Definitions of abnormality, including deviation from social norms, failure to function

adequately, statistical infrequency and deviation from ideal mental health.

● The Statistical infrequency definition of abnormality states that abnormal behaviour is
behaviour that is very rare.
● Statistics are how we measure how common behaviours or traits are when measured in
comparison to the rest of the population. The most uncommon ones are defined a
abnormal.
● For example low IQ is when someone’s intelligence is two standard deviations from the
average. Just 2.28% of the population have low IQ. It is an objective measure of
individuals needing support.
Evaluation
★ Not all statistically infrequent traits are negative. This definition would include high IQ,
but whilst this is statistically rare it is also highly desirable.
★ Where the cut-off point falls results in some people receiving treatment and some not, so
deciding where to put the cut-off is subjective.
★ Some psychopathologies such as depression and anxiety are quite common. Around 1
in 6 adults (17%) surveyed in England by the NHS met the criteria for a common mental
health disorder (CMD) in 2014. The statistical infrequency definition does not match with
the high incidence of mental health disorders within society.

Failure to function adequately

● Failure to function adequately is inability to cope with daily life (interacting with the world
and people around us).
● Rosenhan and Seligman (1989) suggested the following features of failure to function
adequately:
1. Maladaptive behaviour- this is when individuals behave in ways that are against
their long-term interests (i.e: self-harm or unhealthy eating patterns).
2. Personal anguish- suffering from anxiety and distress because of their inability
to cope.
3. Observer discomfort- The person’s behaviour causes distress to the people
around them (i.e: poor personal hygiene or not respecting personal space).
4. Irrationality and unpredictability- behaviour that is hard to understand and/or
seems uncontrolled
5. Unconventionality- behaviours go against normal expectations.
Marbled pigs often irritate uncle
Evaluation
★ Deciding whether an individual is coping or not is a subjective judgement that is affected
by the opinions of the observer, so two observers may not rate a person in the same way
(potential low inter-rater reliability).
★ Some abnormal behaviour is not linked to an inability to cope or intense distress. It is
thought that there are many psychopaths that may be more able to function in certain
roles in society, which may be at the detriment of people other than themselves.
 ★ Not all maladaptive behaviour is an indication of mental illness. For example, smoking
and poor diet are seen as against a person’s long-term interests in their personal health,
but neither of these behaviours are assumed to constitute mental illness.
★ However failure to function does respect and recognises the patient’s own lived
experiences and perspective, which statistical infrequency and deviation from social
norms cannot really address.

Deviation from social norms

● Social norms are unwritten social expectations of behaviour that may differ from
one culture to the next. They often change over time and vary depending on the
context.
● Therefore according to this definition, those who deviate from the society's’ expectations
will be seen as abnormal ‘social deviants’.
● An issue with this explanation of mental illness is that, as norms are a group judgement
on what is acceptable, certain behaviours in one culture that are considered acceptable
may be considered deviant in another culture (i.e: homosexuality, face/hair covering,
queuing, chopsticks, public displays of emotions).
Evaluation
★ It respects cultural differences by not imposing a set definition of abnormality (avoids
western ethnocentrism that would cause other cultures to be viewed as abnormal).
★ It is a clear definition of what is and is not abnormal whilst also taking context into
consideration.
★ Different social classes within the same society may have different social norms. This
could, for example, result in an overdiagnosis of mental health problems in those of
working class backgrounds if most of the psychiatrists are from middle or upper class
backgrounds.
★ Can create problems for people living in a culture that is different from their culture of
origin. For example Cochrane (see the schizophrenia topic) suggests that the there is
7x higher diagnosis rate of schizophrenia for people from Afro-caribbean heritage living
in the UK compared to those native to the UK living in the UK or those native to the
Caribbean who are living there. Fernando considers this to be a “category failure” that
has occurred due to western definitions of mental illness being applied onto non-western
cultures, specifically how hallucinations and religious experiences are interpreted.
★ This definition can result in society imposing punishments to unconventional mentally
healthy people for expressing their individuality, which is unethical

