GENETIC EXPLANATIONS OF AGGRESSION
THE ROLE OF GENETIC FACTORS IN AGGRESSION: XYY KARYOTYPE
The XYY syndrome has attracted significant attention in psychology and criminology. This interest primarily arises from the theory that men with this syndrome may display elevated levels of aggression and a greater inclination toward violent behaviour compared to individuals with the standard XY chromosome pattern.
The "XYY super male karyotype" is a genetic condition found in some male individuals who possess an extra Y chromosome, resulting in a chromosomal pattern of 47, XYY. Typically, males have a 46, XY karyotype, characterized by one X and one Y chromosome. The presence of an additional Y chromosome in individuals with 47 XYY has led to early hypotheses suggesting that they might exhibit exaggerated male characteristics, both physically and behaviorally. This condition is rare, occurring in approximately 1 in 1,000 male births.
The term "super male" was coined based on initial theories proposing that the extra Y chromosome could potentially enhance male traits, possibly due to increased testosterone levels. This hypothesis is rooted in the connection between testosterone and various behavioural aspects, including its role in the development of the brain during prenatal stages. Since the Y chromosome plays a role in testosterone production, it was speculated that having an additional Y chromosome in men with XYY syndrome might lead to elevated testosterone levels. This idea also extended to behavioural aspects, suggesting that XYY males could exhibit heightened aggression and a predisposition for behaviours typically associated with increased testosterone levels.
The XYY syndrome has attracted significant attention in psychology and criminology.
APFS RESEARCH
Several key studies have been conducted to explore the implications of the XYY karyotype. Here are a few notable examples:
Jacobs et al. (1965): This study by Patricia Jacobs and colleagues was among the first to describe the XYY syndrome. They identified the additional Y chromosome in a tall man with an average IQ but severe acne and noted that this might represent a distinct chromosomal abnormality. This research laid the foundation for further studies on men's physical and psychological characteristics with the XYY karyotype.
Court-Brown's Study (1960s): Court-Brown conducted one of the earliest studies investigating the XYY karyotype in the 1960s. He examined patients in high-security psychiatric facilities and found a higher-than-expected frequency of the XYY karyotype among this population. His findings suggested a possible link between the XYY condition and aggressive behaviour, contributing to the early theory that XYY males had a predisposition towards criminal violence.
Theilgaard's Research (1984): Alice Theilgaard conducted a psychological evaluation of XYY and XXY men, comparing them with XY controls. Her findings indicated that XYY men displayed more aggressive responses, rigidity in thinking, higher aggression scores, pessimistic mood, evasiveness, negative relations with others, and a general life of disharmony. These men often experienced less positive childhoods and strained relationships with partners, exhibiting tendencies towards restlessness and impulsiveness.
Moffatt et al. (2002): This longitudinal study looked at the development of antisocial behaviour in a large sample and included an examination of the MAOA gene, which is located on the X chromosome and is related to aggression and criminal behaviour. While not exclusively focused on the XYY karyotype, this study is relevant for understanding the broader context of genetics and behaviour.
S. A. Mednick's in-depth analysis of criminal records involving Danish men provided valuable insights into the behaviour of individuals with the XYY karyotype. Contrary to early hypotheses that suggested XYY individuals might have a higher propensity for violent crimes due to perceived associations with increased testosterone levels, Mednick's research did not support such claims.
Mednick's study involved a comprehensive examination of criminal records, comparing the rates of violent criminal behaviour between men with the XYY chromosomal pattern and those with the typical XY pattern. The findings revealed that there was no significant difference in the likelihood of XYY individuals engaging in violent criminal activities compared to XY individuals.
This research challenged the previously held notion that XYY individuals were more prone to aggression and violent behaviour solely based on their genetic makeup. It highlighted the importance of conducting rigorous scientific investigations to understand the complex interplay between genetics, environment, and behaviour rather than making assumptions based on genetic characteristics alone.
ANALYSIS.
CAUSE AND EFFECT: The initial research carried out in correctional facilities and mental institutions initially hinted at a possible connection between the XYY chromosome pattern and aggressive behaviour. However, these studies later faced criticism due to their misinterpretation of the correlation and causation in the XYY hypothesis. It incorrectly assumed a direct causal link between the presence of an additional Y chromosome and aggressive behaviour. Recognising that correlation does not necessarily imply causation is important, as various factors can influence behaviour.
