Human behaviour is complex.

One of the approaches used in the endeavour to understand its intricacies is a biological or medical model. The biological approachexamines the roles of physiology- the brain and other organs’ reactionsinfluenced by chemicals and the control of certain motor functions, ontogeny -or how a pattern of behaviour develops over a period because of genetics andexperiences, evolution – for instance, the reasons as to why certain functionsexist even though their relevance today is questionable andfunctionality – or why structures have evolved the way they have (Tinbergen1951). Abnormal behaviour, asbroadly defined by the American Psychological Association is the occurrence ofa clinically significant pattern of behaviour that causes distress ordisability which has a greater risk in resulting in death, disability or theloss of one’s freedom. The purpose of this essay is to attempt to explain the occurrence of abnormal behaviour in the context of two biologicalfactors; genes and the role of neurotransmitters. The question as to whethera set of behaviour has been inherited or is a result of environmental factors,or both, has been long debated over. For it to be determined that anindividual’s genotype is indeed the sole reason for the resulting behaviour, itmust be proven that no other environmental contributor is evident as a causalfactor.

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 As referenced by Plomin etal. (1994) research conducted on comparative studies of identical and fraternaltwins, has indicated a greater genetic influence on behavioural disorders suchas schizophrenia, major affective disorders and antisocial personality disorderas opposed to medical conditions such as Parkinson’s disease or RheumatoidArthritis. Further studies conducted in behavioural genetic research alsoindicate that the findings pertaining to the influence of environmental factorsin adoptive sibling studies note that a shared environment has no bearingon the manifestation of psychological traits (Plomin et al – 1994: 1735 and McGue and Bouchard 1998:5).There is no conclusive evidence to date, to suggest that genetics is the onlyconstant in resulting abnormal behaviour.

The reason for this could beattributed to the fact that the study of the approximately 30,000 human genes,is still a work in progress. It has been said that once decoded one would beable to access the data of every aspect of what determines the development ofhuman beings (Human Genome Project 2001) Consider the currentresearch available on anti-social behaviour (ASB) for instance.  There is no denying that genetics play a rolein its occurrence (Raine 2008: 323-324).  In fact, it has been determined that genetic influenceaccounts for more than 50% of resulting anti-social behaviour (Moffit 2005: 535).However the variance at play here is attributed to environmental factors.

Ofthe two methods used to determine the influence of environmental factors inresulting anti-social behavior, is the hypothesis that MZ twins’ genetic construct (being twiceas similar than that of DZ twins), should result in a greater similarity if tested for symptoms of such behaviour. If this didn’t indicate such a similarity, then it is reasonable to assume that that other factors may have influenced theincreased levels of similarity. Although tested positive for several other abnormalities, this didn’t hold true with anti social behaviour. In a study conducted byKendler et al (2003) on the genetic and environmental risk involved in commonpsychiatric and substance use disorders, it was discovered that environmentalinfluence played a more significant role in resultant ASB as opposed toabnormal behaviour and experiences such as anxiety and substance abuse.

Furtherstudies conducted to ascertain ASB in the form of aggression and rule-breakingby using behavioural genetics biometric modelling has indicated that bothgenetics and environment concurrently play a role in its occurrence and whilebetween ages 9 and 10 its effects are a 41% – 40% – 19% split (genetics toshared environment to non-shared environment), with the 14-15 age group this wasfound to shift to a 44% – 79%, environmental factors. It can be said that agetoo therefore, plays a role in resulting ASB (Niv et al 2003).The Serotonin Transportergene is one of the most studied variants in psychiatry and neuroscience. It wasdiscovered that a ‘polymorphism’ in the 5-HTTLPR region of the SerotoninTransporter gene affects the reabsorption of Serotonin after its release. In astudy conducted among 847 participants, the existence of two variants ( long and short), of this gene was discovered. When tested in conditions of highly stressful events experienced by participants aged 21 -26, it wasfound that the individuals with two short forms of the gene had a greatertendency to develop depression when subjected to such stressful event over a period of time.

The short gene by itself didn’t cause depression, butincreased the individuals’ susceptibility to getting it, when faced with stressful events (Caspi et al 2003).  Amore recent gene x environment x mood (GEM) study further revealed that a significant G X E interactionresulted in a greater predisposition for depression. It was also revealed that ageand gender played key roles in resulting depression (olderadolescent carriers of the short allele subjected to peer pressure over timeand females subjected to long term peer pressure, were more prone to bediagnosed with it) (Hankin et al 2015: 804-812).Effects of the existenceof this genetic anomaly has also been observed in individuals with apredisposition to psychopathy. In a study carried out to determine the extentof the role played by the serotonin transporter gene in relation to impulse control ( a commontrait of psychopathy), and its behavior  in relation to  G X E conditions of callousness and narcissism, it was found that individuals carrying the s/s allele rated high onthe APSD (Antisocial Process Screening Device) scale on impulsiveness, whereas those withthe l/l allele raised in low socio-economic  environments indicated a greater disposition towards callousness and narcissism. The research also indicated that nocorrelation was seen to exist between low socioeconomic status and the existence of the genetic anomaly (Sadeh et al 2010:604-608).The premise of the theoriesassociated with neurotransmitters is, that it influences chemical imbalancesthat result in abnormal behaviour (Sue et al 2010:38).

