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IB Psychology studies > Abnormal psychology > Flashcards

Abnormal psychology Flashcards

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1
Q

Biological etiology

A

Genetic vulnerability: The inherited characteristics passed on from parents to children that make it more likely that a person will develop an addiction

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2
Q

Gene-environment interaction (G x E)

A

Concept of genes creating a susceptibility to certain environmental factors (genetic predisposition to MDD, but it’s expressed when exposed to certain environmental factors)

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3
Q

Evidence for Gene-environment interaction (G x E)

A

Longitudinal studies + reductionistic methods

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4
Q

Caspi et al’s year

A

2003

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5
Q

Caspi et al’s aim

A

investigate the role of 5-HTT gene on developing depression as a result of stressful environmental variables

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6
Q

Caspi et al’s sample

A

850 New Zealanders (aged 3 to 26)

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7
Q

Caspi et al’s method + procedure

A

Genetic mapping & questionnaires + life calendars

  1. Used genetic mapping to separate sample into 3 conditions; 2 long-alleles, 2 short alleles and 1 long + 1 short allele
  2. Asked participants to record stressful life events on a calendar and had periodic interviews assessing MDD symptoms exhibited by the sample using DSM-iV criteria
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8
Q

Caspi et al’s findings

A

o Short alleles were more prone to depressive response to stressful events (3+ events at 21 –> MDD at 26)
o No difference in the amount of stressful life events the sample experienced

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9
Q

Caspi et al’s evaluation

A 
\+ large sample size
\+ more holistic 
- self-reported answers
- replications don't show the same results 
- correlational 
- low reliability
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10
Q

Kendler et al’s year

A

2006

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11
Q

Kendler et al’s aim

A

to investigate the heritability rate of MDD, differences between male and female, and whether there are environmental factors that affect MDD overtime

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12
Q

Kendler et al’s sample

A

42000 twin pairs listed in National Swedish Twin Registry (born in 1886 to 1958) from 1998 to 2003

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13
Q

Kendler et al’s method

A

Interview
1. Sample was interviewed over the telephone between 1998 to 2003.
2. Assessed their lifetime major depression by using modified DSM-IV criteria
- 8056 twins met the criteria –> 322 twins voluntarily
discussed a history of antidepressant treatment.
- Asked “shared environment” (when they were living
in the same household) + “individual-specific
environment” (adult personal life events)

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14
Q

Kendler et al’s findings

A

o Heritability ~38% (similar to previous studies 35%-45%)
o Significantly higher in females than males and MZ twins than DZ twins
- MZ(female) - 44%
- MZ(male) - 31%
- DZ(female) - 16%
- DZ(male) - 11%
o No significant differences in the roles of genetic and environmental factors in MDD in the three cohorts spanning birth years 1900-1958 (pre & post WWII)

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15
Q

Kendler et al’s evaluation

A

+ The study appears to confirm previous research, strengthening the reliability of the findings.
+ Very large sample size taken from a single population
- Correlational, no cause and effect relationship can be determined.
- No particular genes were isolated and tested in the study.
- Information about life events and depressive symptoms was self-reported
- Demand characteristics as men might be less reliable in their reporting of lifetime MDD than women –> differences
- The interviewers did not officially diagnose the twins, accepted the diagnoses made by clinicians when it was reported by the interviewee (done over the phone questionable validity)

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16
Q

Biological etiology’s evaluation

A

+ Twin studies have been highly reliable in their results.
+ Modern research has allowed us to actually locate the genetic variations using very large sample sizes.
+ Modern research recognizes the interaction of environmental and biological factors.
- Correlational studies do not establish a causal relationship.
- Population validity (twins) - samples are so small that there is difficulty in generalizing results & different from the experience of the general population.
- Impossible to isolate variables and to separate out social factors.
- Reductionist in nature and does not account for the variations in the symptomology of depression (e.g culture, social factors, cognitive mindset, etc.)
- Not yet clear how the 11 genetic markers interact

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17
Q

Cognitive etiology

A

Beck’s Cognitive Theory of Depression
- Patterns of thinking, cognitive distortions & illogical thinking are responsible for our mental disorders
- Focused attention on the symptoms of one’s distress
- Leads to grim, hopelessness & depression
Kinds of illogical thinking processes:
1. Selective attention - focusing on negative aspects, giving it more weight/ importance to it (leads to rumination)
2. Magnification - exaggerating importance of negative life events
3. Overgeneralization - drawing broad conclusions based on single negative life events
**Being trapped within a negative cognitive triad (oneself, the world & the future) –> overwhelming –> increasing negative thoughts & emotions –> MDD
- Uncontrollable negative thoughts, lack of
motivation, constant sadness, paralysis, despair