WEAK THEORY: The XYY hypothesis rested largely on speculation and lacked robust empirical evidence to support its claims. Its failure can be attributed to the absence of concrete genetic proof, relying instead on an assumption regarding the role of testosterone in aggression. The notion that XYY males were naturally more violent and prone to negative social behaviour gained widespread acceptance and was even included in biology textbooks. Essentially, the hypothesis was a metaphysical assumption, drawing partly from scientific concepts such as the influence of the Y chromosome and androgens on foetal development and partly from conjecture.
POOR METHODOLOGY: Early research on XYY individuals was frequently constrained and poorly executed, yielding inconclusive findings. Moreover, these studies were marred by various potential biases. Many researchers did not delve into the specific nature of crimes committed by individuals with the XYY karyotype. Later analyses revealed that these individuals were predominantly convicted of minor offences like car theft and shoplifting, as opposed to acts of aggression.
Ironically, the prevalence of XYY individuals in prison for these minor offences might suggest that other features associated with this karyotype, such as lower IQ, played a more substantial role in their legal situations. This implies that their cognitive abilities, or lack thereof, might have made them more susceptible to apprehension due to their involvement in petty crimes.
BIAS: Additionally, it became evident that the prison environment itself might inherently bias results towards the identification of aggressive behaviours, regardless of chromosomal patterns. The studies were further hindered by biased sample selection and research settings, as they predominantly focused on XYY individuals who were already incarcerated, neglecting the behaviour of those not in custody.
Most importantly, subsequent research on individuals with the XYY karyotype, often called "supermales," identified certain patterns such as increased height and acne, rather than heightened aggression. The existing evidence does not substantiate an inherent tendency for increased aggression or violence in XYY males.
In conclusion, research findings underscore the importance of avoiding the categorisation of XYY males as inherently dangerous or prone to violent behaviour. Instead, offering them appropriate support and therapy and addressing other issues related to their condition can empower them to lead ordinary lives.
ETHICS:
There was a genuine concern that the overly simplistic theory driven by a flawed interpretation of genetics contributed to stigmatisation and unequal treatment, including stereotyping.
In their time, scientists attempted to reconcile scientific exploration and discovery with the ethical treatment of individuals, especially in light of historical, ethical missteps like the eugenics movement, but unfortunately, they failed. Individuals with the XYY karyotype were treated appallingly. The following are examples of laws and programs implemented based on the hypothesis that XYY caused aggression.
Boston Hospital's Screening Program (1968): In response to growing concerns about the implications of the XYY karyotype, Boston Hospital initiated a screening program for newborn males to identify those with XYY and XXY syndromes. The aim was to study the developmental trajectories of individuals with these conditions. This program was significant as it represented one of the earliest systematic attempts to understand the developmental and behavioural implications of the XYY karyotype from birth. The project was funded by a grant from the Centers for Studies of Crime and Delinquency, a part of the National Institute for Mental Health.
The possibility of terminating pregnancies based on the detection of XYY syndrome raised profound ethical dilemmas at the time. It prompted questions about the value assigned to lives with genetic variations and the potential slippery slope toward neo-eugenics, where genetic selection favoured specific traits while disregarding others. These considerations spurred discussions about the moral standing of fetuses with genetic distinctions and the potential societal repercussions of such decisions.
BALANCE IN ETHICS VERSUS RESEARCH
Balancing Scientific Knowledge and Ethical Concerns:
It was imperative to strike a delicate balance with ethical considerations to navigate the pursuit of genetic knowledge, including studying conditions like XYY syndrome. This required safeguarding individual rights, ensuring informed consent, preserving privacy, and preventing discrimination or marginalization based on genetic data. The challenge lay in harnessing genetic information to improve health and overall well-being while guarding against its potential misuse. Sadly, this did not happen.
DETERMINISM
The debate over genetic determinism – the idea that genes exclusively dictate behaviour and traits – is central to the ethical discussion. The assertion that specific behaviours or tendencies, such as aggression in XYY individuals, are genetically predetermined is contentious and potentially harmful. It can oversimplify complex human traits and behaviours, ignoring the significant role of environmental, cultural, and personal factors.
