Session Two (Phobias)

Question 1

How is a phobia defined?

Answer 1

A strong fear or dislike of a specific stimulus or situation, with associated avoidance behaviour. Specifically is it a fear that cannot be reasonably explained.

Question 2

What are the key features in distinguishing a phobia from a regular fear?

Answer 2

• Phobias are more pronounced, extreme versions of fears (e.g. fearing a tarantula is normal, fearing a house spider is abnormal).
• Has a behavioural component; person changes the way they act to avoid phobia source.

Question 3

At what age to phobias typically manifest?

Answer 3

Simple phobias normally develop in childhood (50% by age 7).

However, many complex phobias such as Agoraphobia or SAD develop in adolescence. (50% by age 13).

Question 4

How is a complex phobia distinguishable from a simple phobia?

Answer 4

Simple phobias revolve around a particular object/animal/situation/activity e.g. dogs, spiders, flying, swimming….

Complex phobias are a disabling fear that occurs to a set of closely linked circumstances linked around a common theme e.g. Social phobia, Agorophobia

Question 5

Where do phobias fit within the DSM?

Answer 5

As an anxiety disorder. ADs are separated into GAD and phobia disorders (which includes SAD).

Question 6

How would you define a panic attack disorder?

Answer 6

Presence of recurrent, unexpected panic attacks followed by at least 1 month of persistent concern about having another PA. Can’t be due to a substance, medication or mental disorder.

High co-morbidity with phobias.

Question 7

What are the symptoms of a panic attack?

Answer 7

Palpitations, High HR, Sweating, Trembling, Shaking, SoB, Choking sensation, Chest pain

Question 8

Describe the relationship between panic disorders and phobias?

Answer 8

Complex. Very high rate of co-occurrence and a seemingly bidirectional relationship (phobias can lead to the development of a panic disorder, and a panic attack can create a phobia of the situation the panic attack occurred in).

Question 9

Describe the prevalence and co-morbidity of phobias?

Answer 9

10-15% over a lifetime.

Very high co-morbidity between panic disorders, GAD, and complex and simple phobias. Complex phobias very easily lead to simple phobias e.g. Agoraphobia leads to a fear of elevators.

Question 10

What are the gender differences in phobias and panic disorders?

Answer 10

Women are more likely to be affected, but men are more likely to harm themselves or commit suicide due to phobias.

Question 11

What are the direct and indirect costs of a psychiatric disease?

Answer 11

Direct = Costs of treatment.

Indirect = Costs not relating to treatment e.g. Time off work.

Question 12

Outline briefly Seligman’s Preparedness theory of phobias?

Answer 12

• Phobias are evolved mechanisms
• Man is born to fear, its in our genetic makeup.
• We are predisposed to react to certain stimuli in a fearful way.
• The majority of common phobias are things we once should have been afraid of (spiders, heights…)
• Natural selection has favoured individuals with a greater propensity for fear of these things.
• In contrast, we do not fear things we legitimately should such as cars and guns, because we haven’t yet evolved these as phobias.

Question 13

What types of studies have provided the most convincing evidence for Preparedness theory?

Answer 13

Twin and Family studies.

Genetic studies have had little success.

Essentially, the evidence suggests there is a genetic link but attempts to find the genes responsible have all failed. This has lead people to study the biochemistry of phobias more closely.

Question 14

How are twin studies used to assess something like the genetic component of phobias?

Answer 14

MZ twins are (in theory) twice as genetically related as DZ twins. If we know the similarity between the two we can treat them as a simultaneous equation.

e.g. if MZ = 0.5, DZ = 0.3 then
(G + F = 0.5) and (0.5G + F = 0.3)
then G = 0.4, F = 0.1

Question 15

How genetically inherited are anxiety disorders?

Hettemma, 2001

Answer 15

Hettemma (2001):
GAD = 32%
Phobias = 20-37%
Panic Disorders = 43%
(remaining variance = unique environment)
Overall, the body of evidence suggests family environment has little to do with phobia development, genetics has something to do with it and personal experiences have a lot to do with it.