Deviation from ideal mental health

● Marie Jahoda (1958) uses humanist principles in not defining abnormality but defining
six features of ideal mental health, suggesting that deviation from these features would
indicate an abnormality. To remember the six features we use the acronym EAR SPA.
1. Environmental mastery- competent in meeting the demands of situations.
Involves flexible thinking.
2. Autonomy- able to act independently of others and rely on their own abilities.
 3. Resisting stress- able to cope with the anxiety caused by the demands of life.
4. Self actualisation- maximising personal growth and development to reach their
potential.
5. Positive attitude towards oneself- positive self-concept (so high self-esteem
and self respect).
6. Accurate perception of reality- realistic view of the world not distorted by
personal biases.
Evaluation
★ A positive holistic approach to diagnosis that identifies areas for personal development.
★ Criteria are culturally biased to reflect an ethnocentric western viewpoint on what ideal
mental health is. This could be an example of a culturally specific (emic) viewpoint being
applied to all people as a universal (etic) construct. For example, many cultures place
less value on the autonomy and personal freedom found in western cultures, seeing
playing a social role as more important.
★ It is very difficult to achieve all of these criteria at the same time, so most people would
be judged as failing to achieve ideal mental health, and would therefore be classed as
abnormal.

The behavioural, emotional and cognitive characteristics of phobias, depression, and

obsessive compulsive disorder (OCD)
● Phobias are extreme irrational fears of certain objects or situations. Examples of
phobias are arachnophobia (fear of spiders) and claustrophobia (a fear of enclosed
spaces).
● Three key behavioural characteristics of phobias are avoidance (behavioural
adaptations made to prevent encountering the phobic object or situation), panic (an
uncontrollable physical response such as screaming, escaping, or hyperventilating),
and failure to function (inability to conduct normal necessary behaviours due to
excessive thoughts of the phobia and/or avoidance).
● Two key emotional characteristics are anxiety (an uncomfortable high arousal state
that inhibits relaxation and pleasurable emotions. Thought is focused on a future
encounter with the phobic object or situation) and fear (an intense emotional state of
panic linked to physiological fight or flight response when presented with the phobic
object or situation).
● Two key cognitive characteristics of phobias are irrational beliefs (sufferers overstate
the potential danger of the phobic object or importance of the social situation) and
reduced cognitive capacity (sufferers focus their attention on the phobic object to
the extent that it interferes with other tasks).
● The three subtypes of phobias are simple/specific phobias (fears of objects), social
phobias (fear of social interactions that could cause rejection or embarrassment) and
agoraphobia (fear of leaving a safe environment).
 ● Obsessive compulsive disorder (OCD) is an anxiety disorder defined by obsessions
(constant intrusive thoughts, usually concerning contamination or safety) and
compulsions (behavioural responses to the obsessions).
● Three key behavioural traits of OCD are compulsions (these often involve checking
behaviour such as repeatedly testing the lights and checking that the door is locked,
and ritual behaviour such as constant hand washing, and hoarding), avoidance
(sufferers avoid behaviour that may lead to obsessive thoughts so may stop using
public toilets for fear of germs), and social impairment (unable to take part in normal
relationships due to excessive anxiety).
● Two key emotional traits of OCD are extreme anxiety (caused by the constant
presence of the persistent obsessive thoughts and the fear associated with them.
Also attempting to resist the urge to carry out compulsions can cause anxiety) and
distress/depression (low mood due to not being able to engage in enjoyable
activities and a feeling of not being in control of own behaviour).
● Two key cognitive traits of OCD are recurrent thoughts (intrusive unpleasant
thoughts that are anxiety-producing. Often of the worst case scenario or something
else that distresses the person) and understanding the irrationality (sufferers know
that the worst case scenarios imagined by their catastrophic thinking are unlikely, but
are still unable to control them).

