Environment, Genetic Variance And Aggression

What can be said for human civilisation

The ongoing battle between genetics and environmental stressors continues, but this theory is outdated and the evidence concludes that nature and nurture can equally share a role in human behaviour. Granted, genetics does play a significant part in the creation of aggression, as seen from an extensive amount of twin and adoption studies. For example, McGuffin and Gottesman who found that the resulting aggressive rate for MZ twins was 87%, whilst for DZ twins was 72% (McGuffin & Gottesman,1985). Thus, clearly suggesting that genetic variance plays an important role. Still if this was true, what can be said of the remaining 13%, as if genetics was the sole cause, it would be 100% of the genes that accord for aggression. This begs the question that the latter 13% must account for some degree of environmental influence.

Extreme violence and aggression is prevalent in society; however, it can be understood that is mostly catalysed from a place of stress and strain on man (Ferguson, 2008). The number of sociopaths and unprovoked spurs of violence are fairly minute compared to provoked violence. The understanding of evolution, such as Darwin’s theory of violence from primates to man, is essential to fully comprehend the behavioural genetics behind innate aggression (Baschetti, 2008; Plokin, 1995). Humans have evolved since the times of ‘hunters’ and ‘gatherers’ into kind and compassionate beings who do have impulse control and can generally filter out negative thoughts and actions. Therefore, high-risk violence is less prevalent in the majority of man.

This review sought to understand the criminal heritability of man through various gene-gene interactions and gene-environment interactions to explain behavioural dysfunctions. Through contextual and clinical understanding of the MAOA genotype many impulsive and severe aggressive traits can be explained which are attributed to both the low expressing MAOA and the childhood maltreatment, but not in carriers of the MAOA-H, who were seen to be less sensitive or vulnerable to the effects of the gene (Caspi et al., 2002; Foley et al., 2004; Fineberg et al.,2014; (Shih, Chen and Ridd, 1999).

The contribution of the environmental element, can therefore increase the risk for violent outcomes or in certain individuals provide a resilience. Discordantly, there have been two substantial studies which have failed to replicate the findings. A clinical sample of males were examined, with a lifetime portrayal of substance abuse and conduct disorder, however no corresponding MAOA genotype was found.

Although there was evidence of childhood maltreatment and subsequent antisocial behaviour, the role of the MAOA-u-VNTR could not be accounted for. This may suggest the advantage that environmental stressors has over genetic variance when childhood adversity is experienced (Haberstick et al., 2005; Young et al., 2006). Previously, many studies have also focused on certain age groups to test the effects of the genotype, mainly from birth to twelve years (Caspi et al., 2002), whilst studies who have focused on later onset delinquency have produced different results (Haberstick et al., 2005; Loeber & Hay, 1997; Tuvblad & Baker ,2011).

This may infer that the effect of the MAOA genotype on childhood maltreatment is age dependant. One of the biggest points to note regarding gene expression, is that manifestation of aggression cannot be put down to one single gene (Rutter, 2006; Ferguson & Beaver, 2009). Multiple gene effects or polygenic effects are more likely to be associated with the output of behaviours and personalities. Therefore, the interactions between the dopaminergic, serotoninergic and the MAOA pathway will all influence one another to create the desired effect. Similarly, the variance of one gene can overpower that of another, creating higher gene expression which is seen in some studies, but that does not necessarily mean that gene codes for high risk behaviours (Watts & McNulty, 2014; Boutwell et al., 2014; Butovskaya et al., 2013; Fernàndez-Castillo & Cormand, 2016)

This can particularly be seen between dopamine pathways, specifically DRD2 and DRD4 genes as they increase reward seeking and risky behaviours. Moving forward, it will be openly necessary to find the causation that the dopaminergic genes have on various other pathways, and to observe these interactions on participants possessing the correct alleles (Boutwell et al., 2014). As previously mentioned, the DRD2 gene has specifically been linked to a range of aggressive traits, from psychopathy (Wu & Barnes,2013) to violent victimisation (Vaske, Wright & Beaver, 2011).

