A01 and Evidence
Biological Explanations of Phobias
CORE IDEAS: combined influence of genes and environmental stimuli causes abnormalities in structure/biochemistry of our nervous system
A02
Genetics
 The main argument from the genetic explanation is that phobic disorders result from faulty genes inherited
from parents. This can affect structure and function of CNS, leading to abnormal thought and behaviour, and
means that disorders should run in families. Therefore the more closely related they are, the more likely
they are to share the disorder.
In terms of evidence numerous family studies have suggested that families who share genes also share
disorders.
Social Phobia
 Reich and Yates (1988) recruited patients from an anxiety treatment centre and found 6.6% rate for
relatives of people with social phobia compared with 2.2% in controls.
 Fyer et al (1993) found that social phobias are considerable more common in the relatives of social phobics
than in the general population. They assessed relatives of 30 patients with social phobias via direct
interview and discovered that 16% of the close relatives of social phobics developed the same disorder,
against only 5% of relatives of individuals without social phobia.
Specific Phobia
 Ost (1992) examined families of people with blood-injection-injury phobia, and found that in 25 blood
phobics, 64% had at least one first degree relative (parent or sibling) with a blood phobia. This is much
higher than the occurrence of a blood-injury-injection phobia in the general population (approx. 3-4%).
Agoraphobia
Harris et al (1983) found that close relatives of agoraphobic patients were more likely to be suffering from
agoraphobia than were the close relatives of non-agoraphobic individuals.
In addition, twin studies have shown that there is a higher concordance for genetically identical monozygotic
(MZ) twins that dzygotic twins (DZ) who share 50% of their genes. These types of study are better than family
studies since both MZ and DZ twins share environments BUT: MZ twins are treated more similarly.
 Kendler et al (1992) administered a structured interview to assess the lifetime history of phobias in 2,163
female twins (MZ and DZ twin pairs). They looked at animal and situational phobia. They found that
genetically identical twins (MZ) are much more likely to both have a specific phobia than non-genetically
identical twins (DZ).
 Torgersen (1983) considered MZ and DZ twins (at least one of whom had panic disorder). The concordance
rate found was 31% in 13 MZ twin pairs for panic disorders and agoraphobia, versus ‘0’ concordance in 16
DZ twin pairs, although none of the concordant twins shared the same phobia.
However
 Kendler et al (1992) interviewed 722 female twins with a lifetime history of phobia. They found that MZ
twins have a significantly lower concordance rates for agoraphobia than DZ twins.
Neurotransmitters: Serotonin/Dopamine and GABA Hypothesis.
 Stein (1998) found that individuals who display the symptoms of phobias seem to have abnormal levels of
the neurotransmitters serotonin and dopamine. This may be related to the increased numbers of serotonin
and dopamine pathways in the limbic system.
 These abnormal levels relate to either too little serotonin (normally inhibitory: calms us) and too much
dopamine (excitory i.e. increases heart rate; associated with rewarding activities/motivation).
 In addition, the GABA hypothesis is proposed to explain the role of neuro transmitters in phobias. It is
proposed specifically to account for phobic disorders and GAD (Bernstein, 1994). Anxiety is believed to
develop from a dysfunction of neurons that normally produce gamma aminobutyric acid (GABA). In normal
functioning, GABA is released automatically is response to high arousal levels. It binds to GABA receptors on
excited neurons, thereby causing them to be inhibited. This results in the reduction of arousal, and
accordingly, a reduction in the experience of anxiety. Those who suffer from phobias, seem to have low
levels of GABA. GABA acts as a natural calming agent in the brain, reducing activity and lessening
physiological arousal. Therefore, phobics may possess less GABA in their systems, resulting in an increase in
their physiological arousal, and this may in turn cause phobics to be more reactive to anxiety provoking
objects or situations. This therefore makes them more likely to develop a phobia. This can exacerbate
phobias by leading to insomnia i.e. inability to calm down, stop worrying and switch off.
Face Validity
The assumption that a person inherits a phobic disorder from their parents makes sense. Therefore, it has face validity because we
do inherit factors such as height, eye colour etc. Consequently, it is logical to assume that we also inherit a genetic predisposition
to be fearful or anxious towards the same object or situation that makes our parents nervous.