● Depression is a category of mood disorders, which is often divided into two main types:
unipolar and bipolar depression, otherwise known as manic-depression.
● Four behavioural traits of depression are weight loss or gain (appetite is reduced or
increases), low energy (lack of desire to participate in normally enjoyable activities such
as sex, exercise, and socialising), self harm (this may be injuring such as cutting or, in
extreme situations, suicide), and poor personal hygiene (low motivation to keep
themselves or their environments clean and tidy).
● Two emotional characteristics of depression are sadness (persistent intense lowered
mood is the defining feature of depression) and reduced self worth (feelings of guilt,
helplessness, or low self esteem).
● Two cognitive features of depression are poor concentration (difficulty in keeping
attention on tasks and indecisiveness) and persistent concern (thoughts biased
towards a negative perspective of events and outcomes).
● Unipolar/major depression effects 25% of women and 12% of men during their
lifetimes, and includes only depressive episodes
● Bipolar/manic depression affects 2% of people. They also have manic episodes
where they have high energy and high moods, engage in risk-taking behaviour, and
potentially have delusions.

The behavioural approach to explaining and treating phobias: the two-process model,
including classical and operant conditioning; systematic desensitisation, including
relaxation and use of hierarchy; flooding
 ● Explaining Phobias- A behaviourist model for explaining phobias is the two-process
model. Behaviourists see all behaviour (including phobias) as learnt via experience. In
the two-process model Mower (1960) suggests that phobias are first acquired (learned)
via association (classical conditioning), and then maintained via reinforcement
(operant conditioning).
● In acquisition (classical conditioning- learning by association) the phobic object(s) are at
first neutral stimulus, not producing the phobic response. However, if the phobic object is
presented with an unconditioned stimulus that produces an unconditioned negative
response, then the neutral stimulus will then be associated with the unconditioned
stimulus and thus the unconditioned response, and so the fear (the phobia) will happen
whenever the neutral stimulus appears. As this point the neutral stimulus becomes the
conditioned stimulus, and the unconditioned response becomes the conditioned
response. This fear will then be passed onto other stimuli similar to the conditioned
stimuli via generalisation (i.e: fear of spiders generalised to all insects).
● In maintenance (operant conditioning- learning by trial and error) the phobic person
avoids situations that may bring the individual with the phobia into contact with the
phobic object. The consequence of this is that anxiety is reduced. This is a pleasant
sensation which acts as a negative reinforcement (removal of negative stimulus).
● Social learning theorists suggest that learning can happen vicariously by observing
models. Observing a fear response in others can then result in the same display of fear,
especially if the behaviour results in reward for the model (i.e: attention).
★ Example for acquisition of a phobia: Bees were originally a neutral stimulus for Laura,
resulting in no fear response. However the pain of being stung (unconditioned stimulus)
produced fear (unconditioned response). Bees (conditioned stimulus) became
associated with the fear (conditioned response) due to the pain of the sting. So even
when not stung there is now fear. However she now feels fear when seeing ants, moths,
and spiders, even though she was never stung by them (generalisation).
★ Example for maintenance of a phobia: Laura has been invited to a summer picnic. As
she approaches the park she sees a number of bees. The thought of sitting near them
causes her anxiety, so she calls her friends to say that an emergency has come up and
she can’t make it. As she heads home, she is sad as she wanted to spend time with
friends, but her anxiety decreases as she didn’t need to be around the bees and the
phobia is thus negatively reinforced.
Evaluation
★ Watson and Rayner (1920) used a child called little Albert to demonstrate how phobias
could be induced in a child. They did this by making a loud noise (by hitting a metal bar
behind the child’s head) when presenting a white rat to the child, and were able to
generalise this fear to other white fluffy objects such as a rabbit.
+ This study acts as evidence for the Two-process model via proving how acquisition and
generalisation of phobias work, however it was a highly unethical study as it caused its
participant (little Albert) emotional harm.
★ Menzies and Clarke (1993) found that only 2% of children with a fear of water could
recall a traumatic experience with water, suggesting that the behaviourist explanation
cannot account for all phobias.
★ Phobias of snakes, birds, and dogs had an evolutionary origin as our very early
ancestors could have been hunted/attacked by these creatures. This could explain why
these are common phobias, when phobias to objects that are more dangerous in the
modern day (i.e: knives, cars) are rare. This is the evolutionary biological theory,
however this nature explanation goes against the nurture explanation of the behavioural
approach.
★ Behaviourist theories of phobia formation and maintenance have lead to effective
counter-conditioning treatments such as flooding and systematic desensitisation (see
below), supporting the behaviourist explanation.

