable number of tandem repeats in the promoter region (5). The varying tandem repeats occur in the genes transcriptional control region and results in high or low activity of the MAOA gene. The monoamine oxidase gene is responsible for the catabolism of monoamines like serotonin, noradrenalin, and dopamine (3). Primary research has shown that there is a link with violent and aggressive behaviors with low activity of MAOA. On the other hand, some research on the high activity genotype may be linked to impulsive aggression. Conclusively, both MAOA genotypes may potentially contribute to violent tendencies or aggressive behaviors with the proper environment (5).

Specifically, the MAOA and -B genes are located on the X chromosome and are made of 15 exons with identical intron-exon organization (3). MAOA and MAOB act at different times and in different ways. MAO-A is involved in a crucial enzyme step which clears serotonin and norepinphrine during brain development. Accordingly, MAO-B activity involves the same type of activity but increases action dramatically after birth (3). In studies with mice, knockouts for MAOA showed to elevate levels of serotonin, norepinphrine and dopamine. Thus, enhancing the organisms amygdale-dependent emotional responses. Male mice given the knockout showed more aggressive behavior (3). There has not been a correlation that all males with low MAOA (MAOA-L) allele will be violent offenders. Through various studies, a connection (not correlation or causation) has been made with low levels of MAOA because the lack of catabolism to monoamine neurotransmitters. Individuals with these neurotransmitters in the brain at high levels than other are susceptible to a high level of compulsivity. This is due to current findings that link amygdale (brain structure - associated with memory of emotional reactions) and medial prefrontal cortices (area of the brain involved in executive functioning and decision making) to be associated with emotion and memory (see Figure 3) . In fact, they are associated with the encoding, retrieval, and extinction of memories (especially negative ones). One study examined the genes of male Finnish alcoholics and violent behavior (inclusively, the research also tested to see how age and differing gene alleles affects violent behavior). Recidivism was tested for 15 years in a sample of 174 Finnish alcoholic offenders (the majority exhibited antisocial or personality disorder behavior). The research gave results that contradict almost all research done on the monoamine oxidase gene. The results suggested that MAOA-H (high activity) genotype in the Finnish alcoholics modulated the effects of alcohol consumption and aging on recidivistic acts of violence (4). Antisocial alcoholic offenders were found to have abnormal metabolisms and neglected nutrition during relapses, which in fact worsened the glucose metabolism and increased the risk for uncontrolled impulsive violence (4). All of these subjects were of the high activity allele, thus the results contradict other research that the low activity allele is responsible for many impulsive violent behaviors. Conclusively, the results demonstrate that other factors (environmental and biological) affect the expression of behavior in an individual (not exclusively dependent upon inherited gene activity), and that there is some gene-by-environment interaction.

Intriguingly, most of the research points to the opposite direction than the previously mentioned study. In another study, 802 white males with the MAOA-H gene and subjected to neglect and child abuse as children, underwent DNA analysis and interviewing to determine behavioral patterns. A composite index of violence was created based upon the individuals diagnostic information (such as arrests or previous criminal activity) and a series of interviews and tests to determine behavioral patterns. The conclusions showed no correlations between the genotype and the individuals indexes in short term (childhood) or long-term (lifespan). Consequently, the MAOA-H gene buffered the effects of neglect and child abuse in whites from becoming risk for violent and impulsive behavior (6). This study also concurred with another study of children with genotype trait for impulsivity followed for 25 years . The longitudinal study predicted violent behavior later in life for MAOA-L males with adverse early experience (1). Rather, these studies in combination suggest deficiency in neural systems responsible for emotional regulation and memory (such as the amygdale and medial prefrontal cortices) can lead to the emergence of violent behavior (3). This was further proved by fMRI studies on subjects who were to match pictures angry and fearful faces. Individuals expressing MAOA-L had significantly increased activity in the left amygdale and decreased response to the ventral cingulated cortex compared to the MAOA-H subjects. Amygdale stimulation in animals has proven to induce violent behavior (2). Since the cingulated cortex has been found to control the amygdale the mechanism of action becomes clear. On the whole, both MAOA genotypes may result in increased violence and impulsivity. The study concludes that gene expression and exhibited behavior can be altered by various aspects, namely the environment. Is there a consensus about the MAOA high and low activity? There is a consensus that both genotypes can create violent behavior, but some depend on environmental factors introduced to the organism (such as the study correlating high MAOA and alcoholism with violence).

