Behavioural issues including violence, aggression and antisocial behaviours cannot be explained by one causative factor; they are not dictated by genetics or environmental issues alone, but rather a complex interplay of them both. The gene x environment interaction can be defined as the expression of a phenotypic characteristic that a person may have due to a genotypic variation, which allows it to be expressed or muted depending on the environmental conditions (Moffit, 2005; Walsh, 2002). Here the square shapes represent the environment either high or low risk, the black circles represent the presence of a risk allele in the individual’s genetics e.g. presence of the MAOA gene. The dashed red line extending to the triangle containing the P, indicates that a low environmental risk, plus the addition of the risk allele equates to a non-significant presentation of the phenotypic characteristics. In the latter box, the parallel is seen, as a high environmental risk plus the presence of the same risk allele is equivalent to a high significant chance of expression of phenotypic characteristics. Thus, the diagram depicts that the expression of ones’ phenotypic traits is based on both the genetics and the environmental they live in. The following equation can be used to further highlight this relationship:
P = G +E + GE
In which P represents the phenotype expressed, which equals to G (genetics) + E (environment) + GE (genetics x environment). Together they will all affect the characteristics of the individual (Baye, 2011).
In humans, the gene x environment relationship is multifaceted, and additional issues need to be considered when genetics are passed down through family and generations, as expression of genes can be amplified or diminished. This can cause severe genetic variation as well as high mutation rates (Gluckman, Hanson & Beedle, 2007) The physical environment a person resides can have an outstanding effect on their overall health and behaviour including mood, personality, disorders and language. Possibly the first instance in which the gene x environment debate began was between R.A Fisher, a statistical geneticist and Lancelot Hogben, an embryologist, in which they both took very different routes to explain the correlation between the two. Fisher approached the discussion by following in the footsteps of Mendelian Laws and arguing the laws of inheritance and variation within man. Hogben vastly disagreed with Fisher, in that he gave credence to the idea that environmental aspects outweighed biological concepts such as social and economical traits (Tabery, 2008).
MAOA X ENVIRONMENT
Countless studies have hypothesised that males with low activity MAOA and who have suffered from childhood maltreatment were significantly more likely to engage in aggression than those with high activity MAOA and/or a stable childhood. Therefore, it has been suggested that the aggression of man is heightened due to the interaction between genetic markers and the environment. The gene x environment interaction was first discussed in literature by Caspi et al, in which maltreated children were observed who possessed the MAOA mutation. It was seen that those who had the high activity MAOA gene and had been mistreated as children were less likely to victimise others compared to those who possessed the low activity gene due to lower effectiveness of neurotransmitter degradation. (Caspi et al., 2002). Follow up studies, also confirmed the positive reaction between the two variables (Foley et al., 2004; Kim-Cohen et al., 2006). Conversely, it is possible that violence may serve as a defence mechanism triggered in situations with adverse environmental conditions, with or without possession of the high or low activity MAOA. This would seek to explain how individuals do not act negatively until placed in a stressful and difficult situation regardless of their genotypes (Manuck et al., 2000). The MAOA gene does not predispose individuals to be maltreated, but instead provided a resilience to those who had been maltreated and possessed the MAOA-H gene, but not the MAOA-L gene. Therefore, it can be insinuated that those who have low activity of MAOA are more sensitive to maltreatment (Baum, 2011), however some environments can prove ‘less challenging’ for some therefore criminal outcomes can be reduced or avoided. This focus on the risk alleles and sensitive to the environment has been termed the diathesis-stress perspective and has been used to explain vulnerability to environmental stressors. Conversely, Belsky (2007) argued that these alleles could prove to be advantageous to society and that some individuals were programmed to be sensitive for ‘better or for worse’ (Belsky et al., 2007).
A fairly recent model was explored by Ferguson, in which he explained the significant relationship between genetics and various environmental factors. This is referred as the Catalyst model. In essence, the model explains the suggestive interaction between genetics i.e. MAOA gene, and adverse environmental elements e.g. family violence to potentially produce a violent and antisocial personality. The model theorises that humans have an innate “impulse control device’ mechanism, in which aggressive and violent reactions are inhibited through self -control. However, if the mechanism is ineffective the actual behaviours produced can be detrimental and violence can be predicted (Ferguson, 2008; Lorenz, 1963). Stress relief if is an important concept surrounding the model, as aggression can be viewed as a factor of that which needs to be expressed in some individuals to allow catharsis. People with high risk personalities and low impulse control will seek violent outcomes, whilst people with low risk will filter out aggressive traits and seek a more appropriate and calm outcome (Ferguson & Beaver, 2009). Therefore, the relationship between genes and the environment is very much shared and equally to do with effective brain functioning and environmental frustrations.
On the contrary, many studies have also found no reasonable interaction between the MAOA genotype and childhood dilemmas, as predictor of antisocial violence in a large sample (n=1002) (Prichard et al., 2008). When determining the relationship between levels of trauma experienced in childhood and MAOA deficiency, it was highlighted in one study that children with severe traumatic experiences showed displays of high aggression regardless of MAOA genotype. A limitation to the study, was that aggression ratings were based on single assessment from one contact e.g. teachers, so it cannot be determined how the level of aggressiveness was rated among varying individuals (Weder et al., 2009).
Multiple risk factor hypothesis
A thirty-year longitudinal study by Ferguson, further examined the G x E interaction examining multiple risk factors e.g. maternal smoking, family deprivation, low IQ, childhood maltreatment. The results conclusively suggested that the combination of both was a precursor to violence (Ferguson et al., 2012). Following on from this, it is plausible that maltreatment during informative years may not be the only environmental stressor which can produce aggressive traits. Specifically, Wakschlag et al, found a reportable G x E interaction between MAOA and maternal smokers (Wakschlag et al., 2010). In females with both negative life experiences as children and anxiety disorder, it was suggested that 39 (of 42) females experienced lower MAOA activity and higher levels of depression and panic disorder, than their healthy counterparts (Domschke et al., 2012). Although some studies have touched upon the interaction between multifaceted gene x environment aspects, many have ignored this and focused solely on childhood maltreatment. Further extensive research should be replicated to further understand the relationship between two or more causative factors, as this has not been largely explored.