This
essay will focus on the behaviour of two members of the Galbraith family. Simon,
a heroin addict and Susannah who has agoraphobia. Two psychological
perspectives will be analysed for each behaviour, key characteristics and its
contribution to understanding the behaviours of each member will be explored. Different
treatment options for their behaviours will be identified and evaluated in
psychological perspectives, including methods of data gathering used to develop
and apply treatment such as therapies and interventions. 

 

The
Diagnostic and Statistical Manual (DSM-V) is a valuable tool widely used by
psychiatrists to diagnose mental disorders, the book contains specific diagnostic
codes to identify each disorder. The DSM-V code for opioid addiction is F11.10 (304.00)
and the code for agoraphobia is F40.00 (300.22).

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Bio-psychologists
explain human behaviour by relating it to the functioning of the brain and
nervous system, they believe humans are a consequence of their genetics and
physiology. The biological approach tends to stress the importance on the nature
side of the Nature and Nurture debate. This perspective involves studying the
brain, immune system, nervous system, neurotransmitters and genetics. This may
include looking at certain types of brain injury, the biological roots that lie
behind such behaviours or may consider the genetic factors contributing to such
behaviours. Various types of brain scanning technology including PET and MRI
can be used to study the structure and functioning of the brain. The
experiments are scientific and measurable, a great deal of quantitative data
can be obtained, it is objective and can be repeated to test for reliability. A
weakness is that it is oversimplified, ignoring life experiences and
psychological factors such as thoughts and feelings.

 

Cherry/Gans
(2017) (online) outline how Charles Darwin (1859) first introduced the idea
that evolution and genetics play a role in human behaviour. Natural selection
is when behaviours which aids survival is passed down while those that prove
dangerous are less likely to be inherited. Therefore, “all that is
psychological is first physiological. All thoughts, feeling & behaviour
ultimately have a biological cause” (McLeod 2015). This indicates an innate
response has evolved a preparedness to fear certain stimuli because such fears
had survival value for ancestors. The key weakness is that it ignores nurture
and over empathises on nature, evolutionary theories are reductionist as they
focus only on one genetic factor.

 

Suzannah’s agoraphobia could be associated with
the fight or flight response, this form of protection prepares the body in
dangerous and stressful situations. The body releases hormones like
adrenalin when feeling anxious or afraid, increasing the breathing and heart
rate. Panic attacks, mood and behaviour can also be affected by an imbalance in
the levels of neurotransmitters in the brain contributing to anxiety. These
neurotransmitters include gamma-aminobutyric acid (GABA), serotonin, dopamine,
and epinephrine. Serotonin is mostly important in feelings and deficiencies of
anxiety and depression. Stress hormones such as cortisol also play a
role. It is also possible that Suzannah is ‘wired’ differently from other
people. Malfunctions in some parts of the brain may cause strong emotion and
fear. Suzannah may have a weak system of spatial awareness resulting in feeling
overwhelmed and not oriented in crowded places. Genetic factors predispose an
individual to develop phobia’s, but life experiences also play an important
part in triggering such responses which the biological approach fail to
recognise.

 

According
to Cardwell & Flanagan (2009) Phobias are among the most common types of
mental disorders. Statistics suggest that 4% of adults suffer from phobias. Cardwell
& Flanagan also refer to the work of Kendler et al (1999) who estimated a
67% heritability rate for Agoraphobia. This oversensitive fear response can be
explained by the functioning of the autonomic nervous system (ANS) which is the
part of the nervous system responsible for control of the bodily functions not
consciously directed, such as breathing, the heartbeat, and digestive
processes. Some individuals may have abnormally high levels of arousal in the
ANS causing increased adrenaline. Alternatively, abnormal levels of dopamine
and serotonin implicated in fear response. Cardwell & Flanagan (2009)
reports that having a family member with a phobia increases the risk in the
individual in developing a similar disorder. Twin studies are used to try to
separate genetic factors from environmental factors. They examine the rate of
concordance between mono-zygotic twins (identical) and di-zygotic twins
(unidentical). Torgerson (1993) compared MZ and same sex DZ pairs (85 in total)
Where one twin (the proband) had an anxiety disorder with panic attacks. Such
disorders were five times more frequent in MZ twin pairs. This study provides
support for the genetic explanation of phobia development with a high
concordance rate. However, this support is limited as the twins did not always have
the same phobia. One other issue with the study is that they fail to control
shared environmental experiences, one way to control this is to study twins who
have been raised apart. Twins only account for 2% of the population and
therefore lacks generalisability. Phobic disorders are not solely genetic and
have some considerable experimental component which is described by the
diathesis-stress model. 

