Lecture 4 + 5 Flashcards
Source of variants in behaviours
Genes - heritability; H2
Shared environment; c2
Non-shared environment; e2
How to study heritability?
Family Studies: similarities due to genetics AND shared environment
Adoption studies: similarities due to shared environment
Twin studies: contribution of genes vs. environment
Molecular studies: genes
Which is higher in heritability; bipolar or unipolar depression?
Bipolar disorder is much more heritable
Heritability of phobias
Seems to be that phobias are heritable, but this can be due to observing our parent fear something and we too end up fearing it from learned behaviour (shared environment)
What are heritable traits?
Factors influence the individual’s risk for placing themselves in or creating potentially hazardous situations
- Neuroticism
- Sensation seeking
- Impulsivity
Difference between genotype and phenotype
Genotype: genetic makeup (the actual alleles)
Phenotype: the expression of the genes (alleles)
Difference between: Genome-Wide association study and Candidate Gene Studies
Genome-Wide: results - no gene has consistently been associated with any psychopathology - don’t replicate well
Candidate approach: examine specific genes/polymorphisms in relation to environment
Genetic variation
arises from mutations or polymorphism
- in mental health mostly look at polymorphisms (ex: serotonin transporter gene 5-HTTLPR)
5-HTTLPR polymorphism
Related to neuroticism
s/s, s/l, l/l
neuroticism seen more in people with the s allele
Impact of Environment on Mental Health
Early adversity is:
bad for health, relatively common, cumulative damage, consequences long-lasting, reduces life-expectancy
Childhood Adversity and Brain Function/Structure
child adversity linked to brain changes at the level of structure and function
- these changes associated with difficulties in social behaviour and emotional regulation
Why is it difficult to measure the changes in brain function/structure due to early adversity
Have to have measurements BEFORE the events
What supports the sensitve period hypothesis; and what is it?
- People are more sensitve to early life stress at specific ages
- Ex: loss of parent before age 9 more predictive of depression than loss of parent after age 13
- Ex: Sexual abuse was linked to reduced hippocampus only when it occured b/w 3-13 y.o and frontal cortex when aged 11-13.
Is depression due to adversity inevitable?
NO
Protective factors help and many are resilient
What is the cumulative stress hypothesis and the mismatch stress hypothesis
Cumulative:
- more early life stress = disease AND more adult stress = disease
Mismatch:
- lots of early life stress can prepare coping mechanisms to deal with adult stress; therefore less affected
What are the disadvantages of human studies on early life stress?
Often based on memory and therefore can be biased or flawed (retrospective study)
Advantages and disadvantages of animal models for early life stress?
Advantages:
- can control for environment
- can control for genes
Disadvantages:
- not necessarily applicable to humans
Longitudinal design
Prospective study - therefore not relying on memory
Gene environment interactions
- Passive: parents provide both genes and environment for child (ex: parents like reading; the house has lots of books)
- Active: your genes allow you to actively choose an environment (ex: an introvert will choose more introverted friends)
- Evocative: your genetic makeup allows people to react a certain way to you (ex: a hyper/temperamental child will evoke frustration from teachers)
The stress-diathesis model
- Influence of genotype is greater in the context of stressors (someone with risky genotype will develop disorder only when stress accumulates)
- Hypothesis: effects of adversity on developmental outcome depends on the genotype (and vice versa)
Main idea from the Capsi paper on the 5-HTTL polymorphism
Short allele of 5-HTTLPR is the risky allele
serotonin transporter gene
Differential susceptibility hypothesis
Same individuals who are affected by the negative environment, flourish in more positive environment
HPA Axis
- Linked to production of cortisol
- Releasing cortisol in response to stress
- However, when you’re under repeated stress – this can get deregulated
- Negative feedback loop to make sure there is less cortisol – under continuous stress the system cannot handle it; therefore negative feedback loop disturbed = continuously either HIGH cortisol levels or LOW cortisol levels (an effect brain, hormones, neurotransmitters…)
Animal studies on the HPA axis
- separation from mother = stress = HPA axis deregulated
- if reunited = normal
- SSRIs reverts the HPA response
What is epigenetics?
How the environment can change the expression of our genes but not the genes themselves
Evidence of epigenetics?
- twin studies
- identical twins already different at birth (therefore prenatal environment affected)
- as MZ twins get older, they become more and more different (as their separate environment have more chances to affect them)
DNA methylation (epigenetic changes) and depressive symptoms
- Depressive symptoms linked to methylation in genes regulating HPA axis and serotonin system
- Maternal depressed mood associated with altered methylation in stress-related genes in the placenta