However, this relationship has not been replicated an extensive amount, potentially leading to inaccuracy of results. In regard to serotonin, all-encompassing evidence has shown the association of low expressing serotonin (5-HTTLPR) and impulsive aggression. There are inconsistencies which are reported widely amongst literature including the discrepancies between the receptors causing decreased aggression in schizophrenics (Cleare and Bond, 2000). However, counteractive results were seen in anti-aggressive mice (Miczek and Fish, 2006). Nevertheless, neuroimaging has still linked 5HT receptors to impulsive violence, aggression, eating disorders and mental illness (Wallner and Machatschke, 2009)

Antisocial behaviours that occur early onset, are normally maladaptive from a series of consequences including, child abuse, inadequate parenting, poor neighbourhoods, poverty and social deprivation (Anderson & Bushman, 2002; Warburton & Anderson, 2015; Loeber & Hay, 1997; Widom, 2017). This can trigger future offending and antisocial behaviour into adulthood, by engaging in more chronic offending and displaying severe deleterious behaviour (DeLisi et al., 2008; Ferguson & Beaver, 2009; Widom, 2017; Kitzmann et al., 2003).

Much of these delinquent acts in young people, are associated with asserting autonomy and the desire to hasten maturity in children and are quite ‘normal’ in the developing teenager years. Stepping into adolescence and adulthood, children tend to socially mature, stabilise and essentially ‘grow out’ of anti-social and delinquent behaviour. The serious concern remains when this does not happen and aggression and offending is carried on into adulthood, indicating a manifestation of deeper and more traumatic issues (Gottfredson & Hirschi, 1990). Through studies of twinships and adoptees, it is evident that home environment can detrimentally effect children differently. However, Hurwitz and Christiansen, commented on the ability to experience home life differently, as some children may be favoured or treated better than other siblings resulting in a negative experience for one but not the other (Hurwitz & Christiansen, 1968; Schwartz & Beaver, 2014).

A reproducing concern in the eyes of the court, is how accountable can someone be for their crimes when they have low genetic expression and predisposing environmental stressors. Free will and responsibility for one’s own actions is a huge constituent in the court system and the idea that an individual may be released or given a shorter sentence can cause much vexation and defeat in the judicial system. Ergo the neuroethical and neurolegal worries need to be solicited in future research and the implication it may have on the criminal justice system (Levitt & Manson, 2007)

Principally, this review sought to explain the mechanisms and fundamental issues behind understanding whether aggression was learned or innate. The conclusion being that both the environment and genetic variance offer substantial contributions to aggression and violent crime.


Despite the fact there were a conglomerate of sound points of comparison mentioned throughout this dissertation, it is still important to highlight points of limitation which can be considered in future research as elements to consider and improve on. Firstly, was the lack of representation of other ethnicities and backgrounds. In many of the gene studies and G x E interpretations only Caucasian males were interviewed and analysed (Xu et al., 2017; Chester et al., 2015; Caspi et al., 2002;). The importance of including other ethnicities and backgrounds is highly stressed as the points of comparison can be vital in understanding any differences in genetics that may occur. In terms of environmental stressors, individuals from different backgrounds may experience cultural, religious and social differences that can influence the G x E outcome.

A second limitation is that of collection methods of data have been multifarious amongst studies and many have not been replicated in the same manner and so certainty cannot be proven. Some studies have chosen the route of self-questionnaires and reviews (Chester et al., 2015; Watts & McNulty,2014; Stetler et al., 2014), whilst some preferred genotyping for desired alleles (Ferguson, Boden and Horwood, 2011; Brunner et al., 1993; Eisenberger et al., 2007; Xu et al., 2017), and strikingly some have chosen administration of hot sauce to prove provoked aggression (McDermott et al., 2009).

In the same vein, the reliability of the self-questionnaires and impulsive test scores cannot be established, as many participants may have chosen to party masquerade the truth, or even decorate the truth hence producing varying results. Furthermore, many of the children and adolescent studies involved parent and teacher confirmations of aggression, which again can be misconstrued information as there has been no clear consensus of replication amongst studies (Byrd & Manuck, 2014; Kinnally et al., 2010). Another limitation is that of gender bias, as a superlative amount of studies have focused on males predominately arguing that this is due to the unrecognised constraint of two female X chromosomes. Nevertheless, the need for female representation in studies is crucial in concurrent events, as female related crimes continue to increase (Guiney, 2017) An eminent amount of reviews have instead chosen to concentrate on banal explanations to human aggression such as menstruation or menopause (Ritter, 2003; Ellis & Austin, 1971; Zygar & Pfundmair, 2017).

Last but by no means least, is the inadequacy of sample sizes used. On the whole, most G x E studies have focused on relatively small sample sizes within the western world, within the range of 100-1000 participants (the latter being very rare) (Chester et al., 2016; Aluja et al., 2015; Rajender et al., 2008; Kulikova et al., 2008; Chester et al., 2015). Overall this gives the study a very low statistical power and cannot be generalised to the rest of the population. This accounts for a huge gap in determining heritability in larger sub-groups and other countries (Manufo, Zammit and Flint, 2014)

03 December 2019
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