Explinations of disorders

Major Depresive Disoder (MDD) is characerized as persistent low moods . diagnosis via the DSM-5 states that paitents needs to have at least 5 symptoms such as constant low mood, loss of ability to feel pleasure from pleasurbale experience, intense feelings of sadness and guilt, apathy, lack of sleep of oversleeping, over or under eating

disorders develop because of biological processes such as genes, neurotransmitters, hormones, or brain function. Some individuals may have a genetic predisposition to developing the disorder. A genetic predisposition means that a person inherits a biological vulnerability,

mental disorders (e.g., depression) result from an interaction between a biological/psychological vulnerability (diathesis) and environmental stressors.

Negative experiences (e.g. abuse, loss, unemployment, trauma) that may trigger depression

Caspi et al 2003

to inevstigate the effect of the size of the 5-HTT gene on likeyhood of MDD

Correlational study, logitiional, quasi
opporunity sample 847 new zealanders that were a part of a cohort of participants who were part of another longitudinal study, When they were 21 using genetic testing to test for varients of the 5-HTT gene and used self-reported measures to measure the exposure to stressful life events and levels of depression until the age for 26
3 groups
2 long allels
1 short and 1 long allele
2 short allele

Paritcipents with one or two short alleles were more likley to develop MDD following stressful life events thus supporting the daithesis stress model and providing evidence as to how genes could be an explination of MDD.

Testable: Researchers could measure: participent genotype, number of stressful life events, symptoms/diganosis for depression, relationship can be emiprically investigated
Empericle: measurable data from: genetic testing, self-reports / assessments of stressful events, diagnostic measures of depression observable evidence rather than theory alone.
Applicable: Helps explain why some people become depressed after stress and others do not, Can improve understanding of risk factors, Supports more personalized mental health interventions, Can reduce stigma by showing depression has a biological vulnerability component
Longitudinal design → can observe development over time

Limits
Construct validity:“ Stressful life events” and “depression symptoms” can be difficult to measure fully, Human depression is complex, so the study may not capture all aspects of the disorder, depression is still a difficult construct to operationalize.
Unbiased: The sample was from New Zealand, so cultural and population bias may limit generalization, Self-reports of life stress may be influenced by memory bias.
Correlational → cannot prove direct causation
Depression is too complex to reduce to one gene
Ethical concern: genetic determinism / labeling
Findings have been debated and not always replicated consistently (Surtees et al., 2006 found no interaction)
May ignore cognitive and environmental factors if used alone

Disorder may be the result of irrational thinking, faulty information processing, and negative schemas

dysfunctional thinking, rather than external events, drives emotional disorders like depression and anxiety
Becks 6 faulty thinking
All-or-nothing thinking – seeing things as black or white
Overgeneralization – seeing a single event as a never-ending pattern
Catastrophizing – expecting the worst outcome
Personalization – blaming yourself for events outside your control
Arbitrary inference: Drawing conclusions based on little to no evidence
Selective abstraction: Drawing conclusions by focusing on a single part of a whole.

Alloy et al (1999)

To investigate whether a person’s thinking style (positive vs. negative cognitive patterns) can predict the development of depression over time.

Longitoonal design
Participants: 473 American college freshmen assessed on their cognitive thinking styles using questionnaires.
Categorized as either having a positive (optimistic) or negative (pessimistic) cognitive style based on their responses
Followed participants for 6 years to see who developed depression.
Researchers periodically assessed participants using standardized diagnostic interviews and self-report measures to track mood changes.

After six years, participants with a negative thinking style were significantly more likely to develop depression than those with a positive style.
The results supported the cognitive vulnerability hypothesis and becks thoery on cognative distortions which states that negative schemas (irrational patterns of thinking) increase susceptibility to depression following stressful events.

This shows that depression has a cognitive explination; negative thinking may increase the chance of getting depression

Strength:
Testabile: ognitive constructs such as negative thinking styles and depressive symptoms were operationalised using standardised questionnaires and structured interviews. This allows hypotheses about the relationship between cognitive biases and depression to be tested empirically
E: provides empircle evidence for becks cognative theory of depression by showing that individuals with negative cognitive styles (e.g. catastrophising and negative attributional styles) were more likely to develop depressive symptoms over time.
A: high practical applicability, particularly in the development of cognitive-based treatments such as Cognitive Behavioural Therapy (CBT). By demonstrating that negative thinking patterns are associated with depression, the study supports interventions that aim to identify and restructure dysfunctional thoughts in patients.
P: high predictive validity, as it suggests that individuals with negative cognitive styles are more likely to develop depressive symptoms in the future. This allows psychologists to identify at-risk individuals and potentially intervene before full clinical depression develops.


Limitation:
C: construct validity may be reduced because depression was measured using self-report questionnaires and diagnostic criteria (DSM). This raises the possibility that the study may not fully capture the complexity of clinical depression, as responses could be influenced by subjective interpretation, social desirability, or misunderstanding of questions. Therefore, it is unclear whether the study is measuring true depression or just reported symptoms.
U: potential bias in self-reported data, particularly recall bias, where participants may inaccurately remember or reinterpret past stressful life events. This could distort the relationship between cognitive style and depression. Additionally, participant bias may occur if individuals respond in ways they believe are expected in psychological research.

Both studies show the explinations behind an indivuals susceptiblity to depression. BUt while caspi explore the biolgical explination; depression may be the results of the interplay between genes and the enviroment, Alloy argues the cognative approach to depression: depression is result of cognative thinking styles and eviroment. As a result its important to take in account multple approaches to gain a full undestanding of depression