All of these studies show a firm understanding of genes and their function; however it also demonstrates the lack of understanding in gene expression and outside influences. Accordingly, a man on trial with a genetic predisposition and a history of family violence should be considered in a court of law. Nevertheless, the consideration of the genetic predisposition is useless unless the accused was aware before the crime occurred. In effect, people cannot be accounted responsible unless a system of genetic testing was catalogued of the entire population. If a man learns early in life that he has a predisposition towards violence, then he can prepare accordingly and make life decisions to stray from a violent path. On the other hand, introducing this methodology of analyzing genotypes for criminal behavior would potentially create bias in the court house. If two men are allegedly accused of murder and one has the genotype eliciting a predisposition to violence, the court would most likely rule in favor of the non predisposed man. Essentially, courts today could use the genotype analysis as further evidence if needed, but not the primary base for conviction. This type of scientific evidence on genes should not yet be used in sentencing, because correlations may not mean causation. For the man on trial, the genetic testing would potentially prove to be useful as many studies have firmly correlated violent behavior to be genetic in families. The court must also be aware of other factors that could be affecting the man's predisposition (for example alcoholism or child abuse). Nonetheless, much of the research that has been done proves to be correct in cases for many violent offenders. Harnessing the power of this technology and research would be to our benefit, as those predisposed could be monitored more closely in society as more is learned about gene effects.

People with known genetic variations must be responsible for their actions. Those with contagious diseases are required to take preventative measures. Thusly, impulsive actions that are more likely to occur in one individual should be accounted for, as genetically predisposed individuals have the capability to do harm to others in a highly emotional event. Moreover, the justice system should genetically test all violent offenders. First, violent offenders can be picked out according to their genetic makeup. This would allow for the potential prediction of violent acts they may commit in the future. Second, mapping the genes of all violent offenders would further the research and understanding the cause of violence. Finally, mapping the genes and monitoring the behavior could elicit useful information in recidivistic violent behavior. Sentencing for predisposed offenders should be looked at differently in the case of repeat offenders. Repeat offenders with a known genetic predisposition are clearly not fit for society. Sterilization in exchange for lighter sentencing is a question of individual good versus the good of society. In effect, genetic analysis and DNA forensics has been targeted for the good of the people in hopes of bringing more criminals to justice. Sterilization thus becomes the good of the individual, as it is an attempt to prevent the person from reproducing. Not allowing the offender to reproduce within society could potentially eliminate the violent associated MAOA genes. However, a full understanding of how genes influence behavior is not fully understood so attempting to eliminate the genes from humans could prove a futile effort.

Conclusively, harsher sentences should be in place for known offenders of the genotype. Cases should be considered on an individual basis as the individual affected with the gene may only be predisposed when exposed to certain exogenous factors. Effectively, repeat offenders with the known genes should be subjected to harsher sentences (life), and first time offenders with known genetic mutation affecting violence should use gene analysis and past history as further evidence in court (but not the sole basis of sentencing a violent offender). Picture a justice system where alleged murderer is in fact innocent, but his gene analysis reveals that he's genetically predisposed with the MAOA-L gene associated with violent behavior. Image the world where an innocent man who has the gene is convicted and worse a guilty man without the gene who is falsely acquitted. It is hard to believe that the MAOA-L gene and full understanding of brain function could have the potential to change many major acquitted offenders.

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Citations

1. Eklund, Jenny, Per Olof Alm, and Britt At Klinteberg. Www.karger.com/Monoamine Oxidase Activity and Tri-lodothryonine Level in Violent Offenders with Early Behavioural Problems. Rep. Karger/Stockholm University, 17 Aug. 2005. Web. 30 Nov. 2009. .

2. Heering, Kees Van, Kurt Audenaert, Lieve Van de Wiele, and Alain Verstraete. Cortisol in violent suicidal behaviour: association with personality and monoaminergic activity. Rep. no. 60. Vol. 60. Gent: Journal of Affective Disorders, Belgium. Print. 181-189.

3. Meyer-Lindenberg, Andreas, Joshua W. Buckholtz, Bhaskar Kolachana, Ahmad R. Hariri, Lukas Pezawas, Guiseppe Blasi, Ashley Wabnitz, Robyn Honea, Beth Verchinski, Joseph H. Callicott, Michael Egan, Venkata Mattay, and Daniel R. Weinberger. Neural Mechanisms of Genetic Risk for Impulsivity and Violence in Humans. Rep. no. 16. PNAS, 18 Apr. 2006. Web. 1 Dec. 2009. .

4. Tikkanen, Roope, Rickard L. Sjoberg, Francesca Ducci, David Goldman, Matti Holi, Jari Tiihonen, and Matti Virkkunen. Effects of MAOA-Genotype, Alcohol Consumption, and Aging on Violent Behavior. Rep. no. 3. Vol. 33. Alcohol Clin Exp Res, 2009. Print. Ser. 3.

5. Viding, Essi, and Uta Frith. Genes for susceptibility to violence lurk in the brain. Rep. no. 16. Vol. 103. London: University College London, 2006. Print. Ser. 16.

6. Widom, Cathy Spatz, and Linda M. Brzustowicz. MAOA and the "Cycle of Violence:" Childhood Abuse and Neglect, MAOA Genotype, and Risk for Violent and Antisocial Behavior. Rep. Vol. 60. Biol Psychiatry, 2006. Print. 684-689.