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18
Q

Theory of rumination

A

Concept that suggests how one focuses their attention on the symptoms of distress, possible causes and consequences, as opposed to its solutions
o Keep ruminators analyzing everything + over-interpreting what others say.
o Leads to feelings of hopelessness about the future and negative evaluations of one’s self.
o Ruminators vacillate between anxiety and depression (uncertainty and hopelessness)
o Prolonged depressed mood –> interferes with good problem solving, and causes friction with friends and family.

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19
Q

Nolen-Hoeksema’s year

A

2000

20
Q

Nolen-Hoeksema’s aim

A

to investigate the role of rumination on symptoms related to MDD via a prospective study

21
Q

Nolen-Hoeksema’s sample

A

1132 randomly selected adults in San Francisco area (via random digit dailing)

22
Q

Nolen-Hoeksema’s method + procedure

A

Interviews
1. Interviewed in person in their own home two times over a period of one year
2. The interview consisted of a clinical interview which lasted for 90 minutes;
o Beck Depression Inventory
o The Hamilton Rating scale for depression
o The SCID
o The Beck Anxiety inventory
3. Given a rumination and coping questionnaire, designed by the researchers
o For example, rate how often they think, “Why do
I react this way”, “I think about how sad I am”, or
“I think that I will lose my job if I don’t get better.”`

23
Q

Nolen-Hoeksema’s findings

A

o Those showing signs of MDD in 1st interview had significantly higher ruminative scores than those who have never been depressed
o Those who had MDD but improved had lower rumination scores than those who remained chronically depressed

24
Q

Nolen-Hoeksema’s evaluation

A

+ Supports Beck’s theory that patterns of cognition can have a negative effect on mental health.

  • Relied on self-report questionnaires rather than diagnoses through clinical interviews
  • Symptoms of depression are not the same as a diagnosis of depression.
  • Small attrition rate (those with the strongest symptoms dropped out –> bias)
  • No information on whether the participants living with depression were receiving treatment or how other protective factors may help them to cope with their disorder.
  • Uncontrolled confounding variables
25
Q

Farb et al’s year

A

2011

26
Q

Farb et al’s aim

A

to investigate the brain activity of formerly depressed patients when watching film clips

27
Q

Farb et al’s sample

A

16 formerly depressed patients & 16 conntrol non-depressed patients

28
Q

Farb et al’s method

A

Longitudinal study + lab experiment w/ fMRI scan

  1. Participants had fMRI scans connected
  2. Participants viewed sad and neutral movie clips
  3. Calculate the correlation between emotional reactivity, neutral responses & relapsing by comparing scans
29
Q

Farb et al’s findings

A

o 10/16 which relapsed during 18-months had more activity in the prefrontal cortex and higher self-reported rumination rates
o Healthy participants only activated their visual cortex
o Within formerly depressed group, viewing sad clips, relapsing patients had higher activity in their medial pre-frontal cortex
Medial prefrontal cortex (mPFC) mediates decision making & retrieval of remote long-term memory
o Exhibits the differences between how formerly depressed people respond to emotional changes
o Tend to obsessively think about negative effects and occurrence (may be connected to LTM)
o Ruminating to understand, analyze & interpret feeling sad –> perpetuating sadness

30
Q

Farb et al’s evaluation

A

+ Provides biological support of the theory of rumination
+ Longitudinal and prospective research
+ Application to treatments on CBT
- Correlational (didn’t isolate any variables & no before-after = no cause-effect inference)
- Small sample size (costly to do large scale fMRIs)
- Lab experimental setting
- Low ecological validity
- Low generalizability
- Researcher bias when interpreting fMRI scans