ALPHA BIAS: The XYY theory exhibits an alpha bias, which can be justified by the prevalence of aggressive acts primarily among males. Additionally, it's important to note that females cannot inherit two Y chromosomes, further supporting the focus on males in this context.
THE ROLE OF GENETIC FACTORS IN AGGRESSION: MONOAMINE OXIDASE A (MAOA)
“In August 2006, news broke that a “warrior” gene was linked to risk-taking, aggression, and criminality in Māori. The story sparked widespread controversy in New Zealand—with journalists, politicians, academics, scientists, and the general community scrambling to express their views publicly.”
The MAOA gene encodes the enzyme monoamine oxidase A, a crucial component in the body's chemical processes. This enzyme belongs to a group that specialises in breaking down a molecule known as monoamines through oxidation, a chemical reaction essential for various bodily functions. Monoamine oxidase A specifically targets certain monoamines that function as neurotransmitters, substances that facilitate signal transmission between nerve cells in the brain. These neurotransmitters, which include serotonin, epinephrine, norepinephrine, and dopamine, are broken down when their signalling role is complete.
MUTATIONS: Mutations in the MAOA gene lead to a deficiency of monoamine oxidase A, an enzyme crucial for normal brain function. This condition predominantly affects males and is characterised by mild intellectual disabilities along with a range of behavioural issues, particularly aggressive and violent outbursts. Exacerbating these symptoms in response to certain foods points towards a dietary influence on the condition.
The deficiency stems from a reduction in monoamine oxidase A activity due to mutations in the MAOA gene. This reduction impairs the normal breakdown of neurotransmitters such as serotonin, leading to their build-up in the brain. Understanding how this build-up results in monoamine oxidase A deficiency symptoms is an active area of research. Research also indicates that decreased monoamine oxidase A activity could impact the development of certain brain regions. For instance, the size of the amygdala, a region associated with processing fear and the fight-or-flight response, might be reduced. Such developmental alterations could contribute to the intellectual and behavioural difficulties experienced by those with this condition. Moreover, the buildup of tyramine in various foods exacerbates symptoms, shedding light on why certain diets might worsen the condition.
Scientists increasingly believe that an excess of specific neurotransmitters, especially serotonin and norepinephrine, may disrupt impulse control, potentially triggering the aggressive behaviours seen in affected individuals.
Neurotransmitters:
Serotonin: Low serotonin levels are often associated with increased aggression. Serotonin helps regulate mood and behaviour, and its deficiency can lead to increased impulsivity and aggression.
Dopamine: This neurotransmitter is linked to reward and motivation systems in the brain. Some studies suggest that dysregulation in dopamine pathways can be associated with increased aggression, particularly impulsive or reward-seeking aggressive behaviours.
Norepinephrine (Noradrenaline): Norepinephrine, involved in the body's fight-or-flight response, can also play a role in aggression, especially in response to stress or threat.
VARIANTS OF MAOA: The MAOA gene has different variants, typically categorised based on their level of activity: high-activity and low-activity. The low-activity variant (MAOA-L) has been associated with aggressive behaviour in some studies, which led to its nickname as the "warrior gene." This association is based on the hypothesis that lower levels of MAOA activity might result in higher neurotransmitters like serotonin, potentially leading to increased impulsivity or aggression.
OTHER VARIATIONS
Variations in the MAOA gene can lead to various disorders. Deletions in the gene may cause developmental delays, weak muscle tone, and repetitive hand movements. When these deletions also affect the MAOB and NDP genes, more severe conditions like Norrie disease, which causes blindness and developmental issues, as well as seizures and autism spectrum disorders, can result.
One key study area is the MAOA-uVNTR polymorphism in the gene's promoter region. The number of repeated DNA building blocks in this region varies, impacting the gene's activity. Alleles with 3.5 or four repeats are considered high-activity, leading to more monoamine oxidase A protein production than low-activity alleles with two or three repeats. The effects of five repeats remain unclear.