According
to Cardwell & Flanagan (2009) the behaviourists believe at birth a human
mind is a blank slate and behaviour is shaped through experience and the
environment. This can be seen through the work of Pavlov and Skinner as
described by Cardwell and Flanagan (2012). Pavlov’s (1849-1936) study explains
how learning takes place through classical conditioning which explains how
people develop responses to certain stimuli that are not naturally occurring
but rather by learning through association. Operant conditioning founded by Skinner (1904-19990)
proposes behaviour is learnt through reward or punishment, if previous
behaviour is followed by pleasant outcomes it is more likely to be repeated. Cardinal & Flanagan (2012)
refer to Watson & Raynor’s (1920) experiment of the 11-month infant “Little
Albert” which explains how fear can be conditioned into a human being
artificially. An incident in childhood may have led to Suzannah’s condition. Her
reward is reaching home, which represents a calm, safe and secure environment.
The hypothesis to this behaviourist theory is that agoraphobia can be traceable
to an original learning experience and possible to condition and decondition
artificially. The strength to this approach is that results are reliable as
experiments are based in controlled scientific settings and involves precise
and objective measurements, quantitative data is gathered as evidence. The
limitations are that genetics are completely ignored, studies are largely based
on animals and doesn’t always explain the complexity of human behaviour.

According to Cardwell & Flannagan (2009) Chemotherapy
is a common biological method of treatments to lower the anxiety levels in agoraphobic
patients. Anti-anxiety drugs such as Benzodiazepines (BZ) reduces anxiety by
enhancing activity of GABA, Beta-blockers reduce blood pressure and
antidepressants such as SSRI’s regulate the mood. The strengths to chemotherapy
is that it can be used to treat many mental conditions, they are effective and
can give a temporary cure however, the drugs focus only on the symptoms and not
the underlying problem and can cause unwanted side effects. Suzannah may
experience headaches, dizziness and nausea when taking them. For Suzannah to confront
her fears Systematic desensitisation can help by gradually changing the
response to relaxation through counterconditioning by working her way up through
a step by step desensitisation hierarchy. She will start with the least
unpleasant stimuli, practice relaxation techniques and then move on to the next
stage when comfortable. According to McLeod (2008 online) therapy usually
requires 4-6 sessions, up to 12 for a severe phobia. Exposure can be done in
two ways; the In vitro method is when the client imagines exposure to the
phobic stimulus and the In vivo method is where the client is exposed to the
phobic stimulus. The strength in this type of therapy is that it is generally a
faster treatment method and requires less effort. Contact with feared stimuli
appears to be more successful than the imagining method. According to Cardwell
and Flanagan (2009), McGrath et al reports that 75% of patients respond to SD,
however Ohman et al (1975) suggest that SD may not be as effective for people
with underlying evolutionary survival component. SD treats the symptoms and not
the causes of the phobia which is a significant weakness.

The treatment suggested for Suzannah’s
agoraphobia is presenting self -improvement methods by developing awareness
about agoraphobia and creating mindfulness of the related condition like panic
attacks and anxiety. Taking regular exercise and a healthy diet plan to help manage
stress levels. Controlled therapeutic step by step measures to expose Suzannah
to the outside world using the in vivo method of exposure and working up the
hierarchy. A low dose of SSRI to help reduce anxiety and increase mood only as
and when needed to prevent dependency.

Key features that could identify a heroin
addict may be that they are taking more than intended, unsuccessful attempts of
wanting to or trying to control, reducing other activities, failing
relationships because of heroin use. Simon may experience withdrawal symptoms such
as sweating, nausea, pain and shakiness when heroin is not taken.

The biological model of addiction includes three
aspects; initiation, maintenance and relapse. Initiation explains how the
behaviour starts, maintenance is why the behaviour is continued and relapse is
what causes the individual to go back to the addictive behaviour after a period
of abstinence from the behaviour. Addiction may be explained through the
chemical imbalances in the brain. Individuals become addicted to drugs that
increase dopamine levels. Dopamine have several different functions and plays a
critical role in the function of the central nervous system (CNS). Dopamine is
linked to motivation, reward and emotional responses. Simon may have low
dopamine levels which makes him more prone to addiction. Heroin builds the
neuronal firing rate of dopamine cells, consequently Simon encounters enhanced
dopamine activity as mood elevation and euphoria. Simon is then highly
motivated to repeat this experience when the heroin is eliminated from the
brain, repeated use of heroin can deplete dopamine from the system. Cardinal
and Flanagan (2009) report studies linking the DRD2 gene to severe heroin and
other addictions. They also refer to Agrawal and Lynskey’s (2006) work who found
illicit drug abuse heritability rate of 45%-79%. The biological approach
explains individual differences in vulnerability to addiction and explain why Simon
may be resistant to treatment and can be generalised to other cultures, however,
genetic factors cannot possibly be solely responsible for the development of
addictive behaviours, it is reductionist by simplifying the explanation of
complex human behaviour. It is deterministic by assuming individuals who have
the gene are bound to become addicted.