Question 16

What are the limitations to using twin studies to investigate genetic link for something like phobias?

Answer 16

• Assuming twins are the same based on their genetic makeup is reductionist.
• Does not take into account the fact they are often treated the same because their twins, creating a number of identical life experiences which could partially explain the link outside of genetic.
• The whole point of twin research is assuming similarities = genetics, differences = personal experience, but much of their similarities likely arise from the similarity of their personal experiences.

Question 17

What do family studies say about phobias?

Answer 17

• Looks to see if specific phobias are more common within specific families.
• Found some evidence to support this, but this could partially be explained by learned behaviour.

Question 18

What are some forms of genetic testing that have been used to study phobias?

Answer 18

• Family linkage studies
• Candidate gene association studies
• Genome wide association studies
• Polygenic risk scores

Question 19

What are family linkage studies and what have they shown us about phobias?

Answer 19

Finds people with phobias, and looks for these phobias in 1st/2nd/3rd degree relatives, then compares broad chromosomal regions.

Some success in proving a genetic link, but nothing concrete and no specific genes identified.

Question 20

What are candidate gene association studies and what have they shown about phobias?

Answer 20

First identified regions along the genome that might have an effect on fear responses (e.g. that code for a protein relating to serotonin transport).
Next found people with and without phobias and compared them at these specific points.

Again, provide some evidence.

Question 21

What are the issues surrounding candidate gene association studies?

Answer 21

• Failure to replicate. Many studies are just too small to provide any reliable conclusions or pick up genes with small effects.
• A further issue is that these theories work around the idea that these genes provide some sort of pre-disposition to phobias, but a participant would still need a triggering life event to actually have the phobia. This makes research very difficult as its hard to identify these factors.

Question 22

What are Genome Wide Association studies and how do they relate to phobia research?

Answer 22

Look at SNPs (single nucleotide polymorphisms), the smallest unit of genetic variation between people.
Look to see if SNP differences affect things like Serotonin activity in the brain (by changing the shape or expression of a transporter, for example).

Question 23

What is the main issue with Genome Wide Association (SNP) research?

Answer 23

Once you get to this level of specificity, looking at single nucleotides, variation between people is bound to crop up, so you need a strong correlation for the evidence to be worthwhile, which hasn’t been found yet.

Question 24

What are Polygenic Risk Scores? What have they shown about anxiety?

Answer 24

A way of looking at genetic links more broadly. Incorporates variation in ALL genes associated with something like anxiety, and gives a person a risk score based on what variant they have.

Found no link between genetics and anxiety. A person’s risk score was not a useful predictor of their anxiety or phobias.

Question 25

What is the supposed link between the Amygdala and Genes in the generation of phobia?

Answer 25

The Amygdala is at least partially responsible for our fear response.

The biological pathway by which these genetic predispositions become full blown phobias may be related to the amygdala.

Question 26

Briefly describe the High and Low roads of fear?

Answer 26

Low Road = Emotional stimulus is picked up by the Sensory Thalamus and crude, archetypal info gets sent straight to the Amygdala, creates an instant response.

High Road = Emotional stimulus still gets sent from the Sensory Thalamus to the Amygdala, but it first passes through the Sensory Cortex which creates a detailed image of the stimulus allowing for a more accurate, measured, but slower. response

Question 27

What evidence is there for the role of the Amygdala in anxiety?

Answer 27

A study found that individuals with social phobia showed a greater degree of activity in the left Amygdaloid-Hippocampal region when they were told they would soon have to speak in front of a crowd when compared to a control (social phobes speaking by themselves).

Question 28

What evidence is there for the role of the Amygdala in phobias specifically?

Answer 28

Dilger (2003)
A study put a group of people with arachnophobia in a FMRI and showed them a variety of images.

Spiders showed greater elevation in activity in the Amygdala, even when compared to other potentially scary images such as snakes.

However there was significant variety amongst participants.