More specifically,studies have revealed that many endogenous compounds such as acetylcholine(ACh), dopamine (DA), serotonin (5HT), gamma aminobutyric acid (GABA) andnorepinephrine (NE) – (among those more commonly referenced), are said toinfluence the occurrence of several abnormal conditions or psychiatric statessuch as schizophrenia, depression (Hanin 1978: 135-138), and more recently inaggressive behaviour (Narvaes et al 2014:601-607) and psychopathy (Buckholtz etal 2010: 419-421).  Consider the complexities of schizophrenia forinstance. After over 1200 studies in trying to understand the reason for itsoccurrence it has been determined that no one gene but the existence of severalsusceptible genes code for varying molecular abnormalities that influenceinsufficient information processing that results in a genetic bias towardsschizophrenia (Stahl 2007 cited in Sue et al 2010: 375).

 In a more recent study conducted to understand theinfluence of underlying genes revealed 14 genes responsible for a combination of neurotransmission and functional inconsistencies in resulting schizophrenia. Of these 14 genes, primarily featuring on the list were three genes associated with the neurotransmission of GABA. This data could explain the abnormal EEG gamma band activity detected in schizophrenic patients. The experiments were carried out by administering PCPand clozapine in a ‘pharmacogenomic mouse model’ and analysed against comparative genetic linkage andpost-mortem brain data to arrive at these findings (Le-Niculescu et al 2007).Depression, has long been asubject of psychiatric research. The monoamine hypothesis of depression wasfirst observed as a result of the effects caused by two monoamine oxidaseinhibitors, namely iproniazid and imipramine, in non-psychiatric patients. Thecompounds had a marked impact on the transmission of serotonin causingsignificant anti-depressant effects.

Furthermore, it was observed thatReserpine caused depressive symptoms in others. To date, antidepressant agentsare designed to influence monoamine transmission by inhibiting either neuralreuptake or degradation.Aggressive behaviour, atrait associated with psychopathy, which in turn results in criminal behaviour,has given cause to greater scientific research as its social and economicburden is immense.

Monetarily in the US alone this is indicative to exceed $1trillion (Buckholtz et al 2010). There is now, documented research confirmingthe roles of neurotransmitters such as GABA, dopamine and serotonin existent in in individuals prone to exhibiting aggression (Narvaes et al 2014). Further to this point, in astudy carried out to determine the hypersensitivity of the dopamine rewardsystem in individuals with psychopathic traits (of which aggression is one), it was discovered that dopaminewas a key determiner in the occurrence of animpulsive-antisocial temperament (aggression) indicatingincreased interaction with the mesolimbic dopamine system in response toreward. Furthermore, several studies conducted on rodents in preclinical tests also indicate mesolimbic dopamine to be critical in the expression of aggression(Buckholtz et al 2010).

                                     In reviewing the geneticand neurochemical premises of abnormal behaviour, we find that neither one northe other can be designated as the sole cause of the resulting abnormal behaviour.There is evidence in several resultant abnormal patterns of behaviour tosuggest that genetic predisposition plays a role in creating susceptibility among individuals in relation to certain chemical functions. As referenced forinstance with schizophrenia the existence of three genes responsible for thetransmission of GABA was observed. With aggressive behaviour and resultantpsychopathy, we see a predisposition towards delinquent behaviour because of apolymorphism of the serotonin transporter gene and a heightened interaction ofthe mesolimbic dopamine system in response to reward. With depression, theexistence of two short alleles of the serotonin transporter gene indicated agreater probability of encountering depression.

Although monoamine basedanti-depressants are the first course of therapeutic measures, certain genepolymorphisms significantly contribute towards a depressed individual’sefficacy in relation to anti-depressants (Uhr et al 2007).Furthermore, although notpreviously discussed in this essay, it should be noted that abnormal behaviour,can also be attributed to other factors. Evolution, for example. Take theevolutionary predisposition to fear certain species such as snakes and spidersresulting in present day phobias of the same (Ohman and Mineka 2001). Abnormal behaviourcan also be the result of the formation or structure of the brain – consideranti-social behaviour for instance; there is mounting evidence to suggestimpairments to the brain’s prefrontal cortex in individuals exhibiting traitsthat constitute for such behaviour (Raine and Yang 2006); in fact, it’s been foundthat murderers show reduced glucose metabolism in this area of the brain whenfaced with a task that’s meant to activate it (Raine 2008).

With schizophrenia,according to the neurodevelopmental hypothesis, abnormalities in the brain is not only attributed to genetics but also to prenatal or postnatal development and environmental influences which have been known to aggravate its symptoms (Weinberger 1996).It was also found that among a group of 390 individuals with schizophrenia,abnormalities were present in the left temporal and frontal areas of the cortexand that the thalamus appeared to be smaller than average(Harmset al 2007).Environmental factors tooplay a key role – some of which was touched on in this essay previously. To further this point, consider that in cases of depression,  although the susceptibility in getting it isgreater among those who have the short serotonin transporter gene, theexistence of other genes that increase the probability of acquiring depression and are triggered by an individual’s traumatic upbringings, have been found to be present in some patients with depression (Bradley et al 2008 and Haeffel et al 2008).Some cases of depression have also been linked to viral infections such asBorna disease (Kalart 2010: 439) and yet some others could be the result ofgiving birth – statistics state that at least 20% (Hopkins et al 1984 cited inKalart 2010: 440) of women report some level of postpartum depression.

Thus, the explanation ofthe complexities of abnormal behaviour must be approached from a broaderperspective, for it to be comprehended to some degree.  


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