Cognitive psychologists assume that behaviour
is the result of information processing adopting a computer metaphor in mind. A
person’s behaviour is determined by the information available from the
environment, how they have learnt to manipulate information and the capacities
for information processing inherent in the type of brain. There are three main
theories contained within the cognitive model, self-medication, the rational
choice theory and the expectancy theory. This approach suggests that Simon’s addiction
is the result of faulty thinking rather than the reality. Sammons (online)
refer to Becks (1996) theory of the computer triad; The self, the future and
the experiences. Simon may be fuelling himself to believe he is a bad person, interpreted
life events negatively and that life is terrible and unlikely to improve, which
may have led Simon to heroin abuse as a way of coping. The initiation of heroin
could have been to seek a sense of escape from life’s negative events or unpleasant
circumstances. Maintenance and relapse occurs as heroin is highly addictive and
therefore tolerance levels build requiring increased amounts to gain effectiveness.
When intake is reduced, withdrawal symptoms and unpleasant feelings is experienced,
resulting in Simon to revert to addiction after trying to stop (relapse). Treatment
can be gained through replacing the dysfunctional beliefs with more positive
ones. The cognitive approach explains the link between faulty thinking
and abnormal behaviour, it is scientific, laboratory experiments is used as key
research methods to producing quantitative data. Case studies are also used to
gather qualitative data. However, this approach is machine reductionist,
computer models are used to explain human behaviour by simplifying human
complexity to a computer system. It lacks ecological validity as it involves tasks
that do not mimic real life experiences.

Harrison (2013 online) highlights a study involving
141 opioid dependent patients randomly selected from the primary care clinic.
The study was based on a 24-week trial, during which all patients received combination
of drugs called buprenorphine and naloxone, and some received an additional CBT
during the first 12 weeks of treatment. Both approaches resulted in a reduction
of opioid use. However, the results did not differ between the two treatment
groups which shows CBT treatment for opioid dependency may not significantly
enhance outcomes compared with medical treatment alone.

Treatment for Simon’s heroin addiction can
include medically assisted heroin detox, cognitive behavioural therapy, 12 step
programs and counselling. Maintenance therapy will allow Simon to switch from
heroin to a substitute such as Methadone which is a slow acting opioid agonist drug.
Buprenorphine/naloxone, relieves drug cravings without producing the “high” or
dangerous side effects of other opioids. Naltrexone, is sedating and does not
result in physical dependence, it can be obtained in an injectable long-acting
formula and be administered once a month. The detox can gradually help to
withdraw from the heroin substitutes until completely drug free. Cognitive-behavioural
therapy helps to modify expectations and behaviours related to drug use and to
increase skills in coping with various life stressors. Treatment durations
varies depending on individual factors. The strength of drug maintenance
therapies is that they are effective methods of treatment, administered on a
medically supervised schedule and will not prevent drug users from living a
normal life. However, treatment drugs are also addictive and unlikely to work
if not used in conjunction with additional therapy such as counselling. Detox
lowers tolerance levels to heroin and therefore the risk of overdosing is
higher if heroin is taken after detoxing.

It is essential for recovering addicts to not
deviate from the medically approved plans for recovery. As Simon is homeless and
there is no one to take care of him, rehabilitation at a residential treatment centre
is recommended to help with withdrawal symptoms. After examination, prescription
of buprenorphine/naloxone to minimize heroin cravings and the accompanying
withdrawal symptoms. Decreasing the dosage after satisfactory stabilisation
followed by intense counselling to help deal with additional underlying issues
such as relationships and childhood deprivation.  

In conclusion, it is possible to reverse learnt
behaviours such as phobias and addiction by applying appropriate intervention
tailored to the individual needs such as changing the way people think and learn.
Research shows that no one type of psychological treatment is superior to
another. Genetics also play a key role in these behaviours. Psychological
therapies appear more effective when combined with pharmaceutical treatment which
can help manage individual vulnerability but should be used as controls instead
of placebo for effective long-term treatment.