FINALS Psych Paper 2 - Etiology of Abnormal psych ✅

MDD

individual experiences at least two weeks of either a depressed mood or a loss of interest and pleasure

symptoms of MDD

insomnia, appetite disturbances, loss of energy, feelings of worthlessness, thoughts of suicide, or difficulty concentrating

Prevalence rates + disorders | K&U | Prevalence rates definition

proportion of a population that has a specific attribute or disease at a given point in time or over a specified period

Prevalence rates + disorders | K&U | Prevalence rates example (men vs. females)

Depression is about 1.5 times more common among women than among men

Prevalence rates + disorders | K&U | Pregnant example (Pregnant female)

>10% pregnant/postpartum women get MDD

Prevalence rates + disorders | Name both studies

Brown and Harris + Caspi (2003)

Brown and Harris | Strengths and Lims

Strengths:

• Large, representative community sample

• Use of both quantitative and qualitative data (surveys + interviews)

• Independent rating of life-event severity increases objectivity

Limitations:

• Only women from South London → limited generalizability

• Correlational, not causal (no manipulation or control group)

• Retrospective self-report may introduce recall bias

Caspi (2003) | Strengths and lims

Strengths:

• Integrates wide range of empirical and cross-cultural studies

• Theoretical depth linking biological, social, and cognitive factors

• Highlights consistent patterns across multiple populations

Limitations:

• Secondary data analysis → relies on quality of existing studies

• Potential publication bias in reviewed literature

• Cannot establish direct causality or measure variables empirically

Prevalence rates and disorders | Critical Thinking

Bidirectional ambiguity 

Potential applications

• Changes in prevalence rates of disorders may lead psychologists to generate new theories about the origins of a disorder

• Targeted solutions/therapies

Caspi (2003)

Topic:

Year:

RM:

Sampling method:

Sample:

Measurement method:

Topic: prevalence rates, bio explanation for disorder

Year: 2003

RM: Longitudinal quasi-experiment (0-26 years old)

Sampling method: Using database

Sample: 847

Measurement method: stressful life events using LHC (Life-history calendar) + frequency of depression using the DIS (Diagnostic Interview Schedule)

Brown and Harris

Topic:

Year:

RM:

Sampling method:

Sample:

Measurement method:

Design:

Topic: Prevalence rates, sociocultural explanation of disorder

Year: 1978

RM: Quasi experimeent

Sampling method: Purposive sampling

Sample: 395 women from south london

Measurement method: Present State Examination (PSE) to measure psychiatric symptoms, life events interview independently rated for severity

Design: Survey + interview

Explanations for disorders | Biological | Genetic Heritability K&U

• Depression tends to run in families; suggesting genetic inheritance may be a factor

• Research from twin studies allows us to investigate the extent to which the predisposition to depression can be inherited

• Comparing concordance rates (rate of probability that two people with shared genes will develop the same behaviour)

Explanations for disorders | Biological | Serotonin hypothesis K&U

• Serotonin hypothesis

• Serotonin is a neurotransmitter that plays a key role in many different physiological and psychological phenomena.

• In psychology it is believed to play an important role in mood stabilization.

• 5HTT transporter gene

Serotonin hypothesis

serotonin plays a role in the onset of MDD

Kendler - Aim

A: To investigate the extent to which genetics influence the development of Major Depressive Disorder (MDD).

Kendler - Method

M: Large-scale twin study using 15,493 complete twin pairs from the Swedish Twin Registry (born 1886–1958) with verified zygosity.

Kendler - Procedure

P: Conducted structured telephone interviews (1998–2003) assessing lifetime MDD using modified DSM-IV criteria and collecting data on shared and individual-specific environmental factors.

Kendler - Results

R: 8,056 twins met MDD criteria; monozygotic twins showed significantly higher concordance rates than dizygotic twins; estimated heritability was 0.38; heritability was higher in women; no link was found between years living together and MDD occurrence.

8000 = depressive symptoms

300 = admitted to history of using antidepressants

Kendler - Conclusion

Genetic factors substantially contribute to MDD, particularly in women, while shared environmental influences appear minimal in comparison to individual-specific experiences.

Kendler - Strength & Limitations

Strengths

• Large Sample Size: enhancing its statistical power and generalizability.

• Longitudinal Nature: a more comprehensive investigation of MDD across different time periods.

• Focus on Genetics: The distinction between MZ and DZ twins provided a clear picture of the genetic influence on MDD.

• Twin studies: can more easily assume a shared environment, isolate the gene aspect more than other events that could have ceased them depression.

Limitation

• Self reported data

• Oversimplification

• Correlational (No cause and effect)

Explanations for disorders | Biological | Critical Thinking

• Gene environment interaction (Caspi)

• Oversimplification 

• No cause and effect

Explanations for disorders | Biological | Evaluate Critical Thinking

• Alt explanation (Socio/Cog)

• Normal discuss BICT

• Equal Environment Fallacy

Explanations for disorders | Cognitive | Beck’s Cognitive vulnerability K&U

1. Automatic thoughts - sub-vocal semi-conscious narratives that accompany everything you do

2. Cognitive triad - a depressed person has three deeply negative beliefs about aspects of reality (The self, The world, The future)

3. Negative self-schemas

4. Faulty thinking patterns - negative beliefs that the person has, leading to cognitive biases that influence how daily experience is processed

Explanations for disorders | Cognitive | Rumination K&U

• Repetitive excessive thoughts on depressive symptoms 

• Can’t think of solution → hopelessness

Joiner et al. (1999) - Aim

To investigate whether dysunctional thinking patterns predict depressive symptoms (but not anxiety) following stressful life events.