Question 29

Why is it difficult to study the Amygdala’s role in panic disorders and is there any evidence?

Answer 29

Unethical to put someone in an FMRI and induce a panic attack.

HOWEVER evidence from people who’ve randomly had a panic attack in an FMRI supports the notion the Amygdala is somehow involved.

Question 30

What anatomical areas of the brain have shown different levels of activity in anxiety disorders?

Answer 30

• Insula
• Anterior Cingulate Cortex
• Amygdala
• Pre-Frontal Cortex
• Orbito-Frontal Cortex

Question 31

What Neurotransmitter is most commonly linked to phobias and what is the evidence for this?

Answer 31

Serotonin.

Stein (1998):

• 187 phobics given an SSRI or a placebo
• 55% of paroxetine group vs 24% of placebo group were much/very much improved on the global improvement score
• Anxiety score and secondary measures also improved

Otto (2001):

• Meta-analysis of drug studies into panic attacks
• Mean effect size of active vs placebo group differences in panic attacks = 0.55
• Indicating medium effect

Question 32

What are the limitations of SSRI studies into phobias to prove Serotonin’s role in phobias?

Answer 32

Backwards research, taking established therapies and using them to prove the MoA of a condition doesn’t make sense, no way of proving the improvement patients experience is due to the Serotonin’s link or another confounding factor.

Hard to draw a valid conclusion.

Question 33

What are Tryptophan Depletion Studies and what have they shown about phobias?

Answer 33

• Tryptophan is an amino acid, the direct dietary precursor to Serotonin.
• Patients given a nutritionally complete meal but without any Tryptophan, who were then told they’d have to speak publicly had higher levels of salivary Amylase (bio marker for ANS activation)
• Patients with anxiety given the same T depletion meals then put in low CO2 conditions (a natural cause of anxiety) reported higher anxiety symptoms than other people in the same conditions (either w anxiety but w/o T, or w/o anxiety but w normal T levels)

Question 34

Explain the Learning (Fear Conditioning) model of phobia development?

(the nurture part of the nature vs nurture debate)

Answer 34

• Phobias develop over the course of our life and are based on experiences.
• Suggests we initially develop a fear through Classical Conditioning, we associated a stimulus with a fearful reaction/situation, creating a phobia.
• Phobia is then maintained through Operant Conditioning, people avoid the stimuli after these events, preventing the fear from naturally extinguishing itself.

Question 35

What is the main study supporting the Learning Theory of phobia?

Answer 35

Little Albert Study:

• Baby was exposed to neutral stimuli, but when that stimuli (a rat) was paired with a fearful experience (a loud noise), he developed a phobic reaction to the item (Classical Conditioning) which he then applied to other similar stimuli (rabbits, fur coats, Santa) he showed the same fear response (Generalisation).
• Doesn’t totally dispute the preparedness theory, as it suggests Albert always had the potential to fear, just that a conditioning experience was also required.

Question 36

What are some criticisms of Learning theory of phobias?

Answer 36

• Most phobics can’t remember the event that lead to their phobia existing. Water/Flying/Dog phobias are often based on a real event, but Spider/Snake fears are some of the most common in light of the fact people have rarely had any serious contact with them.
• HOWEVER phobias can arise from indirect experience e.g something your mother tells you or in a film you saw (Jaws lead to a spike in water phobias).
• Conversely, many people have negative experiences with Water/Dogs and don’t develop phobias.

Question 37

What do Cognitive Approaches to Anxiety suggest about how phobias develop?

Answer 37

Defects in Information-processing (attention, interpretation, memory) create biases in threat cognitions which create phobias and panic.

Abnormal Attention/Interpretation/Memory –> Biases in Threat Cognition –> Phobias/Panic

Simply put, certain people over and misinterpret what is and isn’t a threat, causing them to over react to certain stimuli, creating phobias.

Question 38

What evidence is there to support the existence of attention biases towards threat (and therefore the Cognitive theory of phobia development)?

