Lecture 2/3 Flashcards
methods in psychopathology research
controlled experimental study
quasi-experimental studies
correlational/cross sectional studies
quasi-experimental studies
not randomly assigned by match the experimental group of control
quasi-experimental studies
nto randomly assigned byt match experimental group to control group on as much points as possible
corelational/ cross-sectional study
cant make firm causal explanations
longitudinal designs aim to understand
causailty by trying to establish temporal precedence
types of longitudinal studies
retrospective, follow-up studies, high-risk studies
retrospective studies
collect sample of people with disorder, try to determine what preceded it
what do retrospective studies rely on
self report
why is it problematic to rely on self report
people dont perfectly remember events and mood can influence recall
what does retrospective use in order to avoid problems with self-resports
existing archival data
what are retrospective studies evidence for
current states result in memory biases
what are challenges of retrospective
lack of control over data you get
not everyone has the same records
follow up
follow peopel with the disorder overtime and see what happens
whats something that needs to be present in order for it to be follow-up
already ill sample
what are challenges of follow up
difficult to derive etiological explanations
what are follow up designed for
to understand the course/natural course of the diagnosis
high risk studies
variant of follow-up
identify likley people to develop a disorder
what does high risk study look for and what is it in the basis of
offspring of people with disorder and biological abnormality
what are challenges of high risk studies
if recreuiting offspring may not recruit a representative sample
cons of high risk
genetic: need to find people who have the disorder and also children
biological: associations not well-proven
behavioural: may be a risk factor; early manifestation of the disease
vulnerability markers
something that tells you the person is vulnerable to the disorder
what should vulnerability markers be
traitlike not state-related : should be something that is a characteristic of that person and evident before theyre ill
wha do vulnerability markers have to be
corelated with the disorder, but has to persist beyond the end of the episode
what else has to be done in order for it to be a vulnerability marker
present in a high-risk population and pre-date the disorder
case control
compare one group of people with disorder to a second group of people without the disorder: most helpful if the disorder you’re looking at is fairly rare
cohort
a single large sample of people some of whom have the disorder of interest to multiple control groups
what tends to be common but most useful is the disorder is rare
case control
what is preferable when it is not rare
cohort
patient populations
not representative of people with the disorder int he community. not all disorders people seek treatment
clinical populations
tend to be more severe, have more comorbidities, more likely to be female, and chronic
general population
get a sense of disorder in the wild; what does it look like on average but tends to be closer to the diagnostic threshold: MISDIAGNOSIS MORE LIKELY
if you study people from other ppulations outside of the ones youre studying
allows you to make more specific inferences
match controls on potential confounds
If you are screening people who are healthy controls , you want them to have never had a diagnosis of psychopathology (super healthy controls).You want to typically match your controls on basic demographic variables
why does the above present a danger
systematically mismatching on other variables. It may be impossible to consistently match on every demographic variable of interest .