Joiner et al. (1999) - Method

Natural experiment with 119 American university students enrolled in an abnormal psychology course; questionnaires measured cognitive style and mood.

Joiner et al. (1999) - Procedure

Students completed the Dysfunctional Attitudes Scale (DAS), Cognitive Checklist (CCI), and Beck Depression Inventory (BDI) before and after experiencing a natural stressor—their midterm exams.

Joiner et al. (1999) - Results

Only students with high DAS scores who failed the exam showed a significant increase in BDI scores, indicating higher depressive symptoms; anxiety levels were unaffected

Joiner et al. (1999) - Results

Dysfunctional thinking patterns combined with stressful events increase vulnerability to depression, supporting cognitive vulnerability models of MDD.

Joiner et al. (1999) - Strengths and limitation

+ Cognitive Behavioral Therapy was developed based on the theory = high application of findings

- unclear whether negative cognition cause depression or are a result of depression

Nolen-Hoeksem (2000) - Aim

A: To investigate the role of rumination in the development and maintenance of depressive symptoms over time

Nolen-Hoeksem (2000) - Method

M: Prospective longitudinal study of 1,132 randomly selected adults from the San Francisco area using in-home clinical interviews and standardized psychological tests.

Nolen-Hoeksem (2000) - Procedure

Participants interviewed twice over one year using measures such as the Beck Depression Inventory, Hamilton Rating Scale, SCID, and a researcher-designed rumination questionnaire assessing frequency of self-focused, repetitive thoughts.

Nolen-Hoeksem (2000) - Results

MDD = higher rumination scores

No MDD = lowest scores

Those recovered = lower rumination levels than those who remained chronically depressed.

Nolen-Hoeksem (2000) - Conclusion

Rumination predicts the onset and persistence of depression

women who tend to ruminate more = greater vulnerability to depressive disorders.

Explanations for disorders | Cognitive | Critical Thinking

Applications to reserch

Bi directional ambiguity

Measurement Validity Issues due to self reporting bias

Many studies use BDI or symptom scales, not clinical diagnosis

Reductionism

Explanations for disorders | Sociocultural | Brown’s vulnerability model of depression K&U

• risk factors > protective factors = develop depression

• Risk factor - increase the risk of depression in combination with particularly stressful life events

• Protective factors - decrease the risk of depression in combination with particularly stressful events (ex. relationships)

Brown’s vulnerability model of depression - Risk factors

• three or more children under the age of 14

• lacking employment away from home

• loss of mother before the age of 11

• lack of intimate relationship with a husband or boyfriend

Explanations for disorders | Sociocultural | Diathesis-Stress Model K&U

Present genetic vulnerability (5HTT gene with short alleles) + traumatic life stressors (sociocultural!!) = Develop MDD

a mental disorder develops when an individual has a vulnerability or predisposition combined with exposure to stressful life events

Explanations for disorders | Sociocultural | K&U TOPICS

1. MDD

2. Brown’s vulnerability model of depression

3. Diathesis-stress model

Explanations for disorders | Sociocultural | 2 STUDIES

Brown and Harris + Caspi (2003)

Explanations for disorders | Cognitive | 2 STUDIES

Joiner et al. (1999) + Nolen-Hoeksema (2000)

Explanations for disorders | Cognitive | K&U TOPICS

1. MDD

2. Becks’s Cognitive vulnerability model

3. Rumination

Explanations for disorders | Biological | K&U TOPICS

1. MDD

2. Genetic heritability

3. Serotonin hypothesis

Explanations for disorders | Sociocultural | Critical Thinking

Correlation vs Causation

Stress Is Not Uniformly Experienced

Reductionistic

Contrast BIO + SOCIO explanations for disorders - Critical thinking

• Scope: Bio = internal causes; Socio = external environmental causes.

• Causal layer: Bio = predisposition; Socio = exposure to stress and resources.

• Reductionism vs holism: Bio = reductionist; Socio = more holistic and contextual.

Bio underestimates context; Socio lacks precise internal mechanism

Contrast BIO + COG explanations for disorders - Critical thinking

• Core cause claim: Bio = genes & neurochemistry; Cog = maladaptive thinking patterns

• Reductionism type: Bio = biological reductionism; Cog = psychological reductionism

• Measurement style: Bio = more objective (genotype, concordance); Cog = more subjective (questionnaires, thought reports).

Bio risks genetic determinism; Cog risks directionality ambiguity

Contrast COG + SOCIO explanations for disorders - Critical thinking

• Location of cause: Cog = interpretation of events; Socio = occurrence of events

• Intervention target: Cog = change thought patterns; Socio = change social risk/protection factors