Low-activity alleles are associated with increased aggression, particularly in males, and the risk may be higher for individuals with a history of childhood abuse. Conversely, high-activity alleles may raise the risk of panic disorder in females.
Research on the MAOA gene, including its polymorphisms, extends to conditions like depression, bipolar disorder, alcohol and drug addiction, and more. Scientists are keen to understand how these genetic factors interact with environmental influences, such as childhood abuse, in these disorders.
ALPHA BIASED: The MAOA genes are situated on the X chromosome, which has significant implications for their inheritance. Males with one X and Y chromosome inherit only a single copy of the MAOA gene from their mother. On the other hand, females, who have two X chromosomes, typically do not exhibit symptoms associated with MAOA-related conditions because they have the potential to inherit a functional copy of the gene from either their maternal or paternal line, which can compensate for any genetic abnormalities on the other X chromosome. This dual inheritance in females provides a degree of genetic redundancy that can help mitigate the impact of MAOA gene mutations.
MORE INFORMATION
In summary, monoamine oxidase A deficiency, caused by MAOA gene mutations, presents a complex interplay of genetics, brain chemistry, and dietary factors, highlighting the multifaceted nature of this condition.
The MAO-A gene produces Monoamine Oxidase, a chemical/enzyme involved in the breakdown of the neurotransmitters serotonin, dopamine and noradrenalin in synapses. Consider MAOA-L as the Rubbish, man; it takes the trash away from your brain. It helps remove the waste and keeps your mental streets clean."
Monoamine oxidases (MAOs) are enzymes responsible for breaking down the neurotransmitters—serotonin, dopamine, and adrenalin—and are therefore capable of affecting mood. Indeed, MAO inhibitors (e.g. moclobemide) can effectively treat symptoms of depression and tobacco dependence.
Humans have various forms of the gene, resulting in different levels of enzymatic activity. People with the low-activity form (MAOA-L) produce less of the enzyme, while the high-activity form (MAOA-H) produces more. Low sensitivity is equivalent to low activity.
It is thought that too little of the MAO-A gene leads to the brain being flooded with too much serotonin, noradrenaline and dopamine, eventually lowering sensitivity to these neurotransmitters.
Serotonin is a neurotransmitter. It can be found in the central nervous system (CNS), which has various functions, including mood regulation”.Serotonin has effects all over the body. Low levels of serotonin in the brain can result in impulsive behaviour, aggression, overeating, depression, alcohol abuse and violent suicide.
The activity of MAO enzymes can vary among individuals and is influenced by inherited genetic factors. Understanding the genetic variability of MAO activity and the linkage to drug response traits should assist in the design of more effective treatment options for certain clinical disorders.
The MAOA genes are located on the X chromosome; thus, males inherit only a single maternal copy. Females usually do not show symptoms as they have two copies of the X chromosome. They can inherit from maternal and paternal lines.
APFC RESEARCH
Moffitt et al. Study on Gene-Environment Interaction (2002): Moffitt et al. Study on Gene-Environment Interaction (2002): In 2002, Terrie Moffitt and colleagues conducted a comprehensive longitudinal study involving 422 males in New Zealand. The study focused on various aspects, including their histories of abuse, criminal convictions, tendencies towards violence, and symptoms indicative of antisocial personality disorder. The findings of this landmark study revealed a significant connection between the Monoamine Oxidase A (MAOA) gene and the likelihood of being convicted for a violent crime. However, this association was notably present only in participants who had also experienced childhood abuse. This suggests that the interaction between genetic factors, such as the MAOA gene, and environmental influences, like childhood abuse, plays a crucial role in the development of violent criminal behaviour.
The implication of these findings is profound, suggesting a complex interplay between genetic predispositions and environmental factors in shaping behaviour. Specifically, the study highlights how the presence of the MAOA gene alone may not be a definitive predictor of violent criminal behaviour. Instead, it's the combination of this genetic factor with adverse environmental influences, such as childhood abuse, that significantly heightens the risk of engaging in violent acts.
This research adds to the growing body of evidence that supports a multifactorial approach to understanding aggressive behaviour. It underscores the importance of considering both genetic and environmental elements in the assessment and potential intervention strategies for individuals at risk of violent criminal behaviour.