● Treating Phobias- Behaviourist therapies are based on the idea that phobias are
learnt through association to fear, so therapies attempt to replace the fear
association with one of relaxation/calm.
● Systematic desensitisation is an attempt to use the same classical conditioning
techniques that are thought to have caused the phobia in a process to “counter
condition” the phobia by replacing the association between the phobic object and fear
with an association with relaxation/calm instead.
● The process relies on the theory of reciprocal inhibition, that is, the idea that fear and
relaxation are opposite emotions and so cannot coexist at the same time.
Therefore if you feel calm around the phobic objects then you can’t simultaneously feel
fearful around it, so the fear must have been eradicated.
● The first stage of systematic desensitisation is to break the phobia down into an anxiety
hierarchy, ranking presentations of the stimulus from least feared (a picture of a bee) to
most feared (being in a room with lots of bees).
● Relaxation techniques such as breathing exercises are then taught by the therapist.
● As they are exposed to each stage of the anxiety hierarchy, clients are encouraged to
relax at each stage in a stepped approach (once the client is able to relax at the stage
they feel a bit anxious at, then moving on to the next slightly more anxiety-inducing
situation ..etc). This gradual exposure leads to the extinction (loss of an association)
of the fear association and formation of a new association with relaxation.

➔ Flooding counter conditions phobias by immediate full exposure to the maximum

level of phobic stimulus (i.e: being put in a room with lots of bees). The scenario would
be adjusted to make it safe (i.e: Laura given a beekeeper suit to prevent stings). This
immediate exposure will cause temporary panic in the client while they are bombarded
with fear, and they may even attempt to escape to avoid the phobic stimulus. The
clinician’s job is to prevent avoidance by preventing the client from ending the
treatment. Eventually temporary panic will stop and the client will calm down, anxiety will
have receded and the fear will be extinguished due to exhaustion.
➔ Flooding can be in vivo (real life stimulus) or in vitro (situation is imagined by patient).
Evaluation
★ While both SD and flooding may be effective in the clinical setting, it may be that the
effect is not generalised to the outside world.
★ McGrath et al. (1990) found that 75% of patients with phobias were successfully treated
using systematic desensitisation, when using in vivo techniques (see below). This shows
that systematic desensitisation is effective in treating phobias.
★ Further support comes from Gilroy et al. (2002) who examined 42 patients with
arachnophobia (fear of spiders). Each patient was treated using three 45-minute
systematic desensitisation sessions. When examined three months and 33 months later,
the systematic desensitisation group were less fearful than a control group (who were
only taught relaxation techniques). This provides further support for systematic
desensitisation, as a long-term treatment for phobias.
★ However, systematic desensitisation is not effective in treating all phobias. Patients with
phobias which have not developed through a personal experience (classical
conditioning) for example, a fear of heights, are not effectively treated using systematic
desensitisation. Some psychologists believe that certain phobias, like heights, have an
evolutionary survival benefit and are not the result of personal experience, but the result
of evolution. These phobias highlight a limitation of systematic desensitisation which is
ineffective in treating evolutionary phobias.
★ Systematic desensitisation is often thought to be more successful than flooding as the
client is in control of their progress, not the therapist.
★ Flooding is not appropriate for older people, people with heart conditions, children, or
abuse victims due to ethical concerns, whereas systematic desensitisation is ethically
suitable for almost all people. There are ethical concerns as flooding exposes
participants to emotional harm, and it could also end up reinforcing the phobia if
treatment is ended too soon.
★ One strength of flooding is it provides a cost effective treatment for phobias. Research
has suggested that flooding is comparable to other treatments, including systematic
desensitisation and cognition therapies (Ougrin, 2011), however it is significantly
quicker. This is a strength because patients are treated quicker and it is more cost
effective for health service providers.
★ Although flooding is considered a cost effective solution, it is highly traumatic for patients
and causes a high level of anxiety. Although patients provide informed consent, many do
not complete their treatment because the experience is too stressful and therefore
flooding is sometimes a waste of time and money as many patients do not finish their
therapy. Systematic desensitisation has a higher completion rate, perhaps because it is
a more pleasant experience.
★ Although flooding is highly effective for simple (specific) phobias, the treatment is less
effective for other types of phobia, including social phobia and agoraphobia. Some
psychologists suggest that social phobias are caused by irrational thinking and are
not caused by an unpleasant experiences (or learning through classical conditioning).
Therefore, more complex phobias cannot be treated by behaviourist treatments and may
 be more responsive to other forms of treatment, for example cognitive behavioural
therapy (CBT), which treats the irrational thinking.
★ Alternative treatments for phobias exist, such as drug treatments. These are often used
as a short term solution before talking therapies. Examples are anxiety disorder
tranquilisers such as Benzodiazepines, and beta blockers such as Propranolol.
Antidepressants can also be prescribed, but all of these drugs simply suppress the
symptoms without addressing the underlying cause, and can also cause side-effects. As
talking therapies are more effective in the long term they are the preferred treatment
plan.
★ Both systematic desensitisation and talking therapies take a number of sessions to
complete and require 1:1 time with the therapist, resulting in a substantially higher cost
than for drug treatments.

