Depressive Disorders

Sociocultural Approach
brown and harris (1978)

hays turner and coates (1992)

Vulnerability Model of Depression

Based on the following factors:

1. Protective Factors

Decrease the risk of depression when combined with stressful life events (strong
sense of community or family bonds are strong)

2. Vulnerability Factors

Increase the risk of depression in combo with stressful life events (loss of parent,
lack of confiding relationship, etc.)

3. Provoking Agents

Acute and ongoing stress

This model can be used to link gender differences and class differences in the prevalence of
depression.

Diathesis-Stress Model
Depression may be the result of a hereditary disposition. The vulnerability model falls in line
with this model, which is widely accepted.

Cultural Models of Depression

Parker, Cheah and Roy (2001)

Kirmayer (2001)

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 Evaluation of sociocultural explanations for depression:
Strengths

Modern biological research supports vulnerability models

Vulnerability models acknowledge the interaction of biological and environmental

factors

Explain gender and cultural differences in symptomology

Limitations

Measuring stressful life events may not be a valid measure of stress

Cultural theories are descriptive in nature, don’t explain the origin of the disorder

Cross cultural research is problematic; etic approaches are too ethnocentric and emic
approaches make comparing the disorder difficult

correlational research means cause and effect relationship cannot be established.

Cognitive Approach
Cognitive theories on depression aim to explain why some people are more vulnerable to
depression when confronted with negative events while others only go through mild short-
term distress.
The interpretation people give to their life experiences influences their vulnerability to
depression.

Beck’s Theory of Depression

Depression is rooted in “automatic thoughts,” negative self-schemas centered around failure,
inadequacy, loss, etc. These thoughts are triggered by stimuli that lead to emotional
responses.

1. The Negative Cognitive Triad: depressed patients have negative views of the self, world,
and future.

2. Negative schemas are triggered by negative life events (dysfunctional beliefs)

a. Formed by family problems, social rejection, or having depressed family members.

b. The schemas are activated whenever a person is placed in a situation similar to the
one where this schema was formed.

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 c. Three main schemas:

i. Ineptness—I always fail

ii. Self blame—It is always my fault

iii. Negative self evaluation—I am worthless

3. Engage in cognitive biases (irrational thinking)

Beck’s 6 Types of Faulty Thinking

There are certain patterns of thinking that are common in depressed patients:

1. Arbitrary interference—drawing conclusions based on little or no evidence

2. Dichotomous thinking—all-or-nothing approach to viewing the world (ex. you either

hate me or love me)

3. Exaggeration—also called magnification. Overestimating the significance of negative

events.

4. Overgeneralization—applying a single incident to similar incidents.(ex. an argument

with a friend means that none of your friends care about you)

5. Personalization—assuming other’s behaviours are done to hurt or humiliate you.

6. Selective abstraction—drawing conclusions by focusing in on one small thing (ex.

focusing on one bad grade when you have an A in the class)

Alloy et al. (1999)

Joiner et al (1996)

It isn’t clear if negative thinking patterns are why depression forms or these thinking patterns
are a consequence of having depression.
If these thoughts are the cause, they are attempted to be treated with replacing negative
thinking patterns with positive ones (cognitive-behavioural therapy).

The role of rumination

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 Nolen-Hoeksema learnt that women are likely to amplify depression by ruminating on their
feelings and its possible causes; they think a lot about how they feel and try to understand
why.
Rumination appears to consistently predict the onset of depression rather than how long it
will last. However, rumination alongside negative thinking can predict the duration of
depressive symptoms.

nolen-hoeksema (2000)

farb et al (2011)

Biological Approach
Genetic Explanations for MDD
Researchers argue that genetic predisposition can party explain depression. One of the main
ways to investigate this is through twin studies (Kendler et al (2006)).

Genetic vulnerability: Depression (and other disorders) may be the result of a genetic
predisposition.

Other studies:

Sullivan et al (2000)

Caspi et al (2003)

Cai et al (2015)

Evaluations of genetic explanations for depression:

Strengths

Twin studies are highly reliable

Genetic variations with large samples can be located using modern technology

Modern research does not use a reductionist approach

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 Limitations

Correlational studies don’t establish a cause and effect relationship

Twin studies struggle with population validity—twins don’t necessarily represent the
general population

Variables cannot be isolated

Studies do not account for the variations in symptoms in different cultures

Not clear how genetic markers interact

Serotonin and Cortisol in Depression (Biochemical)

Those with MDD have an imbalance of many neurotransmitters such as noradrenaline,
serotonin, dopamine, and acetylcholine. However, it is difficult to establish a causation and
researchers are left with bidirectional ambiguity (which variable is impacting the other?)

Serotonin Hypothesis

Argues that reduced serotonin leads to an increased predisposition to depression. Low levels
of serotonin result in:

Obsessive thoughts Mood swings

Compulsive behaviours Worrying

Suicidal thoughts Insomnia

Aggressive behaviour Sadness

Caspi’s research on the origins of MDD demonstrate a potential link to serotonin, since the
genes studied were responsible for serotonin transmission.

However, there is the issue that drugs that increase serotonin levels do not have an impact
until 2-4 weeks afterwards, which suggests that there is another factor that is impacting
depression. Additionally, reducing serotonin levels in a person also does not result in
depression, leaving the Serotonin Hypothesis somewhat dubious.
Neurogenesis Theory of Depression

Depression is a result of the cessation of neuron birth int he hippocampus and other neural
networks such as serotonin, dopamine, etc. Cortisol is the reason for this lack of
neurogenesis.

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 MDD patients appear to have HPA-axis hyperactivity, which results in the secretion of too
much cortisol, which leads to reduced serotonin and other neurotransmitters which are linked
to depression.

Studies on Neurogenesis:

Malberg et al (2000)

Videbech and Ravnkilde (2004)

Evaluations of biochemical explanations for depression:

Strengths:

Longitudinal and animal studies support the theories

Practical applications are successful in regards to drug treatment

Limitations:

Causation cannot be established (issue of bidirectional ambiguity again)

Treatment Aetiology Fallacy: Mistaken notion that success of a treatment shows

the cause of the disorder

Biological explanations don’t explain the range of symptoms; might have cultural
and cognitive factors

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