Analyse etiologies (in terms of biological, cognitive and/or sociocultural factors) of one anxiety/affective/eating disorder

Analyse etiologies (in terms of biological, cognitive and/or sociocultural factors) of one anxiety/affective/eating disorder. (8)

Analyse (8) – Break down in order to bring out the essential elements or structure.

Obsessive Compulsive Disorder (OCD) (anxiety disorder)

Biological etiologies of OCD
Genetic predisposition

McKeon and Murray – OCD prevalence
Description	Relatives of OCD patients were more likely than the rest of the population to suffer from anxiety disorders in general, but no more likely to suffer specifically from OCD.

Neurological factor

An affected neurological pathway that regulates aggression, sexuality and bodily excretions.
The pathway includes the following three regions of the brain:
Orbital frontal cortex (later referred to as OFC)
Thalamus
Caudate nucleus
Caudate Nucleus acts as a break, suppressing signals that triggers anxiety (“worry signals”) from the OFC to the Thalamus, preventing it from hyperactivity.
Damaged Caudate Nucleus therefore increases signals between OFC and Thalamus, resulting in increased anxiety.
Patients with OCD display obsessions and compulsions related to aggression, sexuality, and contamination, much like what this neurological pathway deals with.
The primitive nature of this neurological pathway explains why patients with OCD are often irrational.

Baxter et al. – Caudate Nucleus and OCD
[A]	Observe the differences in brain function in patients with OCD before and after successful treatment.
[P]	PET scanning was used to identify active areas of the brain.
[F]	The right Caudate Nucleus became more active in patients after treatment.
[C]	There is a correlation between the activity of the Caudate Nucleus and OCD.

Neurotransmission

Patients with OCD responds positively to SSRI, suggesting that an imbalance of Serotonin maybe the cause of dysregulation of the neurological pathway.
Low Serotonin levels may cause misinterpretation and over-reaction to external stimulus.
Leading to flawed cognition, developing into obsession.
Lowering Serotonin levels with M-CCP (meta-Chlorophenylpiperazine) made the symptoms worse. (Hollander et al.)
Anti-depressants, which increases serotonin levels, can reduce OCD symptoms. (Pigott et al.)

Cognitive etiologies of OCD

Distorted cognition formed during early stages of life may have led to OCD.
The following are false beliefs/schemas which patients with OCD often have:
Exaggerated responsibility in preventing misfortunes or harm to others.
The belief that certain thoughts should be controlled
The belief that having a thought or urge to do something will increase its chances of coming true.
Tendency of overestimating danger.
Perfectionist.
Compulsive routines are responses for the anxiety caused by these obsessions.
Argued to be a learned, conditioned process to neutralise the anxiety.
The relaxing feeling motivates the repetition of the compulsive routines.
Patients with OCD believe that there will be negative consequences if compulsive routines are not carried out.

Cognitive Triad (Theorist: Beck)
Self <=> World <=> Future
Example:

Self – “I am going to do really bad in my coursework”
World – “Everyone probably thinks I suck”
Future – “I am going to fail my course”

Beck’s Cognitive Triad suggests that patients with OCD have choose to generated their own obsessive thoughts.
Since decision making is a cognitive process, it can be seen that OCD may primarily be cause by cognitive distortion.
Leading to compulsive acts as a method of neutralisation.

Socio-cultural etiologies of OCD

Few people believe that the etiology of OCD is based on sociocultural factors.
Hence very few studies have been done to investigate this area.
There are studies that focuses on whether or not “demographic factors…and personal characteristics…[have] an impact on the development of OCD.” (Sullivan, 2008)

Sullivan – Factors Related to OCD
[A]	Examining the relation between academic majors/minors of college students, birth order, gender, level of stress, locus of control and the amount of obsessive-compulsive (OC) behaviors.
[P]	All participants were selected through convenience sampling. A sample of 75 undergraduate students was surveyed. 51 females, 24 males 46 students with science/business majors/minors 26 students with liberal arts/humanities majors/minors 30 first born or only children 43 standing lower in the birth order Questionnaires assessing OC behavior using a 1-7 Likert scale were administered to participants. Questions were based on the Yale-Brown Obsessive Compulsive Scale (Y-BOCS), including 26 questions measuring obsessive thoughts and compulsive behaviors. Relationships between the different demographics and OC behaviour were determined using a t-test or a Pearson Correlation.
[F]	Results supports the following hypothesis: Females reporting more OC behaviors. Participants with greater stress level reporting more OC behaviors. Results do not support the following hypothesis: First born and only children reporting more OC behaviors. Students with external locus of control reporting more OC behaviors. Difference in the amount of OC behaviors among students in Science majors/minors vs. Liberal Arts/humanities majors/minors.
[C]	Greater stress level means higher level of anxiety. Prevalence of OC behaviour in this demographic can arguably be a response to sooth the high anxiety level. Corresponds to previous studies (Bogetto et al., 1999). Most demographics chosen were not equally sampled, and this sample size is not representative of the population.