The cognitive approach to explaining and treating depression: Beck’s negative triad and
Ellis’s ABC model; cognitive behaviour therapy (CBT), including challenging irrational
thoughts
● Cognitive explanations for depression- The cognitive approach suggests that
depression results from faulty cognition/faulty information processing/negative thinking
about events (so disturbances in thinking).
● Cognitive psychologists say that we have a mental framework for objects and events
(schemas) that work as shortcuts in understanding the world. This includes schemas
about ourselves. Depression can result from our self-schemas being negative.

★ One cognitive explanation for depression is Beck’s negative triad. It

states that events are seen by the sufferer with a pessimistic/negative
bias due to the development of negative schemas about the world, the
self, and the future. This can lead to overgeneralisation (problems in one
situation being seen as a problem in others), magnification of problems
(seeing them as more important than they are), selective perception
(focusing on the negative), and absolutist thinking (all or nothing).
Overly magnificent shellfish ass

● Another explanation is Ellis’ ABC model. This model states that people respond in
different ways to stresses and challenges in life. Ellis suggests that this difference
depends on their beliefs, resulting in different consequences for different people.
The activating event (A) is the external situation that there will be a reaction to. The
belief (B) is why the individual thinks that the activating event happened (rational
or irrational). The consequence (C) is the behaviour and emotions caused by the
person’s beliefs about the activating event. In depression the activating event is
blamed for the unhappiness felt.
● Ellis suggests that Musturbatory thinking (thinking in absolutes and that the world
must be a certain way for us) is a common type of belief that leads to unhappiness.
Evaluation
★ Hammen and Krantz (1976) found support for negative cognitive distortions in
depressed female undergraduates compared to a female undergraduate non-depressed
control group when presented with a short story, with the depressed females showing
more errors in logic when interpreting the narrative.
★ Cognitive explanations for depression have been used to develop successful and widely
used CBT and REBT (see below) treatments. The success of these treatments is shown
by March et al (2007) who compared CBT with medication and found an effectiveness
rate of 81% for both treatments, suggesting that the underlying cognitive theory that
depression is due to faulty cognitions is valid as the treatment based on that idea
is effective.
★ The cognitive explanation cannot explain why some depressive patients have manic
phases in which they exhibit a large amount of energy and confidence in short burst
before returning to their depressive state. Also many patients have significant anger
management issues, which the cognitive explanation also fails to explain.
★ Placing the responsibility for depression in the hands of the patient could either empower
the patient to help themselves or potentially be a cause of ‘blaming the victim’, especially
if there are contributing factors like grieving or poverty.
★ There is significant evidence that biological factors play a large role in depression, with
some people being genetically vulnerable and a neurochemical factor being apparent
from the effectiveness of antidepressant medication. This means that the cognitive
explanation cannot be a full explanation.

