Lecture 4 + 5

Question 1

Source of variants in behaviours

Answer 1

Genes - heritability; H2
Shared environment; c2
Non-shared environment; e2

Question 2

How to study heritability?

Answer 2

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

Question 3

Which is higher in heritability; bipolar or unipolar depression?

Answer 3

Bipolar disorder is much more heritable

Question 4

Heritability of phobias

Answer 4

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)

Question 5

What are heritable traits?

Answer 5

Factors influence the individual’s risk for placing themselves in or creating potentially hazardous situations

• Neuroticism
• Sensation seeking
• Impulsivity

Question 6

Difference between genotype and phenotype

Answer 6

Genotype: genetic makeup (the actual alleles)
Phenotype: the expression of the genes (alleles)

Question 7

Difference between: Genome-Wide association study and Candidate Gene Studies

Answer 7

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

Question 8

Genetic variation

Answer 8

arises from mutations or polymorphism

- in mental health mostly look at polymorphisms (ex: serotonin transporter gene 5-HTTLPR)

Question 9

5-HTTLPR polymorphism

Answer 9

Related to neuroticism
s/s, s/l, l/l
neuroticism seen more in people with the s allele

Question 10

Impact of Environment on Mental Health

Answer 10

Early adversity is:

bad for health, relatively common, cumulative damage, consequences long-lasting, reduces life-expectancy

Question 11

Childhood Adversity and Brain Function/Structure

Answer 11

child adversity linked to brain changes at the level of structure and function
- these changes associated with difficulties in social behaviour and emotional regulation

Question 12

Why is it difficult to measure the changes in brain function/structure due to early adversity

Answer 12

Have to have measurements BEFORE the events

Question 13

What supports the sensitve period hypothesis; and what is it?

Answer 13

• 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.

Question 14

Is depression due to adversity inevitable?

Answer 14

NO

Protective factors help and many are resilient

Question 15

What is the cumulative stress hypothesis and the mismatch stress hypothesis

Answer 15

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

Question 16

What are the disadvantages of human studies on early life stress?

Answer 16

Often based on memory and therefore can be biased or flawed (retrospective study)

Question 17

Advantages and disadvantages of animal models for early life stress?

Answer 17

Advantages:

• can control for environment
• can control for genes

Disadvantages:
- not necessarily applicable to humans

Question 18

Longitudinal design

Answer 18

Prospective study - therefore not relying on memory

Question 19

Gene environment interactions

Answer 19

• 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)

Question 20

The stress-diathesis model

Answer 20

• 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)

Question 21

Main idea from the Capsi paper on the 5-HTTL polymorphism

Answer 21

Short allele of 5-HTTLPR is the risky allele

serotonin transporter gene

Question 22

Differential susceptibility hypothesis

Answer 22

Same individuals who are affected by the negative environment, flourish in more positive environment

Question 23

HPA Axis

Answer 23

• 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…)

Question 24

Animal studies on the HPA axis

Answer 24

• separation from mother = stress = HPA axis deregulated
• if reunited = normal
• SSRIs reverts the HPA response

Question 25

What is epigenetics?

Answer 25

How the environment can change the expression of our genes but not the genes themselves

Question 26

Evidence of epigenetics?

Answer 26

• 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)

Question 27

DNA methylation (epigenetic changes) and depressive symptoms

Answer 27

• 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