L02 - Research Methods in Psychopathology Flashcards
What are the three different types of longitudinal studies?
retrospective
follow-up
high risk
What are retrospective studies?
collect a sample of people with a disorder
try to determine what preceded it
self-report
existing archival data
What are follow-up studies?
follow people with the disorder over time
see what happens to them
already-ill sample
difficult to derive etiological explanations
What are high risk studies?
variant of follow-up
identify people who are likely to develop a disorder
- offspring of people with a disorder (genetic)
- on the basis of a biological abnormality
- behavioural variable
follow them over time
What are the cons of high risk studies?
genetic: need to find people who have the disorder and also have children
biological: associations not well-proven
behaviours: may be a risk factor, or may be early manifestation of the disease
What is a vulnerability marker?
should be trait-like, not state-related
has to be correlated with the disorder, but has to persist beyond the end of the episode
- could be a scar
has to be present in a high-risk population
pre-dat disorder
What is the sample issue “case control v. cohort”?
case control: compare one group of people with disorder to a second group without the disorder
cohort: a single large sample of people, some of whom have the disorder
What is the sample issue “patients vs. community”?
patient populations not representative of people with the disorder in the community
clinical populations tend to be more severe, have more comorbidities, more likely to be female, chronic
general population, get a sense of disorder “in the wild”
very expensive
What is the sampling issue with controls?
healthy controls (HC) or Psychiatric controls (PC)?
match on potential confounds?
how do you match on lab tasks?
How do family studies work?
genetic epidemiology
first step:
- identify proband
- assess family members
– interview (Family Study)
– informant report (Family History Study)
many disorders do run in families
subthreshold/symptoms
coaggregation
suggest genetic role, does not prove it
How do adoption studies work?
genetic epidemiology
parent as proband
adoptee as proband
cross-fostering design
- adoption rare event
- selective placement
How do Twin Studies work?
genetic epidemiology
monozygotic (Mz)
dizygotic (Dz)
A = additive genetic component
C = common environment component
E = unique environment
A = 2(rMz - rDz)
Mz concordance = 50%
Dz concordance = 25%
Difference (D) = 25%
2D = 50%
sample specific
higher with less environmental variance
What are the problems with twin studies?
Mz twins often share placenta
Mz twins treated more similarly to one another
Heritability = estimated genetic contirbutions to observed phenotype
not deterministic
often don’t model G x E
What are gene-environment correlations (rGE)?
Passive
- can be addressed in adoption studies
active (niche-picking)
evocative (reactive)
- active and evocative hard to measure - need better understnading of how environment shapes traits
Currently, all rGE attributed to G
caution when interpreting genetic contributions
What is the paradox of intelligence?
IQ highly heritable: 80% (approx.)
IQ also malleable
- Flynn effect:
– developing countries
Higher IQ = seek out “more stimulating” environment
- more stimulating environments available with more development
Heritability varies as a function of what?
heritabiltiy varies as a function of environment
- heritability of IQ increases across development
- among affluent families, heritability of IQ estimated at 0.72
– among less affluent families, little observed additive genetic influence (heritability of 0.10)
- heritability of **alcohol use ** for those residing in a neighbourhood with ten or more alcohol outlets was 74% compared with 16% for those in a neighbourhood with zero outlets
- eating disorder symptoms show minimal heritability before puberty but significant genetic effects (i.e., greater than 50%) during and after puberty
What are quantitative genetics?
mode of transmission
single-gene transmission
polygenic transmission
mixed transmission
What are the problems with single-gene transmission?
single dominant gene, woud expect 50% of relatives to have disorder
no psychiatric disorders show these rates of familial transmission
possible single-gene transmission
- expressed differently in different relatives
no strong evidence
Mendelian disorders very rare
- prevalence about 1 in 10,000
most psychiatric disorders hae prevalence rates at least .5%
monogenic disorders - distinct from “normal”
- e.g., Parkinson’s
psychiatric disorders dimensional, continuously distributed
What is polygenic transmission?
psychological phenotypes likely controlled by more than 1 gene
- skin colour - at least 3 genes
- can be modified by GxG interactions
- GxE interactions
action of multiple genes
- additive or interactive effects
What are some missing heritabilities?
Big Five personality traits have heritability estimates of 0.40 to 0.60
autism spectrum disorder currently estimated at 0.38
schizophrenia at 0.64
estimates so high, explanations provided in quantitative genetics explains very little
where do we get the remaining genetion variation?
What are gene environment interactions?
notion that adverse effects of genes on mental health only expressed under certain environmental conditions
What are epigenetics?
regulation and expression of genes
DNA
action of genes can be regulated
some genes “turn on” at certain developmental periods
under certain environmental circumstances
alterations heritable
What did Michael Meaney study on rats contribute to epigenetics?
good rat mothering associated with better functioning of neuroendocrine stress response
bad rat mothering = high levels of stress and cortisol
cross-fostering
changes in glucorticoid receptor gene
only evident when switch occurred early
What are genotypes-endophenotypes-phenotypes?
genotype –> phenotype
phenotypes very complex phenomena, multiply-determined, often poorly defined
endophenotype: intermediate step between microscopic genes and nerve cells and the experiential and psychological phenotype
- must segregate with illness in the population
- must be heritable
- must not be state-dependent (i.e., manifests whether illness is active or in remission)
- must co-segregate with illness within families
- must be present at a higher rate within affected families than in the population
- must be amenable to reliable measurement, and be specific to the illness of interest