● The cognitive approach to treating depression- Cognitive behavioural therapy

(CBT) is a talking therapy that focuses on identifying and challenging irrational
thoughts. Activities are set to change behaviours.
● Beck’s CBT is a 16-20 week program that focuses on present experiences and
issues. The therapist trains the patient in thought-catching, that is identifying and
recording their automatic negative/irrational thoughts. Once identified the negative
thoughts are challenged and reconstructed to avoid distortion due to the negative
triad.
● The patient can reality-test their irrational thoughts by carrying out homework tasks
such as testing new ways of thinking/behaving and then evaluating the evidence
with the therapist. Diaries may also be used as evidence.
● Patients are encouraged to take part on enjoyable activities that those with depression
often avoid in a process called behavioural activation. This improves emotions and
challenges irrational thoughts.

★ Another form of CBT is Ellis’ Rational Emotive Behavioural Therapy (REBT). In this
therapy Ellis’ ABC model is developed to the ABCDE model, with D being disputation
of irrational beliefs, and E being effective change resulting from the changed
beliefs. REBT is characterised by intensive disputation (arguing against
assumptions underlying irrational beliefs). These arguments can either be logical
(do the beliefs make sense) or empirical (is there evidence for this belief).
Evaluation
★ March et al (2007) compared three groups: those with medication only, those with CBT
only, and those with both over 36 weeks using 327 participants. Found both CBT and
medication alone had 81% effectiveness for depression alone and 86% when combined.
Suggests that CBT is as effective as medication.
★ CBT is not appropriate for patients who are severely depressed as they are
unwilling/unable to engage with the difficult psychological work. In these cases it is more
appropriate to take medication until they improve their mood enough to engage in
therapy.
★ 16-20 sessions with a trained professional is a considerable investment of time and has
considerable costs associated with it. This may mean that access is limited in a health
service, with limited funds making CBT a less viable treatment compared to cheaper and
more accessible antidepressants.
★ CBT could be seen as empowering the patient as in the therapy they act as an engaged
and active force in their own recovery, whereas antidepressant medication places the
patient into a passive role.
★ The success of CBT as a treatment has likely had a positive impact on the wider
economy. People being more in control of their mental health results in fewer sick days
and improves their productivity whilst at work.

The biological approach to explaining and treating OCD: genetic and neural
explanations; drug therapy
● Genetic explanations of OCD- The genetic explanation suggests that OCD may be
inherited, as gene markers predict its presence.
● Individual genes such as Gene 9, COMT, and SERT seem to be present with OCD,
however there may be as many as 230 separate genes that may be involved in the
development of OCD meaning that the disorder is polygenic. It is also aetiologically
heterogeneous as because there are many candidate genes, different gene
combinations could lead to OCD.
● The COMT gene is associated with the regulation of the neurotransmitter dopamine.
One variation of the COMT gene results in higher levels of dopamine and this variation
is more common in patients with OCD, in comparison to people without OCD.
● The SERT gene (also known as the 5-HTT gene) is linked to the neurotransmitter
serotonin and affects the transport of the serotonin (hence Serotonin Transporter),
causing lower levels of serotonin which is also associated with OCD (and
depression).
★ Lewis (1936) examined patients with OCD and found that 37% of the patients with OCD
had parents with the disorder and 21% had siblings who suffered. Research from family
studies, like Lewis, provide support for a genetic explanation to OCD, although it does
not rule out other (environmental) factors playing a role.

● Neural explanations of OCD- Neural explanations of OCD focus on neurotransmitters

as well as brain structures in the development of OCD.
 ● Neurotransmitters- The neurotransmitter serotonin is believed to play a role in OCD.
Serotonin regulates mood and lower levels of serotonin are associated with mood
disorders, such as depression. It may be that serotonin prevents the repetition of
tasks, and that if it is in too low a level, or is removed too quickly from the synaptic
systems, before it is able to inhibit the repetition of an action, and this may result in
obsessive thoughts. Furthermore, some cases of OCD are also associated with the
reduced levels of serotonin, which may be caused by the SERT gene (see above).
Further support for the role of serotonin in OCD comes from research examining
anti-depressants, which have found that drugs which increase the level of serotonin
are effective in treating patients with OCD.
● In addition, the neurotransmitter dopamine has also been implicated in OCD, with higher
levels of dopamine being associated with some of the symptoms of OCD, in
particular the compulsive behaviours.