Empirical Support
One strength of the genetic explanation is that there is further empirical support. For example, (use a study from the evidence
here). This suggests that there is wider academic credibility for the notion that genes play a significant role in the development of
phobias.
Debate: Reductionist
One weakness of the genetic explanation of phobias is that it is reductionist. This is because the model reduces the causes of
phobias down to simple components such as the role of genetics inherited from parents. Although this allows complicated
behaviours to be scientifically tested and allow for future research/explanations to be developed; taking a reductionist approach
does not allow us to look at the development of phobias from the whole individuals’ perspective. For example, it does not
consider the cognitions that helps maintain the fear of a phobia, it does not consider the avoidance coping strategies that
reinforce a phobia and it does not consider the unconscious thoughts that contribute to maintaining a phobia. This suggests that
the biological model of phobias is over simplistic in its approach when explaining phobias.
Debate: Nature Vs Nurture
Another issue is that if phobias were purely genetic, then concordance rates in twin and family studies should be 100%. Therefore
there must be other causal factors. For example, families share the same environments and identical twins tend to be treated more
similarly than non-identical twins, making it difficult to ignore the role of environmental factors, in particular, Social Learning
Theory. It could be that having someone in close proximity with agroaphobia or a social phobia (i.e. in the same house) has led to
close family members imitating the phobic behaviour and the concordance rates are due to social learning and not a genetic link.
Therefore it is difficult to distinguish between the roles of nature Vs nurture. Although twin studies provide strong evidence for the
role of genetic factors, there is a lack of adoption studies to help verify this.
Debate: Biologically Deterministic
Another weakness of the biological explanation of phobias is that it can be said to be biologically deterministic. This is because it
suggests that an individual is pre-determined to develop a phobia if they receive faulty genes inherited from parents. This in
turn, can affect structure and function of CNS, leading to abnormal thoughts, behaviours and fears. Simply because someone has
a genetic predisposition does not mean that they will develop phobias. It could be that the person has a choice over how they
develop a phobia, for example, deciding whether to imitate a same sex role model and their fears, in terms of Social Learning
Theory. This suggests that the biological model does not account for free will.
The use of drugs

One strength of the neurotransmitter explanation in the development of phobias is that symptoms of phobias can be
alleviated using drug therapy. For example, drugs which increase levels of GABA or mimic its effects in the brain are successful
anxiolytics (anxiety reducing drugs) for some people. This suggests that there is indeed at least a contribution of
neurochemistry in phobias, providing support for the explanation.
Neuroanatomical/brain structure
 The main assumptions here are that phobias are the result of abnormalities in the structure of the brain and
nervous system. This means that such abnormalities may be genetic, but they may also be caused by brain
damage through, for example, injury, stress or illness.
The evidence for this comes from differences in structure where the brains of people with disorders are
shown to differ structurally from ‘normal’ brains. However, just a proximate cause has been identified and we
don’t know what caused the difference. In addition, MRI scans and post-mortem studies tell us nothing about
function.
 The amygadala seems to be responsible for emotion, fearful and stressful responses and especially
associations made between the environment and emotions in humans. This is supported by the recent work
of Dilger et al (2003) who found increased amygadala activation in individuals with spider phobias than
controls. This demonstrates the role of the amygadala in certain anxiety disorders.
 Rauch et al (1995) used PET to examine cerebral blood flow in response to specific phobias. They found that
there was and increased amount of blood flow to areas of the brain known as paralimbic structures. The
paralimbic cortex lies close to the limbic structures, and is directly connected with it. There are dense
connections between the paralimbic cortex and core limbic structures, in particular the amygdala. This
therefore suggests that these structures may play a part in the function and development of phobias.
 Fredrikson et al (1995) used PET scans to compare brain reactions in phobic and non-phobic patients. They
used file clips of the feared stimuli with snake and spider phobics. They found that an area in the brain
commonly associated with phobias and other anxiety disorders, the basal ganglia was not activated more by
phobic stimulation. However, the thalamus always reacted to phobia, but not aversive or neutral
stimulation. They concluded that the thalamus could be implicated in the phobia reaction. (Thalamus function includes relaying sensation, spatial sense and motor signals to the cerebral cortex, along with the
regulation of consciousness, sleep and alertness).
