Prevalence Rates
What are the different measures of prevalence rates?
How does the serotonin hypothesis explain the development of MDD?
Serotonin is a mood-regulating neurotransmitter and must be present at optimal levels.
If there are low levels of serotonin, it could lead to depression.
Some people may have genetic mutations that make them vulnerable to serotonin dysregulation, such as the 5HTT serotonin transporter, which increases their vulnerability to depression.
What does Beck's cognitive triad suggest about the development of depression?
What are the three elements of the vulnerability model?
Protective Factors
Vulnerability factors
Provoking agents
Give two reasons why the higher prevalence of MDD in women than men may be biased.
- Reporting biases: Men are less likely to seek mental health support, hence are diagnosed lesser.
- Gender bias in diagnostic systems: Symptoms in men may present differently - lack of impulse control, irritability, loss of libido, substance abuse. They may get diagnosed for substance abuse rather than depression.
What is the Diathesis-Stress Model?
A psychological theory that attempts to explain behavior as a predisposition genetic vulnerability expressed as a result of stress from life experiences
Can negative thinking patterns explain all symptoms of depression?
No, this is one of the drawbacks of cognitive etiologies. It cannot explain atypical symptoms of depression like hallucinations and delusions.
Is there a bidirectional ambiguity in understanding the link between sociocultural factors and depression?
There is also bidirectional ambiguity. It is unclear whether negative life events cause depression or whether the experience of depression can be the cause of negative life changes such as lack of motivation to work and missing deadlines, or withdrawal from a relationship.
What can we learn about prevalence rates from Parkers research?
The lower prevalence of MDD in Asian collectivist countries may be explained by different expression of symptoms-somatic
The short alleles are the genetic mutation that make people vulnerable to depression.
People who have one or two short alleles they have an increased chance of developing depression when triggered by stressful life experiences.
Unclear whether negative thinking patterns cause depression or depression causes negative thinking patterns.
Alloy et al is a longitudinal prospective study. Negative thinking patterns were tested before participants developed depression, which indicates that these thought patterns cause depression.
How are socio-cultural etiologies of depression deterministic?
It suggests that people with greater risk factors than protective factors will develop depression.
However, people may experience the same or similar conditions and still not develop a mental health issue. There are individual differences - biology, cognition that interact.
What can we learn from Brown and Harris's research about prevalence rates?
Women may experience depression at higher rates because of increased socio-cultural pressures.
However, there seems to be an income effect present too. Working class women with children four times more likely to develop depression than middle class women. Confirmation bias?
The serotonin hypothesis is maintained through some degree of treatment-etiology fallacy. How does Andrews et al.'s argument about treatment delay dispute this?
SSRIs change the levels of neurotransmitters in the nervous system within hours of consumption. However, improvements in MDD symptoms are only observed a few weeks later.
SSRIs change the chemistry of the brain and the body tries to regain homeostasis, which may be the reason behind the positive response rather than the SSRI itself.
What are a few strengths of the cognitive triad of explaining MDD?
Significant empirical support for Beck's theory as it is testable.
It does explain the thought patterns of a lot of people with MDD.
Has been applied to develop Cognitive-Behaviour Therapy, which is widely researched and applied by therapists.
What does the vulnerability model suggest about the development of depression?
Our social and cultural environment can be a risk factor triggering the development of depression or a protective factor in preventing the development of depression.
Depression develops when there are more risk factors than protective factors.
What are some issues in the recording of prevalence rates?
Prevalence rates of disorders may not be a result of an official diagnosis, often times psychometric tools and questionnaires are used to indicate MDD.
Reporting biases and lack of mental health resources across different populations.
Time consuming, by the time prevalence reports are produced, they are outdated.
Why is it reductionist and deterministic to link/attribute MDD to the role of one gene/neurotransmitter?
Several genes and other cognitive + socio-cultural factors are involved in the development of depression, too reductionistic. Must adopt an interactionist approach.
Assumed that because a person has a predisposition or vulnerability, they will develop the behaviour. Genes are neither necessary nor sufficient.
Treatment-etiology fallacy: The biased assumption that the success of treatment reveals the cause of the disorder.
There is a lot of empirical support and practice of CBT, indicating that it is effective. This then upholds the cognitive etiology of depression.
What are some drawbacks of Brown and Harris's research?
It is culturally biased. The research is conducted only on women who belong to an individualistic culture, where self-sufficiency is the goal and support from extended family is not as common as in collectivistic cultures.
Self report of MDD symptoms not official diagnosis
Reliability and confirmation bias: The interviews self-reported; it is possible that the participants presented their experiences in a manner that confirmed the role of social and environmental stressors on the development of depression.