➔ Brain structures- Two brain regions have been implicated in OCD, including the basal
ganglia and orbitofrontal cortex.
➔ The basal ganglia is a brain structure involved in multiple processes, including the
coordination of movement. Patients who suffer head injuries in this region often
develop OCD-like symptoms, following their recovery. Furthermore, Max et al. (1994)
found that when the basal ganglia is disconnected from the frontal cortex during surgery,
OCD-like symptoms are reduced, providing further support for the role of the basal
ganglia in OCD.
➔ Another brain region associated with OCD is the orbitofrontal cortex, a region which
converts sensory information into thoughts and actions. It predicts future events
and controls impulses from the limbic system. PET scans have found higher
activity in the orbitofrontal cortex in patients with OCD. One suggestion is that the
heightened activity in the orbitofrontal cortex increases the conversion of sensory
information to actions (behaviours) which results in compulsions. The increased
activity also prevents patients from stopping their behaviours.
➔ There is also abnormal activity in the parahippocampal gyrus, which regulates
unpleasant emotions.
Evaluation
★ One strength of the biological explanation of OCD comes from research from family
studies. Research from family studies, like Lewis, provide support for a genetic
explanation to OCD.
★ While evidence from family studies seem to indicate a strong genetic factor, these
studies cannot fully control for the influence of shared environmental factors such as diet
and social learning theory in their methods. Conversations about and awareness of OCD
will be more common with a sufferer in the household, making other family members
more likely to seek treatment, making this genetic link seem greater than it already is.
★ Further support for the biological explanation of OCD comes from twin studies which
have provided strong evidence for a genetic link. Nestadt et al. (2010) conducted a
review of previous twin studies examining OCD. They found that 68% of identical twins
 and 31% of non-identical twins experience OCD, which suggests a very strong genetic
component.
★ Support for the neural explanations of OCD come from research examining biological
treatments including antidepressants.
★ Hu (2006) found genetic differences between 169 OCD sufferers and 253 controls that
impacted the function of serotonin transporters in the brain, supporting genetic and
neural explanations.
★ Antidepressants typically work by increasing levels of the neurotransmitter serotonin.
These drugs are effective in reducing the symptoms of OCD and provide support for a
neural explanation of OCD.
★ However, no twin study has found a concordance rate of 100% in identical twins, which
means that biological factors are not the only factor contributing to OCD and there must
be environmental factors which also contribute to this disorder.
★ Effectiveness of drug treatments (SSRIs, see below) indicate that the neural
explanations are valid, but drugs that work on the serotonin system simply cover up
symptoms and don’t treat the root cause.
★ The biological explanation could be seen as biologically deterministic as it suggests that
OCD is due to uncontrollable genetic and neuronal factors. However cognitive
explanations say that OCD is due to faulty information processing, and can be cured by
the use of conscious thought in challenging irrational beliefs. Some psychologists
suggest that OCD may be learnt through classical conditioning and maintained through
operant conditioning stimulus (for example, dirt) is associated with anxiety and this
association is then maintained through operant conditioning, where a person avoids dirt
and continually washes their hands. This hand washing reduces their anxiety and
negatively reinforces their compulsions. As OCD symptoms has been shown to be
reduced by cognitive therapies such as CBT, the validity of this deterministic viewpoint
can be questioned.

Drug therapy- Biological treatments for OCD aim to restore biological imbalances, such as too
little serotonin. Drug treatments are based on the assumption that chemical imbalances are the
main cause of the problem. Two types of drug are used for the treatment of OCD: (1)
antidepressants and (2) anti-anxiety drugs.