what is a proband
someone in the family who has been diagnosed with the disorder theyre looking at
what is the function of a family study
look at the relatives of the proband to answer the question if you don’t see higher rates of the disorder in relatives of the proband than you see in the general populations and can conclude its not genetic
interview
family study
infromant report
family history study
if you do see higher rates in the family
does not mean its genetic, need to keep investigating bc its possible has to do with environment
subthreshold and symptoms
run in families ; maybe the disorder itself doesn’t but some underlying liability
what are the challenges to these studies
coaggregation of different illnesses ; if schiz runs in the family they will have higher chance of it and other disorders as well
family studies suggest___ but ___
genetic role but do not prove it
adoption studies 1
biological parent as proband : if they have the disorder and so does the child that they gave up for adoption can infer some genetic cause
adoption studies 2
adoptee as proband: track down their adoptive and biological parent sna d see which one they resemble more
adoption studies 3
cross-fostering designs: where children of control parents might be raised in homes where adoptive parent has a diagnosis of chiz/ and or child of parents has and are raised in homes of control parents
what are the difficulties with adoption studies
adoptions are rare
selective placement
selective placement
most adoptive parents are high SES and are without disorder at time of adoption
A
Additive genetic component; tells us how much more similar are the mono twins than dyz ; refers to the additive effect
what does A represent
the su of all genes that contribute to liability risk
c
common environment component; how much are the twins alike; any environmental factors that make twins similar for the liability/ risk fo the disorder
E
Unique environment; to what extent do you see discrepancies
why is E difficult
because most twins share an environment with another
how do you calculate A
2(rMz- rDz)
MZ concordance
50%
Dz concordance
25%
difference (D)
25%
2D
50%
sample specific
is not absolutely heritability; h estimates differ depending on environment
higher with less environmental variance
IQ is very heritable but less so in lower SES homes where there is more environmental variance
problems with twin studies
Mz often share placenta
Mz twins treated similarily to one another
heritability= estimated genetic contributions to observed phenotype
often do not model GxE
what are the different types of Gene-environment correlations
passive, active, evocative
passive
can be addressed in adoption studies and is not dependent on what the child does
active
niche picking; we behave in ways based on our genetic makeup; often gets stronger as you age
people are major determinants in the type of
environment they are exposed to
evocative
refers to people in their environment will often treat people differently as a function of their underlying genotypes; ways our geentic makeup reacts with others
what is difficult to measure
active and evocative
currently what is attributed to G
all of rGE because the ways in which mz twins are similar then dz is because of their genetic similarity
paradox of intelligence
IQ is highly heritable 80%
but is also malleable
higher IQ= seek out mroe stimulating environments
hertiability varies as a
function of environment
among affluent families
heritibaility approx 0.72
among less afluent families
heritability approc 0.1
what are the different odes of transmission
single gene, polygenic, and mixed
single gene transmission
can be dominant or recessive
what are the problems with single gene transmissions
single dom gene would expect to have 50% of family with disorder but none prove that to be true;
mendelian disorders are very rare but most psychiatric disorders have prevalence of 0.5%
most monogenic disorders have a very clear distinction from what we consider normal but with psychiatric disorders tend to be dimensional and continuously distributed
polygenic transmission
many genes none of which have a large effect but when they come together they form a phenotype; can be modified by GxG interactions ; action of multiple genes additive or interactive effects
mixed transmission
may be largely due to one gene but other genes are associated
missing heritabilities
Big five personality traits have heritabilkity estimates of 0.4 to 0.6
Autism spectrum disorder currently estimated at 0.38%
Schizophrenia at 0.64
explanations for missing heritability
gene-environment interactions, epigenetics, other
gene-environment interactions
notion that adverse effects of genes on mental health only expressed under certain conditions
study by caspi et al
influence of life stress on depression; moderation by a polymorphism in the 5-HTT gene
short allele and long allele three groups
ss
sl
ll
what were the results of caspi et al study
those with two long alleles (ll) even those subject to severe child abuse did not show an increase in depression. they were more at risk than those who never experienced child abuse
SS, when experiencing abuse, much more likely to develop
epigenetics
regulation and expression fo genes
expression of genes is not fixed! DNA is fixed
action of genes can be regulated
some genes can turn on at certain developmental periods or under certain environmental circumstances
alterations heritable
michael meany
Good rat mothering associated with better functioning of neuroendocrine stress response
Bad rate mothering = high levels of stress and cortisol
Changes in glucocorticoid receptor gene
Only evident when switch occurred early
rat cross-fostering
swap babies of good rat moms ☹ and give them to bad rat moms ( even more ☹ ) and vice versa. What you see is that baby with bio good rat moms who end up with bad rat moms show high levels of cortisol in response to high stress situations . This shows that mothering style matters and can in fact have an influence on gene expression. Shows both environmental effect and epigenetic effect
there is a problem with how we measure
phenotype
since phenotypes we are measuring are so broad and inaccurate
might want to look at something in between like endophenotype
endophenotype
intermediate step metween microscopic genes and nerve cells and experiential and psychological phenotype
what must happen if we can determine something a endophenotype
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.
phenotypes
multiply determined; often poorly defined - don’t have great boundaries