Mouse Studies on MAOA Function: Numerous mouse Studies on MAOA Function: Extensive research involving mice has played a pivotal role in elucidating the function of MAOA. Mice genetically modified to lack the MAOA gene (MAOA knockout mice) exhibited heightened aggressive behaviour, altered stress responses, and notable abnormalities in brain chemistry, particularly concerning neurotransmitters such as serotonin. These findings provide conclusive evidence supporting MAOA's role in regulating behaviours associated with neurotransmitter metabolism.
However, it's important to note that mouse aggression may not be directly comparable to human aggression. For instance, mice don't engage in premeditated acts of violence against their species, as humans sometimes do.
Caspi et al. Longitudinal Study (2002):
Avshalom Caspi and his colleagues conducted a longitudinal study in 2002, similar to Moffitt's research, highlighting the interplay between the MAOA gene and environmental factors. Their study revealed that children possessing the low-activity variant of the MAOA gene and who experienced mistreatment during their upbringing were at a higher risk of developing conduct problems and antisocial personality disorder. This further underscores the significance of gene-environment interactions in developing behavioural and personality traits.Godar et al. Study on MAOA and Stress Resilience (2016): This research explored how the high-activity variant of MAOA (MAOA-H) could be associated with better coping and resilience under stress. The study suggested that individuals with the MAOA-H variant might be less likely to develop stress-related psychopathology.
Foley et al. Study on MAOA and Impulsivity (2004): This study linked the low-activity variant of MAOA with impulsivity and higher risk-taking behaviours. It provided insights into how genetic variations might influence personality traits and susceptibility to certain disorders.
Buckholtz and Meyer-Lindenberg Study on MAOA and Brain Structure (2008): This study used neuroimaging to show that individuals with the MAOA-L variant had differences in brain structure and function, particularly in areas related to emotion and social processing. This provided a biological basis for the behavioural differences associated with MAOA variants.
Kim-Cohen et al. Study (2006): This study extended the findings of Caspi and Moffitt by examining the interaction between the MAOA gene and childhood maltreatment in predicting mental health outcomes. The study found that the low-activity MAOA genotype increased the risk of developing antisocial problems in maltreated children but not in non-maltreated children.
McDermott et al. Study on Aggression (2009): This research explored the relationship between MAOA and aggression, finding that individuals with the low-activity form of MAOA were more likely to respond aggressively when provoked. This study helped us understand the situational aspects of aggression related to genetic predispositions.
Widom and Brzustowicz Study (2006): This study examined adults with histories of childhood abuse and neglect, revealing that those with the low-activity MAOA variant were more likely to develop antisocial personality disorder. It highlighted the importance of considering genetic susceptibility and environmental stressors in understanding behavioural outcomes.
Frazzetto et al. Study on Gene-Environment Interaction (2007): This study looked at the interaction between stressful life events and the MAOA gene about antisocial behaviour. It supported the notion that the risk associated with the low-activity MAOA variant is most pronounced in individuals who have experienced significant life stressors.
Alia-Klein et al. Study on Brain Function (2008): Using neuroimaging, this study investigated the brain function of individuals with different MAOA variants. It found that those with the low-activity variant showed heightened brain response in regions associated with emotional regulation, suggesting a biological basis for emotional and behavioural differences.
Beaver et al. Study on Delinquent Peer Association (2013): This research explored how genetic predispositions interact with social environments, particularly regarding delinquent peer associations. The study concluded that individuals with the low-activity MAOA gene were more susceptible to the influence of delinquent peers.
Joseph Newman and his team conducted a notable study exploring the link between the MAOA gene, often called the "warrior gene," and aggressive behaviour. The study involved participants genotyped for the MAOA gene. In a lab setting, these individuals were provoked and allowed to retaliate against their provoker by choosing how much hot chilli sauce to administer, knowing they disliked spicy food. The participants were categorised into high-activity and low-activity variants based on their MAOA genotype. The key finding was that those with the low-activity variant of the MAOA gene tended to choose more chilli sauce, suggesting a greater propensity for aggression. This tendency was especially marked in participants with a history of childhood adversity, aligning with the gene-environment interaction model. The study implies that genetics can predispose individuals to certain behaviours, but environmental factors significantly influence the expression of these behaviours.