Full study report can be found here

Depression (affective disorder)

Socio-cultural etiologies of depression
Diathesis Stress Model
Claims that depression may be a result of inherited predisposition and events from the environment (hence dia-thesis, two explanations).

Lewinsohn et al (2001)
Description	Studied adolescents who experienced many negative life events over a 12 month period. Those who had strongly negative attributions at the start of the study were much more likely to develop major depression. Diathesis Stress Model (Events from the environment)

Vulnerability Model (Theorist: Brown)

Losing either parent at a young age
Lack of confiding relationship
More than three young children at home
Unemployment

Brown & Harris – Social origins of depression in women
[A]	Find out the social origins of depression in women.
[P]	Studied women who received hospital treatment for depression. Sampled 458 women in the general population aged between 18 to 65.
[F]	82% of those who became depressed had recently experienced severe life changing event(s). 33% experienced severe life changing event(s) in the non-depressed group. 23% percent working class women became depressed within the past year. 3% in the middle class. Those with a young children were at higher risk of becoming depressed.
[C]	Life events that resembled previous experiences were more likely to trigger depression.
[E]	Relatively big sample group, representable of the general population, results can be generalised. Cultural factors were not taken into consideration.

Symptoms of depression in different cultures – Marsella

Affective symptoms (sadness, loneliness, isolation) are typical to individualist cultures
Collectivist cultures have a stronger and tighter social network to support individuals
Somatic (physical) symptoms are more common (headache etc.)

Prince – Depression in Africa and Asia
Study brief	Study claims that there were no signs of depression in Africa and parts of Asia. Reported depression rose with westernization in colonial countries.
[E]	Researchers argue that depression is not exactly the same globally. Depression may be expressed differently and may escape the attention of people from different cultures. Asian and African countries tend to be more collectivist. People from collectivist society might not report depression since it might affect others in the social network.

Cognitive etiologies of depression
Learned helplessness and hopelessness (Theorist: Seligman)

Learn that you are helpless therefore lowering one’s self esteem
Explains withdrawal
Link to Faulty Attributions

Seligman – Learned Helplessness Dog Study (Depression)
[A]	Prove that Learned Helplessness can lead to depression.
[P]	A dog was trapped in an enclosed area where the floor was lined with electrodes. The experimenter would activate the electrode once in a while. The dog would jump over a low wall to the other side of the enclosed area where no electrodes were on the floor. The experimenter raised the wall slowly until it was too high for the dog to jump over. Then after a few trials, the experimenter lowered the wall again.
[F]	The dog gave the high wall a few attempts. But after knowing that it is impossible to jump across, the dog gave up and let itself get electrocuted. When the walls were lowered again, the dog did not attempt to jump across.
[C]	The dog learnt that he is incapable of jumping across. Learn that its are helpless therefore lowering its self esteem.
[E]	Low in ecological validity, lab experiment. Controlled, no confounding variable. Animal experiment can provide insight into human behaviour. Unethical, participants did not have rights to withdraw. Induced fear and depression into participants.

Faulty attributions (Theorist: Abramson)

Negative mind set
Explains self blame, guilt
Pessimists
Attribution of negative events to Internal, Stable, and Global hence affecting their self esteem.
Internal: Dispositional attribution
Stable: Happens every time
Global: Happens all the time, every situation

Negative self schema (Theorist: Beck)

Develops early on in life
Relies heavily upon parental influences
Negative self schema, new event interpreted negatively regarding yourself.

Cognitive Triad (Theorist: Beck)
Self <=> World <=> Future
Example:

Self – “I am going to do really bad in my coursework”
World – “Everyone probably thinks I suck”
Future – “I am going to fail my course”

Biological etiologies of depression
Neurotransmitter-Serotonin

Responsible for our Mental Wellbeing (Happiness)/Depression
During the process of neurotransmission, not all Serotonin gets absorbed by the Post-Synaptic neuron.
The extra Serotonin is taken back into the Pre-Synaptic neuron through Active Reuptake; or
The Serotonin gets broken down by Monoamine Oxidase (MAO), which causes a low level of Serotonin being absorbed by the Post-Synaptic neuron.
Low level of serotonin in the Post-Synaptic neuron means impulse cannot be started.
Diathesis Stress Model (Physical vulnerability to stress)

Teuting – Depression and Serotonin study
Description	Individuals with depression were asked to provide urine sample. There was a significantly lower level of Serotonin in the urine sample of participants with depression. Result of MAO breaking down the Serotonin, correlating to the participant’s depression.