Human development of human beings (Human Genome Project

 

Human behaviour is complex.
One of the approaches used in the endeavour to understand its intricacies is a biological or medical model. The biological approach
examines the roles of physiology- the brain and other organs’ reactions
influenced by chemicals and the control of certain motor functions, ontogeny –
or how a pattern of behaviour develops over a period because of genetics and
experiences, evolution – for instance, the reasons as to why certain functions
exist even though their relevance today is questionable and
functionality – or why structures have evolved the way they have (Tinbergen
1951).

Abnormal behaviour, as
broadly defined by the American Psychological Association is the occurrence of
a clinically significant pattern of behaviour that causes distress or
disability which has a greater risk in resulting in death, disability or the
loss of one’s freedom. The purpose of this essay is to attempt to explain the occurrence of abnormal behaviour in the context of two biological
factors; genes and the role of neurotransmitters.

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The question as to whether
a 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 an
individual’s genotype is indeed the sole reason for the resulting behaviour, it
must be proven that no other environmental contributor is evident as a causal
factor.

 

As referenced by Plomin et
al. (1994) research conducted on comparative studies of identical and fraternal
twins, has indicated a greater genetic influence on behavioural disorders such
as schizophrenia, major affective disorders and antisocial personality disorder
as opposed to medical conditions such as Parkinson’s disease or Rheumatoid
Arthritis. Further studies conducted in behavioural genetic research also
indicate that the findings pertaining to the influence of environmental factors
in adoptive sibling studies note that a shared environment has no bearing
on 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 only
constant in resulting abnormal behaviour. The reason for this could be
attributed 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 be
able to access the data of every aspect of what determines the development of
human beings (Human Genome Project 2001)

 

Consider the current
research available on anti-social behaviour (ASB) for instance.  There is no denying that genetics play a role
in its occurrence (Raine 2008: 323-324).  In fact, it has been determined that genetic influence
accounts for more than 50% of resulting anti-social behaviour (Moffit 2005: 535).
However the variance at play here is attributed to environmental factors. Of
the two methods used to determine the influence of environmental factors in
resulting anti-social behavior, is the hypothesis that MZ twins’ genetic construct (being twice
as 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 the
increased levels of similarity. Although tested positive for several other abnormalities, this didn’t hold true with anti social behaviour. 

In a study conducted by
Kendler et al (2003) on the genetic and environmental risk involved in common
psychiatric and substance use disorders, it was discovered that environmental
influence played a more significant role in resultant ASB as opposed to
abnormal behaviour and experiences such as anxiety and substance abuse. Further
studies conducted to ascertain ASB in the form of aggression and rule-breaking
by using behavioural genetics biometric modelling has indicated that both
genetics and environment concurrently play a role in its occurrence and while
between ages 9 and 10 its effects are a 41% – 40% – 19% split (genetics to
shared environment to non-shared environment), with the 14-15 age group this was
found to shift to a 44% – 79%, environmental factors. It can be said that age
too therefore, plays a role in resulting ASB (Niv et al 2003).

The Serotonin Transporter
gene is one of the most studied variants in psychiatry and neuroscience. It was
discovered that a ‘polymorphism’ in the 5-HTTLPR region of the Serotonin
Transporter gene affects the reabsorption of Serotonin after its release. In a
study 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 was
found that the individuals with two short forms of the gene had a greater
tendency to develop depression when subjected to such stressful event over a period of time. The short gene by itself didn’t cause depression, but
increased the individuals’ susceptibility to getting it, when faced with stressful events (Caspi et al 2003).  A
more recent gene x environment x mood (GEM) study further revealed that a significant G X E interaction
resulted in a greater predisposition for depression. It was also revealed that age
and gender played key roles in resulting depression (older
adolescent carriers of the short allele subjected to peer pressure over time
and females subjected to long term peer pressure, were more prone to be
diagnosed with it) (Hankin et al 2015: 804-812).