 However, Mountz et al (1989) found no real difference in cerebral blood flow in individuals with a phobia in
a clam state or a phobic state, and there were no real differences between the cerebral blood flows of
phobic and non-phobic participants, suggesting contradictory evidence for the neuroanatomical explanation.
Issues: Methodological Issues
One problem when looking at PET scans and phobias is that they only tell us there is a correlation between brain activity in
particular areas of the brain and performance on specific tasks. This is an issue because researchers can only identify a
relationship between the amygdala and phobias, meaning that cause and effect cannot be established. Therefore we do not
know whether it is increased blood flow to the amygdala that causes the phobia or whether it is the phobia that causes the
increased blood flow to the amygdala. Furthermore it does not consider third factors such as brain damage, viruses, tumours
which could impact upon the amygdala, or whether it is a contributing factor to the phobias itself. Therefore, this weakens the
neuroanatomical explanation of phobias because the studies it is based upon are invalid. This is because they may not be testing
what they set out to test.
There is evidence to suggest that abnormalities in blood flow in the brain may not be consistent in all phobia sufferers. For
example, Furmark et al (2002) found that while successful treatment of phobias using Citalopram or CBT decreased blood flow in
the anxiety regions of the brain, not all people with phobias show the abnormal blood flows. This means that it is not clear
whether these abnormal blood flows are a causal factor of a phobic disorder or a result of the phobia itself. This weakens the
neuroanatomical explanation of phobias because it shows that its assumptions are unreliable as the presence of abnormal blood
flows are inconsistent in people suffering from phobia.
Debate: Nature Vs Nurture
The neuroanatomical approach may not be the most prominent explanation for the existence of phobias. For example, Mountz et
al (1989) found no real difference in cerebral blood flow in individuals with a phobia in a calm state or a phobic state. There was
no real differences between the cerebral blood flows of phobic and non phobic participants. Therefore because brain structure
alone had no impact on the development of phobias it could be that elements of the enviroment are needed to trigger phobias;
suggesting an interactionist approach (diathasis stress model). The explanation itself is an example of a nature/nurture argument.
It is a nature explanation as it states that phobias are due to structural factors that we inherit through genetics, nevertheless it
does not consider the environment in which the individual is brought up. This weakens the this explanation because there is a
wide amount of evidence suggesting that the environment is more important than structural factors for developing phobias.
Most psychologists currently believe that a more interactionist approach between the two provides a more valid explanation for
phobias. However, most evidence suggests that environmental influence is paramount for phobias.
Overall
Biological explanations identify associations between physical abnormality in structure, function and biochemistry of the nervous system and the presence of disorders. But this does not mean a cause has been identified. Furthermore, it offers only
one ultimate cause, that of genetics. But this view cannot explain the presence of all cases of psychopathologies: some sufferers do not have relatives with the same disorder and concordance rates for MZ twins are never 100 per cent
So, we have to look at sufferers’ experiences to identify other ultimate causes that may have led to a change in biochemistry or neuroanatomy. In addition, biological psychologists suggest that there is a diathesis-stress explanation i.e. that people
may be born with a genetic predisposition to suffer from a psychopathology (or a diathesis). So if people suffer some form of stress from the environment, this predisposition may become a pathological problem. The specific form that this stress
takes may be better explained by psychological approaches.
Exam Questions
1a) Discuss biological explanations of phobias (8 + 16 marks). Here you would explain genetics (A01, and explain the evidence) then evaluate the explanation (A02), the same process for neurotransmitters and brain structure.
2a) Explain biological explanations of phobias (8 marks) Here you would either explain (A01) 2 explanations in detail or 3 in less detail. NO A02 points WHATSOEVER!
2b) Evaluate biological explanations of phobia’s (16 marks) Here you would ONLY give A02 points – NO A01 points WHATSOEVER!! Make sure you refer to which biological explanation you are evaluating in your points.
NB: It is ESSENTIAL that you refer to a range of MAID in your A02 points. These must be elaborated and contextualised to the explanation you are referring to.