Discuss / Evaluate one or more biological etiologies of one disorder (Kendler & Caspi) Flashcards

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1
Q

Define MDD

A

Major Depressive Disorder (MDD) is a mood disorder that is characterized by prolonged (longer than a few weeks) feelings of sadness, loss of interest in daily activities and lack of appetite.

We categorize MDD as abnormal behavior – behavior that is deviant and maladaptive, causes feelings of distress to an individual

The biological etiology provides physiological reasoning behind MDD, genetic arguments which are supported by concordance rate – the % of probability that 2 people with the same genes will develop the same disease

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2
Q

Intro (Explanation of Falconer Model & Serotonin Hypothesis)

A
  • Estimate of the relative contribution of genetic factors vs. environmental factors
  • Genetic heritability determined by
    1. Genetics
    2. Shared environment
    3. Individual environment
  • Researchers believe that genetic vulnerability can make you innately predisposed to experiencing depression through family
  • Researchers also rely on physiological changes in neurobiology – serotonin hypothesis – hypothesizes that low activity of serotonin pathways plays a causal role in the pathophysiology of depression
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3
Q

Thesis (Biological Etiologies)

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The biological etiology of genetic heritability and role of neurotransmitters in the likelihood of developing depression supports and provides an explanation for the origins of depression.

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4
Q

Claim 1 (Genetics)

A

→ Genetic researchers formulate genetic arguments through observing twin studies – hypothesized that since twins share the same genetic link, the ESTIMATED GENETIC HERITABILITY (differences in genes account for difference in traits) can be calculated through the Falconer Model

→ Assumes one’s phenotype (observed characteristics such as the presence of symptoms of MDD) is comprised off GENETICS, SHARED ENVIRONMENT, INDIVIDUAL ENVIRONMENT (I=A+C+E)

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5
Q

Kendler et al Aim

A

Studied 40,000 twins from the Swedish Twin Registry to investigate heritability of depression and genetic and env. factors that change over time

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6
Q

Kendler et al Methods

A
  1. Interviewers used telephone
  2. Assessed Major Lifetime Depression according to the DSM-5 Criteria, around 8000 “diagnosed”
  3. Asked “shared environment” → when they lived tgt and “indiv-specific environment” → any big life events that may have caused their depression
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7
Q

Kendler et al Findings

A

Concordance rate – or correlation of MDD in MONOZYGOTIC twins higher than DIZYGOTIC

Higher for women than men

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8
Q

Kendler et al Link to Genetics

A

This study supports the Falconer Model as it reinforces the correlation between the stronger the genetic link the more susceptibility of developing MDD – identical vs. fraternal

The gene might not be EXPRESSED by one twin – that environment stressors plays a big factor in determining the differences in stress experienced by each twin

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9
Q

Kendler et al Strengths

A

Aligns with previous twin studies research + large sample size, many genetic variations included in study

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10
Q

Kendler et al Weaknesses

A

Correlational study so no cause + effect, diagnoses is afflicted by response bias, Twin studies have the problem of population validity – twin samples do not necessarily represent the general population.

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11
Q

Neurotransmitters and hormones (Claim 2)

A

Neurological phenomenon = neurotransmitters and hormones.

Neurotransmitters released from the Axon Terminal, they transmit electric to chemical charges between neurons in the synaptic cleft

Neuroreceptors OVERSENSITIVE/INSENSITIVE causing too much/too little production

Serotonin Hypothesis: a deficit in serotonin could be the origin of depression. Serotonin plays several roles in your body, including influencing learning, memory, happiness as well as regulating body temperature, sleep, sexual behavior and hunger.

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12
Q

Caspi et al - role of gene mutation and epegenetics aim

A

Study gene-environment interaction in mutation and formation of MDD

Explores diathesis-stress theory of depression states that depression risk lies on a persons vulnerability, altered by their genetic predisposition (release of neurotransmitters in response to stressful situations)

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13
Q

Caspi et al Method

A
  • 847 NZ adults who were assessed for mental health every single year
  • Divided into 3 groups based on their 5-HTT alleles (Group 1: 2 short, Group 2: 1 short, 1 long, Group 3: 2 long) 5-HTT gene has shorter alleles
  • Fill in “Stressful life events” questionnaire about stressors and assessed for depression
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14
Q

Caspi et al Findings

A
  • Version w short allele exhibited depressive and suicidal behavior
  • Strongest effect for those who experienced stressful life events
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15
Q

Caspi et al Link to Neurotransmitters and Hormones

A

Just having the gene mutation is not enough → may increase your susceptibility to depression but it’s the stressful life events that increase likelihood of developing depression.

The length of allele can increase susceptibility to depression eg. there is a reduced availability of serotonin transporter in the synaptic cleft.

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16
Q

Caspi et al Strengths

A

Holistic approach that considers environmental factors good deal of method triangulation (using questionnaires to gather a group for a case study).

Data supports biological evidence - Serotonin (5-HT) neurotransmission has a key role in stress sensitivity and in vulnerability to negative affect.

17
Q

Caspi et al Weaknesses

A

Correlational study so no cause + effect, no evidence that serotonin causes depression, self-reported data

18
Q

Limitations of biological etiology

A
  1. All studies are correlational (no cause and effect of genes and heritability of depression)
  2. Limited research on whether serotonin is the CAUSE of depression
  3. Cultural differences (explanation for somatic symptoms?) Cognitive factors - thought patterns?
19
Q

Cog counter-claim: Nolen-Hoeksema’s Theory of Rumination

A

The cognitive approach argues for patterns of thinking that are responsible for our mental disorders.

→ Gender diff in depression cause of coping styles

→ Men = distraction, women = ruminate feeling, why? What is the meaning for this distress?

→ Neg thinking leads to depressive symptoms (low self-esteem, hopelessness)

20
Q

N-H Aim

A

Role of rumination on depressive symptoms

21
Q

N-H Method

A
  1. 1132 participants in San Fran
  2. Interviewed 2x 1 year with a 90-min clinical interview
  3. Tests – Beck Anxiety and Beck Depression (automatic negative thinking)
  4. Rumination and coping questionnaire (How much are you thinking about your negative feelings?)
22
Q

N-H Findings

A

Potential MDD indivs had higher score of rumination.

Improvement of depression indivs had lowered rumination compared to chronically depressed

23
Q

N-H Strengths

A

Supports N-H Theory, multimethod research - used both questionnaire + interview

24
Q

N-H Weaknesses

A

Correlational, self report – response biases, those with the strongest symptoms dropped out (introducing bias)

25
Q

N-H Link

A

Rumination leads to an increase in exhibited depressive symptoms – persistently thinking negatively about your feelings

26
Q

Bio etiologies conclusion

A

Genetic arguments is one explanation for the origins of depression

  • Rumination leads to an increase in exhibited depressive symptoms – persistently thinking negatively about your feelings – can be explained biologically as environmental factors may have altered how you talk about yourself
  • Different stress responses half genetic half environmental (not having available resources to deal w the situation)
  • Low research if serotonin CAUSES depression
  • Genetic markers are difficult to study (cannot be seen)
  • Biological explanations cannot explain the range of symptoms associated with depression (e.g. lower back pain in Chinese patients). There may be cultural and cognitive factors as well.