Effects of the existence
of this genetic anomaly has also been observed in individuals with a
predisposition to psychopathy. In a study carried out to determine the extent
of the role played by the serotonin transporter gene in relation to impulse control ( a common
trait 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 on
the APSD (Antisocial Process Screening Device) scale on impulsiveness, whereas those with
the l/l allele raised in low socio-economic  environments indicated a greater disposition towards callousness and narcissism. The research also indicated that no
correlation 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 theories
associated with neurotransmitters is, that it influences chemical imbalances
that 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) and
norepinephrine (NE) – (among those more commonly referenced), are said to
influence the occurrence of several abnormal conditions or psychiatric states
such as schizophrenia, depression (Hanin 1978: 135-138), and more recently in
aggressive behaviour (Narvaes et al 2014:601-607) and psychopathy (Buckholtz et
al 2010: 419-421). 

 Consider the complexities of schizophrenia for
instance. After over 1200 studies in trying to understand the reason for its
occurrence it has been determined that no one gene but the existence of several
susceptible genes code for varying molecular abnormalities that influence
insufficient information processing that results in a genetic bias towards
schizophrenia (Stahl 2007 cited in Sue et al 2010: 375). In a more recent study conducted to understand the
influence 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 PCP
and clozapine in a ‘pharmacogenomic mouse model’ and analysed against comparative genetic linkage and
post-mortem brain data to arrive at these findings (Le-Niculescu et al 2007).

Depression, has long been a
subject of psychiatric research. The monoamine hypothesis of depression was
first observed as a result of the effects caused by two monoamine oxidase
inhibitors, namely iproniazid and imipramine, in non-psychiatric patients. The
compounds had a marked impact on the transmission of serotonin causing
significant anti-depressant effects. Furthermore, it was observed that
Reserpine caused depressive symptoms in others. To date, antidepressant agents
are designed to influence monoamine transmission by inhibiting either neural
reuptake or degradation.

Aggressive behaviour, a
trait associated with psychopathy, which in turn results in criminal behaviour,
has given cause to greater scientific research as its social and economic
burden is immense. Monetarily in the US alone this is indicative to exceed $1
trillion (Buckholtz et al 2010). There is now, documented research confirming
the 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 a
study carried out to determine the hypersensitivity of the dopamine reward
system in individuals with psychopathic traits (of which aggression is one), it was discovered that dopamine
was a key determiner in the occurrence of an
impulsive-antisocial temperament (aggression) indicating
increased interaction with the mesolimbic dopamine system in response to
reward. 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 genetic
and neurochemical premises of abnormal behaviour, we find that neither one nor
the other can be designated as the sole cause of the resulting abnormal behaviour.
There is evidence in several resultant abnormal patterns of behaviour to
suggest that genetic predisposition plays a role in creating susceptibility among individuals in relation to certain chemical functions. As referenced for
instance with schizophrenia the existence of three genes responsible for the
transmission of GABA was observed. With aggressive behaviour and resultant
psychopathy, we see a predisposition towards delinquent behaviour because of a
polymorphism of the serotonin transporter gene and a heightened interaction of
the mesolimbic dopamine system in response to reward. With depression, the
existence of two short alleles of the serotonin transporter gene indicated a
greater probability of encountering depression. Although monoamine based
anti-depressants are the first course of therapeutic measures, certain gene
polymorphisms significantly contribute towards a depressed individual’s
efficacy in relation to anti-depressants (Uhr et al 2007).

Furthermore, although not
previously discussed in this essay, it should be noted that abnormal behaviour,
can also be attributed to other factors. Evolution, for example. Take the
evolutionary predisposition to fear certain species such as snakes and spiders
resulting in present day phobias of the same (Ohman and Mineka 2001). Abnormal behaviour
can also be the result of the formation or structure of the brain – consider
anti-social behaviour for instance; there is mounting evidence to suggest
impairments to the brain’s prefrontal cortex in individuals exhibiting traits
that constitute for such behaviour (Raine and Yang 2006); in fact, it’s been found
that murderers show reduced glucose metabolism in this area of the brain when
faced 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 cortex
and that the thalamus appeared to be smaller than average(Harms
et al 2007).

Environmental factors too
play 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 is
greater among those who have the short serotonin transporter gene, the
existence 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 as
Borna disease (Kalart 2010: 439) and yet some others could be the result of
giving birth – statistics state that at least 20% (Hopkins et al 1984 cited in
Kalart 2010: 440) of women report some level of postpartum depression.

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

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