The research findings about genetic influences on aggression and punishment behaviour question the idea that humans always punish wrongdoers purely for the benefit of the group. Instead, these findings support theories suggesting that in a population, there can be a variety of strategies for punishing. This means that some individuals may be punished more than others, and there could be an underlying evolutionary reason for this diversity in punishment behaviour.
Despite its contributions, the study has criticisms, including:
MUNDANE REALISM: The study's setting, where participants administer hot sauce to a supposed partner in a computer-mediated interaction, may not accurately reflect real-world aggression. Actual aggressive encounters often involve more direct interaction and are influenced by various emotional and situational factors. This limitation suggests the study might lack mundane realism, as the experimental setup does not entirely mirror real-life aggression scenarios.
OPERATIONALISATION: The operational definition of aggression in this study, where aggression is measured by the willingness to make someone consume hot sauce, may not encompass the full spectrum of aggressive behaviours seen in everyday life, such as physical or verbal abuse.
Ethical Considerations: While the study was designed with ethical concerns (e.g., simulated hot sauce punishment, no physical harm), it did involve deception, making participants believe they were interacting with a real person. This is a critical ethical aspect, as deception in psychological research requires careful consideration, ethical approval, and thorough debriefing.
.ANALYSIS
NATURE VERSUS NURTURE: Many individuals with these MAOA Lmarkers do not display aggressive behaviour. Research indicates that merely possessing the low-activity version of the MAOA gene does not guarantee a predisposition to a life of aggression. Instead, studies suggest that aggressive tendencies are more likely to manifest in individuals who have both the low-activity MAOA gene and a history of abusive upbringing, as demonstrated by extensive research in this field. Human behaviour, including aggression, results from intricate interactions between genetics, the environment, and personal choices. It's important to note that even if someone possesses a genetic predisposition, such as a low-activity variant of the MAOA gene, it does not guarantee a predetermined outcome. Understanding genetic predispositions can positively impact early intervention and prevention strategies. Suppose an individual is known to have genetic factors that increase the risk of aggressive behaviour. In that case, proactive measures like counselling, education, and creating a positive environment can be implemented to reduce these risks. In this way, genetics can inform strategies to mitigate the potential for aggressive behaviour.
The interplay between nature and nurture in determining aggression is complex, similar to the stress-diathesis model. This model posits that while genetic predispositions (diatheses) may exist, environmental stressors are often necessary to trigger the manifestation of a particular behaviour or psychological condition. In the case of aggression, both genetic capacity and environmental factors interact to shape behaviour.
NON EXPERIMENTS: Overall, research in the MAOA area is often non-experimental. Experimental studies are rare because they face ethical constraints, preventing direct measurement of aggression in controlled laboratory settings.
In summary, while evidence links the low-activity MAOA gene variant to aggression, caution is necessary when interpreting these findings. Much of the research does not show a direct causal link, which limits the ability for certainty. Furthermore, some studies, like the Dutch study mentioned, struggle to disentangle the influences of genetics (nature) from environmental factors (nurture), making it challenging to attribute aggressive behaviour solely to the MAOA-L genotype.
As a result, research on the Monoamine Oxidase A (MAOA) gene has yielded mixed and often conflicting results, with many studies facing challenges in replication.
DETANGLING THE VARAIBLES: A key area of focus is a specific allele (variant) of the MAOA gene, which, when combined with certain life experiences like childhood maltreatment, may impact the development of crucial brain areas, such as the amygdala. This interaction can potentially increase the likelihood of certain behavioural responses. However, pinpointing the exact nature, duration, and timing of abuse that influences brain development remains a significant challenge. Determining the age at which individuals or their brains are most vulnerable to such impacts is also complex.
WHICH NEUROTRANSMITTER: The MAOA gene variant is linked to a less efficient breakdown of several neurotransmitters, including serotonin, norepinephrine, and dopamine. However, the theory does not definitively specify which neurotransmitters are most critical in contributing to aggression. Many studies on MAOA have focused on serotonin due to its known role in mood and social behaviour, this focus may not fully capture the complexity of the gene's influence. The emphasis on serotonin could be due to the extensive research linking serotonin imbalances to various behavioural and psychological disorders, including those involving aggression.
