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PSYC 337 > Lecture 2/3 > Flashcards

Lecture 2/3 Flashcards

1
Q

methods in psychopathology research

A

controlled experimental study
quasi-experimental studies
correlational/cross sectional studies

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2
Q

quasi-experimental studies

A

not randomly assigned by match the experimental group of control

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3
Q

quasi-experimental studies

A

nto randomly assigned byt match experimental group to control group on as much points as possible

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4
Q

corelational/ cross-sectional study

A

cant make firm causal explanations

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5
Q

longitudinal designs aim to understand

A

causailty by trying to establish temporal precedence

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6
Q

types of longitudinal studies

A

retrospective, follow-up studies, high-risk studies

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7
Q

retrospective studies

A

collect sample of people with disorder, try to determine what preceded it

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8
Q

what do retrospective studies rely on

A

self report

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9
Q

why is it problematic to rely on self report

A

people dont perfectly remember events and mood can influence recall

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10
Q

what does retrospective use in order to avoid problems with self-resports

A

existing archival data

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11
Q

what are retrospective studies evidence for

A

current states result in memory biases

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12
Q

what are challenges of retrospective

A

lack of control over data you get
not everyone has the same records

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13
Q

follow up

A

follow peopel with the disorder overtime and see what happens

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14
Q

whats something that needs to be present in order for it to be follow-up

A

already ill sample

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15
Q

what are challenges of follow up

A

difficult to derive etiological explanations

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16
Q

what are follow up designed for

A

to understand the course/natural course of the diagnosis

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17
Q

high risk studies

A

variant of follow-up
identify likley people to develop a disorder

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18
Q

what does high risk study look for and what is it in the basis of

A

offspring of people with disorder and biological abnormality

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19
Q

what are challenges of high risk studies

A

if recreuiting offspring may not recruit a representative sample

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20
Q

cons of high risk

A

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

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21
Q

vulnerability markers

A

something that tells you the person is vulnerable to the disorder

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22
Q

what should vulnerability markers be

A

traitlike not state-related : should be something that is a characteristic of that person and evident before theyre ill

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23
Q

wha do vulnerability markers have to be

A

corelated with the disorder, but has to persist beyond the end of the episode

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24
Q

what else has to be done in order for it to be a vulnerability marker

A

present in a high-risk population and pre-date the disorder

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25
Q

case control

A

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

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26
Q

cohort

A

a single large sample of people some of whom have the disorder of interest to multiple control groups

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27
Q

what tends to be common but most useful is the disorder is rare

A

case control

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28
Q

what is preferable when it is not rare

A

cohort

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29
Q

patient populations

A

not representative of people with the disorder int he community. not all disorders people seek treatment

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30
Q

clinical populations

A

tend to be more severe, have more comorbidities, more likely to be female, and chronic

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31
Q

general population

A

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

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32
Q

if you study people from other ppulations outside of the ones youre studying

A

allows you to make more specific inferences

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33
Q

match controls on potential confounds

A

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

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34
Q

why does the above present a danger

A

systematically mismatching on other variables. It may be impossible to consistently match on every demographic variable of interest .

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35
Q

what is a proband

A

someone in the family who has been diagnosed with the disorder theyre looking at

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36
Q

what is the function of a family study

A

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

37
Q

interview

A

family study

38
Q

infromant report

A

family history study

39
Q

if you do see higher rates in the family

A

does not mean its genetic, need to keep investigating bc its possible has to do with environment

40
Q

subthreshold and symptoms

A

run in families ; maybe the disorder itself doesn’t but some underlying liability

41
Q

what are the challenges to these studies

A

coaggregation of different illnesses ; if schiz runs in the family they will have higher chance of it and other disorders as well

42
Q

family studies suggest___ but ___

A

genetic role but do not prove it

43
Q

adoption studies 1

A

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

44
Q

adoption studies 2

A

adoptee as proband: track down their adoptive and biological parent sna d see which one they resemble more

45
Q

adoption studies 3

A

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

46
Q

what are the difficulties with adoption studies

A

adoptions are rare
selective placement

47
Q

selective placement

A

most adoptive parents are high SES and are without disorder at time of adoption

48
Q

A

A

Additive genetic component; tells us how much more similar are the mono twins than dyz ; refers to the additive effect

49
Q

what does A represent

A

the su of all genes that contribute to liability risk

50
Q

c

A

common environment component; how much are the twins alike; any environmental factors that make twins similar for the liability/ risk fo the disorder

51
Q

E

A

Unique environment; to what extent do you see discrepancies

52
Q

why is E difficult

A

because most twins share an environment with another

53
Q

how do you calculate A

A

2(rMz- rDz)

54
Q

MZ concordance

A

50%

55
Q

Dz concordance

A

25%

56
Q

difference (D)

A

25%

57
Q

2D

A

50%

58
Q

sample specific

A

is not absolutely heritability; h estimates differ depending on environment

59
Q

higher with less environmental variance

A

IQ is very heritable but less so in lower SES homes where there is more environmental variance

60
Q

problems with twin studies

A

Mz often share placenta
Mz twins treated similarily to one another
heritability= estimated genetic contributions to observed phenotype
often do not model GxE

61
Q

what are the different types of Gene-environment correlations

A

passive, active, evocative

62
Q

passive

A

can be addressed in adoption studies and is not dependent on what the child does

63
Q

active

A

niche picking; we behave in ways based on our genetic makeup; often gets stronger as you age

64
Q

people are major determinants in the type of

A

environment they are exposed to

65
Q

evocative

A

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

66
Q

what is difficult to measure

A

active and evocative

67
Q

currently what is attributed to G

A

all of rGE because the ways in which mz twins are similar then dz is because of their genetic similarity

68
Q

paradox of intelligence

A

IQ is highly heritable 80%
but is also malleable
higher IQ= seek out mroe stimulating environments

69
Q

hertiability varies as a

A

function of environment

70
Q

among affluent families

A

heritibaility approx 0.72

71
Q

among less afluent families

A

heritability approc 0.1

72
Q

what are the different odes of transmission

A

single gene, polygenic, and mixed

73
Q

single gene transmission

A

can be dominant or recessive

74
Q

what are the problems with single gene transmissions

A

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

75
Q

polygenic transmission

A

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

76
Q

mixed transmission

A

may be largely due to one gene but other genes are associated

77
Q

missing heritabilities

A

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

78
Q

explanations for missing heritability

A

gene-environment interactions, epigenetics, other

79
Q

gene-environment interactions

A

notion that adverse effects of genes on mental health only expressed under certain conditions

80
Q

study by caspi et al

A

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

81
Q

what were the results of caspi et al study

A

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

82
Q

epigenetics

A

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

83
Q

michael meany

A

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

84
Q

rat cross-fostering

A

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

85
Q

there is a problem with how we measure

A

phenotype

86
Q

since phenotypes we are measuring are so broad and inaccurate

A

might want to look at something in between like endophenotype

87
Q

endophenotype

A

intermediate step metween microscopic genes and nerve cells and experiential and psychological phenotype

88
Q

what must happen if we can determine something a endophenotype

A

 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.

89
Q

phenotypes

A

multiply determined; often poorly defined - don’t have great boundaries

PSYC 337 (11 decks)

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