The genetic explanation of aggression suggests that it is influenced through our genes, and that such behaviour is therefore inherited.
It is thought that aggression is due to a defective gene that is inherited by following generations. One possible gene is the Monoamine Oxidase A gene, which produces Monoamine Oxidase A enzyme that breaks down neurotransmitters associated with aggression. It is thought that a build-up of serotonin and dopamine can cause an individual to act aggressively to stress in the fight or flight response. There are two forms of the gene, MAOA-H (produces a high level of the enzyme) and MAOA-L (produces a low amount of the enzyme). The presence of the MAOA-L gene is related to an increase likelihood of aggression
Research to support the role of the MAOA gene comes from CASES ET AL who disabled the gene in the X chromosome of mice. As no enzyme was produced, the levels of serotonin and dopamine in the brain increased. It was observed that males became highly aggressive (females were unaffected) and by restoring the function of the gene, their behaviour retuned back to normal. This suggests that the gene does in fact increase aggression when not working, supporting the role of genetic factors in aggressive behaviour. However, the research cannot account for aggression in females as they also carry the X chromosome, which implies that other extraneous variables may be interacting with the gene to cause aggression only to occur in the male mice. This is a problem, as we cannot fully conclude that the gene was the sole cause of aggression and therefore it does not fully support the genetic explanation.
One weakness to the theory of the MAOA gene comes from CASPI ET AL, who found that low levels of the enzyme due to the MAOA-L gene did increase aggression but only where individuals had experienced some form of maltreatment during childhood. This implies that aggression may not be purely down to genes, but also the role of an individual’s environment; thus demonstrating the interplay of the external environment and internal genetics.
Another supportive piece of evidence comes from BRUNNER who discovered the defective MAOA gene in a Dutch family with a history of male violence. This therefore suggests that the defective gene does play a role in human aggression as it shows a correlation between aggression and the defective gene. However, as this is only 1 case it is hard to generalise the findings to a wider population, implying that the evidence may be less reliable. The findings also lack ecological validity as this was only observed in a Dutch family and may not be the general trend for everyone. This is a problem as the evidence cannot fully support the theory that genetic factors influence aggression, and implies that more research is needed for a conclusive explanation.
The role of genetic factors in aggression can be tested in twin studies. Genes are identical in sets of monozygotic twins but are different between sets of DZ twins, meaning that if MZ twins are more alike in terms of aggression than DZ twins are, this similarity can be attributed to genetics.
CANTER found a correlation of 0.14 for MZ twins who were raised together. MILES did a meta-analysis and believed heritability plats a 50% roles. RHEE however suggested that there is a huge difference in methodology. They found that aggression levels were lower in studies using self-reports compared to those who reported.
This is a problem as it is a reductionist approach to break down a complex behaviour such as aggression into a simple genetic cause and effect. This suggests the explanation less reliable and implies that a holistic approach is needed.
Adoption studies can help determine the relative contributions of environment and heredity in aggression. Positive correlation between adopted children and their biological parents implies a genetic effect, while positive correlation between the children and their adoptive parents implies an environmental effect. A study of over 14,000 adoptions in Denmark found that a significant number of adopted boys with criminal convictions has biological fathers with criminal convictions, demonstrating a genetic effect – HUTCHINGS AND MEDNICK.
The argument that aggressive predisposition can be inherited has been used as a defence for many criminals. They argue that as their family had a history of violence, they too have inherited this genetic tendency to be so and therefore they should not be held accountable for the crimes that they commit. However, this argument is deterministic as it assumes that everyone who inherited the genetic potential to be aggressive will be so. It does not take into account individual differences of exerting free will over aggressive behaviour, which is a problem as this may lead to implications within the legal system regarding whether or not we can hold a person responsible for their aggressive actions, due to pre-programed genetic information. This is therefore a socially sensitive issue.
Another piece of research to supports the link between genetic factors and aggression comes from LAGERSPERTZ, who bred 25 generations of mice with the most aggressive bred together and least aggressive bred together. This resulted in two different strains of mice; super-aggressive and docile therefore demonstrating how aggressive behaviour is passed down through genetics and supports the role that genes play in influencing such behaviour.
Studies such as this one on non-human animals have an important role in helping us understand aggression in humans, as genes can be manipulated and the effects of these manipulations can be observed. This allows us to precisely identify the role of specific genes. However, commonly-used animals such as mice have a different genome and physiology to humans, so the effects of genes may be different. The use of animals in such studies can also be considered unethical
Another issue that this particular piece of research raises is the problem of defining aggression as it can be displayed in many forms. The researcher may conclude the mice behaviour as “aggressive” simply because this is their personal opinion of what aggressive behaviour consists of, or because they want to produce the dependent variable that they set out to measure in the research, thus showing observer bias. The mice may simply being showing dominant behaviour, which may be a completely separate behaviour to aggression.
This research has an important real-world application. There have been suggestions that if people’s genes predispose them towards aggressive behaviour, genetic engineering should be used to change their genes and reduce this risk. Some have even suggested more extreme measures to prevent the heritability of such genes. However the labelling of an individual as dangerous based on their genetic inheritance poses serious ethical questions.
Many of the studies in this area had focused on individuals convicted of violent crime. However, these results only represent a small minority of those who are regularly involved in aggressive behaviour, as many violent attacks do not results in a conviction. These individuals may also not be habitual offenders; they may usually calm people who were designated as violent for a one-time offence. This may explain why so many studies have found little or no evidence of heritability for violence