HOW DOES IT CAUSE AGGRESSION? More research is needed to work out how the mutation causes aggression. For example, subjects with psychopathic tendencies often exhibit the low-activity version of the MAOA gene, and studies using functional magnetic resonance imaging (fMRI) have revealed that they tend to have smaller amygdalas. Researchers believe that this gene may contribute to issues during fetal development, where the fetus's brain is exposed to an excessive amount of monoamines that it cannot efficiently clear. This overexposure can lead to abnormal amygdala development, a brain region that regulates emotions such as fear and anger. Notably, the amygdala is strongly associated with aggressive behaviour,
OTHER NEUROTRANSMITTERS: The roles of norepinephrine and dopamine are also significant. Norepinephrine is involved in the body's fight-or-flight response and can influence impulsivity, a component of aggressive behaviour. Dopamine, on the other hand, is crucial in reward and motivation systems and has been linked to aggressive behaviour in various studies.
The challenge with the MAOA-L theory is that it doesn't delineate the relative importance of these neurotransmitters in causing aggression. It's a complex interaction where all three neurotransmitters could play a role, and environmental factors like childhood trauma further influence their effects.
SEROTONIN: Asserting that underactive serotonin circuits are solely responsible for aggression is akin to attributing the sound of an entire orchestra to a single instrument. Aggression is a multifaceted behaviour influenced by an intricate network of neurological, genetic, and environmental factors. Just as focusing on one instrument ignores the contributions of the others in an orchestra, focusing solely on serotonin disregards the roles of other neurotransmitters, brain structures, genetic variations, and life experiences that collectively shape aggressive behaviour. Understanding aggression requires a multifaceted approach that includes genetic, environmental, psychological, and cultural factors.
Research over the years has linked underactive serotonin circuits to various conditions, suggesting that serotonin's role is extensive and multifaceted. For instance, articles have associated serotonin imbalances with migraines (July 24, 1996), extreme shyness (May 18, 1999), obsessive-compulsive disorder (February 16, 1997), anxiety and pessimism (November 29, 1996), and restless leg syndrome (April 10, 1996). This wide range of conditions attributed to serotonin suggests that its influence extends far beyond a single behavioural aspect, like aggression. This raises the question of whether serotonin's role in aggression would differ, given its complex network of influence across multiple brain regions.
Understanding serotonin's role in aggression is further complicated by at least sixteen different types of serotonin receptors, each responding distinctly to serotonin. The extent to which neurons prefer serotonin and the implications of this preference remain largely unexplored. Moreover, serotonin-producing neurons in the brainstem has projections extending to various functionally diverse brain regions. These include the amygdala, hypothalamus, hippocampus, cerebellum, and areas within the temporal and prefrontal regions of the cerebral cortex. Given this broad range of influence, it would be surprising if abnormalities in the serotonin system had a specific, uniform impact on aggression. Consequently, the scientific community is still far from understanding how serotonin influences aggression. It is suggested that serotonin's impact on aggressive behaviour is multifaceted, extending beyond the simplistic notion of low serotonin levels.
REDUCTIONISM: it is crucial to understand that genetic factors do not solely determine aggression. Psychological theories like learning theory suggest that experiences shape behaviour, particularly reinforcement and punishment: Social Learning Theory and its emphasis on observational learning. Evolutionary theory (which considers aggression as potentially having an adaptive value in terms of survival and reproduction) offers valuable insights. Additionally, aggression can be influenced by a range of biological and environmental factors.
Simplifying aggression to a single genetic factor ignores human behaviour's complexity and the many influences that shape it. The neuroanatomy of aggressive behaviour is complex and involves at least 38 different brain regions. Research has particularly focused on the role of neurotransmitters, especially serotonin, and areas within the limbic system.
Additionally, observations of human subjects with various head injuries have shown patterns of aggressive behaviour, but these patterns are neither neat nor localised. This lack of specificity challenges the idea of a clearly defined physical pathway for aggression. Thus, pinpointing a specific 'aggression centre' in the brain is challenging due to the intricate interplay of various brain regions and neural pathways involved in aggressive behaviours.