Answer 38

Word Colour Studies:

• Give participants a range of words in different colours.
• Words ranged from neutral (e.g. window, bread) to threatening (e.g. death, failure)
• Ask them to state the colour of the word only. Responses were timed.
• Found that patients with a known anxiety disorder (panic, social, or specific) found it more difficult to give the colour of threat words.

Question 39

What are the limitations and support for Colour Word studies>

Answer 39

Limitations = Simple tests like these may not capture a true attention bias, but more their recall of experiences with that given word. This is crucial as it may suggest the delay was caused by past experiences (Learned theory) not internal cognitions.

However this evidence is in fact supported by probe studies, which showed patients focus lingered on threat words when asked to name the non threat word, causing delays.

Question 40

Aside from probe and word colour studies, what other forms of research have provided support for the Cognitive theory?

Answer 40

• Homophone studies. Ask patients to write a sentence involving a word like mug, most people will assume coffee mug but people with anxiety will go for being mugged or being called a mug.
• Word completion studies show similar results.
• As do Ambiguous Scenario studies, provide someone with an ambiguous scenario and ask them to interpret it. Anxious people will interpret it in a negative way.

All this provides support for the existence of cognitive biases in people prone to anxiety.

Question 41

How do Cognitive Interpretation biases affect a person with anxiety’s interpretation of their own body?

Answer 41

Patients with panic disorders have an enduring tendency to misinterpret bodily sensations as a sign of imminent catastrophe e.g.

• Heart racing = Heart attack
• SoB = Imminent suffocation
• Dizziness = Imminent collapse
• Derealisation = Going crazy

Question 42

How do these interpretation biases lead to panic in people with panic disorders?

Answer 42

• Internal or External trigger leads to…
• Perceived thread out of line with actual threat, leads to…
• Anxiety, which creates…
• Physical or Cognitive symptoms, which the person
• Misinterprets as being far more serious than they are, creating
• More anxiety etc…

Patient is likely to respond to this with ‘Safety Seeking Behaviours’ that provide immediate relief but never allow the misperceptions and misinterpretations to be challenged.

Question 43

Briefly explain how all these theories work together?

Preparedness, Learning, Cognitive

Answer 43

1) Genetic Predisposition leads to
2) Abnormal Neurotransmitter Activity leads to
3) Disrupted Fear Circuitry in the brain, which leads to
4) Involuntary detection and appraisal of threat AND Quicker associations between neutral and aversive stimuli AND an increased chance of generalisation AND Resistance to extinction. All of these factors create
5) Anxiety and Avoidance of the feared stimulus, which worsens the processes created by the disrupted fear circuits.

6) N.B. Personal Aversive experiences can also created these disrupted fear circuits.

Question 44

What are the 3 common forms of treatment for phobias?

Answer 44

• Psychopharmacology (SSRIs)
• CBT
• Complimentary therapies

Question 45

What is the basis of CBT?

Answer 45

• CBT is based on the idea that people’s neurotic disorders are largely based on learning from life experiences and that other learning experiences can be used to correct them.
• CBT focuses on helping people identify and correct faulty cognitions.
• Does not target the cause of the anxiety, but rather the more proximal learned associations/avoidance behaviour/threat cognitions.

Question 46

How does exposure therapy work to cure phobias?

Answer 46

1) Teach relaxation techniques
2) Imagine/view progressively anxiety arousing scenes
3) Use relaxation techniques to control response.
4) Eventually associations between relaxation and stimulus overtake the anxiety associations.

Therapy normally starts with the patient ranking a list of phobia related situations on an anxiety scale and the therapist then judges which to use (not too easy or too difficult).

Question 47

How can phobia exposure therapy be enhanced (supposedly, according to recent studies)?

Answer 47

Through use of D-Cycloserine.

DCS = A partial agonist of the NMDA receptor. A study gave acrophobias (simple) doses of DCS or a placebo and then 2 sessions of exposure therapy, found a statistically significant improvement in symptom reduction in those on the DCS.

Studies into SAD (complex) show similar results.