● Antidepressant drugs- The biological explanation

suggests that OCD (and depression) is the result of low
levels of the serotonin in the brain. SSRIs (selective
serotonin reuptake inhibitors) are one type of
antidepressant drug, which include drugs like Prozac.
● When serotonin is released from the presynaptic
cell into the synapse, it travels to the receptor sites on the
postsynaptic neuron. Serotonin which is not absorbed into
the postsynaptic neuron is reabsorbed into the sending cell
(the presynaptic neuron). SSRIs increase the level of
 serotonin available in the synapse by preventing it from being reabsorbed into the
sending cell. This increases level of serotonin in the synapse and results in more
serotonin being received by the receiving cell (post-synaptic neuron).
● If SSRIs are ineffective then non-selective reuptake drugs called tricyclics (such as
clomipramine) may be used, as may SNRIS that influence noradrenaline, however
these are often second choice due to their more intense side effects.
● Antidepressants (like anti-anxiety drugs) improve mood and reduce anxiety which is
experienced by patients with OCD.

➔ Anti-anxiety drugs- Benzodiazepines (BZs) are a range of anti-anxiety drugs, which

include trade names like Valium and Diazepam.
➔ BZs work by enhancing the action of the neurotransmitter GABA (gamma-aminobutyric
acid).
➔ GABA tells neurons in the brain to ‘slow down’ and ‘stop firing’ and around 40% of the
neurons in the brain respond to GABA. This means that BZs have a general quietening
influence on the brain and consequently reduce anxiety, which is experienced as a result
of the obsessive thoughts.
➔ In severe cases that don’t respond to drugs patients can have surgery to alter the
communication between the orbital frontal cortex and other areas of the brain
(psychosurgery), stopping the loop of continuous checking behaviour. A new
experimental technique is deep brain stimulation, where electrodes are placed within the
brain to interfere with or enhance the function of certain brain regions.
Evaluation
★ In a meta-analysis by Greist (1995) reviewed placebo-controlled trials of the effects of
four drugs on OCD using a total of 1520 participants. All four drugs were found to be
significantly more effective than the placebo, with Clomipramine being the most effective
(the others were fluvoxamine, fluoxetine, and sertraline). So biological treatments for
OCD often have strong evidence such as highly controlled drug trials to show the
effectiveness of biological treatments.
★ Soomro et al. (2008) conducted a review of the research examining the effectiveness of
SSRIs and found that SSRIs were more effective than placebos in the treatment of OCD,
in 17 different trials. This supports the use of biological treatments, especially SSRIs, for
OCD.
★ Cognitive neuroscience applied to OCD is now producing biological treatments that
involve direct deep brain stimulation using electrodes to affected areas of the brain to
reduce the presence of obsessions. It is hoped that these treatments will be able to
replace drugs in severe cases.
★ Publication bias is an issue when considering the effect of drug treatments, as positive
results are more likely to be published than negative, so it is argued that drug companies
often run trials with the financial incentive to show that their drug is effective, potentially
leading to researcher bias and demand characteristics in participants.
★ Another strength of biological treatments is their cost. Biological treatments, including
anti-depressants and anti-anxiety drugs, are relatively cost effective in comparison to
 psychological treatments, like cognitive behavioural therapy (CBT). Consequently, many
doctors prefer the use of drugs over psychological treatments, as they are a cost
effective solution for treating OCD (and depression), which is beneficial for health service
providers.
★ In addition, psychological treatments like CBT require a patient to be motivated. Drugs
however are non-disruptive and can simply be taken until the symptoms subside. As a
result, drugs are likely to be more successful for patients who lack motivation to
complete intense psychological treatments.
★ However, one weakness of drug treatments for OCD is the possible side effects of drugs
like SSRIs and BZs. Although evidence suggests that SSRIs are effective in treating
OCD, some patients experience mild side effects like indigestion, while other might
experience more serious side effects like hallucinations, erection problems and raised
blood pressure. BZs are renowned for being highly addictive and can also cause
increased aggression and long-term memory impairments. As a result, BZs are usually
only prescribed for short-term treatment. Consequently, these side effect diminish the
effectiveness of drug treatments, as patients will often stop taking medication if they
experience these side effects.
★ Finally, drug treatments are criticised for treating the symptoms of the disorder and not
the cause. Simpson (2004) found relapse (symptoms returning) in 45% of OCD cases
within 12 weeks of stopping medication, compared to only 12% of cases for CBT
patients, suggesting that the drugs are not a long term solution as they do not treat the
underlying cause of OCD.