LIMITED GENERALISABILITY: Cultural bias in research, particularly in genetics and behaviour, refers to the tendency to focus on certain cultures, often Western societies, while neglecting others. This bias can lead to a narrow understanding of human behaviour that may not be applicable across different cultural contexts. In the case of the MAOA gene research, focusing predominantly on Maori and Western societies can have several implications: The findings might not be generalisable to other cultural groups if research primarily focuses on specific cultures like Maoris and Western societies. This limitation can lead to a skewed understanding of the genetic factors influencing behaviour, as cultural, environmental, and social contexts can significantly impact how genetic predispositions are expressed.
The MAO-A gene, known to exhibit variations among different ethnic groups, has garnered significant attention due to its socially sensitive implications. For instance, some findings have suggested a predisposition to violence among Maori individuals.
Firstly, the publication of these findings may lead to social stigmatisation, particularly among Maori females who carry the gene. This could potentially result in negative stereotypes and biases against them. Secondly, the research implies a genetic propensity for the MAO-A gene among Maoris. However, it's crucial to note that the presence of this gene in certain populations doesn't exclusively render them susceptible to aggression. Aggressiveness can manifest in any population if specific conditions, such as war, lawlessness, or anarchy, lead to a bottleneck effect in the gene's prevalence. For example, in cases where crime is rampant, women might sexually select aggressive partners, causing a bottleneck effect on the MAO-A gene. In this context, the publication of these findings can be interpreted as a reflection of natural selection that impacts all populations in conflict. In other words,
Besides, critics of the research have raised valid concerns, including using small sample sizes and extrapolating results from non-Maori studies to the Maori population. Additionally, ideological objections and apprehensions about the premature release of these findings have been noted. These criticisms highlight the importance of conducting thorough and culturally sensitive research and exercising caution when communicating potentially sensitive genetic information.
DETERMINISM: This perspective challenges conventional ideas of free will and personal responsibility. Legal and ethical systems typically assume that individuals have some control over their actions, even when biological factors influence behaviour. While genetics may play a role, they usually do not completely negate personal responsibility. In certain legal cases, genetic and psychological evidence have been introduced to argue for reduced responsibility or mitigate sentencing. In specific legal cases, evidence from genetic and psychological sources has been presented to advocate for reduced culpability or lessen the severity of sentencing.
A concrete illustration from a 2009 criminal trial in the United States vividly showcases the practical consequences of having this gene. . In this particular case, the defence crafted an argument based on the conjunction of the "warrior gene" and a documented history of child abuse. As a result, the outcome diverged from a first-degree murder conviction and the death penalty, leading to a 32-year prison sentence for the defendant. This example underscores the profound ramifications of this theory, extending its influence across various facets of society. It pertains not only to political decisions concerning criminal sentencing but also to the intricate ethical debates surrounding topics such as genetic screening and sterilisation.
However, this practice raises significant concerns regarding the principle of equitable treatment within the legal framework and the potential danger of genetic determinism being utilised as an exoneration for one's actions. All people are the result of a complex jigsaw of nature and nurture.
GENDER BIAS: Research that primarily focuses on males may unintentionally reinforce gender stereotypes, suggesting that aggression is an inherently male trait. It's important to note that in the context of the Alpha Theory debate, male-aggressive acts significantly outnumber female-aggressive acts, indicating a notable gender difference in aggressive behaviour.
Critics also emphasize that the preference for male subjects in genetic research is partly due to the simplicity of studying individuals with a single X chromosome. This approach facilitates the observation and analysis of the effects of specific genetic variations, such as those in the MAOA gene.
Moreover, statistically, females are less likely to inherit two faulty X chromosomes carrying the low-activity MAOA gene. At the same time, males only need to inherit one for a similar effect. It's essential to consider that if these genetic bottlenecks are linked to conflicts, females might express the low-activity version of the MAOA gene more prominently.
However, the underrepresentation of females in MAOA research can result in a biased understanding of how these genetic factors influence behaviour across genders.
ne symmetrical structure of two halves within the vertebrate brain, between the neocortex and the midbrain. Some of its functions are relaying sensory and motor signals to the neocortex and regulating consciousness, sleep, and alertness.
