Discuss / Evaluate one or more biological etiologies of one disorder (Kendler & Caspi) Flashcards
Define MDD
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
Intro (Explanation of Falconer Model & Serotonin Hypothesis)
- 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
Thesis (Biological Etiologies)
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.
Claim 1 (Genetics)
→ 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)
Kendler et al Aim
Studied 40,000 twins from the Swedish Twin Registry to investigate heritability of depression and genetic and env. factors that change over time
Kendler et al Methods
- Interviewers used telephone
- Assessed Major Lifetime Depression according to the DSM-5 Criteria, around 8000 “diagnosed”
- Asked “shared environment” → when they lived tgt and “indiv-specific environment” → any big life events that may have caused their depression
Kendler et al Findings
Concordance rate – or correlation of MDD in MONOZYGOTIC twins higher than DIZYGOTIC
Higher for women than men
Kendler et al Link to Genetics
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
Kendler et al Strengths
Aligns with previous twin studies research + large sample size, many genetic variations included in study
Kendler et al Weaknesses
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.
Neurotransmitters and hormones (Claim 2)
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.
Caspi et al - role of gene mutation and epegenetics aim
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)
Caspi et al Method
- 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
Caspi et al Findings
- Version w short allele exhibited depressive and suicidal behavior
- Strongest effect for those who experienced stressful life events
Caspi et al Link to Neurotransmitters and Hormones
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.