31
Q

Beck’s cognitive theory of depression’s evaluation

A

+ “Negative triad” accurately describeshow mostdepressed people think about themselves, the world, and their future.
+ Reflects how depressed people have distorted, illogical thoughts, contributes to helplessness and lack of motivation
+ Suggests it’s possible to change negative thought patterns through therapy –> effectively treat depression.
+ Application to Cognitive Behavioral Therapy (CBT), a method of therapy focused on recognizing and changing illogical negative thoughts, is an effective treatment for depression
+ Suggests an explanation for gender differences in prevalence for MDD
- Unclear why certain people develop negative thoughts in the first place.
- Doesn’t take genetic predispose, or negative life experiences to account
- Genetic factors might be the true “root causes” of depression
- Bidirectional ambiguity: Automatic negative thoughts and cognitive distortions couldcause MDD, or it could be asymptomof MDD
- Alternative explanation is biological factors (levels of neurotransmitters) affecting one’s emotions & negative emotion –> negative thought patterns
- Culturally biased samples and case studies (Western)
- Highly theoretical
- Subjective to treatment etiology fallacy (a belief that a favorable response to CBT proves that cognitive patterns results in MDD)

32
Q

Socio-cultural etiology

A

The origins of MDD are stressors from the environment and the resources available for coping with the stressors.

Vulnerability model

33
Q

Vulnerability model

A

Brown and Harris (1978)
1. Protective factors (e.g. a close family bond)
2. Vulnerable factors (e.g. unemployment)
3. Provoking agents (e.g. acute stress)
o Stress from life events can trigger a predisposition to depression

34
Q

Brown & Harris’s year

A

1978

35
Q

Brown & Harris’s aim

A

to investigate how MDD is linked to social factors and stressful life events

36
Q

Brown & Harris’s sample

A

460 women living in South London

37
Q

Brown & Harris’s method

A

Survey

  1. Surveyed sample on their daily life and depressive episodes (focusing on important biographical details (life events/ difficulties faced by the women)
  2. Rated in severity by independent researchers
38
Q

Brown & Harris’s findings

A

o 8% became clinically depressed in the previous year
o 90% of clinically depressed experienced an adverse life event (e.g. loss) or a serious difficulty (e.g. abusive relationship)
o Only 30% of the women who did not become depressed after an adversity event
o Only 4/37 women became depressed without adversity
**Social class - measured by husband’s occupation, played a significant role in the development of depression in women with children
o Working class women with children were four times more likely than middle-class women with children

39
Q

Brown & Harris’s evaluation

A

+ Semi-structured interview (in-depth understanding on sample’s situation)
+ Results are applied to later studies (Hays et al)
+ High ecological validity (surveyed in their natural setting)
+ Longitude
- Culturally biased sample of South London women
- Low generalizability
- Relies on self-reporting answers
- Low accuracy and reliability
- Correlational studies (no control of external variables + no before & after = no cause-effect relationship)
- Bidirectional ambiguity
- Lacks temporal validity (an external validity, the validity of the findings in relation to the progression of time)

40
Q

Hayes et al’s year

A

1992

41
Q

Hayes et al’s aim

A

To test vulnerability factors on the development of depression by examining the impact of social support on HIV-related condition

42
Q

Hayes et al’s sample

A

508 single gay men participating in the San Francisco Men’s Health Study (ages 25 to 54)

43
Q

Hayes et al’s method + procedure

A

Population-based prospective study

44
Q

Hayes et al’s findings

A

o Those rejected by their family members had higher rates of being diagnosed MDD in gay men with HIV
o Those rejected by family had a faster onset of AIDs
o Lack of protective factors in confiding relationships led to more vulnerability to developing MDD

45
Q

Hayes et al’s evaluation

A

+ High ecological validity (naturalistic conditions)
+ Supports Brown and Harris’s vulnerability model
- Culturally biased sample
- Non-generalizable
- Correlational relationship (no cause-effect inference)
- Unable to control external variables or completely isolate variables

46
Q

Vulnerability model’s evaluation

A

+ Supported by biological research on gene-environment results on the role of stress in MDD’s onset
+ Explains differences in class and gender
+ Researcher triangulation used to increase the validity of findings (i.e Brown and Harris study & Hayes et al’s study)
+ Prospective studies has lead researchers to believe there is a cause and effect relationship
- Difficult to operationalize (express or define to determine, prove or measure) stress
- Impossible to isolate variables
- Does not take into account small stressors/hassles
- Culturally limited (most studies are on individualistic cultures) as cross-cultural research is difficult
o Etic: too ethnocentric
o Emic: too difficult to compare disorders

IB Psychology studies (4 decks)

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